John murtagh's general practice [6, 6 ed.] 9781743760031

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Murtagh's General Practice

NOTICE Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The editors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the editors, nor the publisher, nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete. Readers are encouraged to confirm the information contained herein with other sources. For example, and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this book is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. This sixth edition published 2015 First edition published 1994, second edition published 1998, third edition published 2003, fourth edition published 2007, fifth edition published 2011 Text © 2015 John Murtagh Illustrations and design © 2015 McGraw-Hill Australia Pty Ltd Additional owners of copyright are acknowledged in on-page credits/on the acknowledgments page. Every effort has been made to trace and acknowledge copyrighted material. The authors and publishers tender their apologies should any infringement have occurred. Reproduction and communication for educational purposes The Australian Copyright Act 1968 (the Act) allows a maximum of one chapter or 10% of the pages of this work, whichever is the greater, to be reproduced and/or communicated by any educational institution for its educational purposes provided that the institution (or the body that administers it) has sent a Statutory Educational notice to Copyright Agency Limited (CAL) and been granted a licence. For details of statutory educational and other copyright licences contact: Copyright Agency Limited, Level 15, 233 Castlereagh Street, Sydney NSW 2000. Telephone: (02) 9394 7600. Website: www.copyright.com.au Reproduction and communication for other purposes Apart from any fair dealing for the purposes of study, research, criticism or review, as permitted under the Act, no part of this publication may be reproduced, distributed or transmitted in any form or by any means, or stored in a database or retrieval system, without the written permission of McGraw-Hill Australia including, but not limited to, any network or other electronic storage. Enquiries should be made to the publisher www.mheducation.com.au or marked for the attention of the Permissions editor at the address below. National Library of Australia Cataloguing-in-Publication Data: Creator: Murtagh, John, author. Title: John Murtagh’s general practice / John Murtagh, Jill Rosenblatt. Edition: 6th edition. ISBN: 9781743760031 (hardback) Notes: Includes index. Subjects: Family medicine. Physicians (General practice) Other Creators/Contributors: Rosenblatt, Jill, author. Dewey Number: 610 Published in Australia by McGraw-Hill Australia Pty Ltd Level 2, 82 Waterloo Road, North Ryde NSW 2113 Publisher: Jane Roy Cover design: Christa Moffitt, christabella designs Author photograph: Gerrit Fokkema Photography Internal design: David Rosemeyer Senior production editor: Yani Silvana Permissions editor: Haidi Bernhardt Copy editor: Ali Moore Illustrators: Alan Laver/Shelly Communications and John Murtagh Proofreader: Anne Savage Indexer: Graham Clayton Typeset in Chaparral Pro 10/11.5 by Laserwords Private Ltd, India Printed in China on 70 gsm matt art by 1010 Printing Int. Ltd 987654321

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The authors

Professor John Murtagh AM MBBS, MD, BSc, BEd, FRACGP, DipObstRCOG Emeritus Professor in General Practice, School of Primary Health, Monash University, Melbourne Professorial Fellow, Department of General Practice, University of Melbourne Adjunct Clinical Professor, Graduate School of Medicine, University of Notre Dame, Fremantle, Western Australia Guest Professor, Peking University Health Science Centre, Beijing

John Murtagh was a science master teaching chemistry, biology and physics in Victorian secondary schools when he was admitted to the first intake of the newly established Medical School at Monash University, graduating in 1966. Following a comprehensive postgraduate training program, which included surgical registrarship, he practised in partnership with his medical wife, Dr Jill Rosenblatt, for 10 years in the rural community of Neerim South, Victoria.

He was appointed Senior Lecturer (part-time) in the Department of Community Medicine at Monash University and eventually returned to Melbourne as a full-time Senior Lecturer. He was appointed to a professorial chair in Community Medicine at Box Hill Hospital in 1988 and subsequently as chairman of the extended department and Professor of General Practice in 1993 until retirement from this position in 2010. He now holds teaching positions as Emeritus Professor in General Practice at Monash University, Adjunct Clinical Professor, University of Notre Dame and Professorial Fellow, University of Melbourne. He combines these positions with part-time general practice, including a special interest in musculoskeletal medicine. He achieved the Doctor of Medicine degree in 1988 for his thesis ‘The management of back pain in general practice’. He was appointed Associate Medical Editor of Australian Family Physician in 1980 and Medical Editor in 1986, a position held until 1995. In 1995 he was awarded the Member of the Order of Australia for services to medicine, particularly in the areas of medical education, research and publishing. One of his numerous publications, Practice Tips, was named as the British Medical Association’s Best Primary Care Book Award in 2005. In the same year he was named as one of the most influential people in general practice by the publication Australian Doctor. John Murtagh was awarded the inaugural David de Kretser medal from Monash University for his exceptional contribution to the Faculty of Medicine, Nursing and Health Sciences over a significant period of time. Members of the Royal Australian College of General Practitioners may know that he was bestowed the honour of the namesake of the College library. Today John Murtagh continues to enjoy active participation with the diverse spectrum of general practitioners—whether they are students or experienced practitioners, rural- or urban-based, local or international medical graduates, clinicians or researchers. His vast experience with all of these groups has provided him with tremendous insights into their needs, which is reflected in the culminated experience and wisdom of John Murtagh’s General Practice.

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Murtagh's General Practice

The authors continued

Dr Jill Rosenblatt MBBS, FRACGP, DipObstRCOG, GradDipAppSci General Practitioner, Ashwood Medical Group Adjunct Senior Lecturer, School of Primary Health Care, Monash University, Melbourne

Jill Rosenblatt graduated in medicine from the University of Melbourne in 1968. Following terms as a resident medical officer she entered rural practice in Neerim South, Victoria, in partnership with her husband John Murtagh. She was responsible for inpatient hospital care in the Neerim District Bush

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Nursing Hospital and in the West Gippsland Base Hospital. Her special interests were obstetrics, paediatrics and anaesthetics. Jill Rosenblatt also has a special interest in Indigenous culture and health since she lived at Koonibba Mission in South Australia, where her father was Superintendent. After leaving rural life she came to Melbourne and joined the Ashwood Medical Group, where she continues to practice comprehensive general medicine and care of the elderly in particular. She was appointed Adjunct Senior Lecturer in the Department of General Practice at Monash University in 1980 and a teacher in the GP registrar program. She gained a Diploma of Sports Medicine (RACGP) in 1985 and a Graduate Diploma of Applied Science in Nutritional and Environmental Medicine from Swinburne University of Technology in 2001. Jill Rosenblatt brings a wealth of diverse experience to the compilation of this textbook. This is based on 45 years of experience in rural and metropolitan general practice. In addition she has served as clinical assistant to the Shepherd Foundation, the Menopause Clinics at Prince Henry’s Hospital and Box Hill Hospital and the Department of Anaesthetics at Prince Henry’s Hospital. Jill has served as an examiner for the RACGP for 39 years and for the Australian Medical Council for 16 years. She was awarded a life membership of the Royal Australian College of General Practitioners in 2010 and a Distinguished Service award of the College in 2014.

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Foreword In 1960 a young schoolmaster, then teaching biology and chemistry in a secondary school in rural Victoria, decided to become a country doctor. He was part of the first intake of students into the Medical School of the newly established Monash University, and at the end of his six-year undergraduate medical course and subsequent intern and resident appointments his resolve to practise community medicine remained firm. After more than a decade in country practice with his life partner, Dr Jill Rosenblatt, during which he meticulously documented the cases he treated, in 1977 John Murtagh took up an academic position in the new Department of General Practice at Monash University. He subsequently moved through the ranks of Senior Lecturer, Associate Professor and Professor, now enjoying the title of Emeritus Professor. Through his writing, pedagogy and research, John Murtagh became a national and international authority on the content and teaching of primary care medicine. It was during his tenure as Medical Editor of Australian Family Physician from 1986 to 1995 that the journal became the most widely read medical journal in Australia. This text book provides a distillate of the vast experience gained by a once rural doctor, whose career has embraced teaching; whose abiding interest is in ensuring that disease, whether minor or life-threatening, is recognised quickly; and whose concern is that strategies to match each contingency are well understood. The first edition of this book, published in 1994, achieved remarkable success on both the national and international scene. The second and third editions built on this initial success and the book has become known as the ‘bible of general practice’ in Australia. In addition to being widely used by practising doctors, it has become a popular and standard textbook in several medical schools and also in the teaching institutions for alternative health practitioners, such as chiropractic, naturopathy and osteopathy. In particular, medical undergraduates and graduates struggling to learn English have found the book relatively comprehensible. The fourth and fifth editions were updated and expanded, retaining the successful, user-friendly format including clinical photography and illustrations in colour. Dr Jill Rosenblatt joined John in authoring and editing the fifth and sixth editions. This edition, launched 20 years after the first edition, represents a further milestone in Emeritus Professor John Murtagh’s remarkable career. Having known

John and worked with him for almost three decades, I feel privileged to write this foreword to the sixth edition, adding to earlier forewords by the late Professor Schofield. During this 20-year period I have watched each edition blossom, only to be superseded by a bigger and better replacement. John Murtagh has become a legend nationally and internationally, and in a 2012 Medical Observer survey he was voted the most revered Australian doctor, ahead of Fred Hollows and Victor Chang. This edition retains the time-honoured framework that has made it the seminal text for GPs and students of general practice worldwide. It is to general practice what ‘Harrisons’ is to internal medicine. Although this edition retains the same format, it has a number of significant changes and additions. There is much more on chronic disease, in keeping with the increasing prevalence of chronic disease and the challenges it presents in treating an ageing community. Reflecting John’s lifelong commitment to medical education, he has included more visual material, more practical tips for day-to-day clinical practice and importantly, more on therapeutics supported by references to Therapeutic Guidelines. The expanded volume has necessitated a significant increase in references to original sources to substantiate the evidence base within this text. As expected in contemporary texts, there is also an abundance of online resources. John Murtagh’s works, including this text, have been translated into Italian by McGraw-Hill Libri Italia s.r.l., Portuguese by McGraw-Hill Nova Iorque and Spanish by McGraw-Hill Interamericana Mexico and also into Chinese, Greek, Polish and Russian. In 2009 John Murtagh’s General Practice was chosen by the Chinese Ministry of Health as the textbook to aid the development of general practice in China. Its translation was completed later that year. GC SCHOFIELD OBE, MD, ChB(NZ), DPhil(Oxon), FRACP, FRACMA, FAMA Emeritus Professor of Anatomy Dean of Medicine Monash University, 1977–88 Leon Piterman AM MBBS, MD, MMed, MEdSt, FRCP(Edin), FRACGP Professor of General Practice, Monash University

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Murtagh's General Practice

Contents The authors Foreword Acknowledgments Preface Making the most of your book

Part 1

The basis of general practice

Chapter 1 Chapter Chapter Chapter Chapter Chapter

2 3 4 5 6

Chapter 7 Chapter Chapter Chapter Chapter Chapter Chapter

8 9 10 11 12 13

Chapter 14 Chapter 15 Chapter 16 Chapter 17 Chapter 18

Part 2 Chapter 19 Chapter 20 Chapter 21 Chapter 22 Chapter 23 Chapter 24 Chapter 25 Chapter 26 Chapter 27 Chapter 28 Chapter 29 Chapter 30 Chapter 31

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v vii x xi xii

Chapter 32 Chapter 33

The nature, scope and content of general practice The family Consulting skills Communication skills Counselling skills Difficult, demanding and angry patients Health promotion and patient education The elderly patient Prevention in general practice Nutrition in health and illness Palliative care Pain and its management Research and evidence-based medicine Travel medicine Tropical medicine and the returned traveller Inspection as a clinical skill A safe diagnostic strategy Genetic conditions

Diagnostic perspective in general practice

1

Reviewers Laboratory reference values Normal values: worth knowing by heart Abbreviations

2 7

28 39 44 49 64 75 83 93 106 115 129 141 147 156

175

Depression Diabetes mellitus Drug and alcohol problems Anaemia Thyroid and other endocrine disorders Spinal dysfunction Urinary tract infection Malignant disease HIV/AIDS—could it be HIV? Baffling viral and protozoal infections Baffling bacterial infections Infections of the central nervous system Chronic kidney failure

176 185 202 219 227 239 242 251 259 270 277 290 296

Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter

303 313

Problem solving in general practice 331

Part 3

14 20

Connective tissue disease and the vasculitides Neurological dilemmas

xvi xix xxi xxii

34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70

Abdominal pain Arthritis Anorectal disorders Thoracic back pain Low back pain Bruising and bleeding Chest pain Constipation Cough Deafness and hearing loss Diarrhoea The disturbed patient Dizziness/vertigo Dyspepsia (indigestion) Dysphagia Dyspnoea The painful ear The red and tender eye Pain in the face Fever and chills Faints, fits and funny turns Haematemesis and melaena Headache Hoarseness Jaundice Nasal disorders Nausea and vomiting Neck lumps Neck pain Shoulder pain Pain in the arm and hand Hip, buttock and groin pain Pain in the leg The painful knee Pain in the foot and ankle Walking difficulty and leg swelling Palpitations

332 355 379 387 401 422 432 453 464 478 488 506 525 535 545 549 562 575 591 601 611 620 623 641 645 662 672 678 683 697 710 727 740 758 779 796 803

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Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter

71 72 73 74 75 76 77 78 79

Chapter 80 Chapter 81 Chapter 82 Chapter 83 84 85 86 87 88 89

Part 5 Chapter Chapter Chapter Chapter

817 827

Allergic disorders including hay fever Anxiety disorders Asthma Chronic obstructive pulmonary disease Epilepsy Cardiovascular disease Hypertension Dyslipidaemia Chronic heart failure Osteoporosis

847 854 863 875 888 897

906 914 923

Chapter 94 Chapter 95 Chapter 96 Chapter 97

Part 6

An approach to the child Specific problems of children Surgical problems in children Common childhood infectious diseases (including skin eruptions) Behavioural and developmental issues and disorders in children Child abuse Emergencies in children Adolescent health

Women’s health

Chapter Chapter Chapter Chapter Chapter Chapter

98 99 100 101 102 103

Chapter Chapter Chapter Chapter Chapter Chapter

104 105 106 107 108 109

Cervical cancer screening Family planning Breast pain (mastalgia) Lumps in the breast Abnormal uterine bleeding Lower abdominal and pelvic pain in women Premenstrual syndrome The menopause Vaginal discharge Vulvar disorders Basic antenatal care Infections in pregnancy

High-risk pregnancy Postnatal care

1184 1200

Part 7 Chapter Chapter Chapter Chapter Chapter

Male health 112 113 114 115 116

Part 8 Chapter Chapter Chapter Chapter

1209

Male health: an overview Scrotal pain Inguinoscrotal lumps Disorders of the penis Disorders of the prostate

1210 1214 1219 1230 1238

Sexual health 117 118 119 120

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The subfertile couple Sexual health Sexually transmitted infections Intimate partner violence and sexual assault

1250 1258 1271 1283

935 943 951 955

Part 9

Problems of the skin

Chapter 121

972 977 984

Child and adolescent health 989 90 91 92 93

Chapter 110 Chapter 111

838

Chronic disorders: continuing management 905

Part 4

Chapter Chapter Chapter Chapter Chapter Chapter

Sleep disorders Sore mouth and tongue Sore throat Tiredness/fatigue The unconscious patient Urinary disorders Visual failure Weight gain Weight loss

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990 1000 1017 1028 1041 1054 1062 1077

1085 1086 1094 1105 1110 1122 1130 1143 1147 1154

Chapter Chapter Chapter Chapter Chapter Chapter Chapter Chapter

122 123 124 125 126 127 128 129

Part 10 Chapter 130 Chapter 131 Chapter 132 Chapter 133 Chapter 134 Chapter 135 Chapter 136

Part 11 Chapter 137 Chapter 138 Chapter 139

1162 1170 1179

Appendix Index

1289

A diagnostic and management approach to skin problems Pruritus Common skin problems Acute skin eruptions Skin ulcers Common lumps and bumps Pigmented skin lesions Hair disorders Nail disorders

Accident and emergency medicine Emergency care The doctor’s bag and other emergency equipment Stroke and transient ischaemic attacks Thrombosis and thromboembolism Common skin wounds and foreign bodies Common fractures and dislocations Common sporting injuries

Health of specific groups The health of Indigenous peoples Refugee health Catchy metaphors, similes and colloquial expressions in medicine

1290 1301 1311 1335 1348 1358 1375 1385 1396

1407 1408 1424 1429 1436 1442 1456 1479

1495 1496 1505 1511 1517 1522

CONTENTS

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Murtagh's General Practice

Acknowledgments The author would like to thank the Publication Division of the Royal Australian College of General Practitioners for supporting his past role as Medical Editor of Australian Family Physician, which provided an excellent opportunity to gather material for this book. Acknowledgment is also due to those medical organisations that have given permission to use selected information from their publications. They include the Preventive and Community Medicine committee of the RACGP (Guidelines for Preventive Activities in General Practice), Therapeutic Guidelines Limited (Therapeutic Guidelines series), the Hypertension Guideline Committee: Research Unit RACGP (South Australian Faculty) and the Medical Observer, publishers of A Manual for Primary Health Care, for permitting reproduction of Appendices I–IV. Special thanks to the late Chris Sorrell for his art illustration, and to Nicki Cooper, Jenny Green and Caroline Menara for their skill and patience in typing the manuscript. Many of the quotations at the beginning of chapters appear in either Robert Wilkins (ed), The Doctor’s Quotation Book, Robert Hale Ltd, London, 1991, or Maurice B. Strauss (ed), Familiar Medical Quotations, Little, Brown & Co., New York, 1958. Thanks also to Dr Bruce Mugford, Dr Lucie Stanford, Dr Mohammad Shafeeq Lone, Dr Brian Bedkobar, Dr Joseph Turner and Lesley Rowe for reviewing the manuscript, and to the publishing and production team at McGraw-Hill Education (Australia) for their patience and assistance in so many ways. Finally, thanks to Dr Ndidi Victor Ikealumba for his expert review of General Practice sixth edition and his subsequent contribution.

Photo credits Photographs appearing on the pages below are from The Colour Atlas of Family Medicine 2nd edn by RP Usatine, MA Smith, EJ Mayeaux Jr and H Chumley, McGraw-Hill Education US 2013, with the kind permission of the following people: Dr Richard P Usatine: Fig 16.3, p 144; Fig 35.5, p 364; Fig 72.2, p 830; Fig 72.7, p 835; Figs 91.7 and 91.8, p 1011; Fig 91.9, p 1012; Fig 101.3, p 1112; Fig 106.5, p 1160; Fig 107.1, p 1164; Fig 119.5, p 1279; Fig 123.12, p 1324; Fig 126.20, p 1369; Fig 128.5 and 128.6, p 1391. Dr William Clark: Fig 50.3, p 565; Fig 50.6, p 566; Fig 50.7, p 567; Fig 59.1, p 665. Frontline Medical Communications: Fig 95.4, p 1059; Fig 125.6, p 1356. Paul D. Comeau: Fig 51.6, p 582. DEA: Fig 21.6, p 210. Dr Nicolette Deveneau: Fig 100.2, p 1109. Dr James L Fishback: Fig 138.3, p 1508. Javier La Fontaine DPM: Fig 125.5, p 1355. Reproduced from Gleason, in Tannenbaum: Fig 116.4, p 1245. Dr Michelle Rowe: Fig 21.5, p 210. Dr C. Blake Simpson: Fig 57.1, p 643. Dr Marc Solioz: Fig 16.1, p 142. Dr Eric Kraus: Fig 122.5, p 1305.

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Preface The discipline of general practice has become complex, expansive and challenging, but nevertheless remains manageable, fascinating and rewarding. John Murtagh’s General Practice attempts to address the issue of the base of knowledge and skills required in modern general practice. Some of the basics of primary healthcare remain the same. In fact, there is an everlasting identity about many of the medical problems that affect human beings, be it a splinter under a nail, a stye of the eyelid, a terminal illness or simply stress-related anxiety. Many of the treatments and approaches to caring management are universal and timeless. This text covers a mix of traditional and modern practice with an emphasis on the importance of early diagnosis, strategies for solving common presenting problems, continuing care, holistic management and ‘tricks of the trade’. One feature of our discipline is the patient who presents with undifferentiated problems featuring an overlap of organic and psychosocial components. There is the constant challenge to make an early diagnosis and identify the ever-lurking, life-threatening illness. Hence the ‘must not be missed’ catch cry throughout the text. To reinforce this awareness, ‘red flag pointers’ to serious disease are included where appropriate. The general practice diagnostic model, which pervades all the chapters on problem solving, is based on the authors’ experience, but readers can draw on their own experience to make the model work effectively for themselves. This sixth edition expands on the challenging initiative of diagnostic triads (or tetrads), which act as a brief aide-memoire to assist in identifying a disorder from three (or four) key symptoms or signs. A particular challenge in the preparation of the text was to identify as much appropriate and credible evidence-based information as possible. This material, which still has its limitations, has been combined with considerable collective wisdom from experts, especially from the Therapeutic Guidelines series. To provide updated accuracy and credibility, the authors have had the relevant chapters peer reviewed by independent experts in the respective disciplines. These consultants are acknowledged in the reviewers section. The revised edition also has the advantage of co-authorship from experienced general practitioner Dr Jill Rosenblatt. A comprehensive book such as this one, which presents a basic overview of primary medicine, cannot possibly cover all the medical problems likely to be encountered. An attempt has been made, however, to focus on problems that are common, significant, preventable and treatable. Expanded material on genetic disorders, infectious diseases and tropical medicine provides a glimpse of relatively uncommon presenting problems in first-world practice. John Murtagh’s General Practice is written with the recent graduate, the international medical graduate and the medical student in mind. However, all primary-care practitioners will gain useful information from the book’s content. A summarised form is available in Murtagh’s Flash Cards App.

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Murtagh's General Practice

Making the most of your book Diagnostic strategy models

Key facts and checkpoints

Diagnostic strategy models for common presenting problems form the backbone of this book. General Practice is renowned for this unique and powerful learning feature, which was introduced in the first edition.

Key facts and checkpoints provide accurate statistics and local and global contexts.

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PART THREE

• Problem solving in general practice

The clinical approach Differentiation of coagulation factor deficiencies and platelet disorders as the cause of a bleeding problem can usually be determined by a careful evaluation of the history and physical examination.

History Factors that suggest the presence of a systemic bleeding defect include: • spontaneous haemorrhage • severe or recurrent haemorrhagic episodes e.g. epistaxis • bleeding from multiple sites • bleeding out of proportion to the degree of trauma • cutaneous bleeding • gastrointestinal bleeding • postpartum haemorrhage • bleeding from tooth extraction/oral cavity • menorrhagia • muscle haematomas or haemarthrosis If a bleeding diathesis is suspected it is essential to determine whether local pathology is contributing to the blood loss (e.g. postoperative bleeding, postpartum bleeding, gastrointestinal haemorrhage).

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Diagnostic tips • Platelet abnormalities present as early bleeding following trauma. • Coagulation factor deficiencies present with delayed bleeding after initial haemostasis is achieved by normal platelets. • A normal response to previous coagulation stresses (e.g. dental extraction, circumcision or pregnancy) indicates an acquired problem. • If acquired, look for evidence of MILD: Malignancy, Infection, Liver disease, Drugs. • A diagnostic strategy is outlined in TABLE 39.2. Family history A positive family history can be a positive pointer to the diagnosis: • sex-linked recessive pattern: haemophilia A or B • autosomal dominant pattern: vWD, dysfibrinogenaemias • autosomal recessive pattern: deficiency of coagulation factors V, VII and X Enquire whether the patient has noticed blood in the urine or stools and whether menorrhagia is present in women. A checklist for a bleeding history is

Table 39.2

Key facts and checkpoints

Purpura: diagnostic strategy model

Q. Probability diagnosis A. Simple purpura (easy bruising syndrome) Senile purpura Corticosteroid-induced purpura Immune thrombocytopenic purpura Henoch–Schönlein purpura Liver disease, especially alcoholic cirrhosis Increased intravascular pressure, e.g. coughing, vomiting

• • •

Q. Serious disorders not to be missed A. Malignant disease: • leukaemia • myeloma Aplastic anaemia Myelofibrosis

• •

Severe infections: • septicaemia • meningococcal infection • measles • typhoid • dengue/chikungunya Disseminated intravascular coagulation Thrombotic thrombocytopenic purpura Fat embolism

•

Q. Pitfalls (often missed) A. Haemophilia A, B vWD Post-transfusion purpura Trauma (e.g. domestic violence, child abuse) Rarities: • hereditary telangiectasia (Osler–Weber–Rendu syndrome) • Ehlers–Danlos syndrome • scurvy • Fanconi syndrome

•

Q. The masquerades A. Drugs: examples (see ‘Medication Record’) • sodium valproate • various antibiotics • quinine/quinidine • thiazide diuretics • NSAIDs/salicylates • cytotoxics • oral anticoagulants/heparin Anaemia: • aplastic anaemia Q. Psychogenic factors A. Factitial purpura

mur60035_ch39_422-431.indd 424

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Vertebral dysfunction with nonradicular pain This outstanding common cause of low back pain is considered to be due mainly to dysfunction of the painsensitive facet joint. The precise pathophysiology is difficult to pinpoint.

mur60035_ch42_464-477.indd 464

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Cough is the commonest manifestation of lower respiratory tract infection. Cough is the cardinal feature of chronic bronchitis. Cough is a feature of asthma with sputum production, especially at night. Cough can have a psychogenic basis. Cough may persist for many weeks following an acute upper respiratory tract infection (URTI) as a result of persisting bronchial inflammation and increased airway responsiveness.1 Postnasal drip is the commonest cause of a persistent or chronic cough, especially causing nocturnal cough due to secretions (mainly from chronic sinusitis) tracking down the larynx and trachea during sleep. The commonest causes of haemoptysis are URTI (24%), acute or chronic bronchitis (17%), bronchiectasis (13%), TB (10%). Unknown causes totalled 22% and cancer 4% (figures from a UK study).2

The staff of Asclepius The staff of Asclepius icon highlights diseases for when you are specifically searching for information on a particular disease.

3/4/15 5:09 PM

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John Murtagh's General Practice, Sixth Edition

Red and yellow flags Red and yellow flags alert you to potential dangers. Red is the most urgent, but yellow also requires careful consideration.

g

Yellow flag pointers

Red flag pointers for low back pain

This term has been introduced to identify psychosocial and occupational factors that may increase the risk of chronicity in people presenting with acute back pain. Consider psychological issues if:

There are several so-called ‘red flag’ or precautionary pointers to a serious underlying cause of back pain (see TABLE 38.3). Such symptoms and signs should alert the practitioner to a serious health problem and thus guide selection of investigations, particularly plain films of the lumbar spine.

• • • • • • •

abnormal illness behaviour compensation issues unsatisfactory restoration of activities failure to return to work unsatisfactory response to treatment treatment refused atypical physical signs

Clinical framework

Seven masquerades checklist

Clinical framework based on major steps of clinical features, investigations, diagnosis, management and treatment reflects the key activities in the daily tasks of general practitioners.

This unique feature of the book reminds you of potential and hidden dangers underlying patient presentations. Addison disease

Infections of the central nervous system

Brain abscess4,5 A brain (cerebral) abscess is a focal area of infection in the cerebrum or cerebellum. It presents as a spaceoccupying intracerebral lesion. The infection can reach the brain by local spread or via the bloodstream, for example, endocarditis. There may be no clue to a focus of infection elsewhere but it can follow ear, sinus, dental, periodontal or other infection and also a skull fracture. The organisms are polymicrobial especially microaerophilic cocci and anaerobic bacteria in the non-immunosuppressed. In the immunosuppressed, Toxoplasma, Nocardia sp. and fungi. Clinical features

Raised intracranial pressure • • • •

Headache Nausea and vomiting Altered conscious state Papilloedema

Other • Focal neurological signs such as hemiplegia, dysphasia, ataxia • Seizures (30%) • Fever (may be absent) • Signs of sepsis elsewhere: e.g. teeth, endocarditis Investigations • MRI (if available) or CT scan • FBE, ESR/CRP, blood culture Note: lumbar puncture is contraindicated. • Consider endocarditis Management Management is urgent neurosurgical referral. mur60035_ch34_331-354.indd 333 to guide Aspiration or biopsy is essential antimicrobial treatment which may (empirically) include metronidazole IV and a cephalosporin e.g. ceftriaxone IV.

Spinal subdural or epidural abscess These uncommon focal infections can be extremely difficult to diagnose so an index of suspicion is required to consider such an abscess. The usual organism is Staphylococcus aureus. Clinical features6 • Back pain (increasing) ± radiculopathy • Percussion tenderness over spine

mur60035_ch30_290-295.indd 293

Diagnostic triads

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• Evolving neurological deficit, e.g. gradual leg weakness and sensory loss ± fever (may be absent) Causes • Associated infection: furuncle, decubitus ulcer, adjacent osteomyelitis, discitis, other • Back trauma with haematoma • Post-subdural or epidural anaesthetic block • One-third is spontaneous

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Investigations • Blood culture • MRI scan to localise abscess and spinal cord pressure Management Urgent neurosurgical referral. Empirical therapy while awaiting culture results may include di/flucloxacillin IV, + gentamicin IV, or vancomycin IV. 7,8 mur60035_ch38_401-421.indd Prion transmitted diseases

404

Prions are proteinaceous infected particles devoid of nucleic acid that can present with a wide spectrum of neurological presentations. The feature is transmissible spongiform encephalopathy (TSE) with Creutzfeldt–Jakob disease being the classic example. Other examples of TSE forms affecting humans are variant CJD, kuru (New Guinea) and fatal familial mur60035_ch38_401-421.indd 405 insomnia.

Q. Seven masquerades checklist A. Depression Diabetes (ketoacidosis) Drugs (especially narcotics) Anaemia (sickle cell) Endocrine disorder (thyroid storm, Addison) Spinal dysfunction UTI (including urosepsis) Q. Is the patient trying to tell me something? A. May be very significant. Consider Munchausen syndrome, sexual dysfunction and abnormal stress.

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Creutzfeldt–Jakob disease There are three distinct forms of CJD: sporadic (80– 85%), familial (15%) and iatrogenic (1%). The annual incidence is one per million people. Usual transmission is from contaminated human tissue (e.g. corneal graft), cadaver pituitary human gonadotrophin or eating contaminated beef. There is no specific treatment for the disease.

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DxT fatigue + psychiatric symptoms + myoclonus CJD

Clinical features • Progressive dementia (starts with personality change and memory loss—eventual loss of speech) • Myoclonus/muscle spasms • Fatigue and somnolence • Variable neurological features (e.g. ataxia, chorea)

4/14/15 11:37 AM

Key features that may discriminate between one disease and another are clearly presented.

DxT light-brown skin patches + skin  tumours + axillary freckles   NF1

MAKING THE MOST OF YOUR BOOK

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Evidence-based research

Extensive coverage of paediatric and geriatric care, pregnancy and complementary therapies

Evidence-based research is recognised with a full chapter on research in general practice and evidence base, including more on qualitative models. In addition, substantial references are provided for every chapter.

Extensive coverage of paediatric and geriatric care, pregnancy and complementary therapies is integrated throughout, as well as devoted chapter content providing more comprehensive information in these areas. Pain and its management

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Research and evidencebased medicine

Aspirin Aspirin is not in common use in children and should not be used 10 years since last dose if >5 years for third world travel give CDT 5 years Routine vaccination for all Australians Tetanus, diphtheria, pertussis Hepatitis B Haemophilus influenzae Measles, mumps, rubella Influenza Pneumococcal disease Poliomyelitis Rotavirus Varicella Selected vaccinations based on risk Cholera Hepatitis A Japanese encephalitis Meningococcal disease* Rabies Tick-borne encephalitis Tuberculosis (BCG if mantoux -ve) Typhoid fever Yellow fever* Other Preventive measures against gastrointestinal infections, mosquito bites, malaria (where applicable), sexually transmitted infections * legal requirement in some countries

Japanese B encephalitis This mosquito-borne flavivirus infection presents a real dilemma to the traveller and doctor because it is a very severe infection (mortality rate 20–40%) with high infectivity and high prevalence in endemic countries. The disease is prevalent during the wet season in the region bounded in the west by Nepal and Siberian Russia and in the east by Japan and Singapore, especially in Nepal, Burma, Korea, Vietnam, Thailand, China, eastern Russia and the lowlands of India. Rice paddies and pig farms are areas of risk. The usual preventive measures against mosquito bites are important. DxT febrile illness + vomiting + stupor   Japanese B encephalitis

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Rabies Rabies vaccination is recommended for some international aid workers or travellers going to rabies-endemic areas for periods of more than 1 month or even for short periods of working with affected animals in those areas. The vaccination can be effective after the bite of a rabid animal, so routine vaccination is not recommended for the traveller. Affected animals include dogs, cats, monkeys, camels and feral (wild) animals. A traveller who sustains a bite or scratch or even is licked by an animal in countries at risk should wash the site immediately with soap or a detergent, and then seek medical help. The prebite vaccination does not remove the need for postexposure vaccination.

DxT painful bite + paraesthesia + hydrophobia (pain with drinking)   rabies

Plague Plague is still prevalent in rodents in countries such as Vietnam, Brazil, Peru, Ecuador and Kenya. Although not compulsory, vaccination is recommended for those engaged in field operations in plague areas and rural health workers who may be exposed to infected patients. Two doses are given to adults (three to children 40 years

Age of onset

Usually young 40

Onset

Rapid

Insidious/slow

Presentation

Polyuria, polydipsia weight loss

Milder symptoms, often asymptomatic

Weight at onset

Low (thin)

High (obese)

Ketoacidosis

Yes

Rare

Familial

Weak

Strong

Insulin status

Deficient

Resistant

Complications

Yes

Yes

Note: These are generalisations and the clinical features may vary (e.g. type 2 diabetic patients may be thin and have a rapid onset; type 1 patients may exhibit a weak genetic link).

Key facts and checkpoints •

• • • •

•

In Australians older than 25 years the prevalence of diabetes is 7.5%, with another 10.6% having impaired glucose tolerance.2 About 30% of these people will develop clinical diabetes within 10 years.3 Many type 2 diabetics are asymptomatic. Diabetes can exist for years before detection and complications may be evident. Type 2 diabetes is not a mild disease. About onethird of those surviving 15 years will require insulin injections to control symptoms or complications.4 Blood glucose may be temporarily elevated during acute illness, after trauma or surgery.

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• Diagnostic perspective in general practice • Asymptomatic people of high risk of undiagnosed diabetes should be screened by blood glucose measurement.

Table 20.2

Causes of secondary diabetes

Endocrine disorders Cushing syndrome Acromegaly Phaeochromocytoma Polycystic ovarian syndrome Pancreatic disorders Haemochromatosis Chronic pancreatitis Drug-induced diabetes (transient) Thiazide diuretics

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Oestrogen therapy (high dose—not with low-dose HRT) Corticosteroids Other transient causes Gestational diabetes Medical or surgical stress

Clinical features The classic symptoms of uncontrolled diabetes are: • • • • •

polyuria polydipsia loss of weight (type 1) tiredness and fatigue propensity for infections, especially of the skin and genitals (vaginal thrush)

The young type 1 diabetic person typically presents with a brief 2–10 week history of the classic triad of symptoms:

FIGURE 20.1 Skin signs of diabetes: (a) Recurrent staphylococcus folliculitis (b) Candida albicans erosio interdigitalis (c) Candida albicans balanitis

Complications occur in type 2 diabetes as well as in type 1. • There are several causes of secondary diabetes that are very uncommon (see TABLE 20.2).

DxT thirst + polyuria + weight loss   type 1 diabetes

Other possible symptoms are: • vulvovaginitis • pruritus vulvae • balanitis

}

due to Candida albicans

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Diabetes mellitus • nocturnal enuresis (type 1) • blurred vision/visual changes Symptoms of complications (may be presenting feature) include: • staphylococcal skin infections • polyneuropathy: tingling or numbness in feet, pain (can be severe if present) • impotence • arterial disease: myocardial ischaemia, peripheral vascular disease History The history of a suspected or known diabetic patient should cover the following features including assessment of cardiovascular risks and end-organ damage. • Specific symptoms: — polyuria — polydipsia — loss of weight — polyphagia — tiredness/malaise/fatigue — nocturia • Related general symptom review: — cardiovascular (e.g. chest pain, dyspnoea) — urinary function — sexual function — neurological (e.g. tingling in feet/hands) — vision (e.g. blurred) — infection tendency (e.g. skin, urine, genital) — genital itching • General: — family history — medication — smoking and alcohol — obstetric history (where applicable) — physical activity — nutrition/eating habits Examination The physical examination should ideally follow the protocol for annual review. Initial screening for suspected diabetes should include: • • • • •

general inspection including skin BMI (weight/height) waist circumference visual acuity blood pressure—lying and standing

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• test for peripheral neuropathy: tendon reflexes, sensation (e.g. cotton wool, 10 g monofilament, Neurotips) • urinalysis: glucose, albumin, ketones, nitrites Investigations • Initial: fasting or random blood sugar, follow-up oral glucose tolerance test (OGTT) if indicated • Other tests according to clinical assessment (e.g. glycated haemoglobin (HbA1c), lipids, kidney function, ECG) Risk factors • Age >40 years • Family history • Overweight/obesity • Sedentary lifestyle • Positive obstetric history • Women with polycystic ovarian syndrome PCOS) • Hypertension/ischaemic heart disease • Medication causing hyperglycaemia • Ethnic/cultural groups: Aboriginal and Torres Strait Islanders (ATSIs), Pacific Islanders, people from Indian subcontinent, Chinese, Afro-Caribbeans Screening (type 2)5 • People with impaired fasting glucose/impaired glucose tolerance • Age >40 years • Age >30 years with: family history (firstdegree relative with type 2), obesity (BMI >30), hypertension • Age >20 years from high prevalence ethnic groups (e.g. ATSIs, Pacific Islanders) • Previous gestational diabetes; history of large babies • People on long-term steroids • People on atypical antipsychotics • Polycystic ovarian syndrome, especially if overweight • Cardiovascular disease and other risk factors The optimal frequency is every 3 years from age 40 years using AuSDRISK (www.diabetesaustralia. com.au/Understanding-Diabetes/Are-You-at-Risk/ and annually in very high-risk groups, including ATSIs.6 Diagnosis Diabetes is diagnosed as follows:3,5 1 If symptomatic (at least two of polydipsia, polyuria, frequent skin infections or frequent genital thrush): • fasting venous blood glucose (VBG) ≥7.0 mmol/L on two separate occasions

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or • random VBG (at least 2 hours after last eating) ≥11.1 mmol/L on two separate occasions or • HbAIc >6.5% 2 If asymptomatic: • at least two separate elevated values, either fasting, 2 or more hours post-prandial, or the two values from an oral glucose tolerance test (OGTT)

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Note: If random or fasting VBG lies in an uncertain range (5.5–11.0 mmol/L) in either a symptomatic patient or a patient with risk factors (over 50 years, overweight, blood relative with type 2 diabetes or high blood pressure), perform an OGTT. The cut-off point for further testing has now been reduced to 5.5 mmol/L.5,7 The 2 hour blood sugar on an OGTT is still the gold standard for the diagnosis of uncertain diabetes, i.e. >11.1 mmol/L. The OGTT should be reserved for true borderline cases and for gestational diabetes. A screening (oral glucose challenge) test at 26–30 (usually 28) weeks gestation is sometimes used during pregnancy.

Prediabetes This is the condition where the VPG is elevated above the normal range (i.e. 6.1–6.9) but does not satisfy the type 2 diagnostic criteria. It includes two states: • impaired fasting glucose (IFG) • impaired glucose tolerance (IGT) Urinalysis is unreliable in diagnosis since glycosuria occurs at different plasma glucose values in patients with different kidney thresholds. For a summary of diagnosis of diabetic states refer to FIGURE 20.2.

Table 20.3

Diabetes in children A study by Sinah and colleagues detected impaired glucose tolerance in 25% of 55 obese children (4 to 10 years of age) and 21% of 112 obese adolescents (11 to 18 years of age).9 Type 2 diabetes was identified in 4% of obese adolescents. However, over 30% of newly diagnosed diabetes in children and adolescents is upon presentation with diabetic ketoacidosis. Children with type 1 diabetes usually exhibit the classic features of polyuria, polydipsia, weight loss and lethargy. Be aware of unusual presentations such as urinary disorders including enuresis or daytime wetting accidents when a misdiagnosis of urinary infection or some other condition is sometimes forthcoming. The diagnosis can be made by an elevated random or fasting blood sugar. Oral glucose tolerance tests are inappropriate in the very young. Upon diagnosis it is appropriate to refer the child or adolescent to a multidisciplinary diabetes team.

Gestational diabetes Gestational diabetes is the onset or initial recognition of abnormal glucose tolerance during pregnancy. Pregnancy is diabetogenic for those with a genetic predisposition. All pregnant women should be screened at 28 weeks with an oral glucose challenge test or OGTT. If the blood glucose level is >7.8  mmol/L or if diabetes is otherwise suspected a diagnostic oral glucose tolerance test is indicated. The WHO definition of gestational diabetes is fasting blood sugar of ≥7  mmol/L or a 2-hour level of ≥7.8 mmol/L—refer to CHAPTER 108.

Diabetes in the elderly The incidence of diabetes rises with age. The elderly have increased mortality and morbidity from the

Interpreting diagnostic tests for diabetes8

Test

Normal

Intermediate hyperglycaemia

up to 6 mmol/L

6.1–6.9 mmol/L ≥7 mmol/L

Venous blood glucose concentration

fasting random

up to 6 mmol/L

Oral glucose tolerance test

2-hour venous blood glucose concentration

up to 7.7 mmol/L

HbA1c

Diabetes

≥11.1 mmol/L 7.8–11 mmol/L

≥11.1 mmol/L ≥48 mmol/mol (6.5%)

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Diabetes mellitus

< 5.5

Diabetes unlikely

F: 5.5–6.9 R: 5.5–11.0

F: ≥ 7.0 R:≥ 11.1

Diabetes uncertain

Diabetes likely

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Repeat FBG

Re-test yearly if high risk

Oral glucose tolerance test

3-yearly if increased risk

2 hour glucose levels

7.8–11

< 7.8

Diabetes unlikely

≥ 11.1

Diabetes likely

Impaired glucose tolerance F = fasting

R = random

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FIGURE 20.2 Blood glucose levels—venous plasma (mmol/L) Source: Reproduced with permission from Diabetes Management in General Practice. Guidelines for Type 2 Diabetes. Melbourne: Diabetes Australia & RACGP.5

disease and require careful monitoring, especially with adverse drug effects aggravated by polypharmacy and comorbidities. Special issues include diet, foot care and postural hypotension.

Complications of diabetes Complications may occur in patients with both type 1 and type 2 diabetes, even with early diagnosis and treatment (see FIG. 20.3). Type 1 diabetics still have a significantly reduced life expectancy. The main causes of death are diabetic nephropathy and vascular disease (myocardial infarction and stroke). Diabetes causes both macrovascular and microvascular complications but microvascular disease is specific to diabetes. Special attention should be paid to the ‘deadly quartet’ associated with type 2 diabetes.7,10 Macrovascular complications include: • ischaemic/coronary heart disease • cerebrovascular disease • peripheral vascular disease An analysis of patients with type 2 diabetes in the HOPE study11,12 showed a benefit of ramipril to reduce the risk of: • death (24%) • myocardial infarction (22%)

• stroke (33%) • cardiovascular death (37%) • overt nephropathy (24%) Consider organs/problems affected by diabetes under the mnemonic ‘KNIVES’: • • • • • •

Kidney Nerves Infection Vessels Eyes Skin

Microvascular disease The small vessels most affected from a clinical viewpoint are the retina, nerve sheath and kidney glomerulus. In younger patients it takes about 10 to 20 years after diagnosis for the problems of diabetic retinopathy, neuropathy and nephropathy to manifest.

Nephropathy Prevention of diabetic nephropathy is an essential goal of treatment. Early detection of the yardstick, which is microalbuminuria, is important as the process can be reversed with optimal control. The dipstick method is unreliable. Screening is done simply by an overnight collection (10–12 hours) of all urine, including the first morning sample. It is sent

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• Diagnostic perspective in general practice CVA (increased) General hypoglycaemia hyperglycaemia/ ketoacidosis dyslipidaemia

Blood pressure effects postural hypotension hypertension

Eyes cataract retinopathy ocular palsies (III, VI nerves)

Heart accelerated atherosclerosis myocardial infarction (may be silent) vagal neuropathy arrhythmias

Kidney diabetic nephropathy urinary infection

20

peripheral nerve palsies

small muscle wasting

Skin candidiasis • balanitis • vulvovaginitis staphylococcal infections necrobiosis lipoidica acanthosis nigricans vitiligo

Peripheral (poly) neuropathy paraesthesia muscle weakness reduced reflexes ±pain

FIGURE 20.3 The complications of diabetes

Gastrointestinal gastroparesis diarrhoea

Genitourinary erectile dysfunction/ impotence atonic bladder

amyotrophy (painful wasting)

Peripheral vascular disease macrovascular microvascular

Feet problems ischaemia (rest pain) ulcers gangrene

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Diabetes mellitus to the laboratory to determine the albumin excretion rate. Microalbuminuria is 20–200 mcg/minute (two out of three positive collections). A simpler method is the albumin/creatinine ratio (see CHAPTER 31). ACE inhibitors should be used for evidence of hypertension.

Retinopathy and maculopathy Retinopathy develops as a consequence of microvascular disease of the retina. Its prevalence is related to the duration of illness but up to 20% of people with type 2 diabetes have diabetic retinopathy at the time of diagnosis. The European multicentre study13,14 showed that diabetes is the single most common cause of blindness in European adults in the 16–64 years age groups. It is recommended that patients should undergo fundoscopy each year by an expert. Assessment is by direct ophthalmoscopy (with dilated pupils), retinal photography and fluorescein angiography (depending on the state of the patient’s fundi). Early diagnosis of serious retinopathy is vital since the early use of laser photocoagulation may delay and prevent visual loss.

Neuropathy The following types of neuropathy may occur: • radiculopathy (diabetic lumbosacral radiculoplexopathy) • sensory polyneuropathy • isolated mononeuropathy and multiple mononeuropathy — isolated peripheral nerve lesions (e.g. median nerve) — cranial nerve palsies (e.g. III, VI) — amyotrophy • autonomic neuropathy, which may lead to: — erectile dysfunction — postural hypotension and syncope — impaired gastric emptying (gastroparesis) — diarrhoea — delayed or incomplete bladder emptying — loss of cardiac pain → ‘silent’ ischaemia — hypoglycaemic ‘unawareness’ — sudden arrest, especially under anaesthetic

Infections Poorly controlled diabetics are prone to infections, especially: • skin: mucocutaneous candidiasis (e.g. balanitis, vulvovaginitis), staphylococcal infections (e.g. folliculitis)

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• urinary tract: cystitis (women), pyelonephritis and perinephric abscess • lungs: pneumonia (staphylococcal, streptococcal pneumonia), others; tuberculosis

Diabetic metabolic complications • • • •

Hypoglycaemia Diabetic ketoacidosis Hyperosmolar hyperglycaemia Lactic acidosis

Other complications • • • • •

Cataracts Refractive errors of eye Sleep apnoea Depression Musculoskeletal: neuropathic joint damage (Charcot type arthropathy), tendon rupture • Foot ulcers (related to neuropathy)

Prevention of diabetes Several large studies have demonstrated that it is possible to prevent or delay the onset of diabetes in those at risk.13,14 It involves intensive lifestyle intervention in individuals who are overweight with impaired glucose tolerance or raised fasting blood glucose. One strategy is to follow the SNAP guidelines (Smoking, Nutrition, Alcohol, Physical activity). The essentials are healthy eating, weight loss and physical activity. This represents an important approach that GPs can recommend to their patients at risk.

Management of diabetes mellitus The main objectives for the GP in the optimal management of the diabetic patient, in order to prevent the development of cardiovascular disease and other complications, are:5 1 to achieve strict glycaemic control as measured by (most importantly) glycated haemoglobin (HbA1c) and by blood glucose 2 to achieve blood pressure control (≤130/80 mmHg, supine) 3 to achieve control of blood cholesterol level Note: Refer to the estimations of cardiovascular risk (see FIGS. 85.1 and 85.2 in CHAPTER 85).

Management principles • Provide detailed and comprehensive patient education, support and reassurance.

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• Achieve control of presenting symptoms. • Achieve blood pressure control (≤130/80 mmHg supine). • Develop a diabetic care plan. • Emphasise the importance of the diet: good nutrition, adequate complex carbohydrates, protein, restricted fats and sugars. • Promptly diagnose and treat urinary tract infection. • Treat and prevent life-threatening complications of ketoacidosis or hyperosmolar coma. • Treat and prevent hypoglycaemia in those taking insulin and oral hypoglycaemic agents. • Organise self-testing techniques, preferably blood glucose monitoring. • Detect and treat complications of diabetes— neuropathy, nephropathy, retinopathy, vascular disease.

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Metabolic syndrome8 Beware of the deadly metabolic syndrome (syndrome X or insulin resistance syndrome). • Upper truncal obesity (waist circumference) >102 cm : >88 cm (European population) plus any 2 or more of the following • ↑ triglycerides >1.7 mmol/L • ↓  HDL cholesterol 100 fL • normocytic—MCV 80–100 fL Note: Upper limit of MCV varies from 95–100 fL depending on age and laboratory. TABLE  22.2 outlines a classification of some of the more common causes of anaemia encountered in general practice. There can be an interchange of disorders between the above groups, for example, the anaemia of chronic disorders (chronic infection, inflammation and malignancy) can occasionally be microcytic as well as normocytic; the anaemia of hypothyroidism can be macrocytic in addition to the more likely normocytic; the anaemia of bone marrow disorder or infiltration can also be occasionally macrocytic.

Iron-deficiency anaemia3 Iron deficiency is the most common cause of anaemia worldwide. It is the biggest cause of microcytic anaemia, with the main differential diagnosis of microcytic anaemia being a haemoglobinopathy such as thalassaemia. An understanding of the interpretation of iron studies is important in management. Clinical features • Microcytic anaemia • Serum ferritin level low (NR: F 15–200 mcg/L: M 30–300 mcg/L) • Serum iron level low • Increased transferrin level • Reduced transferrin saturation • Response to iron therapy

Non-haematological effects of chronic iron deficiency • • • • •

Angular cheilosis/stomatitis Glossitis Oesophageal webs Atrophic gastritis Brittle nails and koilonychias

Causes1

Blood loss • Menorrhagia • Gastrointestinal bleeding (e.g. carcinoma, haemorrhoids, peptic ulcer, hiatus hernia, GORD, NSAID therapy) • Frequent blood donations • Malignancy • Hookworm (common in tropics)

Increased physiological requirements • Prematurity, infant growth • Adolescent growth • Pregnancy

Malabsorption • Coeliac disease • Postgastrectomy

MICROCYTIC ANAEMIA—MCV ≤ 80 FL

Dietary

The main causes of microcytic anaemia are iron deficiency and haemoglobulinopathy, particularly thalassaemia. Consider lead poisoning.

• Inadequate intake • Special diets (e.g. fad, vegetarianism) • Pica—eating unnatural food e.g. dirt, ashes

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Anaemia

Table 22.2

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Selected causes and investigations of anaemia

Causes/classification

Primary diagnostic features

Secondary investigations

Iron deficiency

s.Fe ↓; s.ferr ↓; transferrin ↑

Therapeutic trial of iron; GIT evaluation for blood loss

Haemoglobinopathy (e.g. thalassaemia)

s.Fe N or ↑; s.ferr N or ↑

Haemoglobin investigation, e.g. electrophoresis

Sideroblastic anaemia (hereditary)

s.Fe N or ↑; s.ferr N or ↑

Bone marrow examination

s.Fe ↓; s.ferr N or ↑; transferrin ↓

Specific for underlying disorder

Microcytic (MCV 100 fL) (a) With megaloblastic changes Vitamin B12 deficiency Folate deficiency Cytotoxic drugs

IF antibody assay; Schilling test s.B12 ↓; rc.Fol N or ↑ Usually none s.B12 N; rc.Fol ↓ Appropriate setting; s.B12 N; rc.Fol N None

(b) Without megaloblastic changes Liver disease/alcoholism

Appropriate setting; uniform macrocytosis; s.B12 N; rc.Fol N

Liver function tests

Myelodysplastic disorders (including sideroblastic anaemia)

Specific peripheral blood findings; s.B12 N; rc.Fol N

Bone marrow examination

Acute blood loss/occult Anaemia of chronic disease1 Haemolysis

Isolated anaemia; Retic ↑ Appropriate setting; Retic ↓ Specific red cell changes; Retic ↑

Dictated by clinical findings s.Fe ↓  and s.ferr N or ↑ s.Bil and s.LDH ↑; s.hapt ↓  specific tests for cause

Chronic kidney disease Endocrine disorders (e.g. hypothyroidism)

Isolated anaemia; Retic ↓ Appropriate setting; isolated anaemia; Retic ↓

Kidney function Specific endocrine investigation

Normocytic (MCV 80–100 fL)

Abbreviations: MCV = mean corpuscular volume; s.Fe = serum iron; s.ferr = serum ferritin; s.B12 = serum vitamin B12; rc.Fol = red cell folate; IF = intrinsic factor; Retic = reticulocyte count; s.Bil = serum bilirubin; s.LDH = serum lactate dehydrogenase; s.hapt = serum haptoglobin; N = normal; ↓ = reduced; ↑ = elevated; GIT = gastrointestinal Source: Adapted from ‘Anaemia’, MIMS Disease Index,1 with permission of MIMS Australia, a division of MediMedia Australia Pty Limited1

Investigations Investigations are based on the history and physical examination, including the rectal examination. If GIT bleeding is suspected the faecal occult blood test is not considered very valuable but appropriate investigations include gastroscopy and colonoscopy, small bowel biopsy and small bowel enema.

Haematological investigations: typical findings • Microcytic, hypochromic red cells • Anisocytosis (variation in size), poikilocytosis (shape)—pencil-shaped rods

• • • •

Low serum iron level Raised iron-binding capacity Serum ferritin level low (the most useful index) Soluble transferrin receptor factor—this factor is increased in iron deficiency, but not in chronic disease. It is very helpful therefore in differentiating iron deficiency from other forms. It is an indirect marker of what is happening in the bone marrow.4

The state of the iron stores is assessed by considering the serum iron, the serum ferritin and the serum transferrin levels in combination. Typically,

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The interpretation of iron studies2

Table 22.3 Condition

Serum Fe

TIBC

% Transferrin saturation

Ferritin

Iron deficiency

↓ 

N or ↑ 

↓ 

↓  ↓ 

β-thalassaemia

N or ↑ 

N

N or ↑ 

N or ↑ 

↓ 

N or ↓ 

↓ 

N or ↑ 

N or ↑ 

N

N or ↑ 

↑ 

↑ 

↓ 

↑ ↑ 

↑ ↑ 

Anaemia of chronic disease Sideroblastic anaemia Haemochromatosis N = normal

in iron deficiency, the serum iron and ferritin levels are low and the transferrin high, but the serum iron level is also low in all infections—severe, mild and even subclinical—as well as in inflammatory states, malignancy and other chronic conditions. Serum ferritin estimations are spuriously raised in liver disease of all types, chronic inflammatory conditions and malignancy; transferrin is normally raised in pregnancy. Since each of these estimations can be altered in conditions other than iron deficiency, all three quantities have to be considered together to establish the iron status (see TABLE 22.3).2 4

22

Treatment • Correct the identified cause. • Diet—iron-rich foods, vitamin C rich foods (see TABLE 22.4). Iron is present in meat and legumes as Fe+ + + and therefore requires gastric acid for conversion to Fe++. • Iron preparations: — oral iron (ferrous sulphate 1–2 tablets daily between meals for 6 months) e.g. FerroGradumet with orange juice or ascorbic acid until Hb is normal — parenteral iron preferably by IV infusion is probably best reserved for special circumstances (there is a risk of an allergic reaction). Avoid blood transfusions if possible.

Response • Anaemia responds after about 2 weeks and is usually corrected after 2 months (if underlying cause addressed).1 • Oral iron is continued for 3 to 6 months to replenish stores. • Monitor progress with regular serum ferritin levels. • A serum ferritin level >50 mcg/L generally indicates adequate stores.

Table 22.4

Optimal adult diet for iron deficiency

Adults should limit milk intake to 500 mL a day while on iron tablets. Avoid excess caffeine, fad diets and excess processed bread. Eat ample iron-rich foods (especially protein). Protein foods Meats—beef (especially), veal, pork, liver, poultry Fish and shellfish (e.g. oysters, sardines, tuna) Seeds (e.g. sesame, pumpkin) Eggs, especially egg yolk Fruits Dried fruit (e.g. prunes, figs, raisins, currants, peaches) Juices (e.g. prune, blackberry) Most fresh fruit Vegetables Greens (e.g. spinach, silver beet, lettuce) Dried peas and beans (e.g. kidney beans) Pumpkin, sweet potatoes Grains Iron-fortified breads and dry cereals Oatmeal cereal For better iron absorption, add foods rich in vitamin C (e.g. citrus fruits, cantaloupe, Brussels sprouts, broccoli, cauliflower).

Failure of iron therapy Consider: • poor compliance • continuing blood loss • malabsorption (e.g. severe coeliac disease) • incorrect diagnosis (e.g. thalassaemia minor, chronic disease) • bone marrow infiltration

Thalassaemia This inherited condition is seen mainly (although not exclusively) in people from the Mediterranean basin, the Middle East, north and central India and SouthEast Asia, including south China. The heterozygous

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Anaemia form is usually asymptomatic; patients show little if any anaemia and require no treatment. The condition is relatively common in people from these areas. The homozygous form is a very severe congenital anaemia needing lifelong transfusional support but is comparatively rare, even among the populations prone to thalassaemia (refer to CHAPTER 18).2 The key to the diagnosis of heterozygous thalassaemia minor is significant microcytosis quite out of proportion to the normal Hb or slight anaemia, and confirmed by finding a raised HbA2 on Hb electrophoresis. DNA screening analysis is now available. The importance of recognising the condition lies in distinguishing it from iron-deficiency anaemia, for iron does not help people with thalassaemia and is theoretically contraindicated. Even more importantly, it lies in recognising the risk that, if both parents have thalassaemia minor, they run a one in four chance of having a baby with thalassaemia major in every pregnancy, with devastating consequences for both the affected child and the whole family. Treatment of thalassaemia major is transfusion to a high normal Hb with packed cells plus desferrioxamine.

Haemoglobin E This Hb variant is common throughout South-East Asia.4 It has virtually no clinical effects in either the homozygous or heterozygous forms, but these people have microcytosis, which must be distinguished from iron deficiency; moreover, if the HbE gene is combined with the thalassaemia gene, the child may have a lifelong anaemia almost as severe as thalassaemia major. Both genes are well established in the SouthEast Asian populations in Australia as well as in their own countries.

MACROCYTIC ANAEMIA—MCV >100 FL

Alcohol and liver disease Each individually, or in combination, leads to macrocytosis with or without anaemia. The importance of this finding lies in its often being the first indication of alcohol abuse, which can so frequently go unnoticed unless there is a firm index of suspicion. Chronic liver disease due to other causes may also be late in producing specific clinical symptoms.

Drug toxicity Cytotoxic drugs, anticonvulsants in particular, and various others (see TABLE  22.5) may cause macrocytosis. This is of little clinical significance

Table 22.5

223

Drugs causing macrocytosis2,5

Alcohol Cytotoxics/ immunosuppressants Antibiotics

Anticonvulsants

271

Azathioprine Methotrexate 5-fluorouracil Cotrimoxazole Pyrimethamine (incl. Fansidar and Maloprim) Zidovudine Phenytoin Primidone Phenobarbitone

and does not need correction unless associated with anaemia or other cytopaenia.

Myelodysplastic syndromes These conditions have been recognised under a variety of names, such as ‘refractory anaemia’ and ‘preleukaemia’, for a long time, but only relatively recently have they been grouped together. They are quite common in the elderly but may be seen in any age group (refer TABLE 22.2). These conditions frequently present as a macrocytic anaemia with normal serum vitamin B12 and red cell folate, and are unresponsive to these or any other haematinics. They are usually associated with progressive intractable neutropaenia or thrombocytopenia or both, and progress slowly but relentlessly to be eventually fatal, terminating with infection, haemorrhage or, less often, acute leukaemia.

Vitamin B12 deficiency (pernicious anaemia) Although well recognised, this is a much less common cause of macrocytosis than the foregoing conditions. It is usually caused by lack of intrinsic factor due to autoimmune atrophic changes and by gastrectomy. Anaemia does not develop for about 3 years after total gastrectomy. Vitamin B12 deficiency may also be seen together with other deficiencies in some cases of malabsorption and Crohn disease. Vitamin B12 (cobalamin) is found in the normal diet but only in foods of animal origin and consequently very strict vegetarians may eventually develop deficiency. Causes of food vitamin B12 deficiency are:4 • • • • •

atrophic gastritis H. pylori infection H2 receptor blockers PPI drugs other drugs, e.g. OCP, metformin

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• chronic alcoholism • HIV • strict vegan diet

NORMOCYTIC ANAEMIA2 (ANAEMIAS WITHOUT CHANGE IN THE MCV)

The clinical features are anaemia (macrocytic), weight loss and neurological symptoms, especially a polyneuropathy. It can precipitate subacute combined degeneration of the cord. The serum vitamin B12 is below the normal level (normal range 150–700 pmol/L).

This is the most common cause of normocytic anaemia and is usually due to haematemesis and/or melaena.

B12 >220 pmol/L = deficiency unlikely 630 nmol/L) The main cause is poor intake associated with old age, poverty and malnutrition, usually associated with alcoholism. It may be seen in malabsorption and regular medication with anti-epileptic drugs such as phenytoin.6 It is rarely, but very importantly, associated with pregnancy, when the demands of the developing fetus together with the needs of the mother outstrip the dietary intake—the so-called ‘pernicious anaemia of pregnancy’ which, if not recognised and treated immediately, can still be a fatal condition. Unlike vitamin B12, folic acid is not stored in the body to any significant degree and requirements have to be satisfied by the daily dietary intake, which invariably meets the requirement of 5–10 mcg/day. Folic acid is present in most fruit and vegetables, especially citrus fruits, nuts and green leafy vegetables (see CHAPTER 10). Treatment (replacement therapy) Oral folate 5 mg/day to replenish body stores (5–10 mg). This takes about 4 weeks but continue for 4 months. Vitamin B12 is usually given unless levels normal.

Acute haemorrhage

Chronic disease

Chronic inflammation Intercellular iron transport within the marrow is suppressed in inflammation so that, despite normal iron stores, the developing red cells are deprived of iron and erythropoiesis is depressed. If the inflammation is short-lived, the fall in Hb is not noticeable but, if it continues, an anaemia may develop that responds only when the inflammation subsides.

Malignancy Anaemia may develop for the same reasons that apply to chronic inflammation.

Kidney failure This is often associated with anaemia due to failure of erythropoietin secretion and is unresponsive to treatment, other than by alleviating the insufficiency or until erythropoietin is administered.

Haemolysis Suspect haemolytic anaemia if there is a reticulocytosis, mild macrocytosis, reduced haptoglobin, increased bilirubin and urobilinogen. Haemolytic anaemias are relatively infrequent. The more common of the congenital ones are hereditary spherocytosis, sickle cell anaemia and deficiencies of the red cell enzymes, pyruvate kinase and G-6-PD, although most cases of G-6-PD deficiency haemolyse only when the patient takes oxidant drugs such as sulphonamides or eats broad beans—‘favism’. Acquired haemolytic anaemias include those of the newborn due to maternal haemolytic blood group antibodies passing back through the placenta to the fetus, and adult anaemias due to drug toxicity or to acquired auto-antibodies. About half of the latter are idiopathic and half associated with non-Hodgkin lymphomas, and the anaemia may be the presenting sign of lymphoma. Some of these antibodies are active only at cool temperatures—cold agglutinin disease; others act at body temperature and are the more potent cause of autoimmune haemolytic anaemia.

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Anaemia

Bone marrow replacement This may be due to foreign tissue, such as carcinomatous metastases or fibrous tissue as in myelofibrosis; it may also be due to overgrowth by one or other normal elements of the bone marrow, as in chronic myeloid leukaemia, chronic lymphocytic leukaemia and lymphoma, as well as by acute leukaemic tissue. A leuco-erythroblastic picture, in which immature red and white cells appear in the peripheral blood, is often seen when the marrow is replaced by foreign tissue.

Anaemia in children Haemoglobin reference range Infant

term (cord blood) 3–6 months

135–195 g/L 95–135 g/L

Child

1 year 3–6 years 10–12 years

105–135 g/L 105–140 g/L 115–145 g/L

Important causes of anaemia in childhood include iron-deficiency anaemia (quite common), thalassaemia major, sickle-cell anaemia and drug-induced haemolysis. Consider one of the haemoglobinopathies in children of Mediterranean, South-East Asian, Arabic or African–American descent, especially with a family history, normal ferritin level or anaemia resistant to iron therapy. Investigate with Hb electrophoresis. Drugs that can cause haemolysis (the film will have reticulocytosis, spherocytosis and fragmented red cells) include some antibiotics (e.g. sulfamethoxazole, antimalarials and some anti-inflammatories). Think of anaemia in adolescents, especially females with a rapid growth spurt at the menarche and a relatively poor diet.

Iron deficiency in children8 • Iron deficiency is present in up to 10–30% of children in high-risk groups. • It is often subclinical and anaemia develops in relatively few. • It can lead to reduced cognitive and psychomotor performance (even without anaemia). • High-risk groups include those infants 150 per minute), heart  failure and arrhythmias. It is usually precipitated  by surgery or an infection in an undiagnosed patient.

Thyroid crisis (thyroid storm)7

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It requires urgent intensive hospital management with antithyroid drugs; IV saline infusion, IV corticosteroids, anti-heart failure and antiarrhythmia therapy.

When to refer10—hyperthyroidism • Doubt about the diagnosis • Severe hyperthyroidism, especially if there is coexisting thyrocardiac disease • Pregnant patients with hyperthyroidism • Progression of exophthalmos • Ideally all cases

Thyroid nodules A thyroid nodule is defined as a discrete lesion on palpation and/or ultrasonography that is distinct from the rest of the thyroid gland. Causes • Dominant nodule in a multinodular goitre (most likely) • Colloid cyst • True solitary nodule: adenoma, carcinoma (papillary or follicular) Investigations • Ultrasound imaging • Fine-needle aspiration cytology • Thyroid function tests

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Thyroid carcinoma The main presentations are a painless nodule, a hard nodule in an enlarged gland or lymphadenopathy. Papillary carcinoma is the most common malignancy. Although rare compared with non-malignant lesions (such as colloid nodules, cysts, haemorrhage and benign adenomas), it is important not to miss carcinoma because of the very high cure rate with treatment. This often involves total thyroidectomy, ablative 131I treatment, thyroxine replacement and follow-up with serum thyroglobulin measurements, 131 I/thallium scanning and neck ultrasound. Fineneedle aspiration is the investigation of choice.

PITUITARY DISORDERS

Pituitary tumours10 These are invariably benign adenomas. They can present with hormone deficiencies, features of hypersecretory syndromes (e.g. prolactin, GH, ACTH) or by local tumour mass symptoms (e.g. headache, visual field loss).

Hyperprolactinaemia11 The main causes (of many) are a pituitary adenoma (micro- or macro), pituitary stalk damage, drugs— such as antipsychotics, various antidepressants, metoclopramide, cimetidine, oestrogens, opiates, marijuana—and physiological causes such as pregnancy and breastfeeding. Clinical features • Symptoms common to males and females: reduced libido, subfertility, galactorrhoea (mainly females) • Females: Amenorrhoea/oligomenorrhoea • Males: erectile dysfunction, reduced facial hair Diagnosis • Serum prolactin and macroprolactin assays • MRI: consider if headache, etc. Refer for management, which may include a dopamine agonist such as cabergoline or bromocriptine.

Acromegaly Symptoms suggestive of acromegaly include: • • • • • •

excessive growth of hands (increased glove size) excessive growth of tissues (e.g. nose, lips, face) excessive growth of feet (increased shoe size) increased size of jaw and tongue; kyphosis general: weakness, sweating, headaches sexual changes, including amenorrhoea and loss of libido • disruptive snoring (sleep apnoea) • deepening voice

DxT nasal problems + fitting problems (e.g. rings, shoes) + sweating   acromegaly

Diagnosis7,10 • Plasma growth hormone excess • Elevated insulin-like growth factor 1 (IGF-1) (somatomedin)—the key test • X-ray skull and hands • MRI scanning pituitary • Consider associated impaired glucose tolerance/ diabetes Obtain old photographs (if possible). Treatment: pituitary microsurgery.

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Thyroid and other endocrine disorders

Diabetes insipidus and SIADH Impaired secretion of vasopressin (antidiuretic hormone) from the posterior pituitary leads to polyuria, nocturia and compensatory polydipsia resulting in the passage of 3–20 L of dilute urine per day. There are several causes of diabetes insipidus (DI), the commonest being postoperative (hypothalamicpituitary), which is usually transient only. Other causes of cranial DI include tumours, infections and infiltrations. In nephrogenic DI the kidney tubules are insensitive to vasopressin. Differential diagnosis includes compulsive (psychogenic) water drinking. The syndrome of secretion of inappropriate antidiuretic hormone (SIADH) is caused by cancer (e.g. lung, lymphomas, kidney, pancreas), pulmonary disorders, various intracranial lesions and drugs such as carbamazepine and many antipsychotic agents. Management of SIADH is essentially fluid restriction. The treatment of DI is desmopressin, usually given twice daily intranasally. DxT weakness + polyuria + polydipsia diabetes insipidus

Hypopituitarism7 This rare disorder should be considered with: • • • • • •

a history of postpartum haemorrhage symptoms of hypothyroidism symptoms of adrenal insufficiency symptoms suggestive of a pituitary tumour thin, wrinkled skin: ‘monkey face’ pale ‘alabaster’ skin/hairlessness DxT (female): amenorrhoea + loss of axillary and pubic hair + breast atrophy    hypopituitarism DxT (male): ↓ libido + impotence + loss of body hair   hypopituitarism

Investigate with serum pituitary hormones, imaging and triple stimulation test.

ADRENAL DISORDERS It is worth keeping in mind the uncommon disorders of the adrenal cortex, which can also be difficult to diagnose in the early stages, namely: • chronic adrenal insufficiency (Addison disease)— deficiency of cortisol and aldosterone

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• Cushing syndrome—cortisol excess • primary hyperaldosteronism (refer CHAPTER 86)

Addison disease7 Autoimmune destruction of the adrenals is the most common cause. Clinical features • Lethargy/excessive fatigue/weakness • Anorexia and nausea • Diarrhoea/abdominal pain • Weight loss • Dizziness/funny turns, syncope: hypoglycaemia (rare); postural hypotension (common) • Hyperpigmentation, especially mucous membranes of mouth and hard palate, skin creases of hands If Addison disease remains undiagnosed, wasting leading to death may occur. Severe dehydration can be a feature. Delayed diagnosis is a huge problem. DxT fatigue + a/n/v + abdominal pain (± skin discolouration) Addison disease

Diagnosis • Elevated serum potassium, low serum sodium • Low plasma cortisol level (fails to respond to synthetic adrenocorticotropic hormone [ACTH]) • The short synacthen stimulation test is the definitive test • Consider adrenal autoantibodies and imaging ? calcification of adrenals Treatment: corticosteroid replacement— hydrocortisone/fludrocortisone acetate.

Addisonian crisis An Addisonian crisis develops because of an inability to increase cortisol in response to stress, which may include intercurrent infection, surgery or trauma. Clinical features • Nausea and vomiting • Acute abdominal pain • Severe hypotension progressing to shock • Weakness, drowsiness progressing to coma Urgent management • Establish IV line with IV fluids • Hydrocortisone sodium succinate 200 mg IV and 100–200 mg 4–6 hourly • Arrange urgent hospital admission

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Cushing syndrome7 The five main causes are: • iatrogenic—chronic corticosteroid administration • pituitary ACTH excess (Cushing disease) • bilateral adrenal hyperplasia • adrenal tumour (adenoma, adenocarcinoma) • ectopic ACTH or (rarely) corticotrophin-releasing hormone (CRH) from nonendocrine tumours (e.g. oat cell carcinoma of lung) The clinical features (see FIG.  23.5) are caused by the effects of excess cortisol and/or adrenal androgens. Clinical features • Proximal muscle wasting and weakness • Central obesity, buffalo hump on neck • Cushing facies: plethora, moon face, acne • Weakness • Hirsutism • Abdominal striae • Thin skin, easy bruising • Hypertension • Hyperglycaemia (30%) • Menstrual changes (e.g. amenorrhoea) • Osteoporosis • Psychiatric changes, especially depression • Backache

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DxT plethoric moon face + thin extremities + muscle weakness   Cushing syndrome

FIGURE 23.5 62-year-old woman with Cushing syndrome, showing centripetal obesity, hirsutism and virilisation (wearing a wig), ‘moon’ face, thin extremities and plethoric appearance Photo courtesy David Dammery

Diagnosis (apart from iatrogenic cause) • Cortisol excess (plasma or 24-hour urinary cortisol) • Dexamethasone suppression test • Inferior petrosal sinus sampling • Serum ACTH • Radiological localisation: MRI for ACTHproducing pituitary tumours; CT scanning for adrenal tumours

• paraesthesia • polyuria and polydipsia Investigations • aldosterone (serum and urine) ↑ • plasma renin ↓ • Na ↑, K ↓, alkalosis Refer for treatment including possible surgery to excise adenoma.

Primary hyperaldosteronism7 Most commonly due to an adrenal adenoma.

Conn syndrome Usually asymptomatic but any symptoms are features of hypokalaemia: • weakness • cramps

Phaeochromocytoma10 A dangerous tumour of the adrenal medulla. Clinical features are paroxysms or spells of: • • • • •

hypertension headache (throbbing) sweating palpitations pallor/skin blanching

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Thyroid and other endocrine disorders • rising sensation of tightness in upper chest and throat (angina can occur) Investigations • Series of three 24-hour free catecholamines ↑ VMA • Abdominal CT or MRI scan Treatment • Excise tumour, cover with alpha and beta blockers

Congenital adrenal hyperplasia (adrenogenital syndrome)7 An AR condition with 21-hydroxylase deficiency being the most common of several forms. There is inadequate synthesis of cortisol and aldosterone with increased androgenisation. Major problem is adrenal failure ± salt-losing state (SLS). In females, ambiguity of external genitalia and hirsutism before puberty usually occurs. Males may have normal urogenital development but SLS is a concern. Infants of either sex may present with failure to thrive or vomiting and dehydration (SLS). Lifelong glucocorticoid treatment is required. Wearing an alert bracelet or necklace is strongly recommended for these patients.7

Adrenal tumours10 Most of those detected by abdominal imaging are benign and termed ‘incidentalomas’ but serious tumours include adrenal carcinoma, phaeochromocytoma, neuroblastoma, glucocorticoid or a mineral corticoid secreting tumour. Rule: tumours >4 cm require thorough assessment as malignant tumours are large.

CALCIUM DISORDERS

Hypercalcaemia10 Suspect hypercalcaemia if there is weakness, tiredness, malaise, anorexia, nausea or vomiting, abdominal pain, constipation, thirst, polyuria, drowsiness, dizziness, personality changes, muscle aches and pains, visual disturbances. Measure urea and electrolytes (especially calcium), creatinine, albumin. Primary hyperparathyroidism, familial hypercalciuric hypercalcaemia and neoplasia, especially lung and breast (with metastases to bone), account for

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over 90% of cases. Other causes include Paget disease, sarcoidosis and milk-alkali syndrome. Investigations include ESR, serum parathyroid hormone (N: 1.0–7 pmol/L), serum ACE levels, serum alkaline phosphatase, chest X-ray, Sestamibi scan and bone scan. DxT weakness + constipation + polyuria hypercalcaemia DxT cramps + confusion + tetany hypocalcaemia

Primary hyperparathyroidism10 Hyperparathyroidism is caused by an excessive secretion of parathyroid hormone and is usually due to a parathyroid adenoma. The classic clinical features of hyperparathyroidism are due to the effects of hypercalcaemia. Rarely, a parathyroid crisis in a misdiagnosed patient may result in death from severe hypercalcaemia. Classic mnemonic: bones, moans, stones, abdominal groans

Diagnosis • Exclusion of other causes of hypercalcaemia • Serum parathyroid hormone (elevated) • TC-99m Sestamibi scan to detect tumour

Hypocalcaemia7 This usually presents with tetany or more generalised neuromuscular hyperexcitability and neuropsychiatric manifestations. The sensory equivalents are paraesthesia in the hands, feet and around the mouth (distinguish from tetany seen in the respiratory alkalosis of hyperventilation). There may be seizures and cramps. The diagnosis is by measurement of serum total calcium concentration in relation to serum albumin (s. calcium 108 colonyforming units/L), which has not produced symptoms requiring consultation.1 Screening for and treatment of asymptomatic bacteriuria is not recommended except for: • pregnant women because of the risk of pyelonephritis and pregnancy complications (see CHAPTER 109) • patients before urological procedures (e.g. TURP)

• Acute bacterial infection of the kidney produces loin pain and constitutional upset, with fever, rigors, nausea and sometimes vomiting. • The symptoms of acute cystitis are often also present. • The differential diagnosis includes causes of the acute abdomen, such as appendicitis, cholecystitis and acute tubal or ovarian diseases. The presence of pyuria and absence of rebound tenderness are helpful in distinction. The clinical manifestations of UTI are summarised in FIGURE 25.1.

Uncomplicated urinary tract infection This is cystitis occurring in the uninstrumented nonpregnant female without structural or neurological abnormalities.

Complicated urinary tract infection4 This is associated with anatomical or functional abnormalities (e.g. diabetes, urinary calculi) that increase the risk of serious complications or treatment failure.

Urethral syndrome

Symptomatic bacteriuria

The urethral syndrome (sometimes termed abacterial cystitis) is that where the patient presents with dysuria and frequency but does not show a positive urine culture.3

This is defined as the presence of frequency, dysuria and loin pain alone or in combination, together with a significant growth of organisms on urine culture.2 The clinical differentiation between cystitis or lower UTI and kidney or upper UTI cannot be made accurately on the basis of symptoms, except in those patients with well-defined loin pain and/or tenderness.

• 30–40% of adult women with urinary symptoms have this syndrome.3 • Many actually have bacterial cystitis but a negative culture. • The organisms may be anaerobic or fastidious in their culture requirements. • The organisms may include Ureaplasma, Chlamydia and viruses.

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• The urine may have antiseptic contamination or residual antibiotic. • The infection may be undergoing spontaneous resolution at the time of the culture. 3

Interstitial cystitis

This is an uncommon but important cause of the urethral syndrome. • The classic symptoms are frequency day and night and a dull suprapubic ache relieved briefly by bladder emptying. • The feature is small haemorrhages on distension of the bladder.

Symptoms Generalised fever chills sweating rigors headache nausea vomiting diarrhoea

indicate kidney infection

Upper tract loin pain abdominal pain

• Treatment is hydrodistension ± a course of tricyclics, for example amitriptyline.

Laboratory diagnosis The laboratory diagnosis of UTI depends on careful collection, examination and culture of urine.

Collection of urine1 It is best to collect the first urine passed in the morning, when it is highly concentrated and any bacteria have been incubated in the bladder overnight. Preferably the urine should be taken to the laboratory

Physical examination (check the following) General temperature pulse respiration blood pressure

loin tenderness ? mass

25 Lower tract dysuria frequency urgency feeling of incomplete bladder emptying suprapubic discomfort strangury

suprapubic tenderness

haematuria

offensive urine

FIGURE 25.1 Clinical manifestations of urinary tract infection

Consider vaginal examination rectal examination (males)

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immediately, but it can be stored for up to 24 hours at 4°C to prevent bacterial multiplication. • Clean catch midstream specimen of urine (MSU). This is best collected from a full bladder, to allow at least 100 mL of urine to be passed before collection of the MSU. It is important that the urine flow is continuous, and the container is moved in and out of the stream collecting at least 20 mL. — In women, a tampon should first be inserted and the vulva washed with clean water (to avoid contamination with vaginal and vulval organisms). Sit on the toilet and swing one knee to the side as far as possible. The labia are then held apart with the fingers of one hand to prevent contact with the urinary stream while the specimen is collected after passing a small amount of urine into the toilet. — In males, the foreskin (if present) is retracted and the glans washed with clean water. — In children a midstream clean catch (MCC) is useful (although prone to contamination) especially in the hands of experienced collectors. The parent holds the child over a sterile bowl placed under cleansed genitalia. • Catheter specimen of urine (CSU). In women who have difficulty with collecting an uncontaminated MSU (as is commonly the case in the elderly, the infirm and the grossly obese), a short open-ended catheter can be inserted and a specimen collected after 200 mL has flushed the catheter. • Suprapubic aspirate of urine (SPA). This is an extremely reliable way to detect bacteriuria in neonates and in patients where UTI is suspected but cannot be confirmed because of low colony counts or contamination in an MSU. Under local anaesthetic, a needle (lumbar puncture needle in adults) is inserted into the very full bladder about 1–2 cm above the pubic symphysis, and 20 mL is collected by a syringe. Any organisms in an SPA specimen indicate UTI (see FIG. 25.2).

FIGURE 25.2 Suprapubic aspiration of urine in a child

Dipstick testing Dipstick findings of urinary leucocytes or nitrite are suggestive of UTI and may be an indication for empirical treatment if asymptomatic. The reagents in dipstick testing are generally sensitive but have to be interpreted with care. Leucocyte esterase dipsticks are useful in detecting pyuria and give a good guide to infection with a specificity of 94–98% (2–6% false positive) and 74–96% sensitivity (4–26% false negatives).5 Positive nitrite dipsticks give a useful guide to the presence of bacteria. Unexplained haematuria detected by dipstick analysis needs investigation.

Microscopic examination The urine is examined under a microscope to detect pyuria (more than 10 pus cells—WBCs—per highpowered field) but should be examined in a counting chamber to calculate the number of WBCs/mL of urine. In the counting chamber pyuria is >8000  WBC/mL in phase-contrast microscopy. Pyuria is a very sensitive sign of UTI. Vaginal squames and debris indicate contamination.

Urine specimen collection in children

Culture of the urine

All children with a first UTI require investigation. It is diagnosed by significant growth on MSU, CSU, MCC or SPA.

The nature and number of organisms present in the urine are the most useful indicators of UTI.1

• • • • •

Bag specimen: cannot diagnose UTI MSU—usually by 3–4 years when cooperative MCC—practical and reliable SPA—reliable and the best option CSU—for failed SPA or those unable to void on request

• Most common are enteric organisms. Escherichia coli (especially) and Staphylococcus saprophyticus are responsible for over 90% of UTIs, with other Gram-negative organisms (Klebsiella sp. and Proteus sp.), enterococci sp. and Grampositive cocci (Streptococcus faecalis and other staphylococci) also responsible.

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• Infections due to organisms other than E. coli (e.g. Pseudomonas sp.) are suggestive of an underlying kidney tract abnormality. • If >105 colony forming units (cfu) per mL of bacteria are present in an MSU, it is highly likely that the patient has a UTI. • On the other hand, it is most important to realise that up to 30% of women with acute bacterial cystitis have less than 105 cfu/mL in the MSU. For this reason, it is reasonable to treat women with dysuria and frequency even if they have 2 per year • confirmed sterile pyuria • other features of kidney disease, e.g. haematuria Basic investigations include: MCU—microscopy and culture (post-treatment)

Summary: MCU (microscopy and culture urine)

Kidney function tests: plasma urea and creatinine, eGFR

Significant levels for UTI: • Microscopy: WBC >10 per mL (10 × 106/L) • Culture: counts >105 cfu/mL (108/L)

Special considerations:

Other investigations • FBE, ESR/CRP, blood culture (if febrile and unwell), consider U&E, PSA (men)

Acute uncomplicated cystitis Advice to women (especially if recurrent attacks):

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• Keep yourself rested. • Drink a lot of fluid: 2–3 cups of water at first and then 1 cup every 30 minutes. • Try to empty your bladder completely each time. • Gently wash or wipe your bottom from front to back with soft, moist tissues after opening your bowels (for prevention in recurrent attacks). • Use analgesics such as paracetamol for pain. • Make the urine alkaline by taking sodium citrotartrate (4 g orally 6 hourly)—not if taking nitrofurantoin.

UTI: basic management • • • • • • •

Urine dipstick Microculture (clean catch) First-line antibiotics—trimethoprim or cephalexin Alkaliniser for severe dysuria High fluid intake Check sensitivity—leave or change ABs Repeat MCU within 48 hours after AB course

Consider further investigation (see TABLE 25.1)

Intravenous urogram (IVU) and/or ultrasound

In children: micturating cystogram In adult males: consider prostatic infection studies if IVU normal In severe pyelonephritis: ultrasound or IVU (urgent) to exclude obstruction In pregnant women: ultrasound to exclude obstruction

Treatment (non-pregnant women)3 Multiple dose therapy is preferred to single dose therapy. Use for 5 days in women (trimethoprim—3 days). Use for 10 days in women with known urinary tract abnormality: • trimethoprim 300 mg (o) daily for 3 days (first choice) or • cephalexin 500 mg (o) daily for 5 days or • amoxycillin/+ clavulanate 500/125 mg (o) 12 hourly for 5 days or • nitrofurantoin 50 mg (o) 6 hourly for 5 days or • norfloxacin 400 mg (o) 12 hourly for 3 days (if resistance to above agents proven and if susceptible) Caution about tendonopathy, including rupture. Follow-up: MCU 1–2 weeks later. Note: • Avoid using important quinolones—norfloxacin or ciprofloxacin—as first-line agents.

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Urinary tract infection • Cotrimoxazole is not first line because it has no advantage over trimethoprim and has more side effects. • Treatment failures are usually due to a resistant organism or an underlying abnormality of the urinary tract. Pregnant women4 UTI in pregnant women requires careful surveillance. Asymptomatic bacteriuria should always be excluded during early pregnancy because it tends to be blown into a full infection. Treatment of acute cystitis (empirical): • cephalexin 500 mg (o) 12 hourly for 5 days or • nitrofurantoin 100 mg (o) 12 hourly for 5 days or • amoxycillin + clavulanate 500/125 mg (o) 12 hourly for 5 days Repeat MCU at least 48 hours after completion. Asymptomatic bacteriuria should be treated with a week-long course. Refer to CHAPTER 109. Adult males4 Consider the cause (see risk factors above). Investigations: MCU, U&E, ultrasound. Treatment (empirical, while awaiting investigation): • trimethoprim 300 mg (o) daily for 14 days or • cephalexin 500 mg (o) 12 hourly for 14 days or • amoxycillin + clavulanate 500/125 mg (o) 12 hourly for 14 days Note: all males with a UTI should be investigated to exclude an underlying abnormality, e.g. prostatitis, obstruction.

Acute pyelonephritis Mild cases can be treated with oral therapy alone using double the dosage of drugs recommended for uncomplicated cystitis, except for trimethoprim when the same dosage is recommended. Treatment should be continued for 10 days. Ciprofloxacin (500 mg (o) 12 hourly) or norfloxacin (400 mg (o) 12 hourly) is used for 10 days if resistance to these drugs is proven. For severe infection with suspected septicaemia, admit to hospital and treat initially with parenteral antibiotics for 2 to 5 days after taking urine for microscopy and culture and blood for culture.

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• amoxycillin 2 g IV 6 hourly4 plus • gentamicin 4–6 mg/kg/day, single daily IV dose Follow with oral therapy for a total of 14 days. Drug levels of gentamicin require monitoring. Gentamicin can be replaced with IV cefotaxime or ceftriaxone. All patients should be investigated for an underlying urinary tract abnormality.

Recurrent or chronic urinary tract infections Recurrent infections occur as a relapse of a previously treated infection or because of re-infection, often with differing organisms. Persistent (chronic) UTIs indicate that the organism is resistant to the antimicrobial agents employed or that there is an underlying abnormality such as a kidney stone or a chronically infected prostate in the male patient. Such infections may be treated with prolonged courses of an appropriate antibiotic or removal of the focus of infection.6 In men and children, an anatomical abnormality is usual, while recurrent cystitis in women often occurs despite a normal tract. In men, instruction on perineal hygiene, more frequent bladder emptying and post-intercourse voiding may assist in the prevention of re-infection. Treatment4 A 10- to 14-day course of: • amoxycillin/potassium clavulanate (500/125 mg) (o) 12 hourly or • trimethoprim 300 mg (o) once daily or • cephalexin 500 mg (o) 12 hourly or • norfloxacin 400 mg (o) 12 hourly (if proven resistance to above agents) Prevention including antibiotic prophylaxis4 In some female patients with recurrent UTI a single dose of a suitable agent within 2 hours after intercourse is adequate but, in more severe cases, courses may be taken for 3–6 months or on occasions longer. Adult doses given: • trimethoprim 150 mg (o) nocte or • cephalexin 250 mg (o) nocte

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or • norfloxacin 200–400 mg (o) nocte (if proven resistance to others)

Cranberries A recent Cochrane review on the use of cranberries (Vaccinium macrocarpon) for the prevention of UTI concluded that there was evidence to recommend cranberry juice or tablets for the prevention of recurrent symptomatic UTIs in women, but poor evidence for its use in the treatment of UTI, in the management of asymptomatic bacteriuria, or in the prevention of UTIs in children.7,8 An appropriate regimen is 150 mL cranberry juice or one tablet (1:30 parts concentrated juice) twice daily.

Urinary tract infection in children

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By the age of 10 years, about 3% of boys9 and 10% of girls will have had at least one episode of a urinary tract infection. UTI in infants and very young children is often kidney in nature and may be associated with generalised symptoms such as fever, vomiting, diarrhoea and failure to thrive. Offensive urine may be noted. Causes of ‘smelly’ urine in children are urinary infection and/or dehydration especially with gastroenteritis. Symptoms of dysuria and frequency appear only after the age of 2 years when the child is able to indicate the source of the discomfort. In a girl or boy (rare presentation) with symptoms of dysuria and frequency an underlying abnormality is likely to be present with a reported incidence of vesicoureteric reflux (VUR) as high as 40% and scarred kidneys (reflux nephropathy) in 27%.3 Thus the early detection of children with VUR and control of recurrent kidney infection could prevent the development of scars, hypertension and chronic kidney failure. Radiological investigation of children with UTIs shows normal kidneys in approximately 66% and reflux in approximately 33%. It is best to perform the ultrasound first and within the first 3 days for a febrile UTI. A urine specimen is essential before antibiotics are given.

Guidelines for investigation10 •

1 year—ultrasound

The dimercaptosuccinic acid scintigraph scan is the gold standard for diagnosis of kidney scarring and measurement of differential kidney function. It is usually reserved for children with dilating VUR.

Treatment (mild infection in children)4,5 Empirical treatment in children 12 months or more while awaiting culture results. Treatment should be taken orally for 5 days: • trimethoprim 4 mg/kg (max. 150 mg) bd (suspension is 50 mg/5 mL) or • cephalexin 12.5 mg/kg (max. 500 mg) bd or • cotrimoxazole 4/20 mg/kg, (max. 160/800 mg) bd or • amoxycillin/potassium clavulanate 12.5/3.1 mg/kg (max. 500/125 mg) orally bd Norfloxacin and ciprofloxacin should be avoided routinely in children unless required on MCU. Check MCU in 3 weeks. Severe infections in children4 For empirical treatment in those ≥12  months who appear septic or are vomiting, and infants 1 month’s duration); or bronchitis, pneumonitis or oesophagitis • histoplasmosis, disseminated or extrapulmonary • isosporiasis, chronic intestinal (>1 month’s duration) • Kaposi sarcoma • lymphoma, Burkitt (or equivalent term) • lymphoma, immunoblastic (or equivalent term) • lymphoma, primary, of brain • Mycobacterium avium complex of M. kansasii, disseminated or extrapulmonary • Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary) • Mycobacterium, other species or unidentified species, disseminated or extrapulmonary • Pneumocystis jiroveci pneumonia (PJP) General fever night sweats lethargy/malaise anorexia pharyngitis arthralgia myalgia lymphadenopathy

Dermatopathic maculopapular rash roseola-like rash alopecia urticaria (diffuse) desquamation herpes simplex reactivation herpes zoster

• Salmonella septicaemia, recurrent • toxoplasmosis of brain • wasting syndrome due to HIV The Australian AIDS surveillance case definition does not refer to the CD4 cell count although in the US AIDS is also defined by a CD4 cell count of 500 cells/μL)

Immune depletion:

CD4 cell count per μL

1000

fever myalgia arthralgia adenopathy malaise rash meningoencephalitis

500

Guillain-Barré syndrome chronic demyelinating neuropathy

tinea

idiopathic thrombocytopenia

seborrhoeic dermatitis

reactive arthritis

gingivitis polymyositis warts, molluscum contagiosum Bell palsy tuberculosis Sjögren syndrome herpes zoster oral candidiasis sinusitis herpes simplex hairy leucoplakia cryptosporiodiosis Kaposi sarcoma PJP lymphoma (NHL) toxoplasmosis cervical intraepithelial neoplasia cryptococcosis MAC Primary CNS NHL CMV

200

0 0

Intermediate Advanced (500 cells/μL > CD4 > 200 cells/μL) (CD4 < 200 cells/μL)

10 weeks

5 years

10 years

FIGURE 27.3 Chronology of HIV-induced disease correlated with time since infection Source: GJ Steward. Could it be HIV? 1. The challenge: clinical diagnosis of HIV. The Medical Journal of Australia, 1993; 158: 31–4 © Copyright 1993, The Medical Journal of Australia—reproduced with permission.

Management Patients with HIV infection require considerable psychosocial support, counselling and regular assessment from a non-judgmental, caring practitioner. The holistic approach Most people with HIV infection will take ‘natural therapies’. This should be viewed as being complementary to the management suggested by the GP, and the patient should be encouraged to tell his or her doctors of the alternative medicines being taken. Anecdotal reports suggest that 75% of people with HIV regularly use ‘natural therapies’,8 and in the setting of the long-term nature of the condition it is important for doctors to be supportive and create a climate of acceptance around these practices. Positive lifestyle factors include:

27

• a very healthy balanced diet: high fruit and vegetable intake, pure fruit juices, high fibre, low fat, high complex carbohydrates • toxic avoidance: processed foods, caffeine, illicit drugs, alcohol, cigarettes • relaxation and meditation (reduction and selfmonitoring of stress levels)

• appropriate sleep and exercise • consider supplementary antioxidants • support groups and continuing counselling Treatment (medication)8,9,10 Optimal antiretroviral therapy (ART) now depends on the use of combinations of drugs. Monotherapy is no longer accepted practice. The recommendations for the use of antiretroviral therapy are constantly changing. Updated guidelines can be found on the internet at , , or . Viral resistance is the limiting factor, no matter how potent an individual drug may be at reducing viral load initially. The trials of combined zidovudine and lamivudine demonstrated both a more sustained decrease in plasma viral load than either drug did alone, and a more delayed development of viral resistance. There are now many antiretroviral drugs available for use in Australia (see TABLE 27.4) and clinicians have a much wider scope of treatments available. However, many questions remain about combination therapy and further trials using viral load as a clinical endpoint should provide pointers for treatment. Currently

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Table 27.4

313

265

Currently available antiretroviral drugs9

Nucleoside RT* inhibitors Non-nucleoside RT (NRTIs) inhibitors (NNRTIs) • • • • • • • •

abacavir (ABC) zidovudine (AZT) didanosine (DDI) emtricitabine (FTC) stavudine (D4T) lamivudine (3TC) AZT + 3TC (Combivir) AZT + 3TC + abacavir (Trizivir) • tenofovir (TFV)**

• • • • •

nevirapine (NEV) delavirdine (DLV) efavirenz (EFV) etravirine (ETR) rilpivirine (RPV)

Protease inhibitors (HIV PIs)

Fusion (entry) inhibitors

Integrase inhibitors

• • • •

• enfuvirtide (T20) • maraviroc (MVC)≠ 

• raltegravir (RAL)

• • • •

saquinavir (SQV) indinavir (IDV) ritonavir (RTV) fosamprenavir (FAPV) lopinavir/ritonavir (LPV) atazanavir (ATZ) tipranavir (TPV) darunavir (DRV)

Combination of classes • Atripla (TFV, EFV, FTC) • Eviplera (TFV, FTC, RPV)

* RT = reverse transcriptase ** a nucleotide analogue RTI ≠ a CCR5 antagonist

the use of three drugs, referred to as highly active antiretroviral therapy (HAART), is favoured. There are many possible combinations. Side effects, which are often severe—including cardiovascular disease—and affect the quality of life, remain a problem. Resistance to HAART is now a problem. Effective (90%) results have been achieved with TRIO (etravirine, darunavir and raltegravir) therapy.11 Subcutaneous injections of interleukin-2 have been shown to boost immunity.

When to start1,12 This is a controversial issue. CD4 cell count guidelines: • 8 same antibiotics according to weight; 3  days in reasonably well child on antibiotics.3

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Infections of the central nervous system

Table 30.1

339

291

CSF findings in meningitis Bacterial (pyogenic)

Tuberculosis

Viral

CSF appearance

Cloudy/pus

Opalescent

Usually clear

CSF pressure

↑ ↑ ↑

↑ ↑ or N

↑ or N

Predominant cell

Neutrophils

Lymphocytes

Lymphocytes

Cell count/mm3

100–1000 +

50–1000

10–1000

Glucose

↓ ↓ ↓ 

↓ ↓ 

Normal

Fulminating • Dramatic sudden-onset shock, purpura (does not blanch on pressure) ± coma • Usually due to meningococcal septicaemia, also H. influenzae type B, Streptococcus pneumoniae Note: septic shock may ensue without signs of meningitis. FIGURE 30.1 Kernig sign: pain in hamstrings on passive knee extension with hip flexed at 90°

Treatment (suspected meningitis)4 First: oxygen + IV access and consult • Take blood for culture (within 30 minutes of assessment)—ideally prior to hospitalisation • For child give bolus of 10–20 mL/kg of N saline with added bolus up to total 60 ml/kg if signs of hypoperfusion • Admit to hospital for lumbar puncture (preliminary CT scan to assess safety of LP in adults) • Dexamethasone 0.15 mg/kg up to 10 mg IV (start at same time as antibiotics—shown to improve outcome) • Ceftriaxone 4 g (child: 100 mg/kg up to 4 g) IV statim then daily for 4 days or cefotaxime 2 g (child: 50 mg/kg up to 2 g) IV 6 hourly for 3–5 days Note: IV preferable but IM or interosseous better than nothing. Antibiotics of proven effectiveness are cefotaxime, ceftriaxone, meropenem and penicillin. Treatment (meningococcaemia— all ages) Treatment is extremely urgent once suspected (e.g. petechial or purpuric rash on trunk and limbs) (see FIG. 30.3). It should be given before reaching hospital. Empirical treatment is:

FIGURE 30.2 Opisthotonos caused by advanced meningitis

• benzylpenicillin 60 mg/kg IV (max. 2 g) statim (continue for 5 days)

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Encephalitis1,2 Encephalitis is inflammation of the brain parenchyma. It is mainly caused by viruses although other organisms including some bacteria, Mycoplasma, Rickettsia and Histoplasma can cause encephalitis. Suspect it when a viral prodrome is followed by irrational behaviour, altered conscious state and possibly cranial nerve lesions.

30

Clinical features These can vary from mild to severe. FIGURE 30.3 Meningococcaemia with typical early purpuric rash in a 2-year-old child

• if IV access not possible give IM or • ceftriaxone 100 mg/kg IV or IM (max 4 g) statim then daily for 5 days Note: Penicillin dose guide for suspected meningitis in child: 60

Diabetes mellitus

Family history

Hypertension

Aboriginal or Torres Strait Islander origin

Smoking Obesity—BMI ≥30

The clinical approach History A hallmark of early-stage CKF is a non-specific history and examination, and the diagnosis is very difficult in the absence of a known past history of kidney disease. The diagnosis can be established only by kidney function tests. Symptoms from CKF are rare unless the creatinine clearance is less than 20% of normal and only become common when less than 10% of normal. In patients with chronic kidney disease, symptomatic uraemia may be precipitated by prerenal factors, such as fluid loss from vomiting or diarrhoea, infection, antibiotic therapy especially tetracyclines, or increasing hypertension. Symptoms and signs The symptoms and signs of CKF are summarised in FIGURE 31.1. The common early presenting symptoms are generally non-specific and referable to the GIT, presumably due to the formation of ammonia in the upper GIT. However, anaemia is the main cause of symptoms. Such symptoms include: • • • • • • •

malaise anorexia, nausea, vomiting tiredness/lethargy nocturia restless legs pruritus dyspnoea

If a patient presents with these symptoms and has a sallow ‘lemon’ tinge appearance due to a combination of anaemia and brownish pigmentation, then CKF should be highly suspected. DxT  fatigue + a/n/v + sallow skin

CKF

Physical examination6 General inspection of the patient with CKF will usually reveal a sallow complexion with yellow-brown pigmentation in the skin, which is often dry and pruritic. The patient’s mental state should be noted. The respiratory and pulse rates are usually rapid because of anaemia and metabolic acidosis. Other findings may include bruising, uraemic fetor, reduced mental status, pericarditis and peripheral neuropathy. The abdomen should be carefully palpated, especially

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Chronic kidney failure

Anaemia lethargy pallor

Haematological anaemia bruising epistaxis

confusion twitching fits coma

severe uraemia

hyperparathyroidism (secondary) Cardiovascular heart failure hypertension pericarditis

Skin pruritus scratch marks pigmentation purpura yellow tinge

Gastrointestinal tract anorexia, nausea vomiting hiccoughs diarrhoea

Flapping tremor Musculoskeletal muscle weakness bone pain restless legs cramps twitching

Renal polyuria nocturia

Genital erectile impotence infertility amenorrhoea Urine haematuria proteinuria

Periphery peripheral neuropathy oedema

FIGURE 31.1 Clinical features of chronic kidney failure

in the kidney areas. A rectal examination is indicated to detect prostatomegaly or other rectal or pelvic pathology. Ophthalmoscopic examination may show hypertensive or diabetic retinopathy. Urinalysis should test glucose, blood and protein. This involves a dipstick testing on the first morning specimen. Proteinuria should be confirmed with a 24-hour urine protein estimation or (preferably) an albumin creatinine ratio (ACR).

ACR guidelines Normoalbuminuria Men: 35 mg/mmol

Investigations • Urine dipstick (poor sensitivity and specificity)1 • 24-hour urine protein • Albumin creatinine ratio • Microculture of urine

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• Kidney function tests (most appropriate for the GP): — plasma urea — plasma creatinine — creatinine clearance (more precise) — eGFR (the new standard) • Plasma electrolytes: — sodium, potassium, chloride, bicarbonate — calcium and phosphate • Consider: — magnesium, urate, glucose — lipids — prescribed drug level — cardiac studies — full blood count ? anaemia — protein electrophoresis (? myeloma) — ANA for lupus — ANCA for vasculitis • Determination of underlying cause: — imaging of urinary tract—ultrasound — immunological tests — kidney biopsy Biochemical changes—elevation of: — potassium — phosphate — creatinine and urea — urinary protein — hydrogen ions → acidosis; anion group Monitoring CKD The traditional test in identifying and monitoring CKD is the serum creatinine level.7 The normal range is about 40–120 μmol/L (0.04–0.12 mmol/L) but the laboratory will indicate their appropriate reference level. However, serum creatinine is an unreliable and insensitive marker of CKD. To improve detection and management guidelines laboratories now report on estimated glomerular filtration rate (eGFR) using the CKP-EPI (chronic kidney disease epidemiology collaboration) formula with every request for serum creatinine concentration, which is required to calculate to GFR.8 Although common in older people, an eGFR 0.5 g/day

Raynaud’s phenomenon

Arthritis mainly PIP joints of hand

nail-fold hyperaemia

Tendonitis myalgia (muscle pain) Avascular necrosis (e.g. femoral head)

Haematological anaemia leucopenia lymphopenia thrombocytopenia

peripheral neuropathy

Arthritis small joints of feet

FIGURE 32.2 Clinical features of SLE

• dsDNA antibodies—90% specific for SLE but present in only 60% (key test) • ENA antibodies, especially Sm—highly specific • Rheumatoid factor—positive in 50% • LE cell test—inefficient and not used

Management4 • Appropriate explanation, support and reassurance, use of sunscreens (refer to CHAPTER 123) • Refer to consultant rheumatologist for shared care in a multidisciplinary team

The diagnosis cannot be made on blood tests alone. Supportive clinical evidence is necessary.

Treatment2 Based on severity and organ involved.

For suspected SLE, the recommended approach is to perform an ANA test. If positive then order dsDNA and ENA antibodies.

• Mild: NSAIDs (for arthralgia) • Moderate (especially skin, joint serosa involved): low-dose antimalarials (e.g. hydroxychloroquine up to 6 mg/kg once daily) (e.g. 400 mg (o) daily for 3 months, then 200 mg daily long term)

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Connective tissue disease and the vasculitides • Consider: fish body oil 0.2 mg/kg (o) daily • Severe: corticosteroids are the mainstay (e.g. prednisolone 7.5–15 mg (o) daily): immunosuppressive drugs (e.g. azathioprine, methotrexate with folic acid, rituximab) may be used for severe arthralgia • Avoid drugs in those in clinical remission and with normal complement levels. • Other treatments, such as plasma exchange and immunosuppressive regimens, are available for severe disease. • Keep in mind antiphospholipid antibody syndrome, especially with recurrent fetal loss and thrombotic episodes.

Scleroderma (systemic sclerosis) This can present as a polyarthritis affecting the fingers of the hand in 25% of patients, especially in the early stages. Soft tissue swelling produces a ‘sausage finger’ pattern. Scleroderma mainly affects the skin, presenting with Raynaud phenomenon in over 85% of patients (see FIG. 32.3). There are three clinical variants: 1 limited cutaneous disease, for example, morphea 2 cutaneous with limited organ involvement (CREST) 3 diffuse systemic disease (systemic sclerosis)

32 DxT finger discomfort + arthralgia + GORD (± skin tightness) scleroderma

Diagnosis2,5 • ESR may be raised • Normocytic normochromic anaemia may be present • ANA test—up to 90% positive (relatively specific) • Rheumatoid factor—positive in 30% • Anticentromere antibodies—specific (positive in 90% with limited disease and 5% with diffuse)

dysphagia heartburn reflux respiratory symptoms (e.g. fibrosis) Cardiac disorders arrhythmias pericarditis pulmonary artery hypertension renal failure Fingers ‘sausage’ fingers sclerodactyly digital ulceration Raynaud phenomenon telangiectasia calcinosis

FIGURE 32.3 Clinical features of scleroderma

307

Clinical features • Female to male ratio = 3:1 • A progressive disease of multiple organs • Raynaud phenomenon • Stiffness of fingers and other skin areas (see FIG. 32.4) • ‘Bird-like’ facies (mouth puckered) • Dysphagia and diarrhoea (malabsorption) • Oesophageal dysmotility • Respiratory symptoms: pulmonary fibrosis • Cardiac symptoms: pericarditis, etc. • Look for tight skin on chest (Roman breastplate)

Characteristic facies taut and immobile puckering of mouth narrow nose thin lips radial wrinkling upper lip

tight skin on chest

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FIGURE 32.4 Scleroderma showing stiff, taut skin of fingers

• Antitopoisomerase I (anti-Scl-70) antibody is specific but only positive in 20–40% • Skin biopsy—increase in dermal collagen

Clinical features • Any age group • Peak incidence 40–60 years • Female to male ratio = 2:1 • Muscle weakness and wasting proximal limb muscles • Main complaint is weakness • Muscle pain and tenderness in about 50% • Arthralgia or arthritis in about 50% (resembles distribution of rheumatoid arthritis) • Dysphagia in about 50% due to oesophageal involvement • Raynaud phenomenon • Consider associated malignancy: lung and ovary DxT weakness + joint and muscle pain + violaceous facial rash dermatomyositis

heliotrope-coloured photosensitivity rash

Management • Refer to consultant for shared care • Empathic explanation, patient education • Analgesics and NSAIDs for pain • Avoid vasospasm (no smoking, beta blockers, ergotamine): calcium channel blockers such as nifedipine may help Raynaud • Treat malabsorption if present; skin emollients • D-penicillamine can help if there is significant systemic or cutaneous involvement6

proximal muscle weakness and wasting

rash on dorsum of hands

Localised scleroderma • Morphea—plaques of erythema with violaceous periphery, feels hard; mainly on trunk • Linear—may be ‘en coup de sabre’ (a sabre stroke)

CREST syndrome

rash on knees

Clinical features • Calcinosis • Raynaud phenomenon • Oesophageal dysmotility • Sclerodactyly • Telangiectasia • Anticentromere antibody (invariably positive)

Polymyositis and dermatomyositis Polymyositis is an uncommon systemic disorder with inflammation of skin and muscle whose main feature is symmetrical muscle weakness and wasting involving the proximal muscles of the shoulder and pelvic girdles.

FIGURE 32.5 Clinical features of polymyositis/ dermatomyositis

The rash The distinctive rash shows features of photosensitivity. There is heliotrope violet discolouration of the eyelids (see FIG. 32.6), forehead and cheeks, and possible

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DxT dry eyes + dry mouth + arthritis Sjögren syndrome

Diagnosis Autoantibody tests—positive ANA (ENA), Ro (SSA), La (SS-B) Schirmer’s tear test

FIGURE 32.6 Heliotrope discolouration of eyelids in dermatomyositis

erythema resembling sunburn and peri-orbital oedema. There is a characteristic rash on the hands, especially the fingers and nail folds. The knees and elbows are commonly involved. Differential diagnosis: statin-induced necrotising myositis (↑ CK levels). Diagnosis • Muscle enzyme studies (serum creatine kinase and aldolase) • Biopsies—skin and muscle • EMG studies—show characteristic pattern Treatment includes corticosteroids and cytotoxic drugs. Early referral is appropriate.

Sjögren syndrome The under-diagnosed syndrome of dry eyes (keratoconjunctivitis sicca) in the absence of rheumatoid arthritis or any other autoimmune disease is known as primary Sjögren syndrome (SS): • primary SS—limited or multisystem • secondary SS—occurs in association with other CTDs including rheumatoid arthritis (accounts for 50%) Clinical features • Fatigue • Sicca (xerostomia, dry eyes, dry vagina) • Difficulty swallowing food • Increased dental caries; denture dysfunction • Salivary gland enlargement • Xerotrachea → chronic dry cough; hoarseness • Dyspareunia • Arthralgia ± non-erosive arthritis Although considered benign can transform into non-Hodgkin lymphoma (44 times risk).

Management • Referral to rheumatologist • Treatment is symptomatic for dry eyes, mouth and vagina; arthralgia • NSAIDs, hydroxychloroquine or steroids for arthritis

Raynaud phenomenon2 (Refer also to CHAPTER 64.) It is classified as either primary (without associated disease) or secondary (when associated with any CTD). Patients with primary Raynaud may progress to a CTD but the likelihood is low (5–15%) and the delay to diagnosis is long (average of 10 years).2 The more severe the Raynaud, the more likely it is to progress to systemic disease. Raynaud is a clinical syndrome of episodic arteriolar vasospasm usually involving the fingers and toes (one or two at a time). It may also involve the nose, ear or nipple.

THE VASCULITIDES The vasculitides or vasculitis syndromes are a heterogeneous group of disorders involving inflammation and necrosis of blood vessels, the clinical effects and classification depending on the size of the vessels involved. They are a variety of CTD. Small vessel vasculitis is the common type encountered in practice. Medium vessel vasculitis includes polyarteritis nodosa and large vessel vasculitis includes giant cell arteritis. Symptoms suggestive of vasculitis include systemic (malaise, fever, weight loss, arthralgia), skin lesions (e.g. purpura, ulcers, infarction), respiratory (wheeze, cough, dyspnoea), ENT (epistaxis, sinusitis, nasal crusting), chest pain (angina), kidney (haematuria, proteinuria, CKF) and neurological (various e.g. sensorimotor).

Small vessel vasculitis This is associated with many important disorders, such as rheumatoid arthritis, SLE, bacterial endocarditis, Henoch–Schönlein purpura and hepatitis B.

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Skin lesions are usually associated with these disorders and the most common presentation is painless, palpable purpura, such as occurs with Henoch–Schönlein purpura.

Rarer but deadly causes

32

The major vasculitides called systemic vasculitides are polyarteritis nodosa (PN), polymyalgia rheumatica (PR), giant cell arteritis (GCA), Takayasu arteritis, Behçet syndrome, Churg–Strauss vasculitis and Wegener granulomatosis (WG). Unfortunately, many patients die or become terminally ill before the diagnosis is suspected.

Practice tip If a serious ANCA-associated disease is suspected, early diagnosis is life-saving because of sinister kidney damage. Perform a urine examination for haematuria and proteinuria. If positive, order an ANCA test. If positive, refer urgently.

Henoch–Schönlein purpura More details are presented about this vasculitis disorder in CHAPTER 39.

Takayasu arteritis2 Known as ‘pulseless disease’ or ‘aortic arch syndrome’, this vasculitis involves the aortic arch and other major arteries. It typically affects young Japanese female adults. Features include absence of peripheral pulses and hypertension.

Polyarteritis nodosa The hallmark of PN is necrotising vasculitis of the small and medium arteries leading to skin nodules, infarctive ulcers and other serious manifestations. The cause is unknown but associations are found with drug abusers (especially adulterated drugs), B-cell lymphomas, other drugs and hepatitis B surface antigen. It should be suspected in any multisystemic disease of obscure aetiology. Clinical features • Young to middle-aged men • Constitutional symptoms: fever, malaise, myalgia, weight loss • Migratory arthralgia or polyarthritis • Subcutaneous nodules along arterial lines • Livedo reticularis and skin ulcers • Kidney impairment and hypertension

• • • •

Cardiac disorders: arrhythmia, failure, infarction Diagnosis confirmed by biopsy or angiogram ESR raised Treatment with corticosteroids and immunosuppressants • Death is usually from kidney disease DxT arthralgia + weight loss + fever (± skin lesions) polyarteritis nodosa

Giant cell arteritis and polymyalgia rheumatica The basic pathology of this very important disease complex is GCA (synonyms: temporal arteritis, cranial arteritis). The clinical syndromes are polymyalgia rheumatica and temporal arteritis. The clinical manifestations of polymyalgia rheumatica invariably precede those of temporal arteritis, of which there is about a 20% association. The diagnosis is based on clinical grounds. No definite cause has been found. Clinical features (polymyalgia rheumatica) • Pain and stiffness in proximal muscles of shoulder and pelvic girdle, cervical spine (refer FIG. 32.7) • Symmetrical distribution • Typical ages 60–70 years (rare 50 years) polymyalgia rheumatica

Clinical features (temporal arteritis) • Headache—unilateral, throbbing (CHAPTER 56) • Temporal tenderness • Loss of pulsation of temporal artery • Jaw claudication • Biopsy of artery (5 cm) is diagnostic DxT fatigue + headache + jaw claudication temporal arteritis

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possible associated temporal arteritis

main pain distribution

Investigation • No specific test for polymyalgia rheumatica • ESR—extremely high, around 100 • C-reactive protein—elevated • Mild anaemia (normochromic, normocytic) Treatment—for uncomplicated disease

Behçet syndrome is a systemic (multiorgan) vasculitis of unknown aetiology, affecting veins and arteries of all sizes. The main feature is painful oral ulceration and the hallmark is the ‘pathergy’ reaction whereby simple trauma such as a pinprick can cause a papule or pustule to form within a few hours at the site.

There is no specific diagnostic test. Associated problems/complications: repeated uveitis and retinitis → blindness, colitis, venous thrombosis, meningoencephalitis. Treatment: high-dose steroids and specific ulcer treatment. DMARDs may be required.

Practice tip Patients with Behçet eye disease should be referred promptly for an ophthalmological opinion, which may be sight-saving.2

Prednisolone • Starting dose — temporal (giant cell) arteritis: 40–60 mg (o) daily initially for 2–4 weeks (+ aspirin 100 mg/day) then gradual reduction according to ESR/CRP — polymyalgia rheumatica: 15 mg (o) daily for 2–4 weeks, then taper • Taper down gradually to the minimum effective dose (often one lesion separate times

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Other neurological disorders such as infections (e.g. encephalitis), malignancies, spinal cord compression, spinocerebellar degeneration and others must be excluded. Investigation • Lumbar puncture: oligoclonal IgG detected in CSF in 90% of cases14 (only if necessary) • Visual evoked potentials: abnormal in about 90% of cases • MRI scan: usually abnormal, demonstrating MS lesions in about 90% of cases14

33

Course and prognosis • The course is variable and difficult to predict. An early onset (50 mg/L is a feature of appendicitis.6 A particularly severe case of apparent gastroenteritis, especially if persistent, should be regarded as pelvic appendicitis until proved otherwise.

Mesenteric adenitis This presents a difficult problem in differential diagnosis with acute appendicitis because the history can be very similar. At times the distinction may be almost impossible. In general, with mesenteric adenitis localisation of pain and tenderness is not as definite, rigidity is less of a feature, the temperature is higher, and anorexia, nausea and vomiting are also lesser features. The illness lasts about five days followed by a rapid recovery. Comparisons between the two are presented in TABLE 34.5 but if in any doubt it is advisable to consider the problem as acute appendicitis and perhaps proceed to laparoscopy/laparotomy. Mesenteric adenitis can sometimes present an anaesthetic risk and patients are usually quite ill in the immediate postoperative period. Treatment is symptomatic and includes ample fluids and paracetamol.

Recurrent abdominal pain Recurrent abdominal pain (RAP)—three distinct episodes of abdominal pain over 3 or more months— occurs in 10% of school-aged children. In only 5–10% of children will an organic cause be found so that in most cases the cause remains obscure.8 Causes (organic) An organic cause, however, must be considered and excluded. Organic disease is more likely if: • • • • • • •

the pain is other than periumbilical the pain radiates rather than remains localised the pain wakes the child from sleep the pain is accompanied by nausea and vomiting the child is not completely well between attacks there is associated weight loss there is failure to thrive

Table 34.5

389

341

Comparison of the features of acute appendicitis and mesenteric adenitis in children (guidelines only) Acute appendicitis

Mesenteric adenitis

Typical child

Older

Younger

Site of onset of pain

Midline Shifting to right

RIF Can be midline

Preceding respiratory illness

Uncommon

Invariable: URTI or tonsillitis

Anorexia, nausea, vomiting

++

±

Colour

Usually pale

Flushed: malar flush

Temperature

N or ↑ 

↑ ↑  → ↑ ↑ ↑ 

Abdominal palpation

Tender in RIF Guarding ± Rigidity

Tender in RIF Minimal guarding Usually no rigidity

Rectal examination

Invariably tender

Often tender but lesser degree

Psoas and obturator tests

Usually positive

Usually negative

Full blood examination

Leucocytosis

Lymphocytosis

RIF = right iliac fossa

Possible causes • Constipation • Childhood migraine equivalent (pain with extreme pallor) • Lactose intolerance (symptoms related to milk ingestion) • Intestinal parasites (may disturb child about 60 minutes after falling asleep) Investigations • Urine analysis and MSU • FBE and ESR • Plain X-ray (assesses faecal retention)

Non-organic RAP Clinical features Typical clinical features include: • acute and frequent colicky abdominal pain • pain localised to or just above umbilicus

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• Problem solving in general practice

no radiation of pain pain lasts less than 60 minutes nausea frequent and vomiting rare diurnal (never wakes the child at night) minimal umbilical tenderness anxious child obsessive or perfectionist personality one or both parents intense about child’s health and progress

Psychogenic factors Although psychogenic factors are very relevant in individual cases there is scant hard evidence to support the widely held hypothesis8 that such factors account for the vast majority of RAP. Some children will have obvious psychological problems or even be school avoidant, a common factor being family disruption.

34

Management8 • Give explanation, reassurance and support (ensure that the patient is involved in the discussion). • Reassurance can only be given following a careful examination and thoughtfully chosen investigations. • Avoid investigations, especially radiological if possible (FBE and MCU are okay). • Acknowledge that the child has pain. • Emphasise that the disorder is common, and usually traverses childhood without ill effects. • Recommend simple measures (e.g. local warmth, brief rest for painful episodes). • Advise review if episodes change in nature, pain persists for hours or there are new symptoms. • Identify any life stresses and provide insight therapy. • Enquire about family structures and function, and school performance. • Discourage identification with the sick role. • Refer for psychological assessment and counselling if necessary.

• biliary disorders: biliary pain and acute cholecystitis • diverticulitis • sigmoid volvulus • strangulated hernia • intestinal obstruction • cancer, especially of the large bowel • herpes zoster, causing unilateral root pain • constipation and faecal impaction Problems arise with management because the pain threshold is raised (colic in particular is less severe) and there is an attenuated response to infection so that fever and leucocytosis can be absent. Non-specific signs, such as confusion, anorexia and tachycardia, might be the only systemic evidence of infection.

Abdominal aortic aneurysm An AAA may be asymptomatic until it ruptures or may present with abdominal discomfort and a pulsatile mass noted by the patient. There tends to be a family history and thus screening is appropriate in such families. Ultrasound screening is advisable in first-degree relatives over 50 years. The risk of rupture is related to the diameter of the AAA and the rate of increase in diameter. The normal diameter of the abdominal aorta, which is palpated just above the umbilicus, is 10–30 mm, being 20 mm on average in the adult; an aneurysm is greater than 30 mm in diameter.9 Greater than 50 mm is significantly enlarged and is chosen as the arbitrary reference point to operate because of the exponential rise in risk of rupture with an increasing diameter. Refer all cases. The patency of a Dacron graft after 5 years is approximately 95% (see FIG. 34.5). normal

aneurysm

significant

Abdominal pain in the elderly The elderly can suffer from a wide spectrum of disorders. Ischaemic events, emboli, cancer (in particular) and diverticulae of the colon are more common in old age; duodenal ulcer is less so. Those causes of abdominal pain that occur with more frequency include: • vascular catastrophies: ruptured AAA, mesenteric artery occlusion • perforated peptic ulcer

dangerous

3

5

6

Diameter in cm

FIGURE 34.5 Guidelines for normal and abnormal widths of the abdominal aorta in adults (to exact scale)

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Abdominal pain

391

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Investigations • Ultrasound (good for screening) in relatives >50 years (obesity a problem) • CT scan (clearer imaging). Helical/spiral scan is investigation of choice. • MRI scan (best definition)

Rupture of aneurysm This is a real surgical emergency in an elderly person who presents with acute abdominal and perhaps back pain with associated circulatory collapse (see FIG.  34.6). The patient often collapses at toilet because they feel the need to defecate and the resultant Valsalva manoeuvre causes circulatory embarrassment.

? atrial fibrillation

FIGURE 34.7 Typical pain distribution of mesenteric arterial occlusion

pulsatile mass

Clinical features • Abdominal pain—gradually becomes intense (see FIG. 34.7) • Profuse vomiting • Watery diarrhoea—blood in one-third of patients (later) (refer CHAPTER 44) • Patient becomes confused

DxT anxiety and prostration + intense central pain + profuse vomiting ± bloody diarrhoea mesenteric arterial occlusion FIGURE 34.6 Typical pain distribution of a ruptured abdominal aortic aneurysm

The patient should be transferred immediately to a vascular surgical unit, which should be notified in advance. Two important emergency measures for the ‘shocked’ patient are intravenous access for plasma expanding fluid (a central venous line is best if possible) and swift action. DxT intense pain + pale and ‘shocked ± back pain ruptured AAA

Mesenteric artery occlusion Acute intestinal ischaemia arises from superior mesenteric artery occlusion from either an embolus or a thrombosis in an atherosclerotic artery. Another cause is an embolus from atrial fibrillation. Necrosis of the intestine soon follows if intervention is delayed.

Signs • Localised tenderness, rigidity and rebound over infarcted bowel (later finding) • Absent bowel sounds (later) • Shock develops later • Tachycardia (may be atrial fibrillation and other signs of atheroma) Investigations • CRP may be elevated intestinal alkaline phosphatase. • X-ray (plain) shows ‘thumb printing’ due to mucosal oedema on gas-filled bowel. CT scanning gives the best definition while mesenteric arteriography is performed if embolus is suspected. However, it is commonly only diagnosed at laparotomy.

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Management Early surgery may prevent gut necrosis but massive resection of necrosed gut may be required as a lifesaving procedure. Early diagnosis (within a few hours) is essential. Note: • Mesenteric venous thrombosis can occur but usually in patients with circulatory failure. • Inferior mesenteric artery occlusion is less severe and survival more likely.

Acute retention of urine

34

Acute retention of urine usually causes severe lower abdominal pain, which may not be apparent in a senile or demented person. Apart from the common cause of an enlarged prostate or prostatitis it can also result from bladder neck obstruction by faecal loading or other pelvic masses or anticholinergic drugs. It is often precipitated by extreme cold or an excess of alcohol. Neurogenic causes include multiple sclerosis, spinal injury and diabetes. Management • Perform a rectal examination and empty rectum of any impacted faecal material. • Catheterise with size 14 Foley catheter to relieve obstruction and drain (give antibiotic cover). • Have the catheter in situ and seek a urological opinion. Send specimen for MCU. • If there is any chance of recovery (e.g. if the problem is drug-induced), withdraw drug, leave catheter in for 48 hours, remove and give trial of prazosin 0.5 mg bd or terazosin. • Check for prostate cancer and renal impairment.

Faecal impaction Faecal impaction is encountered typically in the aged, bedridden, debilitated patient. It may closely resemble malignant obstruction in its clinical presentation.10 Spurious diarrhoea can occur, which is known as ‘faecal incontinence’ (see CHAPTER 36).

Acute appendicitis Acute appendicitis is mainly a condition of young adults but it affects all ages (although uncommon under 3 years). It is the commonest surgical emergency and special care has to be taken with the very young and the very old. The symptoms can vary because of the different positions of the appendix. It is basically a clinical diagnosis.

Clinical features See FIGURE 34.8. Typical clinical features are: • maximum incidence 20–30 years • initial pain is central abdominal (sometimes colicky) • increasing severity and then continuous • shifts and localises to RIF within 6 hours • may be aggravated by walking (causing a limp) or coughing • sudden anorexia • nausea and vomiting a few hours after the pain starts • ± diarrhoea and constipation

DxT localised RIF pain + a/n/v + guarding  acute appendicitis

Signs • Patient looks unwell • Flushed at first, then pale • Furred tongue and halitosis • May be febrile • Tenderness in RIF, usually at McBurney point • Local rigidity and rebound tenderness • Guarding • ± Superficial hyperaesthesia

First central abdominal pain (visceral pain)

Later RIF pain (somatic pain) McBurney point

FIGURE 34.8 Typical pain distribution of acute appendicitis

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Abdominal pain • ± Psoas sign: pain on resisted flexion of right leg, on hip extension or on elevating right leg (due to irritation of psoas especially with retrocaecal appendix) • ± Obturator sign: pain on flexing patient’s right thigh at the hip with the knee bent and then internally rotating the hip (due to irritation of internal obturator muscle) • Rovsing sign: tenderness in RIF while palpating in LIF • PR: anterior tenderness to right, especially if pelvic appendix or pelvic peritonitis

Variations and cautions • Abscess formation → localised mass and tenderness • Retrocaecal appendix: pain and rigidity less and may be no rebound tenderness; loin tenderness; positive psoas test • Pelvic appendix: no abdominal rigidity; urinary frequency; diarrhoea and tenesmus; very tender PR; obturator tests usually positive • Elderly patients: pain often minimal and eventually manifests as peritonitis; can simulate intestinal obstruction • Pregnancy (occurs mainly during second trimester): pain is higher and more lateral; harder to diagnose; peritonitis more common • Perforation more likely in the very young, the aged and the diabetic Investigations Few investigations including imaging are of value:

345

Small bowel obstruction The symptoms depend on the level of the obstruction (see TABLE 34.6). The more proximal the obstruction, the more severe the pain. Table 34.6

Small bowel obstruction: difference between a high and a low obstruction High

Low

Frequency of spasms

3–5 minutes

6–10 minutes

Intensity of pain

+ + +

+

Vomiting

Early, frequent Violent

Later Less severe

Gastric juices, then green

Faeculent (later)

Dehydration and degree of illness

Marked

Less prominent

Distension

Minimal

Marked

Content:

Main causes • Outside obstruction (e.g. adhesions— commonest cause, previous laparotomy), strangulation in hernia or pockets of abdominal cavity (see FIG. 34.9)—this may lead to a ‘closed loop’ obstruction.13 • Lumen obstructions (e.g. foreign body, trichobezoar, gallstones, intussusception, malignancy).

• blood cell count shows a leucocytosis (75%) with a left shift • urea and electrolytes—to assess hydration prior to surgery • CRP—elevated • plain X-ray may show local distension, blurred psoas shadow and fluid level in caecum • ultrasound shows a thickened appendix (75–90% sensitivity, 80–100% specificity);11 affected by gas shadow • CT scan also accurate and allows other causes, especially in the female pelvis, to be evaluated12 • laparoscopy • β-HCG Management Immediate referral for surgical removal. If perforated, cover with cefotaxime and metronidazole.

393

FIGURE 34.9 Operative findings (corrugated drainage material) in a 65-year-old man with subacute bowel obstruction after a 21-year history of nagging abdominal pain following a cholecystectomy

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Clinical features • Severe colicky epigastric and periumbilical (mainly) pain (see FIG. 34.10) • Spasms last about 1 minute • Spasms every 3–10 minutes (according to level) • Vomiting • Absolute constipation (nil after bowel emptied) • No flatus • Abdominal distension (especially if lower SBO) DxT colicky central pain + vomiting + distension SBO

Management • IV fluids and bowel decompression with nasogastric tube • Laparotomy or hernia repair

Large bowel obstruction The cause is commonly colon cancer (75% of cases), especially on the left side, but it can occur in diverticulitis or in volvulus of the sigmoid colon (10% of cases) and caecum.10 Sigmoid volvulus is more common in older men and has a sudden and severe onset. The pain is less severe than in SBO. Be wary of the non-surgical causes, simple constipation or acute pseudo-obstruction of the colon (Ogilvie syndrome). Consider ileus. Clinical features • Sudden-onset colicky pain (even with cancer) • Each spasm lasts less than 1 minute • Usually hypogastric midline pain (see FIG. 34.11) • Vomiting may be absent (or late) • Constipation, no flatus

34 check umbilicus and hernial orifices

DxT colicky pain + distension ± vomiting LBO

?

FIGURE 34.10 Typical pain distribution of small bowel obstruction

Signs and tests • Patient weak and sitting forward in distress • Visible peristalsis, loud borborygmi • Abdomen soft (except with strangulation) • Tender when distended • Increased sharp, tinkling bowel sounds • Dehydration rapidly follows, especially in children and elderly • PR: empty rectum, may be tender Note: check all hernial orifices, including umbilicus • X-ray: plain erect film confirms diagnosis ‘stepladder’ fluid levels (4–5 for diagnosis) in 3–4 hours — Gastrografin follow-through for precise diagnosis with caution. It can cause severe diarrhoea and may be therapeutic in adhesive obstruction. • ± CT scan (especially if extrinsic causation)

FIGURE 34.11 Typical pain distribution of large bowel obstruction

Signs and tests • Increased bowel sounds, especially during pain • Distension early and marked • Local tenderness and rigidity

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Abdominal pain • PR: empty rectum; may be rectosigmoid cancer or blood. Check for faecal impaction • X-ray: distension of large bowel with separation of haustral markings, especially caecal distension — sigmoid volvulus shows a distended loop — gastrografin enema confirms diagnosis Management • Drip and suction • Surgical referral

Perforated peptic ulcer Perforation of a peptic ulcer can cause acute abdominal pain both with and without a prior history of peptic ulcer. It is an acute surgical emergency requiring immediate diagnosis. Consider a history of drugs, especially NSAIDs and H2-receptor antagonists. Perforated ulcers may follow a heavy meal. There is usually no back pain. May be painless with steroids. The maximal incidence is 45–55 years, most common in males, and a perforated duodenal ulcer is more common than a gastric ulcer. Consider the clinical syndrome in three stages: 1 prostration 2 reaction (after 2–6 hours)—symptoms improve 3 peritonitis (after 6–12 hours) Clinical features See FIGURE 34.12. Typical clinical features are: • sudden-onset severe epigastric pain • continuous pain but lessens for a few hours • epigastric pain at first, and then generalised to whole abdomen

347

• pain may radiate to one or both shoulders (uncommon) or right lower quadrant • nausea and vomiting (delayed) • hiccough is a common late symptom DxT sudden severe pain + anxious, still, ‘grey’, sweaty + deceptive improvement perforated peptic ulcer

Signs and tests (typical of peritonitis) • Patient lies quietly (pain aggravated by movement and coughing) • Pale, sweating or ashen at first • Board-like rigidity • Guarding • Maximum signs at point of perforation • No abdominal distension • Contraction of abdomen (forms a ‘shelf’ over lower chest) • Bowel sounds reduced (silent abdomen) • Shifting dullness may be present • Pulse, temperature and BP usually normal at first • Tachycardia (later) and shock later (3–4 hours) • Breathing is shallow and inhibited by pain • PR: pelvic tenderness • X-ray: chest X-ray may show free air under diaphragm (in 75%)—need to sit upright for prior 15 minutes — limited Gastrografin meal can confirm diagnosis — CT scan is accurate Management • Pain relief • Drip and suction (immediate nasogastric tube) • Broad-spectrum antibiotics • Immediate laparotomy after resuscitation • Conservative treatment may be possible (e.g. later presentation and Gastrografin swallow indicates sealing of perforation)

Ureteric colic Kidney renal colic is not a true colic but a constant pain due to blood clots or a stone lodged at the pelvic– ureteric junction; ureteric colic, however, presents as severe true colicky pain due to stone movement and ureteric spasm. Fortunately, the majority of urinary calculi are small and will pass spontaneously. Guidelines: FIGURE 34.12 Typical features of perforated peptic ulcer with typical pain radiation

395

• loin pain—stone in kidney • kidney/ureteric colic—ureteric stone • strangury—stone in bladder

34

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Clinical features • Maximum incidence 30–50 years (M > F) • Intense colicky pain: in waves, each lasting 30 seconds with 1–2 minutes respite • Begins in loin and radiates around the flank to the groin, thigh, testicle or labia (see FIG. 34.13) • Usually lasts 60 years RA haemophilia spondyloarthropathies sarcoidosis gout Ankle RA spondyloarthropathies gout

FIGURE 35.2 Joints typically affected by various arthropathies

polyarthritis, Lyme disease, rubella, Brucella, hepatitis B, gonococcus, mycoplasma, HIV tests, parvovirus and Barmah Forest virus. In reference to viral serology, a positive immunoglobulin M (IgM) antibody test is presumptive evidence of recent infection and is likely to be of diagnostic significance in this clinical context. However, sometimes IgM antibodies can persist for months or years.6 A positive IgG antibody result indicates previous exposure to the virus but a single positive titre is of no diagnostic significance. Seroconversion or at least a fourfold rise on paired sera confirms recent infection (see FIG. 35.3).

Plain X-ray is invaluable, although in some conditions radiological changes may be apparent only when the disease is well established. Typical X-ray changes for common conditions are presented in FIGURE 35.4. Arthrography has limited value in the diagnosis of polyarthritis but is very useful for specific joints such as the shoulder and the knee. Ultrasound examination for joints such as the shoulder and the hip can be very useful. HLA-B27 should not be used for arthritis screening. It has a high sensitivity for ankylosing spondylitis, but low specificity, and should rarely be ordered.6

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Arthritis

Table 35.2

Appropriate tests can be selected from the following: • urine analysis: blood, protein, sugar • synovial fluid: analysis, culture • radiology—plain X-ray • blood and other cultures • haemoglobin and differential WCC • ESR • C-reactive protein • serum uric acid, creatinine • 24-hour urinary uric acid • rheumatoid factor • anti-CCP (cyclic citrullinated peptide) antibody • antinuclear antibody (screening test for SLE) • dsDNA antibodies • extractable nuclear antigen (ENA) antibodies • HLA-B27 (poor predictive value) • various specific serological tests (e.g. Australian epidemic polyarthritis, rubella, Lyme disease, hepatitis B, Barmah Forest virus, parvovirus) • HIV serology • antistreptolysin O titre • streptococcal anti-DNase B • arthroscopy and biopsy • bone scan

Rheumatoid arthritis cysts joint destruction subluxation erosion joint margins osteoporosis

35 Osteoarthritis

Antibody titre

lgG

periarticular bone sclerosis

marginal osteophytes loss of joint space

cysts

0

weeks

361

Normal joint

Investigations for arthritis

lgM

409

months Time

FIGURE 35.3 Time course of IgG and IgM antibodies in viral arthritis

The various immunological tests for diagnosis of the connective tissue disorders are outlined with the description of each condition. Such screening tests include: • rheumatoid factor and anti-CCP • antinuclear antibodies • dsDNA antibodies The LE cell test has been superseded by the antinuclear, dsDNA and ENA (especially Sm) antibody

Gout

punched out erosions

cyst

FIGURE 35.4 X-rays for common arthritic conditions: typical changes

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tests but the latter should only be performed if there is an elevated ANA test.6

Arthritis in children Arthralgia (joint pain) is a common problem in childhood and, although arthritis is rare, the complaint demands considerable respect because of the many serious problems causing it. Arthritis may be part of an infectious disease such as rheumatic fever, rubella, mumps, varicella, cytomegalovirus infection, erythema infectiosum (human parvovirus), influenza or other viral infection, and is occasionally encountered with Henoch–Schönlein purpura. Actually, viral arthritis is very common in children. An FBE is helpful as it may show lymphopaenia, lymphocytosis or atypical lymphocytes.1 It is worth noting that underlying bone tumours can be present as joint pain if the tumour is adjacent to the joint. A checklist of causes is presented in TABLE 35.3. Note: Acute-onset monoarticular arthritis associated with fever is septic until proven otherwise.

Juvenile idiopathic arthritis

35

JIA, also known as juvenile chronic arthritis and juvenile rheumatoid arthritis (US), is defined as a chronic arthritis persisting for a minimum of 6 weeks (some criteria suggest 3 months) in one or more joints in a child younger than 16 years of age.5 It is rare, affecting only about 1 in 1000 children, but produces profound medical and psychosocial problems. The commonest types of JIA are oligoarticular (pauciarticular) arthritis, affecting four or fewer joints (about 50%), and polyarticular arthritis, affecting five or more joints (about 40%). Systemic onset arthritis, previously known as Still syndrome, accounts for about 10% of cases. It is usually seen in children under the age of 5 but can occur throughout childhood. The children can present with a high remittent fever and coppery red rash, plus other features, including lymphadenopathy, splenomegaly and pericarditis. Arthritis is not an initial feature but develops ultimately, usually involving the small joints of the hands, wrists, knees, ankles and metatarsophalangeal joints. These children should be referred once the problem is suspected or recognised. JIA is not a benign disease—50% have persistent active disease as adults. Rheumatic fever typically occurs in children and young adults, the first attack usually occurring between 5 and 15 years of age.

Table 35.3

Arthritis in children: causes to consider

Infections Rheumatic fever Septic arthritis Meningococcaemia Osteomyelitis Reactive arthritis (post-infectious) Tuberculosis Viral infections (e.g. parvovirus, rubella, HIV) Inflammation—chronic arthritis Juvenile idiopathic/chronic arthritis Subtypes: • Oligo (pauci) articular • Seropositive polyarticular (juvenile RA) • Seronegative polyarticular • Systemic onset arthritis (Still disease) • Enthesitis related arthritis • Psoriatic juvenile arthritis Haematological disorders Thalassaemia Sickle-cell anaemia Haemophilia Neoplasms Leukaemia Lymphoma Neuroblastoma Orthopaedic conditions Perthes disease Slipped upper femoral epiphyses Chondromalacia Others Henoch–Schönlein purpura Kawasaki syndrome Scurvy; rickets Traumatic arthritis Osteochondritis Psychogenic rheumatism Malignant tumour: • bone • cartilage • synovium

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Arthritis in perspective Five per cent of all children complain of recurrent lower limb pain, which often awakens them from their sleep. There may be emotional factors involved and parents need appropriate reassurance. A careful history and physical examination are essential, and perhaps simple basic investigations may be appropriate. As Rudge5 points out, we have to be vigilant against underdiagnosis, misdiagnosis and overdiagnosis. Refer to growing pains (see CHAPTER 91) and postactivity musculoskeletal pain (see CHAPTER 66).

Arthritis in the elderly OA is very common with advancing age and for this reason care has to be taken not to simply attribute other causes of arthritis to OA. Other musculoskeletal conditions that become more prevalent with increasing age are: • • • • • •

polymyalgia rheumatica Paget disease of bone avascular necrosis gout pseudogout (pyrophosphate arthropathy) malignancy (e.g. bronchial carcinoma)

Pseudogout This crystal deposition arthropathy (chondrocalcinosis) is noted by its occurrence in people over 60 years. It usually affects the knee joint but can involve other joints.

Rheumatoid arthritis Although it usually begins between the ages of 30 and 40 it can occur in elderly patients, when it occasionally begins suddenly and dramatically. This is called ‘explosive’ RA and fortunately tends to respond to small doses of prednisolone and has a good prognosis.7 RA in the elderly can present as a polymyalgia rheumatica syndrome.

Rheumatic fever RF is an inflammatory disorder that typically occurs in children and young adults following a group A Streptococcus pyogenes infection. It is common in developing countries and among Indigenous Australians (see CHAPTER 137) but uncommon in first world countries.8 Clinical features • Young person 5–15 years (can be older) • Acute-onset fever, joint pains, malaise

411

363

• Flitting arthralgia mainly in leg (knees, ankles) and arm (elbows and wrists) • One joint settles as the other is affected • May follow a sore throat However, the symptoms depend on the organs affected and arthritis may be absent. Diagnosis Based on clinical criteria: 2 or more major criteria or 1 major + 2 or more minor criteria in the presence of supporting evidence of preceding Group A streptococcal infection.

Major criteria • • • • •

Carditis Polyarthritis Chorea (involuntary abnormal movements) Subcutaneous nodules Erythema marginatum

Minor criteria • • • • •

Fever (≥38°C) Previous RF or rheumatic heart disease Arthralgia Raised ESR >30 mm/hr or CRP >30 mg/L ECG—prolonged PR interval

Investigations A selective combination of: • • • • • • •

FBC throat swab ESR streptococcal ASOT streptococcal anti-DNase B (repeat in 10–14 days) C-reactive protein plus ECG and echocardiogram (if ↑ PR) and CXR.

Treatment • Rest in bed until CRP normal for 2 weeks • Benzathine penicillin 900 mg IM (450 mg in child 0.42 mmol/L in men, > 0.36 mmol/L in women)

Table 35.6

Crystals Monosodium urate

371

Crystal-induced disorders Associated disease/ syndrome Acute gout Tophaceous gout Asymptomatic Chronic gouty arthritis

Calcium pyrophosphate dihydrate (CPPD)

419

Acute pseudogout Destructive arthropathy (like RA)

Typical joints or region affected Metatarsophalangeal joint of big toe Also: other foot joints, ankle, knee and patellar bursa, wrist, fingers Knee, wrist In older people >60 years (average age 72) F >M (2.7:1)

Asymptomatic (most common) Basic calcium phosphate

Acute calcific periarthritis

Shoulder (supraspinatus)

Destructive arthropathy Acute arthritis

• Absence of clinical manifestations • Usually does not warrant treatment Clinical features Typical clinical features of gout include:8 • mainly a disorder of men (5–8% prevalence) • onset earlier in men (40–50) than women (60+) • acute attack: excruciating pain in great toe (see FIG. 35.11), early hours of morning • skin over joint—red, shiny, swollen and hot • exquisitely tender to touch • relief with colchicine, NSAIDs, corticosteroids • can subside spontaneously (3 to 10 days) without treatment Causes/precipitating factors • Alcohol excess (e.g. binge drinking) • Surgical operation • Starvation • Drugs (e.g. frusemide, thiazide diuretics) • Chronic kidney disease • Myeloproliferative disorders • Lymphoproliferative disorders (e.g. leukaemia) • Sugary soft drinks21

35

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• Problem solving in general practice • Elevated serum uric acid (up to 30% can be within normal limits with a true acute attack)19 • X-ray: punched out erosions at joint margins Management Management of gout includes these principles: • • • • •

FIGURE 35.12 Gout showing typical red, shiny, swollen arthritis of the first MTP joint with desquamation of the skin

good advice and patient education information provision of rapid pain relief preventing further attacks prevention of destructive arthritis and tophi dealing with precipitating factors and comorbid conditions (e.g. alcohol dependence, obesity, CKD, polycythaemia vera, diabetes, hypertension)

The acute attack8,21 NSAIDs, in full dosage, are first-line and effective.

• • • •

Cytotoxic agents (tumour lysis) Hypothyroidism Low-dose aspirin Others

The arthritis

35

Monoarthritis in 90% of attacks: • MTP joint great toe—75% • other joints—usually lower limbs: other toes, ankles, knees Polyarticular onset is more common in old men and may occur in DIP and PIP joints of fingers. No synovial joint is immune. Refer to FIGURE 35.13.

Other features • Prone to recurrence • Tophi in ears, elbows (olecranon bursa), big toes, fingers, Achilles tendon (take many years) • Can cause patellar bursitis • Can get cellulitis (does not respond to antibiotics)

Nodular gout Develops in postmenopausal women with kidney impairment taking diuretic therapy who develop pain and tophaceous deposits around osteoarthritic interphalangeal (especially DIP) joints of fingers. Diagnosis • Synovial fluid aspirate → typical uric acid crystals using compensated polarised microscopy; this should be tried first (if possible) as it is the only real diagnostic feature

indomethacin 50 mg (o) tds (if tolerated) until symptoms abate (up to 3–5 days), then taper to 25 mg tds until cessation of the attack If extreme: indomethacin 100 mg (o) statim, 75 mg 2 hours later (if tolerated), then 50 mg (o) tds for 24–48 hours, then 50–75 mg/day. Note: Any other NSAID can be used. Add an antiemetic (e.g. metoclopramide 10 mg (o) tds) or Colchicine: colchicine 0.5 mg (o) statim, then 0.5 mg every 6 or 8 hours until pain relief (usually 24–28 hours) or diarrhoea develops (max. 6 mg/24 hours) Note: • Must be given early • Avoid if kidney impairment • Avoid use with macrolide antibiotics e.g. clarithromycin especially in CKD • Avoid long-term use Consider: • corticosteroids: intra-articular following aspiration and culture (gout and sepsis can occur together); a digital anaesthetic block is advisable. An oral course can be used: start with prednisolone 40 mg/day for 4 days then decrease gradually over 10 days22 • corticotrophin (ACTH) IM in difficult cases (e.g. synthetic ACTH: tetracosactrin 1 mg IM) Note: • Avoid aspirin and urate pool lowering drugs (probenecid, allopurinol, sulphinpyrazone) • Monitor kidney function and electrolytes

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Arthritis Common sites

421

373

Indications:

Less common

• • • •

frequent acute attacks tophi or chronic gouty arthritis kidney stones or uric acid nephropathy hyperuricaemia Adverse effects:

• rash (2%) • severe allergic reaction (rare) Precautions:

DIP joints

knees

metatarsophalangeal joint–great toe

ankles toes

FIGURE 35.13 Gout: possible joint distribution

Long-term therapy When acute attack subsides preventive measures include: • weight reduction • a normal, well-balanced diet • avoidance of purine-rich food, such as organ meats (liver, brain, kidneys, sweetbread), tinned fish (sardines, anchovies, herrings), shellfish and game • reduced intake of alcohol • reduced intake of sugary soft drinks23 • good fluid intake (e.g. water—2 litres a day) • avoidance of drugs such as diuretics (thiazides, frusemide) and salicylates/low-dose aspirin • wearing comfortable shoes Prevention (drug prophylaxis) Allopurinol (a xanthine oxidase inhibitor) is the drug of choice: dose 100–300 mg daily.

• beware of kidney insufficiency and elderly patients—use lower doses • beware of drug interactions: — azathioprine and 6 mercaptopurine— potentially lethal — amoxycillin—prone to rashes

Method: treatment of intercritical and chronic gout • Commence 6–8 weeks after last acute attack. • Start with 50 mg daily for the first week and increase by 50 mg weekly to maximum 300 mg. • Check uric acid level after 4 weeks: aim for level 60 Pseudogout

M = F

>60 especially >70

Knee

Polymyalgia rheumatica

FM 3:1

>60

Morning stiffness and pain ESR ↑ ↑ ↑ in girdles, esp. shoulder Joints normal or osteoarthritic

ESR

Source: After Hart26

Practice tips • • • • • •

•

Morning stiffness and pain, improving with exercise = RA. Flitting polyarthritis and fever = rheumatic fever; ?endocarditis; ?SLE. Polyarthritis (usually PIPs) and rash = viral arthritis or drug reaction. If rheumatoid arthritis involves the neck, beware of atlantoaxial subluxation and spinal cord compression. If the patient is young—think of SLE. If a patient returns from overseas with arthralgia, think of drug reactions, hepatitis, Lyme disease, but if the pain is intense consider dengue fever. Consider the possibility of Lyme disease in people with a fever, rash and arthritis who have been exposed to tick bites in rural areas.

•

•

If a patient presents with Raynaud phenomenon and arthritis, especially of the hands, consider foremost RA, SLE and systemic sclerosis. Avoid the temptation to apply on doubtful grounds a broad label such as arthritis or rheumatoid, or a precise diagnosis such as RA, and introduce drugs.27 TABLE 35.7 presents the diagnostic guidelines.26

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Gout • Osteoarthritis • Rheumatoid arthritis

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References

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1 Hart FD. Practical Problems in Rheumatology. London: Dunitz, 1985: 77. 2 Cormack J, Marinker M, Morrel D. Practice: A Handbook of Primary Health Care. London: Kluwer-Harrop Handbooks, 1980; 3 (61): 1–12. 3 Lassere M, McGuigan L. Systemic disease presenting as arthritis: a diagnostic approach. Aust Fam Physician, 1991; 20: 1683–714. 4 Carroll GJ, Taylor AL. Drug-induced musculoskeletal syndromes. Current Therapeutics, 2000; Feb: 47–50. 5 Rudge S. Joint pain in children: assessing the serious causes. Modern Medicine Australia, 1990; May: 113–21. 6 Barraclough D. Rheumatology symptoms: will investigation make a difference? Aust Fam Physician, 2001; 30 (4): 322–6. 7 Kumar PJ, Clarke ML. Clinical Medicine (7th edn). London: Saunders, 2009: 523–9. 8 Moulds R (Chair). Therapeutic Guidelines: Rheumatology (Version 2). Melbourne: Therapeutic Guidelines Ltd, 2010. 9 Barton S (ed.). Clinical Evidence. London: BMJ Publishing Group, 2001: 808–18. 10 Felson DT. Weight and osteoarthritis. J Rheumatol Suppl, 1995; 43: 7–9. 11 Day R. COX-2 Specific inhibitors: should I prescribe them? Current Therapeutics, 2000; Feb: 9–11. 12 Osteoarthritis—have COX-2s changed its management? NPS News, 2001; 18: 1–6. 13 Reginster JY et al. A controlled trial of glucosamine for osteoarthritis of the knee. Lancet, 2001; 357: 251–6. 14 McAlindon J, Felson DT. Nutrition: risk factors for osteoarthritis. Ann Rheum Dis, 1997; 56: 397–442.

15 Shmerling RH, Delbanco TL. How useful is the rheumatoid factor? An analysis of sensitivity, specificity and predictive value. Arch Intern Med, 1992; 152: 2417–20. 16 Brooks P. Rheumatoid arthritis. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 446–9. 17 Ostor A, McColl G. What’s new in rheumatoid arthritis. Aust Fam Physician, 2001; 30 (4): 314–20. 18 Reilly P, Littlejohn G.  Current treatment concepts in arthritis. Aust Fam Physician, 1989; 18: 1499–1509 19 Cleland LG, James MJ, Proudman SM. Fish oil: what the prescriber needs to know. Arthritis Research and Therapy, 2006; 8 (1): 202–11. 20 Hall S. Crystal arthritis: a clinician’s view. Aust Fam Physician, 1991; 20: 1717–24. 21 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013. 22 Janssens H, Janssen M et al. Use of oral prednisolone or naproxen for treatment of gout arthritis: a double blind randomised equivalence trial. Lancet, 2008; 371 (9627): 1854–60. 23 Choi HK, Curham G. Soft drinks, fructose consumption and the risk of gout in men: prospective cohort study. BMJ online, 31 January 2008: 39449.819271 BE. 24 Edmonds JP. Spondyloarthropathies. Med J Aust, 1997; 166: 214–18. 25 Vilitanen JV et al. Fifteen months follow up of intensive inpatient physiotherapy and exercise in ankylosing spondylitis. Clin Rheumatol, 1995; 14: 413–19. 26 Hart FD. Early clinical diagnosis of 12 forms of arthritis. Modern Medicine Australia, 1989: March: 34–40. 27 Kincaid-Smith P, Larkins R, Whelan G (eds). Problems in Clinical Medicine. Sydney: MacLennan and Petty, 1989: 391.

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Duncan ill with very bad piles—operated on last night, or, since that sounds alarming, lanced. Can’t really sympathise with that particular disease, though the pain is terrible. Must laugh. Virginia Woolf , Diary entry Anorectal problems are common in family practice and tend to cause anxiety in the patient that is often related to the fear of cancer. This fear may be well founded for many instances of rectal bleeding and lumps. It is important to keep in mind the association between haemorrhoids and large bowel cancer. Anorectal problems include: • • • • •

Common anorectal conditions are illustrated in FIGURE 36.1.

ANORECTAL PAIN (PROCTALGIA) The patient may complain that defecation is painful or almost impossible because of anorectal pain.

Causes Pain without swelling:

pain lumps discharge bleeding pruritus

• • • •

anal fissure anal herpes ulcerative proctitis proctalgia fugax

rectal polyp

internal sphincter external sphincter

ischiorectal abscess

dentate line

perianal abscess

ischiorectal fistula

perianal haematoma

FIGURE 36.1 Common anorectal conditions

anal fissure

prolapsed (4th-degree) haemorrhoid

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• solitary rectal ulcer • tenesmus Painful swelling: • • • • •

perianal haematoma strangulated internal haemorrhoids abscess: perianal, ischiorectal pilonidal sinus fistula-in-ano (intermittent)

Anal fissure Anal fissures cause pain on defecation and usually develop after a period of constipation (may be a brief period) and tenesmus. Other associations are childbirth and opioid analgesics.1 Sometimes the pain can be excruciating, persisting for hours and radiating down the back of both legs. Anal fissures, especially if chronic, can cause minor anorectal bleeding (bright blood) noted as spotting on the toilet paper.

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Examination On inspection the anal fissure is usually seen in the anal margin, situated in the midline posteriorly (6  o’clock)—90% of fissures. The fissure appears as an elliptical ulcer involving the lower third of the anus from the dentate line to the anal verge (see FIG. 36.2).1 Digital examination and sigmoidoscopy are difficult because of painful anal sphincter spasm. If there are multiple fissures, Crohn disease should be suspected. These fissures look different, being indurated, oedematous and bluish in colour. In chronic anal fissures a sentinel pile is common and in long-standing cases a subcutaneous fistula is seen at the anal margin, with fibrosis and anal stenosis.1

Red flag pointers for anorectal pain • • • • •

Weight loss Change in bowel habits Fever >38°C Recurrent (consider Crohn disease) Exquisitely painful PR (consider abscess)

Treatment Management is conservative with avoidance of hard stools and warm salt (sitz) baths after bowel movements. A high residue diet and avoidance of constipation (aim for soft bulky stools) may lead to resolution and long-term prevention. A combined local anaesthetic and corticosteroid ointment applied to the fissure can provide relief and promote healing. Topical local anaesthetic applied before passing a stool may relieve pain but not promote healing. Hot baths relax the internal anal sphincter. An acute anal fissure will usually heal spontaneously or within a few weeks of a treatment of high-fibre diet, sitz baths or laxatives.2 A conservative treatment is the application of diluted glyceryl trinitrate ointment (e.g. Rectogesic 2% three times daily for 6 weeks to the lower anal canal) with a gloved finger gently inserted into the anal canal. It achieves healing rates of about 50%.3,4 Transient headache is the main adverse effect. Lateral internal sphincterotomy is indicated in patients with a recurrent fissure and a chronic fissure with a degree of fibrosis and anal stenosis.5 This surgical procedure is very effective. An alternative ‘chemical’ sphincterotomy, which is as effective as surgical treatment, is injection of botulinum toxin into the sphincter.

Proctalgia fugax (levator ani spasm) Clinical features • Episodic fleeting rectal pain • Varies from mild discomfort to severe spasm • Last 3–30 minutes • Often wakes patient from sound sleep • Can occur any time of day • A functional bowel disorder • Affects adults, usually professional males

FIGURE 36.2 Anal fissure with prominent skin tag situated in the mid posterior position of the anal verge: the 6 o’clock position

Management6 • Explanation and reassurance • An immediate drink (preferably hot) and local warmth

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Anorectal disorders • Salbutamol inhaler (2 puffs statim) worth a trial Alternatives include glyceryl trinitrate spray for the symptom or possibly anti-spasmodics, calcium channel blockers and clonidine.

Solitary rectal ulcer syndrome These ulcers occur in young adults; they can present with pain but usually present as the sensation of a rectal lump causing obstructed defecation and bleeding with mucus. The ulcer, which is usually seen on sigmoidoscopy about 10 cm from the anal margin on the anterior rectal wall, can resemble cancer. Management is difficult and a chronic course is common. Treatment includes a high residue diet and the avoidance of constipation.

Tenesmus Tenesmus is an unpleasant sensation of incomplete evacuation of the rectum. It causes the patient to attempt defecation at frequent intervals. The most common cause is irritable bowel syndrome. Another common cause is an abnormal mass in the rectum or anal canal, such as cancer (e.g. prostate, anorectal), haemorrhoids or a hard faecal mass. In some cases, despite intensive investigation, no cause is found and it appears to be a functional problem.

Perianal haematoma A perianal haematoma (thrombosed external haemorrhoid) is a purple tender swelling at the anal margin caused by rupture of an external haemorrhoidal vein following straining at toilet or some other effort involving a Valsalva manoeuvre. The degree of pain varies from a minor discomfort to severe pain. It has been described as the ‘five day, painful, self-curing pile’, which may lead to a skin tag. Management Surgical intervention is recommended, especially in the presence of severe discomfort. The treatment depends on the time of presentation after the appearance of the haematoma. 1 Within 24 hours of onset. Perform simple aspiration without local anaesthetic using a 19 gauge needle while the haematoma is still fluid. 2 From 24 hours to 5 days of onset. The blood has clotted and a simple incision under local anaesthetic over the haematoma with deroofing with scissors (like taking the top off a boiled egg) to remove the thrombosis by squeezing

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is recommended. Removal of the haematoma reduces the chances of the development of a skin tag, which can be a source of anal irritation. 3 Day 6 onwards. The haematoma is best left alone unless it is very painful or (rarely) infected. Resolution is evidenced by the appearance of wrinkles in the previously stretched skin.

Follow-up The patient should be reviewed in 4 weeks for rectal examination and proctoscopy, to examine for any underlying internal haemorrhoid that may predispose to further recurrence. Prevention includes an increased intake of dietary fibre and avoidance of straining at stool. intake of dietary fibre and avoidance of straining at stool.

Strangulated haemorrhoids A marked oedematous circumferential swelling will appear if all the haemorrhoids are involved. If only one haemorrhoid is strangulated, proctoscopy will help to distinguish it from a perianal haematoma. Initial treatment is with rest and ice packs and then haemorrhoidectomy at the earliest possible time. It is best to refer for urgent surgery.

Perianal abscess This is caused by infection by polymicrobial organisms of one of the anal glands that drain the anal canal. Clinical features • Severe, constant, throbbing pain • Fever and toxicity • Hot, red, tender swelling adjacent to anal margin • Non-fluctuant swelling Careful examination is essential to make the diagnosis. Look for evidence of a fistula. Treatment Drain via a cruciate incision, which may need to be deep (with trimming of the corners) over the point of maximal induration. A drain tube can be inserted for 7 to 10 days. Packing is not necessary.

Antibiotics If a perianal or perirectal abscess is recalcitrant or spreading with cellulitis, use: • metronidazole 400 mg (o) 12 hourly for 5–7 days plus • cephalexin 500 mg (o) 6 hourly for 5–7 days7

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Ischiorectal abscess An ischiorectal abscess presents as a larger, more diffuse, tender, dusky red swelling in the buttock. The presence of an abscess is usually very obvious but the precise focus is not always obvious on inspection. Antibiotics are of little help and surgical incision and drainage as soon as possible is necessary. A deep general anaesthetic is necessary.

Pilonidal sinus and abscess Recurrent abscesses and discharge in the sacral region (at the upper end of the natal cleft about 6 cm from the anus) caused by a midline pilonidal sinus, which often presents as a painful abscess. Once the infection has settled it is important to excise the pits, allow free drainage of the midline cavity and lateral tracks and remove all ingrown hair. Antibiotics, which should be guided by culture (e.g. cephalexin and metronidazole), are given to complement surgical drainage only if there is severe surrounding cellulitis. Pilonidal means ‘a nest of hairs’ and the problem is particularly common in hirsute young men (see FIG. 36.3). Refer for excision of the sinus network if necessary.

Fistula-in-ano5

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An anal fistula is a tract that communicates between the perianal skin (visible opening) and the anal canal, usually at the level of the dentate line. It usually arises from chronic perianal infection, especially following discharge of an abscess. It is common in patients with Crohn disease. Symptoms include recurrent abscesses, discharge of blood, pus or serous fluid, swelling and anal pain. A surgical opinion is necessary to determine the appropriate surgical

procedures, which may be complex if it traverses sphincter musculature.

ANORECTAL LUMPS Anorectal lumps are relatively common and patients are often concerned because of the fear of cancer. A lump arising from the anal canal or rectum, such as an internal haemorrhoid, tends to appear intermittently upon defecation, and reduce afterwards.1 Common prolapsing lesions include second- and third-degree haemorrhoids, hypertrophied anal papilla, polyps and rectal prolapse. Common presenting lumps include skin tags, fourthdegree piles and perianal warts (see TABLE 36.1). Table 36.1

Common anal lumps

Prolapsing lumps Second- and third-degree haemorrhoids Rectal prolapse Rectal polyp Hypertrophied anal papilla Persistent lumps Skin tag Perianal warts (condylomata accuminata) Anal cancer Fourth-degree haemorrhoids Perianal haematoma Perianal abscess

Skin tags The skin tag is usually the legacy of an untreated perianal haematoma. It may require excision for aesthetic reasons, for hygiene or because it is a source of pruritus ani or irritation. A tag may be associated with a chronic fissure. Treatment (method of excision) A simple elliptical excision at the base of the skin is made under local anaesthetic. Suturing of the defect is usually not necessary.

Perianal warts It is important to distinguish the common viral warts from the condylomata lata of secondary syphilis. Local therapy includes the application of podophyllin every 2 or 3 days by the practitioner or imiquimod.

Rectal prolapse FIGURE 36.3 Pilonidal sinus revealing a pilonidal sinus and a lateral sinus opening after shaving. It shows the characteristic tuft of hairs protruding from the midline sinus.

This is protrusion from the anus to a variable degree of the rectal mucosa (partial) or the full thickness of the rectal wall. It appears to be associated with

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Anorectal disorders constipation and chronic straining. Features can include mucus discharge, bleeding, tenesmus, a solitary rectal ulcer and faecal incontinence (75%). Visualisation of the prolapse is an important part of the diagnosis. Surgery such as rectopexy (fixing the rectum to the sacrum) is the only effective treatment for a complete prolapse.5 Temporary shrinking of a visible prolapse in an emergency situation can be achieved by a liberal sprinkling of fine crystalline sugar.

Internal haemorrhoids Haemorrhoids or piles are common and tend to develop between the ages of 20 and 50 years. About one out of two Westerners suffers from them by the time 50 is reached.3 Internal haemorrhoids are a complex of dilated arteries, branches of the superior haemorrhoidal artery and veins of the internal haemorrhoidal venous plexus (see FIG.  36.4). The commonest cause is chronic constipation related to a lack of dietary fibre. Anatomically there are three classical sites, namely 3, 7 and 11 o’clock (see FIG. 36.5).

2nd-degree internal haemorrhoid

1st-degree internal haemorrhoid

3rd-degree (prolapsed) internal haemorrhoid

383

Clinical stages and pathology3 • Stage 1: First-degree internal haemorrhoids: three bulges form above the dentate line. Bright bleeding is common. • Stage 2: Second-degree internal haemorrhoids: the bulges increase in size and slide downwards so that the patient is aware of lumps when straining at stool, but they disappear upon relaxing. Bleeding is a feature. • Stage 3: Third-degree internal haemorrhoids: the pile continues to enlarge and slide downwards, requiring manual replacement to alleviate discomfort. Bleeding is also a feature. • Stage 4: Fourth-degree internal haemorrhoids: prolapse has occurred and replacement of the prolapsed pile into the anal canal is impossible. Symptoms Bleeding is the main and, in many people, the only symptom. The word ‘haemorrhoid’ means flow of blood. Other symptoms include prolapse, mucoid discharge, irritation/itching, incomplete bowel evacuation and pain (see FIG. 36.6). Treatment Invasive treatment of haemorrhoids is based on three main procedures: rubber band ligation, cryotherapy and sphincterotomy. Injection is now not so favoured while a meta-analysis concluded that rubber band ligation was the most effective non-surgical therapy.8 Surgery is generally reserved for large strangulated piles. The best treatment, however, is prevention, and softish bulky faeces that pass easily prevent haemorrhoids. People should be advised to have a diet with adequate fibre by eating plenty of fresh fruit, vegetables, whole

perianal haematoma

FIGURE 36.4 Classification of haemorrhoids

FIGURE 36.5 Three sites of primary haemorrhoids, looking into the anus from below

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FIGURE 36.6 Severely prolapsed haemorrhoids requiring surgery

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grain cereals or bran. They should complete their bowel action within a few minutes and avoid using laxatives.

ischaemic colitis

ANAL DISCHARGE Anal discharge refers to the involuntary escape of fluid from or near the anus. The causes may be considered as follows.5 1 Continent • Anal fistula • Pilonidal sinus • STIs: anal warts, gonococcal ulcers, genital herpes • Solitary rectal ulcer syndrome • Cancer of anal margin 2 Incontinent • Minor incontinence—weakness of internal sphincter • Severe incontinence—weakness of levator ani and puborectalis 3 Partially continent • Faecal impaction • Rectal prolapse

Anal (faecal) incontinence 36

Studies have revealed that up to 1 in 10 people suffer some degree of faecal incontinence, which is a common reason for institutionalisation of the elderly.9 Patients may be reluctant to seek medical advice and doctors often do not ask specifically about the condition. The problem is as common in men as in women. Apart from ageing, risk factors include perianal injury, such as childbirth injury, anal surgery, irritable bowel syndrome and neurological disorders. If there are symptoms of anal incontinence postnatally, early referral to a physiotherapist, continence nurse adviser or colorectal surgeon is advisable.10 Among the various possible treatments there are surgical possibilities, which vary from direct sphincter repair, directed injections such as collagen and silicone into the anal sphincter, and an artificial anal sphincter (e.g. Acticon Neosphincter). A colostomy may be the last resort. It is worth keeping in mind asking patients about the possibility of this problem and knowing ‘to whom to refer’.

Rectal bleeding Patients present with any degree of bleeding from a smear on the toilet tissue to severe haemorrhage. Various causes are presented in FIGURE 36.7. Common causes are polyps, colon and rectal cancer, ischaemic colitis, diverticular disease and haemorrhoids.

carcinoma angiodysplasia carcinoma of caecum

diverticulitis

polyp

colitis

carcinoma

solitary ulcer of rectum

anal fissure

haemorrhoids

FIGURE 36.7 Various causes of rectal bleeding

Local causes of bleeding include excoriated skin, anal fissure, a burst perianal haematoma and anal cancer. A characteristic pattern of bright bleeding is found with haemorrhoids. It is usually small nonprolapsing haemorrhoids that bleed. The nature of the blood (e.g. bright red, dark red or black) and the nature of the bleeding (e.g. smear, streaked on stool, mixed with stool, massive) gives an indication of the source of the bleeding (see TABLE  36.2). Black tarry (melaena) stool indicates bleeding from the upper gastrointestinal tract and is rare distal to the lower ileum. Patients with melaena should be admitted to hospital. Frequent passage of blood and mucus indicates a rectal tumour or proctitis, whereas more proximal tumours or extensive colitis present different patterns. Substantial haemorrhage, which is rare, can be caused by diverticular disorder, angiodysplasia or more proximal lesions such as Meckel diverticulum and even duodenal ulcers. Angiodysplasias are 5  mm collections of dilated mucosal capillaries and thick-walled submucosal veins, found usually in the ascending colon of elderly patients who have no other bowel symptoms. The bleeding is persistent and recurrent. The site is identified by technetiumlabelled red cell scan or colonoscopy.

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Anorectal disorders

Table 36.2

Presentation and causes of rectal bleeding6

Bright red blood in toilet separate from faeces

Internal haemorrhoids

Bright red blood on toilet paper

Internal haemorrhoids Fissure Anal cancer Pruritus Anal warts and condylomata

Blood and mucus on underwear

Third-degree haemorrhoids Fourth-degree haemorrhoids Prolapsed rectum Mucosal prolapse Prolapsed mucosal polyp

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sigmoidoscopy3 and by colonoscopy if there are any bowel symptoms or no obvious anal cause or a doubt about a lesion causing the symptoms.

Red flag pointers for rectal bleeding

Blood on underwear (no mucus)

Ulcerated perianal haematoma Anal cancer

Blood and mucus mixed with faeces

Colorectal cancer Proctitis Colitis, ulcerative colitis Large mucosal polyp Ischaemic colitis

Blood mixed with faeces (no Small colorectal polyps mucus) Small colorectal cancer Melaena (black tarry stools)

Gastrointestinal bleeding (usually upper) with long transit time to the anus

Torrential haemorrhage (rare)

Diverticular disorder Angiodysplasia

Large volumes of mucus in faeces (little blood)

Villous papilloma of rectum Villous papilloma of colon

Blood in faeces with menstruation (rare)

Rectal endometriosis

• • • • • • • •

Age >50 years Change of bowel habit Weight loss Weakness, fatigue Brisk bleeding Constipation Haemorrhoids (may be sinister) Family history of cancer

Pruritus ani Pruritus ani, which is itching of the anus, can be a distressing symptom that is worse at night, during hot weather and during exercise. It is seen typically in adult males with considerable inner drive, often at times of stress and in hot weather when sweating is excessive. In children, threadworm infestation should be suspected. It may be part of general itching, such as with a skin disorder, or localised whereby various anorectal disorders have to be excluded. Seborrhoeic dermatitis is a particularly common underlying factor. Consider also the more uncomfortable lichen sclerosus with its ivory white sclerotic plaques, which may also be present in the genital region. Signs The skin changes can vary from minimal signs to marked pathology that can show linear ulceration, maceration or lichenification (see FIG. 36.8). Superficial skin changes can be moist and macerated or dry and scaly. Full anorectal examination is necessary.

Source: Orlay, G. Office Proctology, page 11.11 © Copyright 1987 George Orlay—reproduced with permission

The history should also include an analysis of any associated symptoms such as pain, diarrhoea or constipation, presence of lumps and a sensation of urgency or unsatisfied defecation. The latter symptoms point to a rectal cause. Associated change of bowel habit suggests a diagnosis of cancer of the rectum or left colon. Bleeding from right colon cancer is often occult, presenting as anaemia. The examination includes a general assessment, anal inspection, digital rectal examination and proctosigmoidoscopy. Even if there is an anal lesion, proximal bleeding must be excluded in all cases by

FIGURE 36.8 Lichen chronicus simplex. Lichenification from scratching with longstanding pruritus (see CHAPTER 122)

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Causes and aggravating factors • Psychological factors: — stress and anxiety — fear of cancer • Generalised systemic or skin disorders: — seborrhoeic dermatitis — eczema — lichen sclerosus — diabetes mellitus — candidiasis — psoriasis (look for fissures in natal cleft) — antibiotic treatment — worms: pinworm (threadworm) — diarrhoea causing excoriation • Local anorectal conditions: — piles — fissures — warts • Zealous hygiene • Contact dermatitis: — dyed or perfumed toilet tissue, soap, powder — clothing • Excessive sweating (e.g. tight pantyhose in summer)

36

Diagnosis • Urinalysis (? diabetes) • Anorectal examination • Scrapings and microscopy to detect organisms • Stool examination for intestinal parasites Treatment • Treat the cause (if known). • Avoid local anaesthetics, antiseptics. • Advise aqueous cream to wash anus (instead of soap). • Most effective preparations (for short12 courses): methylprednisolone aceponate 0.1% in a fatty ointment base or hydrocortisone 1% cream/ointment or hydrocortisone 1% cream with clioquinol 3% or clotrimazole 1% (especially if dermatosis and Candida suspected) If an isolated area and resistant, infiltrate 0.5 mL of triamcinolone intradermally. Fractionated X-ray therapy can be used if very severe. Patient education about anal hygiene is essential.

Practice tips for pruritus ani •

• •

• • •

Most cases of uncomplicated pruritus ani resolve with simple measures, including explanation and reassurance. Avoid perfumed soaps and powders. Use bland aqueous cream or a mild soap substitute. Otherwise prescribe a corticosteroid, especially methylprednisolone aceponate 0.1%. Once symptoms are controlled, use hydrocortisone 1%.12 Lifestyle stress and anxiety underlies most cases. In obese patients with intertrigo and excessive sweating strap the buttocks apart with adhesive tape. Consider perianal lichen simplex and lichen sclerosus in patients presenting with ‘a sore bottom’.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Anal fissure • Haemorrhoids • Pruritus ani

References 1 Gold D. Benign anal conditions: how to treat. Australian Doctor, 20 January 2012: 19–25. 2 Utzig MJ, Kroesen AJ, Buhr HJ. Conservative treatment of anal fissure. Am J Gastroenterol, 2003; 98: 968–74. 3 Lund JN, Scholefield JH. A randomised, prospective, double-blind, placebo-controlled trial of glyceryl trinitrate ointment in the treatment of anal fissure. Lancet, 1997; Jan 4: 11–13. 4 Nelson R. Nonsurgical therapy for anal fissure. Cochrane Database Syst Rev. 2006 Oct 18; (4): CD003431. 5 Schnitzler M. Benign perianal conditions. Update. Medical Observer, 23 March 2007: 31–4. 6 Moulds R (Chair). Therapeutic Guidelines: Gastrointestinal (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2011: 163–6. 7 Spicer J (Chair). Therapeutic Guidelines: Antibiotics (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2006: 88–90. 8 MacRae HM, McLeod RS. Comparison of haemorrhoidal treatments: a meta-analysis. Can J Surg, 1997; 40 (1): 14–7. 9 Kalantar JS, Howell S, Talley NJ. Prevalence of faecal incontinence and associated risk factors. Med J Aust, 2002; 176: 54–7. 10 Rieger N. Faecal incontinence: how to treat. Australian Doctor, 15 February 2008: 21–6. 11 Orlay G. Office Proctology. Sydney: Australasian Medical Publishing Company, 1987: 11–52. 12 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 3). Therapeutic Guidelines Ltd, 2009: 141–2.

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The maladies that afflict the clerks aforesaid arise from three causes; first constant sitting, secondly the incessant movement of the hand and always in the same direction, and thirdly the strain on the midline from the effort not to disfigure the books by error or cause loss to their employers. The physician Ramazzini  Thoracic (dorsal) back pain is common in people of all ages, including children and adolescents. It accounts for 10–15% of all spinal pain. Dysfunction of the joints of the thoracic spine, with its unique costovertebral joints (which are an important source of back pain), is very commonly encountered in medical practice, especially in people whose lifestyle creates stresses and strains through poor posture and heavy lifting. Muscular and ligamentous strains may be common, but they rarely come to light in practice because they are self-limiting and not severe. This dysfunction can cause referred pain to various parts of the chest wall and can mimic the symptoms of various visceral diseases, such as angina, biliary colic and oesophageal spasm. In similar fashion, heart and gall bladder pain can mimic spinal pain.

Key facts and checkpoints •

•

•

•

•

• •

The commonest site of pain in the spine is the costovertebral articulations especially the costotransverse articulation (see FIG. 37.1). Pain of thoracic spinal origin may be referred anywhere to the chest wall, but the commonest sites are the scapular region, the paravertebral region 2–5 cm from midline and, anteriorly, over the costochondral region. Thoracic (also known as dorsal) pain is more common in patients with abnormalities such as kyphosis and Scheuermann disease. Trauma to the chest wall (including falls on the chest such as those experienced in body contact sport) commonly lead to disorders of the thoracic spine. Unlike the lumbar spine the joints are quite superficial and it is relatively easy to find the affected (painful) segment. Intervertebral disc prolapse is very uncommon in the thoracic spine. The older patient presenting with chest pain should be regarded as having a cardiac cause until proved otherwise.

•

• •

•

If the chest pain is non-cardiac, then the possibility of referral from the thoracic spine should be considered. The thoracic spine is the commonest site in the vertebral column for metastatic disease. Scheuermann disease, which affects the lower thoracic spine in adolescents, is often associated with kyphosis and recurrent thoracic back pain. Always inspect the thoracic spine of the younger patient for kyphosis and scoliosis, ideally at 9 years of age. Palpation is the most important component of the physical examination.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 37.1.

Probability diagnosis The commonest cause of thoracic back pain is musculoskeletal, due usually to musculoligamentous costotransverse articulation

facet joint

costocentral articulation

intervertebral disc

FIGURE 37.1 The functional unit of the thoracic spine

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Thoracic back pain: diagnostic strategy model

Q. Probability diagnosis A. Musculoligamentous strains (mainly postural) Vertebral dysfunction Q. Serious disorders not to be missed A. Cardiovascular: • myocardial infarction • dissecting aneurysm • pulmonary infarction • epidural haematoma (blood-thinning agents) Neoplasia: • myeloma • lung (with infiltration) • metastatic disease Severe infections: • epidural abscess • pleurisy • infectious endocarditis • osteomyelitis Pneumothorax Osteoporosis

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Q. Pitfalls (often missed) A. Angina Gastrointestinal disorders • oesophageal dysfunction • peptic ulcer (penetrating) • hepatobiliary • pancreatic Herpes zoster Spondyloarthropathies Costochondritis: • Tietze syndrome Fibromyalgia syndrome Polymyalgia rheumatica Chronic infection: • tuberculosis • brucellosis Q. Seven masquerades checklist A. Depression Spinal dysfunction UTI Q. Is this patient trying to tell me something? A. Yes, quite possible with many cases of back pain.

strains caused by poor posture. However, these pains are usually transitory and present rarely to the practitioner. The problems that commonly present are those caused by dysfunction of the lower cervical and thoracic spinal joints, especially those of the midthoracic (interscapular) area.

Arthritic conditions of the thoracic spine are not relatively common although degenerative osteoarthritis is encountered at times; the inflammatory spondyloarthropathies are uncommon. The various systemic infectious diseases such as influenza and Epstein–Barr mononucleosis can certainly cause diffuse backache but should be assessed in context.

Not to be missed A special problem with the thoracic spine is its relationship with the many thoracic and upper abdominal structures that can refer pain to the back. These structures are listed in TABLE 37.2 but, in particular, myocardial infarction and dissecting aneurysm must be considered. A complex problem described by neurosurgeons is the patient presenting with severe sudden thoracic back pain caused by an epidural haematoma related to aspirin or warfarin therapy. Cardiopulmonary problems The acute onset of pain can have sinister implications in the thoracic spine where various life-threatening cardiopulmonary and vascular events have to be Table 37.2

Non-musculoskeletal causes of thoracic back pain

Heart

Myocardial infarction Angina Pericarditis

Great vessels

Dissecting aneurysm Pulmonary embolism (rare) Pulmonary infarction Pneumothorax Pneumonia/pleurisy

Oesophagus

Oesophageal rupture Oesophageal spasm Oesophagitis Oesophageal cancer

Subdiaphragmatic disorders of:

Gall bladder Stomach including ulcers Duodenum Pancreas Subphrenic collection

Miscellaneous infections

Herpes zoster Bornholm disease Infective endocarditis

Psychogenic

}

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Thoracic back pain kept in mind. The pulmonary causes of acute pain include spontaneous pneumothorax, pleurisy and pulmonary infarction. Thoracic back pain may be associated with infective endocarditis due to embolic phenomena. The ubiquitous myocardial infarction or acute coronary occlusion may, uncommonly, cause interscapular back pain, while the very painful dissecting or ruptured aortic aneurysm may cause back pain with hypotension. Osteoporosis Osteoporosis, especially in people over 60 years, including both men and women, must always be considered in such people presenting with acute pain, which can be caused by a pathological fracture. The association with pain following inappropriate physical therapy such as spinal manipulation should also be considered. Acute infections Infective conditions that can involve the spine include osteomyelitis, tuberculosis, brucellosis, syphilis and Salmonella infections. Such conditions should be suspected in young patients (osteomyelitis), farm workers (brucellosis) and migrants from South-East Asia and third world countries (tuberculosis). The presence of poor general health and fever necessitates investigations for these infections. Neoplasia Fortunately, tumours of the spine are uncommon. Nevertheless, they occur frequently enough for the full-time practitioner in back disorders to encounter some each year, especially metastatic disease. The three common primary malignancies that metastasise to the spine are those originating in the lung, breast and the prostate (all paired structures). The less common primaries to consider are the thyroid, the kidney and adrenals and malignant melanoma. Reticuloses such as Hodgkin lymphoma can involve the spine. Primary malignancies that develop in the vertebrae include multiple myeloma and sarcoma. Benign tumours to consider are often neurological in origin. An interesting tumour is the osteoid osteoma, which is aggravated by consuming alcohol and relieved by aspirin. The tumours of the spine are summarised in TABLE 37.3. The symptoms and signs that should alert the clinician to malignant disease are: • back pain occurring in an older person • unrelenting back pain, unrelieved by rest (this includes night pain)

Table 37.3

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Significant tumours affecting the thoracic and lumbar spine Benign

Malignant

Of bone

Osteoid osteoma Haemangioma Osteoblastoma Aneurysmal bone cyst Eosinophilic granuloma

Primary: • multiple myeloma • lymphomas (e.g. Hodgkin) • sarcoma

Spinal

Extradural: • lipoma • neuroma • fibroma Intradural: • neuroma • ependymoma • chordoma • meningioma

Secondary: • breast • lung • prostate • adrenals/kidney • thyroid • melanoma Direct spread: • stomach • large bowel • pancreas • uterus/cervix/ovary

Source: After Kenna and Murtagh2

Red flag pointers for thoracic back pain1 The red flag pointers are similar to those for low back pain (see CHAPTER 38). Fracture pointer Major trauma Minor trauma: • osteoporosis • female >50 years • male >60 years Malignancy pointer Age >50 Past history malignancy Unexplained weight loss Pain at rest Constant pain Night pain Pain at multiple sites Unresponsive to treatment Infection pointer Fever Night sweats Risk factors for infection Other serious conditions Chest pain/heaviness Shortness of breath, cough

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• rapidly increasing back pain • constitutional symptoms (e.g. unexplained weight loss, fever, malaise) • a history of treatment for cancer (e.g. excision of skin melanoma) An ESR and a plain X-ray of the thoracic spine should be the initial screening test in the presence of these pointers. A common trap for the thoracic spine is lung cancer, such as mesothelioma, which can invade parietal pleura or structures adjacent to the vertebral column.

Pitfalls Pitfalls include ischaemic heart disease presenting with interscapular pain, herpes zoster at the preeruption stage and the various gastrointestinal disorders. Two commonly misdiagnosed problems are a penetrating duodenal ulcer presenting with lower thoracic pain and oesophageal spasm, which can cause thoracic back pain. Inflammatory rheumatological problems are not common in the thoracic spine but occasionally a spondyloarthropathy such as ankylosing spondylitis manifests here, although it follows some time after the onset of sacroiliitis.

Seven masquerades checklist

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Spinal dysfunction is the outstanding cause in this checklist, but urinary tract infection may occasionally cause lower thoracic pain. Depression always warrants consideration in any pain syndrome, especially back pain. It can certainly cause exaggeration of preexisting pain from vertebral dysfunction or some other chronic problem.

Psychogenic considerations Psychogenic or non-organic causes of back pain can present a complex dilemma in diagnosis and management. The causes may be apparent from the incongruous behaviour and personality of the patient, but often the diagnosis is reached by a process of exclusion. There is obviously some functional overlay in everyone with acute or chronic pain, hence the importance of appropriate reassurance to these patients that their problem invariably subsides with time and that they do not have cancer.

Anatomical and clinical features The functional unit of the thoracic spine is illustrated in FIGURE  37.1. Although there is scant literature and evidence about the origins of pain in the thoracic spine,3

the strongest evidence indicates that pain from the thoracic spine originates mainly from the apophyseal joints and rib articulations. Any one thoracic vertebra has 10 separate articulations, so the potential for dysfunction and the difficulty in clinically pinpointing the precise joint at a particular level are apparent. The costovertebral joints are synovial joints unique to the thoracic spine and have two articulations— costotransverse and costocentral. Together with the apophyseal joints, they are capable of presenting with well-localised pain close to the midline or as referred pain, often quite distal to the spine, with the major symptoms not appearing to have any relationship to the thoracic spine. Generalised referral patterns are presented in FIGURE 24.2 (see CHAPTER 24), while the dermatome pattern is outlined in FIGURE 37.2. The pain pattern acts as a guide only because there is considerable dermatomal overlap within the individual and variation from one person to another. It has been demonstrated that up to five nerve roots may contribute to the innervation of any one point in the anterior segments of the trunk dermatomes, a fact emphasised by the clinical distribution of herpes zoster.

Upper thoracic pain1 Dysfunction of the joints of the upper thoracic spine usually gives rise to localised pain and stiffness posteriorly but also can cause distal symptoms, probably via the autonomic nervous system. A specific syndrome called the T4 syndrome4 has been shown to cause vague pain and paraesthesia in the upper limbs and diffuse, vague head and posterior neck pain. Examination may reveal hypomobility of the upper thoracic segments. It has been proven to respond to spinal manipulation, which restores full mobility. However, most of the pain, stiffness and discomfort arise from dysfunction of the upper and middle thoracic segments with patients presenting with the complaint of pain between ‘my shoulder blades’.

Costovertebral joint dysfunction1 The unique feature of the thoracic spine is the costovertebral joint. Dysfunction of this joint commonly causes localised pain approximately 3–4  cm from the midline where the rib articulates with the transverse process and the vertebral body. In addition, it is frequently responsible for referred pain ranging from the midline, posterior to the lateral chest wall, and even anterior chest pain.

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Thoracic back pain

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V C2

C3

C3 C4 T2 T3 T4

C4 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1

T5 T6 T7 T8 T9 T10 T11 T12 L1

(a) Anterior

(b) Posterior

FIGURE 37.2 Dermatomes for the thoracic nerve roots, indicating possible referral areas. Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation (2nd edn), Oxford: ButterworthHeinemann, 1997

When the symptoms radiate laterally, the diagnosis is confirmed only when movement of the rib provokes pain at the costovertebral joint. This examination will simultaneously reproduce the referred pain. FIGURE  37.3 presents the pattern of referred pain from these joints and highlights the capacity of the thoracic spine to refer pain centrally to the anterior chest and upper abdomen. Confusion arises for the clinician when the patient’s history focuses on the anterior chest pain and fails to mention the presence of posterior pain, should it be present. The shaded areas on FIGURE 37.3 represent those areas where the patient experiences pain following the injection of hypertonic saline into the posterior elements of the spine.

The clinical approach History The history of a patient presenting with thoracic back pain should include a routine pain analysis, which usually provides important clues for the diagnosis. The age, sex and occupation of the patient are relevant. Pain in the thoracic area is very common in people who sit bent over for long periods, especially working at desks. Students, secretaries and stenographers are

therefore at risk, as are nursing mothers, who have to lift their babies. People who are kyphotic or scoliotic or who have ‘hunchbacks’ secondary to disease such as tuberculosis and poliomyelitis also suffer from recurrent pain in this area. Older people are more likely to present with a neoplastic problem in the thoracic spine and with osteoporosis. Senile osteoporosis is usually a trap because it is symptomless until the intervention of a compression fracture. Symptoms following such a fracture can persist for 3 months. Pain that is present day and night indicates a sinister cause. Features of the history that give an indication that the pain is arising from dysfunction of the thoracic spine include: • Aggravation and relief of pain on trunk rotation. The patient’s pain may be increased by rotating (twisting) towards the side of the pain but eased by rotating in the opposite direction. • Aggravation of pain by coughing, sneezing or deep inspiration. This can produce a sharp catching pain which, if severe, tends to implicate the costovertebral joint. Care must be taken to rule out pneumonia and pleurisy.

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C7

T3

T2

T5 T4 T7

T2

T3

T4

T5

T6 T6

T7 T8

T9

T8 T10

T9

T10 T11

T12

T11

T12

FIGURE 37.3 Kellegren’s (1939) pain referral patterns after stimulation of deep joints of the thoracic spine

• Relief of pain by firm pressure. Patients may state that their back pain is eased by firm pressure such as leaning against the corner of a wall. It is very important to be able to differentiate between chest pain due to vertebral dysfunction and that caused by myocardial ischaemia.

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Key questions • Can you recall injuring your back, such as by lifting something heavy? • Did you have a fall onto your chest or back? • Is the pain present during the night? • Do you have low back pain or neck pain? • Does the pain come on after walking or any strenuous effort? • Does the pain come on after eating or soon after going to bed at night? • Have you noticed a fever or sweating at any time, especially at night? • Have you noticed a rash near where you have the pain? • What drugs are you taking? Do you take drugs for arthritis or pain? Cortisone? • What happens when you take a deep breath, cough or sneeze?

Examination The examination of the thoracic spine is straightforward with the emphasis on palpation of the spine—central and laterally. This achieves the

basic objective of reproducing the patient’s symptoms and finding the level of pain. The ‘LOOK, FEEL, MOVE, X-RAY’ clinical approach is most appropriate for the thoracic spine. Inspection Careful inspection is important since it may be possible to observe at a glance why the patient has thoracic pain. Note the symmetry, any scars, skin creases and deformities, ‘flat spots’ in the spine, the nature of the scapulae or evidence of muscle spasm. Look for kyphosis and scoliosis. Kyphosis may be generalised, with the back having a smooth uniform contour, or localised where it is due to a collapsed vertebra, such as occurs in an older person with osteoporosis. Generalised kyphosis is common in the elderly, especially those with degenerative spinal disease. In the young it may reflect the important Scheuermann disease. The younger person in particular should be screened for scoliosis (see FIG.  37.4), which becomes more prominent on forward flexion (see FIG.  37.6). Look for any asymmetry of the chest wall, inequality of the scapulae and differences in the levels of the shoulders. A useful sign of scoliosis is unequal shoulder levels and apparent ‘winging’ of scapula. When viewed anteriorly a difference in the levels of the nipples indicates the presence of scoliosis, or other problems causing one shoulder to drop. Inspection should therefore take place with posterior, lateral (side) and anterior views.

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Thoracic back pain

high shoulder trunk shift

rib cage prominence scoliosis convex to right

prominent hip

FIGURE 37.4 Adolescent idiopathic scoliosis: typical configuration of the trunk and thoracic spine

Palpation The best position is to have the patient prone on the examination table with the thoracic spine preferably in slight flexion. This is achieved by lowering the top of the table. Test passive extension of each joint with firm pressure from the pad of the thumbs or the bony hand (either the pisiform prominence or the lateral border of the fifth metacarpal). Spring up and down with a few firm oscillations, keeping the elbows straight, but being well above the patient. Ask the patient if the pressure reproduces the pain. Apart from asking the patient ‘Is that the pain?’ note:

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Movements There are four main movements of the thoracic spine to assess, the most important of which is rotation, as this is the movement that so frequently reproduces the patient’s pain where it is facet joint or costovertebral in origin. The movements of the thoracic spine and their normal ranges are: 1 2 3 4

Extension Lateral flexion L and R Flexion Rotation L and R

30° 30° 90° 60°

Ask the patient to sit on the table with hands placed behind the neck and then perform the movements. Check these four active movements, noting any hypomobility, the range of movement, reproduction of symptoms and function and muscle spasm.

Investigations The main investigation is an X-ray, which may exclude the basic abnormalities and diseases, such as osteoporosis and malignancy. If serious diseases such as malignancy or infection are suspected, and the plain X-ray is normal, a radionuclide bone scan may detect these disorders. CT scanning has a minimal role in the evaluation of thoracic spinal pain. Other investigations to consider are: • • • • • •

FBE and ESR/CRP serum alkaline phosphatase serum electrophoresis for multiple myeloma Bence–Jones protein analysis Brucella agglutination test blood culture for pyogenic infection and bacterial endocarditis tuberculosis studies HLA-B27 antigen for spondyloarthropathies ECG or ECG stress tests (suspected angina) gastroscopy or barium studies (peptic ulcer) MRI or CT scanning radionuclide bone scan if neoplastic or metabolic disease is suspected

• the distribution of pain and its change with movement • the range of movement • the type of resistance in the joint • any muscle spasm

• • • • • •

Palpation must follow a set plan in order to reproduce the patient’s pain. The sequence is as follows:

Thoracic back pain in children

1 central—over spinous processes 2 unilateral—over apophyseal joints (2–3 cm from midline) 3 transverse—on side of spinous processes 4 unilateral—costotransverse junctions (4–5 cm from midline) 5 unilateral—over ribs (spring over posterior rib curve with ulnar border of hand, along axis of rib)

The most common cause of thoracic back pain in children is ‘postural backache’, also known as ‘TV backache’, which is usually found in adolescent schoolgirls and is a diagnosis of exclusion. Important, although rare, problems in children include infections (tuberculosis, discitis and osteomyelitis) and tumours such as osteoid osteoma and malignant osteogenic sarcoma.

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Dysfunction of the joints of the thoracic spine in children and particularly in adolescents is very common and often related to trauma such as a heavy fall in sporting activities or falling from a height (e.g. off a horse). Fractures, of course, have to be excluded. Inflammatory disorders to consider are juvenile ankylosing spondylitis and spinal osteochondritis (Scheuermann disease), which may affect adolescent males in the lower thoracic spine (around T9) and thoracolumbar spine. The latter condition may be asymptomatic, but can be associated with back pain, especially as the patient grows older. It is the commonest cause of kyphosis. It is important to screen adolescent children for idiopathic scoliosis, which may be without associated backache.

Kyphosis5

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Kyphosis is the normal curve of the thoracic spine when viewed from the side. The normal range is 20–45° (see FIG.  37.5). An excessive angle (>45– 50°) occurs with a kyphotic deformity. In children a congenital cause is likely (present from infancy); in adolescents it is usually due to Scheuermann disease or is postural; in adults consider ankylosing spondylitis—and osteoporosis in the elderly. Tuberculosis of the spine can cause a gross deformity. Children with significant kyphosis should be referred for management which includes exercises, bracing or surgery.

Scheuermann disease This is a structural saggital plane deformity of unknown cause affecting the T7, 8, 9 or T11, 12 areas. Clinical features • Age 11–17 years • Males > females • Lower thoracic spine • Thoracic pain or asymptomatic • Increasing thoracic kyphosis over 1–2 months • Wedging of the vertebrae • Pain in the wedge, especially on bending (only 20% present with pain) • Short hamstrings • Cannot touch toes • Diagnosis confirmed by X-ray (lateral standing)—shows Schmorl node and anterior vertebral body wedging Treatment • Explanation and support • Extension exercises, avoid forward flexion • Postural correction • Avoidance of sports involving lifting and bending • Consider bracing or surgery if serious deformity • If detected early hyperextension body casts followed by a Milwaukee brace can prevent deformity

Adolescent idiopathic scoliosis A degree of scoliosis is detectable in 5% of the adolescent population.6 The vast majority of curves, occurring equally in boys and girls, are mild and of no consequence. Eighty-five per cent of significant curves in adolescent scoliosis occur in girls.6 Inheritance is a factor. The highest incidence is in first-degree female relatives (12%). The scoliotic deformity develops at 10 years of age. Such curves appear during the peripubertal period, usually coinciding with the growth spurt. The screening test (usually in 12–14 year olds but ideally as early as 9) is to note the contour of the back on forward flexion (see FIG.  37.6). The routine physical screening check of an adolescent should include this area.

FIGURE 37.5 Illustration of kyphosis, which is measured by the angle between the uppermost and lowermost inclined vertebrae on the lateral X-ray

The test The subject stands with the feet parallel and together, and bends forward as far as possible with outstretched hands, palms facing each other, pointed between the great toes.

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Thoracic back pain normal

abnormal

FIGURE 37.6 Screening for adolescent idiopathic scoliosis: testing asymmetry by forward flexion

Investigation A single erect PA spinal X-ray is sufficient;7 the Cobb angle (see FIG. 37.7) is the usual measurement yardstick.

top of vertebra at top end of curve

50° Cobb angle

bottom of vertebra at lower end of curve

FIGURE 37.7 Scoliosis: the Cobb angle method of curve measurement

Management

Aims • To preserve good appearance—level shoulders and no trunk shift • Prevent increasing curve in adult life: less than 45º • Not to produce a straight spine on X-ray

Methods • Braces: — Milwaukee brace (rarely used) — high-density polyethylene underarm orthosis — to be worn for 20–22 hours each day until skeletal maturity is reached.

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• Surgical correction: depends on curve and skeletal maturity Guidelines for treatment • Still growing: 20º

Thoracic back pain in the elderly Thoracic back pain due to mechanical causes is not such a feature in the elderly although vertebral dysfunction still occurs quite regularly. However, when the elderly person presents with thoracic pain, a very careful search for organic disease is necessary. Special problems to consider are: • malignant disease (e.g. multiple myeloma, lung, prostate) • osteoporosis • vertebral pathological fractures • polymyalgia rheumatica • Paget disease (may be asymptomatic) • herpes zoster • visceral disorders: ischaemic heart disease, penetrating peptic ulcer, oesophageal disorders, biliary disorders

Dysfunction of the thoracic spine This is the outstanding cause of pain presenting to the practitioner and is relatively easy to diagnose. It is often referred to as the thoracic hypomobility syndrome with the disorder arising in the facet joints, costovertebral joints and thoracic  musculoligamentous structure, singularly or in combination. The most efficacious treatment  for painful dysfunctional problems varies according to practitioners with a special interest in this area. There is a paucity of studies and evidence supporting the multiplicity of therapies, especially focal injections and physical therapy. Many claim  that special mobilisation and manipulation provides  effective short-term, sometimes immediate, relief.

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Typical profile:2 Age

Any age, especially between 20 and 40 years. History of injury Sometimes slow or sudden onset Site and radiation Spinal and paraspinal— interscapular, arms, lateral chest, anterior chest, substernal, iliac crest Type of pain Dull, aching, occasionally sharp; severity related to activity, site and posture Aggravation Deep inspiration, postural movement of thorax, slumping or bending, walking upstairs, activities (e.g. lifting children, making beds), beds too hard or soft, sleeping or sitting for long periods Association Chronic poor posture Diagnosis confirmation Examination of spine, therapeutic response to manipulation

Management

First-line management

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• Explanation with printed information • Reassurance, including spontaneous recovery likely • Continued activity according to pain level • Back education program • Analgesics (e.g. paracetamol 1 g (o) qid) first line • Posture education • Spinal mobilisation and manipulation (if appropriate)

Spinal mobilisation and manipulation Spinal mobilisation is helpful but the more forceful manipulative therapy produces better and quicker results. There are many techniques that can be employed, the choice depending on which part of the back is affected.7 The sternal thrust (Nelson hold) technique is widely used for upper thoracic segments and the crossed pisiform technique (patient prone) or posteroanterior indirect thrust (patient supine—see FIG. 37.8) is claimed to be the most—effective for the mid-thoracic spine. There is level II evidence that spinal manipulation is effective compared with placebo.8

Thoracic disc protrusion Fortunately, a disc protrusion in the thoracic spine is uncommon. This reduced incidence is related to

FIGURE 37.8 Manipulation of the mid-thoracic spine by the posteroanterior indirect thrust technique Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation (2nd edn). Oxford: Butterworth-Heinemann, 1997

the firm splintage action of the ribcage. Most disc protrusions occur below T9, with the commonest site, as expected, being T11–12. The common presentation is back pain and radicular pain that follows the appropriate dermatome so disc protrusion should be considered in patients with neurological signs at thoracic levels. This may include a flaccid area of the lower abdominal musculature. However, disc lesions in the thoracic spine are prone to produce spinal cord compression, manifesting as sensory loss, bladder incontinence and signs of upper motor neurone lesion. The disc is relatively inaccessible to surgical intervention, but over the past decade there has been a significant improvement in the surgical treatment of thoracic disc protrusions, due to the transthoracic lateral approach.

Syrinx A syrinx usually comes to notice as a radiological finding in the presence of thoracic back pain when it may in fact be asymptomatic. It is a rare, fluid-filled neurological cavity within the spinal cord. It is usually a congenital anomaly, but a neoplasm needs to be excluded. A syrinx usually begins at the cervical level and extends down. Treat conservatively, but refer to an expert who may consider intervention if it is symptomatic.

Muscle injury Muscular injuries such as tearing are uncommon in the chest wall. The strong paravertebral muscles do not appear to be a cause of chest pain, but strains

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Thoracic back pain of intercostal muscles, the serratus anterior and the musculotendinous origins of the abdominal muscles can cause pain. Injuries to these muscles can be provoked by attacks of violent sneezing or coughing or overstrain, for example, lifting a heavy suitcase down from an overhead luggage rack.

SCAPULOTHORACIC JOINT DISORDERS9 The gliding plane between the scapula and thoracic wall permits a considerable range of scapular movement, which contributes significantly to movement of the shoulder. Several muscles including the rhomboids, serratus anterior and levator scapulae help stabilise scapular movement and may be a source of pain in the scapular region.

Snapping scapula The patient complains of a loud cracking or snapping sound upon abduction of the scapula. There is often associated crepitus. Pain is felt along the medial scapular border. The patient may develop a habit (‘tic’) of neurotically clicking the shoulder back and forth. On examination there is usually generalised hypermobility of the scapula, abnormal movement and tenderness to palpation along the medial edge on full abduction. The cause (uncommon) may be an underlying bony abnormality such as a bony spur on the superior border of the scapula or an osteoma. X-rays should include a lateral view of the scapula to search for this possibility. Treatment • Explanation and reassurance (if X-rays normal)— otherwise resect any bone abnormality. • Avoid repeated scapular movement and ‘trick’ movements. • Appropriate exercises under physiotherapy supervision. • Infiltrate any very tender area in the muscle (with care) with local anaesthetic and steroid. • Deep massage to the tender focus.

Scapulocostal syndrome This condition causes localised pain and tenderness, often severe, along the upper part of the medial scapular border, with radiation around the chest wall and shoulder girdle to the neck. Pain is usually worse with prolonged shoulder use towards the end of the day. It is commonly seen in typists, gymnasts and

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other sportspeople. It is related to poor posture. The cause may include friction between the scapula and the thoracic wall, scoliosis, trauma and myofascial strain due to poor posture. Treatment • Avoid the movements producing the pain. • Posture and re-education exercises and scapula stretching. • Deep friction massage. • Local injections of local anaesthetic and corticosteroid into the tender area.

Winging of the scapula The asymmetry may not be apparent until the patient tries to contract the serratus anterior against resistance by pushing the outstretched arm against the wall. There may be parascapular discomfort. The common cause is neurogenic paralysis of the serratus anterior muscle. Paralysis may result from injury to the long thoracic nerve (from C5, 6, 7 nerve roots) such as a neck injury or a direct blow to the suprascapular area and from injury to the brachial plexus such as excessive carrying of heavy packs, severe traction on the arm, forceful cervical manipulation. Most cases settle spontaneously, although it may take 1–2 years.

FIBROMYALGIA, FIBROSITIS AND MYOFASCIAL TRIGGER POINTS Fibromyalgia is relatively uncommon but when encountered presents an enormous management problem. It is not to be confused with so-called fibrositis or tender trigger points. Referral to a specialist with expertise in this condition or to a multidisciplinary pain clinic for the definitive diagnosis is recommended. Fibrositis is not a diagnosis but a symptom, indicating a localised area of tenderness or pain in the soft tissues, especially of the upper thoracic spine. It is probably almost always secondary to upper thoracic or lower cervical spinal dysfunction.

Myofascial trigger points As described by Travell and Rinzler10 a trigger point is characterised by: • circumscribed local tenderness • localised twitching with stimulation of juxtaposed muscle • pain referred elsewhere when subjected to pressure

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Trigger spots also tend to correspond to the acupuncture points for pain relief. Treatment11 Local injection is relatively easy and may give excellent results. Identify the maximal point of pain and inject 5–8 mL of local anaesthetic (LA; e.g. lignocaine/lidocaine 1%) into the painful point (see FIG. 37.9). Post-injection massage or exercises should be performed. Don’t: • use large volumes of LA • use corticosteroids • cause bleeding Do: • use a moderate amount of LA (only)

Fibromyalgia syndrome12 Clinical features The main diagnostic features are: 1 a history of widespread pain (neck to low back) 2 pain in 11 of 18 tender points on digital palpation

FIGURE 37.10 Fibromyalgia syndrome: typical tender points (the tender point map represents the 14 points recommended for use as a standard for diagnostic or therapeutic studies)

These points must be painful, not tender. Smythe and Moldofsky have recommended 14 of these points  on a map as a guide for management12 (see FIG. 37.10).

Other features • Female to male ratio = 4:1 • Usual age onset 29–37 years: diagnosis 44–53 years • Poor sleep pattern • Dermatographia • Fatigue (similar to chronic fatigue syndrome) • Psychological disorders (e.g. anxiety, depression, tension headache, irritable digestive system)

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This disorder is very difficult to treat and is usually unresponsive in the long term to passive physical therapy or injections.13 Patients require considerable explanation, support and reassurance. Best evidence to date supports the value of educational programs and regular aerobic exercise.14

FIGURE 37.9 Injection for myofascial trigger points

Treatment • Explanation, reassurance and counselling • Attention to sleep disorders, stress factors and physical factors • Relaxation program • Rehabilitation: graduated exercise program (e.g. walking, water exercises, swimming or cycling) • Use paracetamol for first-line analgesia

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Thoracic back pain Medication (often disappointing) Antidepressants (of proven short-term value); start low then monthly increments as tolerated:

15,16

amitriptyline 10–75 mg (o) nocte or dothiepin 25–75 mg (o) nocte or duloxetine 30 mg (o) mane, increasing to 60 mg over 2 weeks17 Note: NSAIDs are of no proven benefit.

Serious pitfalls The following points regarding serious vertebral organic disease are worth repeating in more detail.

Metastatic disease18 Secondary deposits in the thoracolumbar spine may be the first presenting symptoms of malignant disease. Any patient of any age presenting with progressive severe night pain of the back should be regarded as having a tumour and investigated with a technetium bone scan as part of the primary investigations. Secondary deposits in the spine can lead to rapid onset paralysis due to spinal cord infarction. Many such metastases can be controlled in the early stages with radiotherapy.

Multiple myeloma Osteoporotic vertebral body collapse should be diagnosed only when multiple myeloma has been excluded. Investigations should include an ESR, Bence–Jones protein analysis, and immunoglobulin electrophoresis. Early treatment of multiple myeloma can hold this disease in remission for many years and prevent crippling vertebral fractures (see CHAPTER 26).

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Strict bed rest with high-dose antibiotic therapy is usually curative. If left untreated, vertebral end plate and disc space collapse is common and extremely disabling. Consider tuberculosis osteomyelitis in people at risk. Suspect an epidural abscess in the presence of persistent and increased back pain. Percuss the spine for localised tenderness (see CHAPTER 30).

When to refer • Persistent pain or dysfunction—refer to a physical therapist. • Evidence or suspicion of a sinister cause (e.g. neoplasia, infective discitis/osteomyelitis in a child). • Suspicion of cardiac or gastrointestinal referred (persistent) pain. • Significant idiopathic adolescent scoliosis or kyphosis (e.g. Scheuermann disease).

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Exercises for your thoracic spine • Fibromyalgia • Scoliosis

Practice tips • • • •

•

Infective discitis, vertebral osteomyelitis and epidural/subdural abscess

•

Severe back pain in an unwell patient with fluctuating temperature (fever) should be considered as infective until proved otherwise. Investigations should include blood cultures, serial X-rays and nuclear bone scanning. Biphasic bone scans using technetium with either indium or gallium scanning for white cell collections usually clinch this diagnosis.

•

•

• •

Feelings of anaesthesia or paraesthesia associated with thoracic spinal dysfunction are rare. Thoracic back pain is frequently associated with cervical lesions. Upper thoracic pain and stiffness is common after ‘whiplash’. The T4 syndrome of upper to mid-thoracic pain with radiation (and associated paraesthesia) to the arms is well documented. Symptoms due to a fractured vertebra usually last 3 months and to a fractured rib 6 weeks. The pain of myocardial ischaemia, from either angina or myocardial infarction, can cause referred pain to the interscapular region of the thoracic spine. Beware of the old trap of herpes zoster in the thoracic spine, especially in the older person. Consider multiple myeloma as a cause of an osteoporotic collapsed vertebra. Examine movements with the patient sitting on the couch and hands clasped behind the neck. Spinal disease of special significance in the thoracic spine includes osteoporosis and neoplasia, continued

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continued while disc lesions, inflammatory diseases and degenerative diseases (spondylosis) are encountered less frequently than with the cervical and lumbar spines. • It is imperative to differentiate between spinal and cardiac causes of chest pain: either cause is likely to mimic the other. A working rule is to consider the cause as cardiac until the examination and investigations establish the true cause. • Always X-ray the thoracic spine following trauma, especially after motor vehicle accidents, as wedge compression fractures (typically between T4 and T8) are often overlooked.

References 1 National Health and Medical Research Council. Evidencebased Management of Acute Musculoskeletal Pain—A Guide for Clinicians. Australian Acute Musculoskeletal Pain Guidelines Group, Canberra: Australian Government, 2004: 30–4. 2 Kenna C, Murtagh J. Back Pain and Spinal Manipulation (2nd edn). Oxford: Butterworth-Heinemann, 1997: 165–74. 3 Chua WL. Thoracic spinal pain—a review. Australasian Musculoskeletal Medicine, 1996; 1: 13–22. 4 McGuckin N. The T4 syndrome. In: Grieve GD (ed.) Modern Manual Therapy of the Vertebral Column. London: Churchill Livingstone, 1986: 370–6. 5 Sponseller P. The 5-minute Orthopaedic Consult. Philadelphia: Lippincott, Williams and Wilkins, 2001: 184–5. 6 Stephens J. Idiopathic adolescent scoliosis. Aust Fam Physician, 1984; 13: 180–4.

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7 Anonymous. The Easter Seal Guide to Children’s Orthopaedics. Toronto: The Easter Seal Society, 1982: 64–7. 8 Schiller L. Effectiveness of spinal manipulation therapy in the treatment of mechanical thoracic back pain. Journal of Manipulative and Physiological Therapeutics, 2001; 24: 394–401. 9 Corrigan B, Maitland G. Practical Orthopaedic Medicine. Sydney: Butterworths, 1986: 384–5. 10 Travell J, Rinzler SH. The myofascial genesis of pain. Postgrad Med, 1952; 11: 425–34. 11 Simons D. Understanding effective treatments of myofascial trigger points. Journal of Bodywork Movement Therapy, 2002; 6: 81–5. 12 Smythe HA, Moldofsky H. Two contributions to understanding of the ‘fibrositis’ syndrome. Bull Rheum Dis, 1977; 28: 928–31. 13 McIndoe R, Littlejohn G. Management of fibromyalgia and regional pain syndromes. Mod Med Aust, 1995; 36 (2): 56–69. 14 McCain GA, Bell DA et al. A controlled study of the effects of a supervised cardiovascular fitness training program on the manifestation of primary fibromyalgia. Arthritis Rheum, 1988; 31: 1135–41. 15 Jaeschke R, Adachi J, Guyatt G et al. Clinical usefulness of amitriptyline in fibromyalgia: the results of 23 N-of-I randomised controlled trials. J Rheumatol, 1991; 18: 447–51. 16 Moulds R (Chair). Therapeutic Guidelines: Rheumatology (Version 2). Melbourne: Therapeutic Guidelines Ltd, 2010: 137–40. 17 Chappell AS, Littlejohn G et al. A 1-year safety and efficacy study of duloxetine in patients with fibromyalgia. Clin J Pain, 2009; 25 (5): 365–75. 18 Young D, Murtagh J. Pitfalls in orthopaedics. Aust Fam Physician, 1989; 18: 653–4.

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Last Wednesday night while carrying a bucket of water from the well, Hannah Williams slipped upon the icy path and fell heavily upon her back. We fear her spine was injured for though she suffers acute pain in her legs she cannot move them. The poor wild beautiful girl is stopped in her wildness at last. Francis Kilvert  Low back pain accounts for at least 5% of general practice presentations. It is a massive problem worldwide. The most common cause is minor soft tissue injury, but patients with this do not usually seek medical help because the problem settles within a few days. Most back pain in patients presenting to GPs is postulated to be due to dysfunction of elements of the mobile segment, namely the facet joint, the intervertebral joint (with its disc) and the ligamentous and muscular attachments. This problem, often referred to as mechanical back pain, will be described as vertebral dysfunction—a general term that, while covering radicular and non-radicular pain, includes dysfunction of the joints of the spine, although the specific origin in most instances cannot be determined. It is therefore appropriate to refer to this as ‘non-specific back pain’.1

Key facts and checkpoints •

• •

•

• •

Back pain accounts for at least 5% of all presenting problems in general practice in Australia and 6.5% in Britain.2 In the US it is the commonest cause of limitation of activity in those under the age of 45.2 Approximately 85–90% of the population will experience back pain at some stage of their lives, while 70% of the world’s population will have at least one disabling episode of low back pain in their lives.2 At least 50% of these people will recover within 2 weeks and 90% within 6 weeks, but recurrences are frequent and have been reported in 40–70% of patients; 2–7% develop chronic pain.3 The most common age groups are the 30s, 40s and 50s, the average age being 45 years.4 The most common cause of back pain is a minor strain to muscles and/or ligaments, but people suffering from this type of back pain usually do not seek medical treatment as most of these soft tissue problems resolve rapidly.

•

The main cause of back pain presenting to the doctor is dysfunction of the intervertebral joints of the spine due to injury, also referred to as mechanical back pain (at least 70%). The second most common cause of back pain is spondylosis (synonymous with osteoarthritis and degenerative back disease). It accounts for about 10% of cases of low back pain. L5 and S1 nerve root lesions represent most of the cases of sciatica presenting in general practice. They tend to present separately but can occur together with a massive disc protrusion. An intervertebral disc prolapse has been proven in only 6–8% of cases of back pain.2

•

•

•

Causes of low back pain To develop a comprehensive diagnostic approach, the practitioner should have a clear understanding of the possible causes of low back and leg pain and of the relative frequency of their clinical presentations. The major causes of low back pain in several hundred patients presenting to the author’s general practice are summarised in TABLE 38.1. Table 38.1

Major causes of low back ± leg pain presenting in the author’s general practice

Patients Vertebral dysfunction Lumbar spondylosis Depression Urinary tract infection Spondylolisthesis Spondyloarthropathies Musculoligamentous strains/tears Malignant disease Arterial occlusive disease Other Total

% 71.8 10.1 3.0 2.2 2.0 1.9 1.2 0.8 0.6 6.4 100.0

Relevant causes are illustrated in FIGURE 38.1.

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Visceral and vascular B—biliary disorders U—penetrating duodenal ulcer P—pancreatitis R—renal disorders

R

U P

Musculoskeletal Scheuermann disease B

pathological fracture metastatic disease

aortic aneurysm (ruptured/dissecting)

spondylolisthesis

retroperitoneal haemorrhage

disc disruption

female pelvic disorders (e.g. endometriosis) prostatitis

facet joint dysfunction spondylosis spinal canal stenosis

abscess (e.g. pilonidal)

sacroiliac dysfunction sacroiliitis trochanteric bursitis gluteus medius bursitis coccydynia ischial bursitis meralgia paraesthetica neurogenic claudication radicular pain

arterial embolism

referred pain

from spinal dysfunction

claudication of arterial occlusive disease

radicular pain

38

FIGURE 38.1 Relevant causes of back pain with associated buttock and leg pain

Anatomical and pathophysiological concepts Recent studies have focused on the importance of disruption of the intervertebral disc in the cause of back pain. A very plausible theory has been advanced by Maigne3 who proposes the existence, in the involved mobile segment, of a minor intervertebral derangement (MID). He defines it as ‘isolated pain in one intervertebral segment, of a mild character, and due to minor mechanical cause’. The MID always involves one of the two apophyseal joints in the mobile segment, thus initiating nociceptive activity in the posterior primary dermatome and myotome.

Maigne points out that the functional ability of the mobile segment depends intimately upon the condition of the intervertebral disc. Thus, if the disc is injured, other elements of the segment will be affected. Even a minimal disc lesion can produce apophyseal joint dysfunction, which is a reflex cause of protective muscle spasm and pain in the corresponding segment, with loss of function (see FIG. 38.2). In theory, any structure with a nociceptive nerve supply may be a source of pain. Such structures include the ligaments, fascia and muscles of the lumbosacral spine, intervertebral joints, facet joints, dura mater and sacroiliac joints.5 Actually, pain can theoretically arise from any innervated structure in the region of the spine. It

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Low back pain minor intervertebral disc disruption

Table 38.2

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Low back pain: diagnostic strategy model

Q. Probability diagnosis A. Vertebral dysfunction especially facet joint and intervertebral disc (mechanical) B E

Musculoligamentous strain/sprain

A

C

D

Spondylosis (degenerative OA) Q. Serious disorders not to be missed A. Cardiovascular: • ruptured aortic aneurysm • retroperitoneal haemorrhage (anticoagulants)

E

D

C

B

A

FIGURE 38.2 Reflex activity from a MID in the intervertebral motion segment. Apart from the local effect caused by the disruption of the disc (A), interference can occur in the facet joint (B) and interspinous ligament (C) leading possibly to muscle spasm (D) and skin changes (E) via the posterior rami. Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 1989

Neoplasia: • myeloma • metastases Severe infections: • vertebral osteomyelitis • epidural abscess • septic discitis • tuberculosis • pelvic abscess/PID Osteoporotic compression fracture Cauda equina compression

can be neurogenic, spondylogenic, viscerogenic, vasculogenic or rarely psychogenic.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 38.2.

Probability diagnosis The commonest cause of low back pain is vertebral dysfunction or mechanical pain, which then has to be further analysed. The term can embrace musculoskeletal strain, discogenic and posterior ligament pain, and facetogenic dysfunction/pain. Degenerative changes in the lumbar spine (lumbar spondylosis) are commonly found in the older age group. This problem, and one of its complications, spinal canal stenosis, is steadily increasing along with the ageing population.

Q. Pitfalls (often missed) A. Spondyloarthropathies: • ankylosing spondylitis • reactive arthritis • psoriasis • bowel inflammation Sacroiliac dysfunction Spondylolisthesis Claudication: • vascular • neurogenic/spinal canal stenosis Paget disease Prostatitis Endometriosis Q. Seven masquerades checklist A. Depression

Serious disorders not to be missed

Spinal dysfunction

It is important to consider malignant disease, especially in an older person. It is also essential to consider infection such as acute osteomyelitis and tuberculosis, which is often encountered in recent immigrants, especially those from Asia and central Africa. The uncommon epidural or subdural abscess

UTI Q. Is this patient trying to tell me something? A. Quite likely. Consider lifestyle, stress, work problems, malingering, conversion reaction Note: Associated buttock and leg pain included.

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should also be kept in mind (see CHAPTER 30). These conditions are considered in more detail under infections of the central nervous system. For pain or anaesthesia of sudden onset, especially when accompanied by neurological changes in the legs, consider cauda equina compression due to a massive disc prolapse and also retroperitoneal haemorrhage. It is important to ask patients if they are taking anticoagulants. See TABLE 38.3. Table 38.3

‘Red flag’ pointers to serious low back pain conditions6

Age >50 years or 37.8°C Constant pain—day and night especially severe night pain Unexplained weight loss Symptoms in other systems, e.g. cough, breast mass Significant trauma Features of spondyloarthropathy, e.g. peripheral arthritis (e.g. age 12 weeks): • beneficial—back exercises, multidisciplinary treatment program • likely benefit—analgesics, NSAIDs, trigger point injections, spinal mobilisation/manipulation

Radiculopathy Radicular pain, caused by nerve root compression from a disc protrusion (most common cause) or tumour or a narrowed intervertebral foramina, typically produces pain in the leg related to the dermatome and myotome innervated by that nerve root. Leg pain may occur alone without back pain and vary considerably in intensity. The two nerve roots that account for most of these problems are L5 and S1 and the commonest disc lesion is L4–5, closely followed by L5–S1. A disc can be confined, extruded or sequestrated. Most settle with time (6–12 weeks). The management is outlined at the end of this chapter and under ‘Sciatica’ (see CHAPTER 66).

Spondylolisthesis About 5% of the population have spondylolisthesis but not all are symptomatic. The pain is caused by extreme stretching of the interspinous ligaments or of the nerve roots. The onset of back pain in many of these patients is due to concurrent disc degeneration rather than a mechanical problem. The pain is typically aggravated by prolonged standing, walking and exercise. The physical examination is quite diagnostic. • Physical examination (significant): stiff waddling gait, increased lumbar lordosis, flexed knee stance, tender prominent spinous process of ‘slipped’ vertebrae, limited flexion, hamstring tightness or spasm • Diagnosis confirmation: lateral X-ray (standing) (see FIG. 38.8) Management This instability problem can be alleviated with relief of symptoms by getting patients to follow a strict flexion exercise program for at least 3 months. The objective is for patients to ‘splint’ their own spine by strengthening abdominal and spinal muscles. Extension of the spine should be avoided, especially hyperextension. Gravity traction might help. Recourse to lumbar corsets or surgery (for spinal fusion) should be resisted although it is appropriate in a few severe intractable cases.

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stress fracture of the pars interarticularis

annular bulge of disc

narrowed spinal canal

osteophytic formation at facet joint

FIGURE 38.8 Spondylolisthesis: illustrating a forward shift of one vertebra on another

Lumbar spondylosis Lumbar spondylosis, also known as degenerative osteoarthritis or osteoarthrosis, is a common problem of wear and tear that may follow vertebral dysfunction, especially after severe disc disruption and degeneration. Stiffness of the low back is the main feature of lumbar spondylosis. Although most people live with and cope with the problem, progressive deterioration can occur, leading to subluxation of the facet joints. Subsequent narrowing of the spinal and intervertebral foramen leads to spinal canal stenosis (see FIG. 38.9). Management • Basic analgesics (depending on patient response and tolerance) • NSAIDs (judicious use) • Appropriate balance between light activity and rest • Exercise program and hydrotherapy (if available)— physiotherapy supervision • Regular mobilisation therapy may help • Consider trials of electrotherapy, such as TENS and acupuncture • Consider decompressive surgery for spinal canal stenosis

THE SPONDYLOARTHROPATHIES The seronegative spondyloarthropathies are a group of disorders characterised by involvement of the sacroiliac joints with an ascending spondylitis and extraspinal manifestations, such as oligoarthritis and enthesopathies (see FIG.  38.10; refer to CHAPTER 35).

narrowed invertebral foramen

subluxation of facet joint

FIGURE 38.9 Lumbar spondylosis with degeneration of the disc and facet joint, leading to narrowing of the spinal canal and intervertebral foramen (spinal canal stenosis)

The pain and stiffness that are the characteristic findings of spinal involvement are typical of inflammatory disease: namely, worse in the morning, may occur at night and improves rather than worsens with exercise. The main disorders in this group are ankylosing spondylitis, psoriatic arthritis, reactive spondyloarthropathies and the inflammatory bowel diseases. Hence the importance of searching for a history of psoriasis, diarrhoea, urethral discharge, eye disorders and episodes of arthritis in other joints. Treatment The earlier the treatment the better the outlook for the patient; the prognosis is usually good (see earlier in chapter). Refer to consultant for shared care. The basic objectives of treatment are: • prevention of spinal fusion in a poor position • relief of pain and stiffness • maintenance of optimum spinal mobility

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(a)

FIGURE 38.10 (a) Ankylosing spondylitis and psoriasis: main target areas on vertebral column and girdle joints (b) Crohn disease and ulcerative colitis: main target areas of enteropathies. Reactive arthritis targets the lumbar spine and sacrolial joints only.

Malignant disease

38

It is important to identify malignant disease and other space-occupying lesions as early as possible because of the prognosis and the effect of a delayed diagnosis on treatment. With respect to the neurological features, more than one nerve root may be involved and major neurological signs may be present without severe root pain. The neurological signs will be progressive. If malignant disease is proved and myeloma is excluded, a search should be made for the six main primary malignancies that metastasise to the spine (see FIG.  38.11). If the bone is sclerotic consider prostatic secondaries, some breast secondaries or Paget disease.

Non-organic back pain Like headache, back pain is a symptom of an underlying functional, organic or psychological disorder. Preoccupation with organic causation of symptoms may lead to serious errors in the assessment of patients with back pain. Any vulnerable aching area of the body is subject to aggravation by emotional factors. Depressed patients are generally less demonstrative than patients with extreme anxiety and conversion

disorders and malingerers, and it is easier to overlook the non-organic basis for their problem. A trial of antidepressants for a minimum of 3 weeks is recommended and quite often a positive response with relief of backache eventuates. Failure to consider psychological factors in the assessment of low back pain may lead to serious errors in diagnosis and management. Each instance of back pain poses a stimulating exercise in differential diagnosis. A comparison of organic and non-organic features is presented in TABLE 38.6. Assessment of the pain demands a full understanding of the patient. One must be aware of his or her type of work, recreation, successes and failures; and one must relate this information to the degree of incapacity attributed to the back pain. Patients with psychogenic back pain, especially the very anxious, tend to overemphasise their problem. They are usually demonstrative, the hands being used to point out various painful areas almost without prompting. There is diffuse tenderness even to the slightest touch and the physical disability is out of proportion to the alleged symptoms. The pain distribution is often atypical of any dermatome and the reflexes are almost always hyperactive. It must be remembered that

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prostate

Main three

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bronchus

breast

} some mainly

osteosclerotic metastases

osteolytic metastases

melanoma

kidney thyroid

FIGURE 38.11 Important primary malignancies metastasising to the spine. Note the difference between sclerotic and osteoporotic metastases; multiple myeloma also causes osteoporotic lesions

patients with psychogenic back pain—for example, depression and conversion disorders—do certainly experience back pain and do not fall for the traps set for the malingerer. Tests for non-organic back pain7 Several tests are useful in differentiating between organic and non-organic back pain (e.g. that caused by depression or complained of by a known malingerer).

Magnuson method (the ‘migratory pointing’ test) 1 Request the patient to point to the painful sites.

2 Palpate these areas of tenderness on two occasions separated by an interval of several minutes, and compare the sites. Between the two tests divert the patient’s attention from his or her back by another examination.

Paradoxical straight leg raising test Perform the usual SLR test. The patient might manage a limited elevation, for example, 30°. Keep the degree in mind. Ask the patient to sit up and swing the leg over the end of the couch. Distract attention with another test or some question, and then attempt to lift the straight leg to the same level achieved on

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Table 38.6

Comparison of general clinical features of organic and non-organic based low back pain8

Symptoms

Organic disorders

Non-organic disorders

Presentation

Appropriate

Often dramatic

Pain

Localised

Bilateral/diffuse Sacrococcygeal

Pain radiation

Appropriate Buttock, specific sites

Inappropriate Front of leg/whole leg

Time pattern

Pain-free times

Constant, acute or chronic

Paraesthesia/anaesthesia

Dermatomal Points with finger

May be whole leg Shows with hands

Response to treatment

Variable Delayed benefit

Patient often refuses treatment Initial improvement (often dramatic) then deterioration (usually within 24 hours)

Observation

Appropriate Guarded

Overreactive under scrutiny Inconsistent

Tenderness

Localised to appropriate level

Often inappropriate level Withdraws from probing finger

Signs

38

Spatial tenderness (Magnuson)

Consistent

Inconsistent

Active movements

Specific movements affected

Often all movements affected

Axial loading test

No back pain (usually)

Back pain

SLR ‘distraction’ test

Consistent

Inconsistent

Sensation

Dermatomal

Non-anatomical ‘sock’ or ‘stocking’

Motor

Appropriate myotome

Muscle groups (e.g. leg ‘collapses’)

Reflexes

Appropriate May be depressed

Brisk hyperactive

the first occasion. If it is possible, then the patient’s response is inconsistent.

2 This will cause no discomfort to (most) patients with organic back pain.

Burn’s ‘kneeling on a stool’ test

Treatment options for back pain

1 Ask the patient to kneel on a low stool, lean over and try to touch the floor. 2 The person with non-organic back pain will usually refuse on the grounds that it would cause great pain or that he or she might overbalance in the attempt. Patients with even a severely herniated disc usually manage the task to some degree.

The axial loading test 1 Place your hands over the patient’s head and press firmly downward (see FIG. 38.12).

General aspects of management1,6 The aim of treatment is to reduce pain, maintain function and minimise disability and work absenteeism and importantly the risk of chronicity. Advice to stay active. Evidence from randomised controlled trials confirms that, in people with acute low back pain, advice to stay active speeds symptomatic recovery, reduces chronic disability and results in less time off work compared with bed rest or usual care.6 Encourage the patient to stay at work or return early if possible. Keep moving despite discomfort.7

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(a)

FIGURE 38.12 The axial loading test

The caring knowledgeable therapist. Evidence supports the positive value of education and reassurance from a confident, supportive and knowledgeable therapist. Relative rest. For acutely painful debilitating back problems, 2 days of strict rest lying on a firm surface is optimal treatment.9 Resting for longer than 3 days does not produce any significant healing, and patients should be encouraged to return to activities of daily living as soon as possible. Patient education. Appropriate educational material leads to a clear insight into the causes and aggravation of the back disorder plus coping strategies. Heat. The application of heat in some form, including heat bags, hot flannels and similar methods, can be of benefit especially in the first 2–4 weeks of acute low back pain. Exercises. An early graduated exercise program as soon as the acute phase settles has been shown to promote healing and prevent relapses.10 All forms of exercise (extension, flexion and isometric) appear to be equally effective (see FIG.  38.13). Swimming is an excellent activity for back disorders. Studies support the use of exercises for chronic back pain rather than acute pain.3

Pharmacological agents Basic analgesics Analgesics such as paracetamol and codeine plus paracetamol (acetaminophen) should be used for pain

(b)

FIGURE 38.13 Examples of exercises for low back pain: (a) rotation exercise; (b) flexion exercise

relief. Paracetamol is recommended as the first-line analgesic. NSAIDs These are useful where there is clinical evidence of inflammation, especially with the spondyloarthropathies, severe spondylosis and in acute radicular pain, to counter the irritation on the nerve root. NSAIDs have been shown to be more effective than placebo in acute back pain for pain relief and overall improvement. There is no evidence to distinguish different NSAIDs.3

Injection techniques Trigger point injection This may be effective for relatively isolated points using 5–8 mL of local anaesthetic. Studies indicate that it is likely to be more beneficial for chronic back pain.3 Chymopapain This enzyme has been advocated for the treatment of acute nuclear herniation that is still intact. The indications are similar for surgical discectomy. However, studies show that although it is more effective than placebo, it is less effective than surgical discectomy.11

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Facet joint injection Corticosteroid injection under radio-image intensification is widely used in some clinics. The procedure is delicate and expertise is required. Best evidence to date does not support the use of these injections. Epidural injections Injections of local anaesthetic with or without corticosteroids are used for chronic pain, especially for nerve root pain. The author favours the caudal (trans-sacral) epidural injection for persistent sciatica using 15 mL of half-strength local anaesthetic only (e.g. 0.25% bupivacaine) (see FIG. 38.14). Others favour the use of steroids and the lumbar epidural approach. The evidence regarding effectiveness is conflicting.5 sacral hiatus

• • • • •

hydrotherapy traction TENS therapeutic ultrasound facet joint injection

end of dural sac

FIGURE 38.14 Caudal epidural injection: the needle should lie free in the space and be well clear of the dural sac

Physical therapy 38

evidence for the efficacy of these modalities is still lacking:

Active exercises are the best form of physical therapy (see FIGS 38.13a, b). Passive spinal stretching at the end range is a safe, effective method (see FIG. 38.15). Spinal mobilisation is a gentle, repetitive, rhythmic movement within the range of movement of the joint. It is safe and quite effective and a variation of stretching. Spinal manipulation is a high velocity thrust at the end range of the joint. It is generally more effective and produces a faster response but requires accurate diagnosis and greater skill. It is more effective for uncomplicated dysfunctional low back pain (without radicular pain), especially acute pain (see FIG.  38.16).3,6,12,13 However, the evidence from controlled trials is conflicting. Adverse effects are uncommon, but can be serious. Other treatments The following treatments have advocates for the management of back pain, although clear-cut

FIGURE 38.15 Lumbosacral spinal stretching technique (for right sided pain): a traditional technique. Illustration of direction of line of force Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 19897

FIGURE 38.16 Lumbar spinal stretching manipulation: illustration of the specific technique for the L4–5 level with arrows indicating the direction of applied force Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 19897

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Low back pain • posterior nerve root (medial branch) blocks with or without denervation (by cryotherapy or radiofrequency) • percutaneous vertebroplasty (injection of bone cement into fractured vertebra of osteoporosis) • deep friction massage (in conjunction with mobilisation and manipulation) • acupuncture (evidence for short-term benefit) • pain clinic (if unresponsive to initial treatments) • biofeedback • gravitational methods (home therapy) • lumbar supports

MANAGEMENT GUIDELINES FOR LUMBOSACRAL DISORDERS (SUMMARY) The management of ‘mechanical’ back pain depends on the cause. Since most of the problems are mechanical and there is a tendency to natural resolution, conservative management is quite appropriate. The rule is: ‘if patients with uncomplicated back pain receive no treatment, one-third will get better within 1 week and by 3 weeks almost all the rest of the other two-thirds are better’.14 Practitioners should have a clear-cut management plan with a firm, precise, reassuring and conservative clinical approach. The problems can be categorised into general conditions for which the summarised treatment protocols are outlined. • Acute pain = pain less than 6 weeks. • Subacute pain = pain 6–12 weeks • Chronic pain = pain greater than 12 weeks

Management of low back pain • • • • •

• • •

Explanation and reassurance Back education program Encouragement of normal daily activities, including work, according to degree of comfort Regular non-opioid analgesics (e.g. paracetamol) Physical therapy: stretching of affected segment, muscle energy therapy, spinal mobilisation or manipulation (if no contraindication)11,13,15 Prescribe exercises (provided no aggravation) Review in about 5 days (probably best time for physical therapy) No investigation needed initially

Acute low back pain6 The common problem of low back pain caused by facet joint dysfunction and/or limited disc

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disruption usually responds well to the following treatment (see box). The typical patient is aged 20–55 years, is well and has no radiation of pain below the knee.15 Most of these patients can expect to be relatively pain free in 14 days and can return to work early (some may not miss work and this should be encouraged). The evidence concerning spinal manipulation is that it reduces the period of disability.

Sciatica with or without low back pain Sciatica is a more complex and protracted problem to treat, but most cases will gradually settle within 12 weeks (refer to CHAPTER 66). Acute6 • Explanation and reassurance • Back education program • Resume normal activities as soon as possible • Regular non-opioid analgesics with review as the patient mobilises • NSAIDs for 10–14 days, then cease and review • If severe pain unrelieved add tramadol 50–100 mg (o) or oxycodone 5–10 mg (o) 4 hourly as necessary, for short-term use6 • Walking and swimming • Weekly or 2-weekly follow-up • Consider: a course of corticosteroids for severe pain,6 e.g. prednisolone 50 mg for 5 days, then 25 mg for 5 days, gradually tapering to 3 weeks in total. or 30 mg daily mane for 3 weeks, tapering to 0 over next 2 weeks (efficacy not clearly established) Chronic • Reassurance that problem will subside (assuming no severe neurological defects) • Consider epidural anaesthesia (if slow response) • Consider amitriptyline 10–25 mg (o) nocte increasing to maximum 75–100 mg Note: An important controlled prospective study comparing surgical and conservative treatment in patients with sciatica over 10 years showed that there was significant relief of sciatica in the surgical group for 1 to 2 years but not beyond that time. At 10 years both groups had the same outcome, including neurological deficits.16

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Sacroiliac dysfunction See CHAPTER 66.

Chronic back pain The basic management of the patient with uncomplicated chronic back pain should follow the following guidelines: • • • • • • • • •

back education program and ongoing support encouragement of normal activity exercise program analgesics (e.g. paracetamol) NSAIDs for 14–21 days (especially if inflammation, i.e. pain at rest—relieved by activity) and review trial of mobilisation or manipulation (at least three treatments)—if no contraindications12,13 consider trigger point injection consider amitriptyline 10–25 mg (o), note increasing to maximum 75–100 mg (o) a multidisciplinary team approach is recommended/back schools

General guidelines for surgical intervention for radiculopathy

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Absolute • Bladder/bowel control disturbance; perineal sensory change • Progressive motor disturbance (e.g. significant foot drop, weakness in quadriceps) Relative • Severe prolonged pain or disabling pain • Failure of conservative treatment with persistent pain (problem of permanent nerve damage) • If all 4 of the following criteria are met:6 — leg pain equal to or worse than back pain — positive straight leg raise test — no response to conservative therapy after 4–6 weeks — imaging shows a lesion corresponding to symptoms

Prevention of further back pain Patients should be informed that an ongoing back care program should give them an excellent outlook. Prevention includes: • education about back care, including a good layperson’s reference • golden rules to live by: how to lift, sit, bend, play sport and so on

• an exercise program: a tailor-made program for the patient • posture and movement training, such as the Alexander technique17 or the Feldenkrais technique18

When to refer Urgent referral • Myelopathy, especially acute cauda equina compression syndrome • Severe radiculopathy with progressive neurologic deficit • Spinal fractures

Other referrals • • • • •

Recalcitrant spinal canal stenosis Neoplasia or infection Undiagnosed back pain Paget disease Continuing pain of 3 months’ duration without a clearly definable cause

Practice tips •

• •

•

•

•

•

• •

Back pain that is related to posture, aggravated by movement and sitting, and relieved by lying down is due to vertebral dysfunction, especially a disc disruption. The pain from most disc lesions is generally relieved by rest. Plain X-rays are of limited use, especially in younger patients, and may appear normal in disc prolapse. Remember the possibility of depression as a cause of back pain; if suspected, consider a trial of antidepressants. If back pain persists, possibly worse during bed rest at night, consider malignant disease, depressive illness or other systemic diseases. Pain that is worse on standing and walking, but relieved by sitting, is probably caused by spondylolisthesis. If pain and stiffness is present on waking and lasts longer than 30 minutes upon activity, consider inflammation. Avoid using strong analgesics (especially opioids) in any chronic non-malignant pain state. Bilateral back pain is more typical of systemic diseases, while unilateral pain typifies mechanical causes.

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Low back pain

•

•

• •

• • • • •

•

Back pain at rest and morning stiffness in a young person demand careful investigation: consider inflammation such as ankylosing spondylitis and reactive arthritis. A disc lesion of L5–S1 can involve both L5 and S1 roots. However, combined L5 and S1 root lesions should still be regarded with suspicion (e.g. consider malignancy). A large central disc protrusion can cause bladder symptoms, either incontinence or retention. Low back pain of very sudden onset with localised spasm and protective lateral deviation may indicate a facet joint syndrome. The T12–L1 and L1–2 discs are the groin pain discs. The L4–5 disc is the back pain disc. The L5–S1 disc is the leg pain disc. Severe limitation of SLR (especially to less than 30º) indicates lumbar disc prolapse. A preventive program for dysfunctional back pain based on back care awareness and exercises is mandatory advice. Remember that most back problems resolve within a few weeks, so avoid overtreatment.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Backache • Exercises for your lower back • Sciatica • Spondylosis

References 1 National Health and Medical Research Council. Evidencebased Management of Acute Musculoskeletal Pain. A Guide for Clinicians. Australian Acute Musculoskeletal Pain Guidelines Group. Canberra: Australian Government, 2004.

2 Sloane P, Slatt M, Baker R. Essentials of Family Medicine. Baltimore: Williams & Wilkins, 1988: 228–35. 3 Barton S (ed.). Clinical Evidence. London. BMJ Publishing Group, 2001: 772–87. 4 Maigne R. Manipulation of the spine. In: Basmajian JV (ed.), Manipulation, Traction and Massage. Paris: RML, 1986: 71–96. 5 Bogduk N. The sources of low back pain. In: Jaysom M, (ed.), The Lumbar Spine and Back Pain (4th edn), Edinburgh: Churchill Livingstone, 1992: 61–88. 6 Moulds R (Chair). Therapeutic Guidelines: Rheumatology (Version 2). Melbourne: Therapeutic Guidelines Ltd, 2010: 109–40. 7 Kenna C, Murtagh J. Back Pain and Spinal Manipulation (2nd edn). Oxford: Butterworth Heinemann, 1997: 70–164. 8 Kamper SJ, Maher CG, Buchbinder R. Non-specific low back pain: manage initially with reassurance, activity and analgesia. Modern Medicine, June 2013: 19–35. 9 Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomised clinical trial. N Engl J Med, 1986; 315: 1064–70. 10 Kendall PH, Jenkins SM. Exercises for backache: a double blind controlled study. Physiotherapy, 1968; 54: 154–7. 11 Gibson JNA et al. Surgery for lumbar disc prolapse. Cochrane Database of Systematic Reviews, Issue 2, 2002. 12 Blomberg S, Svardsudd K, Mildenberger F. A controlled, multicentre trial of manual therapy in low back pain. Scand J Prim Health Care, 1992; 10: 170–8. 13 Royal College of General Practitioners et al. Clinical Guidelines for the Management of Acute Low Back Pain. London: RCGP, 1996. 14 Kuritzky L. Low back pain. Family Practice, Audio-Digest California Medical Association: 1996; 44: 14. 15 Deyo RA. Acute low back pain: a new paradigm for management. Br Med J, 1996; 313: 1343–4. 16 Weber et al. A controlled prospective study with 10 years observation of patients with sciatica. Spine, 1983; 8: 131–40. 17 Hodgkinson L. The Alexander Technique. London: Piatkus, 1988: 1–97. 18 Feldenkrais M. Awareness Through Movement. New York: Harper & Row, 1972.

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Bruising and bleeding

My pa is one mask of brooses both blue and green. Charles Dickens (–), Nicholas Nickleby Many patients present with the complaint that they bruise easily but only a minority turn out to have an underlying blood disorder. Purpura is bleeding into the skin or mucous membranes, appearing as multiple small haemorrhages that do not blanch on pressure. Smaller purpuric lesions that are 2 mm or less in diameter (pinhead size) are termed petechiae, while larger purpuric lesions are called ecchymoses (see FIG. 39.1). Bruises are large areas of bleeding that are a result of subcutaneous bleeding. If bruising is abnormal and out of proportion to the offending trauma, then a disturbance of coagulation is suggested (see FIG. 39.2).

Differential diagnosis ‘Palpable purpura’ due to an underlying systemic vasculitis is an important differential problem. The petechiae are raised so finger palpation is important. The cause is an underlying vasculitis affecting small vessels (e.g. polyarteritis nodosa). The decision to investigate is difficult because decisions have to be made about which patients FIGURE 39.2 Severe bleeding in a diabetic patient with systemic fibrinolysis. Note the bleeding following insulin injections into the abdominal wall and an injection into the shoulder joint. Source: Photo courtesy Hatem Salem

petechiae

purpura

ecchymosis

warrant investigation and whether the haemostatic defect is due to local or systemic pathology.1 The ability to identify a bleeding disorder is important because of implications for surgery, pregnancy, medication and genetic counselling.

Key facts and checkpoints • • FIGURE 39.1 Purpuric rash (petechiae and ecchymoses)

Purpura = petechiae + ecchymoses. Abnormal bleeding is basically the result of disorders of (1) the platelet, (2) the coagulation mechanism or (3) the blood vessel.

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Bruising and bleeding

•

•

•

•

•

• •

•

There is no substitute for a good history in the assessment of patients with bleeding disorders. An assessment of the personal and family histories is the first step in the identification of a bleeding disorder. When a patient complains of ‘bruising easily’ it is important to exclude thrombocytopenia due to bone marrow disease and clotting factor deficiencies such as haemophilia. The commonest cause of an acquired bleeding disorder is drug therapy (e.g. aspirin, NSAIDs, cytotoxics and oral anticoagulants). In general, bleeding secondary to platelet defects is spontaneous, associated with a petechial rash and occurs immediately after trauma or a cut wound.1 The bleeding is usually mucosal (e.g. bleeding from gingiva, menorrhagia, epistaxis and petechiae). Laboratory assessment should be guided by the clinical impression. Bleeding caused by coagulation factor deficiency is usually traumatic and delayed (e.g. haemorrhage occurring 24 hours after a dental extraction in a haemophiliac). The routine screening tests for the investigation of patients with bleeding disorders can occasionally be normal despite the presence of an undeniable bleeding disorder and even a severe haemorrhagic state. Second-line investigations will need to be undertaken.

Causes of clinical disorders The three major mechanisms of systemic bleeding disorders are (the Virchow triad): 1 coagulation deficiencies (reduction or inhibition of circulatory coagulation factors) 2 platelet abnormalities: of platelet number or function 3 vascular defects: of vascular endothelium Bleeding disorders can also be divided into impaired primary or secondary haemostasis. Primary haemostatic disorders which are the most common include von Willebrand disease (vWD), thrombocytopenia and platelet function disorders. Examples of disorders of secondary haemostasis are disorders of fibrin formation and the haemophilias.2 A list of differential diagnoses of systemic bleeding disorders is presented in TABLE 39.1.1

Table 39.1

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Differential diagnoses of systemic bleeding disorders

Vascular disorders (a) Inherited: • hereditary haemorrhagic telangiectasia • Marfan syndrome (b) Acquired: • infection (e.g. meningococcus, measles, dengue) • purpura simplex • senile purpura • Henoch–Schönlein purpura • steroid purpura • vitamin C deficiency (scurvy) Coagulation factor deficiency or inhibitor (a) Inherited: • haemophilia A • haemophilia B • vWD (b) Acquired: • disseminated intravascular coagulation (DIC) • liver disease • vitamin K deficiency • oral anticoagulant therapy or overdosage Thrombocytopenia (a) Inherited: • Fanconi syndrome • amegakaryocytic thrombocytopenia (b) Acquired: (Immune) • immune thrombocytopenic purpura • drug-induced thrombocytopenia (e.g. heparin) • thrombotic thrombocytopenic purpura • post-transfusion purpura (Non-immune) • disseminated intravascular coagulation • bone marrow replacement or failure • splenic pooling Functional platelet disorders (a) Inherited: • Glanzmann thrombasthenia • Bernard–Soulier syndrome • storage pool deficiency (b) Acquired: • drug-induced (e.g. aspirin, NSAIDs) • uraemia /kidney failure • myeloproliferative disorders • dysproteinaemias Source: After Mitchell et al.1 Adapted from Bleeding disorders, MIMS Disease Index (2nd edn) 1996 with permission of MIMS Australia, a division of MediMedia Australia Pty Ltd

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The clinical approach Differentiation of coagulation factor deficiencies and platelet disorders as the cause of a bleeding problem can usually be determined by a careful evaluation of the history and physical examination.

History Factors that suggest the presence of a systemic bleeding defect include: • spontaneous haemorrhage • severe or recurrent haemorrhagic episodes e.g. epistaxis • bleeding from multiple sites • bleeding out of proportion to the degree of trauma • cutaneous bleeding • gastrointestinal bleeding • postpartum haemorrhage • bleeding from tooth extraction/oral cavity • menorrhagia • muscle haematomas or haemarthrosis If a bleeding diathesis is suspected it is essential to determine whether local pathology is contributing to the blood loss (e.g. postoperative bleeding, postpartum bleeding, gastrointestinal haemorrhage).

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Diagnostic tips • Platelet abnormalities present as early bleeding following trauma. • Coagulation factor deficiencies present with delayed bleeding after initial haemostasis is achieved by normal platelets. • A normal response to previous coagulation stresses (e.g. dental extraction, circumcision or pregnancy) indicates an acquired problem. • If acquired, look for evidence of MILD: Malignancy, Infection, Liver disease, Drugs. • A diagnostic strategy is outlined in TABLE 39.2. Family history A positive family history can be a positive pointer to the diagnosis: • sex-linked recessive pattern: haemophilia A or B • autosomal dominant pattern: vWD, dysfibrinogenaemias • autosomal recessive pattern: deficiency of coagulation factors V, VII and X Enquire whether the patient has noticed blood in the urine or stools and whether menorrhagia is present in women. A checklist for a bleeding history is

Table 39.2

Purpura: diagnostic strategy model

Q. Probability diagnosis A. Simple purpura (easy bruising syndrome) Senile purpura Corticosteroid-induced purpura Immune thrombocytopenic purpura Henoch–Schönlein purpura Liver disease, especially alcoholic cirrhosis Increased intravascular pressure, e.g. coughing, vomiting Q. Serious disorders not to be missed A. Malignant disease: • leukaemia • myeloma Aplastic anaemia Myelofibrosis Severe infections: • septicaemia • meningococcal infection • measles • typhoid • dengue/chikungunya Disseminated intravascular coagulation Thrombotic thrombocytopenic purpura Fat embolism Q. Pitfalls (often missed) A. Haemophilia A, B vWD Post-transfusion purpura Trauma (e.g. domestic violence, child abuse) Rarities: • hereditary telangiectasia (Osler–Weber–Rendu syndrome) • Ehlers–Danlos syndrome • scurvy • Fanconi syndrome Q. The masquerades A. Drugs: examples (see ‘Medication Record’) • sodium valproate • various antibiotics • quinine/quinidine • thiazide diuretics • NSAIDs/salicylates • cytotoxics • oral anticoagulants/heparin Anaemia: • aplastic anaemia Q. Psychogenic factors A. Factitial purpura

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Bruising and bleeding

Table 39.3

Checklist for a bleeding history

Skin bruising

Tonsillectomy

Epistaxis

Other operations

Injury

Childbirth

Domestic violence

Haematuria

Menorrhagia

Rectal bleeding

Haemarthrosis

Drugs

Tooth extraction

Family history

Unusual haematomas

Comorbidities (e.g. liver disease, kidney disease)

presented in TABLE 39.3. The actual size and frequency of the bruises should be recorded where possible and if none are present at the time of the consultation the patient should return if any bruises reappear. Key questions • How long has the problem been apparent to you? • Do you remember any bumps or falls that might have caused the bruising? • What sort of injuries cause you to bruise easily? • Have you noticed bleeding from other areas such as your nose or gums? • Has anyone in your family had a history of bruising or bleeding? • What is your general health like? • Do you have any tiredness, weight loss, fever or night sweats? • Did you notice a viral illness or sore throat beforehand? • How much alcohol do you drink? • What happened in the past when you had a tooth extracted? • Have you ever had painful swelling in your joints? Medication record It is mandatory to obtain a complete drug history. Examples of drugs and their responses are: • vascular purpura: — prednisolone/other steroids • thrombocytopenia: — cytotoxic drugs — carbamazepine — gold — sodium valproate — heparin — ranitidine — sulphonamides

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— quinine, quinidine — thiazide diuretics — penicillins, vancomycin — chloramphenicol • functional platelet abnormalities: — aspirin — NSAIDs • coagulation factor deficiency: — warfarin

Examination Careful examination of the skin is important. Note the nature of the bleeding and the distribution of any rash, which is characteristic in Henoch–Schönlein purpura. Senile purpura in the elderly is usually seen over the dorsum of the hands, extensor surface of the forearms and the shins. Purpura on the legs indicates platelet disorders, meningococcal septicaemia and paraproteinaemias; on the fingers and toes indicates vasculitis. Note the lips and oral mucosa for evidence of hereditary telangiectasia. Gum hypertrophy occurs in monocytic leukaemia. Search for evidence of malignancy, such as sternal tenderness, lymphadenopathy and splenomegaly. Examine the ocular fundi for evidence of retinal haemorrhages. Urinalysis, searching for blood (microscopic or macroscopic), is important.

Investigations The initial choice of investigations depends upon the bleeding pattern. If coagulation defect suspected: • • • •

prothrombin time (PT), i.e. INR activated partial thromboplastin time (APTT) fibrinogen level thrombin time (TT) If platelet pathology suspected:

• platelet count • skin bleeding time (of doubtful value) • platelet function analyser (PFA-100) If inherited disorders suspected: • factor VIII • vW factor activity • vW factor antigen The full blood examination and blood film is useful in pinpointing the aetiology. Platelet morphology gives a diagnostic guide to inherited platelet disorders. The skin-bleeding time as a screening test of haemostasis has been shown recently to be severely limited by its lack of specificity and sensitivity and

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its routine use cannot be recommended. It is not a useful predictor of surgical risk of haemorrhage.1,3 Other sophisticated tests, such as von Willebrand’s screen and platelet aggregation (e.g. PFA-100), can be advised by the consulting haematologist. One of considerable value is the bone marrow examination, which is useful to exclude the secondary causes of thrombocytopenia, such as leukaemia, other marrow infiltrations and aplastic anaemia. Other tests to consider: ESR/CRP, autoimmune screening, LFTs, plasma electrophoresis, skin biopsy. Be cautious of pseudo-thrombocytopenia due to laboratory error—exclude on a blood film and consider a repeat collection. A summary of appropriate tests is presented in TABLE 39.4 and of blood changes for some coagulation factor deficiencies in TABLE 39.5.

Abnormal bleeding in children Abnormal bleeding in children is not uncommon and once again the clinical history, particularly the past and family history, provides the most valuable information. It is important to keep non-accidental injury, such as child abuse, in mind in the child presenting with ‘easy bruising’. However, it is appropriate to exclude a bleeding disorder, especially a platelet disorder. Vigorous coughing or vomiting in a child can cause petechiae on or around the eyelids. Coagulation disorders, including haemophilia and vWD, are usually suspected on clinical grounds because of widespread bruising or because of prolonged bleeding following procedures such as circumcision and tonsillectomy. Table 39.4

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Laboratory investigation checklist for the easy bruiser

A common condition is haemorrhagic disease of the newborn, which is a self-limiting disease usually presenting on the second or third day of life because of a deficiency of coagulation factors dependent on vitamin K. The routine use of prophylactic vitamin K in the newborn infant has virtually eliminated this problem. Idiopathic (immune) thrombocytopenic purpura (ITP) is the commonest of the primary platelet disorders in children. Both acute and chronic forms have an immunological basis. The diagnosis is based on the peripheral blood film and platelet count. The platelet count is commonly below 50 000/mm3 (50  ×  109/L). Spontaneous remission within 4 to 6 weeks occurs with acute ITP in childhood.3 The commonest vascular defects in childhood are: • anaphylactoid (Henoch–Schönlein) purpura • infective states • nutritional deficiency (usually inadequate dietary vitamin C)

Henoch–Schönlein purpura HSP is the commonest vasculitis of children. It affects small vessels, producing a leucocytoclastic vasculitis with a classic triad of non-thrombocytopenic purpura, large joint arthritis and abdominal pain. It is diagnosed clinically by the characteristic distribution of the rash (which is a palpable purpura) over the lower limbs, extending onto the buttocks (see FIG. 39.3), but it can also involve the upper limbs, trunk and even the face. The onset of HSP typically follows an upper respiratory tract infection including a group A streptococcal tonsillopharyngitis. The bleeding time, coagulation time and platelet counts are normal. The prognosis is good; most recover fully in a few months.

Full blood count Platelet count Prothrombin time (INR) Thrombin time (TT) Activated partial thromboplastin time

Table 39.5

PT APTT TT

Blood changes for specific coagulation factor disorders Haemophilia A

vWD

Vitamin K deficiency

Normal ↑

Normal ↑

↑ ↑

Normal

Normal

Normal

FIGURE 39.3 Henoch–Schönlein purpura in a 5-year-old boy showing the typical distribution of the rash on the lower limbs

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abdominal pain

haematuria

typical sites of purpura (palpable) arthritis

FIGURE 39.4 Henoch–Schönlein purpura: typical distribution

Clinical features • All ages, mainly in children • Rash, mainly on buttocks and legs (see FIG. 39.4)4 • Rash can occur on hands, arms and trunk • Arthritis: mainly ankles and knees • Abdominal pain—colicky (vasculitis of GIT) • Haematuria (reflects nephritis) Associations • Kidney involvement—deposition of IgA immune complex (a serious complication) • Melaena • Intussusception • Scrotal involvement Investigations • FBE • Urine: protein and blood; spun specimen, micro for casts

Management • Largely symptomatic—analgesics • No specific therapy • Short course of steroids for abdominal pain (if intussusception excluded) • If haematuria: follow-up urine microscopy and kidney function especially if no resolution

DxT arthralgia + purpuric rash ± abdominal pain Henoch–Schönlein purpura

Practice tip Beware of CKF.

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Infective states The purpura associated with severe infections, such as meningococcaemia and other septicaemias, is due primarily to a severe angiitis. Disseminated intravascular coagulation usually follows.3

Abnormal bleeding in the elderly The outstanding causes are senile purpura and purpura due to steroids.5 The cause in both instances is atrophy of the vascular supporting tissue.

VASCULAR DISORDERS The features are: • easy bruising and bleeding into skin • ± mucous membrane bleeding • investigations normal

Simple purpura (easy bruising syndrome) This is a benign disorder occurring in otherwise healthy women usually in their 20s or 30s. The feature is bruising on the arms, leg and trunk with minor trauma. The patient may complain of heavy periods. Major challenges to the haemostatic mechanism, such as dental extraction, childbirth and surgery, have not been complicated by excessive blood loss.

Factitial purpura Unexplained bruising or bleeding may represent selfinflicted abuse or abuse by others. In self-inflicted abuse the bruising is commonly on the legs or areas within easy reach of the patient.

PLATELET DISORDERS

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The features are: • petechiae ± ecchymoses • bleeding from mucous membranes • platelet counts 25% length R wave — occurs normally in leads AVR and V1; III (sometimes) — abnormal if in other leads — occurs also with LBBB, WPW and ventricular tachycardia (VT) — usually permanent feature after full thickness AMI • T wave and ST segment: — transient changes (inversion and elevation respectively) The typical progression is shown in FIGURE 40.18. Note: • Q waves do not develop in subendocardial infarction. • The strategies for management of AMI are based on the distinction between Q wave (transmural) or non-Q wave (subendocardial) infarction. • Q wave infarction has been proved to benefit from thrombolytic therapy but non-Q wave infarction has not. • A normal ECG, especially early, does not exclude AMI. Q waves may take days to develop. 2 Cardiac enzymes. The typical enzyme patterns are presented in FIGURE 40.19. As a rule, large infarcts tend to produce high serum enzyme levels. The elevated enzymes can help time the infarct: • Troponin I or T: — starts rising at 3–6 hours, peaks at 10 hours and persists for about 5–14 days — now the preferred test — positive in unstable angina

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before

Serum enzyme level

troponin

CK

24 minutes afterwards Onset of AMI

48 72 Time in hours

96

120

FIGURE 40.19 Typical cardiac enzyme patterns following myocardial infarction

hours afterwards

4 Echocardiography. This is used to assist diagnosis when other tests are not diagnostic. Note: The clinical diagnosis may be the most reliable, as the ECG and enzymes may be negative.

Management of acute coronary syndromes days afterwards

weeks afterwards

FIGURE 40.18 Typical evolution of ECG changes with myocardial infarction

— may have to wait until 10 hours before recording a negative result — not useful for repeat MI — both proteins, I and T, provide same information — reference interval 15% of total CK; unlike CK, it is not affected by intramuscular injections 3 Technetium pyrophosphate scanning • It is performed from 24 hours to 14 days after onset. • It scans for ‘hot spots’, especially when a posterolateral AMI is suspected and ECG is unhelpful because of pre-existing LBBB.

General principles10,11 • Aim for immediate attendance if suspected. • Pre-hospital: make diagnosis, assess risk, ensure stability. • Call a mobile coronary care unit. • Achieve coronary perfusion and minimise infarct size. • Prevent and treat cardiac arrest; have a defibrillator available to treat ventricular fibrillation. • Optimal treatment is in a modern coronary care unit (if possible) with continuous ECG monitoring (first 48 hours), a peripheral IV line and intranasal oxygen. • Pay careful attention to relief of pain and apprehension. • Establish a caring empathy with the patient. • Give aspirin as early as possible (if no contraindications). • Prescribe a beta blocker and an ACE inhibitor early (if no contraindications). Note: For a STEMI it is important to re-establish flow as soon as possible, usually by either thrombolytic therapy or primary angioplasty (preferably with stenting). Rescue angioplasty is usually used when large infarcts have not perfused at 60–90 minutes.9 Hospital management9,11 • As for first-line management. • Confirm ECG diagnosis: STEMI or NSTEACS.

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• Take blood for cardiac enzymes particularly troponin levels, urea and electrolytes. • Organise an urgent cardiology consultation for risk stratification and a decision whether to proceed to coronary angiography and coronary reperfusion with PCI (or CABG) or with thrombolysis.

Management of STEMI11 The optimal first-line treatment for the patient with a STEMI is urgent referral to a coronary catheter laboratory ideally within 60 minutes (the golden hour) of the onset of pain for assessment after coronary angiography for percutaneous transluminal coronary angioplasty (PTCA). If available and performed by an interventional cardiologist it has the best outcomes (level I evidence). The principle is to achieve rapid reperfusion via primary angioplasty with a stent (optimal stent status currently under evaluation). Adjunct therapy will include aspirin/clopidogrel and heparin and possibly a glycoprotein IIb/IIIa platelet inhibitor such as prasugrel, ticagrelor or abciximab.

First-line management (e.g. outside hospital) •

• • •

• •

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Perform an ECG and classify ACS into STEMI or NSTEACS, and notify the medical facility that will receive the patient (discuss over the telephone). The ECG is the sole test required to select patients for emergency perfusion Oxygen 4–6 L/min (aim to keep PaO2 >90%) Secure an IV line (withdraw blood for tests especially troponin levels) Glyceryl trinitrate (nitroglycerine) 300 mcg (½ tab) SL or spray (every 5 minutes as necessary to maximum of three doses). Beware of sildenafil (Viagra) and related drugs use and bradycardia—correct with atropine Aspirin 300 mg Morphine 2–5 mg IV statim bolus: 1 mg/min until pain relief (up to 15 mg) (If feasible it is preferable to give IV morphine 1 mg/min until relief of pain; this titration is easier in hospital.)

Management of NSTEACS All patients with NSTEACS should have their risk stratified to direct management decisions. Fibrinolytic therapy If angioplasty is unachievable either through timing or the unavailability of the service (such as in rural locations) thrombolysis is an indication for STEMI and the sooner the better, but preferably within 12 hours of the commencement of chest pain.11 The decision should be made by an experienced consultant, especially as PCI is not usually possible once fibrinolytic therapy has been given. Second-generation fibrin-specific agents (reteplase, alteplase or tenecteplase) are the agents of choice. Streptokinase can be used but it is inappropriate for use in Indigenous people and those who have received it on a previous occasion. There are several other contraindications for the use of fibrinolytic agents. Further management strategies include: • Full heparinisation for 24–36 hours (after rt-PA—not after streptokinase), especially for large anterior transmural infarction with risk of embolisation, supplemented by warfarin. • Use LMW heparin (e.g. enoxaparin 1 mg/kg SC bd or unfractionated heparin 5000–7500 units SC 12 hourly). • Beta blocker (if no thrombolytic therapy or contraindications) as soon as possible: atenolol 25–100 mg (o) daily or metoprolol 25–100 mg (o) twice daily • Consider glyceryl trinitrate IV infusion if pain recurs. • Start early introduction of ACE inhibitors (within 24–48 hours) in those with significant left ventricular (LV) dysfunction (and other indications). • Statin therapy to lower cholesterol. • Treat hypokalaemia. • Consider magnesium sulphate (after thrombolysis). • Consider frusemide.

Post-AMI drug management Acceptable time delay guidelines to PCI (from first medical contact to balloon inflation):11 Symptom time:

12 hours

90 minutes

120 minutes

Not recommended

Proven:1,12,13 • beta blockers—within 12 hours • ACE inhibitors—within 24 hours • aspirin 75–150 mg + clopidogrel 75 mg (o) daily (alternatives to clopidogrel: ticagrelor or prasugrel) • lipid-lowering drugs (e.g. statins) • warfarin

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Chest pain Targets: • BP 25% of time • sensation of anorectal obstruction/blockage >25% of time Accordingly it affects more than 1 in 5 in the population.1 However, the emphasis should be on the consistency of the stool rather than on the frequency of defecation; for example, a person passing a hard stool with difficulty once or twice a day is regarded as constipated, but the person who passes a soft

Key facts and checkpoints • • • • • • • • • •

The survey showed 10% of adults and 6% of children reported constipation in the preceding 2 weeks. Up to 20% of British adults take regular laxatives.2 Constipation from infancy may be due to Hirschsprung disorder. Diet is the single most important factor in preventing constipation. Beware of the recent onset of constipation in the middle-aged and the elderly. Bleeding suggests cancer, haemorrhoids, diverticular disorder and inflammatory bowel disease. Unusually shaped stools (small pellets or ribbonlike) suggest irritable bowel syndrome. Always examine the abdomen and rectum. Plain abdominal X-rays are generally not useful in the diagnosis of chronic constipation. The flexible sigmoidoscope is far superior to the rigid sigmoidoscope in investigation of the lower bowel.

•

Intractable constipation (obstipation) is a challenge at both ends of the age spectrum but improved agents have helped with management.

stool comfortably every two or three days is not constipated. Various causes of chronic constipation are summarised in FIGURE 41.1.

A diagnostic approach Using the diagnostic strategy model (see TABLE 41.1), the five self-posed questions can be answered as follows.

Probability diagnosis The commonest is ‘idiopathic’ constipation where there is no structural or systemic disease. This is also referred to as ‘functional’ constipation. Probably the most frequent single factor causing constipation in Western society is deficiency in dietary fibre, including fruit, green leafy vegetables and wholemeal products. The amount of fibre in our diet is directly related to stool weight and to colonic transit time. The average colonic transit time in the large bowel for Westerners is 60 hours; for a rural African on a very high-fibre diet it is 30 hours. Constipation is also a common problem in pregnancy.

Serious disorders not to be missed Neoplasia It is obvious that colonic or anorectal neoplasms must not be missed in a patient, especially middleaged or elderly, presenting with constipation or other change in bowel habit. Most cases present with either complete or incomplete bowel obstruction. Extrinsic malignancy, such as lymphoma or ovarian cancer, compressing or invading the rectum, also has to be considered. Cancer of the large bowel is most prevalent in our society and appropriate screening examinations, including rectal examination, sigmoidoscopy and colonoscopy, must be considered where appropriate.

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• Problem solving in general practice Psychogenic depression anorexia nervosa Neurological disease CVA autonomic neuropathy Parkinson disease Drugs Endocrine/metabolic hypothyroidism hypercalcaemia Idiopathic constipation simple constipation slow transit constipation irritable bowel syndrome

Organic disease of large bowel carcinoma colon diverticular disorder inflammatory bowel disease impacted faeces anorectal disorders carcinoma fissure haemorrhoids Others adynamic bowel Hirschsprung, senility spinal cord injury connective tissue disorders (e.g. scleroderma)

FIGURE 41.1 Causes of chronic constipation

Megacolon In children it is important to detect the presence of megacolon, for example megacolon secondary to Hirschsprung disorder. Symptoms dating from birth suggest Hirschsprung disorder, which occasionally may present for the first time in adult life. Neurological disorders Constipation, often with faecal impaction, is a common accompaniment to paraplegia, multiple sclerosis, cerebral palsy and autonomic neuropathy.

Alarm symptoms

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• • •

Recent constipation in >40 years of age Rectal bleeding Family history of cancer

Pitfalls The pitfalls can be summarised as follows: • impacted faeces • depressive illness

• purgative abuse • local anal lesions • drugs Although patients with impacted faeces usually present with spurious diarrhoea, it is a form of idiopathic constipation and is very commonly encountered in general practice, especially in bedridden elderly people. Anal pain or stenosis, such as fissure-in-ano, thrombosed haemorrhoids, perianal haematoma or ischiorectal abscess, leads to constipation when the patient is hesitant to defecate. General pitfalls and tips • Ensure the patient is truly constipated, and not having unreal expectations of regularity. • Ensure that the anthraquinone group of laxatives, including ‘Ford pills’, is never used long term because they cause melanosis coli and associated megacolon. • Be very wary of alternating constipation and diarrhoea (e.g. colon cancer).

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Constipation • In a busy practice be careful not to let ‘familiarity breed contempt’ (e.g. onset of hyperparathyroidism, cancer). • Avoid relying solely on the rectal examination to exclude cancer.

Seven masquerades checklist Three of the primary masquerades (see TABLE  41.1) are important causes of constipation, namely drugs, depression and hypothyroidism. Many drugs (see TABLE  41.2) may be associated with constipation, especially codeine and its derivatives, antidepressants, aluminium and calcium antacids. A careful drug history is thus mandatory. Fortunately the constipation is usually relieved once the drug

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is withdrawn. Constipation can be a significant symptom in all types of depressive illness and may be aggravated by treatment with antidepressants. Table 41.2

Drugs associated with constipation

Analgesics (inhibitors of prostaglandin synthesis) Antacids (containing calcium carbonate or aluminium hydroxide) Anticholinergic agents, antispasmodics Antidiarrhoeal agents Antiepileptics Antihistamines (H1-receptor blockers)* Antiparkinson drugs*

Table 41.1

Chronic constipation: diagnostic strategy model

Q. Probability diagnosis A. Functional constipation3 • primary—slow transit, dyssynergic defecation • lifestyle—diet, low fluids, bad habits

Antipsychotic drugs* Barbiturates Barium sulphate Benzodiazepines Calcium-channel blockers (verapamil)

Q. Serious disorders not to be missed A. Intrinsic neoplasia: colon, rectum or anus, especially colon cancer Extrinsic malignancy (e.g. lymphoma, ovary) Hirschsprung (children)

Calcium supplements

Q. Pitfalls (often missed) A. Impacted faeces Local anal lesions e.g. fissure, haemorrhoids Drug/purgative abuse Hypokalaemia Depressive illness Acquired megacolon Diverticular disease Rarities: • lead poisoning • hypercalcaemia • hyperparathyroidism • dolichocolon (large colon)/megarectum • Chagas disease • systemic sclerosis

Cytotoxic drugs

Q. Seven masquerades checklist A. Depression Diabetes (autonomic neuropathy) Drugs Thyroid disorder (hypo) Spinal dysfunction (severe only) Q. Is the patient trying to tell me something? A. May be functional (e.g. depression, anorexia nervosa).

Cholestyramine Clonidine Cough mixtures Diuretics that cause hypokalaemia Gabapentin Ganglionic blocking agents Heavy metal (especially lead) Iron supplements Laxatives (chronic use) Monoamine oxidase inhibitors Muscle relaxants Opioid analgesics (e.g. codeine) SSRIs Tricyclic antidepressants* * Denotes anticholinergic effect.

The metabolic causes of constipation include hypothyroidism, hypercalcaemia and porphyria. We occasionally encounter the patient with hypercalcaemia, for example, hyperparathyroidism, but thyroid dysfunction is relatively common in general practice.

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Diabetes rarely can be associated with constipation when an autonomic neuropathy can lead to alternating bouts of constipation and diarrhoea.

Psychogenic considerations Constipation may be a manifestation of an underlying functional problem and psychiatric disorder, such as depression, anorexia nervosa, schizophrenia or drug abuse. Drug abuse must always be considered, keeping in mind that narcotics and laxatives present with rebound constipation. More commonly, it may reflect the inactive lifestyle of the patient and provide a good opportunity for appropriate counselling.

The clinical approach

tested. Digital rectal examination is mandatory, and may reveal a rectal tumour and faecal impaction, as well as testing for rectal size and tone. If there is a history from infancy, a normal or narrow rectum suggests congenital megacolon (Hirschsprung disorder) but, if dilated, acquired megacolon. General signs that may be significant in the diagnosis of constipation are summarised in FIGURE 41.2.

Irregular liver metastases (carcinoma of colon)

History It is important to ask patients to define exactly what they mean by constipation. Some people believe that just as the earth rotates on its axis once a day, so should their bowels open daily to ensure good health. As always, a careful history is appropriate, including stool consistency, frequency, ease of evacuation, pain on defecation and the presence of blood or mucus. A dietary history is very relevant in the context of constipation. Key questions • How often do you go to the toilet? • What are your bowel motions like? • Are they bulky, hard, like rabbit pellets or soft? • Is there pain on opening your bowels? • Have you noticed any blood? • Have you noticed any lumps? • Do you have any soiling on your underwear? • How do you feel in yourself? • What medications are you taking? Diary Ask the patient to keep a 10-day diary recording frequency and nature of stools, and whether any difficulty was experienced when passing stool.

Examination 41

The important aspects are abdominal palpation and rectal examination. Palpation may reveal the craggy mass of a neoplasm, faecal retention (especially in the thin patient) or a tender spastic colon. The perianal region should be examined for localised disease. The patient should be asked to bear down to demonstrate perianal descent, haemorrhoids or mucosal prolapse. Perianal sensation and the anal reflex should be

Distension

Mass in RIF carcinoma Crohn disease

Mass faecal impaction carcinoma

FIGURE 41.2 Possible significant abdominal signs in the patient with constipation

Rectal examination The most important first step is to do the examination.

Method • Explain to the patient what will happen. • After inspection with the patient in the left lateral position and with knees drawn up, a lubricated gloved index finger is placed over the anus. • Part the buttocks. • Ask the patient to concentrate on slow deep breathing.

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Constipation • With gentle backwards pressure the finger is then inserted slowly into the anal canal and then into the rectum (it helps patient comfort if they push down or squeeze to accommodate the finger). • Rotate the finger anteriorly to feel the prostate in males and the cervix in females. • The finger will reach to about 7–8 cm with gentle thrusting into the perineum. • Gently withdraw the finger and examine the whole circumference of the rectum by sweeping the finger from posterior on both sides.

Points to note • Any pain: fissure, proctitis, excoriation from diarrhoea (a rectal examination will not be possible in the presence of a fissure) • Induration from a chronic fissure or fistula in the anal canal • The sphincter tone • The nature of the faeces (? impaction) • The rectal wall: cancer is usually indurated, elevated and ulcerated; a villous adenoma has a soft velvety feel • Posteriorly: the sacrum and coccyx • Laterally: the side walls of the pelvis • Anteriorly: cervix and pouch of Douglas in the female; prostate and rectovesical pouch in the male

Prostate examination • It feels larger if the patient has a full bladder. • The normal prostate is a firm smooth rubbery bilobed structure (with a central sulcus) about 3 cm in diameter. • A craggy hard mass suggests cancer. • An enlarged smooth mass suggests benign hypertrophy. • A tender, nodular or boggy mass suggests prostatitis.

Practice tip on treatment A suitable method of doing a rectal examination on a home visit (in the absence of gloves in the doctor’s bag) is to apply moist soap around the finger and caked under the nail (in case of breakage), then plastic wrap and finally petroleum jelly (e.g. Vaseline). Before resorting to a good old-fashioned ‘3H’ enema (hot water, high and a hell of a lot), use a sorbitol compound (e.g. Microlax 5 mL enema). It can be carried in the doctor’s bag, is very easy to insert and is most effective.

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A common pitfall In the female the cervix or a vaginal tampon can be mistaken for a mobile extrarectal tumour. Endoscopy Sigmoidoscopy—in particular, flexible sigmoidoscopy with examination of the rectosigmoid—is important in excluding local disease; search for abnormalities such as blood, mucus or neoplasia. The insufflation of air sometimes reproduces the pain of the irritable bowel syndrome. It is worth noting that 60% of polyps and cancers will occur in the first 60 cm of the bowel4 and diverticular disorder should be evident with the flexible sigmoidoscope. The presence of melanosis coli is an important sign—it may give a pointer to the duration of the constipation and the consequent chronic intake (perhaps denied) of anthraquinone laxatives.

Investigations These can be summarised as follows: • Haematological: — haemoglobin — ESR • Stools for occult blood • Biochemistry (where suspected): — thyroid function tests — serum calcium — serum potassium — carcinoembryonic antigen (a tumour marker) • Radiological: — CT colonography (virtual colonography) — double contrast barium enema (especially for primary colonic disease, e.g. megacolon) — bowel transit studies, using radio-opaque shapes taken orally and checking progress by abdominal X-ray or stool collection • Physiological tests: — anal manometry—test anal tone — rectal sensation and compliance, using an inflatable rectal balloon — dynamic proctography, to determine disorders of defecation — Rectal biopsy, to determine aganglionia

Constipation in children Constipation is quite common in children but no cause has been discovered in 90–95%. The most common factor is diet. Constipation often begins after weaning or with the introduction of cow’s milk. It is rare with

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breastfeeding. Low fibre intake and a family history of constipation may be associated factors.5 Most children develop normal bowel control by 4 years of age (excluding any physical abnormality). It is normal to have a bowel movement every 2–3 days, providing it is of normal consistency and is not painful. It is important to differentiate between encopresis and constipation: • encopresis or faecal incontinence is the inappropriate passage of normal stool • constipation is difficulty or delay in passing the stool with incomplete emptying of the rectum: this can present as soiling, due to faecal retention with overflow of liquid faeces (paradoxical diarrhoea)

Other important conditions Hirschsprung disorder: • consider if delay in passing first meconium stool and subsequent constipation Anal fissure in infants: • consider if stool hard and associated with pain or bleeding • the mainstay of treatment is dietary manipulation

Principles of treatment of functional constipation

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• Encourage relaxed child–parent interaction with toilet training, such as appropriate encouragement, ‘after breakfast habit’ training. • Introduce psychotherapy or behaviour modification program, especially where ‘fear of the toilet’ exists. • Establish an empty bowel: remove any severely impacted faeces with microenemas (e.g. Microlax), and even disimpaction under anaesthesia if necessary. A good guide if faecal ‘rocks’ are visible on X-ray. • Advice for parents of children over 18 months: — Drink ample non–milk fluids each day— several glasses of water, unsweetened fruit juice or milk. — Use prune juice, which contains sorbitol. — Get regular exercise—walking, running, outside games or sport. — Provide high-fibre foods—high-fibre cereals, wholegrain bread, brown rice, wholemeal pasta, fresh fruit with skins left on where possible, dried fruits such as sultanas, apricots or prunes, fresh vegetables.

• Use a pharmaceutical preparation as a last resort to achieve regularity. First line:6 • paraffin oil (e.g. Parachoc): RCT evidence indicates suitable and better than stimulant laxative osmotic laxative (e.g. lactulose): — 1–5 years: 5 mL bd — 6–12 years: 10 mL bd — >12 years: 15 mL bd or macrogol 3350 with electrolytes: — 2–12 years: 1 sachet Movicol half in 60 mL water once daily — >12 years: 1 sachet Movicol (or 2 Movicol half) daily Severe constipation/faecal impaction: • consider admission to hospital • abdominal X-ray • macrogol 3350 with electrolytes (double above doses and water) • Microlax enema If unsuccessful, add ColonLYTLEY via nasogastric tube or sodium phosphate enema (Fleet Enema) (not 38°C plus at least one respiratory symptom and one systemic symptom • cough (dry) • sore throat • coryza • prostration or weakness • myalgia • headache • rigors or chills

FIGURE 42.2 The main features of influenza

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Cough • Encephalomyelitis (rare) • Depression (a common sequela) Management Advice to the patient includes: • rest in bed until the fever subsides • analgesics: paracetamol and aspirin is effective or codeine and aspirin (or paracetamol), especially if a dry cough • fluids: maintain high fluid intake 12

Antiviral agents

• Neuraminidase inhibitors (cover influenza A and B): zanamivir (Relenza) 10 mg by inhalation bd oseltamivir (Tamiflu) 75 mg (o) bd Both should be commenced within 36 hours of onset and given for 5 days. Note: All the above agents have been shown in RCTs to be beneficial, with a reduction in symptoms by at least 24 hours compared with placebo.12,13 Prevention Influenza vaccination offers some protection for up to 70% of the population for about 12 months.1 (See CHAPTER 9.)

Swine origin flu (The swine variety of H1N1 influenza A) This strain presents with typical influenza symptoms commonly accompanied by gastrointestinal symptoms (especially diarrhoea). Like avian flu it tends to occur in a pandemic and affects the young in particular. The treatment is the same as for influenza in general with neuraminidase inhibitors. A vaccine is now available. Avian (bird) flu due to H5N1 strain: refer to CHAPTER 28.

BRONCHITIS

Acute bronchitis This is acute inflammation of the tracheobronchial tree that usually follows an upper respiratory infection. Although generally mild and self-limiting, it may be serious in debilitated patients. Clinical features Features of acute infectious bronchitis are: • cough and sputum (main symptoms) • wheeze and dyspnoea

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• usually viral infection • can complicate chronic bronchitis—often due to Haemophilus influenzae and Streptococcus pneumoniae • scattered wheeze on auscultation • fever or haemoptysis (uncommon)

Outcome • It improves spontaneously in 4–8 days in healthy patients. Treatment12,14,15 • Symptomatic treatment • Inhaled bronchodilators for airflow limitation • Antibiotics usually not needed in previously healthy adult or child • Use antibiotics only if evidence of acute bacterial infection with fever, increased sputum volume and sputum purulence: amoxycillin 500 mg (o) 8 hourly for 5 days or doxycycline 200 mg (o) statim, 100 mg, especially if mycoplasma suspected daily for 5 days.

Chronic bronchitis This is a chronic productive cough for at least 3 successive months in 2 successive years: • wheeze, progressive dyspnoea • recurrent exacerbations with acute bronchitis • occurs mainly in smokers Refer to COPD (in CHAPTER 83).

PNEUMONIA16 This is inflammation of lung tissue. It usually presents as an acute illness with cough, fever and purulent sputum plus physical signs and X-ray changes of consolidation. However, the initial presentation of pneumonia can be misleading, especially when the patient presents with constitutional symptoms (fever, malaise and headache) rather than respiratory symptoms. A cough, although usually present, can be relatively insignificant in the total clinical picture. This diagnostic problem applies particularly to atypical pneumonia but can occur with bacterial pneumonia, especially lobar pneumonia.

Community-acquired pneumonia12,14 CAP occurs in people who are not or have not been in hospital recently, and who are not institutionalised

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or immunocompromised. The choice of antibiotic is initially empirical. CAP is usually caused by a single organism, especially Streptococcus pneumoniae, which is now becoming resistant to antibiotics.15 Treatment is usually for 5–10 days for most bacterial causes, 2  weeks for Mycoplasma or Chlamydia infection and 2–3 weeks for Legionella. Typical pneumonia The commonest community-acquired infection is with Streptococcus pneumoniae (majority), now becoming resistant to antibiotics, or Haemophilus influenzae.15 Clinical features • Often history of viral respiratory infection • Rapidly ill with high temperature, dry cough, pleuritic pain, rigors or night sweats • 1–2 days later may be rusty-coloured sputum • Rapid and shallow breathing follows • X-ray and examination: focal chest signs, consolidation

Patients can become prostrate with complications. Treat with: azithromycin IV (first-line) or erythromycin (IV or oral) plus (if very severe) ciprofloxacin or rifampicin • Chlamydia pneumoniae: — similar to Mycoplasma • Chlamydia psittaci (psittacosis): — treat with roxithromycin or erythromycin or doxycycline • Coxiella burnetti (Q fever): — treat with doxycycline 200 mg (o) statim then 100 mg daily for 14 days

Antibiotic treatment according to severity11,12 Mild pneumonia This does not require hospitalisation. amoxycillin/clavulanate 875/125 mg (o) 12 hourly for 7 days especially if S. pneumoniae isolated or suspected plus (especially if atypical pneumonia suspected) roxithromycin 300 mg (o) daily for 7 days

The atypical pneumonias Refer to CHAPTER 29. Clinical features • Fever, malaise • Headache • Minimal respiratory symptoms, non-productive cough • Signs of consolidation absent • Chest X-ray (diffuse infiltration) incompatible with chest signs

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• • • • • • •

Diagnostic criteria include:

Neonates Age over 65 years Coexisting illness High temperature: >38°C Clinical features of severe pneumonia Involvement of more than one lobe Inability to tolerate oral therapy Benzylpenicillin 1.2 g IV 4–6 hourly for 7 days or Procaine penicillin 1.5 g IM daily (drugs of choice for S. pneumoniae) or Ceftriaxone 1 g IV daily for 7 days (in penicillinallergic patient) • If not so severe and oral medication tolerated can use amoxycillin/clavulanate or cefaclor or doxycycline • If atypical pneumonia use doxycycline, erythromycin or roxithromycin

prodromal influenza-like illness a dry cough, confusion or diarrhoea very high fever (may be relative bradycardia) lymphopaenia with moderate leucocytosis hyponatraemia

Severe pneumonia The criteria for severity (with increased risk of death) are presented in the box Guidelines for severe pneumonia and hospital admission.14,15,16

Causes • Mycoplasma pneumoniae—the commonest: — adolescents and young adults — treat with: roxithromycin 300 mg (o) daily or doxycycline 100 mg bd for 14 days • Legionella pneumophila (legionnaire disease): — related to cooling systems in large buildings — incubation 2–10 days • • • • •

Moderately severe pneumonia This requires hospitalisation—see box Guidelines for severe pneumonia and hospital admission.

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Cough

Guidelines for severe pneumonia and hospital admission

Pneumonia in children: guidelines for hospitalisation14

• • • • • •

Infants: • RR>70 • Intermittent apnoea • Not feeding

•

Altered mental state/acute onset confusion Rapidly deteriorating course Respiratory rate >30 per minute Pulse rate >125 per minute BP BC

Equal in both ears

Conduction deafness

Negative: BC >AC

Louder in the deaf ear

Very severe conduction deafness

Negative: BC >AC May hear BC only

Louder in the deaf ear

Sensorineural deafness

Positive: AC >BC

Louder in the better ear

Very severe sensorineural deafness

‘False’ negative (without masking)

Louder in the better ear

AC = air conduction; BC = bone conduction

Rinne test The tuning fork is held: • outside the ear (tests air conduction) and • firmly against the mastoid bone (tests bone conduction)

(a)

Audiometric assessment Audiometric assessment includes the following: • • • •

pure tone audiometry impedance tympanometry electric response audiometry oto-acoustic emission testing (b)

FIGURE 43.5 Rinne test comparing air conduction (a) with bone conduction (b)

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Pure tone audiometry4,5

Tympanometry

Pure tone audiometry is a graph of frequency expressed in hertz versus loudness expressed in decibels. The tone is presented either through the ear canal (a test of the conduction and the cochlear function of the ear) or through the bone (a test of cochlear function). FIGURES 43.6 and 43.7 are typical examples of pure tone audiograms.

Tympanometry measures the mobility of the tympanic membrane, the dynamics of the ossicular chain and the middle-ear air cushion. The test consists of a sound applied at the external auditory meatus, otherwise sealed by the soft probe tip.

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FIGURE 43.6 Pure tone audiogram for severe conductive deafness in left ear Source: After Black4 250

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FIGURE 43.7 Pure tone audiogram for unilateral (left) sensorineural deafness. Suspect a viral or congenital origin in children; check adults for acoustic neuroma.

The difference between the two is a measure of conductance. If the two ears have different thresholds, a white noise masking sound is applied to the better ear to prevent it hearing sound presented to the test ear. The normal speech range occurs between 0 and 20 dB in soundproof conditions across the frequency spectrum.

Deafness in children Deafness in childhood is relatively common and often goes unrecognised. One to two of every 1000 newborn infants suffer from SND.1 Congenital deafness may be due to inherited defects, to prenatal factors such as maternal intrauterine infection or drug ingestion during pregnancy, or to perinatal factors such as birth trauma, and haemolytic disease of the newborn. Deafness may be associated with Down syndrome and Waardenburg syndrome. Waardenburg syndrome, which is dominantly inherited, is diagnosed in a patient with a white forelock of hair and different coloured eyes. Acquired deafness accounts for approximately half of all childhood cases. Purulent otitis media and secretory otitis media are common causes of temporary conductive deafness. However, one in 10 children will have persistent middle-ear effusions and mild to moderate hearing loss in the 15–40 dB range.6 Permanent deafness in the first few years of life may be due to virus infections, such as mumps or meningitis, ototoxic antibiotics and several other causes.

Screening1 The aim of screening should be to recognise every deaf child by the age of 8 months to 1 year—before the vital time for learning speech is wasted. Highrisk groups should be identified and screened, for example, a family history of deafness, maternal problems of pregnancy, perinatal problems, survivors of intensive care, very low birthweight and gestation 90% sensitivity and specificity)

• Lymphadenopathy • ± Fever

Associations • Iron-deficiency anaemia • Type 1 diabetes • Pernicious anaemia • Primary biliary cirrhosis • Subfertility • Malignancy, especially lymphoma • Dermatitis herpetiformis • IgA deficiency • Autoimmune thyroid disease • Osteoporosis • Neurological (e.g. seizures, ataxia, peripheral neuropathy) • Down syndrome

Diagnosis • PCR for T. whipplei • Jejunal biopsy—stunted villi

Management • Diet control: high complex carbohydrate and protein, low fat, gluten-free (no wheat, barley, rye and oats) • Treat specific vitamin and mineral deficiencies • Give pneumococcal vaccination (increased risk of pneumococcus sepsis)

Gluten-free diet Avoid foods containing gluten either as an obvious component (e.g. flour, bread, oatmeal), or as a hidden ingredient (e.g. dessert mix, stock cube). Forbidden foods include: • • • • • • •

standard bread, pasta, crispbreads, flour standard biscuits and cakes breakfast cereals made with wheat or oats oatmeal, wheat bran, barley/barley water ‘battered’ or bread-crumbed fish, etc. meat and fruit pies most stock cubes and gravy mixes

Whipple disease This is a rare malabsorption disorder usually affecting white males. It is caused by the bacillus Tropheryma whipplei. It may involve the heart, lungs and CNS. Clinical features • Males >40 years • Chronic diarrhoea (steatorrhoea) • Arthralgia (migratory seronegative arthropathy mainly of peripheral joints) • Weight loss

Treatment IV ceftriaxone for 2 weeks then cotrimoxazole or tetracycline for up to 12 months This produces a dramatic improvement.

Diarrhoea in the elderly The older the patient, the more likely a late onset of symptoms that reflect serious underlying organic disease, especially malignancy. Colorectal cancer needs special consideration. The older the patient, especially the bedridden elderly patient, the more likely the presentation of faecal impaction with spurious diarrhoea. The possibility of drug interactions, including digoxin, should also be considered. Ischaemic colitis must be considered in an elderly patient.

Ischaemic colitis This is due to atheromatous occlusion of mesenteric vessels (low blood flow) (see CHAPTER 34). Clinical features Clinical features include: • sharp abdominal pain in an elderly patient with bloody diarrhoea (low blood flow) or • periumbilical pain and diarrhoea about 15–30 minutes after eating • maybe loud bruits over central abdomen • other evidence of generalised atherosclerosis • barium enema shows ‘thumb printing’ sign due to submucosal oedema • the definitive test is aortography and selective angiography of mesenteric vessels • most episodes resolve—may be followed by a stricture

Diarrhoea in children The commonest cause of diarrhoea in children is acute infective gastroenteritis, but there are certain conditions that develop in childhood and infancy

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Diarrhoea and require special attention. The presentation of small amounts of redcurrant jelly-like stool with intussusception should also be kept in mind. Of the many causes only a few are commonly seen. The two commonest causes are infective gastroenteritis and antibiotic-induced diarrhoea. Important causes of diarrhoea in children are: • • • • • • • • •

infective gastroenteritis antibiotics overfeeding (loose stools in newborn) dietary indiscretions toddler’s diarrhoea sugar (carbohydrate) intolerance food allergies (e.g. milk, soya bean, wheat, eggs) maternal deprivation malabsorption states: cystic fibrosis, coeliac disease

Note: Exclude surgical emergencies (e.g. acute appendicitis), infections (e.g. pneumonia), septicaemia, otitis media 12 mo: 80 mL • Allow for continuing loss. Example: 8 month 10 kg child with 5% dehydration: Fluid loss = 5 × 10 × 10 = 500 mL Maintenance = 100 × 10 = 1000 mL Total 24-hour requirement (min.) = 1500 mL Approximate average hourly requirement = 60 mL • Aim to give more (replace fluid loss) in the first 6 hours. • Rule of thumb: give 100 mL/kg (infants) and 50 mL/kg (older children) in first 6 hours.

Days 2 and 3 Reintroduce your baby’s milk or formula diluted to half strength (i.e. mix equal quantities of milk or formula and water). Their normal food can be continued but do not worry that your child is not eating food. Solids can be commenced after 24 hours. Best to start with bread, plain biscuits, jelly, stewed apple, rice, porridge or non-fat potato chips. Avoid fatty foods, fried foods, raw vegetables and fruit, and wholegrain bread.

Day 4 Increase milk to normal strength and gradually continue reintroduction to usual diet. Breastfeeding. If your baby is not vomiting, continue breastfeeding but offer extra fluids (preferably Gastrolyte) between feeds. If vomiting is a problem, express breast milk for the time being while you follow the oral fluid program. Note: Watch for lactose intolerance as a sequela— explosive diarrhoea after introducing formula. Replace with a lactose-free formula. If acute invasive or persistent Salmonella are present, give antibiotics (ciprofloxacin or azithromycin).

CHRONIC DIARRHOEA IN CHILDREN

Sugar intolerance Synonyms: carbohydrate intolerance, lactose intolerance. The commonest offending sugar is lactose. Diarrhoea often follows acute gastroenteritis when milk is reintroduced into the diet (some recommend

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waiting for 2 weeks). Stools may be watery, frothy, smell like vinegar and tend to excoriate the buttocks. They contain sugar. Exclude giardiasis. A simple test follows. • Line the napkin with thin plastic and collect fluid stool. • Mix 5 drops of liquid stool with 10 drops of water and add a Clinitest tablet (detects lactose and glucose but not sucrose). • A positive result indicates sugar intolerance. Diagnosis: lactose breath hydrogen test Treatment • Remove the offending sugar from the diet. • Use milk preparations in which the lactose has been split to glucose and galactose by enzymes, or use soya protein. Note: Most milk allergies improve with age.

Toddler’s diarrhoea A clinical syndrome of loose, bulky, non-offensive stools with fragments of undigested food in a well, thriving child. The onset is usually between 8 and 20 months. Associated with high fructose intake (fruit juice diarrhoea). Diagnosis by exclusion; treatment by dietary adjustment.

Cow’s milk protein intolerance7 This is not as common as lactose intolerance. Diarrhoea is related to taking a cow’s milk formula and relieved when it is withdrawn. Allergic responses to cow’s milk protein may result in a rapid or delayed onset of symptoms. Delayed onset may be more difficult to diagnose, presenting with diarrhoea, malabsorption or failure to thrive. It is diagnosed by unequivocal reproducible reactions to elimination and challenge. If diagnosed, remove cow’s milk from the diet and replace with either soy milk, a hydrolysed or an elemental formula (see CHAPTER 80).

Inflammatory bowel disorders These disorders, which include Crohn disease and ulcerative colitis, can occur in childhood. A high index of suspicion is necessary to make an early diagnosis. Approximately 5% of cases of chronic ulcerative colitis have their onset in childhood.5

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Chronic enteric infection

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Responsible organisms include Salmonella sp., Campylobacter, Yersinia, G. lamblia and E. histolytica. With persistent diarrhoea it is important to obtain microscopy of faeces and aerobic and anaerobic stool cultures. G. lamblia infestation is not an uncommon finding and may be associated with malabsorption, especially of carbohydrate and fat. Giardiasis can mimic coeliac disease.

Coeliac disease (See earlier in chapter.) Clinical features in childhood: • • • • • •

usually presents at 9–18 months, but any age previously thriving infant anorexia, lethargy, irritability failure to thrive malabsorption—abdominal distension offensive frequent stools Diagnosis: duodenal biopsy (definitive) Treatment: remove gluten from diet

Cystic fibrosis Cystic fibrosis which presents in infancy is the commonest of all inherited disorders (1 per 2500 live births). Refer to CHAPTER 18.

ACUTE GASTROENTERITIS IN ADULTS

Features • Invariably a self-limiting problem (1–3 days) • Abdominal cramps • Possible constitutional symptoms (e.g. fever, malaise, nausea, vomiting) • Other meal sharers affected → food poisoning • Consider dehydration, especially in the elderly • Consider possibility of enteric fever

Traveller’s diarrhoea The symptoms are usually as above but very severe diarrhoea, especially if associated with blood or mucus, may be a feature of a more serious bowel infection such as amoebiasis. Possible causes of diarrhoeal illness are presented in TABLE 14.1, in CHAPTER 14. Most traveller’s diarrhoea is caused by E. coli, which produces a watery diarrhoea within 14 days of arrival in a foreign country. (For specific treatment refer to the section on Traveller’s diarrhoea in CHAPTER 14.)

Persistent traveller’s diarrhoea Any traveller with persistent diarrhoea after visiting less developed countries, especially India and China, may have a protozoal infection such as amoebiasis or giardiasis. If there is a fever and blood or mucus in the stools, suspect amoebiasis. Giardiasis is characterised by abdominal cramps, flatulence and bubbly, foulsmelling diarrhoea.

Principles of treatment of diarrheoa Acute diarrhoea • Maintenance of hydration: Antiemetic injection (for severe vomiting) prochlorperazine IM, statim or metoclopramide IV, statim • Antidiarrhoeal preparations: (avoid if possible: loperamide preferred) loperamide (Imodium) 2 caps statim then 1 after each unformed stool (max: 8 caps/day) or diphenoxylate with atropine (Lomotil) 2 tabs statim then 1–2 (o) 8 hourly General advice to patient

Rest Your bowel needs a rest and so do you. It is best to reduce your normal activities until the diarrhoea has stopped.

Diet Eat as normally as possible but drink small amounts of clear fluids such as water, tea, lemonade and yeast extract (e.g. Marmite). Then eat low-fat foods such as stewed apples, rice (boiled in water), soups, poultry, boiled potatoes, mashed vegetables, dry toast or bread, biscuits, most canned fruits, jam, honey, jelly, dried skim milk or condensed milk (reconstituted with water). At first, avoid alcohol, coffee, strong tea, fatty foods, fried foods, spicy foods, raw vegetables, raw fruit (especially with hard skins), Chinese food, wholegrain cereals and cigarette smoking. On the third day introduce dairy produce, such as a small amount of milk in tea or coffee and a little butter or margarine on toast. Add also lean meat and fish (either grilled or steamed).

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Diarrhoea Treatment (antimicrobial drugs)3 Bacterial diarrhoea in adults and older children is usually self-limiting and does not require antibiotic treatment (they may be used to shorten the course of a persistent infection). Campylobacter, Salmonella, Shigella and E. coli are the most common causes. As a rule, use oral rehydrate solution 2–3 L orally over 24 hours if mild to moderate dehydration. If severe, intravenous rehydration with N saline is recommended. It is advisable not to use antimicrobials except where the following specific organisms are identified. The drugs should be selected initially from the list below or modified according to the results of culture and sensitivity tests.3 Only treat if symptoms have persisted for more than 48 hours. Adult doses are shown for the following enteric infections.

Cotrimoxazole (double strength) 1 tab (o) 12 hourly for 5 days: use in children (children’s doses) or norfloxacin 400 mg (o) 12 hourly for 5 days (preferred for adults) or ciprofloxacin 500 mg (o) bd for 5 days

Giardiasis This protozoal infestation is often misdiagnosed. It should be considered for a persistent profuse, watery, bubbly, offensive diarrhoea (see CHAPTER 15). Tinidazole 2 g (o), single dose (may need repeat) or metronidazole 400 mg (o) tds for 7 days (in children: 30 mg/kg/day [to max. 1.2 g/day] as single daily dose for 3 days)

Salmonella enteritis Antibiotics are not generally advisable but if severe or prolonged use: ciprofloxacin 500 mg (o) bd for 5–7 days or azithromycin 1 g (o) day, then 500 mg for 6 days or ceftriaxone IV or ciprofloxacin IV if oral therapy not tolerated Note: Salmonella is a notifiable disease; infants under 15 months are at risk of invasive Salmonella infection.

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Campylobacter A zoonosis that is usually self-limiting. Antibiotic therapy indicated in severe or prolonged cases: azithromycin 500 mg (o) 12 hourly for 3 days or ciprofloxacin 500 mg (o) 12 hourly for 3 days or norfloxacin 400 mg (o) 12 hourly for 5 days

Cryptosporidium species Usually self-limiting, may need fluid and electrolytes and anti-motility agents. If severe, nitazoxamide (shared care).

Amoebiasis (intestinal) See CHAPTER 15.

Shigella dysentery (moderate to severe)

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metronidazole 600–800 mg (o) tds for 6–10 days plus diloxanide furoate 500 mg (o) tds for 10 days

Blastocystitis hominis (a parasitic infection) Pathogenicity is disputed: give therapy only if severe. Associated with poor hygiene (travel, pets, dam/tank water, oysters). metronidazole for 7 days Specialist advice should be sought. Treatment for special enteric infections

Typhoid/paratyphoid fever See CHAPTER 15. azithromycin 1 g (o) daily for 7 days or (if not acquired in the Indian subcontinent or SE Asia) ciprofloxacin 500 mg (o) 12 hourly for 7–10 days (use IV if oral therapy not tolerated) If ciprofloxacin is contraindicated (e.g. in children) or not tolerated, then use: ceftriaxone 3 g IV daily until culture and sensitivities available, then choose oral regimens If severe: administer same drug and dosage IV for first 4–5 days.

Cholera Antibiotic therapy reduces the volume and duration of diarrhoea. Rehydration is the key.

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azithromycin 1 g (child 20 mg/kg up to 1 g)(o) as a single dose or ciprofloxacin 1 g (o) as a single dose

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For pregnant women and children: amoxycillin (child: 10 mg/kg up to) 250 mg (o) 6 hourly for 4 days

INFLAMMATORY BOWEL DISEASE3 Inflammatory bowel disease (IBD) should be considered when a young person presents with: • bloody diarrhoea and mucus • colonic pain and fever • constitutional symptoms including weight loss and malaise • extra-abdominal manifestations such as arthralgia, low back pain (spondyloarthropathy), eye problems (iridocyclitis), liver disease and skin lesions (pyoderma gangrenosum, erythema nodosum) Investigations include FBE, vitamin B12 and folate, LFTs (abnormal enzymes), HLA B27, faecal calprotectin (if normal, no intestinal inflammation; if abnormal, needs colonoscopy) and lactoferrin. Two important disorders are ulcerative colitis (UC) and Crohn disease, which have equal sex incidence and can occur at any age, but onset peaks between 20 and 40 years.

Ulcerative colitis Clinical features • Mainly a disease of Western societies • Mainly in young adults (15–40 years) • High-risk factors—family history, previous attacks, low-fibre diet • Recurrent attacks of loose stools • Blood, or blood and pus, or mucus in stools • Abdominal pain slight or absent • Fever, malaise and weight loss uncommon • Begins in rectum (continues proximally)—affects only the colon: it usually does not spread beyond the ileocaecal valve • An increased risk of carcinoma after 7–10 years Main symptom • Bloody diarrhoea Diagnosis • Faecal calprotectin: a sensitive test

• Proctosigmoidoscopy: a granular red proctitis with contact bleeding • Barium enema: characteristic changes Prognosis • 5% mortality in an acute attack • Recurrent attacks common

Crohn disease Synonyms: regional enteritis, granulomatous colitis. The cause is unknown but there is a genetic link. Clinical features • Recurrent diarrhoea in a young person (15–40 years) • Blood and mucus in stools (less than UC) • Colicky abdominal pain (small bowel colic) • Right iliac fossa pain (confused with appendicitis) • Constitutional symptoms (e.g. fever, weight loss, malaise, anorexia, nausea) • Signs include perianal disorders (e.g. anal fissure, fistula, ischiorectal abscess), mouth ulcers • Skip areas in bowel: ½ ileocolic, ¼ confined to small bowel, ¼ confined to colon, 4% in upper GIT Main symptom • Colicky abdominal pain Diagnosis • Sigmoidoscopy: ‘cobblestone’ appearance (patchy mucosal oedema) • Colonoscopy: useful to differentiate from UC • Biopsy with endoscopy Prognosis Less favourable than UC with both medical and surgical treatment. Management principles of both • Education and support including support groups • Treat under consultant supervision • Treatment of acute attacks depends on severity of the attack and the extent of the disorder: — mild attacks: manage out of hospital — severe attacks: hospital, to attend to fluid and electrolyte balance • Role of diet controversial: consider a high-fibre diet but maintain adequate nutrition • Pharmaceutical agents (the following can be considered): — 5-aminosalicylic acid derivatives (mainly UC): sulfasalazine (mainstay), olsalazine, mesalazine

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Diarrhoea — corticosteroids (mainly for acute flares): oral, parenteral, topical (rectal foam, suppositories or enemas) — for severe disease, immunomodifying drugs (e.g. azathioprine, cyclosporin, methotrexate) and biological agents (e.g. infliximab) • Surgical treatment: reserve for complications; avoid surgery if possible

diarrhoea and/or constipation

abdominal pain bloating

ALTERNATING DIARRHOEA AND CONSTIPATION

flatulence

Alternating diarrhoea and constipation are wellknown symptoms of incomplete bowel obstruction (cancer of colon and diverticular disease) and irritable bowel syndrome.

Irritable bowel syndrome (IBS)3,8 Clinical features • Typically in younger women (21–40 years) • Any age or sex can be affected • May follow attack of gastroenteritis/traveller’s diarrhoea • Cramping abdominal pain (central or iliac fossa)—FIGURE 44.4 • Pain usually relieved by passing flatus or by defecation • Variable bowel habit (constipation more common) • Diarrhoea usually worse in morning—several loose, explosive bowel actions with urgency • The Bristol stool chart was devised to assist with the subclassification of stool types and bowel habits • Often precipitated by eating • Faeces sometimes like small, hard pellets or ribbon-like • Anorexia and nausea (sometimes) • Bloating, abdominal distension, borborygmi • Tiredness common The Rome III diagnostic criteria for IBS are presented in TABLE 44.11. IBS is a diagnosis of exclusion. A thorough physical examination, investigations (FBE, ESR and stool microscopy or culture) and colonoscopy are necessary. Insufflation of air at colonoscopy may reproduce the abdominal pain of IBS. Possible related causes Bowel infection, food irritation (e.g. spicy foods), lactose (milk) intolerance, low-fibre diet, high

FIGURE 44.4 Classic symptoms of irritable bowel syndrome

Table 44.11

Rome III diagnostic criteria for irritable bowel syndrome*9,10

In the preceding 3 months, the patient has had abdominal discomfort for at least 3 days per month with two of the following three features: • relieved by defecation • onset associated with a change in stool frequency • onset associated with a change in form (appearance) of stool (loose, watery or pellet-like) Symptoms that cumulatively support the diagnosis of irritable bowel syndrome: • abnormal stool frequency (for research purposes may be defined as more than three bowel movements per day and less than three bowel movements per week) • abnormal stool form (lumpy/hard or watery/mushy) • abnormal stool passage (straining, urgency or feeling of incomplete evacuation) • passage of mucus • bloating or feeling of abdominal distension Note: Red flags must be excluded * in absence of structural or metabolic abnormalities to explain symptoms

fatty foods, laxative overuse, use of antibiotics and codeine-containing analgesics, psychological factors. Management The patient must be reassured and educated with advice that the problem will not cause malignancy or inflammatory bowel disease and will not shorten life

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Red flag pointers for non-IBS disease9

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• • • • • • • • • • • •

Age of onset >50 years Fever Unexplained weight loss Rectal bleeding Pain waking at night Persistent daily diarrhoea/steatorrhoea Recurrent vomiting Major change in symptoms Mouth ulcers ↑ CRP, ESR Anaemia Family history bowel cancer or IBD

expectancy. The basis of initial treatment is simple dietary modification (FODMAPs), exercise, fluids (2–3 L water daily) and non-fermentable fibre. Self-help advice to the patient Anyone with IBS should try to work on the things that make the symptoms worse. If you recognise stresses and strains in your life, try to develop a more relaxed lifestyle. You may have to be less of a perfectionist in your approach to life. Try to avoid any foods that you can identify as causing the problem. You may have to cut out smoking and alcohol and avoid laxatives and codeine (in painkillers). A high-fibre (non-fermentable) and low-carbohydrate diet and 2–3 L of water a day may be the answer to your problem. A low FODMAP diet can produce good benefits.11 FODMAP refers to fermentable oligosaccharides, disaccharides, monosaccharides and polyols, which are poorly absorbed. All of these carbohydrates need to be eliminated (under a dietitian’s guidance) then reintroduced one at a time. See , available as an app—the Monash University low FODMAP Diet.

Diverticular disorder Diverticular disorder is a problem of the colon (90% in descending colon) and is related to lack of fibre in the diet. It is usually symptomless. Clinical features • Typical in middle aged or elderly—over 40 years • Increases with age • Present in one in three people over 60 years (Western world) • Diverticulosis—symptomless

• Diverticulitis—infected diverticula and symptomatic (refer CHAPTER 34) • Constipation or alternating constipation/diarrhoea • Intermittent cramping lower abdominal pain in LIF • Tenderness in LIF • Rectal bleeding—may be profuse (± faeces) • May present as acute abdomen or subacute obstruction • Usually settles in 2–3 days Complications (of diverticulitis) • Abscess • Perforation • Peritonitis • Obstruction (refer CHAPTER 34) • Fistula—bladder, vagina Investigations • WBC and ESR—to determine inflammation • Sigmoidoscopy • Barium enema Management • It usually responds to a high-fibre diet. • Avoidance of constipation. Advice to the patient The gradual introduction of fibre with plenty of fluids (especially water) will improve any symptoms you may have and reduce the risk of complications. Your diet should include: 1 cereals, such as bran, shredded wheat, muesli or porridge 2 wholemeal and multigrain breads 3 fresh or stewed fruits and vegetables Bran can be added to your cereal or stewed fruit, starting with 1 tablespoon and gradually increasing to 3 tablespoons a day. Fibre can make you feel uncomfortable for the first few weeks, but the bowel soon settles to your improved diet.

When to refer Children with diarrhoea • Infant under 3 months • Moderate to severe dehydration • Diagnosis of diarrhoea and vomiting in doubt (e.g. blood in vomitus or stool, bile-stained vomiting, high fever or toxaemia, abdominal signs suggestive of appendicitis or obstruction) • Failure to improve or deterioration • A pre-existing chronic illness

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Diarrhoea

Adults • Patient with chronic or bloody diarrhoea • Any problem requiring colonoscopic investigation • Patients with anaemia • Patients with weight loss, abdominal mass or suspicion of neoplasia • Patients with anal fistulae • Patients not responding to treatment for giardiasis • Infection with E. histolytica • Long-term asymptomatic carrier of typhoid or paratyphoid fever • Patient with persistent undiagnosed nocturnal diarrhoea • Patients with IBS with a significant change in symptoms • Patients with inflammatory bowel diseases with severe exacerbations, possibly requiring immunosuppressive therapy and with complications • Patients with ulcerative colitis of more than 7 years’ duration (screening by colonoscopy for carcinoma)

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Coeliac disease in adults • Coeliac disease in children • Diarrhoea—acute diarrhoea in adults • Gastroenteritis in children

Practice tips •

•

Oral antidiarrhoeal drugs are contraindicated in children; besides being ineffective they may prolong intestinal recovery. Anti-emetics can readily provoke dystonic reactions in children, especially if young and dehydrated.

•

•

• • •

• •

Acute diarrhoea is invariably self-limiting (lasts 2–5 days). If it lasts longer than 7 days, investigate with culture and microscopy of the stools. If diarrhoea is associated with episodes of facial flushing or wheezing, consider carcinoid syndrome. Recurrent pain in the right hypochondrium is usually a feature of IBS (not gall bladder disease). Recurrent pain in the right iliac fossa is more likely to be IBS than appendicitis. Beware of false correlations or premature conclusions (e.g. attributing the finding of diverticular disorder on barium meal to the cause of the symptoms). Undercooked chicken is a common source of enteropathic bacterial infection. Consider alcohol abuse if a patient’s diarrhoea resolves spontaneously on hospital admission.

References 1 Bolin T, Riordan SM. Acute and persistent diarrhoea. Current Therapeutics, 2001; May: 47–57. 2 Sandler G, Fry J. Early Clinical Diagnosis. Lancaster: MTP Press, 1986: 25–30. 3 Moulds R (Chair). Therapeutic Guidelines: Gastrointestinal (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2011. 4 Dalton C. Foodborne illness: how to treat. Australian Doctor, 15 April: 2005; 39–46. 5 Robinson MJ, Roberton DM. Practical Paediatrics (5th edn). Edinburgh: Churchill Livingstone, 2003: 675–90. 6 Oberklaid F. Management of gastroenteritis in children. In: The Australian Paediatric Review. Melbourne: Royal Children’s Hospital, 1990: 1–2. 7 Thomson K, Tey D, Mark M. Paediatric Handbook (8th edn). Oxford: Wiley-Blackwell, 2009: 343–4. 8 Ellard K, Malcolm A. Irritable bowel syndrome. Medical Observer, 30 March 2007: 29–32. 9 NICE. Irritable bowel syndrome in adults: diagnosis and management of irritable bowel syndrome in primary care, 2008. 10 Gibson PR. Irritable bowel syndrome. Australian Doctor, 13 April 2012: 17–34. 11 Gibson PR, Shepherd SJ. Evidence based dietary management of functional gastrointestinal symptoms: the FODMAP approach. J Gastroenterol Hepatology, 2010; Feb 25 (2): 2528.

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The disturbed patient

There is not a sight in nature so mortifying as that of a Distracted Person, when his imagination is troubled, and his whole soul is disordered and confused. Joseph Addison (–) The disturbed and confused patient is a complex management problem in general practice. The cause may be a single one or a combination of several abnormal mental states (see TABLE  45.1).1 The cause may be an organic mental disorder, which may be a long-term insidious problem such as dementia, or an acute disorder (delirium), often dramatic in onset. On the other hand, the cause of the disturbance may be a psychiatric disorder such as panic disorder, mania, major depression or schizophrenia. The manifestations of the disturbance are many and include perceptual changes and hallucinations,

Table 45.1

A general classification of psychiatric disorders1

Organic mental disorders • acute organic brain syndrome (delirium) • chronic organic brain syndrome (dementia) Psychoactive and substance use disorders • toxic states • drug dependency • withdrawal states Schizophrenic disorders Mood disorders: • major depression • bipolar (manic depressive) disorder • adjustment disorders with depressed mood • dysthymia Anxiety disorders • generalised anxiety disorder • panic disorder • obsessive–compulsive disorder • phobic disorders • post-traumatic stress disorder

Key facts and checkpoints •

• • •

•

•

•

• • •

Depression affects 15% of people over 65 and can mimic or complicate any other illness, including delirium and dementia.1 Elderly patients with depression are at a high risk of suicide. Always search vigorously for the cause or causes of delirium. Seeing patients in their home is the best way to evaluate their problem and support systems. It allows opportunities for a history from close contacts and for checking medication, alcohol intake and other factors. The diagnosis of dementia can be overlooked: a Scottish study showed that 80% of demented patients were not diagnosed by their GP.2 Patients with a chronic brain syndrome (dementia) are at special risk of an acute brain syndrome (delirium) in the presence of infections and many prescribed drugs.1 Consider prescribed and illicit substances, including the severe anticholinergic delirium syndrome. The key feature of dementia is impaired memory. The two key features of delirium are disorganised thought and attention. Hallucination guidelines: — Auditory: psychoses e.g. schizophrenia — Visual: almost always organic disorder — Olfactory: temporal lobe epilepsy — Tactile: cocaine abuse, alcohol withdrawal

disorientation, changes in consciousness, changes in mood from abnormally elevated to gross depression, agitation and disturbed thinking, including delusions.

Disorders specific to children Other disorders: • postpartum psychiatric illness • eating disorders • personality disorders • body dysmorphic disorder

A diagnostic approach A summary of the diagnostic strategy model for the disturbed or confused patient is presented in TABLE 45.2.

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The disturbed patient

Glossary of terms Alzheimer disease A term used for both senile and presenile dementia, which has characteristic pathological degenerative changes in the brain. Cognition The mental functions of perception, thinking and memory. It is the process of ‘knowing’. Compulsions Repeated, stereotyped and seemingly purposeful actions that the person feels compelled to carry out but resists, realising they are irrational (most are associated with obsessions). Confusion Disorientation in time, place and person. It may be accompanied by a disturbed conscious state (TABLE 75.1, CHAPTER 75). Conversion The process by which thoughts or experiences unacceptable to the mind are repressed and converted into physical symptoms. Delirium (also termed ‘toxic confusional state’) A relatively acute disorder in which impaired consciousness is associated with abnormalities of perception or mood. Delusions Abnormal, illogical or false beliefs that are held with absolute conviction despite evidence to the contrary. Dementia An acquired, chronic and gradually progressive deterioration of memory, intellect and personality. Presenile dementia or early onset dementia is dementia under 65 years of age. Senile dementia refers to older patients (usually over 80 years). Dissociation A psychological disorder in which unpleasant memories or emotions are split off from consciousness and the personality and buried into the unconsciousness. Depersonalisation An alteration in the awareness of the self—the person feels unreal. Hallucinations Disorders of perception quite divorced from reality. Features: • mostly auditory or visual • a false perception—not a distortion • perceived as normal perceptions • independent of the person’s will Illusions False interpretations of sensory stimuli such as mistaking people or familiar things. Obsessions Recurrent or persistent thoughts, images or impulses that enter the mind despite efforts to exclude them. Somatisation The conversion of mental experiences or states into bodily symptoms, with no physical causation.

Table 45.2

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The disturbed mind: diagnostic strategy model

Q. Probability diagnosis A. The 4 Ds: • dementia • delirium (look for cause) • depression • drugs: toxicity, withdrawal Q. Serious disorders not to be missed A. Cardiovascular: • CVAs • cardiac failure • arrhythmia • acute coronary syndromes Neoplasia: • cerebral • cancer (e.g. lung) Severe infections: • septicaemia • HIV infection • infective endocarditis Hypoglycaemia Bipolar disorder/mania Schizophrenia states Anxiety/panic Subdural haematoma Q. Pitfalls (often missed) A. Illicit drug withdrawal Fluid and electrolyte disturbances Faecal impaction (elderly) Urinary retention (elderly) Hypoxia Pain syndromes (elderly) Rarities: • hypocalcaemia • kidney failure • hepatic failure • prion diseases (e.g. Creutzfeldt–Jakob disease) Q. Seven masquerades checklist (all possible) A. Depression Diabetes Drugs Anaemia Thyroid disorder Spinal dysfunction (severe pain in elderly) UTI Q. Is the patient trying to tell me something? A. Consider anxiety, depression, emotional deprivation or upset, change in environment, serious personal loss.

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Probability diagnosis The diagnosis depends on the age and presentation of the patient. In a teenager the probable causes of acute confusion or irrational behaviour include drug toxicity or withdrawal, schizophrenia, severe depression or a behavioural disorder. It is the elderly who commonly present with confusion. The questions that must be asked are:

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• Is the problem one of the 4 Ds—dementia, delirium, depression, drugs or something else? • If delirium is the problem, what is the cause? Depression affects 15% of people over 65 and can mimic other causes of confusion and behavioural disturbance. Significant prescribed drugs include hypnotics, sedatives, oral hypoglycaemics, antihypertensives, digoxin, antihistamines, anticholinergic drugs and antipsychotics.

Serious disorders not to be missed There are many serious underlying disorders that must be considered, especially with delirium (see  TABLE  45.3). Cerebral organic lesions, including  space-occupying lesions (e.g. cerebral tumour, subdural haematoma), severe infection (systemic or intracerebral) and cancer at any site, especially lung, breast, bowel, or lymphoma, must be ruled out. The sudden onset of delirium may suggest angina, myocardial infarction or a cerebrovascular accident. Twenty per cent of patients with delirium also have underlying heart failure.3

Pitfalls There are many pitfalls, especially with drug toxicity or withdrawal from the so-called illicit drugs. In the elderly in particular, fluid and electrolyte disturbances, such as dehydration, hypokalaemia, hyponatraemia and hypocalcaemia, can cause delirium. Bowel disturbances such as faecal impaction or constipation can cause delirium and incontinence of both faeces and urine.

Seven masquerades checklist All the following disorders can cause disturbed or confused behaviour, particularly in the elderly: • depression: a very important cause of ‘pseudodementia’ • drugs: toxicity or withdrawal (see TABLE 45.4)

Table 45.3

Important causes of delirium (typical examples of each group

Drug intoxication and drug sensitivity Anticholinergics Antidepressants Sedatives Alcohol, opioids, etc. Withdrawal from substances of abuse and prescribed drugs Alcohol Opioids Amphetamines Cannabis Sedatives and anxiolytics Infections Specific:

Intracranial: Systemic:

Urinary tract Lower respiratory (e.g. pneumonia) Otitis media Cellulitis Meningitis Encephalitis Infective endocarditis Septicaemia HIV virus Other viral infections Malaria

Metabolic disturbances Uraemia, hepatic failure Electrolyte disturbances Dehydration Endocrine disturbances Diabetic ketoacidosis, hypoglycaemia Hypothyroidism/hyperthyroidism Nutritional and vitamin deficits Vitamin B complex deficiency (esp. B6, B12) Wernicke encephalopathy Hypoxia Respiratory failure, cardiac failure, anaemia Vascular CVA Acute coronary syndromes Head injury and other intracranial problems Seizures Complex partial seizures ‘Subtle’ causes Pain (e.g. herpes zoster) Emotional upset Environmental change Peri-operative Faecal impaction Urinary retention

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The disturbed patient

Table 45.4

Prescribed drugs that can cause delirium

Anticholinergic: • antiparkinsonian (e.g. benztropine) • tricyclic antidepressants Tranquillisers and hypnotics: • major tranquillisers (e.g. chlorpromazine) • minor tranquillisers (e.g. diazepam) • hypnotics • lithium Anti-epileptics Antihistamines 1 and 2 Antihypertensives Corticosteroids Cardiac drugs: • digoxin • diuretics • beta blockers Opioids Sympathomimetics

• diabetes: especially hypoglycaemia, which can occur with type 2 • anaemia: often from self-neglect or chronic blood loss • thyroid disorders: both hyperthyroidism and hypothyroidism can present with disturbed behaviour; ‘myxoedemic madness’ may be precipitated by atropine compounds • urinary tract infection: causes or contributes to 20% of cases of hallucinations or illusions2 • spinal dysfunction: with its many severe pain syndromes, such as sciatica, can be a significant factor

Psychogenic factors Apart from the primary psychiatric disorders of anxiety, depression, mania and schizophrenia, relatively simple and subtle social problems, such as loneliness, boredom, a domestic upset, financial problem or similar issue, can trigger a confusional state.

The clinical approach

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When communicating with the patient, speak slowly and simply (avoid shouting), face the patient and maintain eye contact. Important features are the past history and recent psychosocial history, including recent bereavement, family upsets and changes in environment. Search for evidence of depression and note any organic symptoms such as cough, constipation and so on. Mental status examination The most practical bedside screening test of mental function is the Mental Status Questionnaire of Kahn and colleagues,4 which includes 10 simple questions. 1 2 3 4 5 6 7 8 9 10

What is the name of this place? What city are you in now? What year is it? What month is it? What is the date today? What year were you born? When is your birthday? How old are you? Who is the prime minister/president? Who was the prime minister/president before him?

(Interpretation: normal 9–10; mildly impaired 8–9; confused/demented 7 or less.) Other MMSEs are presented in CHAPTER 8.

Examination The patient’s general demeanour, dress and physical characteristics should be noted at all times. Assess the patient’s ability to hear, see, speak, reason, obey commands, stand and walk. Any problems related to the special senses can cause confusion. Look for features of alcohol abuse, Parkinson disease and hypothyroidism. Examine the neurological system and keep in mind the possibility of a subdural haematoma, which may have followed a forgotten fall. Don’t omit the rectal examination to exclude faecal impaction, melaena, cancer and prostatomegaly (in males), and also check the bladder for evidence of chronic retention.

Investigations

History

Investigations to consider for delirious or demented patients (unknown cause):

Developing rapport with the disturbed or confused patient is essential and can be helped by a warm handshake or a reassuring pat on the shoulder. The basis of the history is a careful account from relatives or witnesses about the patient’s behaviour.

• • • • •

urinalysis and microscopy cultures of blood and urine total and differential blood count; ESR blood glucose urea and creatinine and electrolytes

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calcium and phosphate vitamin D thyroid function tests liver function tests serum vitamin B12 and folate levels ECG/troponin (? acute coronary syndrome) chest X-ray cerebral CT scan, especially non-contrast CT syphilis serology HIV arterial blood gases

Behavioural emergencies: management of the acutely disturbed patient5 Delirious or psychotic patients can be paranoid and respond defensively to the world around them. This behaviour can include aggressive and violent behaviour resulting in danger to themselves, their friends and family and to their medical attendants. Dangerousness should be assessed from features such as the patient’s past history (especially previous dangerous behaviour), age and sex, recent stress, victim behaviour, muscle bulk, presence of weapons, degree of overactivity and the manner of handling of the present distress by others. The patient may be in a state of acute panic and trying to flee a situation or in an agitated psychotic state prepared to confront the situation. It should be emphasised that most violent individuals are not mentally ill. Most cases require an injection (the ideal intravenous administration can be extremely difficult and hazardous), which is often interpreted as a physical attack. It may not be possible to diagnose the cause of the problem before giving the injection.

Approach to management • Assess the environment and don’t move into the patient’s space until in a position of control. • React calmly. Communicate calmly and simply. • State your task firmly and simply. • Try to control the disturbed patient gently. • Ensure the safety of all staff and make certain that heroics are not attempted in dangerous circumstances. • An adequate number of staff to accompany the doctor is essential—six is ideal (one for immobilisation of each limb, one for the head and one to assist with drugs).1 • Patients should be placed on the floor in the prone position.

Principles of sedative administration1 • Use the safest possible route of administration whenever possible (i.e. oral in preference to parenteral but often impractical). Intravenous administration has the lowest margin of safety. • Parenteral administration should be restricted to severely disturbed patients. • Closely monitor vital signs during and after sedative administration. • Avoid intramuscular diazepam because of poor absorption. • Be cautious of intravenous midazolam (Hypnovel) in such patients because of the risk of respiratory depression. • Avoid benzodiazepines in patients with respiratory insufficiency. Haloperidol is an alternative. • Patients have died from cardiopulmonary arrest after repeated sedative administration (especially benzodiazepines), so intensive monitoring is essential. Monitor the following adverse effects: • • • •

respiratory depression hypotension dystonic reactions, including choking neuroleptic malignant syndrome

Treatment options1,5 The treatment in acute medical and psychiatric settings depends on the appropriate mode of administration. Benzodiazepines are generally the drugs of first choice over antipsychotics in tranquillisation.5 However, the IV route allows titration to the desired degree of sedation and has a more immediate effect. Oral medication diazepam 5–20 mg (o), repeated every 2–6 hours (max: 120 mg/24 hours) or lorazepam 1–2 mg (o), repeated every 2–6 hours (max: 10 mg/24 hours) If sedation is not achieved, add an antipsychotic medication e.g. olanzapine 5–10 mg initially or risperidone 0.5–1 mg initially Intravenous medication diazepam or midazolam 2.5–5 mg increments IV, repeated every

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The disturbed patient 3–4 minutes until required level of sedation (rousable drowsiness) is reached—up to a maximum of 20–30 mg, when specialist advice is needed especially if further boluses are necessary and/or droperidol 5–10 mg IV Intramuscular medication If this route considered appropriate: midazolam 5–10 mg IM or (if history of benzodiazepine tolerance) droperidol 5–10 mg IM or olanzapine 5–10 mg repeated every 2–4 hours or combination midazolam/droperidol (These first two injections can be repeated in 20 minutes if required. Droperidol is similar to haloperidol but more sedating. Keep in mind the rare but potentially fatal laryngeal dystonia with high doses—cover with benztropine 2 mg IM.)

Postdisturbance evaluation Determine the likely cause, such as: • acute organic brain syndrome: toxic causes, infection • alcohol or drugs (illicit or prescribed): intoxication, withdrawal • manic illness • severe depression • schizophrenic syndrome • severe panic

Acute organic brain syndrome (delirium) The many labels of acute organic brain syndrome include: • • • • •

delirium acute confusional state toxic confusional state confusional episode acute brain syndrome

Main clinical features • Clouding of conscious state • Disorientation • Impaired attention • Impaired memory • Global cognitive defect—onset over days/hours Refer to the box.

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DSM-5 criteria for delirium6 Diagnosis of delirium requires evidence of: A Disturbance of consciousness, attention and awareness B Clinical features appearing over a short period C A change in cognition: • perceptual disturbance • incoherent speech • disorientation • memory impairment/deficit D A & C not better explained by another disorder E Evidence of a cause

Other clinical features1 • The patients are usually elderly. • Anxiety and agitation can be severe but in hypoactive deliria (usually due to metabolic disturbance) the conscious state can vary from drowsiness to coma. • Odd behaviour with mood swings can occur. • Psychotic symptoms can occur. • Delusions are usually fleeting. • The disturbance is usually worse at night and may be aggravated by sedation. • Visual hallucinations are a feature of alcohol withdrawal. • Attacks on bystanders may result (uncommon). Always seek a cause.1 A list of causes is presented in TABLE 45.3. The most important causes are: • infections (usually in urinary tract, lungs or ear, or systemic in young or elderly) • prescribed drugs

Anticholinergic delirium Consider this cause (from drugs with anticholinergic properties or illicit substances). Features include hyperactivity, marked thought disorder, vivid visual hallucinations and very disturbed behaviour.

Differential diagnosis of delirium In the earlier stages it may mimic the various psychiatric disorders, including anxiety, depression, various hallucinatory states, particularly agitated schizophrenia (rarely), extreme manic states, complex partial seizures, dementia. Consider deafness. Delirium is common in the hospital setting.

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Investigations Investigations are those listed under ‘The clinical approach’ earlier in the chapter. Treatment Principles:

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• Acute delirium is a medical emergency. • Establish normal hydration, electrolyte balance and nutrition. • Consider alcohol withdrawal and give a trial of thiamine when the cause of delirium is unknown. • Attend to helpful environmental factors (e.g. calm atmosphere, a night-light, orientation clues, presence of friends and relatives). • Give oxygen if hypoxic e.g. respiratory distress

Medication Medication1 may not be needed but will be if there are symptoms of anxiety, aggression or psychotis. For psychotic behaviour: haloperidol 0.5 mg (o) as a single dose or olanzapine 2.5–10 mg (o) daily in 1 or 2 doses If oral administration is not possible or when parenteral medication is required (cover with benztropine 2 mg (o) or IM): haloperidol 0.5 mg IM as single dose or olanzapine 2.5 mg IM as single dose For anticholinergic delirium: tacrine hydrochloride 15–30 mg with caution by slow IV injection (an antidote) Note: • Avoid benzodiazepines, especially in children and in patients with respiratory insufficiency. • Consider necessity for pain relief. • Use lower doses of parenteral medications in the very old and frail.

Dementia (chronic organic brain syndrome) Dementia or neurocognitive disorder is an important diagnosis to consider in the elderly patient. The DSM criteria for dementia are presented in CHAPTER 8. The main feature of dementia is impairment of memory, especially recent memory, when the person

cannot remember what has happened a few hours (or even moments) earlier but may clearly remember the events of the past. The more serious behavioural changes encountered with dementia tend to occur in the advanced stages. However, these disturbances may be  precipitated by  illness such as infections, emotional upset and drugs. These serious disturbances include: • uninhibited behaviour • hallucinations (generally uncommon) • paranoid delusions If a stable patient becomes acutely disturbed, delirium should be suspected.

Presenile dementia—Alzheimer type The main features are: • • • • • •

onset in late 50s and early 60s insidious onset early loss of short-term memory progressive decline in intellect death in 5–10 years more common in Down syndrome

Differential diagnosis of dementia There are two approaches to the differential diagnosis, including consideration of the classic causes of disturbed behaviour as summarised in the mnemonic in TABLE 45.5.7 However, the foremost differential diagnosis should be ‘pseudodementia’ caused by severe depression. A simple comparison between schizophrenia and dementia is shown in TABLE 45.6. A vigorous search for a possible cause of dementia is warranted since there are a significant number of reversible causes. In particular, it is important to exclude the psychiatric conditions that may mimic dementia. Treatment • To control psychotic symptoms or disturbed behaviour: risperidone 0.5–2 mg (o) daily or olanzapine 2.5–10 mg (o) daily in 1 or 2 doses • To control symptoms of anxiety and agitation: oxazepam 15 mg (o) 1 to 4 times daily. Avoid benzodiazepines for more than 2 weeks.

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The disturbed patient

Table 45.5

Differential diagnosis of dementias

D = Delirium drugs (see toxic)

Table 45.7

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Causes of psychoses8

Functional psychoses:

E = Emotional disorder = depression endocrine = thyroid M = Memory = benign forgetfulness E = Elective = anxiety disorders/neuroses N = Neurological: • CVA • head trauma

• schizophrenia • schizoaffective disorder (core symptoms of schizophrenia + mood symptoms) • bipolar mood disease (depressed or manic phase) Drug-induced psychoses Organic based psychoses Other: • delusional disorder (paranoid psychoses) • brief psychotic disorder • folie à deux (psychosis occurring simultaneously in two close associates)

T = Toxic: • drugs/medication • metabolic disease I = Intellect—low or retarded A = Amnesic disorders—Korsakov syndrome S = Schizophrenia (chronic)

intervention leads to improved outcomes. Early or prodromal symptoms include the following:

Source: After McLean6

Table 45.6

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Comparison of schizophrenia and dementia Dementia

Schizophrenia

Onset

Middle-aged or elderly

Young

Memory

Always impaired

Usually unaffected

Delusions

Rare

Frequent

Hallucinations

Uncommon

Frequent

Thought broadcasting

Never

Frequent

The acute psychotic patient Acute psychosis is the presence of the mental state where appreciation of reality is impaired as evidenced by the presence of typical psychotic symptoms such as delusions, hallucinations, mood disturbance and bizarre behaviour.8

• • • • • • • • •

social withdrawal reduced attention and concentration reduced drive and motivation depressed mood anxiety irritability/agitation suspiciousness sleep disturbance deterioration in role functioning

It is appropriate to ask the correct questions in order to elicit psychotic symptoms. These are presented in TABLE 45.8.

Table 45.8

Questions for eliciting psychotic symptoms

Anxiety

Have you been feeling especially nervous or fearful? Have you felt tense and shaky, or experienced palpitations?

Depressed mood

Have you been feeling sad or ‘down in the dumps’ recently, not enjoying activities as much as before?

Elevated mood

Have you been feeling especially good in yourself, more cheerful than usual and full of life?

The differential diagnoses of patients presenting with psychoses is presented in TABLE 45.7.

Early diagnosis Early recognition of a psychosis, particularly schizophrenia, is extremely important, as early

continued

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Table 45.8 continued Auditory hallucinations

Do you hear voices of people talking to you even when there is no-one nearby?

Thought insertion

Have you felt that thoughts are being put into your mind? Do you experience telepathy?

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Thought withdrawal

Have you experienced thoughts being taken out of your mind?

Thought broadcasting

Have you felt that other people are aware of your thoughts?

Thought echo

Have you experienced voices or people echoing your thoughts?

Delusion of control

Have you felt under the control or influence of an outside force?

Delusions of reference

Do programs on the television or radio hold special meaning for you?

Delusions of persecution

Do you feel that you are being singled out for special treatment? Is there a conspiracy against you?

Delusions of grandeur

Do you feel special, with unusual abilities or power?

Delusions of guilt

Do you believe that you have sinned or have done something deserving punishment?

The term ‘schizophrenia’ (Bleuler 1911) refers to a group of severe psychiatric illnesses characterised by severe disturbances of emotion, language, perception, thought processes, volition and motor activity. The causes of schizophrenia disorders are unknown, but genetic factors and drug abuse are implicated. Signs and symptoms of schizophrenia • Positive — delusions — hallucinations — thought disorder — disorganised speech and behaviour • Negative — flat affect — poverty of thought — lack of motivation — social withdrawal — reduced speech output • Cognitive — distractibility — impaired working memory — impaired executive function (e.g. planning) — impaired insight • Mood — mania (elevation) — depression Other features include:

Reproduced with permission 5

Source: Moulds

DSM-5 key diagnostic criteria6— schizophrenia A Two or more of following, each present for a significant portion of time during a one-month period 1 2 3 4 5

Schizophrenia and associated disorders

delusions hallucinations at least one of these disorganised speech grossly disorganised or catatonic behaviour negative symptoms e.g. flat effect



B Social, learning or occupational dysfunction C Continuous signs of disturbance for at least 6 months D No evidence of other psychoses e.g. bipolar E Not attributable to effects of substance abuse or other medical condition

• • • •

bizarre behaviour subject to tension, anxiety or depression deterioration in work and study performance peak incidence 15–25 years9—smaller peak at 40 years • lifetime prevalence 1 in 100 • equal sex incidence • high risk of suicide Differential diagnosis Organic factors need to be excluded, especially drugs: • amphetamines • hallucinogens (e.g. LSD) • marijuana A comparison of delirium, dementia and functional psychosis is presented in TABLE 45.9. Management Drug treatment is only a part of total management. Explanation and appropriate reassurance to the

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The disturbed patient

Table 45.9

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Comparison of the clinical features of delirium, dementia and acute functional psychoses9

Feature

Delirium

Dementia

Acute psychosis

Onset

Rapid

Slow—insidious

Rapid

Duration

Hours to weeks

Months to years

Depends on response to treatment

Course over 24 hours

Fluctuates—worse at night

Minimal variation

Minimal variation

Consciousness

Reduced

Alert

Alert

Perception

Misperceptions common, especially visual

Misperceptions rare

May be misperceptions

Hallucinations

Common, visual (usually) or auditory

Uncommon

Common, mainly auditory

Attention

Distractable

Normal to impaired

Variable—may be impaired

Speech

Variable, may be incoherent

Difficulty finding correct words

Variable: normal, rapid or slow

Organic illness or drug toxicity

One or both present

Often absent

Usually absent

family with patient and family supportive care is obviously essential. Supportive psychotherapy is important in all phases. A team approach is necessary to cope with the disorder, which usually has a devastating effect on the family. Referral for specialist care is appropriate.

Acute phase • Hospitalisation usually necessary • Drug treatment for the psychosis1 Drug treatment may include the first-generation (typical or conventional) antipsychotics such as haloperidol and chlorpromazine, which are effective for managing the ‘positive’ symptoms, or the second generation (atypical) antipsychotics such as risperidone, olanzapine, quetiapine, clozapine, amisulpride and aripiprazole, which in addition are more effective at treating the ‘negative’ and other symptoms of schizophrenia.10 The usual practice rule is to start with a secondgeneration antipsychotic at a low dose and titrate upwards at a rate and to a level that is optimal for the patient. Patients with a first psychotic episode may respond to lower than usual doses.6 1 When oral medication is possible, first-line treatment is one of (with starting doses):5,6,11 amisulpride 100 mg nocte asenapine 5 mg sublingual bd aripiprazole 10 mg once daily olanzapine 5 mg nocte paliperidone 3 mg once daily quetiapine 50 mg bd → 200 mg bd (by day 5)

risperidone 0.5–1 mg nocte → 2 mg nocte sertindole 4 mg (o) once daily ziprasidone 40 mg bd → 80 mg bd If response is inadequate in 3 weeks increase the dose according to prescribing guidelines. If no response after 4–6 weeks consider a change to: • an alternative second-generation agent (above) or • a first-generation antipsychotic such as: chlorpromazine 200 mg once daily → 500 mg haloperidol 1.5 mg once daily → 7.5 mg trifluoperazine 2 mg bd 2 Parenteral medication should be avoided if possible in acute care but if required: haloperidol 2.5–10 mg IM, initially, up to 20 mg in 24 hours, depending on the response or olanzapine 5–10 mg IM initially (do not use with benzodiapines concurrently) add benztropine 1–2 mg (o) bd (to avoid dystonic reaction) or zuclopenthixol acetate 50–150 mg IM as a single dose If dystonic reaction: benztropine 1–2 mg IV or IM If very agitated use: diazepam 5–10 mg (o) up to 40 mg/day or 5–10 mg IV

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Chronic phase Long-term antipsychotic medication is recommended to prevent relapse.1 • Examples of oral medication regimens:11

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olanzapine 10–20 mg (o) nocte or risperidone 1–2 mg (o) bd or quetiapine 150 mg (o) bd • Aim for lowest possible dose to maintain control. • Chlorpromazine is not recommended for long-term use because of photosensitivity reactions. • Use depot preparations if compliance is a problem:5,11 fluphenazine decanoate 12.5 mg IM, statim then 12.5–50 mg every 2–4 weeks or haloperidol decanoate 50 mg IM, statim then 50–200 mg every 4 weeks or flupenthixol decanoate 10 mg IM, statim then 20–40 mg every 2–4 weeks or risperidone 25–50 mg IM every 2 weeks, titrated to clinical response or zuclopenthixol 100 mg IM, statim then titrated to 200–400 mg every 2–4 weeks Tips with depot preparations: • Start with IM test doses and then titrate to recommended controlling levels (half or full starting dose). • May take 2–4 months to produce a stable response, so oral supplements may be necessary. • Not as effective as oral therapy. • Give as deep IM injection with 21 gauge needle in buttock. • Use lowest possible dose to avoid tardive dyskinesia. • Reassess at least every 3 months. • Closely monitor patient for movement disorders.

Drug-resistant schizophrenia Consider other causes (e.g. substances abuse). ECT may help the agitated patient, especially if catatonic. Consider a trial of clozapine (300–600 mg daily) with strict monitoring for blood dyscrasias or olanzapine (5–20 mg daily).

Movement disorders from antipsychotic medication1

Acute dystonias • Usually bizarre muscle spasms affect face, neck, tongue and trunk • Oculogyric crises, opisthotonos and laryngeal spasm Treatment: benztropine 1–2 mg IV or IM

Akathisia • Subjective motor restlessness of feet and legs • Generally later onset in course of treatment Treatment: • reduce dosage until akathisia less troublesome or substitute thioridazine • can use oral propranolol, diazepam or benztropine as a short-term measure

Parkinsonian • Seen relatively early in treatment • The akinesia can be confused with drug-induced depression Treatment: • use lower dose or substitute a phenothiazine in low dosage • alternatively, use benztropine or benzhexol

Tardive dyskinesia Tardive dyskinesia is a syndrome of abnormal involuntary movements of the face, mouth, tongue, trunk and limbs. This is a major problem with the use of long-term antipsychotic drugs and may occur months or years (usually) after starting treatment and with drug withdrawal. Avoid prolonged use of metoclopramide. Differential diagnosis: • • • •

spontaneous orofacial dyskinesia senile dyskinesia ill-fitting dentures neurological disorders causing tremor and chorea

If drug withdrawal is ineffective, use tetrabenazine 12.5 mg (o) daily, increasing as necessary.12 The risks and benefits of continuing therapy have to be weighed. Note: Because of the difficulty with managing tardive dyskinesia, prevention in the form of using the lowest possible dosage of antipsychotic

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The disturbed patient medication is essential. This involves regular review and adjustment if necessary.

A Distinct period for at least 1 week of abnormal and persistent elevated, expansive or irritable mood B Three or more of these unusual features: 1 inflated self-esteem or grandiosity 2 decreased need for sleep 3 talkative/accelerated speech 4 racing thoughts or flights of ideas 5 distractability as reported or observed 6 increased goal-directed activity or psychomotor agitation 7 excessive activity with ‘painful’ consequences C Marked impaired social or occupational functioning or need for hospitalisation or psychotic features D Episode not due to substance abuse or other medical condition

This is a potentially fatal adverse effect that can develop at any time. It develops in hours to days. Syndrome: high temperature, muscle rigidity, altered consciousness. Milder variants can occur (refer to CHAPTER 53). Treatment: • discontinue medication • ensure adequate hydration with IV fluids • if life-threatening: bromocriptine 2.5 mg (o) bd, gradually increasing to 5 mg (o) tds and dantrolene 50 mg IV every 12 hours for up to 7 doses

A–D = a manic episode: at least one in a lifetime for diagnosis

• consultant referral

Cardiac dysfunction

Bipolar disorder The mood disorders are divided into depressive disorders and bipolar disorders. Bipolar is a broad term to describe a recurrent illness with episodes of either mania or depression with return to normal function in between. The swing in moods in bipolar

mania manic phase

hypomania mild euphoria

normal mood minor depression moderate depression

depressive phase

major depression

FIGURE 45.1 Bipolar disorder (manic depression): possible mood swings

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DSM-5 criteria for a manic episode

Neuroleptic (antipsychotic) malignant syndrome

Various psychotrophic agents, particularly the phenothiazines, are prone to cause the adverse effect of prolongation of the QT interval with potential severe outcomes.

565

disorders (manic depressive disorders) is illustrated in FIGURE 45.1. It affects 1%–2% of the population. Bipolar I disorder has one fully fledged manic or mixed episode and usually depressive episodes. Bipolar II disorder is defined as a major depressive episode with at least one hypomanic episode but no classic manic episodes. The symptoms of mania may appear abruptly. Typical inherent features include: • • • • • •

reckless behaviour, overspending hasty decisions (e.g. job resignation, hasty marriages) impaired judgment increased sexual drive and activity poor insight into the problem variable psychotic symptoms—paranoia, delusions, auditory hallucinations

Note: The peak onset is in early adult life. There is a strong hereditary basis. Episodes may be precipitated by stress. ‘Hypomania’ is the term used to describe the symptoms of mania that are similar to but less severe (without criterion C) and of shorter duration. The subsequent major depressive phase is associated with a high risk of suicide. Good questions to ask the patient with suspected ‘bipolar’ disorder: • How have you been feeling in yourself? • Have you felt especially good about yourself?

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• Do you feel that you are special or have special powers? • Have you been spending more than usual? • Have you been needing less sleep than usual?

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Management of acute mania This is a medical emergency requiring hospitalisation for protection of both family and patient. Involuntary admission is usually necessary. It may be a first episode or a relapse due to poor treatment compliance or substance abuse. A recent metaanalysis indicates that antipsychotics are the most efficacious drugs. Treatment First line: olanzapine 5 mg (o) nocte initially or risperidone 0.5–1 mg (o) nocte initially Second line: haloperidol or other first-generation antipsychotic or lithium carbonate 750–1000 mg (o) daily in 2 or 3 divided doses increasing according to serum levels or sodium valproate 200–400 mg (o) bd initially or carbamazepine 100–200 mg (o) bd initially Failure to respond to treatment: • ensure maximum concentration of first drug • switch to a different drug e.g. olanzapine to lithium • combine drugs e.g. second-degree antipsychotic + lithium • ECT is of proven benefit for recalcitrant patients Remember to provide supportive psychotherapy with appropriate psychosocial interventions.

Prophylaxis for recurrent bipolar disorder (Over 90% will have a recurrence at some time: consider medication if two or more episodes of either mania or depression in the previous 4 years.)

Recommended prophylactic agents5 lithium 125–500 mg (o) bd then adjusted or second-generation antipsychotic agent or (if depression prominent) lamotrigine or carbamazine or sodium valproate

Use long-term lithium (e.g. 3–5 years). Target plasma level for maintenance is usually 0.6–0.8 mmol/L. A US study recommended lithium as the prime mood stabiliser.14 • If poor response, use another agent. • Unwanted side effects of lithium include: — a fine tremor — muscle weakness — weight gain — gastrointestinal symptoms • With anti-epileptics adjust dosage according to clinical response and toxicity.

Management of bipolar depression11,15 This is a difficult component to treat and antidepressants should not be used alone.11 Many mood-stabilising agents appear to have a bimodal (antidepressant and antimania) effect and can be useful in the absence of classical antidepressants.15 A recommended regimen is: lithium, valproate, carbamazepine, quetiapine, lamotrigine or olanzapine plus an antidepressant (e.g. SSRI, SNRI or MAOI) Antidepressants are usually withdrawn within 1–2 months because of a propensity to precipitate mania. ECT is an effective treatment for bipolar depression while psychological therapies such as CBT and psychoeducation have proven efficacy. Bipolar I patients usually recover but proceed to have further episodes of depression or mania.11

Body dysmorphic disorder5 Body dysmorphic disorder is characterised by a preoccupation with the belief that some aspect of physical appearance is abnormal, unattractive or diseased. The person’s concern and distress is out of proportion to any imagined or actual defect and usually not amenable to reassurance. This preoccupation causes significant functional impairment. The condition rarely presents directly and may be over-represented in the area of dermatology or plastic surgery. It begins in late childhood or early adolescence. The person’s focus is on the face, head or secondary sexual characteristics. Patients may be helped by counselling and psychotherapy including CBT. There is clinical evidence that SSRIs help if the symptoms suggest an obsessive–compulsive disorder. An antipsychotic agent may help where beliefs are delusional or in the context of a psychotic disorder.

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The disturbed patient

Depression Depression is very common and presents in a great range of severity. In the context of ‘the disturbed patient’ depression can be confused with dementia or a psychosis, particularly if the following are present: • • • •

psychomotor agitation psychomotor retardation delusions hallucinations

Assessment1 The following questions need to be addressed: • Is the depression primary (i.e. not secondary to another psychiatric condition such as schizophrenia or anxiety disorder)? • Is it part of a bipolar disorder? Has there been a previous manic or hypomanic episode? If so, a different approach to treatment is required. • Is the depression caused by another illness or physical factor (e.g. hypothyroidism, cerebrovascular disease or medication)? • Is the patient psychotic? • Is the patient a suicide risk? The treatment of depression is presented in CHAPTER 19.

PSYCHOACTIVE SUBSTANCE USE DISORDERS It is important for the GP to be aware of the effects of self-administration of psychoactive substances, especially their toxic or withdrawal effects. They form significant consideration for the differential diagnosis of disturbed patient behaviour. The following substances can cause these effects.

Management1 Undertake withdrawal with medical supervision as an inpatient. Transfer the patient to phenobarbitone or diazepam. phenobarbitone 120 mg (o) hourly until sedation or phenobarbitone 30 mg for each 100 mg of shorter-acting barbiturate reduce the dose gradually over 10 to 14 days or diazepam 20–40 mg orally, daily reduce the dose gradually over 10 to 14 days

Benzodiazepine dependence Withdrawal symptoms in the dependent patient include anxiety, restlessness, irritability, palpitation and muscle aches and pains, but delirium and seizures are uncommon except with very high doses. The shorter the half-life, the greater the dependence. Withdrawal is best achieved by supervising a gradual reduction in dosage aided by relaxation techniques and behavioural strategies to help patients cope with insomnia and anxiety. Refer to CHAPTER 21 for the effects of opioid dependence, stimulant substance abuse, hallucinogen abuse and cannabis use and dependence.

PSYCHIATRIC DISORDERS OF CHILDHOOD AND ADOLESCENCE1 The following disturbance problems do occur and must be taken seriously, especially the potential for suicide in the second decade. Many of these disorders are presented in more detail in CHAPTER 94.

Alcohol Toxic and withdrawal effects, including delirium tremens, are outlined in CHAPTER 21. Abrupt withdrawal can cause symptoms ranging from tremors, agitation and dysphoria (feeling thoroughly miserable) to fully developed delirium tremens. Epileptic seizures may also occur.

Barbiturate dependence Tolerance and symptoms on withdrawal are the main features. Barbiturate withdrawal is a very serious, life-threatening problem and may be encountered in elderly people undergoing longstanding hypnotic withdrawal. Symptoms include anxiety, tremor, extreme irritability, twitching, seizures and delirium.

Attention deficit hyperactivity disorder Clinical features: • • • • •

short attention span distractibility overactivity impulsiveness antisocial behaviour

Depression Major depression follows the same criteria as for adults. Suicidal ideation has to be considered and taken very seriously if present. Imipramine is probably the drug of choice.

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Bipolar disorders Mania is seldom diagnosed before puberty. Adolescents may present (uncommonly) with symptoms of mania or hypomania.

Schizophrenia and related disorders Schizophrenia is rare before puberty. The criteria for diagnosis are similar to adults:

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• • • •

delusion thought disorder hallucinations 6 months or more of deterioration in functioning

Autism Aggression and irritability can be a feature, especially during adolescence.

Tourette syndrome Behavioural problems can be part of this syndrome, which requires the attention of an experienced consultant.

Obsessive–compulsive disorders In about one-third of cases the onset is between 5 and 15 years of age.

VIOLENCE AND DANGEROUSNESS Dangerousness has been defined as a ‘propensity to cause serious physical injury or lasting psychological harm to others’ and, in the context of the mentally abnormal, ‘the relative probability of their committing a violent crime’.16 Dangerousness is not related only to mental illness and, interestingly, most offenders have no psychiatric diagnosis. It is not an inherited, immutable characteristic of an individual but tends to surface on impulse in a particular context given a whole range of situational factors. Prediction of the risk of violence is not straightforward. Various groups have been identified as contributing risk factors for violent conduct.16 • Schizophrenic psychoses, including: older male paranoid schizophrenics; younger males prone to act violently and impulsively, presumably due to hallucinatory commands • Morbid jealousy: associated with delusions of infidelity • Antisocial personality disorder • Mood disorder: violence, usually associated with depression (rarely mania); married women with severe depression (violence against young children); history of suicide attempts in depression

• Episodic discontrol syndrome (similar to intermittent explosive disorder) • Intellectual disability combined with personality disorder and behavioural disturbances • Alcohol abuse or dependency • Amphetamine or benzodiazepine abuse or dependency From a management viewpoint, homicidal threats must be taken very seriously.

SUICIDE AND PARASUICIDE The haunting issue of suicide and parasuicide is presented in CHAPTER 19. The disturbed patient is always a suicide risk rather than a homicide risk. The importance of recognising depression with an associated suicide risk in the elderly patient has been emphasised heavily in this chapter.

Facts and figures17 • More than 90% of suicides occur without underlying chronic conditions but most people are significantly depressed at the time. • In Australia suicide is the second most common cause of death between the ages of 11 and 25 years. Children as young as 5 years of age have committed suicide. • Those who talk about suicide may attempt it later. • About half those committing suicide have seen a doctor within their last month of life. • Around 80–90% of suicides have given clear or subtle warnings to family, friends or doctors. • There is no evidence that asking patients about suicidal ideation provokes suicidal acts. • Doctors in Australia and other Western countries have a high suicide rate.

Suicide risk Blumenthal’s18 overlapping model lists five groups of risk factors (see FIG. 45.2): 1 Psychiatric disorders: • affective disorder and alcohol abuse in adults • schizophrenia • depression and conduct disorder in young people 2 Personality traits: • impulsiveness and aggression 3 Environmental and psychosocial factors: • poor social supports • chronic medical illness (e.g. AIDS) • significant loss

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The disturbed patient

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Overlap model (five domains) 5 Biology

45 3 Psychosocial life events, and chronic medical illness

1 Psychiatric disorder

4 Family history and genetics

2 Personality traits

FIGURE 45.2 Overlap model for understanding suicidal behaviour. Source: After Blumenthal SJ, Kupfer DJ, Generalised treatable strategies for suicidal behaviour, Annals New York Academy of Science, 1986; 487: 327–40.

4 Family history and genetics (both nature and nurture): • emulation of relatives • specific ethnic groups in custody 5 Biological factors: • possible serotonin deficiency

Parasuicide Parasuicide is attempted suicide; in many cases patients are drawing attention to themselves as a ‘plea for help’. It is important for the GP to take an active role in the support of the patient and family after discharge from hospital, but preferably in conjunction with a psychiatric or counselling service. Arrange frequent consultations at first and ensure adequate follow-up, especially for missed appointments.

PERSONALITY DISORDERS People with personality disorders may become very distressed and acutely disturbed under stress or provocation, and this may involve dramatic scenes, including public suicide threats. It is important to recognise personality disorders because they usually

cause considerable distress to the patients, their family, society and GPs. The prevalence is estimated as 11–12%.5 In practice the personality disorders of most concern are those that present with hostility, either verbal or physical, particularly if a suicide or homicide threat is involved. It is a mistake to assume that those patients who manifest violent or psychopathic behaviour have a personality disorder or, conversely, the meek and mild are free from personality disorder. The diagnosis of personality disorder can be difficult. As practitioners we tend to have a ‘gut feeling’ about the diagnosis but often find it difficult to classify the personality of the patient and then to manage it appropriately. The main characteristics of a personality disorder are:5 • lack of confidence and low self-esteem • long history from childhood • difficulties with interpersonal relationships and society • recurrent maladaptive behaviour • relatively fixed, inflexible and stylised reaction to stress

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Table 45.10

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Summary of main personality disorders

Main cluster group

Subtypes

Main features of disorder

A Withdrawn

Paranoid

Suspicious, oversensitive, argumentative, defensive, hyperalert, cold and humourless

Synonyms: • odd • eccentric

Schizoid

Shy, emotionally cold, introverted, detached, avoids close relationships

Schizotypal Odd and eccentric, sensitive, suspicious and superstitious, socially isolated, odd speech, thinking and behaviour. Falls short of criteria for schizophrenia

B Antisocial Synonyms: • dramatic • emotional • sociopathic • flamboyant • erratic

Antisocial (sociopathic, psychopathic)

Histrionic (hysterical)

Narcissistic (‘prima donna’)

Borderline (‘hell-raiser’)

Impulsive, insensitive, selfish, callous, superficial charm, lack of guilt, low frustration level, doesn’t learn from experience, relationship problems (e.g. promiscuous), reckless disregard for safety of self and others Self-dramatic, egocentric, immature, vain, dependent, manipulative, easily bored, emotional scenes, inconsiderate, seductive, craves attention and excitement Morbid self-admiration, exhibitionist, insensitive, craves and demands attention, exploits others, preoccupied with power, lacks interest in and empathy with others, bullying, insightless Confused self-image/identity, impulsive, reckless, emptiness, ‘all or nothing’ relationships—unstable and intense, damaging reckless behaviour, full of anger and guilt, lacks self-control, uncontrolled gambling, spending etc. Note: High incidence suicide and parasuicide; drug abuse

C Dependent

Avoidant (anxious)

Anxious, self-conscious, fears rejection, timid and cautious, low self-esteem, overreacts to rejection and failure

Synonyms: • anxious • fearful • inhibited

Dependent

Passive, weak willed, lacks vigour, lacks self-reliance and confidence, overaccepting, avoids responsibility, seeks support

Obsessional (obsessive– compulsive)

Rigid, perfectionist, pedantic, indecisive, egocentric, preoccupied with orderliness and control

Passive–aggressive

Procrastinates, childishly stubborn, dawdles, sulks, argumentative, clings, deliberately inefficient and hypercritical of authority figures

Hypochondrial

Health-conscious, disease fearing, symptom preoccupation

Depressive (dysthymic, cyclothymic)

Pessimistic, anergic, low self-esteem, gloomy, chronic mild depression

Other (unofficial categories)

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The disturbed patient • minimal insight • perception of difficulties as external to themselves The medical/psychiatric significance: • maladaptive relationships with GPs and society • problem of sexually dysfunctional lives • risk of substance abuse and self-destructive behaviour • prone to depression and anxiety (usually low grade) • susceptible to ‘breakdown’ under stress Personality is the result of a genetic template and the continuing interaction of the person with outside influences (peer pressures, family interactions, influential events) and personal drives in seeking an identity. The outcome is a unique behaviour pattern manifest as a personality trait or character reflective of the individual’s self-image and fundamental to his or her sense of personal identity.19 Although personality is unique, it is possible to make a hypothesis that one is normal or abnormal. If abnormal, it is possible to stereotype it according to the predominant symptoms or behaviours. Using the International Classification of Disease (ICD-10) and the DSM-5 classification, various subtypes are readily identifiable (see TABLE  45.10),6 which can be considered in three main groups. There is a considerable overlap between the subtypes within a group20 and it is more important to understand the specific features of a person’s personality rather than categorise them.21 The antisocial personality disorders (ASPD) group (1–2% of population) tend to come to the attention of GPs more frequently, with some individuals representing ‘heart-sink’ patients because of demanding, angry or aggressive behaviour. They are more common among people in prison. The withdrawn group are typically withdrawn, suspicious and socially isolated but fall short of a true psychotic syndrome. GPs have problems communicating with them because they are often suspicious, which can make proper physical examination and management difficult. In the dependent and inhibited groups, which may overlap with an anxiety state, the main features are nervousness, timidity, emotional dependence and fear of criticism and rejection. They are frequent attenders (the ‘fat file’ syndrome) and are often accompanied by friends and relatives because of their insecurity.

Management The best treatment is a supportive, ‘therapeutic’ community and an understanding and supportive GP. Psychotherapies are the key to long-term treatment. It is vital to understand that people with personality disorders perceive the world from a fundamentally different perspective. Problematic patients, if agreeable, may respond well to psychological intervention and behavioural techniques, especially operant conditioning (reinforcing acceptable behaviour) and averse conditioning (correcting inappropriate behaviour).5,19 CBT has the most to offer. The borderline and narcissistic disorders in particular respond well to specific types of psychotherapeutic intervention. Patients’ selfesteem needs careful support while maladaptive modes of behaviour are confronted. Hospitalisation is rarely required except for those at risk of suicide (e.g. antisocial patients). Medication has limitations but may be useful to treat those individuals who temporarily decompensate into a psychosis, an anxiety state or depression. One study has shown that antipsychotic medication in low dosage (e.g. haloperidol 5 mg daily) is effective in treating the problematic behaviours in paranoid and some antisocial personality disorders.22 There are dangers to the therapist and it is important not to ‘buy into’ a particular psychopathy, especially with seductive, manipulative or paranoid patients.18

When to refer17 Indications for referral to a psychiatrist: • • • •

severe depression high suicide risk actual suicide attempt: recent or in the past suspected psychiatric disorders in the elderly: ?depression or schizophrenia; ?depression or dementia • failure to improve with treatment • poor family and social supports

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Bipolar disorder • Personality disorders • Schizophrenia

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References

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1 Dowden J (Chair). Therapeutic Guidelines: Psychotropic (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2003: 65–94. 2 Biro G. Dementia. Australian Doctor Weekly, 1990; 16 February: I–VIII. 3 Biro G. Delirium in the elderly. Australian Doctor Weekly, 1989; 1 December: I–VIII. 4 Kahn RL et al. Brief objective measures of the determination of mental status in the aged. Am J Psychiatry, 1960; 117: 326–9. 5 Moulds R (Chair). Therapeutic Guidelines: Psychotropic (Version 7). Melbourne: Therapeutic Guidelines Ltd, 2012: 7. 6 Kupfer DJ (Chair). Diagnostic and Statistical Manual of Mental Disorder (5th edn). Washington DC: American Psychiatric Publishing, 2013. 7 McLean S. Is it dementia? Aust Fam Physician, 1992; 21: 1762–6. 8 Keks N, Blashki G. The acutely psychotic patient: assessment and initial management. Aust Fam Physician, 2006; 35 (3): 90–4. 9 Norman T, Judd F. Schizophrenia. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 455–7. 10 Lovric K. Schizophrenia: update. Medical Observer, 17 September; 2004: 31–2. 11 Blashki G, Judd F, Piterman L. General Practice Psychiatry. Sydney: McGraw-Hill, 2007: 189–90.

12 Moulds R (chair) Therapeutic Guidelines: Neurology (Version 4). Melbourne. Therapeutic Guidelines Ltd, 2011: 121. 13 Smith LA, Cornelius V et al. Pharmacological intervention for acute bipolar mania: a systematic review of randomised placebo controlled trials. Bipolar Disorders, 2007; 9 (6): 551–60. 14 Sachs GS. A 25-year-old woman with bipolar disorder. JAMA, 2001; 285: 454–62. 15 Lovic K. Bipolar affective disorder: update. Medical Observer, 25 November 2005: 25–8. 16 Beaumont PJV, Hampshire RB. Textbook of Psychiatry. Melbourne: Blackwell Scientific Publications, 1989: 283–4. 17 Biro G. Suicide. Australian Doctor Weekly, 1991; 26 April: I–VIII. 18 Blumenthal S. Suicide—a guide to risk factors, assessment and treatment of suicidal patients. Med Clin North Am, 1988; 72: 937–63. 19 Papadakis MA, McPhee SJ et al. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013: 1051–2. 20 Pullen I, Wilkinson G et al. Psychiatry and General Practice Today. London: RC Psych & RCGP, 1994: 180–3. 21 Kaplan R. Personality disorders: diagnoses and treatment. Medical Observer, 24 August; 2001: 32–3. 22 Soloff PH et al. Progress in pharmacotherapy of borderline disorders: a double blind study of amitriptyline, haloperidol and placebo. Arch Gen Psychiatry, 1986; 43: 691–7.

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Dizziness/vertigo

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I got my giddiness in 1690 (at the age of 23) by eating 100 golden pippins at a time at Richmond. Four years later at a place 20 miles further on in Surrey I got my deafness; and these two ‘friends’ have visited me one or other year since, and being old acquaintances have often sought fit to come together. Jonathan Swift (–), describing his Ménière syndrome When patients complain of ‘dizziness’, they can be using this term to describe many different phenomena, and hence a careful history is required to unravel the problem. Other patients may use different terms to explain the same sensation, for example, ‘giddiness’, ‘swimming in the head’, ‘my brain spinning’, ‘whirling’ and ‘swinging’. ‘Dizzy’ comes from an old English word, dysig, meaning foolish or stupid. Strictly speaking, it means unsteadiness or lightheadedness—without movement or motion or spatial disorientation. ‘Vertigo’, on the other hand, comes from the Latin vertere (to turn) and -igo for a condition. It should describe a hallucination of rotation of self or the surroundings in a horizontal or vertical direction.1 The term ‘dizziness’, however, is generally used collectively to describe all types of equilibrium disorders and, for convenience, can be classified as shown in FIGURE 46.1.

Key facts and checkpoints •

• •

•

•

•

Approximately one-third of the population will have suffered from significant dizziness by age 65 and about a half by age 80.2 The commonest causes in family practice are postural hypotension and hyperventilation. The ability to examine and interpret the sign of nystagmus accurately is important in the diagnostic process. A drug history is very important, including prescribed drugs and others such as alcohol, cocaine, marijuana and illicit drugs. Ménière syndrome is overdiagnosed. It has the classic triad: vertigo–tinnitus–deafness (sensorineural). Vertebrobasilar insufficiency is also overdiagnosed as a cause of vertigo. It is a rare cause but may result in dizziness and sometimes vertigo but rarely in isolation.

vertigo

giddiness or lightheadedness dizziness

pseudovertigo

fainting or syncopal episodes

disequilibrium

FIGURE 46.1 Classification of dizziness

Defined terminology Vertigo Vertigo is defined as an episodic sudden sensation of circular motion of the body or of its surroundings or an illusion of motion, usually a rotatory sensation. Other terms used by the patient to describe this symptom include ‘everything spins’, ‘my head spins’, ‘the room spins’, ‘whirling’, ‘reeling’, ‘swaying’, ‘pitching’ and ‘rocking’. It is frequently accompanied by autonomic symptoms such as nausea, retching, vomiting, pallor and sweating. Vertigo is characteristically precipitated by standing or turning the head or by movement. Patients have to walk carefully and may become nervous about descending stairs or crossing the road and usually seek support. Therefore the vertiginous patient is usually very frightened and tends to remain immobile during an attack. Patients may feel as though they are being impelled by some outside force that tends to pull them to one side, especially while walking.

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True vertigo is a symptom of disturbed function involving the vestibular system or its central connections. It invariably has an organic cause. Important causes are presented in TABLE  46.1, while FIGURE  46.2 illustrates central neurological centres that can cause vertigo. Nystagmus is often seen with vertigo and, since 80–85% of causes are due to an ear problem, tinnitus and hearing disorders are also associated. In acute cases there is usually a reflex autonomic discharge producing sweating, pallor, nausea and vomiting.

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Giddiness Giddiness is a sensation of uncertainty or ill-defined lightheadedness. Other terms used by patients include ‘a swimming sensation’, ‘walking on air’ and ‘ground going beneath me’. It usually contains no elements of rotation, impulsion, tinnitus, deafness, nausea or vomiting. The patient with giddiness, although fearful of falling or swooning, can nonetheless walk without difficulty if forced to do so. Giddiness is a typical psychoneurotic symptom.

Syncopal episodes Syncope may present as a variety of dizziness or lightheadedness in which there is a sensation of

Table 46.1

Causes of vertigo

Peripheral disorders Labyrinth: • labyrinthitis: viral or suppurative • Ménière syndrome • benign paroxysmal positional vertigo (BPPV) • drugs • trauma • chronic suppurative otitis media Eight nerve: • vestibular neuronitis • acoustic neuroma • drugs Cervical vertigo Central disorders Brain stem (TIA or stroke): • vertebrobasilar insufficiency • infarction Cerebellum: • degeneration • tumours Migraine Multiple sclerosis

temporal lobe: tumour focal epilepsy

eye (disorders causing diplopia)

labyrinth: labyrinthitis Ménière syndrome vestibular nerve: acoustic neuroma vestibular neuronitis brain stem: multiple sclerosis vascular insufficiency

cerebellum: tumours inflammation posterior inferior cerebellar artery: thromboembolism

vertebral artery: thromboembolism

FIGURE 46.2 Diagrammatic illustration of central centres that can cause vertigo

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Dizziness/vertigo impending fainting or loss of consciousness. Common causes are cardiogenic disorders and postural hypotension, which are usually drug-induced.

Disequilibrium Disequilibrium implies a condition in which there is a loss of balance or instability while walking, without any associated sensations of spinning. Other terms used to describe this include ‘unsteadiness on feet’, ‘the staggers’, ‘swaying feeling’ and ‘dizzy in the feet’. Disequilibrium is usually of neurogenic origin.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 46.2.

Probability diagnosis In medical school we gain the wrong impression that the common causes of dizziness or vertigo are the relatively uncommon causes, such as Ménière syndrome, aortic stenosis, Stokes–Adams attacks, cerebellar disorders, vertebrobasilar disease and hypertension. In the real world of medicine, one is impressed by how often dizziness is caused by relatively common benign conditions, such as hyperventilation associated with anxiety, simple syncope, postural hypotension due to drugs and old age, inner ear infections, wax in the ears, post head injury, motion sickness and alcohol intoxication. In most instances making the correct diagnosis (which, as ever, is based on a careful history) is straightforward, but finding the underlying cause of true vertigo can be very difficult. The common causes of vertigo seen in general practice are benign paroxysmal positional vertigo (BPPV, so often related to cervical vertebral dysfunction), accounting for about 25% of cases, acute vestibulopathy (vestibular neuronitis) and vestibular migraine. Viral labyrinthitis is basically the same as vestibular neuronitis, except that the whole of the inner ear is involved so that deafness and tinnitus arise simultaneously with severe vertigo. The most common causes of recurrent spontaneous vertigo are Ménière syndrome and vestibular migraine.

Serious disorders not to be missed Neoplasia The important serious disorders to keep in mind are space-occupying tumours, such as acoustic neuroma, medulloblastoma and other tumours (especially posterior fossa tumours) capable of

Table 46.2

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Q. Probability diagnosis A. Anxiety-hyperventilation (G) Postural hypotension (G/S) Simple faint—vasovagal (S) Acute vestibulopathy (V) Benign paroxysmal positional vertigo (V) Motion sickness (V) Vestibular migraine (V) Cervical dysfunction/spondylosis Q. Serious disorders not to be missed A. Neoplasia: • acoustic neuroma • posterior fossa tumour • other brain tumours, primary or secondary Intracerebral infection (e.g. abscess) Cardiovascular: • arrhythmias • myocardial infarction • aortic stenosis Cerebrovascular: • vertebrobasilar insufficiency • brain stem infarct (e.g. PICA thrombosis) Multiple sclerosis Carbon monoxide poisoning Q. Pitfalls (often missed) A. Ear wax—otosclerosis Arrhythmias Hyperventilation Alcohol and other drugs Cough or micturition syncope Vestibular migraine/migrainous vertigo Parkinson disease Ménière syndrome (overdiagnosed) Rarities: • Addison disease (CHAPTER 23) • neurosyphilis • autonomic neuropathy • hypertension • subclavian steal • perilymphatic fistula • Shy–Drager syndrome Q. Seven masquerades checklist A. Depression Diabetes (possible: hypo/hyper) Drugs Anaemia Thyroid disorder (possible) Spinal dysfunction UTI (possible) Q. Is the patient trying to tell me something? A. Very likely. Consider anxiety and/or depression. G = giddiness; S = syncope; V = vertigo

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causing vertigo, intracerebral infections and cardiovascular abnormalities. It is important to bear in mind that the commonest brain tumour is a metastatic deposit from lung cancer.3

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The lesions of multiple sclerosis may occur in the brain stem or cerebellum. Young patients who present with a sudden onset of vertigo with ‘jiggly’ vision but without auditory symptoms should be considered as having multiple sclerosis. Five per cent of cases of multiple sclerosis present with vertigo.

Red flags for dizziness/vertigo

Pitfalls

• • • • •

A list of conditions causing dizziness that may be misdiagnosed is presented in TABLE 46.2. Wax in the ear certainly causes dizziness, though its mechanism of action is controversial. Cough and micturition syncope do occur, although they are uncommon. Ménière syndrome is a pitfall in the sense that it tends to be overdiagnosed.

neurological signs ataxia out of proportion to vertigo nystagmus out of proportion to vertigo central nystagmus central eye movement abnormalities

Acoustic neuroma This uncommon tumour should be suspected in the patient presenting with the symptoms shown in the diagnostic triad below. Headache may occasionally be present. DxT (unilateral) tinnitus + hearing loss + unsteady gait   acoustic neuroma

Diagnosis is best clinched by high-resolution MRI. Audiometry and auditory evoked responses are also relevant investigations. Cardiac disorders Cardiac disorders that must be excluded for giddiness or syncope are the various arrhythmias, such as Stokes–Adams attacks caused by complete heart block, aortic stenosis and myocardial infarction. Cerebrovascular causes The outstanding cerebrovascular causes of severe vertigo are vertebrobasilar insufficiency and brain stem infarction. Vertigo is the commonest symptom of transient cerebral ischaemic attacks in the vertebrobasilar distribution.1 Severe vertigo, often in association with hiccoughs and dysphagia, is a feature of the variety of brain stem infarctions known as the lateral medullary syndrome due to posterior inferior cerebellar artery (PICA) thrombosis. There is a dramatic onset of vertigo with cerebellar signs, including ataxia and vomiting. There are ipsilateral cranial nerve (brain stem) signs with contralateral spinothalamic sensory loss of the face and body. Diagnosis is by CT or MRI scanning. Neurological causes Important neurological causes of dizziness are multiple sclerosis and complex partial seizures.

Seven masquerades checklist Of these conditions, drugs and vertebral dysfunction (of the cervical spine) stand out as important causes. Depression demands attention because of the possible association of anxiety and hyperventilation. Diabetes mellitus has an association through the possible mechanisms of hypoglycaemia from therapy or from an autonomic neuropathy. Drugs Drugs usually affect the vestibular nerve rather than the labyrinth. Drugs commonly associated with dizziness are presented in TABLE 46.3.

Table 46.3

Drugs that can cause dizziness

Alcohol Antibiotics: streptomycin, gentamicin, kanamycin, tetracyclines Antidepressants Anti-epileptics: phenytoin Antihistamines Antihypertensives Aspirin and salicylates Cocaine Diuretics in large doses: intravenous frusemide, ethacrynic acid Glyceryl trinitrate Quinine-quinidine Tranquillisers: phenothiazines, phenobarbitone, benzodiazepines

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Dizziness/vertigo Cervical spine dysfunction It is not uncommon to observe vertigo in patients with cervical spondylosis or post cervical spinal injury. It has been postulated4 that this may be caused by the generation of abnormal impulses from proprioceptors in the upper cervical spine, or by osteophytes compressing the vertebral arteries in the vertebral canal. Some instances of BPPV are associated with disorders of the cervical spine.

Psychogenic considerations This may be an important aspect to consider in the patient presenting with dizziness, especially if the complaint is giddiness or lightheadedness. An underlying anxiety, particularly agoraphobia and panic disorder, may be the commonest cause of this symptom in family practice and clinical investigation of hyperventilation may confirm the diagnosis. The possibility of depression must also be kept in mind.5 Many of these patients harbour the fear that they may be suffering from a serious disorder, such as a brain tumour or multiple sclerosis, or face an impending stroke or insanity. Appropriate reassurance to the contrary is often positively therapeutic for that patient.

The clinical approach The essentials of the diagnostic approach include careful attention to the history and physical examination, and judicious selection of specific office tests and special investigations.

History It is important to get patients to explain the precise nature of the symptoms, even asking their opinion as to the cause of their dizziness. Key questions The following questions should be addressed: • Is it vertigo or pseudovertigo? • Symptom pattern: — paroxysmal or continuous? — effect of position and change of posture? • Any aural symptoms? Tinnitus? Deafness? • Any visual symptoms? • Any neurological symptoms? • Any nausea or vomiting? • Any symptoms of psychoneurosis? • Any recent colds? • Any recent head injury (even trivial)?

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• Any drugs being taken? — alcohol? — marijuana? — hypotensives? — psychotropics? — other drugs?

Examination A full general examination is appropriate with particular attention being paid to the cardiovascular and central nervous systems and the auditory and vestibular mechanisms. Guidelines Examination guidelines are: 1 ear disease: • auroscopic examination: ? wax ? drum • hearing tests • Weber and Rinne tests 2 the eyes: • visual acuity • test movements for nystagmus 3 cardiovascular system: • evidence of atherosclerosis • blood pressure: supine, standing, sitting • cardiac arrhythmias 4 cranial nerves: • 2nd, 3rd, 4th, 6th and 7th • corneal response for 5th • 8th—auditory nerve 5 the cerebellum or its connections: • gait • coordination • reflexes • Romberg test • finger nose test: ? past pointing 6 the neck, including cervical spine 7 general search for evidence of: • anaemia • polycythaemia • alcohol dependence Office tests for dizziness • Ask the patient to perform any manoeuvre that may provoke the symptom. • Carry out head positional testing to induce vertigo and/or nystagmus (e.g. Hallpike manoeuvre) (see FIG. 46.3). Avoid if prominent spontaneous vertigo and nystagmus. • Take blood pressure measurements in three positions.

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• Perform forced hyperventilation (20 to 25 breaths per minute) for 2 minutes. • Carry out palpation of carotid arteries and carotid sinus (with care).

Investigations Appropriate laboratory tests should be selected from TABLE 46.4. Table 46.4

Investigations

Haemoglobin

46

Blood glucose ECG: ? Holter monitor Audiometry Brain-stem evoked audiometry Caloric test Visual evoked potentials (MS) Electrocochleography Electro-oculography (electronystagmography) Rotational tests Radiology: • chest X-ray (? bronchial carcinoma) • cervical spine X-ray • CT scan • MRI (the choice to locate acoustic neuroma or other tumour—may detect MS and vascular infarction)

Diagnostic guidelines • A sudden attack of vertigo in a young person following a recent URTI is suggestive of vestibular neuronitis. • Dizziness is a common symptom in menopausal women and is often associated with other features of vasomotor instability. • Phenytoin therapy can cause cerebellar dysfunction. • Postural and exercise hypotension are relatively common in the older atherosclerotic patient. • Acute otitis media does not cause vertigo but chronic otitis media can, particularly if the patient develops a cholesteatoma, which then erodes into the internal ear causing a perilymphatic fistula.

Dizziness in children Dizziness is not a common symptom in children. Vertigo can have sinister causes and requires referral

because of the possibility of tumours, such as a medulloblastoma. A study by Eviatar and Eviatar6 of vertigo in children found that the commonest cause was a seizure focus particularly affecting the temporal lobe. Other causes included psychosomatic vertigo, vestibular migraine and vestibular neuritis. Apart from the above causes it is important to consider: • infection (e.g. meningitis, meningoencephalitis, cerebral abscess) • trauma, especially to the temporal area • middle-ear infection • labyrinthitis (e.g. mumps, measles, influenza) • BPPV (short-lived attacks of vertigo in young children between 1 and 4 years of age: tends to precede adulthood migraine)7 • hyperventilation • drugs—prescribed • illicit drugs (e.g. cocaine, marijuana) • cardiac arrhythmias • alcohol toxicity A common trap is the acute effect of alcohol in curious children who can present with the sudden onset of dizziness.

Dizzy turns in girls in late teens • These are commonly due to blood pressure fluctuations. • Give advice related to reducing stress, lack of sleep and excessive exercise. • Reassure that it settles with age (rare after 25 years).

Dizziness in the elderly Dizziness is a relatively common complaint of the elderly. Common causes include postural hypotension related mainly to drugs prescribed for hypertension or other cardiovascular problems. Cerebrovascular disease, especially in the areas of the brain stem, is also relevant in this age group. True vertigo can be produced simply by an accumulation of wax in the external auditory meatus, being more frequent than generally appreciated. Middle-ear disorder is also sometimes the cause of vertigo in an older person but disorder of the auditory nerve, inner ear, cerebellum, brain stem and cervical spine are common underlying factors. Malignancy, primary and secondary, is a possibility in the elderly. The possibility of cardiac arrhythmias as a cause of syncopal symptoms increases with age.

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Dizziness/vertigo

Dizzy turns in elderly women If no cause such as hypertension is found, advise them to get up slowly from sitting or lying, and to wear firm elastic stockings.

Acute vestibulopathy (vestibular failure) Causes: • vestibular neuritis • stroke—AICA or PICA Vestibular neuritis covers both vestibular neuronitis and labyrinthitis, which are considered to be a viral infection of the vestibular nerve and labyrinth respectively, causing a prolonged attack of vertigo that can last for several days and be severe enough to require admission to hospital.8 It is analogous to a viral infection of the 7th nerve causing Bell palsy. The attack is similar to Ménière syndrome except that there is no hearing disturbance. DxT acute vertigo + nausea + vomiting  vestibular neuritis

It is basically a diagnosis of exclusion. Treatment • Rest in bed, lying very still • Gaze in the direction that eases symptoms The following drugs can be used (see TABLE 46.5): prochlorperazine (Stemetil) 12.5 mg IM (if severe vomiting) but may slow recovery or 5–10 mg (o) tds

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or promethazine 10–25 mg IM or slow IV then 10–25 mg (o) for 48 hrs or (recommended as best) diazepam (which decreases brain-stem response to vestibular stimuli)2 5–10 mg IM for the acute attack, then 5 mg (o) tds for 2–3 days A short course of corticosteroids often promotes recovery (e.g. prednisolone 1 mg/kg (up to 100 mg) (o) daily in morning for 5 days, then taper over 15 days and cease).1, 10

Table 46.5

Symptomatic relief of acute vertigo9: pharmaceutical options

Anti-emetics: • prochlorperazine • metoclopramide Antihistamines: • promethazine • betahistine Benzodiazepines (short period use for vertigo): • diazepam • lorazepam

DxT same symptoms + hearing loss ± tinnitus  acute labyrinthitis

Characteristic features • single attack of vertigo without tinnitus or deafness • usually preceding ‘flu-like’ illness • mainly in young adults and middle age • abrupt onset with vertigo, ataxia, nausea and vomiting • generally lasts days to weeks • examination shows lateral or unidirectional nystagmus—rapid component away from side of lesion (no hearing loss) • caloric stimulation confirms impaired vestibular function

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Outcome Both are self-limiting disorders and usually settle over 5–7 days or several weeks. Labyrinthitis usually lasts longer and during recovery rapid head movements may bring on transient vertigo.

Benign paroxysmal positional vertigo BPPV is a common type of acute vertigo that is induced by changing head position—particularly tilting the head backwards, changing from a recumbent to a sitting position or turning to the affected side. Features • Affects all ages, especially the elderly • The female to male ratio is 2:1 • Recurs periodically for several days • Each attack is brief, usually lasts 10–60 seconds, and subsides rapidly • Severe vertigo on getting out of bed • Can occur on head extension and turning head in bed

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• Attacks are not accompanied by vomiting, tinnitus or deafness (nausea may occur) • In one large series 17% were associated with trauma, 15% with viral labyrinthitis, while about 50% had no clear predisposing factor other than age. One accepted theory of causation is that fine pieces of floating crystalline calcium carbonate deposits (otoconia) that are loose in the labyrinth settle in the posterior semicircular canal and generate endolymphatic movement.11 It may also be a variation of cervical dysfunction. • Diagnosis is confirmed by head position testing. From a sitting position the patient’s head is rapidly taken to a head-hanging position 30° below the level of the couch—do three times, with the head (1) straight, (2) rotated to the right, (3) rotated to the left. Hold on for 30 seconds and observe the patient carefully for vertigo and nystagmus. There is a latent period of few seconds before the onset of the symptoms—see FIGURE 46.3. • Tests of hearing and vestibular function are normal • There is usually spontaneous recovery in weeks (most return to regular activity after 1 week) • Recurrences are common: attacks occur in clusters

Management • Give appropriate explanation and reassurance • Avoidance measures: encourage the patient to move in ways that avoid the attack • Drugs are not recommended • Special exercises • Cervical traction may help

Particle repositioning manoeuvres Patient-performed exercises. Most patients appear to benefit from exercise, such as the Brandt and Daroff procedure12 or the Cawthorne–Cooksey exercises9 that consist essentially of repeatedly inducing the symptoms of vertigo. Rather than resorting to avoidance measures, the patient is instructed to perform positional exercises to induce vertigo, hold this position until it subsides, and repeat this many times until the manoeuvre does not precipitate vertigo. The attacks then usually subside in a few days. Therapist-performed exercises. Physical manoeuvres performed as an office procedure include the Epley and Semont manoeuvres (refer ).

Surgical treatment Rarely surgical treatment is required; it involves occlusion of the posterior semicircular canal rather than selective neurectomy.

Ménière syndrome This is caused by a build-up of endolymph.

FIGURE 46.3 Hallpike manoeuvre: positional testing for benign paroxysmal positional vertigo (head rotated to 45° then taken rapidly from a sitting position to a hanging position).Repeat with head turned to the opposite side. A positive response is the onset of symptoms ± nystagmus with the affected ear lowermost.

• It is commonest in the 30–50 years age group. • It is characterised by paroxysmal attacks of vertigo, tinnitus, nausea and vomiting, sweating and pallor, deafness (progressive). • Onset is abrupt—patient may fall and then be bedridden for 1–2 hours. Patient doesn’t like moving head. • Attacks last 30 minutes to several hours. • There is a variable interval between attacks (twice a month to twice a year). • Nystagmus is observed only during an attack (often to side opposite affected inner ear). • Examination: — sensorineural deafness (low tones) — caloric test: impaired vestibular function — audiometry: sensorineural deafness, loudness recruitment — special tests • There are characteristic changes in electrocochleography.

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Dizziness/vertigo

DxT vertigo + vomiting + tinnitus + sensorineural deafness   Ménière syndrome

Treatment The aim is to reduce endolymphatic pressure by reducing the sodium and water content of the endolymph.

Acute attack13 Anticipation of attack (fullness, tinnitus): prochlorperazine 25 mg suppository or 30 g urea crystals in orange juice (preferably 30 minutes before in prodromal phase) Treatment: diazepam 5 mg IV ± prochlorperazine 12.5 mg IM. Consider betahistine 8 mg (o) tds if persistent or episodic

Long term • Reassurance with a careful explanation of this condition to the patient, who often associates it with malignant disease • Excess intake of salt, tobacco and coffee to be avoided • A low-salt diet is the mainstay of treatment (10% Vomiting Older age >50 years Chronic NSAID use Severe frequent symptoms Family history of upper GIT or colorectal cancer Short history of symptoms

Complications • Oesophagitis ± oesophageal ulcer • Iron-deficiency anaemia • Oesophageal stricture

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• Respiratory: chronic cough, asthma, hoarseness • Barrett oesophagus (from prolonged reflux)

Barrett oesophagus • Usually a metaplastic response to prolonged reflux • A premalignant condition (adenocarcinoma) • Lower oesophagus lined with gastric mucosa (at least 3 cm) • Prone to ulceration • Needs careful management • Consider 2 yearly endoscopies with biopsies

• Antacids (see TABLES 47.4 and 47.5): best is liquid alginate/antacid mixture e.g. Gaviscon/Mylanta plus 20 mL on demand or 1–2 hours before meals and bedtime Table 47.4

Antacids in common use

Antacids Water soluble:

Calcium carbonate Sodium: • bicarbonate • citrotartrate

Investigations6

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• Endoscopy (see Red flag pointers)—perform prior to empirical therapy. Limited role—about one third negative • Barium swallow and meal • 24-hour ambulatory oesophageal pH monitoring

Note: Excess is prone to cause alkalosis—apathy, mental changes, stupor, kidney dysfunction, tetany Water insoluble:

Management of GORD6,7,8,9

Stage 1 • Patient education/appropriate reassurance • Consider acid suppression or neutralisation • Attend to lifestyle: — reduce weight if overweight (this alone may abolish symptoms) — reduce or cease smoking — reduce or cease alcohol (especially with dinner) — avoid fatty foods (e.g. pastries, french fries) — reduce or cease coffee, tea and chocolate — avoid coffee and alcohol late at night — avoid gaseous drinks — leave at least 3 hours between the evening meal and retiring — increase fibre intake (e.g. high fibre cereals, fruit and vegetables) — small regular meals and snacks — eat slowly and chew food well — sleep on the left side — main meal at midday; light evening meal — avoid spicy foods and tomato products • Drugs to avoid: anticholinergics, theophylline, calcium-channel blockers, doxycycline. Pillinduced oesophagitis occurs, especially with tetracyclines, slow-release potassium, iron sulphate, corticosteroids, NSAIDs—avoid taking dry; use ample fluids • Elevation of head of bed or wedge pillow: if GORD occurs in bed, sleep with head of bed elevated 10–20 cm on wooden blocks or use a wedge pillow (preferable)

Aluminium: • hydroxide • glycinate • phosphate Magnesium: • alginate • carbonate • hydroxide • trisilicate

Combination antacids Antacid + alginic acid Antacid + oxethazaine Antacid + simethicone

Table 47.5

Side effects of common antacids

Aluminium hydroxide:

Constipation

Magnesium trisilicate:

Diarrhoea

Sodium bicarbonate:

Alkalosis Milk alkali syndrome Aggravation of hypertension

Calcium carbonate:

Alkalosis Constipation Milk alkali syndrome Hypercalcaemia

Antacids are appropriate for rapid relief of mild intermittent or occasional breakthrough symptoms but are ineffective for long-term management.

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Dyspepsia (indigestion) Stage 26 If no relief after several weeks, the following approaches are recommended by the Gastroenterological Society of Australia (GESA).6 Reduce acid secretion. Select from: • Proton-pump inhibitor (PPI) for 4 weeks (preferred agent) 30–60 minutes before food lansoprazole 30 mg mane or omeprazole 20 mg mane or pantoprazole 40 mg mane or esomeprazole 20 mg mane or rabeprazole 20 mg mane • H2-receptor antagonists (oral use for 8 weeks) famotidine 20 mg bd or nizatadine 150 mg bd or 300 mg nocte or ranitidine 150 mg bd pc or 300 mg nocte

Proton-pump inhibitor (PPI) H2-receptor antagonist lifestyle modification ± antacids

Step down

Step up

Although the more traditional step-up approach of 1. Antacids → 2. H2-receptor antagonists → 3. PPI can be used, there has been a change to favour a high level (more potent) initial therapy with PPIs at standard dose (a step-down approach; see FIG. 47.1). This is based on the grounds of outcomes, speed of response and total cost. Surgery is usually for young patients with severe reflux. The gold standard is a short loose 360-degree fundoplication.

FIGURE 47.1 The stepwise approach to the management of dyspeptic symptoms7

Functional (non-ulcer) dyspepsia7, 10 This term applies to the 60% of patients presenting with dyspepsia in which there is discomfort on eating in the absence of demonstrable organic disease. This

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can be considered in two categories (although there is overlap): • ulcer-like dyspepsia or • dysmotility-like dyspepsia

Ulcer-like dyspepsia Treat as for GORD. A practical approach is to commence with a 4-week trial of a PPI or an H2receptor antagonist and cease if symptoms resolve.7

Dysmotility-like dyspepsia Clinical features • Discomfort with early sense of fullness on eating • Nausea • Overweight • Emotional stress • Poor diet (e.g. fatty foods) • Similar lifestyle guidelines to GORD Management • Treat as for GORD (stage 1). • Include antacids. • If not responsive: — Step 1: H2-receptor antagonists — Step 2: prokinetic agents domperidone 10 mg tds or metoclopramide 10 mg tds

Peptic ulcer disease10,11 Features (general) • Common: 10–20% incidence over a lifetime • Point prevalence of ulcer disease: 3–5% • DU:GU = 4:1 • DUs common in men 3:1 • Cumulative mortality of 10% • Risk factors: — male sex — family history — smoking (cause and delayed healing) — stress — common in blood group O — NSAIDs 2–4 times increase in GU and ulcer complications — H. pylori: if absent and no NSAIDS, no ulcer • Unproven risk factors: — corticosteroids — alcohol (except for gastric erosion) — diet (does reduce recurrence of PU)

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• Types of ulcers: — lower oesophageal — gastric — stomal (postgastric surgery) — duodenal Clinical features • Episodic burning epigastric pain related to meals (1–2 hours after) • Relieved by food or antacids (generally) • Dyspepsia common • May be ‘silent’ in elderly on NSAIDs • Physical examination often unhelpful

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Investigations • Endoscopy (investigation of choice):12 92% predictive value • Barium studies: 54% predictive value • Serum gastrin (consider if multiple ulcers) • H. pylori test: serology or urea breath test; diagnosis usually based on urease test performed at endoscopy Complications • Perforation • Bleeding → haematemesis and melaena • Obstruction—pyloric stenosis • Anaemia (blood loss) • Cancer (in GU) • Oesophageal stenosis

Bleeding peptic ulcer This can be treated with endoscopic haemostasis with heater probe or injection of adrenaline or both. Also IV omeprazole 80 mg bolus, then 8 mg/hr IV infusion for 3 days. Surgery is an option. Management of peptic ulcer disease Aims of treatment: • • • •

relieve symptoms accelerate ulcer healing prevent complications minimise risk of relapse

The treatment of a GU is similar to that for a DU except that GUs take about 2 weeks longer to heal and the increased risk of malignancy has to be considered.

Stage 17 General measures: (lifestyle and symptom relief) • same principles as for GORD • stop smoking

• avoid irritant drugs: NSAIDs, aspirin • normal diet but avoid foods that upset • antacids If H. pylori positive—eradicate with combined therapy. Confirm eradication with a urea breath test (DU) or repeat gastroscopy (GU) and repeat if still present.8 If H. pylori negative—treat with full-dose PPI. Proton-pump inhibitors (PPIs) provide more potent acid suppression and heal GUs and DUs more rapidly than H2-receptor antagonists. • 4–8-week oral course Use with caution in: • the elderly • those on drugs, especially warfarin, anticonvulsants, beta blockers • liver disease

Therapy to eradicate Helicobacter pylori 13 This organism has a proven link with PU disease (both DU and benign non-drug induced GU), gastric cancer and maltoma (a gastric lymphoma) because of mucosal infection. This hypothesis is supported by a very low relapse of DU in subjects eradicated of H. pylori. Most infected people are asymptomatic but infection leads to a lifetime risk of peptic ulcer disease in 15–20% and of gastric cancer in up to 2%.10 Twenty per cent of people have a variety of symptoms including those from gastritis and duodenitis. Treatment is based on combination triple or quadruple therapy, which can achieve a successful eradication rate of 85–90%. Drug treatment regimens (examples)7 First-line therapy: PPI (e.g. omeprazole or esomeprazole 20 mg) plus clarithromycin 500 mg plus amoxycillin 1 g All orally twice daily for 7 days and is the preferred regimen. Available as a combination pack. or PPI + clarithromycin + metronidazole 400 mg (twice daily for 7 days)—if hypersensitive to penicillin or other combinations: quadruple therapy e.g. bismuth + PPI + tetracycline + metronidazole (for failed triple combination)

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Dyspepsia (indigestion) Note: Resistance to metronidazole is common (>50%) and to clarithromycin is increasing (about 5% plus) but uncommon with tetracycline and amoxycillin.6 Maintenance anti-secretory therapy is usually unnecessary for H. pylori ulcers after successful eradication.7

Surgical treatment Indications (now uncommon) include: • failed medical treatment after 1 year • complications: — uncontrollable bleeding — perforation — pyloric stenosis • suspicion of malignancy in GU • recurrent ulcer after previous surgery

NSAIDs and peptic ulcers7,14 1 Ulcer identified in NSAID user: • stop NSAID (if possible) • check smoking and alcohol use • try alternative anti-inflammatory analgesic: — paracetamol — COX-2 selective drug — enteric-coated, slow-release aspirin — corticosteroids intra-articular or oral • PPI for 4 weeks (gives best results) Note: Healing time is doubled if NSAID continued.2 About 90% heal within 12 weeks. Check healing by endoscopy at 12 weeks. Do H. plyori test. 2 Prevention of ulcers in NSAID user:14 Primary prophylaxis is usually reserved for those at significantly increased risk, for example older persons (>75 years) and past history PU. Use one of the following PPIs: esomeprazole 20 mg daily or omeprazole 20 mg daily or pantoprazole 40 mg daily Increased dietary fibre assists DU healing and prevention. Note: Do H. pylori test and if present, it should be eradicated with combination therapy.

Autoimmune gastritis7 This is an inflammatory condition with antibodies to parietal cells and intrinsic factor. It is asymptomatic

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and may lead to pernicious anaemia. Diagnosis is confirmed by histology or endoscopy. H. pylori is absent. Treat with iron and vitamin B12.

Stomach cancer Clinical features • Male to female ratio = 3:1 • Usually asymptomatic early • Consider if upper GIT symptoms in patients over 40 years, especially weight loss • Recent-onset dyspepsia in middle age • Dyspepsia unresponsive to treatment • Vague fullness or epigastric distension • Anorexia, nausea, ± vomiting • Dysphagia—a late sign • Onset of anaemia • Changing dyspepsia in GU • Changing symptoms in pernicious anaemia • H. pylori now implicated as a cause Risk factors: ↑ age, blood group A, smoking, atrophic gastritis Limited physical findings • Palpable abdominal mass (20%) • Signs (see FIG. 47.2) in advanced cases DxT malaise + anorexia + dyspepsia + weight loss   stomach cancer

DxT triple loss of appetite + weight + colour   stomach cancer

Investigations • Endoscopy and biopsy is optimal test • Barium meal—false negatives Treatment • Surgical excision: may be curative if diagnosed early but overall survival is poor

When to refer • Infants with persistent gastro-oesophageal reflux not responding to simple measures • Failure to respond to stage 1 therapy for heartburn, when endoscopy is required • Patients with persistent or recurrent ulcers • Any patient with a PU complication, such as haemorrhage, obstruction or perforation

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• • anaemia

hepatomegaly —hard and irregular

enlarged supraclavicular lymph node (Troisier sign)

epigastric mass

• •

Keep in mind the malignant potential of a GU. A change in the nature of symptoms with a GU suggests the possibility of malignant change. Avoid the long-term use of water-soluble antacids. Investigate the alarm symptoms—dysphagia, bleeding, anaemia, weight loss, waking at night, pain radiating to the back.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Heartburn • Hiatus hernia • Peptic ulcer • Reflux disease • Reflux in infants

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References

FIGURE 47.2 Late signs of stomach cancer

Practice tips • • • • • •

Scleroderma is a rare but important cause of oesophagitis. Advise patients never to ‘dry swallow’ medications. Dysphagia always warrants investigation, not observation. Beware of attributing anaemia to oesophagitis. Epigastric pain aggravated by any food, relieved by antacids = chronic GU. Epigastric pain before meals, relieved by food = chronic DU.

1 Smallwood R. Dyspepsia. Medical Observer, 1991; 27 September; 1991: 33–4. 2 Pritchard P. The management of upper gastrointestinal problems in patients taking NSAIDs. Aust Fam Physician, 1991; 20: 1739–41. 3 McGarity B, Morgia M. Peptic ulcer disease: an update on diagnosis and treatment. Medicine Today, 2001; December: 33–7. 4 Sewell J. Gastro-oesophageal reflux. Australian Paediatric Review, 1991; 3: 2. 5 Thomson K, Tey D, Mark M. Paediatric Handbook (8th edn). Oxford: Wiley-Blackwell, 2009: 345–6. 6 Gastro-Oesophageal Reflux Disease in Adults: Guidelines (5th edn). Sydney: Gastroenterological Society of Australia, 2011. 7 Moulds R (Chair). Therapeutic Guidelines: Gastroenterology (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2011: 61–119. 8 GORD and Non-Ulcer Dyspepsia. NPS News, 2001; PPR review No. 11. 9 Fock KM et al. Asia-Pacific consensus on the management of gastroesophageal reflux disease: update. J Gastroenterol Hepatol, 2008; 23: 8–22. 10 Katelaris P. Dyspepsia: update. Australian Doctor, 2005; 7 October; 2005: 23–5. 11 Madge S, Yeomans N. Stomach and duodenal ulcers. Current Therapeutics, 2001; September: 69–72. 12 Korman M, Sievert W. Peptic ulcers. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 400–2. 13 Ford A, Delaney B et al. Eradication therapy for peptic ulcer disease in Helicobacter positive patients. Cochrane Database System Review, 2004 (4): CD003840. 14 Chan FK, To KF, Wu JC. Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long term treatment with NSAIDs: a randomised trial. Lancet, 2002; 359 (9300): 9–13.

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We swallow approximately 1200 times daily, largely subconsciously. While we take the fundamental function for granted, disordered swallowing can be a devastating condition, with substantial morbidity for those affected. Ian Cook  Dysphagia is difficulty in swallowing. It is a common problem affecting up to 22% of patients in the general practice setting.1 It is usually associated with a sensation of hold-up of the swallowed bolus and is sometimes accompanied by pain. Its origin is considered as either oropharyngeal or oesophageal. Oropharyngeal dysphagia is usually related to neuromuscular dysfunction and is commonly caused by stroke. Oesophageal dysphagia is usually due to motor disorders, such as achalasia or diffuse oesophageal spasm, and to peptic oesophageal strictures often secondary to reflux. In this type of dysphagia there is a sensation of a hold-up, which may be experienced in either the cervical or retrosternal region.1 Causes are usually classified as functional, mechanical and neurological (see TABLE 48.1).

Table 48.1

Causes of dysphagia

Functional

Examples: muscle tension, ‘express swallowing’

Neurological

Examples: stroke, myasthenia, MND

Mechanical • luminal • mural • extramural

Example: foreign body Example: stricture, tumour Example: extrinsic compression (i.e. goitre)

Dysphagia must not be confused with globus sensation, which is the sensation of the constant ‘lump in the throat’ although there is no actual difficulty swallowing food. If dysphagia is progressive or prolonged then urgent attention is necessary. There are only a few common causes of dysphagia and these are usually readily diagnosed on the history and two or three investigations. A careful history is very important, including a drug history and psychosocial factors.

Diagnostic guidelines • Any disease or abnormality affecting the tongue, pharynx or oesophagus can cause dysphagia. • Patients experience a sensation of obstruction at a definite level with swallowing food or water; hence, it is convenient to subdivide dysphagia into oropharyngeal and oesophageal. • Pain from the oropharynx is localised to the neck. • Pain from the oesophagus is usually felt over the T2–6 area of the chest. • Oropharyngeal causes: difficulty initiating swallowing; food sticks at the suprasternal notch level; regurgitation; aspiration. • Oesophageal causes: food sticks to mid to lower sternal level; pain on swallowing solid foods, especially meat, potatoes and bread, and then eventually liquids. • A pharyngeal pouch usually causes regurgitation of undigested food and gurgling may be audible over the side of the neck. • Neurological disorders typically result in difficulty swallowing or coughing or choking due to food spillover, especially with liquids. • Dysphagia for solids only indicates a structural lesion, such as a stricture or tumour. • Dysphagia for liquids and solids is typical of an oesophageal motility disorder, namely achalasia.2 • GORD tends to exclude achalasia.

Red flag pointers for dysphagia • • • • • • • • •

Age >50 years Recent or sudden onset Unexplained weight loss Painful swallowing Progressive dysphagia Dysphagia for solids Hiccoughs Hoarseness Neurological symptoms/signs

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• Gastroenterologists claim that the big three common causes referred to them are benign peptic stricture, cancer and achalasia.3 • Intermittent dysphagia for both liquids and solids is characteristic of a motility disorder such as oesophageal achalasia. • Malignant oesophageal obstruction is usually evident when there is a short history of rapidly progressive dysphagia and significant weight loss.4 A summary of the diagnostic strategy model is presented in TABLE 48.2.

Examination

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It is worthwhile focusing on the following features: • general examination including hands and skin ? scleroderma • assess nutritional status including BMI • mouth, pharynx, larynx (look for paralysis) ? dentition • neck, especially for lymph nodes and thyroid • neurological, especially cranial nerve function and muscle weakness disorders or evidence of stroke • special oesophageal obstruction test: — hand the patient a glass of water and place a stethoscope over the left upper quadrant of abdomen — measure time between swallowing and murmur produced by bolus passing the cardia (normal: 7–10 seconds) • assess aspiration risk e.g. through having a sip of water1

Investigations • Full blood examination: ? anaemia • Neurological cause: oesophageal motility study (manometry) • Mechanical: — extrinsic compression (e.g. barium swallow, CT scan, chest X-ray) — intrinsic (e.g. endoscopy ± barium swallow) — PET scan: good for identifying oesophageal cancer and gastro-oesophageal function The primary investigation in suspected pharyngeal dysphagia is a video barium swallow5 while endoscopy is generally the first investigation in cases of suspected oesophageal dysphagia. Barium swallow should precede endoscopy in the latter when there is a suspected oesophageal ‘ring’ and suspected

Table 48.2

Dysphagia: diagnostic strategy model (excluding oropharyngeal infections and strokes)

Q. Probability diagnosis A. Functional (e.g. ‘express’ swallowing, psychogenic) Tablet-induced irritation Pharyngotonsillitis Reflux oesophagitis Q. Serious disorders not to be missed A. Neoplasia: • cancer of the pharynx, oesophagus, stomach • extrinsic tumour AIDS (opportunistic oesophageal infection) Stricture, usually benign peptic stricture Scleroderma Neurological causes: • pseudobulbar palsy • multiple sclerosis/myasthenia gravis • motor neurone disease (amyotrophic sclerosis) • Parkinson disease Q. Pitfalls (often missed) A. Foreign body Drugs (e.g. phenothiazines, bisphosphanates) Subacute thyroiditis Extrinsic lesions (e.g. lymph nodes, goitre) Upper oesophageal web (e.g. Plummer–Vinson syndrome) Eosinophilic oesophagitis Oesophageal candidiasis Radiotherapy Achalasia Upper oesophageal spasm (mimics angina) Rarities (some): • Sjögren syndrome • aortic aneurysm • aberrant right subclavian artery • lead poisoning • cervical osteoarthritis (large osteophytes) • other neurological causes • other mechanical causes Q. Seven masquerades checklist A. Depression Drugs Thyroid disorder Q. Is this patient trying to tell me something? A. Yes. Could be functional ? globus sensation.

oesophageal dysmotility. If endoscopy and radiology are negative, consider oesophageal motility studies to look specifically for achalasia or other less common motility disorders.

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Dysphagia SPECIFIC CONDITIONS

Benign peptic stricture • Fibrous stricture of lower third oesophagus (can be higher) • Follows years of reflux oesophagitis • Usually older patients • Dysphagia with solid food • Diagnosis confirmed by endoscopy and barium swallow Treatment • Dilate the stricture • Treat reflux vigorously

Oesophageal cancer • Dysphagia at beginning of meal • Dysphagia for solid food steadily progressive over weeks • Can remain silent and tends to be invasive when diagnosed • Hiccoughs may be an early sign • Hoarseness and cough (upper third) • Discomfort or pain—throat, retrosternal, interscapular • Weight loss can be striking • Associations: GORD, tobacco, Barrett oesophagus • Diagnosis confirmed by barium swallow and endoscopy • Both SCC (commonest) and adenocarcinoma • Adenocarcinoma associated with Barrett mucosa • Treatment is usually palliative surgery

DxT fatigue + progressive dysphagia +  weight loss  oesophageal cancer

Achalasia • A disorder of oesophageal motility • Widely dilated oesophagus • Empties poorly through a smoothly tapered lower end • Gradual onset of dysphagia for both liquids and solids • Fluctuating symptoms • Diagnosis confirmed by barium swallow or manometry • Manometry is the only way to diagnose with certainty1

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Treatment • Conservative in the elderly (e.g. nifedipine/or endoscopic botulinum toxin injection into the sphincter)6 • Pneumatic dilatation of lower oesophageal sphincter or surgical myotomy Note: Prokinetic drugs have no place in treatment.

Drug-induced oesophageal ulceration3 • Tetracycline, especially doxycycline, can cause painful ulceration in all age groups. • Delayed passage of some drugs (due to preexisting disorders) can cause local ulceration, even perforation (especially in elderly) (e.g. iron tablets, slow-release potassium, aspirin, NSAIDs, bisphosphonates, zidovudine, antibiotics). • The elderly are prone to the problem if they ingest drugs upon retiring to bed with insufficient liquid washdown.

Globus sensation (cricopharyngeal spasm) Also referred to as ‘globus hystericus’ or ‘lump in the throat’, it is the subjective sensation of a lump in the throat. It appears to be associated with psychological stress (e.g. unresolved hurt, grief, non-achievement). Suppression of sadness is most often implicated.6 No specific aetiology or physiological mechanism has been established. The symptom can be associated with GORD, from frequent swallowing or emotionally based dry throat. Clinical features • Sensation of being ‘choked up’ or ‘something stuck’ or lump—a very real sensation • Not affected by swallowing • Eating and drinking may provide relief • Normal investigations Approach to patient • Careful history and examination • Exclude organic cause (refer TABLE 48.2) • May require investigations if doubtful diagnosis Management • Usually settles with education, reassuring support and time (up to several months) • Avoid swallowing very hot drinks • No drug of proven value • Treat any underlying psychological disorder

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Odynophagia Pain on swallowing is basically caused by irritation of an inflamed or ulcerated (in particular) mucosa by the swallowed food bolus. Important causes include: • GORD (the commonest cause) with associated oesophagitis • oesophageal spasm • oesophageal candidiasis, especially in the immunosuppressed • herpes simplex oesophagitis, also in the immunosuppressed • cytomegalovirus oesophagitis, in the immunosuppressed • pill-induced oesophagitis/ulceration • oesophageal cancer • achalasia

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Eosinophilic oesophagitis7,8 Eosinophilic oesophagitis is increasingly being recognised as a cause of dysphagia, gastro-oesophageal reflux and acute food bolus obstruction in both children (particularly) and adults. It may present as infant colic.8 It should be considered in those who regularly experience food getting stuck in their throat. It is associated with allergic disorders such as hay fever, cow’s milk allergy and asthma. The IgE is elevated. Refer to gastroscopy, which may show eosinophilic infiltrates in the oesophagus on mucosal biopsies. However, symptoms usually resolve within 72 hours of eliminating the offending food. A six-food elimination diet (cow’s milk protein, wheat, soy, eggs, seafood and peanuts) has been shown to reduce symptoms in up to 90%.1 Treatment of the acute attack includes IM buscopan and a swallowed topical corticosteroid aerosol e.g. fluticasone twice daily for 8 weeks.9

Practice tips •

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Although dysphagia is a common psychogenic symptom it must always be taken seriously and investigated. Mechanical dysphagia represents cancer until proved otherwise.

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•

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Progressive dysphagia and weight loss in an elderly patient is oesophageal cancer until proved otherwise. Oesophageal cancer usually causes pain, wasting and regurgitation. Globus sensation or hystericus, an anxiety disorder, should not be confused with dysphagia. It is the subjective sensation of a lump or mass in the throat. Usually seen in young women. Cancer-induced achalasia occurs with tumours at the gastro-oesophageal junction usually due to adenocarcinoma of the stomach. Severe oesophageal reflux predisposes to adenocarcinoma. Oesophageal strictures can be benign, usually secondary to chronic reflux oesophagitis, or due to malignancy. Be careful of a change of symptoms in the presence of long-standing reflux. Consider stricture or cancer. A prominent hard lymph node in the left supraclavicular fossa (Troisier sign) is suggestive of cancer of the stomach. Dysphagia can be caused by a tight fundoplication and can be diagnosed by manometry or barium swallow.1

References 1 Kuo P, Holloway R. Dysphagia: how to treat. Australian Doctor, 8 February 2013: 21–8. 2 Trate DM, Parkman HP, Fisher RS. Dysphagia: evaluation, diagnosis and treatment. Primary Care, 1996; 23: 417–32. 3 Breen K. A practical approach to patients with dysphagia or pain on swallowing. Modern Medicine Australia, 1992; 3: 50–6. 4 Abeygunasekera S. Difficult and painful swallowing: a guide for GPs. Medicine Today, 2003; 4 (10): 33–40. 5 Cook I. Swallowing disorders. Current Therapeutics, 1996; 37: 81–5. 6 Beers M, Berkow R (eds). The Merck Manual (18th edn). Merck Research Laboratories, 2006: 69–70. 7 Kakakios A, Heine R. Eosinophilic oesophagitis. Med J Aust, 2006; 185 (7): 401. 8 Thomson K, Tey D, Marks M. Paediatric Handbook (8th edn). Oxford: Wiley-Blackwell, 2009: 232. 9 Moulds R. Therapeutic Guidelines: Gastrointestinal (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2011: 42.

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Dyspnoea

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When man grows old . . . there is much gas within his thorax, resulting in panting and troubled breathing. Huang Ti (– BC), The Yellow Emperor’s Classic of Internal Medicine Dyspnoea is the subjective sensation of breathlessness that is excessive for any given level of physical activity. It is a cardinal symptom affecting the cardiopulmonary system and can be very difficult to evaluate. Appropriate breathlessness following activities such as running to catch a bus or climbing several flights of stairs is not abnormal but may be excessive due to obesity or lack of fitness.

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Determination of the underlying cause of dyspnoea in a given patient is absolutely essential for effective management. The main causes of dyspnoea are lung disease, heart disease, obesity and functional hyperventilation.1 The most common cause of dyspnoea encountered in family practice is airflow obstruction, which is the basic abnormality seen in chronic asthma and chronic obstructive pulmonary disease (COPD).2 Wheezing, which is a continuous musical or whistling noise, is an indication of airflow obstruction. Some patients with asthma do not wheeze and some patients who wheeze do not have asthma. Other important pulmonary causes include restrictive disease, such as fibrosis, collapse and pleural effusion. Dyspnoea is not inevitable in lung cancer but occurs in about 60% of cases.3 Normal respiratory rate is 12–16 breaths/minute.

Terminology It is important to emphasise that dyspnoea or breathlessness is a subjective sensation of the desire for increased respiratory effort and must be considered in relation to the patient’s lifestyle and individual tolerance of discomfort. It also depends on the age, physical fitness and physical expectations of the person. Patients may complain of tightness in the chest and this must be differentiated from angina.

The New York Heart Association functional and therapeutic classification applied to dyspnoea is: Grade 1 Grade 2 Grade 3 Grade 4

No breathlessness Breathlessness on severe exertion Breathlessness on mild exertion Breathlessness at rest

Glossary of terms Hyperpnoea An increased level of ventilation (e.g. during exertion). Hyperventilation Overbreathing. Orthopnoea Breathlessness lying down flat. Paroxysmal nocturnal dyspnoea Inappropriate breathlessness causing waking from sleep. Tachypnoea An increased rate of breathing.

Difference between heart and lung causes The distinguishing features between dyspnoea due to heart disease and to lung disease are presented in TABLE 49.1. The history is a good indication and a useful guideline is that dyspnoea at rest is typical of lung disease, especially asthma, while it tends to be present on effort with heart disease as well as with COPD.

Wheezing Wheezing is any continuous musical expiratory noise heard with the stethoscope or otherwise. Wheeze includes stridor, which is an inspiratory wheeze.

Common causes of wheezing Localised: • partial bronchial obstruction: — impacted foreign body — impacted mucus plugs — extrinsic compression

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• Problem solving in general practice

Comparison of distinguishing features between dyspnoea due to heart disease and lung disease

Comparison of asthma and COPD Asthma

COPD

Symptoms 30  g/L; lactic dehydrogenase >200 IU/L

Causes • Infection—bacterial pneumonia, pleurisy, empyema, TB, viral • Malignancy—bronchial carcinoma, mesothelioma, metastatic • Pulmonary infarction • Connective tissue diseases (e.g. SLE, RA) • Acute pancreatitis • Lymphoma • Sarcoidosis • HIV with parasitic pneumonia Management Aspiration if symptomatic: may require repeats and pleurodesis. Treat the underlying cause.

Dyspnoea in children 49

There are numerous causes of dyspnoea in children but the common causes are asthma, bronchiolitis and pulmonary infections. The important infections that can be fatal—croup, epiglottitis and myocarditis— must be kept in mind and intensively managed. Bronchiolitis is an important cause of respiratory distress in infants under 6–12 months. It should not be confused with asthma (refer to CHAPTER 96). Sudden breathlessness or stridor may be due to an inhaled foreign body. Signs of lobar collapse may be present but physical examination may be of little help and a chest X-ray is essential. Cardiovascular disorders, including congenital heart disease, can cause dyspnoea. Extra respiratory causes include anaemia, acidosis, aspiration, poisoning and hyperventilation.

Dyspnoea in the elderly Dyspnoea in the elderly is common and is caused usually by heart failure and COPD. The other associations with ageing, such as lung cancer, pulmonary fibrosis and drugs, are relevant. The classic problem of the aged is acute heart failure that develops typically in the early morning hours. The acute brain syndrome is a common presentation of all these disorders.

Respiratory disease in the elderly The respiratory system, like most other bodily systems, matures until about the age of 25 years and subsequently slowly loses efficiency due to a variety

of factors such as disease, smoking, pollution and ageing. There is a decline in lung function and gas exchange and decreased ventilatory responses to hypoxia and hypercapnia.

Heart failure Heart failure occurs when the heart is unable to maintain sufficient cardiac output to meet the demands of the body. Dyspnoea is a common early symptom as pulmonary congestion causes hypoxia (increased ventilation) and decreased compliance (increased work). The incidence of congestive cardiac failure (CCF) has been increasing steeply, partly due to the ageing population. Symptoms • Increasing dyspnoea progressing to (in order): — fatigue, especially exertional fatigue — paroxysmal nocturnal dyspnoea — weight change: gain or loss It is convenient to divide heart failure into left and right heart failure but they rarely occur in isolation and often occur simultaneously. Right failure is invariably secondary to left failure. Furthermore, some cardiologists stress the importance of differentiating between systolic and diastolic dysfunction. Both present in the same way clinically and hence referral for cardiac studies to obtain measurement of the left ventricular function is required. This permits an accurate diagnosis and guide to treatment and an accurate prognosis. Refer to Chronic heart failure (CHAPTER 88).

Chronic obstructive pulmonary disease Chronic bronchitis and emphysema should be considered together as both these conditions usually coexist to some degree in each patient. An alternative, and preferable, term—chronic obstructive pulmonary disease (COPD)—is used to cover chronic bronchitis and emphysema with chronic airflow limitation.6 For more detail on the management of COPD refer to CHAPTER 83.

INTERSTITIAL LUNG DISEASES Interstitial lung diseases comprise a group of disorders that have the common features of inflammation (pneumonitis) and fibrosis of the interalveolar septum, representing a non-specific reaction of the lung to injury of various causes.8

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Dyspnoea In many there is a hypersensitivity reaction to various unusual antigens. The fibrosis may be localised as following unresolved pneumonia, bilateral as with tuberculosis or widespread. Consider possibility of fibrosis of lungs in chronic dyspnoea and a dry cough with normal resonance. Causes of widespread interstitial pulmonary fibrosis include: • sarcoidosis • idiopathic pulmonary fibrosis • extrinsic allergic alveolitis (hypersensitivity pneumonitis) • drug-induced • lymphangitis carcinomatosis • various occupational lung disorders • rheumatoid arthritis • acute pulmonary oedema • immunological (e.g. connective tissue disorders, vasculitis) Common clinical features: • dyspnoea and dry cough (insidious onset) • fine inspiratory crackles at lung base with faint breath sounds • cyanosis and finger clubbing may be present • PFTs: — restrictive ventilatory deficit — decrease in gas transfer factor • characteristic X-ray changes High-resolution CT scanning has been a major advance in diagnosis. May show ‘honeycomb lung’.

Sarcoidosis Sarcoidosis is a multisystemic disorder of unknown aetiology which is characterised by non-caseating granulomatous inflammation that involves the lung in about 90% of affected patients. A characteristic feature is bilateral hilar lymphadenopathy, which is often symptomless and detected on routine chest X-ray (CXR). Radiological lung involvement can

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be associated with or occur independently of hilar lymphadenopathy. Clinical features8,9 • May be asymptomatic (one-third) • Onset usually third or fourth decade (but any age) • Bilateral hilar lymphadenopathy (on CXR) • Cough • Fever, malaise, arthralgia • Erythema nodosum • Ocular lesions (e.g. anterior uveitis) • Other multiple organ lesions (uncommon) • Overall mortality 2–5% Erythema nodosum with an acute swinging fever, malaise and arthralgia in a young adult female is diagnostic of sarcoidosis. Diagnosis Histological evidence from biopsy specimen, usually transbronchial biopsy (essential if an alternative diagnosis, e.g. lymphoma, cannot be excluded) or skin biopsy in cases of erythema nodosum. A better modern diagnostic method is biopsy via videoassisted thoracoscopy. Supporting evidence: • elevated serum ACE (non-specific) • PFTs: restrictive pattern; impaired gas transfer in advanced cases • ±ve Kveim test (not recommended these days) • serum calcium Treatment Sarcoidosis may resolve spontaneously (hilar lymphadenopathy without lung involvement does not require treatment). Indications for treatment with corticosteroids: • no spontaneous improvement or worsening after 3–6 months • symptomatic pulmonary lesions • eye, CNS and other systems involvement

Glossary of terms Chronic airflow limitation A physiological process measured as impairment of forced expiratory flow which is the major cause of dyspnoea in these patients. Chronic bronchitis A clinical condition characterised by a productive cough on most days for at least 3 months of the year for at least 2 consecutive years in the absence of any other respiratory disease that could be responsible for such excessive sputum production (such as tuberculosis or bronchiectasis).

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COPD A chronic, slowly progressive disorder characterised by the presence of airway obstruction which may (or may not) be partially reversible by bronchodilator therapy.8 Emphysema This is defined in pathological rather than clinical terms, as permanent dilatation and destruction of lung tissue distal to the terminal bronchioles.

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• hypercalcaemia, hypercalciuria • erythema nodosum with arthralgia • persistent cough

Corticosteroid treatment9 • Prednisolone 20–40 mg (o) daily for 6–8 weeks, then reduce to lowest dose that maintains improvement.9 If there is no response, taper the dose to zero. If there is a response, taper the dose to 10–15 mg (o) daily as a maintenance dose for 6–12 months.9 • Prednisolone 20–30 mg for 2 weeks for erythema nodosum of sarcoidosis.

Idiopathic pulmonary fibrosis

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Idiopathic pulmonary fibrosis, also known as idiopathic fibrosing interstitial pneumonia and cryptogenic fibrosing alveolitis, is the most common diagnosis among patients presenting with interstitial lung disease. Patients usually present in the fifth to seventh decade with the clinical features as outlined under interstitial lung diseases such as slowly progressive dyspnoea over months to years. Chest X-ray abnormalities are variable but include bilateral diffuse nodular or reticulonodular shadowing favouring the lung bases. High-resolution CT scans are effective for diagnosis. Open lung biopsy may be needed for diagnosis and staging. The usual prognosis is poor with death occurring about 2–5 years after diagnosis. The usual treatment is high doses of oral corticosteroids with azathioprine and no smoking.9

Table 49.7

Various causes of extrinsic allergic alveolitis

Occupation/disease

Source of antigen

Farmer’s lung

Mouldy hay, grain and straw

Bagassosis

Mouldy sugar cane fibre (bagasse)

Bird fancier’s lung

Avian proteins: dropping dust (e.g. from pigeons); ‘bloom’ on budgerigar feathers

Mushroom workers

Mushroom compost

Cheese washer’s lung

Moulds or mites on cheese

Wheat weevil lung

Infested wheat flour (insect)

Ventilator pneumonitis

Humidified hot air system Air-conditioning system

Wood pulp worker’s disorder

Contaminated wood dust

Detergent worker’s disorder

Proteolytic enzymes

Suberosis

Mouldy cork bark

Rat handler’s lung

Rat urine and serum

Malt worker’s lung

Mouldy barley

Coffee worker’s lung

Coffee dust

Sisal worker’s lung

Sisal dust

Sericultural workers

Silkworms

Furrier’s lung

Fur dust

Sausage workers

Dust

Prawn workers

Prawn fumes

Extrinsic allergic alveolitis Extrinsic allergic alveolitis (hypersensitivity pneumonitis) is characterised by a widespread diffuse inflammatory reaction in both the small airways of the lung and the alveoli, due to the inhalation of allergens, which are usually spores of microorganisms such as thermophilic actinomycetes in ‘farmer’s lung’ or (more commonly) avian protein from droppings or feathers in ‘bird fancier’s lung’. Occupational causes of extrinsic alveolitis have been described by Molina10 (see TABLE 49.7). Illness may present as acute or subacute episodes of pyrexia, chills and malaise with dyspnoea and a peripheral neutrophil several hours after exposure.10 Management is based on prevention, namely avoiding exposure to allergens or wearing protective, finemesh masks. Prednisolone can be used (with caution) to control acute symptoms. It should be pointed out that this allergic disorder is different from the infection psittacosis.

Drug-induced interstitial lung disease9 Drugs are an important cause of this disorder and have three main effects: 1 Alveolitis with or without pulmonary fibrosis. This is mainly due to cytotoxic drugs, nitrofurantoin and amiodarone. The drug should be removed and consideration given to prescribing prednisolone 50 mg (o) daily for several weeks, depending on response. 2 Eosinophilic reactions. This is presumably an immunological reaction, which may present as wheezing, dyspnoea, a maculopapular rash and pyrexia. The many implicated drugs include various antibiotics, NSAIDs, cytotoxic agents, major tranquillisers and antidepressants, and anti-epileptics. Treatment is drug removal and a

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Dyspnoea short course of prednisolone 20–40 mg (o) daily for 2 weeks. 3 Non-cardiogenic acute pulmonary oedema. This is rare and has been reported to occur with opioids, aspirin, hydrochlorothiazide, β2-adrenoceptor agonists (given IV to suppress premature labour), cytotoxics, interleukin-2, heroin.

OCCUPATIONAL PULMONARY DISEASE Various types of acute and chronic pulmonary diseases are related to exposure to noxious substances such as dusts, gases and vapours in the workplace. Common chemical causes include formaldehyde used in processed woods, e.g. chipboard and medium-density fibre. GPs have a crucial role in the identification of the possible work-relatedness of lung disease. Disorders due to chemical agents include: • obstructive airways disorders, such as occupational asthma, acute bronchitis, (chronic) industrial bronchitis, byssinosis (asthma-like condition due to cotton dust) • extrinsic allergic alveolitis • pulmonary fibrosis (pneumoconiosis) due to mineral dust • lung cancer due to industrial agents such as asbestos, various hydrocarbons • pleural disorders, usually associated with asbestosis

Table 49.8

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Selected pneumoconioses

Fibrotic lung disease

Agent

Typical occupations

Coal dust

Coal mining

Metallic iron or iron oxide

Mining

Coal dust Coal worker’s pneumoconiosis Metal dust Siderosis

Welding Foundry work Inorganic dusts Silicosis

Silica (silicon dioxide)

Quarrying Rock mining Stone cutting Sandblasting

Silicate dusts Asbestosis

Asbestos

Mining Shipbuilding Insulation Power stations Wharf labouring

Pneumoconiosis The term ‘pneumoconiosis’ refers to the accumulation of dust in the lungs and the reaction of tissue to its presence, namely chronic fibrosis. The main cause worldwide is inhalation of coal dust, a specific severe variety being progressive massive fibrosis (complicated coal worker’s pneumoconiosis) in which the patient suffers severe dyspnoea of effort and cough often productive of black sputum. TABLE  49.8 summarises the important causes. Of particular concern are diseases caused by inhalation of fibres of asbestos, which is a mixture of silicates of iron, magnesium, cadmium, nickel and aluminium. The diseases include asbestosis, diffuse pleural thickening, pleural plaques, mesothelioma and increased bronchial carcinoma in smokers. Pulmonary asbestosis has classic X-ray changes but highresolution CT scans may be required to confirm the presence of calcified pleural plaques. It usually takes 10–20 years from exposure for asbestosis to develop and 20–40 years for mesothelioma to develop,8 while bronchial carcinoma is caused by the synergistic effects of asbestosis and cigarette smoking.

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Acute respiratory distress syndrome (ARDS) ARDS, also known as acute lung injury and formerly called ‘adult respiratory distress syndrome’, refers to acute hypoxaemic respiratory failure following a pulmonary or systemic insult with no apparent cardiogenic cause of pulmonary oedema. This occurs about 12–48 hours after the event.11 The most common cause is sepsis which accounts for about onethird of ARDS patients. The mortality rate is 30–40% increasing if accompanied by sepsis. Management is based on early diagnosis, early referral, identification and treatment of the underlying condition and then optimal intensive care.12

Clinical features • • • •

Sudden onset of respiratory distress Stiff lungs—reduced lung compliance Bilateral pulmonary infiltrates on X-ray No apparent evidence of heart failure

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• Absence of elevated left atrial pressure • Specific gas exchange abnormalities • Signs: tachypnoea, laboured breathing, rib retraction, central cyanosis, fine crackles on auscultation The differential diagnoses are pneumonia and acute heart failure. Common risk factors/associations for ARDS include (indirectly—systemic)—sepsis, shock, trauma, burns, drug overdose (e.g. heroin), multiple transfusions, obstetric complications (e.g. eclampsia, amniotic fluid embolism), and many direct causes such as pulmonary aspiration, toxic gas inhalation, blast injury and pneumonia (e.g. SARS).

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Severe acute respiratory syndrome (SARS)

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SARS is a respiratory illness of varying severity (mild to severe) with a known mortality rate of about 10% of clinically established cases. All cases to date exhibit a high fever of >38°C. It is considered to be an atypical pneumonia caused by a quite unique coronavirus. Cases have acquired SARS following exposure to endemic areas of South-East Asia. Severe cases (up to 10% mortality) can progress to ARDS. Suspected case = fever >38°C  + cough, breathing difficulty or dyspnoea + contact with SARS person/ area. Plain X-rays may show pulmonary infiltrates while high-resolution CT scans may show typical patterns.

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Remember to order a chest X-ray and pulmonary function tests in all doubtful cases of dyspnoea. All heart diseases have dyspnoea as a common early symptom. Increasing dyspnoea on exertion may be the earliest symptom of incipient heart failure. Several drugs can produce a wide variety of respiratory disorders, particularly pulmonary fibrosis and pulmonary eosinophilia. Amiodarone and cytotoxic drugs, especially bleomycin, are the main causes. Dyspnoea in the presence of lung cancer may be caused by many factors, such as pleural effusion, lobar collapse, upper airway obstruction and lymphangitis carcinomatosis. The abrupt onset of severe dyspnoea suggests pneumothorax or pulmonary embolism. If a patient develops a relapse of dyspnoea while on digoxin therapy, consider the real possibility of digoxin toxicity and/or electrolyte abnormalities leading to left heart failure. Recurrent attacks of sudden dyspnoea, especially waking the patient at night, are suggestive of asthma or left heart failure. Causes of hyperventilation include drugs, asthma, thyrotoxicosis and panic attacks/anxiety.

Key features • Symptoms of atypical pneumonia: fever, cough, dyspnoea • Associated may be myalgia, diarrhoea, headache, sore throat, rhinorrhoea, confusion, malaise, rash • Virulent virus—droplet spread • Incubation period 2–7 days • Crackles and wheezes may be present on auscultation but no hallmark sign • Non-specific X-ray signs • Prime CT scans may show typical changes • Diagnosis confirmed by PCR studies or isolation of the virus on culture • Complications appear to be confined to the lung

Bronchial carcinoma

Optimal treatment for SARS by drugs is still being evaluated. Preventive measures, including wearing of face masks (NIOSH standard mask best) and appropriate infection control procedures, are important. Wear a mask, gloves, goggles and gown for clinical assessment of suspected cases and switch off air-conditioning (refer to CHAPTER 28).

• Patients with acute onset of severe dyspnoea • All patients with heart failure resistant to initial therapy or where the diagnosis is in doubt • Patients with pulmonary disease of uncertain aetiology, especially those requiring respiratory function tests • Those in whom lung cancer is suspected

Dyspnoea is associated with about 60% of cases of lung cancer3 (see CHAPTER 42). It is not a common early symptom unless bronchial occlusion causes extrinsic collapse. In advanced cancer, whether primary or secondary, direct spread or metastases may cause dyspnoea. Other factors include pleural effusion, lobar collapse, metastatic infiltration, upper airway obstruction due to superior vena cava (SVC) obstruction and lymphangitis carcinomatosis. A special problem arises with coexisting chronic bronchitis and emphysema.

When to refer

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Dyspnoea

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Asthma • Asthma in children • Chronic obstructive airways disease • Dangerous asthma • Heart failure

References 1 Sandler G. Common Medical Problems. London: ADIS Press, 1984: 31–56. 2 Cormack J, Marinker M, Morrell D. Practice: A Handbook of Primary Health Care. London: Kluwer-Harrap Handbooks, 1980; 3 (29): 3. 3 Walsh TD. Symptom Control. Boston: Blackwell Scientific Publications, 1989: 157–64. 4 Beck ER, Francis JL, Souhami RL. Tutorials in Differential Diagnosis (3rd edn). Edinburgh: Churchill Livingstone, 1993: 37.

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5 Kelly DT. Cardiac failure. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 97–9. 6 Kumar PJ, Clark ML. Clinical Medicine (7th edn). London: Elsevier, 2009: 819–28. 7 Beers MH, Porter RS. The Merck Manual (18th edn). Whitehouse Station: Merck Research Laboratories, 2006: 307. 8 Papadakis MA, McPhee SP. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013: 1602. 9 Moulds R (Chair). Therapeutic Guidelines: Respiratory (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 175–88. 10 Molina C. Occupational extrinsic allergic alveolitis. In: Pepys J (ed.), Clinics in Immunology and Allergy. London: WB Saunders, 1984: 173–90. 11 Papadakis MA, McPhee SP. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013; 322–3. 12 Ware LB et al. The acute respiratory distress syndrome. N Engl J Med, 2000; 342: 1334.

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The painful ear

The ears should be kept perfectly clean; but it must never be done in company. It should never be done with a pin, and still less with the fingers, but always with an ear picker. St Jean Baptiste de la Salle (–) Pain in the ear (otalgia) is a common symptom in general practice. It affects all ages, but is most prevalent in children, where otitis media is the commonest cause. Ear pain may be caused by disorders of the ear or may arise from other structures, and in many instances the precise diagnosis is difficult to make. Important causes of ear pain are summarised in TABLE 50.1.1 A patient with a painful ear often requests urgent attention, and calls in the middle of the night from anxious parents of a screaming child are commonplace. Infants may present with nothing except malaise, vomiting or screaming attacks.

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Of patients presenting with earache, 77% can be expected to have acute otitis media and 12% otitis externa.2 Approximately one of every 25 patients in general practice will present with an earache. Two-thirds of children will sustain at least one episode of otitis media by their second birthday; one in seven children will have had more than six episodes by this age.3 Otitis media is unlikely to be present if the tympanic membrane (TM) is mobile. Pneumatic otoscopy greatly assists diagnosis since the most valuable sign of otitis media is absent or diminished motility of the TM. Bullous myringitis, which causes haemorrhagic blistering of the eardrum or external ear canal, is an uncommon cause of severe pain. It is caused by a virus, probably influenza.4 The antibiotic of first choice for acute otitis media (children and adults) is amoxycillin. Otitis externa can be distinguished from otitis media by pain on movement of the pinna.

A diagnostic approach The five self-posed questions can be answered using the diagnostic strategy model (see TABLE 50.2).

Table 50.1

Causes of ear pain

1 Ear External ear: • Perichondritis • Otitis externa: — Candida albicans — Aspergillus nigra — Pseudomonas spp. — Staphylococcus aureus • Furunculosis • Trauma • Neoplasia • Herpes zoster (Ramsay–Hunt syndrome) • Viral myringitis • Wax-impacted Middle ear: • Eustachian insufficiency • Eustachian tube dysfunction • Barotrauma • Acute otitis media • Chronic otitis media and cholesteatoma • Acute mastoiditis 2 Periotic cause Dental disorders Upper cervical spinal dysfunction TMJ arthralgia Parotitis Temporal arteritis Lymph node inflammation Other referred causes Pharyngeal disorders Tonsillitis Glossopharyngeal neuralgia

Probability diagnosis The commonest cause of ear pain is acute otitis media. Chronic otitis media and otitis externa are also common. In the tropics, ‘tropical ear’ due to acute bacterial otitis is a particular problem.

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The painful ear

Table 50.2

The painful ear: diagnostic strategy model

Q. Probability diagnosis A. Otitis media (viral or bacterial) Otitis externa (fungal, viral or bacterial) TMJ arthralgia Eustachian tube dysfunction Q. Serious disorders not to be missed A. Neoplasia of external ear Cancer of other sites (e.g. tongue, nasopharynx) Herpes zoster (Ramsay–Hunt syndrome) Acute mastoiditis Cholesteatoma Necrotising otitis externa Q. Pitfalls (often missed) A. Foreign bodies in ear Hard ear wax Barotrauma Dental causes (e.g. abscess) Referred pain: neck, throat Unerupted wisdom tooth and other dental causes TMJ arthralgia Facial neuralgias, esp. glossopharyngeal Chondromalacia nodularis helicies Furuncles of canal or pinna Post tonsillectomy: • from the wound • from TMJ due to mouth gag

attic perforation

superior margin of tympanic membrane

lateral process of malleus

FIGURE 50.1 Infected ear: unsafe perforation

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Q. Is the patient trying to tell me something? A. Unlikely, but always possible with pain. More likely in children. Consider factitious pain. FIGURE 50.2 Infected ear: safe perforation

Serious disorders not to be missed As always, it is important not to overlook malignant diseases, especially the obscure ones, such as cancer of the tongue, palate or tonsils, which cause referred pain. Locally destructive cholesteatoma associated with chronic otitis media must be searched for. It signifies the ‘unsafe’ ear (see FIG.  50.1) that must be distinguished from the so-called ‘safe’ ear (see FIG. 50.2).

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Herpes zoster should be considered, especially if it does not erupt on the pinna and is confined to the ear canal (usually the posterior wall), and especially in the older person.

Q. Seven masquerades checklist A. Depression Spinal dysfunction (cervical)

Temporomandibular joint (TMJ) arthralgia, which may be acute or chronic, is also common and must be considered, especially when otitis media and otitis externa are excluded.

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Pitfalls The medical aphorism ‘more things are missed by not looking than by not knowing’ applies particularly to the painful ear—good illumination and focusing the auroscope are mandatory. Particular attention should be paid to the external canal—look for hard wax, otitis externa, furuncles and foreign objects such as insects. It may not be possible to visualise the TMs so it is important to clean the canal to permit this (if possible, on the first visit). Otitis media may coexist with otitis externa. Barotrauma should be considered, especially if pain follows air travel or diving.

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General pitfalls • Failing to visualise the TM before diagnosis and treatment • Not checking out possible referral sites such as the oropharynx and teeth • Overlooking common musculoskeletal causes such as TMJ arthralgia and cervical spondylosis • Failing to recognise the unsafe ear

Red flag pointers for painful ear • • • • • •

Offensive discharge >9 days Downward displacement of pinna Swelling behind ear Neurological symptoms (e.g. headaches, drowsiness) Older person: unexplained, intractable ear pain Persistent fever

Seven masquerades checklist

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Of the conditions in the checklist, depression and dysfunction of the upper cervical spine have to be considered. Depressive illnesses should be considered in any patient complaining of chronic pain. Disorders of the upper cervical spine are a commonly overlooked cause of periotic pain. Pain from the C2 and C3 levels is referred to the posterior region of the ear.

Psychogenic considerations Such factors are unlikely, unless the pain causes discomfort in the periotic region, which is likely to be magnified by a depressive state.

The clinical approach History In assessing the painful ear the relevant features are: • • • •

site of pain and radiation details of the onset of pain nature of the pain aggravating or relieving factors, especially swimming • associated features such as deafness, discharge, vertigo, tinnitus and irritation of the external ear, sore throat Agonising pain may be caused by perichondritis or furunculosis of the external ear and by the rare problem of herpes zoster (Ramsay–Hunt syndrome).5 Movement of the pinna markedly increases the

pain of acute otitis externa and perichondritis, and movement of the jaw usually causes an exacerbation of TMJ arthralgia or severe otitis externa. Key questions (especially children) • Where is the pain? • Is it in the ear, behind or below it? • Is it in one ear or both ears? • Have you noticed any other symptoms such as sore throat, fever or vomiting? • Has anyone hit you over the ear? • Has there been a discharge from the ear? • Have you noticed any deafness? • Are you allergic to penicillin? • Have you been swimming in a spa, and where? • Have you been in an aeroplane?

Examination The patient’s general state and behaviour is observed during the history taking. Sudden, jabbing pain may indicate neuralgia, particularly glossopharyngeal neuralgia or a severe infection. The external ear is carefully inspected and the pinna manipulated to determine any tenderness. Palpate the face and neck and include the parotid glands, regional lymph nodes and the skin. Inspect the TMJs—tenderness from dysfunction typically lies immediately in front of the external auditory meatus. Palpate the TMJ over the lateral aspect at the joint disc. Ask the patient to open the mouth fully when tenderness is maximal. The TMJ can be palpated posteriorly by inserting the little finger into the external canal. Inspect both ear canals and TMs with the auroscope, using the largest earpiece that comfortably fits into the canal. Better visualisation of the TM can be achieved by pulling the pinna back in young children and up and back in older children—see FIGURE  50.3 for normal appearance. Impacted wax may not explain the otalgia. If herpes zoster involves the facial nerve, vesicles may be noted in and around the external auditory meatus (notably the posterior wall). If the diagnosis is still doubtful look for causes of referred pain; inspect the cervical spine, the nose and postnasal space and the mouth, including the teeth, pharynx and larynx. Pharyngeal and mandibular causes of periotic pain are summarised in FIGURES 50.4 and 50.5. Inspect sites supplied by the nerves V2, IX, X, XI, C1, C2 and C3 to exclude other causes of referred pain.

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wisdom teeth caries

apical abscess carcinoma

FIGURE 50.5 Mandibular causes of otalgia Source: Courtesy of Bruce Black

Swabs from discharge, especially to determine bacterial causes, such as Staphylococcus aureus or Pseudomonas spp. infection, may be necessary. However, swabs are of no value if the TM is intact. Radiology and CT/MRI scanning may be indicated for special conditions such as a suspected extraotic malignancy.

FIGURE 50.3 Normal right tympanic membrane

glossopharyngeal neuralgia

Ear pain in children trauma

carcinoma palate tonsil tongue

aphthous ulcers

tonsils tonsillitis quinsy tonsillectomy

Important causes of primary otalgia in children include otitis media, otitis externa, external canal furuncle or abscess, chronic eczema with fissuring of the auricle, impacted wax, foreign body, barotrauma, perichondritis, mastoiditis and bullous myringitis. Secondary otalgia includes pharyngeal lesions, dental problems, gingivostomatitis, mumps and postauricular lymphadenopathy. Peritonsillar abscess (quinsy) may cause ear pain.

Foreign bodies

Investigations

Foreign bodies (FBs) are frequently inserted into the ear canal (see FIG.  50.6). They can usually be syringed out or lifted with thin forceps. Various improvised methods can be used to remove FBs in cooperative children. These include a probe to roll out the FB or a rubber catheter used as a form of suction or otherwise a fine sucker.6

Investigations are seldom necessary. Hearing tests are essential, especially for children. Simple tests such as speech discrimination, hair rubbing and tuning fork tests can be used. Otherwise audiometry can be used. Audiometry combined with tympanometry and physical measurement of the volume of the ear canal can be performed in children, irrespective of age.

Probe method This requires good vision using a head mirror or head light and a thin probe. The probe is inserted under and just beyond the FB. Lever it in such a way that the tip of the probe ‘rolls’ the foreign body out of the obstructed passage.

FIGURE 50.4 Pharyngeal causes of otalgia Source: Courtesy of Bruce Black

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• Problem solving in general practice • The commonest organisms are Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis • Fever, irritability, otalgia and otorrhoea may be present • The main symptoms in older children are increasing earache and hearing loss • Pulling at the ears is a common sign in infants • Removal of wax is necessary in about 30% to visualise the TM

Visualisation of the tympanic membrane

FIGURE 50.6 Foreign body (bead) in ear canal of a 3-year-old child, showing reactive tissue in ear canal

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Rubber catheter suction method The only equipment required for this relatively simple and painless method is a straight rubber catheter (large type) and perhaps a suction pump. The end of the catheter is cut at right angles, a thin smear of petroleum jelly is applied to the rim and this end is applied to the FB. Suction is applied either orally or by a pump. Gentle pump suction is preferred but it is advisable to pinch closed the suction catheter until close to the FB as the hissing noise may frighten the child. Insects in the ear Live insects should be immobilised by first instilling Aquaear drops or olive oil, and then syringing the ear with warm water. Dead flies that have originally been attracted to pus are best removed by suction. Note: If simple methods such as syringing fail to dislodge the FB it is important to refer for examination and removal under microscopic vision. Syringing should not be performed if there is a possibility of the FB perforating the TM.

Use the largest ear speculum that will comfortably fit in the child’s ear. A good technique to enable the examination of the ears (also nose and throat) in a reluctant child is where the child is held against the parent’s chest while the parent’s arm embraces the child’s arm and trunk. Note the following features of the TM: translucency, colour, position and motility. Treatment Many children with viral URTIs have mild reddening or dullness of the eardrum and antibiotics are not warranted particularly in the absence of systemic features (fever and vomiting).7 Best practice at this stage is symptomatic relief with analgesics and either watchful waiting or antibiotics.8 In contrast, where the eardrum is red or yellow and bulging, with loss of anatomical landmarks, antibiotic therapy is indicated. The debate about the role of antibiotics in acute otitis media is controversial. An Australian study revealed that antibiotics provided only modest benefit: up to 20 children must be treated to prevent one child from experiencing pain by 2–7 days after presentation.8,9 A North American survey concluded: ‘treat children who are very ill (approximately 15%) with antibiotics immediately. Treat all others for pain and pain only and follow up according to age. Treat with antibiotics if more serious symptoms develop, or the fever, pain and other symptoms do not resolve within the time frame’.10

Otitis media in children Otitis media is very common in children and is the most common reason a child is brought in for medical attention. Persistent middle ear effusions may follow and affect the language and cognitive development of young children. Clinical features • Two peaks of incidence: 6–12 months of age and school entry • Seasonal incidence coincides with URTIs • Bacteria cause two-thirds of cases7

Possible clinical indications for antibiotics in children with painful otitis media8 • • • • • • •

3  months, arrange for a hearing assessment and consider referral to an ENT surgeon for possible tympanostomy tubes (grommets).13 Note: a proposed S. pneumoniae and H. influenzae conjugate vaccine may be an effective preventive measure for childhood otitis media.

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Antibiotic prevention of acute otitis media is indicated (arguably) if it occurs more often than every other month or for three or more episodes in 6 months or >4 in 12 months:14 chemoprophylaxis (for about 4 months) amoxycillin twice daily (first choice) or cefaclor twice daily Consider Pneumococcus vaccine in children over 18 months of age (if not already given) in combination with the antibiotic. Avoid smoke exposure (cigarettes and wood fires) and group child care. Consider review by ENT consultant.

Viral infections Most children with viral URTIs have mild reddening or dullness of the eardrum and antibiotics are not warranted. If painful bullous otitis media is present, either prick the bulla with a sterile needle for pain relief, or instil dehydrating eardrops such as anhydrous glycerol.

Ear pain in the elderly Causes of otalgia that mainly afflict the elderly include herpes zoster (Ramsay–Hunt syndrome), TMJ arthralgia, temporal arteritis and neoplasia. It is especially important to search for evidence of malignancy.

Acute otitis media Acute otitis media causes deep-seated ear pain, deafness and often systemic illness (see FIG. 50.8). The sequence of symptoms is a blocked ear feeling, pain

FIGURE 50.8 Acute otitis media causing true otalgia. The ear drum bulges laterally due to pus in the middle ear. Perforation and otorrhoea imminent.

and fever. Discharge may follow if the TM perforates, with relief of pain and fever. The commonest organisms are viruses (adenovirus and enterovirus), and the bacteria H. influenzae, S. pneumoniae, Moraxella (previously Neisseria catarrhalis) and β-haemolytic streptococci. The two cardinal features of diagnosis are inflammation and middle ear effusion. Appearance of the tympanic membrane (all ages) Translucency. If the middle ear structures are clearly visible through the drum, otitis media is unlikely. Colour. The normal TM is a shiny pale-grey to brown: a yellow colour is suggestive of an effusion. Diagnosis The main diagnostic feature is the redness of the TM. The inflammatory process usually begins in the upper posterior quadrant and spreads peripherally and down the handle of the malleus (see FIG.  50.9). The TM will be seen to be reddened and inflamed with engorgement of the vessels, particularly along the handle of the malleus. The loss of light reflex follows and anatomical features then become difficult to recognise as the TM becomes oedematous. Bulging of the drum is a late sign. Blisters are often seen on the TM and this is thought to be due to a viral infection in the epidermal layers of the drum.

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Treatment of acute otitis media (adults) • Analgesics to relieve pain • Adequate rest in a warm room • Nasal decongestants for nasal congestion • Antibiotics until resolution of all signs of infection • Treat associated conditions (e.g. adenoid hypertrophy) • Follow-up: review and test hearing audiometrically

Antibiotic treatment7 First choice: erythema of prominent blood vessels progressing down handle of malleus normal drum

amoxycillin 750 mg (o) bd for 5 days7 or 500 mg (o) tds for 5 days A longer course (up to 10 days) may be required depending on severity and response to 5-day course. Alternatives: doxycycline 100 mg (o) bd for 5–7 days (daily for milder infections) or cefaclor 250 mg (o) tds for 5–7 days or (if resistance to amoxycillin is suspected or proven) amoxycillin/potassium clavulanate 500/125 mg (o) tds for 5 days (the most effective antibiotic) Consider surgical intervention for failed therapy.

CHRONIC OTITIS MEDIA progressive erythema loss of light reflex

There are two types of chronic suppurative otitis media and they both present with deafness and discharge without pain. The discharge occurs through a perforation in the TM: one is safe (see FIG. 50.10a), the other unsafe (see FIG. 50.10b).

Chronic discharging otitis media (safe)7 If aural discharge persists for >6 weeks after course of antibiotics, treatment can be with topical steroid and antibiotic combination drops, following ear toilet. The toileting can be done at home by dry mopping with rolled tissue spear. If persistent, referral to exclude cholesteatoma or chronic osteitis is advisable.

Recognising the unsafe ear bulging pars flaccida red pars tensa anatomical structures unidentifiable

FIGURE 50.9 The appearances of the left tympanic membrane in the progressive development of acute otitis media

Examination of an infected ear should include inspection of the attic region, the small area of drum between the lateral process of the malleus, and the roof of the external auditory canal immediately above it. A perforation here renders the ear ‘unsafe’ (see FIG.  50.1); other perforations, not involving the drum margin (see FIG. 50.2), are regarded as ‘safe’.13

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(a)

Cholesteatoma is visible through the hole as white flakes, unless it is obscured by discharge or a persistent overlying scab. Either type of perforation can lead to chronic infective discharge, the nature of which varies with its origin. Mucus admixture is recognised by its stretch and recoil when this discharge is being cleaned from the external auditory canal. The types of discharge are compared in TABLE 50.3.

Table 50.3

(b)

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Comparison of types of discharge Unsafe

Safe

Source

Cholesteatoma

Mucosa

Odour

Foul

Inoffensive

Amount

Usually scant, never profuse

Can be profuse

Nature

Purulent

Mucopurulent

Management If an attic perforation is recognised or suspected, specialist referral is essential. Cholesteatoma cannot be eradicated by medical means: surgical removal is necessary to prevent a serious infratemporal or intracranial complication.

Otitis externa

FIGURE 50.10 (a) Chronic otitis media with loss of the tympanic membrane; this is ‘safe ear’ (b) Unsafe ear: chronic otitis media with attic cholesteatoma.

Cholesteatoma13 Refer CHAPTER 43. The status of a perforation depends on the presence of accumulated squamous epithelium (termed cholesteatoma) in the middle ear, because this erodes bone. An attic perforation contains such material; safe perforations do not. Red flags for cholesteatoma include meningitistype features, cranial nerve deficits, sensorineural hearing loss and persistent deep ear pain.

Otitis externa (see FIG.  50.11), also known as ‘swimmer’s ear’, ‘surfer’s ear’ and ‘tropical ear’, is common in a country whose climate and coastal living leads to extensive water sports. It is more prevalent in hot humid conditions and therefore in the tropics. Predisposing factors are allergic skin conditions, ear canal trauma, water penetration (swimming, humidity, showering), water and debris retention (wax, dermatitis, exostoses), foreign bodies, contamination from swimming water including spas, and use of Q tips and hearing aids. Common responsible organisms • Bacteria: — Pseudomonas sp. — Escherichia coli — S. aureus — Proteus sp. — Klebsiella sp. • Fungi: — Candida albicans — Aspergillus sp.

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Dressings

swollen inflamed skin of outer ear canal

soggy debris and wax

Dressings are essential in all but the mildest forms. After cleaning and drying, insert 10–20 cm of 4 mm Nufold gauze impregnated with a steroid and antibiotic cream. For severe otitis externa, a wick is important and will reduce the oedema and pain in 12 to 24 hours (see FIG.  50.12). The wick can be soaked in an astringent (e.g. aluminium acetate 4% solution or glycerin and 10% ichthammol). The wick needs replacement daily until the swelling has subsided.

FIGURE 50.11 Otitis externa

Clinical features • Itching at first • Otalgia/pain (mild to intense) in 70% • Fullness in ear canal • Scant discharge • Hearing loss Signs • Oedema (mild to extensive) • Tenderness on moving auricle or jaw • Erythema • Discharge (offensive if coliform) • Pale cream ‘wet blotting paper’ debris— C. albicans • Black spores of Aspergillus nigra • TM granular or dull red Obtain culture, especially if resistant Pseudomonas sp. suspected, by using small ear swab. Note: ‘Malignant’ otitis externa occurs in diabetics due to Pseudomonas infection at base of skull. Management

Aural toilet Meticulous aural toilet by gentle suction and dry mopping with a wisp of cotton wool on a fine broach under good lighting is the keystone of management. This enables topical medication to be applied directly to the skin.

FIGURE 50.12 Insertion of a wick; it is packed gradually by short back-and-forth movements of the forceps. Source: Courtesy of Bruce Black

Topical antimicrobials7 The most effective, especially when the canal is open, is an antibacterial, antifungal and corticosteroid preparation such as Kenacomb or Sofradex drops (2–3 drops tds), Locacorten-Vioform drops (2–3 drops bd) or Ciproxin HC (3 drops bd). Be cautious of ear drops with neomycin (hypersensitivity). The tragus should be pumped for 30 seconds after instillation by pressing on it repeatedly, within the limitation of any pain.

Other measures • Strong analgesics are essential • Antibiotics have a minimal place in treatment unless a spreading cellulitis has developed (refer if in doubt) • Prevent scratching and entry of water • Use a wick soaked in combination steroid and antibiotic ointment for more severe cases

Practice tip for severe ‘tropical ear’

Syringing

Prednisolone (o) 15 mg statim then 10 mg 8 hourly for 6 doses followed by:

This is appropriate in some cases but the canal must be dried meticulously afterwards. For most cases it is not recommended.

• •

Merocel ear wick topical Kenacomb or Sofradex drops

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Prevention • Keep the ear dry, especially those involved in water sports • Protect the ear with various water-proofing methods: — cotton wool coated with petroleum jelly — use an antiseptic drying agent (eg. ethanol) after swimming and showering — tailor-made ear plugs (e.g. EAR foam plugs) — silicone putty or Blu-Tack — a bathing cap pulled well forward allows these plugs to stay in situ • Avoid poking objects such as hairpins and cotton buds in the ear to clean the canal • If water enters, shake it out or use Aquaear drops (spirit drops help dry the canal)

Necrotising otitis externa This severe complication usually due to Pseudomonas aeruginosa can occur in the immunocompromised, diabetic or elderly patient. It involves cartilage and bone and should be considered with treatment failure, severe persistent pain, fever and visible granulation tissue. Urgent referral is advisable.

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Ear exostoses (‘surfer’s ear’) These periosteal bony overgrowths are usually caused by water retention in the ear. They are often multiple. They tend to trap keratin, wax and water, leading to infection. Prevention • Use plugs or Blu-Tack to waterproof ear. • Dry thoroughly with hair dryer after swimming. They may require surgical removal.

Furunculosis Furunculosis is a staphylococcal infection of the hair follicle in the outer cartilaginous part of the ear canal. It is usually intensely painful. Fever occurs only when the infection spreads in front of the ear as cellulitis. The pinna is tender on movement—a sign that is not a feature of acute otitis media. The furuncle (boil) may be seen in the external auditory meatus (see FIG. 50.13). Management • If pointing, it can be incised after a local anaesthetic or freezing spray • Warmth (e.g. use hot face washer, hot water bottle) • If fever with cellulitis—dicloxacillin

FIGURE 50.13 Furuncle (boil) in hair-bearing area at opening of the ear canal

Perichondritis Perichondritis is infection of the cartilage of the ear characterised by severe pain of the pinna, which is red, swollen and exquisitely tender. It is rare and follows trauma or surgery to the ear. As the organism is frequently P. pyocaneus the appropriate antibiotics must be carefully chosen (e.g. ciprofloxacin).

Infected ear lobe The cause is most likely a contact allergy to nickel in an earring, complicated by a S. aureus infection. Management • Discard the earrings • Clean the site to eliminate residual traces of nickel • Swab the site and then commence antibiotics (e.g. flucloxacillin or erythromycin) • Instruct the patient to clean the site daily, and then apply the appropriate ointment • Use a ‘noble metal’ stud to keep the tract patent • Advise the use of only gold, silver or platinum studs in future

Eustachian tube dysfunction This is a common cause of discomfort.15 Symptoms include fullness in the ear, pain of various levels and impairment of hearing. The most common causes of dysfunction are disorders causing oedema of the tubal

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The painful ear lining, such as viral URTI and allergy when the tube is only partially blocked; swallowing and yawning may elicit a crackling or popping sound. Examination reveals retraction of the TM and decreased mobility on pneumatic otoscopy. The problem is usually transient after a viral URTI. Treatment • Systemic and intranasal decongestants (e.g. pseudoephedrine or corticosteroids in allergic patients) • Autoinflation by forced exhalation against closed nostrils (avoid in active intranasal infection) • Avoid air travel, rapid altitude change and underwater diving

Otic barotrauma Barotrauma is damage caused by undergoing rapid changes in atmospheric pressure in the presence of an occluded Eustachian tube (see FIG.  50.14). It affects scuba divers and aircraft travellers.

Prevention Flying. Perform repeated Valsalva manoeuvres during descent. Use decongestant drops or sprays before boarding the aircraft, and then 2 hours before descent. Diving. Those with nasal problems, otitis media or chronic tubal dysfunction should not dive.

Penetrating injury to tympanic membrane A penetrating injury to the TM can occur in children and adults from various causes such as pencils and slivers of wood or glass. Bleeding invariably follows and infection is the danger. Management • Remove blood clot by suction toilet or gentle dry mopping • Ensure no FB is present • Check hearing • Prescribe a course of broad spectrum antibiotics (e.g. cotrimoxazole) • Prescribe analgesics • Instruct patient not to let water enter ear • Review in 2 days and then regularly • At review in 1 month the drum should be virtually healed • Check hearing 2 months after injury

Temporomandibular joint arthralgia

Source: Courtesy of Bruce Black

The symptoms include temporary or persisting pain, deafness, vertigo, tinnitus and perhaps discharge. Inspection of the TM may reveal (in order of seriousness): retraction; erythema; haemorrhage (due to extravasation of blood into the layers of the TM); fluid or blood in the middle ear; perforation. Perform conductive hearing loss tests with tuning fork. Treatment Most cases are mild and resolve spontaneously in a few days, so treat with analgesics and reassurance. Menthol inhalations are soothing and effective. Refer

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if any persistent problems for consideration of the Politzer bag inflation or myringotomy.

Complete healing can be expected within 8 weeks in 90–95% of such cases.16

FIGURE 50.14 Mechanism of barotrauma, with blocking of the Eustachian tube due to increased pressure at the sites indicated.

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If rheumatoid arthritis is excluded, a set of special exercises, which may include ‘chewing’ a piece of soft wood over the molars, invariably solves this problem (see CHAPTER 52). If an obvious dental malocclusion is present, referral is necessary.

When to refer Otitis media • Incomplete resolution of acute otitis media • Persistent middle ear effusion for 3 months after an attack of acute otitis media • Persistent apparent or proved deafness • Evidence or suspicion of acute mastoiditis or other severe complications • Frequent recurrences (e.g. four attacks a year) • Presence of craniofacial abnormalities

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Other ear problems • Attic perforation/cholesteatoma • FBs in ear not removed by simple measures such as syringing • No response to treatment after 2 weeks for otitis externa • Suspicion of carcinoma of the ear canal • Acute TM perforation that has not healed in 6 weeks • Chronic TM perforation (involving lower twothirds of TM)

Practice tips • •

•

•

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• • •

•

The pain of acute otitis media may be masked by fever in babies and young children. A red TM is not always caused by otitis media. The blood vessels of the drum head may be engorged from crying, sneezing or nose blowing. In crying babies, the TM as well as the face may be red. In otitis externa, most cases will resolve rapidly if the ear canal is expanded and then cleaned meticulously. If an adult presents with ear pain but normal auroscopy, examine possible referral sites, namely TMJ, mouth, throat, teeth and cervical spine. Consider mastoiditis if foul-smelling discharge is present over 7 + days. Antibiotics have no place in the treatment of otic barotrauma. It is good medicine to make relief of distressing ear pain a priority. Adequate analgesics must be given. There is a tendency to give too low a dose of paracetamol in children. The installation of nasal drops in infants with a snuffy nose and acute otitis media can indirectly provide amazing relief of pain. Spirit ear drops APF are a cheap and simple agent to use for recurrent otitis externa where wetness of the ear canal is a persistent problem.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Earache in children • Ear infection (otitis media) • Ear: otitis externa • Ear: wax in your ear

References 1 Black B. Otalgia. Aust Fam Physician, 1987; 16: 292–6. 2 Shires DB, Hennen BK, Rice DI. Family Medicine (2nd edn). New York: McGraw-Hill, 1987: 86–93. 3 Jarman R. Otitis media. Australian Paediatric Review, 1991; 4: 1–2. 4 Ludman H. ABC of Otolaryngology (3rd edn). London: BMJ, 1993. 5 Sandler G, Fry J. Early Clinical Diagnosis. Lancaster: MTP Press, 1986: 285–7. 6 Murtagh J. Practice Tips (6th edn). Sydney: McGraw-Hill, 2013: 134–6. 7 Moulds R (Chair). Therapeutic Guidelines: Antibiotics (Version 14). Melbourne: Therapeutic Guidelines Ltd, 2010; 269–73. 8 Morris PS, Leach AJ. Managing otitis media: an evidencebased approach. Australian Prescriber, 2009; 32 (6): 155–9. 9 Del Mar C, Glasziou P, Hayem M. Are antibiotics indicated for the initial treatment of acute otitis media in children? A meta analysis. BMJ, 1997; 314: 1526–9. 10 Rosser W, Shafir M. Evidence-Based Family Medicine. Hamilton: BC Decker, 1998: 111–13. 11 Gunasekera H. Otitis media in children: how to treat. Australian Doctor, 18 July 2008: 33–40 12 Van Dongen TM, van der Heijden GJ et al. Treatment of otitis media in children under 2 years of age. N Eng J Med, 2014; 370: 723–33. 13 Black B. Otitis media: how to treat. Australian Doctor, 29 November; 2002: I–VIII. 14 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013: 386–7. 15 Papadakis MD, McPhee SJ. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013; 201–2. 16 Kruger R, Black B. Penetrating injury eardrum. Aust Fam Physician, 1986; 15: 735.

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Those with sore eyes . . . find the light painful, while the darkness, which permits them to see nothing, is restful and agreeable. Dio Chrysostom (–) A red eye accounts for at least 80% of patients with eye problems encountered in general practice.1 An accurate history combined with a thorough examination will permit the diagnosis to be made in most cases without recourse to specialist ophthalmic equipment. A summary of the diagnostic strategy model is presented in TABLE 51.1. Table 51.1

The red and tender eye: diagnostic strategy model

Q. Probability diagnosis A. Conjunctivitis: • bacterial • adenovirus • allergic Q. Serious disorders not to be missed A. Acute glaucoma Uveitis: • acute iritis • choroiditis Corneal ulcer Herpes simplex keratitis Microbial keratitis (e.g. fungal, amoebic, bacterial) Herpes zoster ophthalmicus Penetrating injury Endophthalmitis Orbital cellulitis Q. Pitfalls (often missed) A. Scleritis/episcleritis Foreign body Trauma—contusion, penetrating injury Ultraviolet light ‘keratitis’ Blepharitis Cavernous sinus arteriovenous fistula Q. Seven masquerades checklist A. Drugs (hypersensitivity) Thyroid disorder (hyperthyroidism) Q. Is the patient trying to tell me something? A. Unlikely.

Key facts and checkpoints • • • • •

•

•

•

Acute conjunctivitis accounts for over 25% of all eye complaints seen in general practice.2 A purulent discharge indicates bacterial conjunctivitis.3 A clear or mucous discharge indicates viral or allergic conjunctivitis. Viral conjunctivitis can be slow to resolve and may last for weeks. Pain and visual loss suggest a serious condition such as glaucoma, uveitis (including acute iritis) or corneal ulceration. Beware of the unilateral red eye—think beyond bacterial or allergic conjunctivitis. It is rarely conjunctivitis and may be a corneal ulcer, keratitis, foreign body, trauma, uveitis or acute glaucoma.4 Keratitis (inflammation of the cornea) is one of the most common causes of an uncomfortable red eye. Apart from the wellknown viral causes (herpes simplex, herpes zoster, adenovirus and measles), it can be caused by fungal infection (usually on a damaged cornea), bacterial infection or inflammatory disorder such as ankylosing spondylitis.5 Herpes simplex keratitis (dendritic ulcer) often presents painlessly as the neurotrophic effect grossly diminishes sensation.

The clinical approach The five essentials of the history are: • history of trauma, especially as indicator of intraocular foreign body (IOFB) • vision • the degree and type of discomfort • presence of discharge • presence of photophobia

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The social and occupational history is also very important. This includes a history of exposure to a ‘red eye’ at school, work or home; incidents at work such as injury, welding, foreign bodies or chemicals; and genitourinary symptoms. When examining the unilateral red eye keep the following diagnoses in mind: • • • • • •

trauma foreign body, including IOFB corneal ulcer iritis (uveitis) viral conjunctivitis (commonest type) acute glaucoma

The manner of onset of the irritation often gives an indication of the cause. Conjunctivitis or uveitis generally has a gradual onset of redness, while a small foreign body will produce a very rapid hyperaemia. Photophobia occurs usually with uveitis and keratitis. It is vital to elicit careful information about visual acuity. The wearing of contact lenses is very important as these are prone to cause infection or the ‘overwear syndrome’, which resembles an acute ultraviolet (UV) burn.

The key eye symptoms The key eye symptoms are:

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• • • •

itch irritation pain (with pus or watering) loss of vision (red or white eye) — red = front of eye — white = back of eye

Key questions • Have you noticed blurring of your vision? • Have you been in close contact with others with the same condition? • Have you had a cold or running nose recently? • Do you wear contact lenses? • Can you recall scratching or injuring your eye? • What were you doing at the time you noticed trouble? • Have you been putting any drops, ointments or cosmetics in or around your eye? • Do you suffer from hay fever? • Do you have any problems with your eyelids? • Had your eyes been watering for some time beforehand? • Have you had any other problems? • Have you been exposed to arc welding?

Red eye red flags (urgent ophthalmic referral)3,6 • • • • • • • • • •

Severe ocular pain Severe orbital pain Reduction of vision Loss of vision Diplopia Dilated pupil Abnormal corneal signs Globe displacement Endophthalmitis Microbial keratitis ± contact lens use

Loss of vision in the red eye Consider: • • • •

iritis (uveitis) scleritis acute glaucoma (pain; nausea and vomiting) chemical burns

The painful red eye Causes to consider: • • • • • • • • • • •

keratitis uveitis (iritis) episcleritis scleritis acute glaucoma hypopyon (pus in the anterior chamber) endophthalmitis (inflammation of internal structures—may follow surgery) corneal abrasion/ulceration Pain with discharge: keratitis Pain with photophobia: uveitis episcleritis

Examination The basic equipment: • • • • • • • • • •

eye testing charts at 45 cm (18 in) and 300 cm (10 ft) multiple pinholes torch (e.g. Cobalt blue) magnifying aid (e.g. binocular loupe) glass rod or cotton bud to aid eyelid eversion fluorescein sterile paper strips anaesthetic drops Schiotz tonometer ophthalmoscope Ishihara colour vision test

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The red and tender eye The four essentials of the examination are: • • • •

testing and recording vision meticulous inspection under magnification testing the pupils testing ocular tension4

papillae of allergic (vernal) conjunctivitis

foreign body

625

577

lymphoid follicles of viral conjunctivitis ciliary flush

conjunctival vessels

irregular pupil

Also: • local anaesthetic test • fluorescein staining • subtarsal examination Inspection A thorough inspection is essential, noting the nature of the inflammatory injection, whether it is localised (episcleritis) or diffuse, viewing the iris for any irregularity, observing the cornea, and searching for foreign bodies, especially under the eyelids, and for any evidence of penetrating injury. No ocular examination is complete until the eyelid is everted and closely inspected. Both eyes must be examined since many patients presenting with conjunctivitis in one eye will have early signs of conjunctivitis in the other. Use fluorescein to help identify corneal ulceration. Local anaesthetic drops instilled prior to the examination of a painful lesion are recommended. The local anaesthetic test is a sensitive measure of a surface problem—if the pain is unrelieved a deeper problem must be suspected. Palpate for enlarged pre-auricular lymph nodes, which are characteristic of viral conjunctivitis. The nature of the injection is important. In conjunctivitis the vessels are clearly delineated and branch from the corners of the eye towards the cornea, since it involves mainly the tarsal plate. Episcleral and scleral vessels are larger than conjunctival vessels and are concentrated towards the cornea (see FIG. 51.1). Ciliary injection appears as a red ring around the limbus of the cornea (the ciliary flush), and the individual vessels, which form a parallel arrangement, are not clearly visible. Ciliary injection may indicate a more serious deep-seated inflammatory condition such as anterior uveitis or a deep corneal infection. The presence of fine follicles on the tarsal conjunctivae indicates viral infection while a cobblestone appearance indicates allergic conjunctivitis. Note: Slit lamp examination is ideal for the examination of the eye. Investigations These include: • swab of discharge for micro and culture or for viral studies

dendritic ulcer blepharitis

episcleral vessels mucopurulent discharge —bacterial conjunctivitis

FIGURE 51.1 Physical signs to search for in a patient with a red eye (eyelids everted)

• ESR/CRP • HLA B27 antigen • imaging

Red eye in children Children can suffer from the various types of conjunctivitis (commonly), uveitis and trauma. Of particular concern is orbital cellulitis, which may present as a unilateral swollen lid and can rapidly lead to blindness if untreated. Bacterial, viral and allergic conjunctivitis are common in all children. Conjunctivitis in infants is a serious disorder because of the immaturity of tissues and defence mechanisms. Serious corneal damage and blindness can result.

Neonatal conjunctivitis (ophthalmia neonatorum) This is conjunctivitis in an infant less than 1 month old and is a notifiable disease. Chlamydial and gonococcal infections are uncommon but must be considered if a purulent discharge is found in the first few days of life.7 In both conditions the parents must be investigated for associated venereal infection and treated accordingly (this includes contact tracing) (see CHAPTER 137). Chlamydia trachomatis accounts for 50% or more of cases. Its presentation in neonates is acute, usually 1–2 weeks after delivery, with moderate mucopurulent discharge. It is a systemic disease and may be associated with pneumonia. The diagnosis is confirmed by PCR tests on the conjunctival secretions. Treatment is with oral erythromycin for 21 days and local sulfacetamide eye drops.

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Neisseria gonorrhoeae conjunctivitis, which usually occurs within 1–2 days of delivery, requires vigorous treatment with intravenous cephalosporins or penicillin and local sulfacetamide drops. The discharge is highly infectious and the organism has the potential for severe corneal infection or septicaemia.7 Other common bacterial organisms can cause neonatal conjunctivitis, and herpes simplex virus type II can cause conjunctivitis and/or eyelid vesicles or keratitis.2

Trachoma More than 6 million people worldwide have trachomacaused blindness. Trachoma is a chlamydial conjunctivitis that is prevalent in outback areas and in the Indigenous population. C. trachomatis is usually transmitted by human contact between children and mothers and also by flies, especially where hygiene is inadequate. It is the most common cause of blindness in the world. Recurrent and untreated disease leads to lid scarring and inturned lashes (entropion) with corneal ulceration and visual loss. It is important to commence control of the infection in childhood. Treatment • Prevention/community education • Antibiotics—azithromycin • Surgical correction (where relevant)

51

Blocked nasolacrimal duct Delayed development of the nasolacrimal duct occurs in about 6% of infants,7 resulting in blocked lacrimal drainage; the lacrimal sac becomes infected, causing a persistent discharge from one or both eyes. In the majority of infants, spontaneous resolution of the problem occurs by the age of 6 months. Management • Local antibiotics for infective episodes • Bathing with normal saline • Frequent massage over the lacrimal sac • Referral for probing of the lacrimal passage before 6 months if the discharge is profuse and irritating or between 6 and 12 months if the problem has not self-corrected (refer CHAPTER 91)

Red eye in the elderly In an elderly patient there is an increased possibility of acute glaucoma, uveitis and herpes zoster. Acute angle closure glaucoma should be considered in any

patient over the age of 50 presenting with an acutely painful red eye. Eyelid conditions such as blepharitis, trichiasis, entropion and ectropion are more common in the elderly.

ACUTE CONJUNCTIVITIS Acute conjunctivitis is defined as an episode of conjunctival inflammation lasting less than 3 weeks.2 The two major causes are infection (either bacterial or viral) and acute allergic or toxic reactions of the conjunctiva (see TABLE 51.2). Clinical features • Diffuse hyperaemia of tarsal or bulbar conjunctivae • Absence of ocular pain, good vision, clear cornea • Infectious conjunctivitis is bilateral (usually) or unilateral (depending on the cause), with a discharge, and a gritty or sandy sensation

Bacterial conjunctivitis Bacterial infection may be primary, secondary to a viral infection or secondary to blepharitis. History Purulent discharge with sticking together of eyelashes in the morning is typical. It usually starts in one eye and spreads to the other. There may be a history of contact with a person with similar symptoms. The organisms are usually picked up from contaminated fingers, face cloths or towels. Clinical features • Gritty red eye • Purulent discharge • Clear cornea Examination There is usually a bilateral mucopurulent discharge with uniform engorgement of all the conjunctival blood vessels and a non-specific papillary response (see FIG. 51.2). Fluorescein staining is negative. Causative organisms These include: • • • • • •

Streptococcus pneumoniae Haemophilus influenzae Staphylococcus aureus Streptococcus pyogenes N. gonorrhoeae (a hyperacute onset) Pseudomonas aeruginosa

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The red and tender eye

Table 51.2

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Major causes of a red eye Site of inflammation

Pain

Discharge

Vision

Photophobia Pupil

Cornea

Ocular tension

Bacterial conjunctivitis

Conjunctiva, including lining of lids (usually bilateral)

Irritation— gritty

Purulent, lids stuck in the morning

Normal

No

Normal

Normal

Normal

Viral conjunctivitis

Conjunctiva, Gritty lining of lids often follicular (uni or bilateral)

Watery

Normal

No

Normal

Normal

Normal

Allergic (vernal) conjunctivitis

Conjunctiva, papillary swellings on lid linings (bilateral)

Gritty— itching

Watery

Normal

No

Normal

Normal

Normal

Contact hypersensitivity (dermatoconjunctivitis)

Conjunctiva and eyelids Oedema

Itching

Watery

Normal— No may be blurred

Normal

Normal

Normal

Subconjunctival haemorrhage

Beefy red area fading at edge (unilateral)

No

No

Normal

No

Normal

Normal

Normal

Herpes simplex keratitis

Yes—gritty Unilateral— circumcorneal Dendritic ulcer

No, reflex Blurred, lacrimation but variable, depends on site

Yes

Normal

Abnormal Normal

Corneal ulcer

Yes Unilateral— circumcorneal (exclude foreign body)

No, reflex Blurred, lacrimation but variable, depends on site

Yes

Normal

Abnormal Normal

Scleritis/episcleritis

Localised deep redness Tender area

Yes

No

Normal

No

Normal

Normal

Normal

Acute uveitis/iritis

Maximum around cornea

Yes— radiates to brow, temple, nose

No, reflex Blurred lacrimation

Yes

Constricted, Normal may be irregular

Normal or low

Acute glaucoma

Yes, severe No, reflex Haloes Diffuse but lacrimation around with maximum lights circumcorneal nausea and vomiting

Yes

Dilated Absent light reflex

51

Hazy

Hard, elevated

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• Problem solving in general practice • Chlamydia trachomatis—may be sexually transmitted. Shows a brick red follicular conjunctivitis with a stringy mucus discharge.

Viral conjunctivitis The most common cause of this very contagious condition is adenovirus.

FIGURE 51.2 Acute bacterial conjunctivitis with mucopurulent discharge, no corneal stain

Diagnosis is usually clinical but a swab should be taken for smear and culture with:2 • hyperacute or severe purulent conjunctivitis • prolonged infection • neonates Management Limit the spread by avoiding close contact with others, use of separate towels and good ocular hygiene.

Mild cases

51

Mild cases may resolve with saline irrigation of the eyelids and conjunctiva but may last up to 14 days if untreated.8 An antiseptic eye drop such as propamidine isethionate 0.1% (Brolene) 1–2 drops, 6–8 hourly for 5–7 days can be used.

History It is commonly associated with URTIs and is the type of conjunctivitis that occurs in epidemics (pink eye).1 The conjunctivitis usually has a 2–3 week course; it is initially one-sided but with cross-infection occurring days later in the other eye. It can be a severe problem with a very irritable, watering eye. Examination The examination should be conducted with gloves. It is usually bilateral with diffuse conjunctival infection and productive of a scant watery discharge. Viral infections typically but not always produce a follicular response in the conjunctivae (tiny, pale lymphoid follicles) and an associated pre-auricular lymph node (see FIG.  51.3). Subconjunctival haemorrhages may occur with adenovirus infection. High magnification, ideally a slit lamp, may be necessary to visualise some of the changes, such as small corneal opacities, follicles and keratitis.

More severe cases Chloramphenicol 0.5% eye drops, 1–2 hourly for 2 days,1 decrease to 4 times a day for another 7 days (max. 10 days—cases of aplastic anaemia have been reported with long-term use). Use also chloramphenicol 1% eye ointment each night or framycetin 0.5% eye drops 1–2 drops, every 1 to 2 hours for first 24 hours, decreasing to 8 hourly until discharge resolves for up to 7 days.

Practice tip Brick red eye—think of chlamydia.

FIGURE 51.3 Viral conjunctivitis: watery eye, lid swelling, typical eyelid follicles, associated local lymphadenopathy

Specific organisms

Diagnosis is based on clinical grounds and a history of infected contacts. Viral culture and serology can be performed to identify epidemics.

• Pseudomonas and other coliforms: use topical gentamicin and tobramycin. • N. gonorrhoeae: use appropriate systemic antibiotics.

Treatment • Limit cross-infection by appropriate rules of hygiene and patient education.

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The red and tender eye • Treatment is symptomatic—cool compress and topical lubricants (artificial tear preparations), naphazoline (e.g. Albalon), vasoconstrictors (e.g. phenylephrine) or saline bathing. • Do not pad; avoid bright light. • Watch for secondary bacterial infection. Avoid corticosteroids, which reduce viral shedding and prolong the problem.

Primary herpes simplex infection This viral infection produces a follicular conjunctivitis. About 50% of patients have associated lid or corneal ulcers/vesicles which are diagnostic.2 Only a minority (less than 15%) develop corneal involvement with the primary infection. Dendritic ulceration highlighted by fluorescein staining is diagnostic (see FIG. 51.4). Antigen detection or culture may allow confirmation. Treatment (herpes simplex keratitis) • Attend to eye hygiene • Aciclovir 3% ointment, 5 times a day for 14 days or for at least 3 days after healing8 • Atropine 1% 1 drop, 12 hourly, for the duration of treatment will prevent reflex spasm of the pupil (specialist supervision) • Debridement by a consultant

neonates: erythromycin for 3 weeks children over 6 kg and adults: azithromycin 1 g (o) as single dose Note: Partner must be treated in cases of STI.

ALLERGIC CONJUNCTIVITIS Allergic conjunctivitis results from a local response to an allergen. It includes: • vernal (hay fever) conjunctivitis, and • contact hypersensitivity reactions, e.g. reaction to preservatives in drops

Vernal (hay fever) conjunctivitis This is usually seasonal and related to pollen exposure.  There is usually associated rhinitis (see CHAPTER 80). Treatment Tailor treatment to the degree of symptoms. Antihistamines may be required but symptomatic measures usually suffice. Treatment options: 1 Topical antihistamines/vasoconstrictors 2 Mast cell stabilisers, e.g. sodium cromoglycate 2% drops, 1–2 drops per eye 4 times daily or ketotifen 3 Combination of 1 and 2 4 Topical steroids (severe cases)

Contact hypersensitivity

Chlamydial conjunctivitis Chlamydial conjunctivitis is encountered in three common situations: • neonatal infection (first 1–2 weeks) • young patient with associated venereal infection • isolated Aboriginal people with trachoma

581

Take swabs for culture and PCR testing. Systemic antibiotic treatment:8

Artificial tear preparations may give adequate symptomatic relief.

FIGURE 51.4 Herpes simplex keratitis—gritty, watery eye with typical dendritic ulcer, stained with fluorescein

629

Common topical allergens and toxins include topical ophthalmic medications, especially antibiotics, contact lens solutions (often the contained preservative) and a wide range of cosmetics, soaps, detergents and chemicals. Clinical features include burning, itching and watering with hyperaemia and oedema of the conjunctiva and eyelids. A skin reaction of the lids usually occurs. Treatment • Withdraw the causative agent. • Apply normal saline compresses. • Treat with naphazoline or phenylephrine. • If not responding, refer for possible corticosteroid therapy.

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Subconjunctival haemorrhage Subconjunctival haemorrhage, which appears spontaneously, is a beefy red localised haemorrhage with a definite posterior margin (see Fig. 51.5). If it follows trauma and extends backwards it may indicate an orbital fracture. It is usually caused by a sudden increase in intrathoracic pressure such as coughing and sneezing. It is not related to hypertension but it is worthwhile measuring the blood pressure to help reassure the patient.

Clinical features Episcleritis: • • • • •

no discharge no watering vision normal (usually) often sectorial usually self-limiting Treat with topical or oral steroids.

Scleritis: • painful loss of vision • urgent referral History A red and sore eye is the presenting complaint. There is usually no discharge but there may be reflex lacrimation. Scleritis is much more painful than episcleritis3 and the eye becomes intensely red. Examination With scleritis there is a localised area of inflammation that is tender to touch (FIG.  51.6), and more extensive than with episcleritis, being uniform across the eye. The inflamed vessels are larger than the conjunctival vessels.

FIGURE 51.5 Subconjunctival haemorrhage: this is usually localised haemorrhage that appears spontaneously. It is pain free. If traumatic and extends posteriorly it may indicate an orbital fracture.

51

Management No local therapy is necessary. The haemorrhage absorbs over 2 weeks. Patient explanation and reassurance is necessary. If haemorrhages are recurrent a bleeding tendency should be excluded.

Episcleritis and scleritis Episcleritis and scleritis present as a localised area of inflammation (see FIGS 51.1 and 51.6). The episclera is a vascular layer that lies just beneath the conjunctiva and adjacent to the sclera. Both may become inflamed but episcleritis (which is more localised) is essentially self-limiting while scleritis (which is rare) is more serious as the eye may perforate.3 Both conditions may be confused with inflammation associated with a foreign body, pterygium or pinguecula. There are no significant associations with episcleritis, which is usually idiopathic, but scleritis may be associated with connective tissue disease, especially rheumatoid arthritis and herpes zoster and rarely sarcoidosis and tuberculosis.

FIGURE 51.6 Episcleritis showing inflammation of the conjunctival and episclerical tissue only. Note the absence of violaceous colour that is seen in scleritis.

Management An underlying cause such as an autoimmune condition should be identified. Refer the patient, especially for scleritis. Corticosteroids or NSAIDs may be prescribed.

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The red and tender eye

Uveitis (iritis) The iris, ciliary body and the choroid form the uveal tract, which is the vascular coat of the eyeball.7 Anterior uveitis (acute iritis or iridocyclitis) is inflammation of the iris and ciliary body and this is usually referred to as acute iritis (see FIG.  51.7). The iris is sticky and sticks to the lens. The pupil may become small because of adhesions, and the vision is blurred. ocular (bulbar) conjunctiva eyelid

sclera choroid

cornea (keratitis)

retina

posterior uveitis anterior iris uveitis ciliary body

FIGURE 51.7 Diagrammatic representation of eye structures involved in inflammatory disorders

Causes include autoimmune-related diseases such as the seronegative arthropathies (e.g. ankylosing spondylitis), SLE, IBD, sarcoidosis and some infections (e.g. toxoplasmosis and syphilis). Clinical features • Eye redness, esp. around edge of iris • Eye discomfort or pain • Increased tearing • Blurred vision • Sensitivity to light • Floaters in the field of vision • Small pupil The examination findings are summarised in The affected eye is red with the injection being particularly pronounced over the area covering the inflamed ciliary body (ciliary flush). However, the whole bulbar conjunctivae can be injected. The patient should be referred to a consultant. Slit lamp examination aids diagnosis. TABLE 51.2.

583

Management involves finding the underlying cause. Treatment includes pupil dilatation with atropine drops and topical steroids to suppress inflammation. Systemic corticosteroids may be necessary. The prognosis of anterior uveitis is good if treatment and follow-up are maintained, but recurrence is likely. Posterior uveitis (choroiditis) may involve the retina and vitreous. Blurred vision and floating opacities in the visual field may be the only symptoms. Pain is not a feature. Referral to detect the causation and for treatment is essential.

Acute glaucoma

episclera (episcleritis)

blepharitis

631

Acute glaucoma should always be considered in a patient over 50 years presenting with an acutely painful red eye. Permanent damage will result from misdiagnosis. The attack characteristically strikes in the evening when the pupil becomes semidilated.3 Clinical features • Patient >50 years • Pain in one eye • ± Nausea and vomiting • Impaired vision • Haloes around lights • Hazy cornea • Fixed semidilated pupil • Eye feels hard Management Urgent ophthalmic referral is essential since emergency treatment is necessary to preserve eyesight. If immediate specialist attention is unavailable, treatment can be initiated with acetazolamide (Diamox) 500 mg IV and pilocarpine 4% drops to constrict the pupil or pressure-lowering drops.

Keratoconjunctivitis sicca Dry eyes are a common problem, especially in elderly women. Lack of lacrimal secretion can be functional (e.g. ageing), or due to systemic disease (e.g. rheumatoid arthritis, SLE, Sjögren syndrome), drugs (e.g. β-blockers) or other factors, including the menopause. Up to 50% of patients with severe dry eye have Sjögren syndrome. Clinical features • A variety of symptoms • Dryness, grittiness, stinging and redness

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• Sensation of foreign body (e.g. sand) • Photophobia if severe • Slit light examination diagnostic with special stains Treatment • Treat the cause. • Bathe eyes with clean water. • Use artificial tears: hypromellose (e.g. Tears Naturale), polyvinyl alcohol (e.g. Tears Plus). • Be cautious of adverse topical reactions. • Refer severe cases.

EYELID AND LACRIMAL DISORDERS There are several inflammatory disorders of the eyelid and lacrimal system that present as a ‘red and tender’ eye without involving the conjunctiva. Any suspicious lesion should be referred.

FIGURE 51.9 Steaming the painful eye: allow steam to rise from a thermos onto the closed eye for 10–15 minutes

Stye (external hordeolum) A stye is an acute abscess of a lash follicle or associated glands of the anterior lid margin, caused usually by S. aureus. The patient complains of a red tender swelling of the lid margin, usually on the medial side (see FIG.  51.8). A stye may be confused with a chalazion, orbital cellulitis or dacryocystitis.

51

FIGURE 51.8 Hordeolum—a stye. This is a focal staphylococcal infection of the root of an eyelash.

Management • Use heat to help it discharge by using direct steam from a thermos (see FIG. 51.9) onto the enclosed eye or by hot compresses. • Perform lash epilation to allow drainage of pus (incise with a size 11 blade if epilation does not work). • Use chloramphenicol ointment if the infection is spreading locally.3

Chalazion (meibomian cyst) Also known as internal hordeolum, this granuloma of the meibomian gland in the eyelid may become inflamed and present as a tender irritating lump in the lid. Look for evidence of blepharitis. Differential diagnoses include sebaceous gland carcinoma and basal cell carcinoma. Management Conservative treatment may result in resolution. This involves heat either as steam from a thermos or by applying a hot compress (a hand towel soaked in hot water) followed by light massage and the application of chloramphenicol ointment for 5 days. If the chalazion is very large, persistent or uncomfortable, or is affecting vision, it can be incised and curetted under local anaesthesia. This is best performed through the inner conjunctival surface using a chalazion clamp (blepharostat) (see FIG. 51.10). Meibomianitis is usually a staphylococcal microabscess of the gland and oral antistaphylococcal antibiotics (not topical) are recommended (e.g. di/ flucloxacillin 500 mg (o) 6 hourly (adult)). Surgical incision and curettage may also be necessary.

Blepharitis This common chronic condition is characterised by inflammation of the lid margins and is commonly associated with secondary ocular effects such as styes, chalazia and conjunctival or corneal ulceration (see FIG.  51.11). Blepharitis is frequently associated with seborrhoeic dermatitis (especially) and atopic

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The red and tender eye

FIGURE 51.10 Excision of a meibomian cyst, using a chalazion clamp and curette

ulcers on eyelids

633

585

Management • Eyelid hygiene is the mainstay of therapy. The crusts and other debris should be gently cleaned with a cotton wool bud dipped in a 1:10 dilution of baby shampoo or a solution of sodium bicarbonate, once or twice daily. Application of a warm water or saline soak with gauze for 20 minutes is also effective. • For chronic blepharitis short-term use of a corticosteroid ointment (e.g. hydrocortisone 0.5%) can be very effective. • Ocular lubricants such as artificial tear preparations may greatly relieve symptoms of keratoconjunctivitis sicca (dry eyes). • Control scalp seborrhoea with regular medicated shampoos. • Treat infection with an antibiotic ointment smeared on the lid margin (this may be necessary for several months) (e.g. tetracycline hydrochloride 1% or framycetin 0.5% or chloramphenicol 1% ointment to lid margins 3–6 hourly).8 • Systemic antibiotics such as flucloxacillin may be required for lid abscess. • Avoid wearing make-up and contact lenses if inflammation is present.

Dacryocystitis conjunctivitis stye

greasy scaly skin on eyelids

FIGURE 51.11 Blepharitis: common complicating features

dermatitis, and less so with rosacea.9 There is a tendency to colonisation of the lid margin with S. aureus, which causes an ulcerative infection. The three main types are: • seborrhoeic blepharitis • staphylococcal blepharitis • blepharitis associated with rosacea Clinical features9 • Persistent sore eyes or eyelids • Irritation, grittiness, burning, dryness and ‘something in the eye’ sensation • Lid or conjunctival swelling and redness • Crusts or scales around the base of the eyelids • Discharge or stickiness, especially in morning • Inflammation and crusting of the lid margins

Acute dacryocystitis is infection of the lacrimal sac secondary to obstruction of the nasolacrimal duct at the junction of the lacrimal sac (see FIG.  51.12). Inflammation is localised over the medial canthus.  There is usually a history of a watery eye for months beforehand. The problem may vary from being mild (as in infants) to severe with abscess formation. Management • Use local heat: steam or a hot moist compress. • Use analgesics. • In mild cases, massage the sac and duct, and instil astringent drops (e.g. zinc sulfate + phenylephrine). • For acute cases systemic antibiotics are best guided by results of Gram’s stain and culture but initially use di/flucloxacillin or cephalexin. • Measures to establish drainage are required eventually. Recurrent attacks or symptomatic watering of the eye are indications for surgery such as dacryocystorhinostomy.

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• Problem solving in general practice sinus tenderness normal eye

swollen red eyelids

restricted eye movement

FIGURE 51.13 Important signs in the patient presenting with orbital cellulitis

FIGURE 51.12 Acute dacryocystitis with abscess formation. Associated obstruction of the nasolacrimal duct at the junction of the lacrimal sac, which has become infected.

Dacroadenitis Dacroadenitis is infection of the lacrimal gland presenting as a tender swelling on the outer upper margin of the eyelid. It may be acute or chronic and has many causes. It is usually caused by a viral infection (e.g. mumps), which is treated conservatively with warm compresses. Bacterial infection is treated with appropriate antibiotics.

Orbital cellulitis

51

Orbital cellulitis includes two basic types—peri-orbital (or preseptal) and orbital (or postseptal) cellulitis. The latter is a potentially blinding and life-threatening condition. It is especially important in children in whom blindness may develop in hours. The patient, often a child, presents with unilateral swollen eyelids that may be red. Ask about a history of sinusitis, peri-ocular trauma, surgery, bites and immunocompromise. Features to look for in orbital cellulitis include:3 • • • • •

a systemically unwell patient proptosis peri-ocular swelling and erythema tenderness over the sinuses ocular nerve compromise (reduced vision, impaired colour vision or abnormal pupils) • restricted and painful eye movements (see FIG. 51.13) In peri-orbital cellulitis, which usually follows an abrasion, there is no pain or restriction of eye movement (see FIG. 51.14). Immediate referral to hospital for specialist treatment is essential for both types. Treatment is

FIGURE 51.14 Peri-orbital cellulitis following an abrasion to the eye. Treat this as an urgent condition.

with IV cefotaxime until afebrile, then amoxycillin/ clavulanate for 7–10 days for peri-orbital cellulitis and  for orbital cellulitis, IV cefotaxime + di(flu) cloxacillin together followed by amoxycillin/ clavulanate (o) 10 days.8

Herpes zoster ophthalmicus Herpes zoster ophthalmicus (shingles) affects the skin supplied by the ophthalmic division of  the trigeminal nerve. The eye may be affected if the nasociliary branch is involved. Ocular problems include conjunctivitis, uveitis, keratitis and glaucoma. Immediate referral is necessary if the eye is red, vision is blurred or the cornea cannot be examined. Apart from general eye hygiene, treatment usually

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The red and tender eye includes one of the oral anti-herpes virus agents such as oral aciclovir 800 mg, 5 times daily for 10 days or (if sight is threatened) aciclovir 10 mg/kg IV slowly 8 hourly for 10 days (provided this is commenced within 3 days of the rash appearing)5,8 and topical aciclovir ointment 4 hourly (see CHAPTER 124).

Pinguecula and pterygium10 Pinguecula is a yellowish elevated nodular growth on either side of the cornea in the area of the palpebral fissure. It is common in people over 35 years. The growth tends to remain static but can become inflamed—pingueculitis. Usually no treatment is necessary unless they are large, craggy and uncomfortable, when excision is indicated. If irritating, topical astringent drops such as naphazoline compound drops (e.g. Albalon) can give relief. Pterygium is a fleshy overgrowth of the conjunctiva onto the nasal side of the cornea and usually occurs in adults living in dry, dusty, windy areas. Excision of a pterygium by a specialist is indicated if it is likely to interfere with vision by encroaching on the visual axis, or if it becomes red and uncomfortable or disfiguring.

CORNEAL DISORDERS11 Patients with corneal conditions typically suffer from ocular pain or discomfort and reduced vision. The common condition of dry eye may involve the cornea while contact lens disorders, abrasions/ulcers and infection are common serious problems that threaten eyesight. Inflammation of the cornea—keratitis— is caused by factors such as UV light, e.g. ‘arc eye’, herpes simplex, herpes zoster ophthalmicus and the dangerous microbial keratitis. Bacterial keratitis is an ophthalmological emergency which should be considered in the contact lens wearer presenting with pain and reduced vision. Topical corticosteroids should be avoided in the undiagnosed red eye.

Corneal abrasion and ulceration There are many causes of abrasions, particularly trauma from a foreign body embedded on the corneal surface or ‘cul-de-sac’ FB, contact lenses, fingernails including ‘french nails’, and UV burns. The abrasion may be associated with an ulcer, which is a defect in the epithelial cell layer of the cornea. Common causes of a corneal ulcer are listed in TABLE 51.3.

Table 51.3

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Corneal ulceration: common causes

Trauma Contact lens wear/injury Infection—microbial keratitis: • bacterial (e.g. Pseudomonas [contact lens]) • viral (e.g. herpes simplex [dendritic ulcer], herpes zoster ophthalmicus) • fungal • protozoal (e.g. Acanthamoeba) Neurotrophic (e.g. trigeminal nerve defect) Immune related (e.g. rheumatoid arthritis) Spontaneous corneal erosion Chronic blepharitis Overexposure (e.g. eyelid defects)

Symptoms • Ocular pain • Foreign body sensation • Watering of the eye (epiphoria) • Blepharospasm • Blurred vision Diagnosis is best performed with a slit lamp using a cobalt blue filter and flourescein staining. Management (corneal ulcer) • Stain with fluorescein. • Check for a foreign body. • Treat with chloramphenicol 1% ointment ± homatropine 2% (if pain due to ciliary spasm). • Double eye pad (if not infected). • Review in 24 hours. • A 6 mm defect heals in 48 hours. • Consider specialist referral.

Superficial punctate keratitis Punctate keratopathy presents as scattered small lesions on the cornea which stain with fluorescein if they are deep enough. It is a non-specific finding and may be associated with blepharitis, viral conjunctivitis, trachoma, keratitis sicca (dry eyes),

Practice tips •

•

Think corneal abrasion if the eye is ‘watering’ and painful (e.g. caused by a large insect like a grasshopper or other foreign body) If a slit lamp is unavailable, the direct ophthalmoscope can be used to provide illumination as well as blue light for corneal examination. Magnifying loupes can then be used for viewing the illuminated cornea.

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UV light exposure (e.g. welding lamps, sunlamps), contact lenses and topical ocular agents. Management involves treating the cause and careful follow-up.

Microbial keratitis This is responsible for at least 1.5 million new cases of blindness every year in the developing world and for significant morbidity in developed countries. Risk factors • Contact lens wear • Corneal trauma, especially agriculture trauma • Corneal surgery • Post-herpetic corneal lesion • Dry eye • Corneal anaesthetic • Corneal exposure (e.g. VII nerve lesion) • Ocular surface disease including ulceration Pseudomonas aeruginosa is the most common causative organism in contact lens wearers. Acanthamoeba is associated with bathing or washing in contaminated water. Urgent referral to an ophthalmologist or eye clinic is needed to avoid rapid corneal destruction with perforation especially with bacterial keratitis. An appropriate ‘covering’ topical antibiotic is ciprofloxacin 0.3% ointment.

Problems with contact lenses

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Because a contact lens is a foreign body, various complications can develop and a history of the use of contact lenses is important in the management of the red eye. Infection Infection is more likely to occur with soft rather than hard lenses. They should not be worn for sleeping since this increases the risk of infection 10-fold.12 One cause is Acanthamoeba keratitis acquired from contaminated water that may be used for cleaning the lenses.

Hard lens trauma This may cause corneal abrasions with irreversible endothelial changes or ptosis, especially with the older polymethyl-methacrylate-based lenses. Patients should change to modern gas permeable hard lenses. Lost lenses Patients should be reassured that lenses cannot go behind the eye. The edge of the lens can usually be seen by everting the upper lid.

Preventive measures13 • Wash hands before handling lenses. • Do not use tap water or saline. • Clean lenses with disinfecting solution. • Store overnight in a clean airtight case with fresh disinfectant. • Change the lens container solution daily. • Discard disposable lenses after 2 weeks. • Do not wear lenses while sleeping. • Do not wear lenses while swimming in lakes, rivers or swimming pools. Refer to an ophthalmologist if a painful red eye develops, especially if a discharge is present.

Flash burns A common problem, usually presenting at night, is bilateral painful eyes caused by UV ‘flash burns’ to both corneas some 5–10 hours previously. The mechanism of injury is UV rays from a welding machine causing superficial punctate keratitis. Other sources of UV light such as sunlamps and snow reflection can cause a reaction. Management • Local anaesthetic (long-acting) drops: once-only application (do not allow the patient to take home more drops). • Instil homatropine 2% drops statim or other short-acting ocular dilating agent (be careful of glaucoma). • Use analgesics (e.g. codeine plus paracetamol) for 24 hours. • Use broad spectrum antibiotic eye ointment in lower fornix (to prevent infection). • Use firm eye padding for 24 hours, when eyes reviewed (avoid light). The eye usually heals completely in 48 hours. If not, check for a foreign body. Note: Contact lens ‘overwear syndrome’ gives the same symptoms.

Cavernous sinus arteriovenous fistula Such a fistula produces conjunctival hyperaemia but no inflammation or discharge. The lesion causes raised orbital venous pressure. The fistula may be secondary to head injuries or may arise spontaneously, particularly in postmenopausal women. They need radiological investigation.

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The red and tender eye The classic symptom is a ‘whooshing’ sound synchronous with the pulse behind the eye, and the sign is a bruit audible with the stethoscope placed over the orbit.

Penetrating eye injuries

— — — — — — — — — — — — — —

X-ray tetanus prophylaxis transport by land injection of anti-emetic (e.g. metoclopramide)

Use no ointment or eye drops, including local anaesthetic. If significant delay is involved give one dose (in adults) of:8 gentamicin 1.5 mg/kg IV plus cefotaxime 1 g or ceftriaxone 1 g IV (can give ceftriaxone IM but with lignocaine 1%) or vancomycin IV + oral ciprofloxacin

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• Emergency referral is also necessary for hyphaema, hypopyon, penetrating eye injury, acute glaucoma, severe chemical burn • Herpes zoster ophthalmicus: if the external nose is involved then the internal eye may be involved • Summary for urgent referral:

These require urgent referral to an ophthalmologist. Consider: • • • •

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trauma (significant)/penetrating injury hyphaema >3 mm corneal ulcer severe conjunctivitis uveitis/acute iritis Behçet syndrome acute glaucoma giant cell arteritis orbital cellulitis (pre- and post-) acute dacryocystitis keratitis episcleritis/scleritis endophthalmitis herpes zoster ophthalmicus

Note: As a general rule never use corticosteroids or atropine in the eye before referral to an ophthalmologist.

Endophthalmitis This is an intra-ocular bacterial infection which may complicate any penetrating injury including intra-ocular surgery. It should be considered in patients with such a history presenting with a red painful eye. Pus may be seen in the anterior chamber (hypopyon). Urgent referral is mandatory. If significant delay, use ciprofloxacin (o) + vancomycin IV.8

Practice tips •

When to refer

•

• Uncertainty about the diagnosis • Patients with uveitis, acute glaucoma, episcleritis/scleritis or corneal ulceration • Deep central corneal and intra-ocular foreign bodies • Prolonged infections, with a poor or absent response to treatment or where therapy may be complicating management • Infections or severe allergies with possible ocular complications • Sudden swelling of an eyelid in a child with evidence of infection suggestive of orbital cellulitis—this is an emergency

• •

• •

Avoid long-term use of any medication, especially antibiotics (e.g. chloramphenicol: course for a maximum of 10 days).2 Note: Beware of allergy or toxicity to topical medications, especially antibiotics, as a cause of persistent symptoms. As a general rule avoid using topical corticosteroids or combined corticosteroid/antibiotic preparations. Never use corticosteroids in the presence of a dendritic ulcer. To achieve effective results from eye ointment or drops, remove debris such as mucopurulent exudate with bacterial conjunctivitis or blepharitis by using a warm solution of saline (dissolve a teaspoon of kitchen salt in 500 mL of boiled water) to bathe away any discharge from conjunctiva, eyelashes and lids. A gritty sensation is common in conjunctivitis but the presence of a foreign body must be excluded.3 Beware of the contact lens ‘overwear syndrome’, which is treated in a similar way to flash burns.

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Red eye golden rules • • • • • • • • • • • •

Always test and record vision Beware of the unilateral red eye Conjunctivitis is almost always bilateral Irritated eyes are often dry Never use steroids if herpes simplex is suspected A penetrating eye injury is an emergency Consider an intra-ocular foreign body Beware of herpes zoster ophthalmicus if the nose is involved Irregular pupils: think iritis, injury and surgery Never pad a discharging eye Refer patients with eyelid ulcers If there is a corneal abrasion look for a foreign body

Source: Based on J Colvin and J Reich4

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Blepharitis • ‘Bloodshot’ eye • Chalazion (meibomian cyst) • Conjunctivitis • Foreign body in the eye • Stye

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References 1 McDonnell P. Red eye: an illustrated guide to eight common causes. Modern Medicine Australia, 1989; October: 37–9. 2 Della NG. Acute conjunctivitis. In: MIMS Disease Index. Sydney: IMS Publishing, 1991–92: 113–15. 3 Kuzniarz M. Red eye. Medical Observer, 11 May 2012: 27–30. 4 Colvin J, Reich J. Systematic examination of the red eye. Aust Fam Physician, 1976; 5: 153–65. 5 Maclean H. Keratitis (viral and fungal). In: MIMS Disease Index. Sydney: IMS Publishing, 1991–92: 301–3. 6 Robinson MJ, Roberton DM. Practical Paediatrics (5th edn). Melbourne: Churchill Livingstone, 2003: 759. 7 Moulds R (Chair). Therapeutic Guidelines: Antibiotics (Version 14). Melbourne: Therapeutic Guidelines Ltd, 2010: 87–100. 8 Barras CW. Blepharitis. In: MIMS Disease Index. Sydney: IMS Publishing, 1991–92: 80–2. 9 Colvin J. Painful eye: an emergency call. Aust Fam Physician, 1985; 14: 1258. 10 Watson SL. Common corneal conditions. Medicine Today, 2005; 6 (5): 22–30. 11 Schein OD, Poggio EC. Ulcerative keratitis in contact lens wearers. Cornea, 1990; 9 (1): 55–8. 12 Lazarus MG. Complications of contact lenses. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 121–3. 13 Sehu W, Zagora S. The red eye. Australian Doctor. 12 October 2012: 23–30.

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Pain in the face

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It’s as though the devil suddenly thrust red hot electric needles through my right cheek towards my ear. Patient (Anonymous), describing ‘tic douloureux’ When a patient complains of pain in the face rather than the head, the physician has to consider foremost the possibilities of dental disorders, sinus disease, especially of the maxillary sinuses, temporomandibular Joint (TMJ) dysfunction, eye disorders, lesions of the oropharynx or posterior third of the tongue, trigeminal neuralgia and chronic paroxysmal hemicrania. The key to the diagnosis is the clinical examination because even the most sophisticated investigation may provide no additional information. A basic list of causes of facial pain is presented in 1 TABLE 52.1. The causes can vary from the simple, such as aphthous ulcers, herpes simplex and dental caries, to serious causes, such as carcinoma of the tongue, sinuses and nasopharynx or osteomyelitis of the mandible or maxilla.

Key facts and checkpoints •

• • • •

•

Dental disorders are the commonest cause of facial pain, accounting for up to 90% of pain in and about the face.2 The most common dental disorders are dental caries and periodontal diseases. The mean age of onset of trigeminal neuralgia is 50–52 years. There is a similarity in the ‘occult’ causes of pain in the ear and in the face (refer to FIGS 50.4 and 50.5). Sinusitis occurs mainly as part of a generalised upper respiratory infection. Swimming is another common predisposing factor. Dental root infection must be sought in all cases of maxillary sinusitis.

Table 52.1

Diagnoses to consider in orofacial pain

Positive physical signs Cervical spinal dysfunction Dental pathology Erysipelas Eye disorders Herpes zoster Nasopharyngeal cancer Oropharyngeal disorders: • ulceration (aphthous, infective, traumatic, others) • cancer • gingivitis/stomatitis • tonsillitis • erosive lichen planus Paranasal sinus disorders Parotid gland: • mumps • sialectasis • cancer • pleomorphic adenoma TMJ dysfunction Temporal arteritis Absent physical signs Atypical facial pain Chronic paroxysmal hemicrania Depression-associated facial pain Facial migraine (lower half headache) Glossopharyngeal neuralgia

A diagnostic approach

Migrainous neuralgia (cluster headache)

A summary of the diagnostic strategy model is presented in TABLE 52.2.

Trigeminal neuralgia (tic douloureux)

Probability diagnosis The commonest cause of facial pain is dental disorders, especially dental caries. Another common cause is sinusitis, particularly maxillary sinusitis.

TMJ dysfunction causing TMJ arthralgia is a very common problem encountered in general practice and it is important to have some simple basic strategies to give the patient.

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Pain in the face: diagnostic strategy model

Q. Probability diagnosis A. Dental pain: • caries • periapical abscess • fractured tooth Maxillary/frontal sinusitis TMJ dysfunction Q. Serious disorders not to be missed A. Cardiovascular: • myocardial ischaemia • aneurysm of cavernous sinus • internal carotid aneurysm • ischaemia of posterior inferior cerebellar artery Neoplasia: • cancer: mouth, sinuses, nasopharynx, tonsils, tongue, larynx • metastases: orbital, base of brain, bone Severe infections: • herpes zoster • erysipelas • periapical abscess → osteomyelitis • acute sinusitis → spreading infection Temporal arteritis

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Q. Pitfalls (often missed) A. TMJ dysfunction Migraine variants: • facial migraine • chronic paroxysmal hemicrania Eye disorders: • glaucoma • iritis • optic neuritis Chronic dental neuralgia Salivary gland: infection, calculus, obstruction, cancer Acute glaucoma (upper face) Cranial nerve neuralgias: • trigeminal neuralgia • glossopharyngeal neuralgia Q. Seven masquerades checklist A. Depression Spinal dysfunction (cervical spondylosis) Q. Is the patient trying to tell me something? A. Quite probably. Atypical facial pain has underlying psychogenic elements.

Red flag pointers for pain in the face • • • • •

Persistent pain: no obvious cause Unexplained weight loss Trigeminal neuralgia: possible serious cause Herpes zoster involving nose Person >60 years: consider temporal arteritis, malignancy

Serious disorders not to be missed It is important not to overlook cancer of various structures, such as the mouth, sinuses, nasopharynx, tonsils, tongue, larynx and parotid gland, which can present with atypical chronic facial pain. It is important therefore to inspect these areas, especially in the elderly, but lesions in the relatively inaccessible nasopharynx can be easily missed. Nasopharynx cancer spreads upwards to the base of the skull early and patients can present with multiple cranial nerve palsies before either pain or bloody nasal discharge.1 Tumours may arise in the bones of the orbit, for example, lymphoma or secondary cancer, and may cause facial pain and proptosis. Similarly, any spaceoccupying lesion or malignancy arising from the region of the orbit or base of the brain can cause facial pain by involvement (often destruction) of trigeminal sensory fibres. This will lead to a depressed ipsilateral corneal reflex. Also, aneurysms developing in the cavernous sinus1 can cause pain via pressure on any of the divisions of the trigeminal nerve, while aneurysms from the internal carotid arising from the origin of the posterior communicating artery can cause pressure on the oculomotor nerve. Temporal arteritis typically causes pain over the temporal area but can cause ischaemic pain in the jaws when chewing.

Pitfalls Commonly overlooked causes of facial pain include TMJ arthralgia and dental disorders, especially of the teeth, which are tender to percussion, and oral ulceration. Diagnosing the uncommon migraine variants, particularly facial migraine and chronic paroxysmal hemicrania, often presents difficulties, including differentiating between the neuralgias. Glossopharyngeal neuralgia, which is rare, causes pain in the back of the throat, around the tonsils and adjacent fauces. The lightning quality of the pain of neuralgia gives the clue to diagnosis.

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Pain in the face Common pitfalls • Failing to refer unusual or undiagnosed causes of facial pain • Overlooking infective dental causes, which can cause complications • Failing to consider the possibility of malignant disease of ‘hidden’ structures in the older patient

Seven masquerades checklist Of these, depression and cervical spinal dysfunction must be considered. The upper cervical spine can cause facial pain from lesions of C2 or C3 via the lesser occipital or greater auricular (see FIG.  52.1) nerves, which may give pain around the ear. It is important to remember that the C2 and C3 nerves share a common pathway with the trigeminal nerve (see CHAPTER 62).

C2

overlap area

C3

Depressive illness can present with a variety of painful syndromes and facial pain is no exception. The features of depression may be apparent and thus antidepressants should be prescribed. Usually the facial pain and the depression subside concomitantly.

Psychogenic considerations Psychogenic factors have to be considered in every painful condition. They are considered to be high in patients with atypical facial pain.

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The clinical approach History Diagnosis of nearly all types of facial pain must be based almost entirely on the history. It is often difficult to delineate the exact nature and distribution of the pain. The history should include the typical analysis of pain, especially noting the site and radiation of the pain.

Examination The patient’s general state and behaviour should be noted. Any sudden jabbing pain in the face causing the characteristic ‘tic’ may indicate neuralgia. Palpate the face and neck to include the parotid glands, eyes, regional lymph nodes and the skin. Inspect the TMJs and cervical spine. Carefully inspect the nose, mouth, pharynx and postnasal space. In particular inspect the teeth, percussing each tooth if dental disorder is suspected. Bimanual palpation of the floor of the mouth is performed to detect induration or submandibular and submental lymph node enlargement. The sinuses, especially the maxillary sinuses, should be inspected and a torch light should be placed inside the mouth to test transillumination of the maxillary sinuses. It works best when one symptomatic side can be compared with an asymptomatic side. Perform a neurological examination on the cranial nerves with special emphasis on the trigeminal, oculomotor and glossopharyngeal nerves.

Investigations

FIGURE 52.1 Dermatomes of C2 and C3, with the overlap area indicated

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If investigations are being contemplated referral may be appropriate. The association of multiple sclerosis and tumours with neuralgias may have to be investigated. Radiological investigations include plain X-rays of the paranasal sinuses, CT scans, MRI and orthopantomograms.

Facial pain in children Apart from trauma, facial pain in children is almost invariably due to dental problems, rarely migraine variants and occasionally childhood infections such as mumps and gingivostomatitis. A serious problem sometimes seen in children is orbital cellulitis secondary to ethmoiditis. Sinusitis occurs in children, especially older children, and it should be suspected with persistent bilateral mucopurulent rhinorrhoea (beyond 10 days).

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Facial pain in the elderly Many of the causes of facial pain have an increased incidence with age, in particular trigeminal neuralgia, herpes zoster, cancer, glaucoma, TMJ dysfunction and cervical spondylosis. Glossopharyngeal neuralgia does not seem to have a particular predilection for the elderly. Xerostomia due to decreased secretions of salivary glands may cause abrasion with minor trauma. It may aggravate the pain of glossitis, which is common in the elderly.

Dental treatment will usually alleviate the problem; however, if severe: amoxycillin 500 mg (o) tds for 5 days If unresponsive: amoxycillin/clavulanate 875/125 mg (o) bd (adjust to children’s dose) add metronidazole 400 mg (o) 12 hourly for 5 days

DENTAL DISORDERS

For patients hypersensitive to penicillin:

Dental caries

clindamycin 300–450 mg (o) 8 hourly for 5 days

Dental caries, impacted teeth, infected tooth sockets and dental roots can cause pain in the maxillary and mandibular regions. Caries with periapical and apical abscess formation produce pain from infection extending around the apex of the tooth into the alveolar bone. Retention of a fractured root may cause unilateral paroxysmal pain. Impacted third molars (wisdom teeth) may be associated with surrounding soft tissue inflammation (pericoronitis), causing pain that may be localised to the mandible or radiate via the auriculotemporal nerve to the ear. Candida albicans, which is an oral commensal, may colonise dentures causing hyperaemia and painful superficial ulceration of the denture-bearing mucosa.

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Tooth abscess, inflamed wisdom tooth or root canal infection4

Features of dental caries • Pain is usually confined to the affected tooth but it may be diffuse. • Pain is almost always aggravated by thermal changes in the mouth: — cold—if dental pulp vital — hot—if dental pulp is necrotic • Pain may be felt in more than one tooth. • Dental pain will not cross the midline. Treatment of dental pain • Arrange urgent dental consultation • Pain relief:3 aspirin 600 mg (o), 4–6 hourly or paracetamol 0.5–1 g (o), 4–6 hourly If pain is severe add: codeine 30 mg (o), 4–6 hourly

Gingivitis and periodontitis Refer to CHAPTER 72.

Alveolar osteitis (dry socket) Refer for specialised toileting. This usually heals naturally in 14 days. Antibiotics are of no proven use (see FIG. 52.2).4

FIGURE 52.2 Dry tooth socket: this is a very painful condition mainly in the lower molars unrelieved by analgesics following a tooth extraction 1–3 days earlier. The socket has few or no blood clots and sensitive bone surfaces covered by a greyish layer of necrotic tissue.

Ludwig angina This is a rapidly swelling cellulitis occurring in both the sublingual and submaxillary spaces without abscess formation, often arising from a root canal infection. It resembles an abscess and should be treated as one. It is potentially life-threatening as it can compromise the airway.

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Pain in the face Management • Culture and sensitivity testing • Specialist consultation • Empirical treatment: amoxycillin 2 g IV, 6 hourly plus metronidazole 500 mg IV, 12 hourly

Pain from paranasal sinuses Infection of the paranasal sinuses may cause localised pain. Localised tenderness and pain may be apparent with frontal or maxillary sinusitis. Sphenoidal or ethmoidal sinusitis causes a constant pain behind the eye or behind the nose, often accompanied by nasal blockage. Chronic infection of the sinuses may be extremely difficult to detect. The commonest organisms are Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Expanding lesions of the sinuses, such as mucocoeles and tumours, cause local swelling and displace the contents of the orbit—upwards for maxillary, laterally for the ethmoids and downwards for the frontal.

Maxillary sinusitis

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Some simple office tests Diagnosing sinus tenderness6 To differentiate sinus tenderness from non-sinus bone tenderness palpation is useful. This is best done by palpating a non-sinus area first and last (see FIG.  52.3), systematically exerting pressure over the temporal bones (T), then the frontal (F), ethmoid (E) and maxillary (M) sinuses, and finally zygomas (Z), or vice versa.

T

T F F

E

F

E

Z

Z M

M

The maxillary sinus is the one most commonly infected.5 It is important to determine whether the sinusitis is caused by stasis following a URTI or acute rhinitis, or due to dental root infection. Most episodes are of viral origin. Clinical features (acute sinusitis) • Facial pain and tenderness (over sinuses) • Toothache • Headache • Purulent postnasal drip • Nasal discharge • Nasal obstruction • Rhinorrhoea • Cough (worse at night) • Prolonged fever • Epistaxis Suspect bacterial cause if high fever and purulent nasal discharge. Clinical features (chronic sinusitis) • Vague facial pain • Offensive postnasal drip • Nasal obstruction • Toothache

FIGURE 52.3 Diagnosing sinus tenderness: T (temporal) and Z (zygoma) represent no sinus bony tenderness, for purposes of comparison

Differential tenderness both identifies and localises the main sites of infection (see FIG. 52.3). Diagnosing unilateral sinusitis A simple way to assess the presence or absence of fluid in the frontal sinus, and in the maxillary sinus (in particular), is the use of transillumination. It works best when one symptomatic side can be compared with an asymptomatic side. It is necessary to have the patient in a darkened room and to use a small, narrow-beam torch. For the maxillary sinuses remove dentures (if any). Shine the light inside the mouth (with lips sealed), on either

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side of the hard palate, pointed at the base of the orbit. A dull glow seen below the orbit indicates that the antrum is air-filled. Diminished illumination on the symptomatic side indicates sinusitis. A CT scan may show mucosal thickening without fluid levels. Plain films are not indicated. Management (acute bacterial sinusitis)

Principles • • • •

Exclude dental root infection. Control predisposing factors. Use appropriate antibiotic therapy. Establish drainage by stimulation of mucociliary flow and relief of obstruction.

Guidelines for antibiotic therapy Consider therapy for severe cases displaying at least three of the following: • persistent mucopurulent nasal discharge (>7–10 days) • facial pain • poor response to decongestants • tenderness over the sinuses especially maxillary • tenderness on percussion of maxillary molar and premolar teeth that cannot be attributed to by a single tooth

Measures

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• Analgesics • Antibiotics:4 amoxycillin 500 mg (o) tds for 7 days or (if sensitive to penicillin) doxycycline 100 mg (o) bd for 7 days or cefaclor 500 mg (o) tds for 7 days or amoxycillin + clavulanate 875/125 mg (o) tds for 7–14 days if poor response to above (indicates resistant H. influenzae) • In complicated or severe disease, use intravenous cephalosporins or flucloxacillin • Nasal decongestants (oxymetazoline-containing nasal drops or sprays)5 for 5–10 days only if congestion • Inhalations (a very important adjunct) • Nasal saline irrigation

Inhalations for sinusitis The old method of towel over the head and inhalation bowl can be used, but it is better to direct the vapour at the nose. Equipment needed is a container, which can be an old disposable bowl, a wide-mouthed bottle or tin, or a plastic container. For the inhalant, several household over-thecounter preparations are suitable such as Friar’s Balsam (5 mL), Vicks VapoRub (1 teaspoon), or menthol (5 mL). The cover can be made from a paper bag (with its base cut out), a cone of paper or a small cardboard carton (with the corner cut away).

Method 1 Add 5 mL or 1 teaspoon of the inhalant to 0.5 L (or 1 pint) of boiled water in the container. 2 Place the paper or carton over the container. 3 Get the patient to apply nose and mouth to the opening and breathe in the vapour deeply and slowly through the nose, and then out slowly through the mouth. 4 This should be performed for 5–10 minutes, three times a day, especially before retiring. After inhalation, upper airway congestion can be relieved by autoinsufflation.

Chronic sinusitis Chronic sinusitis or recurrent sinusitis may arise from chronic infection or allergy. It may be associated with nasal polyps and vasomotor rhinitis, but is frequently associated with a structural abnormality of the upper airways. Refer to CHAPTER 59. It does not usually cause pain unless an acute infection intervenes. The acute or chronic attack is treated as for the acute attack but with 14 days of antibiotics. Those with an allergic mucous membrane may respond to intranasal corticosteroids. Surgical intervention will benefit chronic recurrence with mechanical blockage.

TMJ dysfunction

Antihistamines and mucolytics are of no proven value.

This condition is due to abnormal movement of the mandible, especially during chewing. The basic cause is dental malocclusion. The pain is felt over the joint and tends to be localised to the region of the ear and mandibular condyle but may radiate forwards to the cheek and even the neck.

Invasive methods Surgical drainage may be necessary by atrial lavage or frontal sinus trephine.

Examination • Check for pain and limitation of mandibular movements, especially on opening the mouth.

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Pain in the face • Palpate about the joint bilaterally for tenderness, which typically lies immediately in front of the external auditory meatus; palpate the temporalis and masseter muscles. • Palpate the TMJ over the lateral aspect of the joint disc. • Ask the patient to open the mouth fully when tenderness is maximal. The TMJ can be palpated posteriorly by inserting the little finger into the external canal. • Check for crepitus in mandibular movement. Treatment If organic disease such as rheumatoid arthritis and obvious dental malocclusion is excluded, a special set of instructions or exercises can alleviate the annoying problem of TMJ arthralgia in about 3 weeks.

Method 1: ‘Chewing’ the piece of soft wood • Obtain a rod of soft wood approximately 15 cm long and 1.5 cm wide. An ideal object is a large carpenter’s pencil. • Instruct the patient to position this at the back of the mouth so that the molars grasp the object with the mandible thrust forward. • The patient then rhythmically bites on the object with a grinding movement for 2–3 minutes at least 3 times a day.

Method 2: The ‘six by six’ program This is a specific program recommended by some dental surgeons. The six exercises should be carried out six times on each occasion, six times a day, taking about 1–2 minutes. Instruct the patient as follows: 1 Hold the front one-third of your tongue to the roof of your mouth and take six deep breaths. 2 Hold the tongue to the roof of your mouth and open your mouth six times. Your jaw should not click. 3 Hold your chin with both hands keeping the chin still. Without letting your chin move, push up, down and to each side. Remember, do not let your chin move. 4 Hold both hands behind your neck and pull chin in. 5 Push on upper lip so as to push head straight back. 6 Pull shoulders back as if to touch shoulder blades together. These exercises should be pain-free. If they hurt, do not push them to the limit until pain eases.

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Treatments Injection into the TMJ7 • Indications: painful rheumatoid arthritis, osteoarthritis or TMJ dysfunction not responding to conservative measures. Inject a 1 mL solution of local anaesthetic and corticosteroid in equal parts. • Dental management that may be required for malfunction of the bite includes dental occlusal splinting. • NSAIDs: A trial of NSAIDs, e.g. ibuprofen 400 mg (o) tds for 10 days, for TMJ inflammation may need consideration. Cease if no response after 10 days.

Inflammatory or ulcerative oropharyngeal lesions A variety of ulcerative conditions and infections of structures such as gingivae, tongue, tonsils, larynx and pharynx can cause facial pain (refer to CHAPTER 72). Gingivostomatitis, herpes labialis (cold sores) and aphthous ulceration are common examples. Lesions of the posterior third of the tongue, the oropharynx, tonsils and larynx may radiate to the region of the ear via the tympanic branch of the ninth nerve or the auricular branch of the tenth nerve.

Trigeminal neuralgia Trigeminal neuralgia (tic douloureux) is a condition of often unknown cause that typically occurs in patients over the age of 50, affecting the second and third divisions of the trigeminal nerve and on the same side of the face. Brief paroxysms of pain, often with associated trigger points, are a feature. Clinical features • Site: sensory branches of the trigeminal nerve (see FIG. 52.4) almost always unilateral (often right side) • Radiation: tends to commence in the mandibular division and spreads to the maxillary division and (rarely) to the ophthalmic division • Quality: excruciating, searing jabs of pain like a burning knife or electric shock • Frequency: variable and no regular pattern • Duration: seconds to 1–2 minutes (up to 15 minutes) • Onset: spontaneous or trigger point stimulus • Offset: spontaneous • Precipitating factors: talking, chewing, touching trigger areas on face (e.g. washing, shaving, eating), cold weather or wind, turning onto pillow

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trigeminal ganglion

opthalmic nerve

maxillary nerve V1

V2

V3

mandibular nerve

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FIGURE 52.4 Typical cutaneous sensory distribution of the trigeminal nerve and its branches

FIGURE 52.5 Trigeminal neuralgia: typical trigger points

• Aggravating factors: trigger points usually in the upper and lower lip, nasolabial fold or lower eyelid (see FIG. 52.5) • Relieving factors: nil • Associated features: rarely occurs at night; spontaneous remissions for months or years • Signs: there are no signs, normal corneal reflex

Alternative drugs if carbamazepine not tolerated or ineffective (but question the diagnosis if lack of response):

Causes • Unknown • Local pressure on the nerve root entry zone by tortuous pulsatile dilated small vessels (probably up to 75%) • Multiple sclerosis • Neurosyphilis • Tumours of the posterior fossa Note: Precise diagnosis is essential. MRI may be helpful. Treatment • Patient education, reassurance and empathic support is very important in these patients.

Medical therapy carbamazepine (from onset of the attack to resolution)8 50 mg (elderly patient) or 100 mg (o) bd initially; gradually increase the dose to avoid drowsiness every 7 days to 200 mg bd (maintenance); higher dosage to maximum 600 mg bd may be necessary

gabapentin 300 mg daily initially, then increase lamotrigine 400 mg (o) daily phenytoin 300–500 mg daily clonazepam baclofen sodium valproate

Surgery • Refer to a neurosurgeon if medication ineffective • Possible procedures include: — decompression of the trigeminal nerve root (e.g. gel foam packing between the nerve and blood vessels) — if severe, refer for neuroblative treatment, e.g. thermocoagulation/radiofrequency neurolysis — surgical division of peripheral branches

Glossopharyngeal neuralgia8,9 This is an uncommon condition of the ninth cranial nerve and branches of the vagus nerve with similar clinical features of severe, lancinating pains, particularly felt in one ear, the base of the tongue or beneath the angle of the jaw. The pain usually lasts 30–60 seconds. • Sites: back of throat around tonsillar fossa and adjacent fauces deep in ear

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Pain in the face • Radiation: ear canal, neck • Triggers: swallowing, coughing, talking, yawning, laughing • Treatment: as for trigeminal neuralgia

Migrainous neuralgia (cluster headache) As described in CHAPTER 56, the pain is unilateral and centred around the eye with associated lacrimation and stuffiness of the nose.

Facial migraine (lower half headache)8 Migraine may rarely affect the face below the level of the eyes, causing pain in the area of the cheek and upper jaw. It may spread over the nostril and lower jaw. The pain is dull and throbbing, and nausea and vomiting are commonly present. The treatment is as for other varieties of migraine with simple analgesics or ergotamine for infrequent attacks.

Chronic paroxysmal hemicrania In the rare condition of chronic or episodic paroxysmal hemicrania there is a unilateral facial pain that can resemble chronic cluster headache but the duration is briefer, about 15 minutes, and it may recur many times a day even for years. It responds dramatically to indomethacin.10

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Treatment Trial of an antidepressant8, e.g.: amitriptyline 10–75 mg nocte or dothiepin 25–150 mg nocte or carbamazepine

Temporal arteritis This may produce mild or severe unilateral or bilateral headache. There may be ischaemic pain in the jaws when chewing. There may be marked scalp tenderness over the affected arteries. See CHAPTER 32 for management.

Erysipelas Classical erysipelas is a superficial form of cellulitis involving the face. It usually presents with the sudden onset of butterfly erythema with a welldefined edge (see FIG.  52.6). It often starts around the nose and there may be underlying sinus or dental infection which should be investigated. There is an associated ‘flu like’ illness and fever. It is invariably caused by Streptococcus pyogenes. Treatment is by phenoxymethylpenicillin or di/flucloxacillin for 7–10 days.

Herpes zoster and postherpetic neuralgia Refer to CHAPTER 123. Herpes zoster may present as hyperaesthesia or a burning sensation in any division of the fifth nerve, especially the ophthalmic division.

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Atypical facial pain This is mainly a diagnosis of exclusion whereby patients, usually middle-aged to elderly women, complain of diffuse pain in the cheek (unilateral or bilateral) without demonstrable organic disease. The pain does not usually conform to a specific nerve distribution (although in the maxillary area), varies in intensity and duration and is not lancinating as in trigeminal neuralgia. It is usually described as deepseated and ‘boring’, severe, continuous and throbbing in nature. It is a very confusing and difficult problem to treat. These patients tend to show psychoneurotic tendencies but caution is needed in labelling them as functional.

FIGURE 52.6 Erysipelas: typical spreading distribution of the infection

When to refer • Severe trigeminal neuralgia • Unusual facial pain, especially with a suspicion of malignancy • Positive neurological signs, such as impaired corneal reflex, impaired sensation in a trigeminal dermatome, slight facial weakness, hearing loss on the side of the neuralgia

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• Possible need for surgical drainage of sinusitis— indications for surgery include failure of appropriate medical treatment, anatomical deformity, polyps, uncontrolled sinus pain5 • Dental root infection causing maxillary sinusitis • Other dental disorders

Practice tips • •

• •

Malignancy must be excluded in the elderly with facial pain. Problems from the molar teeth, especially the third (wisdom), commonly present with periauricular pain without aural disease and pain in the posterior cheek. Facial pain never crosses the midline; bilateral pain means bilateral lesions. If no obvious cause of persistent pain, refer to exclude sinister cause: don’t overdiagnosis sinusitis.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Sinusitis • Temporomandibular joint dysfunction

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References 1 Beck ER, Francis JL, Souhami RL. Tutorials in Differential Diagnosis. Edinburgh: Longman Cheshire, 1987: 161–4. 2 Gerschman JA, Reade PC. Orofacial pain. Aust Fam Physician, 1984; 13: 14–24. 3 Mashford ML (Chair). Therapeutic Guidelines: Analgesic (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2002: 298–300. 4 Spicer J (Chair). Therapeutic Guidelines: Antibiotic (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2006: 167–243. 5 Stevens M. The diagnosis and management of acute and chronic sinusitis. Modern Medicine Australia, 1991; April: 16–26. 6 Bridges-Webb C. Diagnosing sinus tenderness: practice tip. Aust Fam Physician, 1981; 10: 742. 7 Murtagh J. Practice Tips (6th edn). Sydney: McGraw-Hill, 2013: 139–40. 8 Moulds R (Chair). Therapeutic Guidelines: Neurology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2011: 69–72. 9 Mendelsohn M, Lance J, Wheatley D. Facial pain: how to treat. Australian Doctor, 7 November; 2003: 31–6. 10 Burns R. Pitfalls in headache management. Aust Fam Physician, 1990; 19: 1825.

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Why! the fever itself is nature’s instrument. Thomas Sydenham (–), Medical Observations Although fever is a sign of disease and usually occurs in response to infection (mainly viral), its presence is recognised as playing an important role in the individual’s defence against infection. The infecting pathogen triggers hypothalamic receptors, causing the thermostatic mechanisms to be reset to maintain core temperature at a higher level. The elevation in temperature results from increased heat production (e.g. shivering) or decreased loss (e.g. peripheral vasoconstriction). The elevation in body temperature activates T-cell production, increases the effectiveness of interferons and limits the replication of some common viruses.1

•

• •

Key facts and checkpoints • • •

• • •

•

• • • • •

Fever plays an important physiological role in the defence against infection. Normal body temperature (measured orally midmorning) is 36–37.2°C (average 36.8°C). Fever can be defined as an early morning oral temperature >37.2°C or a temperature >37.8°C at other times of day.2 Oral temperature is about 0.4°C lower than core body temperature. Axillary temperature is 0.5°C lower than oral temperature. Rectal, vaginal and ear drum temperatures are 0.5°C higher than oral and reflect core body temperature. There can be a normal diurnal variation of 0.5–1°C (lowest in early morning and highest in late afternoon). Fevers due to infections have an upper limit of 40.5–41.1°C (105–106°F). Hyperthermia (temperature above 41.1°C) and hyperpyrexia appear to have no upper limit. Infection remains the most important cause of acute fever.3 Symptoms associated with fever include sweats, chills, rigors and headache. General causes of fever include infections, malignant disease, mechanical trauma (e.g. crush

•

•

•

injury), vascular accidents (e.g. infarction, cerebral haemorrhage), immunogenic disorders (e.g. drug reactions, SLE), acute metabolic disorders (e.g. gout), and haemopoietic disorders (e.g. acute haemolytic anaemia).3 Drugs can cause fever, presumably because of hypersensitivity.3 Important examples are allopurinol, antihistamines, barbiturates, cephalosporins, cimetidine, methyldopa, penicillins, isoniazid, quinidine, phenolphthalein (including laxatives), phenytoin, procainamide, salicylates and sulphonamides. Drug fever should abate by 48 hours after discontinuation of the drug.4 Infectious diseases at the extremes of age (very young and aged)3 often present with atypical symptoms and signs. Their condition may deteriorate rapidly. Overseas travellers or visitors may have special, even exotic infections and require special evaluation (refer to CHAPTER 15). Immunologically compromised patients (e.g. AIDS patients) pose a special risk for infections, including opportunistic infections. A febrile illness is characteristic of the acute infection of HIV: at least 50% have an illness like glandular fever. Think of it!

Chills/rigors2 The abrupt onset of fever with a chill or rigor is a feature of some diseases. Examples include: • bacteraemia/septicaemia • pneumococcal pneumonia • pyogenic infection with bacteraemia • lymphoma • pyelonephritis • visceral abscesses (e.g. perinephric, lung) • malaria • biliary sepsis (Charcot triad—jaundice, right hypochrondial pain, fever/rigors) Features of a true chill are teeth chattering and bed shaking, which is quite different from the chilly

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sensations that occur in almost all fevers, particularly those in viral infections. The event lasts 10–20 minutes. Other features: • shaking cannot be stopped voluntarily • absence of sweating • cold extremities and pallor (peripheral vascular shutdown) • dry mouth and pilo-erection: lasts 10–20 minutes

Hyperthermia Hyperthermia or hyperpyrexia is a temperature greater than 41.1°C (106°F). A more accurate definition is a state when the body’s metabolic heat production or environmental heat load exceeds normal heat loss capacity. Hyperthermia may be observed particularly in the tropics, in malaria and heatstroke. It can occur with CNS tumours, infections or haemorrhages because of its effect on the hypothalamus.

Heatstroke (sunstroke, thermic fever)5 This is the sudden onset of hot, dry, flushed skin with a rapid pulse, temperature above 40°C, and confusion or altered conscious state in a person exposed to a very hot environment. The BP is usually not affected initially but circulatory collapse may precede death. It is a life-threatening emergency. The diagnosis is clinical. Differential diagnoses include severe acute infection, toxic shock, food, chemical and drug poisoning. The elderly and debilitated are susceptible as are children left in cars.

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Treatment • Immediate effective cooling water applied to skin • Icepacks at critical points (e.g. axillae, neck, head) • Ice water bath if possible • Aim to bring down temperature by 1°C every 10 minutes

Malignant hyperthermia This is a rare hereditary disorder characterised by rapidly developing hyperpyrexia, muscular rigidity and acidosis in patients undergoing major surgery.

Sweats Sweating is a heat loss mechanism, and diffuse sweating that may soak clothing and bedclothing permits rapid release of heat by evaporation. In

febrile patients the skin is usually hot and dry— sweating occurs in most when the temperature falls. It is characteristic of only some fevers (e.g. septic infections and rheumatic fever).

Factitious fever Factitious fever is usually encountered in hospitalised patients attempting to malinger. The situation is usually suspected when: • a series of high temperatures is recorded to form an atypical pattern of fluctuation • there is excessively high temperature (41.1°C) and above • a recorded high temperature is unaccompanied by warm skin, tachycardia and other signs of fever such as a flushed face and sweating • there is an absence of diurnal variation The patient may have surreptitiously dipped the thermometer in warm water, placed it in contact with a heat source or heated the bulb by friction with bedclothes or even mucous membranes of the mouth.

Neuroleptic malignant syndrome This is often confused with ‘malignant’ hyperthermia and heat stroke. The syndrome includes high temperature, muscle rigidity, autonomic dysfunction and altered consciousness. It is a rare and potentially lethal reaction in patients taking antipsychotic drugs, particularly occurring with haloperidol alone or with other drugs especially lithium carbonate. Refer to CHAPTER 45.

Measurement of temperature Temperature can be measured by several methods, including the mercury thermometer, the liquid crystal thermometer and the electronic probe thermometer. The mercury thermometer, however, is probably still the most widely used and effective temperaturemeasuring instrument.

Basic rules of usage 1 Before use, shake down to 35–36°C. 2 After use: — shake down and store in antiseptic — do not run under hot water — wipe rectal thermometer with alcohol and store separately 3 Recording time is 3 minutes orally and 1–2 minutes rectally.

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Fever and chills Oral use 1 Place under the tongue at the junction of the base of the tongue and the floor of the mouth to one side of the frenulum—the ‘heat’ pocket. 2 Ensure that the mouth is kept shut. 3 Remove dentures. Note: This is unsuitable for children 4 years and under, especially if irritable. Rectal use This is an appropriate route for babies and young children under the age of 4 years but should be used with care. The rule is ‘3 cm in for 3 minutes’ and some authorities claim that this method is the gold standard, especially in infants.

Method 1 Lubricate the stub with petroleum or KY jelly. 2 Insert for 3 cm past anal verge. 3 Keep the thermometer between the flexed fingers with the hand resting on the buttocks (see FIG. 53.1).

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Groin use This route is not ideal but is more reliable than the axilla. It closely approximates oral temperature. In infants, the thigh should be flexed against the abdomen. Vaginal use This is mainly used as an adjunct to the assessment of ovulation during the menstrual cycle. It should be placed deeply in the vagina for 5 minutes before leaving bed in the morning. Infrared eardrum use Otic thermography is now accepted standard practice. The tympanic membrane (TM) accurately reflects hypothalamic temperature, which in turn reflects core body temperature. The TM is also immune from the effects of eating, drinking and smoking. A systematic review in the Cochrane study describes the tympanic temperature as being inaccurate and unreliable.8 However, some Australian authorities believe that in general practice the benefits of convenience outweigh lack of accuracy.9 The normal range is the same as for rectal temperature. Skin use Plastic strip thermometers placed on the forehead are very inaccurate and should not be used.

Accidental breakage in the mouth If children bite off the end of a mercury thermometer there is no need for alarm, as the small amount of mercury is non-toxic and the piece of glass will usually pass in the stool.

The clinical approach

FIGURE 53.1 Rectal temperature measurement in infants

Don’t: • dig thermometer in too hard • hold it too rigidly • allow the child to move around Axillary use This is unreliable with poor sensitivity and generally should be avoided but may be practical in young children.6,7 If used, place high in the axilla for 3 minutes. Fever is present if the temperature is above 37.2°C.

The initial approach is to evaluate the severity of the problem and the nature of the illness. Some infections, particularly bacterial infections, are lifethreatening and this requires urgent diagnosis and hospital admission. According to Yung and Stanley3 it is helpful to consider fever in three categories: less than 3 days duration; between 4 and 14 days duration; and protracted fever (more than 14 days).

Fever of less than 3 days duration This is very commonly encountered in family practice, often due to a self-limiting viral infection of the respiratory tract. It is important, however, to be vigilant for other infections, so evidence of an infectious disease, urinary tract infection, pneumonia

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or other infection should be sought. A routine urine examination, especially in females, is an important screening investigation. The majority of patients can be managed conservatively.

Fever present for 4 to 14 days If fever persists beyond 4–5 days a less common infection should be suspected since most common viral infections will have resolved by about 4 days.3 A checklist of causes is presented in TABLE 53.1. The careful history is mandatory, as outlined later in the chapter for fever of unknown origin (FUO). The basic examination and investigations are along similar lines. Table 53.1

Common causes of fever of 4–14 days duration

Influenza Sinusitis Epstein–Barr mononucleosis (EBM) Enteroviral infection Infective endocarditis Dental infections Hepatobiliary infections: hepatitis, cholecystitis, empyema of gall bladder Abscess Pelvic inflammatory disease Cytomegalovirus infection Lyme disease Travel-acquired infection: typhoid, dengue, hepatitis, malaria, amoebiasis Zoonosis: brucellosis, Q fever, leptospirosis, psittacosis Drug fever

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Temperature chart Charting the patterns of fever may be a diagnostic help because some febrile conditions follow a predictable temperature pattern.10 Examples are presented in FIGURE 53.2. Intermittent fever This is a fever in which the temperature rises for a few hours each day and then returns to normal (see FIG.  53.2a). Examples include various pyogenic infections, cytomegalovirus and lymphoma. Relapsing fever The fever returns to normal for days before rising again. Malaria is the classic example of periodic

relapsing fever: in quartan fever, caused by Plasmodium malariae (see FIG.  53.2a), the attacks occur every 72 hours (the term quartan means every 4th day by inclusive counting). This compares with tertian fever from Plasmodium vivax in which paroxysms of malaria occur every 48 hours. Remittent fever This is a fever in which the temperature returns towards normal for a variable period but is always elevated (see FIG.  53.2d). Common examples are collections of pus (e.g. pelvic abscess, wound infection, empyema and carcinoma). It is a common feature of empyema. Undulant fever Undulant fever is characterised by bouts of continuous or remittent fever for several days, followed by afebrile remissions lasting a variable number of days. It is commonly a feature of brucellosis infection but is also seen in the lymphomas, especially Hodgkin lymphoma (see FIG.  53.2b). The latter is referred to as Pel–Ebstein fever with fevers lasting 3 to 10 days followed by afebrile periods of 3 to 10 days. Continuous fever pattern This is common with viral infections such as influenza (see FIG. 53.2c). Quotidian fever In this pattern the fever recurs daily (see FIG. 53.2d). Daily fever spikes in the morning are characteristic of Pseudomonas infection (e.g. pulmonary superinfection); afternoon spikes are indicative of cytomegalovirus infection; and evening spikes suggest localised collection of pus (e.g. empyema of the gall bladder). Double quotidian fever (two fever spikes in a day) is caused by adult Still syndrome, gonococcal endocarditis and visceral leishmaniasis. If risk factors are present, especially if taking antibiotics, consider the investigations outlined in TABLE 96.1, in CHAPTER 96. Postoperative fever This is fever occurring within 24 hours after surgery— common with abdominal surgery. Causes to consider: • • • • •

pulmonary atelectasis (common) wound haematoma deep venous thrombosis myocardial infarction allergic drug reaction

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(a)

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39 38 37

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2

3

4

5

6

7

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10 11 12 13 14 15 16 17 18 19 20 21

Periodic relapsing fever: quartan fever of malaria (a 4-day pattern with fever peaks every third day)

(b)

39 38 37

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10 11 12 13 14 15 16 17 18 19 20 21

Undulant fever: due to lymphoma

(c)

39 38 37

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Continuous pattern

(d)

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10 11 12 13 14 15 16 17 18 19 20

Quotidian fever pattern and intermittent fever (e.g. empyema of gall bladder)

FIGURE 53.2 Examples of fever patterns from temperature charts

21

Days

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Septic problems related to the operation usually develop after several days.

Fever in children In children, most authorities would consider a fever of 38.5°C and above to be significant and warrant close scrutiny.11 The fever is usually a response to a viral infection. Fever itself is not harmful until it reaches a level of 41.5°C.1 Hyperthermia is uncommon in children. Temperatures above 41°C are usually due to CNS infection or the result of human error, for example:

Febrile convulsions Refer to CHAPTER 96.

• shutting a child in a car on a hot day • overwrapping a febrile child

Fever in the elderly

Complications include dehydration (usually mild) and febrile convulsions, which occur in 5% of febrile children between 6 months and 5 years. Febrile convulsions are triggered by a rapid rise in temperature rather than its absolute level. Note: Teething does not cause fever.

The elderly tend to have a problem with impaired thermoregulation and so they may not develop a fever in response to suppurative infection compared with younger people. This can be misleading in the diagnostic process.

Approach to the febrile infant It is important to decide whether the child looks well or seriously ill. Identification of the very ill child is presented in CHAPTER 96. If the child is well and has no risk factors (e.g. unreliable caregiver, poor access to treatment, medical risk factors, taking antibiotics) treat expectantly. The only test required is urine microscopy and culture. Educate the caregiver about review if serious signs develop. Treat the fever as outlined in TABLE 96.1, in CHAPTER 96.

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Advice to parents • Dress the child in light clothing (stripping off is unnecessary). • Do not overheat with too many clothes, rugs or blankets. • Give frequent small drinks of light fluids, especially water. • Sponging with cool water and using fans is not effective.

Management • Treatment of low-grade fevers should be discouraged. • Treatment of high-grade fevers includes: — treatment of the causes of the fever (if appropriate) — adequate fluid intake/increased fluids — paracetamol (acetaminophen) is the preferred antipyretic since aspirin is potentially dangerous in young children (use if temperature >38.5°C). The usual dose of 10–15 mg/kg every 4–6 hours may represent undertreatment. Use 20 mg/kg as a loading dose and then 15 mg/kg maintenance — evidence favours tepid sponging for first 30 minutes combined with paracetamol12 — ibuprofen 5–10 mg/kg every 6 hours is a suitable antipyretic

Important facts • Any fever in the elderly is significant. • Viral infection is a less common cause of fever in the elderly. • Fever in the elderly is sepsis until proven otherwise (common sites are the lungs and urinary tract). The elderly are more vulnerable to hyperthermia and hypothermia. Heatstroke classically occurs in epidemic form during a heatwave. The syndrome consists of hyperpyrexia, decreased sweating, delirium and coma. The core temperature is usually over 41°C.

‘Alarm bell’ signs In many patients the existence of a life-threatening infective illness is obvious and prompt action is essential. In others the diagnosis is not clear-cut but there are certain warning signs (see Red flags box). These ‘red flag’ symptoms and signs are obviously super ‘sensitive’. Patients with some of these features may have potentially life-threatening diseases, but this list would include many with viral infections.

Fever of undetermined origin Fever of undetermined origin (FUO), also referred to as pyrexia of unknown origin (PUO), has the following criteria:13 • illness for at least 3 weeks • fevers >38.3°C (100.9°F) • undiagnosed after 1 week of intensive study

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Fever and chills

Red flag pointers for fever • • • • • • • • • • • • •

High fever Repeated rigors Drenching night sweats Severe myalgia (? sepsis) Severe pain anywhere (? sepsis) Severe sore throat or dysphagia (? Haemophilus influenzae epiglottitis) Altered mental state Incessant vomiting Unexplained rash Jaundice Marked pallor Tachycardia Tachypnoea

Most cases represent unusual manifestations of common diseases and not rare or exotic diseases. Examples are tuberculosis, bacterial endocarditis, hepatobiliary disease and lung cancer.14 Keep in mind that the longer the duration of fever, the less likely the diagnosis is to be infectious—fevers that last greater than 6 months are rarely infectious (only 6%). One study showed that 9% are factitious.15 Patients with FUO in definite need of further investigation are: • • • • • •

babies 40°C adults >50 years diabetics the immunocompromised travellers

A diagnostic approach A knowledge of the more common causes of FUO is helpful in planning a diagnostic approach (refer to TABLE 53.2). History The history should include consideration of past history, occupation, travel history, sexual history, IV drug use (leads to endocarditis and abscesses), animal contact, medication and other relevant factors. Symptoms such as pruritus, a skin rash and fever patterns may provide clues for the diagnosis. The average patient with a difficult FUO needs to have a careful history taken on at least three separate occasions.16 Examination A common mistake is the tendency to examine the patient only once and not re-examine. The patient

Table 53.2

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Common causes of FUO

Common examples of each group selected Infection (up to 40%) Bacteria: • pyogenic abscess (e.g. liver, pelvic) • urinary infection • biliary infection (e.g. cholangitis) • chronic septicaemia • infective endocarditis • Lyme disease • tuberculosis • brucellosis • osteomyelitis • typhoid/paratyphoid fever Viral, rickettsial, Chlamydia: • Epstein–Barr mononucleosis • cytomegalovirus • HIV virus infection (primary HIV, AIDS, ARC) • Q fever • psittacosis Parasitic: • malaria • toxoplasmosis • amoebiasis Malignancy (up to 30%) Reticuloendothelial: • leukaemia • lymphomas Solid (localised) tumours: • kidney • liver • pancreas • stomach • lung • sarcoma Disseminated Immunogenic (up to 20%) Drug fever Connective tissue diseases/vasculitides: • rheumatic fever • rheumatoid arthritis • SLE • polyarteritis nodosa/Wegener granulomatosis • giant cell arteritis/polymyalgia rheumatica Sarcoidosis Inflammatory bowel disease (e.g. Crohn) Factitious (1–5%) Hyperthyroidism (0.5–1%) Remain unknown (5–25%) Source: After Kumar and Clark16,17

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should be examined regularly (as for history taking) as physical signs can develop eventually. HIV infection must be excluded. Special attention should be paid to the following (see FIG. 53.3):

• • • •

• • • • •

Investigations Basic investigations include:

skin—look for rashes, vesicles and nodules the eyes and ocular fundi temporal arteries sinuses teeth and oral cavity—? dental abscess, other signs • heart—murmurs, pericardial rubs • lungs—abnormalities including consolidation, pleuritic rub • abdomen—enlarged/tender liver, spleen or kidney

• • • • • • •

rectal and pelvic examination (note genitalia) lymph nodes, especially cervical (supraclavicular) blood vessels, especially of the legs—? thrombosis urine (analysis)

haemoglobin, red cell indices and blood film white cell count ESR/C-reactive protein chest X-ray and sinus films urine examination (analysis and culture) routine blood chemistry blood cultures

Factitious fever Drugs

Lung abscess TB sarcoidosis carcinoma Pyogenic abscess lung subphrenic liver perinephric empyema gall bladder Malignancy liver kidney stomach pancreas lymphoma leukaemia

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FIGURE 53.3 Sites to consider in FUO (malignancy is indicated by a star)

Sinus chronic sinusitis Wegener granulomatosis Dental abscess Lymphadenopathy lymphoma leukaemia HIV infection sarcoidosis EBM Heart infective endocarditis pericarditis Splenomegaly myeloproliferative disorder bacterial endocarditis

Perianal lesions sepsis Crohn disease

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Fever and chills Further possible investigations: • stool microscopy and culture • culture of sputum (if any) • specific tests for malaria, typhoid, EBM, Q fever, brucellosis, psittacosis, cytomegalovirus, toxoplasmosis, syphilis, various tropical diseases and others • NAAT (e.g. PCR) tests • HIV screening • tests for rheumatic fever • tuberculin test • tests for connective tissue disorders (e.g. DNA antibodies, C-reactive protein) • upper GIT series with small bowel follow-through • CT and ultrasound scanning for primary and secondary neoplasia: — gall bladder functioning — occult abscesses • MRI—best for detecting lesions of the nervous system • echocardiography—for suspected endocarditis • isotope scanning for specific causes • aspiration or needle biopsy • laparoscopy for suspected pelvic infection • tissue biopsies (e.g. lymph nodes, skin, liver, bone marrow) as indicated

FUO in children Fever in children is usually a transient phenomenon and subsides within 4–5 days. At least 70% of all infections are viral. Occasionally a child will present with FUO which may be masked from antibiotic administration. Common causes of prolonged fever in children differ from those in adults. Most cases are not due to unusual or esoteric disorders,18 the majority representing atypical manifestation of common diseases. A summary of the common causes (with the most common ranked first) is as follows.18 Infectious causes (40%) • Viral syndrome • Urinary tract infection • Pneumonia • Pharyngitis • Sinusitis • Meningitis Collagen–vascular disorders (15%) • Rheumatic arthritis • Systemic lupus erythematosus

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• Rheumatic fever • Henoch–Schönlein syndrome Neoplastic disorders (7%) • Leukaemia • Reticulum cell sarcoma • Lymphoma Inflammatory diseases of the bowel (4%)

Septicaemia The diagnosis of septicaemia can be easily missed, especially in small children, the elderly and the immunocompromised, and in the absence of classic signs, which are: • • • • •

fever rash (suggestive of meningococcus) tachycardia tachypnoea cool extremities

Patients with septicaemia require urgent referral as it has a very high mortality rate. Investigations should include two sets of blood cultures and other appropriate cultures (e.g. urine, wound, sputum). Empirical initial treatment (after blood cultures) is di/flucloxacillin 2 g IV 1 gentamicin 4–6 mg/kg IV (statim).19

Glossary of terms Bacteraemia The transient presence of bacteria in the blood (usually asymptomatic) caused by local infection or trauma. Septicaemia (sepsis) The multiplication of bacteria or fungi in the blood, usually causing a systemic inflammatory response (SIRS). SIRS is defined as 2 or more of (in adults): • • • •

temperature >38°C or 20/min heart rate >90/min WCC >12 × 109/L or 50 years Post head injury

Inspect the head, temporal arteries and eyes. Areas to palpate include the temporal arteries, the facial and neck muscles, the cervical spine and sinuses, the teeth and temporomandibular joints. Search especially for signs of meningeal irritation and papilloedema. A mental state examination is mandatory and includes looking for altered consciousness or cognition and assessment of mood, anxiety–tension–depression, and any mental changes. Neurological examination includes assessment of visual fields and acuity, reactions of the pupils and eye movements in addition to sensation and motor power in the face and limbs and reflexes, including the plantar response. ‘Red flag’ pointers from physical examination are given in the box.

Special signs • Upper cervical pain sign. Palpate over the C2 and C3 areas of the cervical spine, especially two finger breadths out from the spinous process of C2. If this is very tender and even provokes the headache it indicates headache of cervical origin. • Ewing sign for frontal sinusitis. Press your finger gently upwards and inwards against the orbital roof medial to the supra-orbital nerve. Pain on pressure is a positive finding and indicates frontal sinusitis. • The invisible pillow sign. The patient lies on the examination table with head on a pillow. The examiner then supports the head with his or her hands as the pillow is removed. The patient is instructed to relax the neck muscles and the examiner removes the supporting hands. A positive test indicating tension from contracting neck muscles is when the patient’s head does not readily change position. This is uncommon.

Investigations Investigations can be selected from: • • • •

haemoglobin ? anaemia WCC: leucocytosis with bacterial infection ESR/CRP: ? temporal arteritis radiography: — chest X-ray, if suspected intracerebral malignancy — cervical spine — skull X-ray, if suspected brain tumour, Paget disease, deposits in skull — sinus X-ray, if suspected sinusitis — CT scan: detection of brain tumour (most effective), cerebrovascular accidents (valuable), SAH — radioisotope scan (technetium-99m) to localise specific tumours and haematoma — MRI: very effective for intracerebral pathology but expensive; produces better

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definition of intracerebral structures than CT scanning but not as sensitive for detecting bleeding; detects intracranial vasculitis in temporal arteries — lumbar puncture: diagnosis of meningitis, suspected SAH (only if CT scan normal) Note: Dangerous if raised intracranial pressure.

Headache in children

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Respiratory infections and febrile illnesses are common causes of headache in children but there are other causes that reflect the common causes in adults. Many childhood headaches are isolated but are chronic in a significant number. Migraine is relatively common before adolescence, while tension or muscle contraction headache is more common after adolescence. Consider often overlooked causes such as hair traction, eye strain (measure and record vision) and hypoglycaemia. Children who have long periods without regular eating are prone to headache including exacerbations of migraine. They should not skip breakfast.8 Young children rarely experience sinus headache and this should not really be considered until the sinuses develop, around 5 years for the frontal sinuses. From 1% of children aged 7 years to 5% or more of children aged 15 years suffer from migraine, with girls developing it at a higher rate2 with increasing age. There is a strong family history. As a rule the prognosis is good as the majority will have no migraines in the long term. The type is mainly common migraine with symptoms such as malaise or nausea: classic migraine with the typical aura is not a feature of childhood migraine. The rather dramatic migraine, such as vertebrobasilar migraine, is frequent in adolescent girls and hemiplegia occurs in infants and children, especially with their first migraine attack.9 Vomiting is not necessarily an associated symptom in children. The possibility of cerebral space-occupying lesions requires due consideration, especially if the headaches are progressive. These are present typically in the morning and are associated with symptoms such as vomiting, dizziness, diplopia, ataxia, personality changes and deterioration of school performance. Symptoms that indicate a cerebral tumour or other serious problem are outlined in TABLE 56.3. Neonates and children aged 6–12 months are at the greatest risk from meningitis and it is important to keep this in mind.

Table 56.3

Pointers to serious causes of headache in children

Headache features Persistent or recurrent Present first thing in morning Wakes child at night No past history No family history Associated poor health Associated neurological symptoms Unilateral localisation Source: After Wright2

Management of the non-serious causes of headache includes reassurance (especially of parents), discouragement of excessive emphasis on the symptom and simple medications, such as paracetamol for the younger child and aspirin for the adolescent. Patients with undiagnosed and/or problematic headache should be referred. Pharmacological treatment in children9 Tension headache and migraine: paracetamol 20 mg/kg (o) statim then 15 mg/kg 4–6 hourly up to 90 mg/kg/day (max. 4 g daily) or ibuprofen 5–10 mg/kg (o) statim up to 40 mg/kg/ day (not for children 2 hours (max. 30 mg/24 hours) or • eletriptan 40–80 mg (o) up to 160 mg/24 hours Avoid triptans in patients with coronary artery disease, Prinzmetal angina, uncontrolled hypertension or during pregnancy. Do not use with ergotamine simultaneously and cease if chest pain develops, albeit transient in a young patient. Use with caution in patients taking SSRIs, MAOIs and lithium.

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Treatment of the severe attack (If other preparations ineffective.)

Caution: Do not use ergotamine preparations if sumatriptan used in previous 6 hours, and do not use sumatriptan if ergotamine preparations used in previous 24 hours.

Practice tips for severe classic migraine: • •

IV metoclopramide + 1 litre N saline IV in 30 minutes + oral aspirin or paracetamol Continue high fluid intake

Status migrainosus (persistent migraine): IV dihydroergotamine 0.25–1 mg—over 2 minutes (may have to be given 8 hourly over 3–7 days in hospital) or chlorpromazine 0.1 mg/kg IV, repeated every 15 minutes for up to 3 doses (if necessary). Consider corticosteroids (e.g. dexamethasone 10–20 mg IV statim and then taper). Prophylaxis Non-drug self-management with avoidance of any known trigger factors is the key. Consider prophylactic therapy for frequent attacks that cause disruption to the patient’s lifestyle and well-being, a rule of thumb being two or more severe migraine attacks per month; certainly consider it for weekly attacks and a poor response to therapy for the acute attack. Do not give ergotamine.10 The most commonly used drugs include: • beta blockers—propranolol 40 mg (o) bd or tds (max. 320 mg/day), metoprolol, atenolol*

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Headache • • • • • • • • • • • • •

tricyclic antidepressants—amitriptyline* sodium valproate* pizotifen 0.5–2.0 mg at night cyproheptadine (ideal for children) clonidine methysergide (reserve for unresponsive severe migraine) 1 mg tds after food—up to 4 months only calcium-channel blockers—nifedipine, verapamil NSAIDs—naproxen, indomethacin, ibuprofen MAOIs—phenelzine, moclobemide sumatriptan gabapentin topiramate botulinum toxin

* first line

Menstrual migraine Naproxen 550 mg (o) bd, 48 hours before expected attack for 4–10 days or oestradiol gel 1.5 mg transdermally, once daily for 7 days. Guidelines9,13 Select the initial drug according to the patient’s medical profile: • • • • • • •

if low or normal weight—pizotifen if hypertensive—a beta blocker if depressed or anxious—amitriptyline if tension—a beta blocker if cervical spondylosis—naproxen food-sensitive migraine—pizotifen menstrual migraine—naproxen or mefenamic acid or ibuprofen or oestradiol transdermal gel

Commonly prescribed propranolol or pizotifen:10

first-line

drugs

are

propranolol 40 mg (o) bd or tds (at first) increasing to 320 mg daily (if necessary) pizotifen 0.5–1 mg (o) nocte (at first) increasing to 3 mg a day (if necessary) Each drug should be tried for 2 months before it is judged to be ineffective. Amitriptyline 50 mg nocte can be added to propranolol, pizotifen (beware  of weight gain) or methysergide and may convert a relatively poor response to very good control.3

Cluster headache Cluster headache is also known as migrainous neuralgia. It occurs in paroxysmal clusters of

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unilateral headache that typically occur nightly, usually in the early hours of the morning, although patients may have headaches that occur at other times. A hallmark is the pronounced cyclical nature of the attacks and at least 5 attacks. It occurs typically in males (6:1 ratio) and is rare in childhood. There are no visual disturbances or vomiting. DxT retro-orbital headache + rhinorrhoea + lacrimation cluster headache

Management Acute attack (brief treatment seldom effective): • consider 100% oxygen 10 L/min for 15 min (usually good response) • sumatriptan 6 mg SC injection (or 20 mg intranasal) or • metoclopramide 10 mg IV + dihydroergotamine 0.5 mg IV slowly or 1 mg IM • consider local anaesthetic—greater occipital nerve block Avoid alcohol during cluster. Prophylaxis (once a cluster starts) Consider the following: • methysergide 1 mg (o) once daily up to 3 mg bd • prednisolone 50 mg/day for 10 days then taper over 3 weeks (as a bridging treatment) • lithium 250 mg (o) bd • verapamil SR 160 mg (o) daily up to 320 mg • pizotifen • indomethacin (helps confirm diagnosis) • sodium valproate Note: Some of the above can be used long term for frequent clusters. Clinical features Site: Radiation: Quality: Frequency: Duration:

over or about one eye (see FIG. 56.5); always same side frontal and temporal regions severe one every other day and 8 per day for more than half the time 15 minutes to 180 minutes (average 30 minutes); the clusters last 4–6 weeks (can last months) continued

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continued Onset:

Offset: Aggravating factors: Relieving factors: Associated features:

suddenly during night (usually), same time about 2–3 hours after falling asleep; the ‘alarm clock’ headache (e.g. 2–4 am) spontaneous alcohol (during cluster) drugs family history; rhinorrhoea and/or congestion, ipsilateral nose; lacrimation; flushing and/or sweating of forehead and cheek; redness of ipsilateral eye; eyelid oedema; miosis and/or ptosis; sensation of fullness in ear; a sense of restlessness or agitation (see FIG. 56.6)

Cervical dysfunction/spondylosis Headache from neck disorders, often referred to as occipital neuralgia or cervicogenic, is far more common than realised and is very rewarding to treat by physical therapy, including mobilisation and manipulation and exercises in particular. See CHAPTERS 24 and 62. Headache can be caused by abnormalities in any structure innervated by the upper two cervical nerves C2, C3 (usually the C1–2, C2–3 facet joints). Pain from cervical structures can be referred retroorbitally and over one-half of the head. The headache is often incorrectly diagnosed as migraine but clinical examination of the neck helps differentiation.14 The neck may be responsible for so-called ‘tension’ headache but clinical differentiation can be more difficult. Clinical features The pain is usually sited in the occipital region with possible radiation to the parietal region, vertex of skull and behind the eye (see FIG. 56.7). It is usually present on waking and settles during the day. There is usually a history of trauma including an MVA or blow to the head. Associated features include stiffness and grating of the neck. On examination there is usually tenderness to palpation over the C1, C2 and/or C3 levels of the cervical spine, especially on the side of the headache.

FIGURE 56.5 Typical distribution of pain in cluster headache

Treatment • Physiotherapy modalities: hydrotherapy, muscle energy therapy, mobilisation, manipulation (from experts) and neck exercises (very important) • Supportive neck pillow • NSAIDs for cervical spondylosis • For intractable cases consider mobilisation under general anaesthesia, injections of corticosteroids around, or surgical section of, the greater occipital nerve14

ptosis (Horner syndrome)

lacrimation

nasal discharge

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FIGURE 56.6 Features of an attack of cluster headache: ptosis, lacrimation and a discharge from the nostril on the side of pain

FIGURE 56.7 Typical distribution of pain in cervical dysfunction (right side)

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Headache

Combination headache Combined (also known as mixed) headaches are common and often diagnosed as psychogenic headache or a typical migraine. They have a combination of various degrees of: • • • •

tension and/or depression cervical dysfunction vasospasm (migraine) drugs: analgesics (rebound), alcohol, nicotine, caffeine, NSAIDs

The headache, which has many of the features of tension headache, is usually described as a heavy deep ache ‘as though my head is ready to burst’. It tends to be constant, being present throughout every waking moment. It tends to last for days (average 3–7) but can last for weeks or months. It is often related to stress and adverse working conditions, and sometimes follows an accident. Management An important strategy is to evaluate each possible component of the headache as a stepwise trial by an elimination process: • • • • •

drug evaluation and modification cervical dysfunction—physical therapy if present depression tension and stress other psychogenic factors (e.g. conversion reaction) • vasospasm Treatment includes cognitive therapy, reassurance that the patient does not have a cerebral tumour, and lifestyle modification. The most effective medication is amitriptyline or other antidepressant. Propranolol and the antiepileptics can be considered.

Temporal arteritis TA is also known as giant cell arteritis or cranial arteritis. There is usually a persistent unilateral throbbing headache in the temporal region and scalp sensitivity with localised thickening, with or without loss of pulsation of the temporal artery. It is related to polymyalgia rheumatica—20% of sufferers will develop TA. See CHAPTER 32. TA is a type of collagen disease causing inflammation of extracranial vessels, especially the superficial temporal artery. It usually presents as a unilateral intermittent headache in a person over 50 years.

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Clinical features Age: Site: Radiation: Quality: Frequency: Duration: Onset: Offset: Aggravating factors: Relieving factors: Associated features:

Other pointers:

over 50 years (mean age 70 years) forehead and temporal region (unilateral) (see FIG. 56.8) down side of head towards occiput severe burning pain daily, a constant ache usually constant (getting worse) non-specific, tends to be worse in morning nil stress and anxiety nil malaise, vague aches and pains in muscles (especially of neck), weight loss intermittent blurred vision tenderness on brushing hair jaw claudication on eating polymyalgia rheumatica hypertension abnormal emotional behaviour

TA may also involve the intracranial vessels, especially the ophthalmic artery or posterior ciliary arteries, causing optic atrophy and blindness. Vision is impaired in about one-half of patients at some stage. Once the patient goes blind it is usually irreversible. Diagnosis Diagnosis is by biopsy and histological examination of the superficial temporal artery. The ESR is usually markedly elevated but may be normal. The biopsy may be normal as TA has a focal nature. MRI has a high sensitivity and specificity. Note: Consider it with any ‘new’ headache.

56 FIGURE 56.8 Typical distribution of pain in temporal arteritis (right side)

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Treatment TA is very responsive to corticosteroids; start treatment immediately to prevent permanent blindness. Initial medication is prednisolone 40–60 mg orally daily in two divided doses initially for 2–4 weeks. Dose reduction and progress is monitored by the clinical state and ESR and CRP levels.10 Concomitant use of H2-receptor antagonists may be appropriate initially. Temporal arteritis may take 1–2 years to resolve.

Frontal sinusitis The headache of frontal sinusitis can be a diagnostic problem especially in the absence of, or a lapse in time since, an obvious upper respiratory infection or vasomotor rhinitis. Some patients do not have a history of a preceding respiratory infection, nor any signs of nasal obstruction or fever. Contrary to popular belief, sinusitis is a relatively uncommon source of headache. Clinical features It presents typically as a frontal or retro-orbital headache (see FIG. 56.9). A characteristic is its diurnal variation, developing in the morning around 9 am, being most intense in the middle of the day, then subsiding to offset around 6 pm. Examination There is tenderness over the frontal sinus and pain on percussion over the sinus. Ewing sign may be elicited. Fever and oedema of the upper eyelid may be present. Management

Principles of treatment • Drain the sinus conservatively using steam inhalations • Antibiotics: amoxycillin or amoxycillin/ clavulanate or cefaclor or doxycycline • Analgesics

Referral If resolution cannot be accomplished by conservative means then referral to an ENT specialist is advisable. Acute purulent sinusitis can be treacherous if it persist and spreads, causing collections of pus in the extradural or subdural space, cerebral abscess or blood-borne spread of infection.

Complications • • • •

Orbital cellulitis Subdural abscess Osteomyelitis Cavernous sinus thrombosis Symptoms indicating spread of infection:

• • • • • •

increase in fever and chills vomiting oedema of the eyelids and forehead visual disturbances dulling of the sensorium convulsions

Raised intracranial pressure Important causes of a space-occupying lesion include a cerebral tumour and subdural haematoma. Sometimes it is not possible to differentiate between a subdural and an extradural haematoma, although the latter classically follows an acute injury (see CHAPTER  75). Typical features are generalised headache, usually worse in the morning, aggravated by abrupt changes in intra-cranial pressure and later associated with vomiting and drowsiness. Headache is an uncommon presenting symptom of a cerebral tumour.

DxT drowsiness + vomiting + seizure raised intracranial pressure

Clinical features

56 FIGURE 56.9 Typical distribution of pain of frontal sinusitis (right side)

Site:

generalised, often occipital

Radiation:

retro-orbital

Quality:

dull, deep steady ache

Frequency:

daily

Duration:

may be hours in morning

Onset:

worse in mornings, usually intermittent, can awaken from sleep

Offset:

later in day (if at all)

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Headache Aggravating factors: Relieving factors: Associated features:

coughing, sneezing, straining at toilet analgesics (e.g. aspirin), sitting, standing vomiting (without preceding nausea); vertigo/dizziness; drowsiness; seizures; confusion (later); neurological signs (depending on side)

Examination • Focal CNS signs • Papilloedema (see FIG. 56.10) (but may be absent)

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Approximately 75% will present with an acute severe headache and the remainder with loss of consciousness. Clinical features • Sudden severe ‘thunderclap’ headache • Occipital location • Localised at first, then generalised • Pain and stiffness of the neck follows • Vomiting and loss of consciousness often follow • Confusion or a lowered consciousness level • ± seizures • Kernig sign positive (see CHAPTER 30) • Neurological deficit may include: hemiplegia (if intracerebral bleed), third nerve palsy (partial or complete) (see FIG. 56.11) About one-third of patients experience a ‘sentinel’ headache. DxT occipital headache + vomiting + neck stiffness SAH

FIGURE 56.10 Papilloedema with swollen optic disc of the ocular fundus due to raised intracranial pressure

Intracerebral tumours • Incidence is 5–10 per 100 000 population • Two peaks of incidence: children 55 years presenting with unaccustomed headache has an organic disorder such as TA, intracerebral tumour or subdural haematoma until proved otherwise. The ESR is an excellent screening test to diagnose TA but occasionally can be normal in the presence of active TA. If a patient presents twice within 24 hours to the same practice or hospital with headache and vomiting, consider other causes apart from migraine before discharging the patient.8 If migraine attacks are severe and unusual (e.g. always on the same side) consider the possibility of cerebral vascular malformation. CT scans and MRI have superseded other investigations in the diagnosis of cerebral tumours and intracranial haemorrhage but should be ordered sparingly and judiciously. If a headache is occipital in origin or accompanied by neck pain, consider the likely possibility of cervical dysfunction and refer to the appropriate therapist once the diagnosis is established. For recurrent migraine sufferers emphasise the importance of trigger factor avoidance and of taking aspirin and metoclopramide medication at the earliest warning of an attack. A severe headache of sudden onset is SAH until proved otherwise. It is overlooked sometimes. SAH is overlooked sometimes, mainly because it is not considered in the differential diagnosis. Suspect with very severe and protracted headache, drowsiness and neck stiffness. Medical evidence indicates that most headaches are related to fatigue, stress or migraine triggers and respond to application of heat or cold, exercise and common analgesics, including aspirin and ibuprofen.15 If women with migraine demand the oral contraceptive, use a low-dose oestrogen preparation and monitor progress. The use of narcotics for migraine treatment (such as pethidine and codeine) is to be avoided whenever possible—the frequent use of ergotamine, analgesics or narcotics can transform episodic migraine into chronic daily headache.4

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Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Migraine • Tension headache

References 1 Cormack J, Marinker M, Morrell D. The patient complaining of headache. In: Practice. London: Kluwer Medical, 1982: 3–12. 2 Wright M. Recurrent headaches in children. Australian Paediatric Review, 1991; 1 (6): 1–2. 3 Anthony M. Migraine and tension headache. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 313–16. 4 Stark R. Management of headache. Proceedings of 25th update course for GPs. Monash University, 2003. 5 Lance JW. Headache and facial pain. Med J Aust, 2000; 172: 450–5.

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6 Davis A, Bolin T, Ham J. Symptom Analysis and Physical Diagnosis. Sydney: Pergamon, 1990. 7 Lance JW. Mechanism and Management of Headache (3rd edn). London: Butterworths, 1978: 109–12. 8 Smith L. Childhood headache. In: Australian Doctor Education, GP Paediatrics, 2005. 9 Moulds R (Chair). Therapeutic Guidelines: Neurology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2011: 73–99. 10 Burns R. Pitfalls in headache management. Aust Fam Physician, 1990; 19: 1821–6. 11 IHS Classification ICHD-3: 2013. Refer or . 12 Day TJ. Migraine and other vascular headaches. Aust Fam Physician, 1990; 19: 1797–804. 13 Heywood J, Zagami A. Treating acute migraine attack. Current Therapeutics, 1997; 37 (12): 33–7. 14 Anthony M. The treatment of migraine—old methods, new ideas. Aust Fam Physician, 1993; 22: 1401–05. 15 Rosser W, Shafir MS. Evidence-based Family Medicine. Hamilton: BC Decker Inc., 1998: 164–6.

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Hoarseness results from imperfect phonation due to impairment of normal vocal cord mobility or vibration. It is an important symptom as it may signal a serious cause such as malignancy or a disease with potential for airway obstruction.1 Raymond L Carroll  Hoarseness (dysphonia) is defined as an altered voice due to a laryngeal disorder.2 It is an important symptom of laryngeal disease presenting in general practice, and ranges from the very common, trivial, self-limiting condition of viral upper respiratory tract infection to a life-threatening disorder (see TABLE 57.1). It may be of sudden presentation lasting only a few days or develop gradually and persist for weeks or months. The cut-off point between acute and chronic hoarseness is three weeks duration, by which time most self-limiting conditions have resolved. Hoarseness pertains to harsh, raspy, gravelly or rough tones of voice rather than pitch or volume. Rarely, hoarseness can be a functional or deliberate symptom referred to as ‘hysterical aphonia’.3 In this condition, patients purposely hold the cords apart while speaking. Table 57.1 Hoarseness: diagnostic strategy model Q. Probability diagnosis A. Viral URTI: acute laryngitis Non-specific irritative laryngitis (Reinke oedema) Vocal abuse (shouting, screaming, etc.) Nodules and polyps of cords Presbyphonia in elderly: ‘tired’ voice Acute tonsillitis Q. Serious disorders not to be missed A. Cancer: larynx, lung, including recurrent laryngeal nerve palsy, oesophagus, thyroid Imminent airway obstruction (e.g. acute epiglottitis, croup) Other rare severe infections (e.g. TB, diphtheria) Foreign body Motor neurone disease Aortic arch aneurysm Myasthenia gravis Q. Pitfalls A. Toxic fumes Vocal abuse Benign tumours of vocal cords (e.g. polyps, ‘singer’s nodules’, papillomas)

Gastro-oesophageal reflux → pharyngolaryngitis Goitre Vocal cord palsy Dystonia Physical trauma (e.g. post-intubation), haematoma Fungal infections (e.g. Candida with steroid inhalation, immunocompromised) Allergy (e.g. angioedema) Leucoplakia Systemic autoimmune disorders (e.g. SLE, Wegener granulomatosis) Q. Masquerades A. Consider: • drugs: antipsychotics, anabolic steroids • smoking → non-specific laryngitis • hypothyroidism, acromegaly Q. Is the patient trying to tell me something? A. Consider: • functional aphonia • functional stridor

Key facts and checkpoints •

• •

•

•

In acute hoarseness the diagnosis is usually obvious from the history alone. Examples include acute upper respiratory tract infection (URTI) or vocal overuse. Think ‘hypothyroidism’ if unusual hoarseness develops. Laryngeal cancer must be excluded if hoarseness persists for longer than 3 weeks in an adult. It can arise intrinsic or extrinsic to the vocal cords. Intermittent hoarseness is invariably secondary to a benign disorder. Constant or progressive hoarseness suggests malignancy. Non-malignant vocal cord lesions, which include polyps, vocal nodules, contact ulcers, granulomas, other benign tumours and leucoplakia, account for about half of all voice disorders. continued

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continued

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•

In cases of chronic hoarseness the larynx must be visualised for diagnosis but the following are common: — children—‘screamer’s nodules’ — adults—non-specific irritant laryngitis • Acute laryngeal oedema may develop as a component of the life-threatening acute angioedemic allergic response. • Elderly or debilitated patients may exhibit a shaky or soft ‘pseudohoarse’ voice due to a weakened respiratory effort. This is termed phonaesthenia or presbyphonia. • Contact ulcers of the larynx occur on the posterior third of the vocal cords where the mucosa is thin. The resultant weak hoarse voice may be accompanied by painful phonation. The ulcers may develop into granulomas. Apart from intubation, the condition is usually found in forceful orators who misuse their larynx when attempting to lower the pitch of their voice.3

The clinical approach History Note the nature and duration of the voice change. Inquire about corticosteroid inhalations, excessive or unaccustomed voice straining (especially singing), recent surgery, possible reflux, smoking or exposure to environmental pollutants. Elicit associated respiratory or general symptoms such as cough and weight loss. Consider symptoms of hypothyroidism.

Examination Palpate the neck for enlargement of the thyroid gland or cervical nodes. Perform a simple oropharyngeal examination except if epiglottitis is suspected. Check for signs of hypothyroidism, such as coarse dry hair and skin, slow pulse and mental slowing. Perform indirect laryngoscopy if skilled in the procedure.

Investigations The following need to be considered: • Thyroid function tests. • Chest X-ray if it is possibly due to lung cancer with recurrent laryngeal nerve palsy. • Indirect laryngoscopy (the gag reflex may preclude this). • Direct laryngoscopy with a flexible fibre-optic endoscope with possible biopsy (the most sensitive investigation). • The choice of imaging to detect suspected neoplasia or laryngeal trauma is special CT scan.

Management principles Acute hoarseness • Treat according to cause. • Advise vocal rest or minimal usage at normal conversational level. • Avoid irritants (e.g. dust, tobacco, alcohol). • Consider inhalations and cough suppressants in cases of acute URTI and coughing paroxysms. Chronic hoarseness • Establish the diagnosis. • Consider referral to ENT specialist.

Hoarseness in children • It is worth bearing in mind that stridor in infants can be caused by a congenital abnormality of the larynx, including laryngomalacia (congenital laryngeal stridor), which is particularly noticeable when the child is asleep; laryngeal stenosis (congenital laryngeal narrowing); and laryngeal paralysis due to birth trauma of the vagus nerve. Vocal cord paralysis/palsy is the most common laryngeal abnormality in children (20% of cases) after laryngomalacia.3 • In children exclude the acute infections— laryngotracheobronchitis (croup), tonsillitis and epiglottitis. • Persistent hoarseness in children is due commonly to vocal cord nodules related to vocal abuse, such as screaming and yelling, often due to noisy children’s games. • It is important to exclude a juvenile papilloma in a hoarse child.4

SPECIFIC CONDITIONS

Acute laryngitis Most cases are caused by the respiratory viruses— rhinovirus, influenza, para-influenza, Coxsackie, adenovirus and respiratory syncytial virus, resulting in vocal cord oedema (be cautious of group A Streptococcus). The main symptom is hoarseness, which usually persists for 3–14 days and leads to loss of voice. Even speaking can be painful. Aggravating factors include smoking, excessive alcohol drinking, and exposure to irritants and pollutants, airconditioning systems and very cold weather. Management • Rest at home, including voice rest (the best treatment).

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Hoarseness • • • • • •

Use the voice sparingly, avoid whispering. Use a warm sialagogue (e.g. hot lemon drinks). Drink ample fluids, especially water. Avoid smoking, passive smoke and alcohol. Have hot, steamy showers as humidity helps. Use steam inhalations (e.g. 5 minutes, three times a day). • Use cough suppressants, especially mucolytic agents. • Use simple analgesics, such as paracetamol or aspirin, for discomfort. • Antibiotics are of no proven use unless there is evidence of bacterial infection. Corticosteroids are rarely indicated.

Chronic laryngitis: ‘barmaid syndrome’ This typically occurs in a heavy smoker who works in a heavy smoking environment, who is a heavy drinker and continually talks or sings. It is a combination of vocal abuse and chemical irritation. Hoarseness often comes and goes. Treatment involves modification of these factors and screening for vocal cord tumours. Chronic laryngitis due to laryngopharyngeal reflux is treated with an 8–12 week empirical course of proton-pump inhibitors as well as dietary and lifestyle modification.2

Benign tumours of the vocal cords These include nodules (most common) (see FIG.  57.1), polyps (number 2), cysts and papules. Vocal cord nodules, including ‘singer’s nodules’,

may respond well to conservative measures such as a voice rest and vocal therapy. If not, they can be removed by microlaryngeal surgery or laser therapy. Dependent polyps and papillomas are removed by microsurgery.

Laryngeal cancer Squamous cell carcinoma usually occurs in patients with a history of chronic laryngitis, smoking and alcohol use. Symptoms include hoarseness, stridor, haemoptysis and dysphagia. It may be preceded by leucoplakia, which is treated by vocal cord stripping under microsurgery. The diagnosis based on persistent hoarseness is made after fibre-optic laryngoscopy and biopsy by a specialist. The patient may present with an unexplained cervical lymph node. The condition is curable if detected early. Small local tumours can be treated by radiotherapy or laser therapy. Larger tumours usually require laryngectomy and perhaps dissection of the cervical lymph nodes (Commando operation). Such radical surgery demands considerable patient support, including education about speech, eating and tracheostomy care.

When to refer1 • Acute cases that are unexplained, fail to respond by 3–4 weeks or recur. • All chronic cases. • Any case with stridor or non-tender cervical lymphadenopathy. • Patients requiring voice therapy when vocal abuse is identified.

Practice tips •

nodules

•

•

• • FIGURE 57.1 Vocal cord nodules

Consider intubation as a possible cause of transient hoarseness, especially in these times of day surgery.5 Consider gastro-oesophageal reflux disease in the elderly but avoid such a diagnosis without specialist investigation for other causes. If stridor is present with acute hoarseness, the airway is compromised. Be on stand-by for possible emergency intervention. Prevention is the best treatment for laryngeal cancer (i.e. quit smoking). Recurrent laryngeal nerve palsy may be associated with cancer of the lung and mediastinum, or diabetes, or may be idiopathic.

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References 57

1 Carroll RL. Hoarseness. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 239–40. 2 Bova R, McGuinness J. Hoarseness: a guide to voice disorders. Medicine Today, 2007; 8 (2): 38–44.

3 Priestly J, Havas TE. Benign vocal fold lesions. Medical Observer, 19 November 2012: 1–3. 4 Birman C, Fitzsimons, Quayle S. Little voices: therapy update. Australian Doctor, 7 May 2004: 49–50. 5 Hopcroft K, Forte V. Symptom Sorter (4th edn). Oxford: Radcliffe Publishing, 2011; 316–8.

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The disease is produced by black bile when it flows into the liver. The symptoms are these: ‘an acute pain in the liver, also below the breast, a feeling of suffocation is strong during these days and becomes less strong later’. The liver is tender to palpation and the complexion of the patient is somewhat livid. These are symptoms that occur in the beginning but as the disease progresses, the fever diminishes in strength and the patient feels sated after ingesting a little amount of food. He must drink melikration [a mixture of water and honey]. Hippocrates on hepatitis Jaundice is a yellow discolouration of the skin and mucosal surfaces caused by the accumulation of excessive bilirubin.1 It is a cardinal symptom of hepatobiliary disease and haemolysis. Important common causes include gallstones, hepatitis A, hepatitis B, hepatitis C, drugs, alcohol and Gilbert syndrome. The commonest clinical encounter with jaundice, especially physiological jaundice, is in the newborn. As for all patients, the history and examination are paramount, but investigations are essential to clinch the diagnosis of jaundice. The three major categories of jaundice are (see FIG. 58.1): • obstructive: — extrahepatic — intrahepatic • hepatocellular • haemolytic

Key facts and checkpoints • • • •

•

• •

Jaundice is defined as a serum bilirubin level exceeding 19 μmol/L.2 Clinical jaundice manifests only when the bilirubin level exceeds 50 μmol/L.1 However, jaundice is difficult to detect visually below 85 μmol/L if lighting is poor. It can be distinguished from yellow skin due to hypercarotenaemia (due to dietary excess of carrots, pumpkin, mangoes or pawpaw) and hypothyroidism by involving the sclera. The most common causes of jaundice recorded in a general practice population are (in order) viral hepatitis, gallstones, pancreatic cancer, cirrhosis, pancreatitis and drugs.3 Always take a full travel, drug and hepatitis contact history in any patient presenting with jaundice. Acute hepatitis is usually self-limiting in patients with hepatitis A and in adults with hepatitis B but

•

progresses to chronic infections with hepatitis C and children with hepatitis B.4 A fatty liver (steatosis) can occur not only with alcohol excess but also with obesity, diabetes and starvation. There is usually no liver damage and thus no jaundice.

Table 58.1 Abbreviations used in this chapter Hepatitis A virus

HAV

Hepatitis A antibody

anti-HAV

Immunoglobulin M

IgM

Immunoglobulin G

IgG

Hepatitis B virus

HBV

Hepatitis B surface antigen

HBsAg

Hepatitis B surface antibody

anti-HBs

Hepatitis B core antibody

anti-HBc

Hepatitis Be antigen

HBeAg

Hepatitis C virus

HCV

Hepatitis C virus antibody

anti-HCV

Hepatitis D (Delta) virus

HDV

Hepatitis E virus

HEV

Hepatitis F virus

HFV

Hepatitis G virus

HGV

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 58.2.

Probability diagnosis The answer depends on the age and social grouping of the patient, especially if the patient indulges in risktaking behaviour or has travelled overseas.

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red blood cells liver

58 unconjugated bilirubin spleen

conjugated bilirubin urobilinogen

kidneys

gut bilirubin oxidised by bacteria in gut to urobilinogen urobilinogen excreted in faeces as sterocobilin

urinary urobilin

FIGURE 58.1 The jaundice pathway

Viral hepatitis A, B or C account for the majority of cases of jaundice. In the middle-aged and elderly group, a common cause is obstruction from gallstones or cancer. It is common for older people to have painless obstructive jaundice; bear in mind that the chances of malignancy increase with age. Alcoholic liver disease is common and may present as chronic alcoholic cirrhosis with liver failure or as acute alcoholic hepatitis. It is worth emphasising that such patients can make a dramatic recovery when they cease drinking alcohol. In family practice we encounter many cases of drug-induced jaundice, especially in the elderly. These drugs are outlined later in the chapter, under ‘Seven masquerades checklist’.

Serious disorders not to be missed Malignancy must always be suspected, especially in the elderly patient and those with a history of chronic active hepatitis (e.g. post hepatitis B or C infection). The former is more likely to have carcinoma of the

head of the pancreas and the latter, hepatocellular carcinoma (hepatoma). Metastatic cancer must be kept in mind, especially in those with a history of surgery, such as large bowel cancer, melanoma and stomach cancer. An enlarged, knobbly, hard liver is a feature. Hepatic failure can be associated with severe systemic infection (e.g. septicaemia and pneumonia), and after surgery in critically ill patients. A patient who has the classic Charcot triad of upper abdominal pain, fever (and chills) and jaundice should be regarded as having ascending cholangitis until proved otherwise. Wilson syndrome, although rare, must be considered in all young patients with acute hepatitis. A history of neurological symptoms, such as a tremor or a clumsy gait, and a family history is important. If Wilson syndrome is suspected an ocular slit lamp examination, serum ceruloplasmin levels (low in 95% of patients) and a liver biopsy should be performed. Early diagnosis and treatment mean a better prognosis. Reye syndrome is a rare and severe complication of influenza and some other viral diseases, especially

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Jaundice

Table 58.2

Jaundice (adults): diagnostic strategy model

Q. Probability diagnosis A. Hepatitis A, B, C (mainly B, C) Gallstones in common bile duct Alcoholic hepatitis/cirrhosis Q. Serious disorders not to be missed A. Malignancy: • pancreas • biliary tract • hepatocellular (hepatoma) • metastases Severe infections: • septicaemia • ascending cholangitis • fulminant hepatitis • HIV/AIDS Rarities: • Wilson syndrome • Reye syndrome • acute fatty liver of pregnancy Q. Pitfalls (often missed) A. Gallstones Gilbert syndrome Cardiac failure Primary biliary cirrhosis Autoimmune chronic active hepatitis Primary sclerosing cholangitis Chronic viral hepatitis Haemochromatosis Viral infections (e.g. CMV, EBV) Leptospirosis Q. Seven masquerades checklist A. Drugs Anaemia Q. Is the patient trying to tell me something? A. Not usually applicable.

in children when given aspirin. There is rapid development of hepatic failure and encephalopathy.

Pitfalls Gallstones, especially in the absence of upper abdominal pain, can be overlooked, so this possibility should be kept in mind in the elderly. Gilbert syndrome is worth considering, especially as it is the commonest form of unconjugated hyperbilirubinaemia. It affects at least 3% of the population. Cardiac failure can present as jaundice with widespread tenderness under the right costal

margin. It can be insidious in onset or manifest with gross acute failure. It can be confused with acute cholecystitis. The biochemical abnormalities seen are very variable. Usually there is a moderate rise in bilirubin and alkaline phosphatase and sometimes, in acute failure, a marked elevation of transaminase may occur, suggesting some hepatocellular necrosis. There are many other pitfalls for a family doctor, who may encounter the conditions very rarely, if at all. Such disorders include: • inherited conjugated hyperbilirubinaemias (Dubin–Johnson and Rotor syndromes) caused by faulty excretion by liver cells • haemochromatosis (associated pigmentation and diabetes) • chronic active hepatitis • primary biliary cirrhosis • primary sclerosing cholangitis (associated with ulcerative colitis) General pitfalls • Excluding jaundice by examining the sclera in artificial light • Not realising that the sclera in elderly patients often have an icteric appearance (without jaundice) • Omitting to take a careful history, including illicit drugs • A liver biopsy is essential in all patients with chronic hepatitis

Seven masquerades checklist Of this group the haemolytic anaemias and drugs have to be considered. Drug-related jaundice Drug-induced jaundice is common and many drugs are implicated. The patterns of drug-related liver damage include cholestasis, necrosis (‘hepatitis’), granulomas, chronic active hepatitis, cirrhosis, hepatocellular tumours and veno-occlusive disease.4,5 Some drugs, such as methyldopa, can initiate haemolysis. The important drugs to consider are presented in TABLE  58.3. Antibiotics, especially flucloxacillin, amoxycillin  +  clavulanate and erythromycin, are commonly implicated. Haemolysis The patient may present with the symptoms of underlying anaemia and jaundice with no noticeable change in the appearance of the urine and stool. The degree of haemolysis may vary from the

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Table 58.3 Drugs that can cause jaundice Haemolysis Methyldopa

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Hepatocellular damage Dose-dependent: • paracetamol (can cause acute hepatic necrosis) • salicylates • tetracycline Dose-independent: • anaesthetics (e.g. halothane) • antidepressants (e.g. MAOIs) • anti-epileptics (e.g. phenytoin, sodium valproate, carbamazepine) • antibiotics (e.g. penicillins, sulphonamides) • antimalarials (e.g. Fansidar) • antituberculosis (e.g. isoniazid) • anti-inflammatories (e.g. NSAIDS, various) • carbon tetrachloride • cardiovascular (e.g. amiodarone, methyldopa, perhexiline) • statins (e.g. simvastatin) Cholestasis Antithyroid drugs Chlorpromazine

lemon-yellow tinge of pernicious anaemia in an elderly patient to a severe haemolytic crisis precipitated by drugs or broad beans (favism) in a patient with an inherited red cell deficiency of glucose-6phosphate dehydrogenase (G6PD). More common causes include the hereditary haemolytic anaemias, such as congenital spherocytosis and thalassaemia major. Acquired causes include incompatible blood transfusions, malignancies (such as lymphoma), severe sepsis and some drugs. Splenomegaly occurs in most patients with haemolytic anaemia, and decreased red cell survival can be measured.

Psychogenic considerations This is not really applicable for an organic problem such as jaundice. Nevertheless, the cause may be related to factors in the patient’s lifestyle, such as homosexuality, sexual promiscuity or intravenous drug abuse, and the patient may be reluctant to offer this information. Discreet, concerned probing will be necessary.

Red flag pointers for jaundice • • • •

Unexplained weight loss Progressive jaundice including painless jaundice Oedema Cerebral dysfunction (e.g. confusion, somnolence)

The clinical approach

Erythromycin estolate

History

Penicillins, esp. flucloxacillin

The history should include questioning about the following:

Gold salts Oral contraceptives/oestrogens Synthetic anabolic steroids (e.g. methyltestosterone) Hypoglycaemic drugs (e.g. chlorpropamide) Amitriptyline Others Allopurinol Cimetidine (aggravated by alcohol) Cytotoxics (e.g. methotrexate, azathioprine) Etretinate Hydralazine Nitrofurantoin Vitamin A (mega dosage) Various complementary medicines (e.g. herbal agents)

• • • • • • • • • • • • • •

any episodes of jaundice change in colour of faeces and urine anorexia, sore throat, weight loss, pruritus abdominal pain residence and members of household contact with patients with hepatitis or jaundice recent overseas travel exposure to blood or blood products needle-stick injuries or exposure to needles, such as acupuncture, tattooing and intravenous drugs dietary history—shellfish, drinking water sexual history—evidence of promiscuity drug history, including alcohol, paracetamol recent medical history, including surgery family history—family contacts who have had jaundice, haemolytic disease and other genetic liver diseases

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Jaundice • ethnic history—liable to haemolytic disease, contact with hepatitis B • occupational history—exposure to hazards

wasting, and testicular atrophy and gynaecomastia. Test for hepatic flap (asterixis) and fetor, which indicate liver failure. Search for lymphadenopathy, which may be indicative of malignancy. The examination should include dipstick urine testing for bilirubin and urobilinogen. A summary of the possible findings is presented in FIGURE 58.2.

Significance of various symptoms • Pain in the right hypochondrium: — gallstones — acute hepatitis (a constant ache) — cholecystitis • Anorexia, dark urine, fever: — viral hepatitis probable — alcoholic liver disease possible — drug-induced hepatitis possible • Pruritus: — cholestasis probable — possible with all liver diseases • Arthralgia, rash: — viral hepatitis — autoimmune hepatitis

Investigations The main investigations are FBE and the standard LFTs and viral serology for the infective causes, particularly hepatitis A, B and C virus (also EBV and CMV). A summary of the general findings for liver function tests is shown in TABLE  58.4. Consideration should be given to ordering fractionalisation of bilirubin to determine whether it is conjugated or unconjugated (important in diagnosis of Gilbert syndrome).

Examination

Diagnostic markers for hepatitis • Hepatitis A: IgM antibody (HAV Ab) • Hepatitis B: surface antigen (HBsAg) • Hepatitis C: HCV antibody (HCV Ab)

The abdominal examination is very important. The liver should be palpated carefully for enlargement, consistency and tenderness under the right costal margin. Search for enlargement of the gall bladder and the spleen. The gall bladder lies in the transpyloric line. A palpable gall bladder indicates extrahepatic biliary obstruction, and splenomegaly may indicate haemolytic anaemia, portal hypertension or viral hepatitis. Test for ascites. Skin excoriation may indicate pruritus, which is associated with cholestatic jaundice. Look for evidence of chronic liver disease, such as palmar erythema, easy bruising, spider naevi and muscle

Table 58.4

Hepatobiliary imaging Tests to identify causes such as malignancy or gallstones are now sophisticated and should be chosen with care. • X-ray: a plain abdominal X-ray shows up to 10% of gallstones • Transabdominal ultrasound (US): the most useful investigation for detecting gallstones

Characteristic liver function tests for selected types of liver disease Liver metastases/ abscess

Liver function tests (serological)

Hepatocellular (viral) Haemolytic hepatitis jaundice

Bilirubin

↑ to ↑ ↑ ↑

↑ ↑ to ↑ ↑ ↑ unconjugated

↑ up to 50 ↑ to N unconjugated

↑ to N

Alkaline phosphatase

↑ 2N

N

↑ ↑ to ↑ ↑ ↑

↑

Alanine transferase (ALT)

↑ ↑ ↑ >5N

N

N or ↑

N

↑

↑

Gamma glutamyl transferase

N or ↑

N

↑ ↑

N

↑

↑ ↑ ↑

Albumin

N or ↓

N

N

N

N to ↓

N to ↓ ↓

Globulin

N or ↑

N

N

N

N

N to ↑

N: is within normal limits

Obstruction

Gilbert syndrome

Alcoholic liver disease

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General jaundice loss of body hair fever

alcoholic facies parotid enlargement spider naevi

58

Epstein–Barr mononucleosis lymphadenopathy tonsillitis

scratch marks (if obstructive jaundice) gynaecomastia

Liver large or small

? splenomegaly needle marks

enlarged gall bladder (carcinoma head pancreas)

dilated abdominal veins (if cirrhosis)

liver palms

Tremor Wilson syndrome hepatic flap

leuconychia

testicular atrophy

FIGURE 58.2 Possible findings on examining the jaundiced patient

• • • •

and dilatation of the common bile duct; also detects liver metastases and other diffuse liver diseases HIDA scintiscan: useful in diagnosis of acute cholecystitis CT scan: for diagnosis of enlargement of the head of the pancreas and other pathology; indicated if US unsatisfactory PTC: percutaneous transhepatic cholangiography: shows imaging of biliary tree ERCP: endoscopic retrograde cholangiopancreatography; PTC and ERCP (best) determine the cause of the obstruction and relieves it by sphincterotomy and removal of CBD stones

• MRCP: magnetic resonance cholangiography provides non-invasive planning for obstructive jaundice • Liver isotopic scan: useful for liver cirrhosis, especially of the left lobe Specific tests Some specific tests include: • autoantibodies for autoimmune chronic active hepatitis and primary biliary cirrhosis • carcinoembryonic antigen to detect liver secondaries, especially colorectal • serum iron studies, especially transferrin saturation—elevated in haemochromatosis

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Jaundice in children JAUNDICE IN THE INFANT Jaundice in the newborn is clinically apparent in 50% of term babies and more than 80% of preterm.6 Icterus is therefore common and invariably physiologically benign. However, it is a cause for concern as there are many other causes and investigation is needed to determine whether the bilirubin is conjugated (always pathological) or unconjugated. If conjugated, consider the serious biliary atresia (stools are white); also a cyst obstructing the bile duct or neonatal hepatitis. Prompt referral is essential. Jaundice occurring in the first 24 hours after birth is not due to immature liver function but is pathological and usually due to haemolysis consequent on blood group incompatibility. In primigravidas it is usually due to ABO incompatibility.

Bilirubin encephalopathy Unconjugated bilirubin can be regarded as a neurological poison. With increasing serum levels an encephalopathy (which may be transient) can develop, but if persistent can lead to the irreversible brain damage known as kernicterus. The level of bilirubin causing kernicterus is totally unpredictable, but a guideline as a cause for concern in babies with Rh disease is a serum unconjugated bilirubin of 340 μmol/L (20 mg/dL). Guidelines for treatment for hyperbilirubinaemia (at 24–36 hours)—an example • >285 μmol/L—phototherapy • >360 μmol/L—consider exchange transfusion An example of a normogram is presented in FIGURE 58.3.

Physiological jaundice This mild form of jaundice, which is very common in infants, is really a diagnosis of exclusion. In a term infant the serum bilirubin rises quickly after birth to reach a maximum by day 3–5, then declines rapidly over the next 2–3 days before fading more

550

exchange transfusion and phototherapy

500 exchange transfusion if phototherapy fails

450 Serum bilirubin (mol/l)

• alpha-fetoprotein—elevated in hepatocellular carcinoma; mild elevation with acute or chronic liver disease (e.g. cirrhosis) • serum ceruloplasmin level—low in Wilson syndrome • liver biopsy • EBV/cytomegalovirus serology (consider if hepatitis serology negative)

651

58

400 possible haemolysis

phototherapy

350

300

250

200 0

24

46

72

96

Time after birth (h)

FIGURE 58.3 Typical normogram for decision making in healthy infants with jaundice

slowly for the next 1–2 weeks. Management includes phototherapy.

Pathological jaundice There are many causes of pathological jaundice, including: • haemolysis (e.g. blood grouping incompatibilities, ABO or Rhesus, G6PD deficiency, hereditary spherocytosis) • polycythaemia (e.g. intrauterine growth retardation) • inherited conjugation defects (e.g. uridyl diphosphate glucuronyl transferase deficiency) • breast milk jaundice • drugs • sepsis • hypothyroidism • biliary atresia Such cases require referral for evaluation and management.

ABO blood group incompatibility This is antibody-mediated haemolysis (Coomb test positive): • Mother is O • Child is A or B Jaundice develops within first 24 hours.

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Treatment • Perform a direct Coomb test on infant. • Phototherapy is required immediately. • These children require follow-up developmental assessment including audiometry.

Breast milk jaundice If the secondary causes of prolonged jaundice are excluded, the baby is well and breastfeeding, the likely cause of unconjugated elevated bilirubin is breast milk jaundice. It occurs in 2–4% of breastfed infants. It usually begins late in the first week and peaks at 2–3 weeks. Diagnosis is confirmed by suspending (not stopping) breastfeeding for 24–48 hours. The serum bilirubin falls and then breastfeeding can continue. The mother, who can express milk for this short period, must be reassured that there is nothing wrong with the milk and advised to resume. Some doctors recommend continuation of breastfeeding.

JAUNDICE IN OLDER CHILDREN Viral infection is the commonest cause of jaundice in the older child, especially hepatitis A and hepatitis B. It is uncommon for viral hepatitis to become chronic in childhood.

Jaundice in the elderly If an elderly person presents with jaundice the usual causes and investigations have to be considered. Obstructive jaundice is the commonest form of jaundice in the elderly and may be caused by gallstones blocking the common bile duct (may be painless) and carcinoma of the head of the pancreas, the biliary tract itself, the stomach or multiple secondaries for other sites. While it is not uncommon for a gallstone to produce marked obstructive jaundice and yet be painless, it is appropriate to adhere to the old adage that painless obstructive jaundice is due to neoplasm—particularly if the gall bladder is palpable (Courvoisier’s law). Alcoholic liver disease, although most frequently affecting patients between 40 and 60 years, can present for the first time over age 60 years. The commonest cause of hepatocellular jaundice in the elderly is probably alcoholic cirrhosis; hepatitis A is still relatively uncommon in old persons. Drugs do not cause jaundice in the elderly as frequently as they once did, particularly as phenothiazines, especially chlorpromazine, are not prescribed as often as previously. However, drugs should be considered as a potential cause and a careful check of the drug history is important.

Infective causes of jaundice A generation ago hepatitis A (infectious hepatitis or yellow jaundice) was the commonest recognised form of viral hepatitis, presenting usually with an abrupt onset of fever, anorexia, nausea and vomiting. It usually occurred in epidemics and hence was common in overcrowded institutions and camps. Now hepatitis B and C are the most commonly reported types of viral hepatitis with an onset that is more insidious and with a longer incubation period.4,7 Symptoms include malaise, anorexia, nausea and polyarthritis. Acute hepatitis C is often subclinical. The various forms of hepatitis are summarised in TABLE  58.5. All forms of hepatitis are common in developing countries and travellers are at risk of contracting these infections: hepatitis A and E from faeco-oral transmission; and hepatitis B, C, D and G from intravenous drugs and bodily fluids (from sexual transmission, in particular, for hepatitis B). Evidence points to more viruses causing non-ABC hepatitis.8 Hepatitis F virus has been claimed to be transmitted enterically while the newly designated hepatitis G virus (HGV) is transmitted parenterally. It does not appear to cause a severe illness in recipients. It can be predicted that the hepatitis alphabet will continue to expand. In hepatitis A, liver damage is directly due to the virus, but in hepatitis B and C it is due to an immunologic reaction to the virus. Other infections that can present with jaundice as part of a systemic disease are malaria, Epstein– Barr mononucleosis, cytomegalovirus, Q fever, toxoplasmosis, leptospirosis and, rarely, measles, varicella, yellow fever, rubella, herpes simplex, dengue fever, Lassa fever and Marburg and Ebola virus.

Hepatitis A Hepatitis A is becoming relatively less prevalent in first world countries. It is enterically transmitted and arises from the ingestion of contaminated food, such as shellfish, or water. There is no carrier state and it does not cause chronic liver disease. Hepatitis A most often causes a subclinical or self-limited clinical illness. Clinical features Pre-icteric (prodromal) phase: • • • •

anorexia, nausea ± vomiting malaise headache distaste for cigarettes in smokers

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Table 58.5

653

Characteristic profiles of viral hepatitis A–E

Characteristic

Hepatitis A

Hepatitis C

Hepatitis D

Hepatitis E

Pseudonyms

Infectious hepatitis Serum hepatitis

Parenterally transmitted non-A, non-B

Delta hepatitis

Enterically transmitted non-A, non-B

Agent (virus)

27 nm RNA

42 nm DNA

50 nm RNA

35 nm RNA

30 nm RNA

Transmission

Faecal–oral

Blood and other body fluids

Blood ? Other body fluids

Blood and other body fluids

Faecal–oral

Incubation period

15–45 days

40–180 days

14–180 days

30–50 days

15–45 days

Severity of acute illness

Mild to moderate; Mild to moderate; Mild to severe; often subclinical— jaundice common; often subclinical arthralgia and no jaundice rash common

Moderate to severe; high mortality; usually jaundice

Mild to moderate; often subclinical

Chronic liver disease

No

Yes 5–10%

Yes 20–50%

Yes Potentially worst

No

Carrier state

No

Yes

Yes

Yes

No

Risk in travellers

Yes, applies to all A–E: East and South-East Asia, Asian subcontinent (e.g. India), South Pacific Islands (e.g. Fiji), sub-Saharan Africa, Mexico, Russia, other developing countries. A and E with poor sanitation; B, C, D also with IV drug use; B, D sexual contact.

Antigens

HAV Ag

HBsAg, HBcAg, HBeAg

HCV Ag

HDV Ag

?

Serology

IgM anti-HAV diagnosis (HAV IgM)

HBsAg diagnosis anti-HBs— exposure immunity

anti-HCV (antibody) HCVRNA (PCR) HCV genotype

HBsAg +ve HDsAg +ve anti-HDV (antibody)

HEV IgM

Immunoprophylaxis

Normal Ig

HB Ig

? Ig effective

None

None

Vaccine

Hepatitis A vaccine

Hepatitis B vaccine

None

Hepatitis B vaccine

None

Hepatitis B

• mild fever • ± diarrhoea • ± upper abdominal discomfort Icteric phase (many patients do not develop jaundice):

infection, and IgG antibodies, which means past infection and lifelong immunity and which is common in the general population. Ultrasound is useful to exclude bile duct obstruction, especially in an older patient.

Recovery usually in 3–6 weeks. Fulminant hepatitis with liver coma and death may occur but is rare.

Outcome and treatment Hepatitis A has an excellent prognosis with most patients making a complete recovery, and patients should be reassured. The mortality is less than 0.5%. Admission to hospital is not usually necessary. There is no specific treatment, so management is as follows.

Investigations LFTs and viral markers confirm the diagnosis. The antibodies to HAV are IgM, which indicates active

• Provide appropriate reassurance and patient education. • Rest as appropriate. • Follow a fat-free diet.

• • • •

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dark urine pale stools hepatomegaly splenomegaly (palpable in 10%)

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• Avoid alcohol, smoking and hepatotoxic drugs (until recovery). • Advise on hygiene at home to prevent spread to close contacts and family members. • Wash hands carefully after using the toilet and disinfect them with antiseptic. • Do not handle food for others with your fingers. • Do not share cutlery and crockery during meals. • Do not use tea-towels to dry dishes.

Table 58.6

Higher-risk groups for contracting hepatitis B (vaccination advisable)7

Babies born to hepatitis B positive (carrier) mothers Garbage collectors Health care workers Household contacts of hepatitis B carriers Institutionalised intellectually disabled patients Intravenous drug users

Prevention Simple health measures such as good sanitation, effective garbage disposal and hand washing are probably responsible for the major decrease in the disease. Immune serum globulin (0.03–0.06 mL/kg IM) confers satisfactory passive immunity for close contacts (within 2 weeks of contact) and for travellers to endemic areas for up to 3 months. An active vaccine consisting of a two-dose primary course is the best means of prevention.

Hepatitis B Hepatitis B has protean clinical manifestations. Transmission is by blood spread, percutaneous, sexual transmission, perinatal spread or by close prolonged family contact. Infection may be subclinical or selflimited acute hepatitis. Fulminant hepatitis is rare. Five per cent of subjects go on to become chronic carriers of the virus. Most are ‘healthy carriers’ but some may develop chronic active hepatitis, cirrhosis and hepatoma. The serology of hepatitis B involves antibody responses to the four main antigens of the virus (core, DNA polymerase, protein X and surface antigens). Passive and active vaccines are available, and should be used freely in groups at risk, including babies of infected mothers. High-risk groups are presented in TABLE  58.6. The clinical features are the same as those found in hepatitis A infection but may be less abrupt in onset but more severe in the long term.7 A serum sickness-like immunological syndrome may be seen with transient rashes (e.g. urticaria or a maculopapular rash), and polyarthritis affecting small joints in up to 25% of cases in the prodromal period. Investigations5,9,10 The main viral investigation for HBV is HBsAg (surface antigen), which is searched for routinely. If detected, indicating hepatitis B positive or carrier, a full viral profile is then formed. HBsAg may disappear or persist. Its presence indicates a current or chronic infection as well as

Kidney dialysis patients Male homosexuals Prisoners Recipients of blood or blood products (prior to testing) Sex industry workers Sexual partners of hepatitis B carriers (especially acute HBV) Travellers to endemic areas

a carrier state (see FIG.  58.4). Chronic hepatitis B (carriage) is defined as the presence of HBsAg for at least 6 months. HBeAg is a soluble protein from the pre-core and core. Antibodies develop to both HBsAg and HBeAg.

Serological patterns Acute hepatitis HBsAg +ve, anti-HBcIgM + anti-HBs -ve Chronic hepatitis HBsAg +ve, anti-HBcIgG + anti-HBs -ve

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702

HBsAg

Anti-HBC lgM)

Anti-HBS

HBeAg Anti-HBe 0

1

2

3

4

5

6

Months

FIGURE 58.4 Time course of acute hepatitis B infection

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Jaundice Monitoring and outcome9, 10 The possible course of events is shown in FIGURE 58.5. The majority of patients recover completely with the outcome depending on several factors, including the virulence of the virus and the immune state and age of the patient. Some will develop chronic hepatitis, some will develop a fulminant course, and others will become asymptomatic carriers and present a health risk to others. Monitor progress with 6–12 monthly LFTs, HBeAg and HBV DNA. • Negative HBsAg and HBV DNA (with anti-HBe) = resolving, with anti-HBs = full recovery. • Positive HBsAg and HBV DNA = replicating and infective—refer. • Monitor LFTs every 6 months. Refer if ALT elevated. Treatment5 There is no specific treatment initially—appropriate reassurance and patient education are necessary. Advise avoidance of alcohol. Avoid certain drugs, e.g. sedatives, NSAIDs, OCP, until recovery (normal LFTs). Advise about prevention of transmission

(a)

Serology guidelines HBsAg = acute or persistent infection anti-HBs = past infection and immunity HBeAg = highly infectious HBV DNA = circulating and replicating virus anti-HBc IgM = recent and continuing infection anti-HBc IgG = past infection anti-HBe = seroconversion

(b)

Acute hepatitis B infection 95% of infant-acquired infections

especially safe sex and sharing needles. Treatment of chronic hepatitis B infection (abnormal LFTs) is with the immunomodulatory and antiviral agents— pegylated interferon alpha and entecavir or tenofir. This is expensive but it achieves permanent remission in 25% of patients, and temporary remission in a further 25%.7 Liver transplantation has been performed, but is often followed by recurrence of hepatitis B in the grafted liver. Follow up with regular LFTs and alpha-fetoprotein screening. It is appropriate to refer any HBsAg positive patient with an abnormal ALT and/or signs of chronic liver disease to a specialist since the evaluation of chronic hepatitis B can be complex.4

Acute hepatitis C infection

3–6% of adult-acquired infections

chronic HBV infection

20–40% spontaneously clear infection

60–80% are chronically infected

chronic hepatitis 15–40% lifetime risk 1.3–2.5% per annum cirrhosis 6–15% in 5 years

hepatocellular carcinoma

chronic hepatitis— minimal to severe inflammation and fibrosis bridging fibrosis

20–23% in 5 years

liver failure

1–4% per cirrhosis in 10–25% annum develops over 20–30 years

liver transplant

hepatocellular carcinoma

liver transplantation

liver failure

FIGURE 58.5 Natural history of (a) hepatitis B infection; (b) hepatitis C infection. Source: W Sievert, B Katz, Department of Gastroenterology, Monash Medical Centre

death

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Prevention Active immunisation through hepatitis B vaccination has been a major breakthrough in the management of this serious illness. There is a course of three injections. If there is a negative antibody response after 3 months, revaccinate with a double dose. If the response is positive, consider a test in 5 years with a view to a booster injection. For non-immune patients at risk (e.g. after a needle-stick injury), hepatitis B immunoglobin (HBIg), which contains a high level of HBV surface antibody, is appropriate. Prenatal screening of pregnant women and appropriate use of HBIg and HB vaccine is useful in preventing perinatal vertical transmission of HBV. Refer CHAPTER 109.

HCV RNA Anti-HCV antibody exposure

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0

ALT

1

2

3

4

5

6

Months

FIGURE 58.6 Time course of active hepatitis C infection

Hepatitis C5,9,11,12 Hepatitis C virus is responsible for most cases of viral hepatitis in Australia. It is primarily contracted from intravenous drug use or tattooing. It does not seem to be spread very readily by sexual contact although there is a small risk during heterosexual and homosexual intercourse. It is also not readily spread perinatally. Clinical symptoms of hepatitis C are usually minimal (often asymptomatic), and the diagnosis is often made after LFTs are found to be abnormal. An important feature is that there are at least six major genotypes of HCV and treatment decisions are based on the genotype; thus, patients with acute hepatitis C should have HCV genotype testing. Hepatitis C infection may be self-limiting, but more commonly (in about 70% of cases) causes a slow, relentless progression to chronic hepatitis, cirrhosis (20%) and also hepatoma.7 See FIGURE 58.6. The severity of hepatic fibrosis can be assessed by liver biopsy or, preferably, by a non-invasive device called a FibroScan that assesses ‘hardness or stiffness’ of the liver via the technique of transient elastography. A raised ALT level that is tested three times over the next 6 months implies disease activity. HCV RNA (a PCR test) is present when the ALT becomes abnormal while the anti-HCV rises more slowly and may not be detectable for several weeks. If the PCR test is negative, the hepatitis C infection has resolved.

• HCV-RNA +ve = chronic viraemia –ve = spontaneous clearance • CD4/HCV = viral load • ALTs on LFTs indicate disease activity (tested 3 times over next 6 months) ALT persistently normal = good prognosis ALT ↑ ↑ = requires referral for treatment • If PCR +ve + significant viral load + ALT ↑ perform HCV genotype—determines treatment • PCR –ve, ALT –ve = infection clear

Diagnosis and progress This is by serology:

Those at increased risk of having hepatitis B and C • Blood transfusion recipients (prior to HBV and HCV testing)

• HCV Ab (anti-HCV) +ve = exposure (current or past)

Treatment5,12 The current standard treatment for chronic hepatitis C is ribavirin orally daily and pegylated alphainterferon by weekly SCI—genotypes 1, 4, 5, 6 for 48 weeks; genotypes 2, 3 for 24 weeks. The combination therapy, which can cure many cases of hepatitis C, has considerable side effects, ranging from flu-like symptoms to depression to significant anaemia. At present the determination of the genotype and the viral load will identify those groups most likely to respond to therapy, for example, genotype 1 infected patients will have a good response while an excellent response including cure can be expected in genotypes 2 and 3. Acute hepatitis C can be treated with pegylated alphainterferon but the acute stage is difficult to recognise clinically. There is no vaccine yet available. These patients should be tested for hepatitis A and B and immunised if not immune. They should avoid alcohol.

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Jaundice • • • • • •

Intravenous drug users (past or present) Male homosexuals who have practised unsafe sex Kidney dialysis patients Sex industry workers Those with abnormal LFTs with no obvious cause Tattooed people/body piercing

Prevention of transmission of hepatitis B and C viruses Advice to those who are positive for HCV: • Do not donate blood or any body organs or tissues. • Do not share needles. • Advise health care workers, including your dentist. • Do not share intimate equipment such as toothbrushes, razors, nail files and nail scissors. • Wipe up blood spills in the home with household bleach. • Cover up cuts or wounds with an adequate dressing. • Dispose of bloodstained tissues, sanitary napkins and other dressings safely. • Use safe sex practices such as condoms. • Avoid tattooing.

Hepatitis D Hepatitis D is a small defective virus that lacks a surface coat. This is provided by hepatitis B virus, and so hepatitis D infection occurs only in patients with concomitant hepatitis B. It is usually spread parenterally and if chronic is usually associated with progressive disease with a poor prognosis. Treatment with interferon has a poor success rate. Antibodies to the delta virus, both anti-HDV and anti-HDV IgM (indicating a recent infection) as well as HDV Ag can be measured.13

Hepatitis E Hepatitis E is an enterically transmitted virus that occurs in outbreaks in certain countries with a poor water supply, such as some Asian subcontinent countries. Epidemiologically, HEV behaves like HAV, with well-documented water-borne epidemics in areas of poor sanitation. There is a high case fatality rate (up to 20%) in pregnant females.

Hepatitis F Researchers claim to have identified HGF virus, which is spread enterically.14

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Hepatitis G HGV has been identified as a transfusion-spread virus. It has subsequently been found to be prevalent among Queensland blood donors.10,15

Cholestatic jaundice Cholestasis refers to the syndrome of biliary obstructive jaundice whereby there is obstruction to the flow of bile from the hepatocyte to the duodenum, thus causing bilirubin to accumulate in the blood. It is classified into two main groups: • intrahepatic cholestasis—at the hepatocyte or intrahepatic biliary tree level • extrahepatic cholestasis—obstruction in the large bile ducts by stones or bile sludge The significant causes are listed in TABLE 58.7.

Table 58.7 Significant causes of cholestasis in adults Intrahepatic Alcoholic hepatitis/cirrhosis Drugs Primary biliary cirrhosis Viral hepatitis Extrahepatic Cancer of bile ducts Cancer of pancreas Other cancer: primary or secondary spread Cholangitis Primary sclerosing cholangitis (? autoimmune) Common bile duct gallstones Pancreatitis Post-surgical biliary stricture or oedema

Symptoms • Jaundice (greenish tinge) • Dark urine and pale stools • Pruritus—worse on palms and soles • Pain varies from nil to severe Gallstones and jaundice Gallstones can be found in the following (see FIG. 58.7): • gall bladder (asymptomatic up to 75%)—the majority remain here

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Carcinoma of head of the pancreas

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common hepatic duct stone impacted in cystic duct or gall bladder neck biliary pain or acute cholecystitis stone in common bile duct biliary pain obstructive jaundice cholangitis

asymptomatic stones or symptomatic

Pancreatic cancer is the fourth commonest cause of cancer death in the UK and US.13 Clinical features • M > F • Mainly >60 years of age • Obstructive jaundice • Pain (over 75%)—epigastric and back • Enlarged gall bladder (50–75%)

Possible features ampulla of Vater

duodenum

FIGURE 58.7 Clinical presentation of gallstones

• neck of gall bladder (biliary ‘colic’ or acute cholecystitis) • cystic duct (biliary ‘colic’ or acute cholecystitis) • common bile duct—may cause severe biliary ‘colic’, cholestatic jaundice or cholangitis Acute cholecystitis is accompanied by mild jaundice in 25% of cases, due to accompanying common duct stones.13 Common bile duct stones may be asymptomatic or may present with any one or all of the triad of abdominal pain, jaundice and fever. The jaundice varies, depending on the amount of obstruction. The liver is moderately enlarged if the obstruction lasts for more than a few hours. The investigations of choice for cholestatic jaundice are ultrasound and ERCP.

Acute cholangitis This is due to bacterial infection of the bile ducts secondary to abnormalities of the bile duct, especially gallstones in the common duct. Other causes are neoplasms and biliary strictures. Charcot triad (present in 70%) is shown in the diagnosis box. DxT fever (often with rigor) + upper abdominal  pain + jaundice   acute cholangitis

• • • •

Weight loss, malaise, diarrhoea Migratory thrombophlebitis Palpable hard, fixed mass Metastases (e.g. left supraclavicular gland of Troisier) • Occult blood in stool • Glycosuria Diagnosis • Scanning by ultrasound or CT scan may show mass • ERCP

DxT jaundice + constitutional symptoms (malaise, anorexia, weight loss) + epigastric pain (radiating to back)   pancreatic cancer

Prognosis Prognosis is very poor: 5-year survival is 5%.

Cirrhosis of the liver Cirrhosis is accompanied by jaundice as a late and serious manifestation with the exception of primary biliary cirrhosis, where jaundice appears before advanced liver failure. The development of jaundice usually indicates that there is minimal hepatic reserve and is therefore found in conjunction with other signs of liver failure (see FIG. 58.8). Causes Common: • alcohol excess • chronic viral hepatitis (esp. HBV, HCV)

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Jaundice alcohol facies telangiectasia plethora rhinophyma bloatedness angular chelitis suffused conjunctiva

parotid enlargement spider naevi

jaundice gynaecomastia splenomegaly (possible)

hepatomegaly

dilated veins (caput medusae) sparse pubic hair

ascites (possible) palmar erythema

soft atrophic testes

Dupuytren contractur e

flapping tremor (asterixis) clubbing leuconychia (white nails)

bruising

? peripheral neuropathy ? peripheral oedema

FIGURE 58.8 Possible features of chronic alcoholic liver disease

• • • • • •

autoimmune chronic active hepatitis primary biliary cirrhosis (autoimmune) haemochromatosis Wilson syndrome drugs (e.g. methotrexate) cryptogenic (no cause found)

Clinical features • Anorexia, nausea ± vomiting • Swelling of legs • Abdominal distension • Bleeding tendency • Drowsiness, confusion or coma (if liver failure)

659

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fetor, breath

Others:

707

Signs • Spider naevi (distribution of superior vena cava) • Palmar erythema of hands • Peripheral oedema and ascites • Jaundice (obstructive or hepatocellular) • Enlarged tender liver (small liver in long-term cirrhosis) • Ascites • Gynaecomastia • ± Splenomegaly (portal hypertension) Complications • Ascites • Portal hypertension and GIT haemorrhage

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• Portosystemic encephalopathy • Hepatoma • Kidney failure

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Autoimmune chronic active hepatitis (ACAH)5 Also termed idiopathic ACAH, this usually affects young females (10–40 years) who present insidiously with progressive fatigue, anorexia and jaundice. Diagnosis is made by abnormal LFTs, positive smooth muscle antibodies, a variety of other autoantibodies and a typical liver biopsy. If untreated, most patients die within 3–5 years. Treatment is with prednisolone orally, monitored according to serum alanine aminotransferase levels, and supplemented with azathioprine or mercaptopurine. About 80% respond while 20% develop chronic liver disease.

Primary sclerosing cholangitis5 This uncommon inflammatory disorder of the biliary tract presents with progressive jaundice and other features of cholestasis such as pruritus. It is often associated with ulcerative colitis. Diagnosis is based on characteristic cholangiopancreatography findings. There is no specific therapy, but refer for possible ERCP.

Primary biliary cirrhosis5 This is an uncommon cause of chronic liver disease that often presents with pruritis, malaise and an obstructive pattern of liver biochemistry. Treatment is with ursodeoxycholic acid orally.

Alcoholic liver disease The main effects of alcohol excess on the liver are: • acute alcoholic liver disease • fatty liver • alcoholic hepatitis (progresses to cirrhosis if alcohol consumption continues) • alcoholic cirrhosis If diagnosed, patients are advised to stop drinking alcohol for life except for fatty liver when small amounts can be drunk later.

Fatty liver Alcohol can cause hepatic steatosis (fatty liver), which is almost universal in obese alcoholics. Nonalcoholic causes include obesity, diabetes mellitus,

hypertriglyceridaemia and corticosteroids. A significant number with this very common condition (one in five Australians) will develop cirrhosis. Fatty liver is usually asymptomatic but some complain of malaise and tiredness. Serology is unhelpful. Diagnosis is by liver biopsy and perhaps CT scan. The treatment is weight loss through diet, which improves liver function and reduces fatty deposits.

Special patient groups The returned overseas traveller The overseas traveller presenting with jaundice may have been infected by any one of the viruses— hepatitis A, B, C, D or E. All are prevalent in developing countries, especially in south-eastern and eastern Asia, some Pacific islands and Africa. Other causes to consider are malaria, ascending cholangitis and drug-induced hepatic damage due to, for example, the antimalarials, including mefloquine (Lariam) and Fansidar. Refer CHAPTERS 14 and 15.

The pregnant patient Important hepatic disorders in pregnancy leading to jaundice are cholestasis of pregnancy, acute fatty liver of pregnancy and severe pre-eclampsia. Refer to CHAPTER 109.

Postoperative jaundice There are many possible causes of postoperative jaundice either in the immediate or the long-term postoperative phase. Hypoxia associated with shock in a severely ill patient or in a patient with cardiopulmonary disease may lead to transient abnormalities in liver function. Other causes include: • • • • • •

post-transfusion hepatitis coincident viral hepatitis drugs, including anaesthetics transfusion overload (haemolysis) sepsis unmasked chronic liver disease and biliary tract disease • cholestasis: post major abdominal surgery

Neonates of HBeAg positive mothers The neonates should have the following (see CHAPTER 109): • hepatitis B immunoglobulin IM within 24 hours of birth • hepatitis B vaccine at birth, 1 month and 6 months

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Jaundice This is not 100% effective because some infants can be infected in utero.

When to refer • • • • • • • •

All patients with fulminant hepatitis All patients with chronic liver disease Painless obstructive jaundice Evidence of malignancy Symptomatic gallstones Patients with cirrhosis Acute fatty liver of pregnancy (very urgent) Suspected rare conditions (e.g. Wilson syndrome)

Practice tips • •

• • •

• •

•

• •

All drugs should be suspected as potential hepatotoxins. With hepatitis A the presence of IgM antibodies reflects recent infection, and IgG antibody indicates past infection and lifelong immunity. There is no chronic carrier state of hepatitis A and E. All patients with jaundice should be tested for hepatitis B surface antigen (HBsAg). Hepatitis B infection is usually benign and shortlived, but it can be fatal if chronic hepatitis develops, which may lead later to cirrhosis and hepatocellular carcinoma. Up to 5% of patients with hepatitis B will become chronic carriers (especially drug addicts). Such carriers are identified by persistent titres of HBsAg and possibly HBeAg, the latter indicating the presence of the whole virus, and active replication and high infectivity. A raised gamma glutamyl transferase accompanied by a raised MCV is a good screening test for alcohol abuse. A systolic murmur may be heard over the liver in alcoholic hepatitis and hepatoma. A distaste for smoking (with jaundice) suggests acute viral hepatitis.

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Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Gallstones • Hepatitis A • Hepatitis B • Hepatitis C

References 1 Kincaid-Smith R, Larkins R, Whelan G. Problems in Clinical Medicine. Sydney: McLennan & Petty, 1989: 251. 2 Coffman D, Chalstrey J, Smith-Laing G. Gastrointestinal Disorders. Edinburgh: Churchill Livingstone, 1986: 106. 3 Sandler G, Fry J. Early Clinical Diagnosis. Lancaster: MTP Press, 1986: 468–90. 4 Croagh C, Desmond D. Viral hepatitis: an A, B, C guide. Medicine Today, 2007; 8 (7): 47–56. 5 Moulds R (Chair). Therapeutic Guidelines: Gastrointestinal (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2011: 169–205. 6 Thomson K, Tey D, Mark M. Paediatric Handbook (8th edn). Melbourne: Blackwell Science, 2009: 438–9. 7 Ruff TA, Gust I. Hepatitis, viral (acute and chronic). In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 226– 30. 8 Bowden DS, Moaven LD, Locarnini SA. New hepatitis viruses: are there enough letters in the alphabet? Med J Aust, 1996; 164: 87–9. 9 Cossart Y. Recent advances in diagnosis and management of viral hepatitis. Common sense pathology. RCPA + Australian Doctor, 2006: 2–8. 10 McCaughan G, Levy M. Hepatitis B infection: how to treat. Australian Doctor, 16 January 2004: 28–32. 11 Singal DK, George J. Chronic hepatitis C. Australian Doctor, 15 February 2001: i–viii. 12 Mahady S, George J. Hepatitis C infection. Australian Doctor, 5 February 2010: 19–26. 13 McPhee SJ, Papadakis MA et al. Current Medical Diagnosis and Treatment (49th edn). New York: The McGraw-Hill Companies, 2010: 636. 14 Deka N, Sharma MD, Mukerjee R. Isolation of the novel agent from human stool that is associated with sporadic human hepatitis. J Virol, 1994; 68: 7810–15. 15 Moaven LD et al. Prevalence of hepatitis G virus in Queensland blood donors. Med J Aust, 1996; 165: 369–71.

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Nasal disorders

The face of Mrs Gamp—the nose in particular—was somewhat red and swollen, and it was difficult to enjoy her society without becoming conscious of the smell of spirits. Charles Dickens (–), Martin Chuzzlewit Disorders of the nose, which include the everyday problems of rhinitis, postnasal drip, epistaxis, folliculitis and disorders of smell, are very common in everyday general practice. The main functions of the nose are: • airflow • filtration—of dust, organisms and other air-borne particles • olfaction (smell) • self-cleansing and moisturising of the mucous membrane • humidification and warming of air in its passage to the lungs • vocal resonance The main symptoms of nasal disorders are discharge, blockage, sneezing, anosmia, itching, postnasal drip, bleeding and snoring (see TABLE 59.1).1 Nasal discharge is a common and important symptom to evaluate. The characteristics of nasal discharge are summarised in TABLE 59.2. Table 59.1

Typical symptoms for nasal disorders2

Foreign body

Unilateral discharge, unilateral blockage

Acute sinusitis

Facial pain, toothache, nasal discharge, postnasal drip

Allergic rhinitis

Sneezing, rhinorrhoea, itch, eye irritation

Infective rhinitis

Blockage, purulent discharge, postnasal drip

Deviated septum

Blockage, postnasal drip

Nasal polyps

Blockage, reduced sense of smell

Nasal tumour

Blockage, unilateral discharge, epistaxis

Adenoidal hypertrophy

Bilateral blockage, snoring, halitosis

Nasal vestibulitis

Local pain, crusting, malodour

Table 59.2

Characteristics of nasal discharge

Nature of discharge Think of: Blood

Neoplasia, trauma, bleeding disorder, rhinitis, infection, hypertension

Mucopurulent

Bacterial rhinitis, foreign body

Serosanguineous

Neoplasia, foreign body

Watery/mucoid

Viral rhinitis, allergic rhinitis, vasomotor rhinitis, CSF

A major presenting problem is nasal obstruction with the complaint of a blocked or ‘stuffy’ nose. Common causes are physiological (the nasal cycle), rhinosinusitis (allergic or non-allergic), polyps, adenoid hypertrophy and mechanical such as septal deformity.

Red flag pointers for nasal disorders • • • • • •

Unilateral nasal ‘polyp’ Unilateral blood-stained discharge Toddler with offensive nasal discharge esp. unilateral Post-traumatic periseptal swelling Rhinitis medicamentosa Chronic sinusitis + LRTI = ? Wegener granulomatosis

Disorders of smell The basic sense of smell is detected in the olfactory region by the olfactory nerve (cranial nerve I) while irritant sensors in the nose, mediated by the maxillary branch of the trigeminal nerve (cranial nerve V), detect some noxious odours. The disorders can be classified as:3 • anosmia—no smell • hyposmia—reduced smell

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Nasal disorders • hyperosmia—increased sensitivity to odours • dysosmia—distortion of smell perception — cacosmia—normal odours seem foul or unpleasant — parosmia—a perverse sense of smell Disorders of smell can be caused by conductive or sensorineural disturbances or considered as idiopathic (see TABLE  59.3). Conductive disorders present as anosmia or hyposmia, while sensorineural disorders can present with all of the above disorders.3 Most cases of idiopathic anosmia are considered to be viral neuropathies and may last from a few days to several months. Head trauma, which can cause conductive or sensorineural disturbances, is considered to be caused either from a fracture of the skull involving the cribriform plate or, more commonly, by posterior head trauma. Some patients will never recover their sense of smell. Patients with anosmia lack flavour discrimination and often have accompanying loss of sense of taste. They are also vulnerable to an unawareness of smoke, gas, dangerous chemicals and unhealthy food. Table 59.3

Causes of reduced sense of smell

Conductive defects Head trauma Nasal polyps Septal deviation Rhinitis and sinusitis Rare (not to be missed) Nasal tumour Wegener granulomatosis Central/sensorineural defects Ageing Chemicals (e.g. benzene, chlorine, formaldehyde, cement dust) Cigarette and other smoking/inhalation Drugs Endocrine disorders (e.g. diabetes, hypothyroidism) Frontal lobe tumour Parkinson disease Head trauma Kallmann syndrome (anosmia + hypogonadism) Nutritional deficiencies Viral infections

The clinical approach • History: head injury or surgery, recent URTI, drugs, occupation including chemical exposure

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• Physical examination, including inspection via a Thudicum nasal speculum • Sniff test—qualitative and quantitative odours (e.g. coffee, cloves, lemon, peppermint, water placebo). Ammonia (for irritant sensation) • Investigations (e.g. CT scan for sinus disease, nasal polyps)

Treatment2,4 • Explanation and reassurance • Education about smoke detectors, caution about chemicals including gas, excessive perfume, food safety including milk and meat contamination • Consider dietary supplement with daily zinc sulphate, vitamin A and thiamine For chronic anosmia following an URTI: • prescribe a nasal decongestant such as Spray-Tish Menthol for 5–7 days

Rhinitis Rhinitis is inflammation of the nose causing sneezing, nasal discharge or blockage for more than an hour during the day. Rhinitis is subdivided into various types: • According to time span: — seasonal rhinitis: occurs only during a limited period, usually springtime — perennial rhinitis: present throughout the year • According to pathophysiology: — allergic rhinitis: an IgE-mediated atopic disorder — vasomotor rhinitis: due to parasympathetic overactivity Both allergic and vasomotor rhinitis have a strong association with asthma. The classification can be summarised as: • seasonal allergic rhinoconjunctivitis = hay fever • perennial rhinitis — allergic (usually due to house dust mites) — non-allergic = vasomotor: eosinophilic, noneosinophilic Note: allergic rhinitis (hay fever) is presented in detail in CHAPTER 80. Clinical features Nasal symptoms: • sneezing • nasal obstruction and congestion • hypersecretion—watery rhinorrhoea, postnasal drip

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• reduced sense of smell • itching nose (usually allergic) Throat symptoms: • dry and sore throat • itching throat

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Irritated eyes (allergic) Abnormal nasal mucous membrane—pale, boggy, mucoid discharge. A transverse nasal crease indicates nasal allergy, especially in a child.

Allergens • • • • •

Pollens from trees (spring) and grass (in summer) Moulds House dust mites (perennial rhinitis) Hair, fur, feathers (from cats, dogs, horses, birds) Some foods (e.g. cow’s milk, eggs, peanuts, peanut butter)

Diagnosis Allergic rhinitis—nasal allergy: • detection of allergen-specific IgE antibodies (not specific) • RAST test or skin testing for specific allergens (can get false negatives)

RHINOSINUSITIS

Acute sinusitis Acute sinusitis is acute inflammation in the mucous membranes of the paranasal sinuses. About 5% of URTIs are complicated by an acute sinusitis,4 which is mainly viral initially while secondary bacterial infection commonly follows. Any factor that narrows the sinus openings into the nasal cavity (the ostia) will predispose to acute sinusitis. The two prime clinical presentations are: 1 an URTI persisting for longer than 10 days 2 an URTI that is unusually severe with pyrexia and a purulent nasal discharge Refer to CHAPTER 52 for features of acute maxillary sinusitis.

Chronic sinusitis Chronic sinusitis is the most common complication of acute sinusitis. In chronic sinusitis the symptoms and signs of inflammation persist for more than 8–12 weeks and are more likely to be associated with factors that impair drainage via the osteomeatal complex, including nasal polyps.

Vasomotor rhinitis—a diagnosis of exclusion. Other causes of rhinitis • Chronic infection (viral, bacterial, fungal) • Rhinitis of pregnancy • Rhinitis medicamentosa—following overuse of OTC decongestant nasal drops or oxymetazoline sprays • Drug-induced rhinitis: — various antihypertensives — aspirin — phenothiazines — oral contraceptives — cocaine, marijuana • Chemical or environmental irritants (vasomotor rhinitis): — smoke and other noxious fumes — paints and sprays — cosmetics Factors aggravating rhinitis (vasomotor) • Emotional upsets • Fatigue • Alcohol • Chilly damp weather • Air-conditioning • Sudden changes in temperature and humidity

Treatment • Amoxycillin 500 mg (o) 8 hourly for 10–14 days, possibly for longer periods of 3–6 weeks5 • Consider decongestant spray (e.g. xylometazoline) for maximum of 5 days and intranasal steroids • Steam inhalations three times daily • Nasal saline sprays

Chronic rhinosinusitis If the above therapies are ineffective a mechanical saline sinus irrigation procedure to remove stagnant mucus is beneficial.6 Refer urgently: • for surgical drainage if there is no response to the above regimen • those with orbital or facial cellulitis

Nasal polyps Nasal polyps are round, soft, pale, pedunculated outgrowths arising from the nasal or sinus mucosa. They are basically prolapsed, congested, oedematous mucosa, described by some as ‘bags of water’ (FIG 59.1). They occur in patients with all types of rhinitis, but

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Nasal disorders Treatment The initial treatment should be medical.7 A medical ‘polypectomy’ can be achieved with oral steroids, for example, prednisolone 50 mg daily for 7 days. Supplement this with a corticosteroid spray such as betamethasone, starting simultaneously and continuing for at least 3 months. Give antibiotics for any purulent nasal discharge. Simple polyps can be readily snared and removed, but referral to a specialist surgeon is advisable for surgical intervention since the aim is to remove the polyp with the mucosa of the sinuses (often ethmoidal cells) from which it arises. This complex procedure reduces the incidence of recurrence. FIGURE 59.1 Nasal polyp in right nasal cavity in a patient with inflamed mucosa from allergic rhinitis

sinuses

Epistaxis This common emergency should, in some instances, be treated as a life-threatening problem. The common situation is intermittent anterior bleeding from Little area, seen in children and the young adult (90% of episodes), while posterior epistaxis (10%) is more common in the older hypertensive patient. It has a strong association with higher URTI (rhinitis, sinusitis), hot dry climates and trauma. Neoplasms should be kept in mind. Bleeding often occurs at night due to vascular vasodilation. Systemic factors include hypertension, atherosclerotic vascular disease, bleeding disorders and the rare hereditary haemorrhagic telangiectasia (see TABLE 59.4). The secret

nasal cavity polyp from maxillary sinus

nasal septum

FIGURE 59.2 Cross-section of nose, demonstrating origin of nasal polyps

especially in allergic rhinitis (see FIG.  59.2). Polyps usually arise from the middle meatus and turbinates. Symptoms include nasal obstruction, watery discharge, postnasal drip and loss of smell. Note: • Nasal polyps may be associated with asthma and aspirin sensitivity. • Cystic fibrosis should be considered in any child with nasal polyps. • A polyp that does not have the typical smooth pale appearance may be malignant. • A unilateral ‘polyp’ may be a neoplasm. • If there is a purulent discharge, swab and give antibiotics.

Table 59.4

Causes of epistaxis

Local causes Idiopathic (spontaneous) Intracranial tumours Rhinitis Trauma including nose picking, nasal fracture URTIs: • common cold • influenza • sinusitis Systemic causes Blood disorders (e.g. leukaemia, thrombocytopenia) Cardiovascular disorders: • arteriosclerosis • hypertension Drugs: anticoagulants, aspirin, others Hereditary haemorrhagic telangiectasia Systemic febrile infections (e.g. malaria) Toxic agents

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of good management is to have the right equipment, good lighting and effective local anaesthesia. Ideal equipment Head light, Thudicum nasal speculum, Tilley nasal packing forceps, suction cannula and tubing, CoPhenylcaine forte spray ± 5% cocaine solution.

Tamponade options (for difficult bleeding)

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Merocel expandable pack, Kaltostat, BIPP (bismuth iodoform paraffin paste) with ribbon gauze, Foley catheter (no. 12, 14 or 16) with a 30 mL balloon and self-sealing rubber stopper, anterior/posterior balloon, Epistat catheter with or without Kaltostat. Treatment Simple tamponade: • Pinch ‘soft’ part of nose below the nasal septum between thumb and finger for 5 minutes • Apply ice packs to bridge of nose Simple cautery of Little area (see FIG. 59.3) (under local anaesthetic e.g. Co-Phenylcaine forte nasal spray ± 5% cocaine solution): • use one of three methods: electrocautery trichloracetic acid or silver nitrate stick (preferred)

Persistent anterior bleed Merocel (surgical sponge) nasal tampon or Kaltostat pack

‘Trick of the trade’ for intermittent minor anterior epistaxis: topical antibiotic (e.g. Aureomycin ointment) bd or tds for 10 days or (better option) Nasalate nasal cream tds for 7–10 days or Rectinol ointment or Vaseline Avoid digital trauma and nose blowing.

Severe posterior epistaxis Use a Foley catheter or an Epistat catheter.

Nasal vestibulitis Infection of the nasal vestibule can cause a tender, irritating, crusty problem. Low-grade infections and folliculitis, which are evident on inspection, cause localised pain, crusts and bleeding, especially if picked from habit. Treatment is with bacitracin or preferably mupirocin (intranasal) ointment topically for 5–7 days. Furunculosis of the nasal vestibule is usually due to Staphylococcus aureus. It starts as a small superficial abscess in the skin or the mucous membrane and may develop into a spreading cellulitis of the tip of the nose. The affected area becomes tender, red and swollen. It is best treated by avoidance of touching, hot soaks and systemic antibiotics such as dicloxacillin or as determined by culture from swabs of the vestibule.

anterior ethmoid artery

Little area

septal branch of the sphenopalatine artery

branch from superior labial greater palatine artery

FIGURE 59.3 Little area on the nasal septum where several blood vessels anastomose. Bleeding is common here, especially in young people

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Nasal disorders Tip: Staphylococcus aureus colonises the nose of 20–30% of the population.8 Carriers are prone to transmit nosocomial infection and have an increased risk of serious infections in the presence of serious medical disorders. Treatment includes strict hygiene and eradication with an agent such as mupirocin ointment (match-head size) 2–3 times daily for 5–7 days (max. 10 days).6 Fissure: Painful fissures often develop at the mucocutaneous junction. They may become crusted and chronic. Fissures can be treated by keeping the area moist with petroleum jelly (Vaseline) or saline gel, using hot compresses and the use of an antibiotic or antiseptic ointment if necessary. Offensive smell from nose This may be caused by vestibulitis but ensure no foreign body is present. Treatment • Take nasal swab for culture. consider mupirocin 2% nasal ointment, instilled 2 to 3 times a day for 10 days or Kenacomb ointment, instil 2 to 3 times a day

Rhinophyma This disfiguring swelling of the nose is due to hypertrophy of the nasal sebaceous glands. There is no specific association with alcohol. It is almost exclusive to men over the age of 40 years. Rhinophyma may be associated with rosacea. Treatment • Good control of rosacea may reduce the risk (see CHAPTER 123). • If surgical correction is warranted refer to a specialist. • Carbon dioxide laser therapy is the treatment of choice. • Shave excision is another effective therapy.

Nasal septal deviation This causes blockage as a solitary symptom. Mild septal deviation tends to cause alternating blockage while severe deviation causes persistent blockage on one side. The septum can be divided into anterior and posterior segments. The anterior portion is necessary to support the cartilaginous pyramid of the nose whereas the posterior portion has no supporting role and can be removed without disturbing the support of

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the nose. The classic submucous resection operation is therefore suitable for posterior septal deviations. Repair of anterior septal deviations is more complex. Nasal cosmetic surgery Rhinoplasty is undertaken to improve the function of an obstructed nasal airway or for cosmetic reasons. In counselling for rhinoplasty it is important to undertake careful planning with realistic anticipated outcomes. The GP should provide non-judgmental support for the patient's decision for cosmetic surgery before referral to an expert in rhinoplasty. Each case has to be assessed individually and the surgery tailored to the deformity. Attention to surgery to the airway is important, otherwise the nose may become partially obstructed and stuffy after cosmetic surgery alone.

Septal perforation A hole in the nasal septum is caused commonly by chronic infection including tuberculosis, repeated trauma such as vigorous nose ‘picking’ or following nasal surgery. It is a known occupational hazard particularly among chrome workers and is seen in drug users who sniff cocaine. In about 5–10% of cases perforation is a result of malignant disease.4 The condition may be asymptomatic depending on the cause, but there is often an irritating nasal crust and a whistling sound on nasal inspiration. It can be demonstrated by looking in one nares while a light is shone in the opposite one. The cartilaginous part is usually involved. If not due to a serious cause, treat with Vaseline or saline gel and topical antibiotics for any infection. Refer if malignancy is suspected, otherwise treat symptomatically.

Nasal fractures2,9 Fractures of the nose can occur in isolation or combined with fractures of the maxilla or zygomatic arch. They may result in nasal bridge bruising, swelling, non-alignment and epistaxis. Always check for a compound fracture or head injury and, if present, leave alone and refer. If the patient is seen immediately (such as on a sports field) with a straightforward lateral displacement, reduction may be attempted ‘on the spot’ with digital manipulation before distortion from soft tissue swelling. This involves simply using the fingers to push laterally on the outside of the nose towards the injured side.2 Tips: • X-rays are generally unhelpful unless excluding other facial skeletal injuries.

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• If a deformity is present refer the patient within 7 days, ideally from days 3–5. • Skin lacerations, i.e. compound fracture, usually require early repair. • The optimal time to reduce a fractured nose is about 10 days after injury. There is a window period of 2–3 weeks before the fracture unites. • Closed reduction under local or general anaesthetic is the preferred treatment. • Open reduction is more suitable for bilateral fractures with significant septal deviation, bilateral fractures with major dislocations or fractures of the cartilaginous pyramid. Refer: • uncontrolled epistaxis • recurrent epistaxis • concern about cosmetic alignment

Haematoma of nasal septum Septal haematoma following injury to the nose can cause total nasal obstruction. It is easily diagnosed as a marked swelling on both sides of the septum when inspected through the nose (see FIG. 59.4). It results from haemorrhage between the two sheets of mucoperiosteum covering the septum. It may be associated with a fracture of the nasal septum.

Treatment • Remove blood clot through an incision, under local anaesthetic. • Prescribe systemic (oral) antibiotics (e.g. penicillin or erythromycin). • Treat as a compound fracture if X-ray reveals a fracture. • ENT specialist advice as necessary.

Stuffy, running nose in adults For simple post-URTI rhinitis, blow the nose hard into disposable paper tissue or a handkerchief until clear, instil a nasal decongestant for 2 to 3 days and also have steam inhalations with Friar's Balsam or menthol preparations.

RHINORRHOEA This can be normal or abnormal. There is a ‘nasal cycle’ in which there is nasal congestion and decongestion that alternates from side to side and leads to rhinorrhoea. Other causes of normal discharge include vasomotor reactions to external environmental stimuli, such as cold wind and irritants, and postnasal drip (2 L of mucus pass down the back of the nose each day).

Senile rhinorrhoea This is a common, distressing problem in the elderly, caused by failure of the vasomotor control of the mucosa. It may be associated with a deviated septum and dryness of the mucosa. There are few physical signs apart from the nasal drip. The treatment is to keep the nasal passages lubricated with an oily based preparation, for example, insufflation with an oily mixture (a sesame oil based preparation, e.g. Nozoil, is suitable) or petroleum jelly. Topical decongestants cause serious side effects in the elderly.

CSF rhinorrhoea FIGURE 59.4 Inferior view of nasal cavity showing bilateral swelling of septal haematoma

Note: This is a most serious problem as it can develop into a septal abscess. The infection can pass readily to the orbit or the cavernous sinus through thrombosing veins and may prove fatal, especially in children. Otherwise it may lead to necrosis of nasal septal cartilage followed by collapse and nasal deformity.

Following head injury, clear dripping fluid (+ve for glucose) may indicate a fracture of the roof of the ethmoid. Refer for assessment although spontaneous healing can occur.

Neoplasia Malignant nasal disease, which is uncommon, may cause nasal discharge which may be clear at first, becoming thick and offensive. Malignancy should be suspected in the presence of blood. The growth may be in the nasal fossa, sinus or nasopharynx.

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Nasal disorders Benign tumours include papilloma, fibroma, osteoma, fibroangioma of puberty and nasal polyps. Fibroangiomas occur exclusively in males between the ages of 9 and 24. Patients present with unilateral nasal obstruction and recurrent epistaxis. Malignant tumours include nasopharyngeal carcinoma, with the maxillary sinus being the most common site. Squamous cell carcinoma is the most common, followed by adenocarcinoma melanoma and lymphoma. Malignant or non-healing granuloma, sometimes called ‘midline granuloma’, is a slowly progressing ulceration of the face starting in the region of the nose.4 It may represent a form of T cell malignant lymphoma, which responds to radiotherapy. The differential diagnosis is Wegener granulomatosis (see CHAPTER 32). Diagnosis is by CT scan and biopsy. Treatment of nasopharyngeal and sinonasal carcinoma depends on the site, size and histology, but usually involves a combination of surgery and postoperative radiotherapy.

NASAL DISORDERS IN CHILDREN Nasal problems, especially nasal discharge (rhinorrhoea), are very common in children but the pattern of presentation is usually different from that of adults. Sinusitis is uncommon in children under the age of 10 and allergic nasal polyps are relatively rare. If a child presents with polyps, consider the possibility of cystic fibrosis or neoplasia. Rhinitis, epistaxis and nasal foreign bodies are common. Abnormal causes • Adenoid hypertrophy causing post-nasal space obstruction • Foreign body in nose—usually unilateral discharge • Allergic rhinitis • Unilateral choanal atresia • Sinusitis (possible but rare) • Tumour (also rare—consider fibroangioma) Diagnosis may be enhanced by spraying with a vasoconstricting agent and getting the child to blow the nose. A tumour, foreign body or polyp may become visible.

Choanal atresia Acute bilateral nasal obstruction may occur in newborns with congenital bilateral choanal atresia. This leads to anterior nasal discharge and to acute respiratory distress. Immediate investigation and relief are essential and a finger in the corner of the mouth can be life-saving as can passing a nasal probe down one nostril and perforating the membrane.

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Sinusitis Although rare, sinusitis can represent a serious emergency. Red flags requiring consideration include a sick child, pyrexia, rapid onset, unilateral and deteriorating airway obstruction.

Blocked nose and snoring The above causes of nasal blockage may lead to snoring, mouth breathing, reduced sense of smell, dribbling and possibly obstructive sleep apnoea.

Nasal trauma and fractures10 Areas of concern associated with nasal fractures, which are uncommon, are possible child abuse, open fracture, septal haematoma or abscess and eye or facial changes. If a fracture is undisplaced the treatment is pain relief, ice compresses and rest. If displaced refer for closed reduction under general anaesthetic within 1–2 weeks (ideally at 10 days).10 If associated epistaxis does not settle with pressure, temporary packing may be required.

Epistaxis Epistaxis is usually intermittent anterior bleeding from Little area and may follow trauma including nose picking. Bleeding often occurs at night due to vascular vasodilatation. At first, try correction with simple measures (see earlier in chapter) such as pinching below the nasal septum for 5 minutes, supplemented by cold packs. Vaseline applied in the nose at night tends to prevent bleeding while an antibiotic ointment twice daily for 7–10 days may help. If problematic, refer for an ENT appointment. Tip: Think of a bleeding disorder or a tumour, e.g. juvenile angiofibroma.

Snoring and obstructive sleep apnoea In normal children these problems are almost always due to adenotonsillar hypertrophy and most cases are relieved by surgery; CPAP is rarely necessary. Sleep studies are performed to confirm clinical features and allay parental concerns. See CHAPTER 71.

The snuffling infant Snuffling in infants is usually caused by rhinitis due to an intercurrent viral infection. The presence of yellow or green mucus should not usually be cause for concern.

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Treatment Reassure the parents.

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• Paracetamol mixture or drops for significant discomfort. • Get the parents to perform nasal toilet with a salt solution (1 teaspoon of salt dissolved in some boiled water); using a cotton bud, gently clear out nasal secretions every 2 waking hours. • Once the nose is clean, saline nose drops or spray (e.g. Narium nasal mist) can be instilled. • Stronger decongestant preparations are not advised unless the obstruction is causing a significant feeding problem, when they can be used for up to 4–5 days.

Foreign bodies in the nose The golden rule is ‘a child with unilateral nasal discharge has a foreign body (FB) until proved otherwise’. Such foreign bodies usually consist of beads, pebbles, peas, pieces of rubber, plastic and paper or other small objects handled by the child. A rhinolith may develop in time on the foreign body. In adults, foreign bodies are often rhinoliths, which are sometimes calcium deposits on pieces of gauze or other material that has been used to pack the nose. Removal of foreign bodies Removal of FBs from the nose in children is a relatively urgent procedure because of the risks of aspiration. A disc/button battery such as a hearing aid battery in the nose is a medical emergency requiring urgent removal under anaesthetic.10 The nose should be examined using a nasal speculum under good illumination. The tip of the nose should be raised and pressed with the tip of a thumb. At first spray a topical decongestant into the nose and see if the child can blow it out after waiting 10 minutes. Do not attempt to remove FBs from the nose by grasping with ‘ordinary forceps’.

Methods of removal 1 Spray with decongestant, wait 10 minutes, then ask the child to blow out the FB. 2 It is best to pass an instrument behind the FB and pull or lever it forward. Examples of instruments are: • a Eustachian catheter • a probe to roll out the FB

• a bent hairpin • a bent paperclip 3 Snaring the FB This is the appropriate method for soft irregular FBs such as paper, foam rubber and cottonwool that are clearly visible. Examples of instruments are: • a foreign-body remover • crocodile forceps • fine nasal forceps 4 Glue on a stick Apply SuperGlue to the plastic end of a swab stick. Apply it to the FB, wait about 1 minute and then gently extract the FB. 5 Rubber catheter suction technique The only equipment required is a straight rubber catheter (large type) and perhaps a suction pump. The method involves cutting the end of the catheter at right angles, smearing the rim of the cut end with petroleum jelly and applying this end to the FB, then providing suction. Oral suction may be applied for a recently placed or ‘clean’ object, but gentle pump suction, if available, is preferred. 6 Irritation of the nose Some practitioners sprinkle white pepper into the nose to induce sneezing. 7 The ‘kiss and blow’ technique This mouth-to-mouth method is used for a cooperative child with a firm, round foreign body such as a bead impacted in the anterior nares. It is best to supervise the child's mother to perform the technique, but the practitioner or practice nurse can perform it.

Method • Use a nasal decongestant spray. • After 20 minutes lay the child on an examination couch with a pillow under the head. • Obstruct the normal nostril with a finger from the side. • Place the mouth over the child’s mouth, blowing into it until a slight resistance is felt (this indicates that the glottis is closed). • Then blow hard with a high velocity puff to cause the FB to ‘pop out’. To encourage cooperation with the technique the child can be asked to give mother (or other) a ‘kiss’. More than one attempt may be needed but it is usually very successful and avoids the necessity for a general anaesthetic.

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Nasal disorders

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Hay fever • Nosebleed • Nose: stuffy, running nose • Sinusitis

References 1 Kalish L, Da Cruz M. Nasal obstruction. Medicine Today, March 2009; 10 (3): 41–52. 2 Mendelsohn M, Ruhno J. The nose—form and function. Australian Doctor, 2 October 2004: 31.

3 Porter RS, Kaplan JL. The Merck Manual of Diagnoses and Therapy (19th edn). New Jersey: Merck, Sharp & Dohme Corp., 2011: 466–8. 4 Burton M (ed.). Hall and Coleman's Diseases of the Ear, Nose and Throat (15th edn). Edinburgh: Churchill Livingstone, 2000: 107–17. 5 Moulds R (Chair). Therapeutic Guidelines: Respiratory (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 137–150. 6 Harvey RJ. Differentiating chronic sino-nasal complaints. Australian Doctor, 6 February 2009: 27–32. 7 Lund JL. Diagnosis and treatment of nasal polyps. BMJ, 1995; 311: 1411–4. 8 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty. Ltd, 2013: 366. 9 Oates K, Currow K, Hu W. Child Health: A Practical Manual for General Practice. Sydney: MacLennan & Petty, 2001: 328–30. 10 Hansen G. Practice Tips. Aust Fam Physician, 1982; 11: 867.

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Nausea and vomiting

Nausea, retching and hypersalivation frequently precede the act of vomiting, which is a highly integrated sequence of involuntary visceral and somatic motor events. Harrison’s Principles of Internal Medicine,  Vomiting or emesis is a rather dramatic event with a diverse number of causes. It is usually preceded by nausea.

Definitions Haematemesis Vomiting of blood. It is presented in CHAPTER 55. Nausea The unpleasant sickly sensation that can herald the onset of vomiting or can be present without vomiting. Regurgitation The effortless passage of gastric contents into the mouth in the absence of nausea and without diaphragmatic muscular contractions. Retching An involuntary act with all the movements of vomiting without the expulsion of gastric contents because the cardiac orifice remains closed. Rumination The effortless regurgitation of recently ingested food into the mouth, followed by rechewing and reswallowing or spitting out.1 Vomiting The forceful expulsion of gastric contents through a relaxed upper oesophageal sphincter and out of the mouth.

The clinical approach History A careful history is essential with an emphasis on drug intake, possible psychogenic factors, including self-induced emesis, weight loss, other GIT symptoms or symptoms suggestive of systemic disease.

Examination If fever is present possible sources of infection (e.g. middle ear, meninges and urinary tract) should be checked. A careful abdominal examination is appropriate in most instances and this includes urinalysis. Look

Key facts and checkpoints •

• •

•

•

•

Nausea and vomiting have a wide range of potential causes emanating from every body system. The common cause of acute nausea and vomiting in most age groups is gastroenteritis. The most common causes of vomiting in children are infections—viral (especially) and bacterial— including otitis media and urinary infection. Drug ingestion is a common cause of nausea and vomiting; thus, a drug history is vital in assessment. Vomiting is commonly associated with migraine and may be the only symptom of a variety of migraine. Children with cyclical vomiting syndrome may have a genetic association with migraine. The nature of the vomitus provides a clue: — faecalent = intestinal obstruction — blood = bleeding from oesophagus, stomach or duodenum (mostly) — coffee-grounds = bleeding from stomach or duodenum

particularly for scars indicating previous surgery. Look for a succussion splash—this indicates pyloric obstruction. A neurological examination needs to be considered, including ophthalmoloscopy. Consider raised intracranial pressure. No examination is complete without assessment of the patient's physical fitness, including the level of hydration, especially in infants and the very old. In these age groups the history may be difficult to obtain and the consequences of fluid loss are more complicated. Always be mindful of the possibility of pregnancy in the female patient. Look for acid dental erosion as a marker of bulimia.

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Investigations These should consider the underlying cause and also biochemical abnormalities resulting from fluid and electrolyte loss. The following need to be considered: • • • • • •

pregnancy test (all females of child-bearing age) microscopy and culture of stools radiology of GIT endoscopy oesophageal motility studies neurological investigation for suspected intracranial pressure (e.g. CT scan, MRI) • drug toxicity studies • biochemistry • cortisol/short synacthen test

Red flags for vomiting • • • • •

Marked pallor Signs of hypovolaemia Peritoneal signs Headache, stiff neck, confusion Distended tympanic abdomen

Diagnostic guidelines • Surgical GIT causes are unlikely in the absence of abdominal pain. • Vomiting without bile-stained vomitus = pyloric obstruction. • Vomiting of bile = obstruction below duodenal ampulla. • Vomiting of ingested food = oesophageal obstruction. • Vomiting without nausea and possibly projectile =  ↑  intracranial pressure. A summary of the diagnostic strategy model is presented in TABLE 60.1.

Vomiting in infancy Is the vomiting bile-stained? • Green vomiting = urgent surgical referral for possible intestinal malrotation with volvulus (6 hours leeway before gangrene of bowel)2 Other causes: meconium ileus, small bowel atresia • Non bile-stained vomitus (curdled milk): consider pyloric stenosis, GORD, feeding problems, concealed infection (e.g. UTI, meningitis). Both pyloric stenosis and GORD cause projectile vomiting.

Table 60.1

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Vomiting: diagnostic strategy model

Q. Probability diagnosis A. All ages: acute gastroenteritis, motion sickness, drugs, various infections Neonates: feeding problems Children: viral infections/fever, otitis media, UTI Adults: gastritis, alcohol intoxication, other toxins, pregnancy, migraine Q. Serious disorders not to be missed A. Bowel obstruction: • oesophageal atresia (neonates) • pyloric obstruction 40 years, esp. >70 years Nodes >2.5 cm Nodes >3–4 cm ? malignancy Tender mass Purple discolouration (collar-stud abscess) Single, gradually enlarging node Fixed to skin without punctum Associated dysphagia Hard midline thyroid lump Patient at risk of malignancy and HIV Exposure to tuberculosis

The 20:40 and 80:20 rules3 • The age of the patient is a helpful guide, as causes of neck lumps can be roughly categorised by the ‘20:40 rule’: — 0–20 years: congenital, inflammatory, lymphoma, tuberculosis — 20–40 years: inflammatory, salivary, thyroid, lymphoma — >40 years: lymphoma, metastases • Most neck lumps (80%) are benign in children while the reverse applies to adults. • Imaging techniques that may assist diagnosis include axial CT scan (especially in fat necks), MRI scan (distinguishes a malignant swelling from scar tissue or oedema), tomogram of larynx (laryngocele or malignancy), barium swallow (pharyngeal pouch), sialogram and carotid angiogram.4 A basic suggested approach for the patient presenting with a neck lump is summarised in FIGURE 61.2.

CERVICAL LYMPHADENOPATHY • There are many causes, varying from local infections to lymphoproliferative disorders. • Most malignant nodes in the supraclavicular area have their primary tumour below the clavicle. • Eighty-five per cent of malignant nodes in the anterior triangle have their primary tumour in the head and neck.2

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preauricular (ear, scalp)

postauricular (ear, scalp)

preparotid (parotid, ear) tonsillar (tonsils)

occipital (scalp)

submandibular (tongue, floor of mouth) Posterior triangle submental (lip, mouth)

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posterior cervical

anterior cervical (thyroid, larynx) Anterior triangle supraclavicular

(lung, breast)

(stomach)

FIGURE 61.1 Lymph glands (site of the nodes) of the neck including common sources of adenopathy (excluding lymphomas)

History

Clinical examination

• Hodgkin lymphoma usually presents with rubbery, painless nodes in the neck. • Most swellings are lateral.

Consistency of enlarged nodes FNAB

CT scan

? Specialists/ multidisciplinary clinic

Rules of thumb are:5 • • • •

hard: secondary carcinoma rubbery: lymphoma soft: sarcoidosis or infection tender and multiple: infection

Causes of cervical lymph node enlargement (lateral cervical swelling)

FIGURE 61.2 A basic approach for patients presenting with a neck lump4

Acute cervical lymphadenitis • Acute viral lymphadenitis • Acute bacterial lymphadenitis—coccal infection

• Always search for: — other nodes at distant sites — possible primary source of infections or neoplasia — hepatosplenomegaly

Chronic lymph node infection • MAIS lymphadenitis (atypical tuberculosis) • Tuberculosis • Viral infection, for example, EBM (see FIG. 61.3), rubella, cytomegalovirus, HIV

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Anterior triangle • Branchial cyst (in upper part): — usually adulthood (20–25 years) • Carotid body tumour: — opposite thyroid cartilage — smooth and pulsatile — can be moved laterally but not vertically — usually 40–60 years — requires excision (with care) • Carotid aneurysm • Lateral thyroid tumours FIGURE 61.3 Cervical lymphadenopathy associated with Epstein–Barr mononucleosis

• Toxoplasma gondii infection • Cat scratch disease—Bartonella henselae infection Neoplastic lymphadenopathy • Lymphomas, esp. Hodgkin lymphoma • Leukaemia Metastatic • Check mouth, pharynx, sinuses, larynx, scalp, oesophagus, stomach, breast, lungs, thyroid and skin. A working rule is upper neck—from skin to upper aerodigestive tract; lower neck—from below clavicles (e.g. lung, stomach, breast, colon). • Examples: — occipital or pre-auricular—check scalp — submental—check mouth, tongue, teeth — submandibular—check floor of mouth — left supraclavicular (under sternomastoid)— consider stomach (Troisier sign) — deep anterior cervical—consider larynx, thyroid, oesophagus, lungs

NECK LUMPS NOT DUE TO LYMPH NODE SWELLING6

Types and causes Widespread • Sebaceous cysts • Lipomas Midline • Thyroid nodule (moves upon swallowing) • Thyroglossal cysts (moves upwards on tongue protrusion) • Dermoid cyst (beneath chin)

Posterior triangle • Developmental remnants: — cystic hygroma — bronchial sinuses and cysts • Pancoast tumour (from apex lung) • Cervical rib Submandibular swellings • Submandibular salivary gland • Cervicofacial actinomycosis (lumpy jaw syndrome): — chronic granulomatosis infection due to Gram-positive Actinomyces israelii — forms a multilocular abscess (pus has ‘sulphur granules’) — infection follows dental extraction or poor dental hygiene, esp. severe caries — treat with high-dose penicillin G, 4 months Sternomastoid tumour Refer CHAPTER 91. Pharyngeal pouch • A soft, squelchy, indefinite mass • Base of left neck • History of difficulty in swallowing Thyroid nodule The most likely cause of a solitary thyroid nodule is the dominant nodule in a multinodular goitre. Other causes include a true solitary nodule— adenoma, follicular carcinoma or solitary carcinoma— and a colloid cyst. Malignancy must be excluded.

Investigations • Ultrasound • FNAB (may resolve a cystic lesion) • TFTs

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Neck lumps in children Eighty per cent of neck lumps are benign while 20% are malignant. Benign lumps usually occur in the anterior triangle, while malignant lumps are more likely in the posterior triangle. The common midline lump in children is the thyroglossal cyst.3 Consider sternomastoid tumour (fibrosis) in infants (see CHAPTER 92).

Acute bacterial lymphadenitis

Lymphadenopathy

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• Common sites are submandibular, tonsillar and pre-auricular nodes • Invariably unilateral, confined to one lymph node group • No pulmonary involvement • Unresponsive to antimicrobials: treatment is by surgical excision of abscess and underlying lymph nodes

• Most enlarged lymph nodes are either ‘normal’ or local infections (mainly viral), especially if 50 years Constant pain (day and night) Fever >38°C Anterior neck (throat) pain History of cancer Unexplained weight loss Neurological deficit Radicular pain in arm Rheumatoid arthritis Down syndrome

Pitfalls There are many pitfalls in the clinical assessment of causes of neck pain, many of them related to inflammation. Rheumatoid arthritis is the prime severe inflammatory arthropathy that involves the neck but the neck can be affected by the seronegative spondyloarthropathies, particularly ankylosing spondylitis, psoriasis and the inflammatory bowel disorders. While polymyalgia rheumatica affects mainly the shoulder girdle, pain in the lower neck, which is part of the symptom complex, is often overlooked. Diffuse neck pain in myofascial soft tissue with tender trigger areas is part of the uncommon but refractory fibromyalgia syndrome. General pitfalls • Failing to appreciate how often the benign problem of facet joint dysfunction occurs in the neck, causing pain and limited movement. This involves failure to appreciate the value of physical therapy, especially exercise programs, in alleviating the problem.

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• Failing to adhere to the idiom: one disc—one nerve root. Involvement of more than one nerve root in the upper limb may mean a neoplastic disorder such as metastatic disease, lymphoma in the thoracic outlet and similar serious diseases. • Missing the insidious onset of myelopathy, especially the spasticity component, caused by rheumatoid arthritis, osteophytic overgrowth or, rarely, a soft disc prolapse.

Seven masquerades checklist

62

Cervical spinal dysfunction is the obvious outstanding cause. Thyroiditis may cause neck pain, as in the extremely rare cases of acute specific infection in the thyroid (e.g. syphilis, pyogenic infections), which cause severe pain; non-specific thyroiditis (de Quervain thyroiditis) produces painful swelling with dysphagia. The association between depression and neck pain is well documented.

Psychogenic considerations

• Do you have trouble reversing your car? • Can you recall an injury to your head or neck such as hitting your head on an overhead bar? • Does your neck grate or get stiff? • Do you get headaches or feel dizzy? • Is the pain present day and night? • Do you get pain or pins and needles or numbness in your arms? • Does the pain come on with activity? • Does the pain wake you at night? • Do you feel pain on both sides of your neck and over your shoulders? • Do your hands or arms feel weak or clumsy?

Examination It is appropriate to follow the traditional rule for examination of any joint or complex of joints: look, feel, move, measure, test function, look  elsewhere and X-ray. Careful examination of  the cervical spine is essential for the correct diagnosis and for specific treatment at the painful level. Three objectives of the examination are to:

The neck is one of the commonest areas for psychological fixation following injury. This may involve perpetuation or exaggeration of pain because of factors such as anxiety and depression, conversion reaction and secondary gain. The psychological sequelae that can follow a whiplash injury and chronic neck problems such as spondylosis serve as a reminder that the state of the patient's cervical spine can profoundly affect his or her life and that we should always be aware of the whole person. A feeling of depression is a very common sequel to such an injury and these patients demand our dutiful care and understanding.

• reproduce the patient’s symptoms • identify the level of lesion or lesions • determine the cause (if possible)

The clinical approach

• • • •

History It is important to analyse the pain into its various components, especially the nature of its onset, its site and radiation, and associated features. The diurnal pattern of the pain will provide a lead to the diagnosis (refer to FIG. 38.3: the patterns are similar to low back pain). Key questions • Can you point to exactly where in your neck you get the pain? • Do you wake up with pain in the morning? • Does the pain come on when you have to look up for a while?

A neurological examination is essential if radicular pain is present, or weakness or other upper limb symptoms, including any pain or paraesthesia that extends below the elbow. Inspection The patient should be examined sitting on a couch, rather than on a chair. The body should be fully supported with the hands resting on the thighs. The following should be noted: willingness to move the head and neck level of the shoulders any lateral flexion contour of the neck from the side

In the patient with torticollis the head is held laterally flexed with, perhaps, slight rotation to one  side—usually away from the painful side. Patients  suffering from whiplash injury and severe spondylosis tend to hold the neck stiff and the head forward, and tend to turn the trunk rather than rotate the neck. Palpation For this vital component of the examination it is essential to know the surface anatomy of the neck so that the affected level can be determined.

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Neck pain Method The patient lies prone on the examination couch with the forehead resting on the hands (palms up). The neck should be flexed forward and the shoulders relaxed. 1 Central digital palpation Systematically palpate the first spinous processes of the cervical vertebrae. • C2 (axis) is the first spinous process palpable beneath the occiput. • C7 is the largest ‘fixed’ and most prominent process—situated at the base of the neck. • C6 is also prominent but usually ‘disappears’ under the palpating finger with extension of the neck. • The spinous processes of C3, C4 and C5 are difficult to palpate because of cervical lordosis but their level can be estimated (see FIG. 62.2). Standing at the patient's head, place opposed pulps of the thumbs on the spinous processes (starting at C2) and then move down the middle line to C7. Press firmly over each and with arms straight oscillate with moderate firmness three or four times to assess pain, stiffness or muscle spasm. 2 Lateral digital palpation The facet joints lie in sequence (called the articular pillar) about 2 to 3 cm from the midline. Press with opposed thumbs against this pillar in a systematic manner on either side of the midline (top to base) to determine any painful area. Palpation should be extended to include the anterior neck, searching for evidence of lymphadenitis, muscle spasm, thyroid disorder and other problems.

Movement Active movements are observed with the patient sitting on the couch. The movements are as follows with normal range indicated: • • • •

flexion—45° extension—50° lateral flexion (R and L)—45° rotation (R and L)—75°

If there is a full range of pain-free movement, apply overpressure slowly at the end range and note any pain. The range of movements can be plotted on a special grid called a direction of movement (DOM) diagram (see FIG. 62.3). This provides a ready reference for serial assessments. F

R

62

LF

LF

left

right

R

E

FIGURE 62.3 Direction of movement diagram to record movements of the neck. This record shows restricted and painful movements (indicated by II) in right lateral flexion and right rotation; the other movements are free.

Neurological examination A neurological examination for nerve root lesions (C5 to T1) is indicated if the clinical assessment identifies the presence of neurological symptoms and signs such as pain, paraesthesia or anaesthesia in the arm. Nerve root pressure is indicated by: C2

C6 C7

FIGURE 62.2 Relative sizes of spinous processes of the cervical spine

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• pain and paraesthesia along the distribution of the dermatome • localised sensory loss • reduced muscular power (weakness or fatigue or both) • hyporeflexia (reduced amplitude or fatigue or both) It is necessary to know the sensory distribution for each nerve root and the motor changes. This is summarised in TABLE  62.3. The dermatomes are illustrated in FIGURE 62.4.

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Table 62.3

• Problem solving in general practice

Cervical nerve root syndromes

Nerve root

Sensory change

Muscle power

Power loss

Reflex

C5

Outer arm

Deltoid

Abduction arm

Biceps jerk (C5, 6)

C6

Outer forearm/thumb/ index finger

Biceps

Elbow flexion Extension wrist

Biceps + brachioradialis (C5, 6)

C7

Hand/middle and ring fingers

Triceps

Elbow extension

Triceps (C7–8)

C8

Inner forearm/little finger

Long flexors finger, long extensors thumb

Grip

Fingers (C8)

T1

Inner arm

Interossei

Finger spread

• HLA-B27 antigen • radiology:

V cranial nerve

— plain X-ray (not indicated in absence of red flags and major trauma) — CT scan (good for bone definition) — CT scan and myelogram (if cervical disc surgery contemplated) — radionucleide bone scan (for suspected metastatic disease) — MRI: the investigation of choice for cervical radiculopathy, myelopathy, suspected spinal infection and tumour

C3

62

C5

C5 T2

These should be selected conservatively. CT imaging has high radiation levels. T1

C6

C6

Neck pain in children C7

C8 C7

C8

FIGURE 62.4 Dermatomes of the upper limb, head and neck

Investigations The investigations are directed to diagnosing the painful condition and determining if suspected or true organic disease is present in the spine. It is inappropriate to perform sophisticated investigations such as CT scans on most patients. Scanning should be reserved where surgery is contemplated and serious disease is suspected but not confirmed by plain X-ray. Investigations to consider include: • haemoglobin, film and WCC • ESR/CRP • rheumatoid arthritis factor

In children and adolescents, neck pain, often with stiffness, may be a manifestation of infection or inflammation of cervical lymph nodes, usually secondary to an infected throat—for example, tonsillitis or pharyngitis. However, it is vital to consider the possibility of meningitis. Sometimes a high fever associated with a systemic infection or pneumonia can cause meningism. In the presence of fever the rare possibility of poliomyelitis should be kept in mind. In both children and adults the presence of cerebral pathology, such as haemorrhage, abscess or tumour are uncommon possibilities.5 Acute torticollis is quite common in this age group and the neck may be involved in chronic juvenile arthritis.

Neck pain in the elderly In adults the outstanding causes are dysfunction of the joints and spondylosis, with the acute febrile causes encountered in children being rare. However, cerebral and meningeal disorders may cause pain and stiffness in the neck.5

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Neck pain Rheumatoid arthritis is the prime severe inflammatory arthropathy that involves the neck, but the neck can be affected by the spondyloarthropathies (e.g. ankylosing spondylitis). The painful, acute wry neck can affect all ages and is considered to be caused mainly by acute disorders of the apophyseal joints rather than disc prolapse. However, disc lesions do occur and can cause referred pain or radicular pain. In the elderly, radicular pain can also be caused by impingement of the nerve root in the intervertebral foramen that has become narrowed from the degenerative changes of longstanding spondylosis. Problems with a higher probability with increasing age include: • cervical spondylosis with radiculopathy or myelopathy • atlantoaxial subluxation complicating rheumatoid arthritis • polymyalgia rheumatica • metastatic cancer • Pancoast tumour of the lung • angina and myocardial infarction • pharyngeal and retropharyngeal infection and tumour

Clinical problems of cervical spinal origin Pain originating from disorders of the cervical spine is usually, although not always, experienced in the neck. The patient may experience headache, or pain around the ear, face, arm, shoulder, upper anterior or posterior chest.5 Possible symptoms include: • • • • • • • • • • • • • •

neck pain neck stiffness headache migraine-like headache facial pain arm pain (referred or radicular) myelopathy (sensory and motor changes in arms and legs) ipsilateral sensory changes of scalp ear pain (peri-auricular) scapular pain anterior chest pain torticollis dizziness/vertigo visual dysfunction

FIGURE 24.1 in CHAPTER 24 indicates typical directions of referred pain from the cervical spine. Pain in the arm (brachialgia) is common and tends to cover the shoulder and upper arm as indicated.

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CERVICAL DYSFUNCTION Dysfunction of the 35 intervertebral joints that comprise the cervical spine complex is responsible for most cases of neck pain. The problem can occur  at all ages and appears to be caused by disorder (including malalignment) of the many facet joints, which are pain-sensitive. Dysfunction of these joints, which may also be secondary to intervertebral disc disruption, initiates a reflex response of adjacent muscle spasm and myofascial tenderness.

Acute neck pain Acute neck pain (ANP) is most commonly idiopathic or due to a whiplash accident. Serious causes are rare.6 Dysfunction can follow obvious trauma such as a blow to the head or a sharp jerk to the neck, but can be caused by repeated trivial trauma or activity such as painting a ceiling or gentle wrestling. People often wake up with severe neck pain and blame it on a ‘chill’ from a draught on the neck during the night. This is incorrect because it is usually caused by an unusual twist on the flexed neck for a long period during sleep. Clinical features • Typical age range 12–50 years • Dull ache (may be sharp) in neck • May radiate to occiput, ear, face and temporal area (upper cervical) • May radiate to shoulder region, especially suprascapular area (lower cervical) • Rarely refers pain below the level of the shoulder • Pain aggravated by activity, improved with rest • Various degrees of stiffness • Neck tends to lock with specific movements, usually rotation • Localised unilateral tenderness over affected joints • Variable restriction of movement but may be normal • X-rays usually normal: plain X-rays are not indicated for the investigation of ANP in the absence of ‘red flags’ and a history of trauma6 Management The aim of treatment is to reduce pain, maintain function and minimise the risk of chronicity. • Provide appropriate reassurance, information and support.

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• Give advice to the patient about rules of living including the following: Do: — Stay active and resume normal activities. — Keep your neck upright in a vertical position for reading, typing and so on. — Keep a good posture—keep the chin tucked in. — Sleep on a low firm pillow or a special conforming pillow. — Sleep with your painful side on the pillow. — Use heat and massage: massage your neck firmly three times a day using an analgesic ointment. Don’t: — Look up in a strained position for long periods. — Twist your head often towards the painful side (e.g. when reversing a car). — Lift or tug with your neck bent forwards. — Work, read or study with your neck bent for long periods. — Become too dependent on ‘collars’. — Sleep on too many pillows. • Monitor the patient's progress without overtreatment. • Analgesia:7 — first line: paracetamol 1 g (o) qid — second: paracetamol + codeine or an NSAID (o) — third: tramadol 50 mg tds (avoid opioids if possible) — ± tricyclic antidepressant for night pain • Prescribe an exercise program as early as possible; start with gentle exercises and maintain them at home. Suitable exercises are shown in FIGURE 62.5. • Refer to an appropriate therapist for cervical mobilisation for persisting pain. Mobilisation combined with exercises can be effective treatment. Occasionally, manipulation may help with a stubborn ‘locked’ neck but should be left to an expert. If manipulation, which carries the rare but real risk of vertebral artery dissection and stroke, is to be performed, informed consent and an experienced therapist are required.8

Evidence of benefit (in summary)6 • • • •

Staying active: resuming normal activities Exercises Combined cervical passive mobilisation/ exercises Pulsed electromagnetic therapy (up to 12 weeks)

(a)

(b)

(c)

FIGURE 62.5 Examples of exercises for the neck: (a) resisted side bending, (b) rotation, (c) chin retraction

Approximately 40% of patients recover fully from acute idiopathic ANP, about 30% continue to have mild symptoms while 30% continue to have moderate or severe symptoms.6 Chronic pain (lasting more than 3 months)7 Additional treatment modalities to consider include: • • • • •

a course of antidepressants TENS, especially when drugs are not tolerated hydrotherapy acupuncture (may provide short-term relief) corticosteroid facet injections (ideally under image intensification) • facet joint denervation with percutaneous radiofrequency (if nerve block provides relief) • multidisciplinary rehabilitation program

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Neck pain

Cervical spondylosis7 Cervical spondylosis following disc degeneration and apophyseal joint degeneration is far more common than lumbar spondylosis and mainly involves the C5–6 and C6–7 segments. The consequence is narrowing of the intervertebral foramen with the nerve roots of C6 and C7 being at risk of compression. Cervical spondylosis is generally a chronic problem  but it may be asymptomatic. In some patients the pain may lessen with age, while stiffness increases. Clinical features • Dull, aching suboccipital neck pain (see FIG. 62.6) • Stiffness • Worse in morning on arising and lifting head • Improves with gentle activity and warmth (e.g. warm showers) • Deteriorates with heavy activity (e.g. working under car, painting ceiling) F LF

LF

left

right

R

E

Treatment • Provide appropriate reassurance, information and support. • Refer for physiotherapy, including warm hydrotherapy. • Use regular mild analgesics (e.g. paracetamol). • Use NSAIDs: a trial for 2 weeks and then review. • Prescribe gentle mobilising exercises as early as possible. • Give passive mobilising techniques. • Outline general rules to live by, including advice regarding sleeping and pillows, and day-to-day activities.

• Radiculopathy (unilateral or bilateral) • Myelopathy—pressure on spinal cord • Spinal canal stenosis

Acute torticollis Torticollis (acute wry neck) means a lateral deformity of the neck. This is usually a transient self-limiting acutely painful disorder with associated muscle spasm of variable intensity.

FIGURE 62.6 Cervical spondylosis: typical pain distribution with direction of movement diagram indicating painful and restricted movements

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• Usually unilateral pain—may be bilateral • Pain may be referred to head, arms and scapulae • May wake patient at night with paraesthesia in arms • C6 nerve root most commonly involved • Acute attacks on chronic background • Aggravated by flexion (reading) and extension • Associated vertigo or unsteadiness • Restricted tender movements, especially rotation/lateral flexion • Joints tender to palpation • X-ray changes invariable

Complications R

739

Clinical features • Age of patient between 12 and 30 years • Patient usually awakes with the problem • Pain usually confined to neck but may radiate • Deformity of lateral flexion and slight flexion/ rotation • Deformity usually away from the painful side • Loss of extension • Mid-cervical spine (C2–3, C3–4, C4–5) • Any segment between C2 and C7 can cause torticollis • Usually no neurological symptoms or signs

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The exact cause of this condition is uncertain, but both an acute disc lesion and apophyseal joint lesion are implicated, with the latter the more likely cause. Acute torticollis is usually a transient and selflimiting condition that can recover within 48 hours. Sometimes it can last for about a week. Encourage heat massage and early mobility. Avoid cervical collars. Management by mobilisation and muscle energy therapy is very effective.

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Muscle energy therapy This amazingly effective therapy relies on the basic physiological principle that the contracting and stretching of muscles leads to automatic relaxation of agonist and antagonist muscles.9 Lateral flexion or rotation or a combination of movements can be used but treatment in rotation is preferred. The direction of contraction can be away from the painful side (preferred) or towards the painful side, whichever is most comfortable for the patient.

(a)

motion barrier

resisted contraction

limit of movement reduced motion barrier (b)

Method 1 Explain the method to the patient, with reassurance that it is not painful. 2 Rotate the patient's head passively and gently towards the painful side to the limit of pain (the motion barrier). 3 Place your hand against the head on the side opposite the painful one. The other (free) hand can be used to steady the painful level—usually C3–4. 4 Request the patient to push the head (in rotation) as firmly as possible against the resistance of your hand. The patient should therefore be producing a strong isometric contraction of the neck in rotation away from the painful side (see FIG. 62.7A). Your counterforce (towards the painful side) should be firm and moderate (never forceful) and should not ‘break’ through the patient's resistance. 5 After 5–10 seconds (average 7 seconds) ask the patient to relax; then passively stretch the neck gently towards the patient's painful side (see FIG. 62.7B). 6 The patient will now be able to turn the head a little further towards the painful side. 7 This sequence is repeated at the new improved motion barrier. Repeat three to five times until the full range of movement returns. 8 Ask the patient to return the following day for treatment although the neck may be almost normal. The patient can be taught self-treatment at home using this method.

FIGURE 62.7 Muscle energy therapy for acute torticollis: (a) isometric contraction phase for problem on the left side, (b) relaxation phase towards the affected (left) side

Acceleration hyperextension (whiplash) injury Patients with the whiplash syndrome, preferably referred to as an acceleration hyperextension injury, present typically with varying degrees of pain-related loss of mobility of the cervical spine, headache and emotional disturbance in the form of anxiety and depression. The problem can vary from mild temporary disability to a severe and protracted course. The injury occurs as a consequence of hyperextension of the neck followed by recoil hyperflexion, typically following a rear-end collision between motor vehicles. There is reversal of sequence of these movements in a head-on collision. In addition to hyperextension, there is prolongation or anterior stretching plus longitudinal extension of the neck.8 It can also occur with other vehicle accidents and in contact sports such as football. Whiplash causes injury to soft tissue structures including muscle, nerve roots, the cervical sympathetic chain, ligaments, apophyseal joints and their synovial capsules and intervertebral discs. Damage to the apophyseal joints appears to be severe, with possible microfractures (not detectable on plain X-ray) and long-term dysfunction.

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Neck pain Pain and stiffness of the neck are the most common symptoms. The pain is usually experienced in the neck and upper shoulders but may radiate to the sub-occipital region, the interscapular region and down the arms. The stiffness felt initially in the anterior neck muscles shifts to the posterior neck. Headache is a common and disabling symptom that may persist for many months. It is typically occipital but can be referred to the temporal region and the eyes. Nerve root pain can be caused by a traction injury of the cervical nerve roots or by inflammatory changes or direct pressure subsequent to herniation of a disc. Paraesthesia of the ulnar border of the hand, nausea and dizziness are all relatively common symptoms. Delayed symptoms are common. A patient may feel no pain until 24 (sometimes up to 96) hours later; most experience symptoms within 6 hours. Complications of whiplash are summarised in TABLE 62.4. Table 62.4

Complications of whiplash

Referred pain (headache, arm pain) Visual problems Vertigo Dysphagia Depression Compensation neurosis Disc rupture increasing to nerve root pain Osteoarthritis becomes symptomatic

The Canadian guidelines (1995) for whiplash are: • Grade I—neck pain, stiffness or tenderness • Grade II—neck symptoms + musculoskeletal signs (e.g. decreased range of motion, point tenderness) • Grade III—neck symptoms + neurological signs • Grade IV—neck symptoms + fracture or dislocation Management principles The objective of treatment is to obtain a full range of free movement of the neck without pain by attending to both the physical and the psychological components of the problem. Other objectives include an early return to work and discouragement of unnecessary and excessive reliance on cervical collars and legal action. Treatment • Establish an appropriate empathy and instil patient confidence with a positive, professional approach. Discourage multiple therapists.

• Provide appropriate reassurance and patient education. • Encourage normalisation of activities as soon as possible. • Compare the problem with a sprained ankle, which is a similar injury. • Inform that an emotional reaction of anger, frustration and temporary depression is common (lasts about 2 weeks). • X-ray is required. • Prescribe rest only for grades II and III (max. 4 days). • Use a cervical collar (limit to 2 days) for grades II and III. Provide collar and refer for grade IV. • Use analgesics (e.g. paracetamol)—avoid narcotics. • Use NSAIDs for 14 days. • Use tranquillisers, mild—up to 2 weeks. • Refer for physiotherapy. • Provide neck exercises (as early as possible). • Use heat and massage—‘spray and stretch’— or ice. • Give passive mobilisation (not manipulation). Recovery can take any time from 1 to 2 weeks up to about 3 months. A valuable reference is Update Quebec Task Force Guidelines for the Management of Whiplash—Associated Disorder at

Cervical disc disruption Disruption of a cervical disc can result in several different syndromes. 1 Referred pain over a widespread area due to pressure on adjacent dura mater. Note: A disc disruption is capable of referring pain over such a diffuse area (see FIG. 62.8) that the patient is sometimes diagnosed as functional (e.g. hysterical). 2 Nerve root or radicular pain (radiculopathy). The pain follows the dermatomal distribution of the nerve root in the arm. 3 Spinal cord compression (myelopathy).

Radiculopathy Apart from protrusion from an intervertebral disc, nerve root pressure causing arm pain can be caused by osteophytes associated with cervical spondylosis. Uncommon causes include various tumours involving the vertebral segment, the meninges and nerves or their sheaths. The pain follows neurological patterns

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severe C5–6 disc protrusion

Investigations • Plain X-ray (AP, lateral extension and flexion, oblique views to visualise foramina); not good for diagnosis or for surgery • Plain CT scan • CT scan and myelogram—excellent visualisation of structures but invasive • MRI—excellent but expensive, sometimes difficult to distinguish soft disc from osteophytes • Electromyography—may help delineate lesions requiring surgery Treatment Many patients respond to conservative treatment, especially from a disc prolapse. It is basically a selflimiting disorder—about 10% remain severely disabled:10 • • • •

62 FIGURE 62.8 Zone of possible referred pain distribution caused by a cervical disc lesion on the right side

down the arm, being easier to localise with lower cervical roots, especially C6, C7 and C8. 1 The cervical roots exit above their respective vertebral bodies. For example, the C6 root exits between C5 and C6 so that a prolapse of C5–6 intervertebral disc or spondylosis of the C5–6 junction affects primarily the C6 root (see FIG. 62.4). 2 One disc—one nerve root is the rule. 3 Spondylosis and tumours tend to cause bilateral pain (i.e. more than one nerve root). Clinical features • A sharp aching pain in the neck, radiating down one or both arms • Onset of pain may be abrupt, often precipitated by a sudden neck movement on awakening • Paraesthesia in the forearm and hand (in particular)—in 90% with proven disc prolapse9 • Stiffness of neck with limitation of movement • Nocturnal pain, waking patient during night • Pain localised to upper trapezius and possible muscle spasm

bed rest soft cervical collar analgesics (according to severity—see CHAPTER 38) consider a course of corticosteroids for severe neck radicular pain • tranquillisers, especially at night • traction (with care) • careful mobilisation (manipulation is contraindicated)

CERVICAL SPONDYLITIC MYELOPATHY Sometimes the presence of large or multiple osteophytes or in the presence of a narrowed spinal canal symptoms of spinal cord involvement may develop.11,12 The common cause is a hard mass of material projecting from the posterior aspect of the vertebral body to indent the spinal cord and possibly the nerve roots at the exit foramina. This resultant spinal cord compression may result in several different clinical presentations, notably myelopathy in particular, but also central cord and anterior cord syndrome. A full neurological assessment is necessary. Clinical features • Older patients, typically men >50 years • Insidious onset—symptoms over 1–2 years • Numbness and tingling in fingers • Leg stiffness • Gait disturbance • Numb, clumsy hands, especially with a high cervical lesion

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Neck pain • Signs of UMN: spastic weakness, increased tone and hyper-reflexia (arms > legs) ± clonus • Neurological deficit, which predicts the level with reasonable accuracy • Bowel and bladder function usually spared Note: LMN signs occur at the level of the lesion, and UMN signs and sensory changes occur below this level. Causes • Cervical spondylosis • Atlantoaxial subluxation: rheumatoid arthritis, Down syndrome • Primary spinal cord tumours (e.g. meningiomas) • Metastasis to cervical spine → epidural spinal cord compression Investigations • MRI scan • CT scan with myelogram (most accurate)

Central cord syndrome12 This rather bizarre condition occurs classically in a patient with a degenerative cervical spine following a hyperextension injury that causes osteophytes to compress the cord anteriorly and posteriorly simultaneously. The maximum damage occurs in the central part of the cord, leading to sensory and motor changes in the upper limbs with relative sparing of the lower limbs due to the arrangements of the long tracts in the cord. Fortunately, the prognosis is good with most patients achieving a good neurological recovery.

Anterior cord syndrome The anterior cord syndrome occurs with hyperflexion injuries that produce ‘tear drop’ fractures of the vertebral bodies or extrusion of disc material. The syndrome can also be produced by comminuted vertebral body fractures. It is characterised by complete motor loss and the loss of pain and temperature discrimination below the level of the injury, but deep touch, position and vibration sensation remain intact. Because it is probably associated with obstruction of the anterior spinal artery, early surgical intervention to relieve pressure on the front of the cord may enhance recovery. Otherwise the prognosis for recovery is poor.

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Down syndrome One of the more sinister problems with trisomy 21 syndrome is hypoplasia of the odontoid process, leading to C1–2 subluxation and dislocation. If unrecognised in the early stages, sudden death can occur in these children. If suspected, flexion– extension lateral views of the cervical spine will highlight the developing instability and the need for early specialist opinion.

Rheumatoid arthritis7 Involvement of the cervical spine is usually a late manifestation of rheumatoid arthritis (RA). It is important to be aware of the potentially lethal problem of C1–2 instability due to erosion of the major odontoid ligaments in the rheumatoid patient. These patients are especially vulnerable to disasters when under general anaesthesia and when involved in motor vehicle accidents. Early cervical fusion can prevent tragedies, especially with inappropriate procedures such as cervical manipulation. It is imperative to perform imaging of the cervical spine of all patients with severe RA before major surgery to search for C1–2 instability. Lateral plain X-rays in flexion and extension may reveal increased distance in the atlanto–dens interval. This can be assessed further with MRI or CT scanning in a specialist clinic. Treatment of spondylitic myelopathy Conservative (may help up to 50%):2 • soft cervical collar • physiotherapy for muscle weakness • analgesics and/or NSAIDs Surgery is indicated when the myelopathy interferes with daily activities. One procedure is the ‘Cloward’ method, which is anterior decompression with discectomy and fusion. The aim of surgery is to halt deterioration.

When to refer • Persisting radicular pain in an arm despite conservative treatment • Evidence of involvement of more than one nerve root lesion in the arm • Evidence of myelopathy, such as weakness, numbness or clumsiness of the upper limbs • Evidence, clinical or radiological, of cervical instability in post-accident victims, or people with Down syndrome or rheumatoid arthritis

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•

• • •

‘One disc—one nerve root’ is a working rule for the cervical spine. The patient should sit on the couch with the thighs fully supported for inspection and movements of the neck. Be alert for patients with RA and Down syndrome who have cervical instability. Physical treatments such as cervical manipulation may easily cause quadriplegia. All acutely painful conditions of the cervical spine following trauma should be investigated with a careful neurological examination of the limbs, sphincter tone and reflexes. Plain film radiology is mandatory. In conscious patients, flexion and extension lateral cervical spinal plain films are useful for diagnosing instability of spinal segments with or without associated spinal fractures. The so-called ‘whiplash’ syndrome is a diagnosis of exclusion of spinal fractures or severe ligamentous disruption causing instability, and even then, for medicolegal and psychological reasons, would best be termed a ‘soft tissue injury of the cervical spine’. Most ‘soft tissue cervical spine injuries’ heal within 3 months with conservative treatment. If severe pain persists, follow-up investigations may be required. Dysfunction of the cervical spine is an underestimated cause of headache. Always consider dysfunction of the cervical spine as a possible cause of shoulder pain. Strains and fractures of the apophyseal joints, especially after a whiplash injury, are difficult to detect, and are often overlooked causes of neck and referred pain.

Patient education resources Hand-out sheets from Murtagh's Patient Education 6th edition: • Exercises for your neck • Neck: painful neck • Whiplash • Wry neck (torticollis)

References 1 Gordon SJ, Trott P, Grimmer KA. Waking cervical pain and stiffness, headache, scapula or arm pain: gender and age effects. Australian Journal of Physiotherapy, 2002; 48 (1): 9–15. 2 Cohen ML. Neck pain. Modern Medicine Australia, 1989; November: 44–53. 3 Payne R. Neck pain in the elderly: a management review. Modern Medicine Australia, 1988; July: 56–67. 4 Bogduk N. Neck pain. Aust Fam Physician, 1984; 13: 26–9. 5 Hart FD. Practical Problems in Rheumatology. London: Dunitz, 1985: 10–14. 6 Australian Acute Musculoskeletal Pain Guidelines Group, National Health and Medical Research Council. EvidenceBased Management of Acute Musculoskeletal Pain: A Guide for Clinicians. Canberra: Australian Government, 2003: 36–43. 7 Moulds R (Chair). Therapeutic Guidelines: Rheumatology (Version 2). Melbourne: Therapeutic Guidelines Ltd, 2010. 8 Beran RG et al. Serious complications with neck manipulation and informed consent. Med J Aust, 2000; 173: 213–14. 9 Kenna C, Murtagh J. Back Pain and Spinal Manipulation (2nd edn). Oxford: Butterworth-Heinemann, 1997: 83–99. 10 Bogduk N. Medical Management of Acute Cervical Radicular Pain: An Evidence Based Approach. Newcastle: Newcastle Bone and Joint Institute, 1999: 5–59. 11 Porter RS, Kaplan JL. The Merck Manual (19th edn). Whitehorse Station: Merck, Sharpe & Dohme Corp., 2011: 1808–9. 12 Young D, Murtagh J. Pitfalls in orthopaedics. Aust Fam Physician, 1989; 18: 645–6.

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Search for clues—difficulty reaching into the hip pocket to remove a wallet may indicate loss of function due to total rupture of the supraspinatus tendon, while a complete rotator-cuff tear may lead the patient to lift the affected limb to the clothes line and leave it suspended there by the hand while hanging out the laundry. Michael Hayes  The painful shoulder is a relatively common and sometimes complex problem encountered in general practice. The diagnostic approach involves determining whether the disorder causing the pain arises from within the shoulder structures or from other sources such as the cervical spine (see FIG. 63.1), the acromioclavicular (AC) joint or diseased viscera, especially the heart, lungs and sub-diaphragmatic structures.

Key facts and checkpoints •

•

•

•

•

Virtually all shoulder structures are innervated by the fifth cervical vertebra (C5) nerve root. Pain present in the distribution of the C5 nerve can arise from the: — cervical spine — upper roots of brachial plexus — glenohumeral joint — rotator cuff tendons, especially supraspinatus — biceps tendon — soft tissue (e.g. polymyalgia rheumatica) — viscera, especially those innervated by the phrenic nerve (C3, C4, C5) The visceral diseases causing a painful shoulder include cardiac disorders, such as angina and pericarditis; lung diseases, especially Pancoast tumour; mediastinal disorders; and diaphragmatic irritation, as from intra-abdominal bleeding or a subphrenic abscess. A careful history should generally indicate whether the neck or the shoulder is responsible for the patient’s pain. By the age of 50 about 25% of people have some wear and tear of the rotator cuff, making it more injury-prone.1 Disorders of the rotator cuff are common, especially supraspinatus tendonopathy. The most effective tests to diagnose these problems are the resisted movement tests.1

•

•

Injections of local anaesthetic and long-acting corticosteroid produce excellent results for inflammatory disorders around the shoulder joint, especially for supraspinatus tendonopathy. The diagnosis is usually made on the history and examination. Blood tests are usually not necessary and imaging has a limited place and value.2

Note: The term tendonopathy or tendonosis is preferred to tendonitis since it has been shown that overuse tendon conditions generally have a noninflammatory pathology.

FIGURE 63.1 Typical pain zone arising from disorders of the shoulder joint and the lower cervical spine (C5 level)

Functional anatomy of the shoulder A working knowledge of the anatomical features of the shoulder is essential for understanding the various disorders causing pain or dysfunction of the  shoulder. Apart from the AC joint there are two most significant functional joints— the glenohumeral (the primary joint) and the subacromial complex (the secondary joint) (see FIG. 63.2). The glenohumeral joint is a ball and socket

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joint enveloped by a loose capsule. It is prone to injury from traumatic forces and develops osteoarthritis more often than appreciated. Two other relevant functional joints are the scapulothoracic and sternoclavicular joints. The clinically important perihumeral space lies above the glenohumeral joint between the head of the humerus and an arch formed by the bony acromion, the thick coracoacromial ligament and the coracoid process. This relatively tight compartment houses the subacromial bursa and the rotator cuff, particularly the vulnerable supraspinatus tendon.3 Excessive friction and pinching in this space render these structures prone to injury. There is a critical zone of relative ischaemia that appears to affect the rotator cuff about 1 cm medial to the attachment of the supraspinatus tendon,4 and this area is compromised during adduction and abduction of the arm due to pressure on the rotator cuff tendons from the head of the humerus. The socalled ‘impingement interval’ is the space between the undersurface of the acromion and the superior aspect of the humeral head. This space is normally narrow (6–14 mm), especially when the arm is abducted. Such factors are largely responsible for the many rotator cuff syndromes, including subacromial bursitis and lesions of the supraspinatus tendon and also bicipital tendonopathy.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 63.1.

Probability diagnosis The commonest causes of pain in the shoulder zone (see FIG. 63.1) are cervical disorders and periarthritis (i.e. soft tissue lesions involving the tendons around the glenohumeral joint). The outstanding common disorders of the shoulder joint are the rotator cuff disorders and adhesive capsulitis. Of these, supraspinatus tendon disorders are the commonest. It is obvious that the supraspinatus tendon is subjected to considerable friction and wear and tear. For acute shoulder pain presentation consider rotator cuff disorders (including calcific tendonitis and an acute tear) and adhesive capsulitis.

Serious disorders not to be missed As usual it is important to exclude any malignancy or septic infection, be it septic arthritis or osteomyelitis. Lung cancer (Pancoast syndrome), myeloma and bony metastases should be kept in mind. For pain in the region of the left shoulder the possibility of myocardial ischaemia has to be considered. Referred pain to the right shoulder from myocardial ischaemia is rare, occurring about once for every 20 episodes of left shoulder referral.

acromioclavicular joint acromion

clavicle subacromial bursa supraspinatus

attachment of supraspinatus tendon

glenohumeral joint

capsule

deltoid muscle

long head biceps tendon

FIGURE 63.2 The basic anatomical structures of the shoulder joint

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Shoulder pain

Table 63.1

Shoulder pain: diagnostic strategy model

Q. Probability diagnosis A. Cervical spine dysfunction (referred pain) Rotator cuff tendonopathy ± a tear Adhesive capsulitis Glenoid labral tears Q. Serious disorders not to be missed A. Cardiovascular: • angina • myocardial infarction Neoplasia: • Pancoast tumour • primary or secondary in humerus Severe infections: • septic arthritis (especially children) • osteomyelitis Axillary vein thrombosis Rheumatoid arthritis Intra-abdominal pathology e.g. bleeding Q. Pitfalls (often missed) A. Polymyalgia rheumatica Cervical dysfunction Gout/pseudogout (uncommon) Osteoarthritis of acromioclavicular joint Winged scapula—muscular fatigue pain Q. Seven masquerades checklist A. Depression Diabetes Drugs Thyroid disorder (rarely) Spinal dysfunction Q. Is the patient trying to tell me something? A. Shoulder is prone to (uncommonly) psychological fixation for secondary gains, depression and conversion reaction.

Referred pain from the diaphragm and intraabdominal disorders (e.g. biliary, perforated ulcer, splenic rupture) should be kept in mind. With an acute onset of painful capsulitis the possibility of rheumatoid arthritis (or even gout) is worth considering.

Pitfalls The shoulder is notorious for diagnostic traps, especially for referred pain from visceral structures, but polymyalgia rheumatica is the real pitfall. A good rule is to consider it foremost in any older person (over 60) presenting with bilateral shoulder girdle pain that is worse in the morning.

• • • •

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Specific pitfalls include: misdiagnosing posterior dislocation of the shoulder joint misdiagnosing recurrent subluxation of the shoulder joint overlooking an avascular humeral head (post fracture) misdiagnosing rotator cuff tear or degeneration

Seven masquerades checklist Of the seven primary masquerades, spinal dysfunction and depression are those most likely to be associated with shoulder pain. The degree to which cervical spondylosis is associated with shoulder pain is not always appreciated. It is important to realise that patients’ perception of pain in the ‘shoulder’ may be amazing. For example, pain in the lower border of the scapula may be referred to as shoulder pain. Diabetics have a higher incidence of adhesive capsulitis. Drugs are relevant as corticosteroids can cause avascular necrosis of the humeral head and anabolic steroids (weight-lifters) can cause osteolysis of the AC joint. A summary of common shoulder conditions is presented in TABLE 63.2.

The clinical approach History In analysing the pain pattern it is appropriate to keep the various causes of shoulder pain in mind (see TABLE  63.3). Many of these conditions, such as rheumatoid arthritis, osteoarthritis and gout, are relatively uncommon. A careful history should generally indicate whether the neck or the shoulder (or both) is responsible for the patient’s pain. Enquire about features of movement: • stiffness and restriction • excessive movement/instability • weakness • rough versus smooth

Red flag pointers for shoulder pain6 • • • • • •

Fever (septic arthritis, osteomyelitis) Skin redness or swelling History of trauma (dislocation, fracture, rotary cuff tear) History of inflammatory arthritis Past history cancer Motor or sensory loss in arm

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Table 63.2 Common shoulder conditions (after Murrell)5 Problem

Structure affected

Typical age group

Symptoms

Diagnostic pointers

Instability

Labrum/capsule

15–35

Dislocations

History of dislocation, apprehension sign

Stiffness

Capsule

40–60

Pain, night pain, loss of movement

Loss of external rotation

Impingement

Rotator cuff (fatigue)

30–60

Night pain, pain with overhead activities

Impingement signs

Rotator cuff tear

Rotator cuff esp. supraspinatus

50 + 

As above

Impingement signs, weakness external rotation, weakness supraspinatus

AC joint pain

AC joint cartilage

25–45

Localised AC joint pain

Paxinos sign

Arthritis

Glenohumeral joint cartilage

70 + 

Pain, loss of movement

Crepitus

Table 63.3

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Causes of shoulder pain (excluding trauma, fractures and dislocations)

— psoriatic arthropathy • osteoarthritis

Cervical:

• avascular necrosis

• dysfunction

• septic arthritis

• spondylosis

Winged scapula—muscular fatigue pain

Cervical radiculopathy

Malignant disease:

Polymyalgia rheumatica (bilateral)

• primary or secondary in humerus

Acromioclavicular joint:

• Pancoast (referred from lung)

• dysfunction

Referred pain

• osteoarthritis

Cardiac:

Shoulder complex

• ischaemic heart disease

Extracapsular:

• pericarditis

• subacromial bursitis

Gall bladder

• rotator cuff disorders:

Lung

— supraspinatus tendonopathy

• mediastinum, including oesophagus

— infraspinatus tendonopathy

• diaphragmatic irritation

— subscapularis tendonopathy

Herpes zoster

• bicipital tendonopathy Intracapsular (glenohumeral joint): • adhesive capsulitis: — idiopathic — blunt trauma — diabetes — others • rheumatoid inflammation: — rheumatoid arthritis — ankylosing spondylitis

Key questions • Did you have any injury, even very minor, before your pain started? • Does the pain keep you awake at night? • Do you have pain or stiffness in your neck? • Do you have pain or restriction when clipping or handling your bra or touching your shoulder blades? (indicates painful internal rotation and a problem of capsular restriction or a disorder of the acromioclavicular joint)

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Shoulder pain • Do you have trouble combing or attending to your hair? (indicates problematic external rotation and also a disorder of the capsule, e.g. adhesive capsulitis) • Is the pain worse when you wake in the morning? (indicates inflammation) • Do you have aching in both your shoulders or around your hips? • Do you get pain associated with sporting activity, including weight training, or with housework, dressing or other activities? • Do you think you can throw a ball underhand for 10–20 m and/or overhead for 20–25 m with your affected arm? • Can you lift a full 2 L container (e.g. milk) to the level of your shoulder without bending your elbow (or to the top of your head)? • Can you carry a 20–30 kg weight (e.g. full suitcase) by your side?

Examination The diagnosis is based on systematic examination of the cervical spine followed by examination of the shoulder joint. For details of examination of the cervical spine, refer to CHAPTER 62. Examination of the shoulder3,6 For the examination of the shoulder it is important to understand the functional anatomy of all important tendons. The tendon disorders are diagnosed by pain on resisted movement (see TABLE 63.4). A knowledge of the anatomical attachments of the rotator cuff tendons to the head of the humerus (see FIG. 63.3) provides an understanding of the shoulder movements powered by these muscles. supraspinatus (abduction)

(external rotation)

infraspinatus teres minor

posterior aspect

subscapularis (internal rotation)

anterior aspect

FIGURE 63.3 The attachments of the rotator cuff tendons to the head of the humerus Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 1989

Table 63.4

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Tendon disorders: determining resisted movements

Painful resisted movement at shoulder

Affected tendon

1 Abduction

Supraspinatus

2 Internal rotation

Subscapularis

3 External rotation

Infraspinatus Teres minor* Biceps*

4 Adduction

Pectoralis major Latissimus dorsi*

* Lesser role

With tendon disorders (rotator or biceps) there is usually painful movement in one direction, but with subacromial bursitis there is usually most directions.

cuff tendons restriction of capsulitis and restriction in

Inspection Observe the shape and contour of the shoulder joints and compare both sides. Note the posture and the position of the neck and scapula. The position of the scapula provides considerable clinical information. Note any deformity, swelling or muscle wasting. Palpation Stand behind the patient and palpate significant structures such as the AC joint, the subacromial space, the supraspinatus tendon and the long head of biceps. The subacromial bursa is one area where it is possible to localise tenderness with inflammation. Feel also over the supraspinatus and infraspinatus muscles for muscle spasm and trigger points. The axilla should be palpated for lymphadenopathy. Movements The movements of the shoulder joint are complex and involve the scapulothoracic joint as well as the glenohumeral joint, with each joint accounting for about half the total range. Significant signs of a painful capsular pattern can be gained by determining the movements of flexion, abduction, external rotation and internal rotation. For each movement, note: • • • •

the range of movement any pain reproduction any trick movement by the patient scapulothoracic rotation

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Movements should be tested bilaterally and simultaneously wherever possible. Look for impingement, which is the sign of fleeting interruption of free movement by ‘catching’ of a tendon upon bone.

1 Active movements • Flexion (anterior elevation) 180° • Extension (posterior elevation) 50° With the palm facing medially the patient moves the arm upwards through 180° to a vertical position above the head and then backwards through this plane. • Abduction—180° • Adduction—50° (from neutral position)

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180 glenohumeral: pectoralis major 120 painful arc (due to phase when greater tuberosity negotiates the subacromial space)

scapulohumeral: serratus anterior trapezius 90

60

glenohumeral component: supraspinatus deltoid

FIGURE 63.4 The painful arc syndrome

Abduction, which is initiated by the deltoid, is possible only if the arm is fully externally rotated. It is a key combined glenohumeral and scapulothoracic movement, which should reach 180°, and these components should be differentiated if the movement is limited. This is done by fixing the scapula with one hand holding the scapula at its inferior angle and noting the degree of movement of each component (initial glenohumeral range 85–100°). Look for the presence of a painful arc, which occurs usually between 60° and 120° of abduction (see FIG. 63.4). The commonest cause is supraspinatus tendonopathy. Other causes include infraspinatus tendonopathy and subacromial bursitis (milder degree).

‘emptying the can’ position (90° of abduction, 30° horizontal flexion and full internal rotation). Internal rotation (subscapularis test). The examiner stands behind the patient and grasps the palmar surface of the patient’s wrists (with the arm by the side and elbow at 90°). The patient attempts to move the forearm internally (medially) against resistance. External rotation (infraspinatus test). With the examiner and patient adopting a similar position to that for internal rotation, the examiner grasps the dorsal surface of the forearm near the wrist and asks the patient to press outwards, using the forearm as a lever to produce external rotation. This test is also positive for a C5 nerve root lesion.

• Internal rotation—90° • External rotation—90°

3 Special tests

These movements are tested with the arm by the side and the elbow flexed to 90° with the palm facing medially. The hand is carried outwards to test external rotation and inwards towards the abdomen for internal rotation.

2 Resisted movements3 Resisted movements (isometric contractions of a muscle) are important ways of testing capsulitis and for pinpointing tenderness of muscle insertions around the shoulder joint, and no examination of the shoulder is complete without them (see TABLE 63.4). Abduction (supraspinatus test). With the arm abducted to no more than 15° the patient pushes the elbow away from the side while the examiner’s hands resist and prevent the movement, holding for 5 seconds. Compare both sides and note any reproduction of the patient’s pain. A better and more specific test for supraspinatus impingement is testing resisted elevation in the

Supraspinatus/infraspinatus rapid differentiation test. A quick test that helps to differentiate between a lesion of either of these tendons causing a painful arc syndrome is the ‘thumbs up/thumbs down’ abduction test. To test the supraspinatus, perform abduction with thumbs pointing upwards, and then with the thumbs pointing downwards to test the infraspinatus. Long head of biceps test. The best test is opposed forward elevation of the arm with the elbow at right angles. A positive test is reproduction of pain in the bicipital groove. Another useful test is resisted supination at the wrist (Yergason test). The brachial plexus tension test. This test, devised by Elvey,8 tests the nerve roots and sheaths of the brachial plexus without implicating the cervical spine and the glenohumeral joint. The upper cervical roots of the plexus are sometimes injured in accidents, so this test is an effective differentiation test. Impingement test for supraspinatus lesions. See later in this chapter.

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Shoulder pain

Investigations Appropriate investigations for shoulder pain include: • • • • •

ESR (especially for polymyalgia rheumatica)/CRP rheumatoid factor and anti-CCP serum uric acid (acute pain) ECG (if IHD suspected) radiology: — X-ray of a specific part of the shoulder—AC joint, axillary view of glenohumeral joint (best view to show osteoarthritis) — X-ray of cervical spine and chest (if relevant) — radionuclide bone scan—to assess bone tumours — shoot-through axillary views (posterior dislocation) — high-resolution ultrasound—modern techniques make this an appropriate test to assess shoulder pain due to rotator cuff lesions, especially tears and capsulitis, especially if surgery is contemplated. However this test as sometimes reported can be misleading. — arthrogram of shoulder (beware of false negatives) — CT scan (limited use) — MRI—a useful imaging method but not routinely required except for the unstable joint — arthroscopy

Shoulder tip pain Pain at the shoulder tip may be caused by local musculoskeletal trauma or inflammation or can be referred from blood or other irritants in the peritoneal cavity. Referred causes where the pain is unchanged by shoulder movement include: • • • • • • • • •

peptic ulceration diaphragmatic irritation (e.g. pneumonia) ruptured viscus (e.g. perforated ulcer) intraperitoneal bleeding (e.g. ruptured spleen) pneumothorax/pneumonia post laparoscopy (intraperitoneal gas) myocardial infarction/pericarditis ectopic pregnancy gall bladder disease

Shoulder pain in children Shoulder pain in children is not a common presenting problem but the following require consideration: • septic arthritis/osteomyelitis • swimmer’s shoulder (supraspinatus dysfunction)

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Swimmer’s shoulder Although it occurs in adults, shoulder pain is the most common complaint in swimmers in the teenage years (over 12 years of age). American studies of college and national competition swimmers showed 40–60% had suffered significant pain.9 Refer to CHAPTER 136. The problem, which is considered to be associated with abnormal scapular positioning and cervicothoracic dysfunction, occurs in the supraspinatus tendon where an avascular zone is compressed by the greater tuberosity when the arm is abducted and relieved when adducted. Swimmers’ shoulders are forced through thousands of revolutions each day, so the susceptible area tends to impinge on the coracoacromial arch, leading to the impingement syndrome, which can progress with continued stress and age.10 Symptoms • Stage 1: pain only after activity • Stage 2: pain at beginning only, then after activity • Stage 3: pain during and after activity, affects performance Management • Early recognition is important. • Discuss training program with coach. • Consider alteration of technique. • Application of ICE after each swim. • Use NSAIDs. • Avoid corticosteroid injections. • Refer for physiotherapy for scapular stabilisation and cervicothoracic mobilisation.

Shoulder pain in the elderly As a rule most of the shoulder problems increase with age. Special features in the elderly are: • polymyalgia rheumatica (increased incidence with age) • supraspinatus tears and persistent ‘tendonitis’ • other rotator cuff disorders • stiff shoulder due to adhesive capsulitis • osteoarthritis of AC and glenohumeral joints • cervical dysfunction with referred pain • the avascular humeral head Since the rotator cuff is prone to degeneration with age, there is a high incidence of rotator cuff tears in the elderly that are mostly asymptomatic.

The avascular humeral head The humeral head may become avascular after major proximal humeral fractures. With experience, it is

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usually possible to predict the fractures at special risk. Early humeral head replacement with a prosthesis can lead to excellent pain relief and to a return of good function. Once the head has collapsed, there is secondary capsular contracture. Prosthetic replacement of the head is then rarely associated with an adequate return of joint movement. Thus, early referral of comminuted proximal humeral fractures for an expert opinion in all age groups is good practice. Early replacement can improve the functional outcome.11

Rotator cuff tendonopathy6 Rotator cuff tendonopathy, also referred to as ‘impingement syndrome’, is the commonest cause of shoulder pain. It can be associated with inflammation (tendonitis), a tear in a tendon or impingement under the acromion. It may involve one tendon, usually the supraspinatus, or more of the rotator cuff tendons. It is most frequently encountered in young people engaged in sport involved in overhead activities and people over 50 years, in whom rotator cuff tears occur most often. The diagnosis can usually be made on the history and physical examination.

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Supraspinatus tendonopathy Supraspinatus tendonopathy can vary in intensity from mild to extremely severe. The severe cases usually involve calcification (calcific periarthritis) of the tendon, which has a very rapid onset, and spread to the subacromial bursa (subacromial bursitis). The impingement tests5 These are effective tests for supraspinatus lesions as they force impingement of the rotator cuff and bursa under the acromion. One of these tests is the ‘emptying the can’ resistance test. The arm is placed in the ‘emptying the can’ position (90° of abduction, 30° of horizontal flexion and full internal rotation). Elevation of the arm is resisted against the therapist’s downward push. This also tests the strength of supraspinatus. Impingement can also be tested in external rotation when the arm is abducted to 90° and externally rotated. Other tests include those of Speed, Neer and Hawkin.6 Treatment12 Systematic reviews to date have a lack of sufficient information to provide conclusive evidence-based recommendations for treatment.13 NSAIDs might provide some relief from pain while corticosteroid injections and physiotherapy could improve range of movement. Experienced therapists believe that peritendon and subacromial corticosteroid injections are efficacious in selected patients.

• Rest during the acute painful phase • Analgesics and NSAIDs (up to 4 weeks) • Peritendon or subacromial injection (if no tears on ultrasound) • Physiotherapy—an active program including scapular stabilising exercises and rotator cuff strengthening Injection technique The ideal injection is a specific injection onto the tendon rather than general infiltration into the subacromial space. As a rule the therapeutic result is quite dramatic after one or two days of initial discomfort (often severe). The tendon can be readily palpated as a tender cord anterolaterally as it emerges from beneath the acromion to attach to the greater tuberosity of the humerus. This identification is assisted by depressing the shoulder via a downward pull on the arm and then externally and internally rotating the humerus. This manoeuvre allows the examiner to locate the tendon readily.

Method • Identify and mark the tendon. • Place the patient’s arm behind the back, with the back of the hand touching the far waistline. This locates the arm in the desired internal rotation and forces the humeral head anteriorly. • Insert a 23-gauge 32-mm needle under the acromion along the line of the tendon, and inject around the tendon just under the acromion (see FIG. 63.5). If the gritty resistance of the tendon is encountered, slightly withdraw the needle to ensure that it lies in the tendon sheath. • The recommended injection is 1 mL of a soluble or long-acting corticosteroid with 5 mL of 1% lignocaine.

Persistent supraspinatus tendonopathy There are three factors to consider with this problem: 1 A very tight subacromial space. Refer for subacromial decompression by division of the thickened coracoacromial ligament. Even in younger patients this procedure (with or without acromioplasty) may be indicated for those with pain persisting beyond 12 months. 2 Rotator cuff tear or degeneration. In middle-aged and elderly patients, persisting tendonitis is usually due to rotator cuff tear and degeneration, an underdiagnosed condition. Excellent clinical and functional results can be achieved if surgery is performed when the tear is small.

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753

705

Other rotator cuff lesions

acromion

The patient may present with dominant signs of subscapularis or infraspinatus lesions, or a combination of two or three tendinous lesions, including the supraspinatus. This problem could be confused with milder adhesive capsulitis, hence the value of investigations such as ultrasound. coracoid process XX Palpate for: (1) tenderness (2) site of injections

bicipital groove

Management A subacromial space injection of 1 mL of corticosteroid and 2–3 mL of 1% local anaesthetic, using the posterior approach, generally achieves a good result for multiple affected rotator cuff tendons with or without subacromial bursitis.

Method FIGURE 63.5 Injection placement for supraspinatus tendonopathy

3 Calcification of the tendon. This problem usually settles but occasionally surgical intervention is necessary. Typical pain profile—supraspinatus tendonopathy Site:

the shoulder and outer border of arm; maximal over deltoid insertion

Radiation:

to elbow

Quality:

throbbing pain, can be severe

Frequency:

constant, day and night

Duration:

constant

Onset:

gradual or sudden, such as straining the shoulder (e.g. dog on leash, working under car, fall onto outstretched arm)

Offset:

nil

Aggravation:

specific movements, putting on shirt, toilet activity, lying on shoulder (unable to sleep)

Relief:

analgesics only

Associated features:

trigger point over supraspinatus origin

Examination (typical features):

— — — — —

Diagnosis:

high-resolution ultrasound

painful resisted abduction painful arc painful resisted external rotation positive impingement test positive ‘emptying the can’ sign

With the patient sitting upright the large posterior gap between the medial acromial ridge and the humeral head is identified by palpation from behind. The needle (23 gauge, 32 or 38 mm long) is inserted into this gap just inferior to the acromion. The solution should flow into this space without resistance.

Rotator cuff tears Asymptomatic rotator cuff tears are common, being present in 4% of people 18 months—open reduction and possible osteotomy Note: Despite early treatment some cases progress to acetabular dysplasia (underdevelopment of the ‘roof’ of the hip joint) and to premature osteoarthritis. Thus a follow-up X-ray of the pelvis during teenage years should be considered for anyone with a history of DDH.

Perthes disease Perthes disease results in the femoral head becoming partly or totally avascular (i.e. avascular necrosis). Clinical features • Males:females = 4:1 • Usual age 4–8 years (rarely 2–18 years) • Sometimes bilateral • Presents as a limp and aching (hip or groin pain) • May be knee pain • ‘Irritable’ hip early • Limited movement in abduction and IR X-ray. Joint space appears increased and femoral head too lateral: typical changes of sclerosis, deformity and collapse of the femoral capital epiphysis may be delayed.

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Management • Refer urgently (provide crutches) • Aim is to keep femoral head from becoming flat • Choice of treatment depends on severity of the condition and age of the patient If untreated, the femoral head usually becomes flat over some months, leading to eventual osteoarthritis. Some untreated cases of Perthes disease heal and have a normal X-ray.

• • • •

Limp and irritability of hip on movement Anterior hip (groin) pain Knee pain Hip rotating into external rotation on flexion and often lies in external rotation (ER) • Most movements restricted, especially IR Any adolescent with a limp or knee pain should have X-rays (AP and frog view) of both hips (see FIG. 65.6). Otherwise, this important condition will be overlooked. SCFE is graded I to IV.

Transient synovitis This common condition is also known as ‘irritable hip’ or observation hip6 and is the consequence of a self-limiting synovial inflammation. Clinical features • Child aged 3–8 years (usually 6 years) • Sudden onset of hip pain and a limp • Child can usually walk but with pain (some may not) • May be history of trauma or recent URTI or viral illness • Painful limitation of movements, especially abduction and rotation • Blood tests and X-rays normal (may be soft tissue swelling); ESR may be mildly elevated • Ultrasound shows fluid in the joint

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Differential diagnosis. This includes septic arthritis, JCA, Perthes disease. Outcome. It settles to normal within 7 days, without sequelae. Treatment. Refer early. Treatment is bed rest or the use of crutches and analgesics. Follow-up X-ray is needed in 4 to 6 months to exclude Perthes disease. Aspiration under general anaesthetic may be needed to exclude septic arthritis.

Slipped capital femoral epiphysis One problem of the displaced capital epiphysis of the femoral head (SCFE) is when some patients develop avascular necrosis despite expert treatment. Diagnosis of the condition before major slipping is important. This necessitates early consultation with the teenager experiencing hip or knee discomfort and then accurate interpretation of X-rays. Clinical features • Adolescent 10–15 years, often obese • Most common in the oversized and undersexed (e.g. the heavy prepubertal boy) • Bilateral in 20%

normal hip

SCFE

FIGURE 65.6 Appearance of a slipped capital femoral epiphysis; note that, in the normal state, a line drawn along the superior surface of the femoral neck passes through the femoral head, but passes above it with SCFE

Management • Cease weight-bearing and refer urgently to an orthopaedic surgeon. Also refer if the clinical signs indicate SCFE but the X-rays look normal. • If acute slip, gentle reduction via traction is better than manipulation in preventing later avascular necrosis. • Once reduced, pinning is performed.

Septic arthritis Septic arthritis of the hip should be suspected in all children with acutely painful or irritable hip problems. These patients may not be obviously sick on presentation, particularly in infants 90% achieve a good result. Most replacements last 15–20 years.

Groin pain

65

All conditions involving the hip joint, especially osteoarthritis, can present with groin pain (see CHAPTER 136). Consider an unrecognised fracture neck of femur, psoas abscess, Paget disease, osteitis pubis and hernias. Also consider hip labral or chondral lesions. Hip labral injuries present with inguinal pain or upper anterior thigh pain, and require investigation and referral.

Osteitis pubis See CHAPTER 136.

Hip labral tears10 Acetabular labral tears are becoming better recognised in motor accident victims, dancers and athletes, especially with the use of MRI and hip arthroscopy. Patients may complain of sharp impingement pain in the hip and/or groin and of painful clicking, catching or locking. The impingement test should be performed (see earlier in chapter). X-rays will exclude bony hip pathology while MRI is the radiological investigation of choice. According to Paoloni, examination after hip joint anaesthetic injection is the gold standard for diagnosing hip pathology.11 Refer for possible surgical treatment through hip arthroscopy.

Sacroiliac pain Pain arising from SIJ disorders is normally experienced as a dull ache in the buttock but can be referred to the groin or posterior aspect of the thigh. It may mimic pain from the lumbosacral spine or the hip joint. The pain may be unilateral or bilateral. It is worse in loading situations e.g. walking, running, getting in and out of cars. There are no accompanying neurological symptoms such as paraesthesia or numbness but it is common for more severe cases to cause a heavy aching feeling in the upper thigh. Causes of SIJ disorders • Inflammatory (the spondyloarthropathies) • Infections (e.g. TB, Staphylococcus aureus—rare) • Osteitis condensans ilii • Degenerative changes • Mechanical disorders • Post-traumatic, after sacroiliac disruption or fracture • Childbirth—in postnatal period Examination The SIJs are difficult to palpate and examine but there are several tests that provoke them. Direct pressure. With the patient lying prone a rhythmic springing force is applied directly to the upper and lower sacrum respectively. Winged compression test. With the patient lying supine and with arms crossed, ‘separate’ the iliac crests with a downwards and outwards pressure. This compresses the SIJs. Lateral compression test. With hands placed on the iliac crests, thumbs on the ASISs and heels of hand on the rim of the pelvis, compress the pelvis. This distracts the SIJs. Patrick or FABERE test. This method can provoke the hip as well as the SIJ. The patient lies supine on the table and the foot of the involved side and extremity is placed on the opposite knee (the hip joint is now flexed, externally rotated and abducted). The knee and opposite ASIS are pressed downwards simultaneously (see FIG. 65.7). If low back or buttock pain is reproduced the cause is likely to be a disorder of the SIJ. Unequal sacral ‘rise’ test. Squat behind the standing patient and place hands on top of the iliac crests and thumbs on the posterior superior iliac spines (PSIS). Ask the patient to bend slowly forwards and touch the floor. If one side moves higher relative to the other a

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Greater trochanteric pain syndrome13

FIGURE 65.7 The Patrick (FABERE) test for right-sided hip or sacroiliac joint lesion, illustrating directions of pressure from the examiner

problem may exist in the SIJs (e.g. a hypomobile lesion in the painful side if that side’s PSIS moves higher). Mechanical disorders of the SIJ These problems are more common than appreciated and can be caused by hypomobile or hypermobile problems. Hypomobile SIJ disorders are usually encountered in young people after some traumatic event, especially women following childbirth (notably multiple or difficult childbirth), or after a heavy fall onto the buttocks, as well as in those with structural problems (e.g. shortened leg). Pain tends to follow rotational stresses of the SIJ (e.g. tennis, dancing). Excellent results are obtained by passive mobilisation or manipulation, such as the non-specific rotation technique with the patient lying supine, as described in Practice Tips by the author.12 Hypermobile SIJ disorders are sometimes seen in athletes with instability of the symphysis pubis, in women after childbirth and in those with a history of severe trauma to the pelvis (e.g. MVAs, horse riders with foot caught in the stirrups after a fall). The patient presents typically with severe aching pain in the lower back, buttocks or upper thigh. Such problems are difficult to treat and manual therapy usually exacerbates the symptoms. Treatment consists of relative rest, analgesics and a sacroiliac supportive belt.

Pain around the lateral aspect of the hip is a common disorder, and is usually seen as lateral hip pain radiating down the lateral aspect of the thigh in older people engaged in walking exercises, tennis and similar activities. It is analogous in a way to the shoulder girdle, where supraspinatus tendonitis and subacromial bursitis are common wear-andtear injuries. The cause is tendonopathy of the gluteus medius tendon (considered to be the main pathology), where it inserts into the lateral surface of the greater trochanter of the femur and/or gluteus minimus tendon with or without inflammation of the trochanteric bursa. The degenerative tendon may tear, rupture or become detached. The pain of this condition tends to occur at night, especially after activity such as long walks and gardening. X-rays are usually normal but ultrasound may demonstrate the pathology. Clinical features • Female >45–50 years • Pain on outside hip referred to as far as foot • Pain on lying on hip at night • Pain climbing stairs, getting in and out of car • Limp Treatment A trial of NSAIDs (weigh the risks) is worthwhile and physiotherapy involving hip-strengthening exercises is first-line treatment. Injection therapy, ideally under ultrasound, is also worthwhile.

Method of injection without ultrasound • Determine the points of maximal tenderness over the trochanteric region and mark them. (For tendonitis, this point is immediately above the superior aspect of the greater trochanter—see FIG. 65.8). • Inject aliquots of a mixture of 1 mL of longacting corticosteroid with 5–7 mL of local anaesthetic into the tender area, which usually occupies an area similar to that of a standard marble. The injection may be very effective. Follow-up management includes sleeping with a small pillow under the involved buttock, sleeping on a sheepskin

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gluteus medius tendonitis

trochanteric bursitis

FIGURE 65.8 Injection technique for gluteus medius tendonitis (into area of maximal tenderness)

rug and stretching the gluteal muscles with knee– chest exercises. Advise the patients to walk with the feet turned out—‘the Charlie Chaplin gait’. One or two (maximum) repeat injections over 6 or 12 months may be required. Surgical intervention such as iliotibial band release ± bursectomy may be necessary. Local application of ice and massage therapy may provide relief.

Fascia lata syndrome

65

Pain in the lateral thigh can be caused by inflammation of the fascia lata. It is often due to overuse or weak musculature around the hip. Treatment is relative rest and physiotherapy.

Ischial bursitis

Snapping or clicking hip (coxa saltans) Some patients complain of a clunking, clicking or snapping hip, either palpable and/or audible. This represents an annoying problem that may cause pain in the groin or thigh. It is more common in females with a wide pelvis. Causes • A taut iliotibial band (tendon or tensor fascia femoris) slipping backwards and forwards over the prominence of the greater trochanter or • The iliopsoas tendon snapping across the iliopectineal eminence at the anterior brim of the pelvis • The gluteus maximus sliding across the greater trochanter • Joint laxity Treatment The basics of treatment are: • explanation and reassurance • exercises to stretch the iliotibial band14 Occasionally surgery is necessary to lengthen the iliotibial band.

Exercises • The patient lies on the ‘normal’ side and flexes the affected hip, with the leg straight and a weight around the ankle (see FIG. 65.9), to a degree that produces a stretching sensation along the lateral aspect of the thigh. • This iliotibial stretch should be performed for 1–2 minutes, twice daily.

Tailor’s bottom or ‘weaver’s bottom’, which is occasionally seen, is a bursa overlying the ischial tuberosity. Irritation of the sciatic nerve may coexist and the patient may appear to have sciatica. Clinical features • Severe pain when sitting, especially on a hard chair • Tenderness at or just above the ischial tuberosity Treatment • Infiltration into the tender spot of a mixture of 4 mL of 1% lignocaine and 1 mL of LA corticosteroid (avoid the sciatic nerve) • Foam rubber cushion with two holes cut out for the ischial prominences

weight around ankle

FIGURE 65.9 One treatment for the clicking hip

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Hip, buttock and groin pain

When to refer

Patient education resources

• Clinical evidence or suspicion of severe childhood disorders: DDH, Perthes disease, septic arthritis, SCFE or osteomyelitis • Undiagnosed pain, especially night pain • Any fractures or suspicion of fractures such as impacted subcapital fracture or stress fracture of the femoral neck • Patients with true claudication in buttock, whether it is vascular from aortoiliac occlusion or neurogenic from spinal canal stenosis • Patients with disabling osteoarthritis of the hip not responding to conservative measures; excellent results are obtained from surgery to the hip • Any mass or lump

Hand-out sheets from Murtagh’s Patient Education 6th edition: • Bursitis and tendonitis of outer hip • Hip: osteoarthritis

Practice tips •

• •

• •

Training on a plastic DDH model should be essential for all neonatal practitioners in order to master the manoeuvres for examining the neonatal hip. True hip pain is usually felt in the groin, thigh and medial aspect of the knee. The name of the FABERE test is an acronym for Flexion, Abduction, External Rotation and Extension of the hip. Night pain adds up to inflammation, bursitis or tumour. The hip joint can be the target of infections such as Staphylococcus aureus or tuberculosis or inflammatory disorders such as rheumatoid and the spondyloarthropathies, but these are rare numerically compared with osteoarthritis.

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References 1 Cyriax J. Textbook of Orthopaedic Medicine, Vol. 1 (6th edn). London: Balliere Tindall, 1976: 568–94. 2 Cormack J, Marinker M, Morell D. Hip problems. Practice. London: Kluwer-Harrap Handbooks, 1980; 3.65: 1–6. 3 Wood T (Coordinator). Sports Medicine. Check Program 453. Melbourne: RACGP, 2009: 11–13. 4 Anonymous. The Eastern Seal Guide to Children’s Orthopaedics. Toronto: Eastern Seal Society, 1982. 5 Robinson MJ. Practical Paediatrics (5th edn). Melbourne: Churchill Livingstone, 2003: 239–40. 6 Corrigan B, Maitland G. Practical Orthopaedic Medicine. Sydney: Butterworths, 1986: 103–24. 7 Larkins PA. The little athlete. Aust Fam Physician, 1991; 20: 973–8. 8 Young D, Murtagh J. Pitfalls in orthopaedics. Aust Fam Physician, 1989; 18: 654–5. 9 Corrigan B, Maitland G. Practical Orthopaedic Medicine. Sydney: Butterworths, 1986: 324–31. 10 Wood TQ, Young DA. Labral tears: understanding the significance of rim lesions. Medicine Today, 2008; 9: 71–5. 11 Paoloni J. Hip and groin injuries in sport. Medical Observer, 9 March 2007: 27. 12 Murtagh J. Practice Tips (6th edn). Sydney: McGraw-Hill, 2013: 174. 13 Walsh MJ, Solomon MJ. Trochanteric bursitis: misnomer and misdiagnosis. Medicine Today, 2006; 7 (12): 62–3. 14 Sheon RP, Moskowitz RW, Goldberg VM. Soft Tissue Rheumatic Pain (2nd edn). Philadelphia: Lea & Febiger, 1987: 211–12.

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Pain in the leg

Thou cold sciatica Cripple our senators, that their limbs may halt As lamely as their manners. William Shakespeare (–), Timon of Athens Pain in the leg has many causes, varying from a simple cramp to an arterial occlusion. Overuse of the legs in the athlete can lead to a multiplicity of painful leg syndromes, ranging from simple sprains of soft tissue to compartment syndromes. A major cause of leg pain lies in the source of the nervous network to the lower limb, namely the lumbar and sacral nerve roots of the spine. It is important to recognise radicular pain, especially from L5 and S1 nerve roots, and also the patterns of referred pain, such as from apophyseal (facet) joints and sacroiliac joints (SIJs).

Key facts and checkpoints •

• • •

•

• • • •

Always consider the lumbosacral spine, the SIJs and hip joints as important causes of leg pain. Hip joint disorders may refer pain around the knee only (without hip pain). Nerve root lesions may cause pain in the lower leg and foot only (without back pain). Nerve entrapment is suggested by a radiating burning pain, prominent at night and worse at rest. Older people may present with claudication in the leg from spinal canal stenosis or arterial obstruction or both. Think of the hip pocket wallet as a cause of sciatica from the buttocks down. Acute arterial occlusion to the lower limb requires relief within 4 hours (absolute limit of 6 hours). The commonest site of acute occlusion is the common femoral artery. Varicose veins can cause aching pain in the leg.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 66.1.

Table 66.1

Pain in the leg: diagnostic strategy model

Q. Probability diagnosis A. Muscle cramps Nerve root ‘sciatica’ Osteoarthritis (hip, knee) Exercise-related pain (e.g. Achilles tendonitis), muscular injury (e.g. hamstring) Q. Serious disorders not to be missed A. Vascular: • peripheral vascular disease • arterial occlusion (embolism) • thrombosis popliteal aneurysm • deep venous thrombosis • iliofemoral thrombophlebitis Neoplasia: • primary (e.g. myeloma) • metastases (e.g. breast to femur) Infection: • osteomyelitis • septic arthritis • erysipelas • lymphangitis • gas gangrene Q. Pitfalls (often missed) A. Osteoarthritis hip Osgood–Schlatter disorder Spinal canal stenosis → neurogenic claudication Herpes zoster (early) Greater trochanteric pain syndrome Nerve entrapment e.g. meralgia paraesthetica ‘Hip pocket nerve’: from wallet pressure Iatrogenic: injection into nerve Sacroiliac disorders Sympathetic dystrophy (causalgia) Peripheral neuropathy Rarities: • osteoid osteoma • polymyalgia rheumatica (isolated) • Paget disease • popliteal artery entrapment • tabes dorsalis • Ruptured Baker cyst

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Pain in the leg

Q. Seven masquerades checklist A. Depression Diabetes Drugs (indirect) Anaemia (indirect) Spinal dysfunction Q. Is the patient trying to tell me something? A. Quite possible. Common with work-related injuries.

Probability diagnosis Many of the causes, such as foot problems, ankle injuries and muscle tears (e.g. hamstrings and quadriceps), are obvious and common. There is a wide range of disorders related to overuse syndromes in athletes. A very common cause of acute severe leg pain is cramp in the calf musculature, the significance of which escapes some patients as judged by middle-ofthe-night calls. One of the commonest causes is nerve root pain, invariably single, especially affecting the L5 and S1 nerve roots. Tests of their function and of the lumbosacral spine for evidence of disc disruption or other spinal dysfunction will be necessary. Should multiple nerve roots be involved, other causes, such as compression from a tumour, should be considered. Remember that a spontaneous retroperitoneal haemorrhage in a patient on anticoagulant therapy can cause nerve root pain and present as intense acute leg pain. The nerve root sensory distribution is presented in FIGURE 66.1. Other important causes of referred thigh pain include ischiogluteal bursitis (weaver’s bottom) and gluteus medius tendonitis or trochanteric bursitis.

Serious disorders not to be missed Neoplasia Malignant disease, although uncommon, should be considered, especially if the patient has a history of one of the primary tumours, such as breast, lung or kidney. Such tumours can metastasise to the femur. Consider also osteogenic sarcoma and multiple myeloma, which are usually seen in the upper half of the femur. The possibility of an osteoid osteoma should be considered with pain in a bone relieved by aspirin.

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Superficial infections such as erysipelas and lymphangitis occur occasionally. Vascular problems Acute severe ischaemia can be due to thrombosis or embolism of the arteries of the lower limb. Such occlusions cause severe pain in the limb and associated signs of severe ischaemia, especially of the lower leg and foot. Chronic ischaemia due to arterial occlusion can manifest as intermittent claudication or rest pain in the foot due to small vessel disease.1 Various pain syndromes are presented in FIGURE  66.2. It is important to differentiate vascular claudication from neurogenic claudication (see TABLE 66.2). L1 L23

T12 L1

S4 S5

S2 S3

L2 L2 S2 L3

L3 L4

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L4 L4

L5

L5

S1

S1

S1 L5 L4

Infections Severe infections are not so common, but septic arthritis and osteomyelitis warrant consideration.

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FIGURE 66.1 Dermatomes of the lower limb, representing approximate cutaneous distribution of the nerve roots

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buttock and thigh claudication

calf claudication

calf claudication

foot claudication or rest pain in foot if small vessels involved high obstruction (abdominal–pelvic)

obstruction in thigh (superficial femoral)

peripheral obstruction

FIGURE 66.2 Arterial occlusion and related symptoms according to the level of obstruction

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Venous disorders The role of uncomplicated varicose veins as a cause of leg pain is controversial. Nevertheless, varicose veins can certainly cause a dull aching ‘heaviness’ and cramping, and can lead to painful ulceration. Superficial thrombophlebitis is usually obvious, but it is vital not to overlook deep venous thrombosis. These more serious conditions of the veins can cause pain in the thigh or calf.

Pitfalls There are many traps and pitfalls in the painful leg. Herpes zoster at the pre-eruption phase is an old trap and more so when the patient develops only a few vesicles in obscure parts of the limbs. In future we can expect to encounter more cases of spinal canal stenosis (secondary to the degenerative changes) in the elderly. The early diagnosis can be difficult, and buttock pain on walking has to be distinguished from vascular claudication due to a high arterial obstruction. The many disorders of the SIJ and hip region can be traps, especially the poorly diagnosed yet common

gluteus medius tendonitis. Another more recent phenomenon is the ‘hip pocket nerve syndrome’, where a heavy wallet crammed with credit cards can cause pressure on the sciatic nerve. One of the biggest traps, however, is when hip disorders, particularly osteoarthritis, present as leg pain, especially on the medial aspect of the knee. Nerve entrapments (see FIG. 66.3) are an interesting cause of leg pain, although not as common as in the upper limb. Some entrapments to consider include: • lateral cutaneous nerve of thigh, known as meralgia paraesthetica • common peroneal nerve • posterior tibial nerve at ankle (the ‘tarsal tunnel’ syndrome) • obturator nerve, in obturator canal • femoral nerve (in inguinal region or pelvis) Then there are the rare causes. One overlooked problem is complex regional pain syndrome I (sympathetic dystrophy), which may follow even minor trauma to the limb. This ‘causalgia’ syndrome manifests as burning or aching pain with vasomotor

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Pain in the leg

Table 66.2

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Comparison of the clinical features of neurogenic and vascular claudication Neurogenic claudication

Vascular claudication

Cause

Spinal canal stenosis

Aortoiliac arterial occlusive disease

Age

Over 50 Long history of backache

Over 50

Pain site and radiation

Proximal location, Initially lumbar, buttocks and legs Radiates distally

Distal location Buttocks, thighs and calves (especially) Radiates proximally

Type of pain

Weakness, burning, numbing or tingling (not cramping)

Cramping, aching, squeezing

Onset

Walking (uphill and downhill) Distance walked varies Prolonged standing

Walking a set distance each time, especially uphill

Relief

Lying down Flexing spine (e.g. squat position) May take 20–30 minutes

Standing still—fast relief Slow walking decreases severity

Associations

Bowel and bladder symptoms

Impotence Rarely, paraesthesia or weakness

Peripheral pulses Lumbar extension

Present Aggravates

Present (usually) Reduced or absent in some, especially after exercise No change

Neurological

Saddle distribution Ankle jerk may be reduced after exercise

Note: abdominal bruits after exercise

Diagnosis confirmation

Radiological studies

Duplex ultrasound Ankle brachial index Arteriography

Physical examination

instability in the limbs. The essential feature is the disparity between the intensity of the pain and the severity of the inciting injury. General pitfalls • Overlooking beta blockers and anaemia as a precipitating factor for vascular claudication • Overlooking hip disorders as a cause of knee pain • Mistaking occlusive arterial disease for sciatica • Confusing nerve root syndromes with entrapment syndromes

Seven masquerades checklist The outstanding cause of leg pain in this group is spinal dysfunction. Apart from nerve root pressure due to a disc disruption or meralgia paraesthetica, pain can be referred from the apophyseal (facet) joints. Such pain can be referred as far as the mid-calf (see FIG. 66.4).

The other checklist conditions—depression, diabetes, drugs and anaemia—can be associated with pain in the leg. Depression can reinforce any painful complex. Diabetes can cause discomfort through a peripheral neuropathy that can initially cause localised pain before anaesthesia predominates. Drugs such as beta blockers, and anaemia, can precipitate or aggravate intermittent claudication in a patient with a compromised circulation.

Psychogenic considerations Pain in the lower leg can be a frequent complaint (maybe a magnified one) of the patient with non-organic pain, such as the malingerer, the conversion  reaction  patient (hysteria) and the depressed. Sometimes regional pain syndrome (reflex or post-traumatic) is incorrectly diagnosed as functional.

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lateral femoral cutaneous nerve of thigh

obturator nerve

superficial peroneal posterior tibial at tarsal tunnel (causes pain on sole of foot) deep peroneal

FIGURE 66.3 Distribution of pain in the leg from entrapment of specific nerves; the sites of entrapments are indicated by an X

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The clinical approach Careful attention to basic detail in the history and examination can point the way of the clinical diagnosis.

History In the history it is important to consider several distinctive aspects, outlined by the following questions. • Is the pain of acute or chronic onset? • If acute, did it follow trauma or activity? — If not, consider a vascular cause: vein or artery; occlusion or rupture. • Is the pain ‘mechanical’ (related to movement)? — If it is unaltered by movement of the leg or a change in posture, it must arise from a soft tissue lesion, not from bone or joints.

FIGURE 66.4 Possible referred pain patterns from dysfunction of an apophyseal joint, illustrating pain radiation patterns from stimulation by injection of the right L4–5 apophyseal joint Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 1989

• Is the pain postural? — Analyse the postural elements that make it better or worse. — If worse on sitting, consider a spinal cause (discogenic) or ischial bursitis. — If worse on standing, consider a spinal cause (instability) or a local problem related to weight-bearing (varicose veins). — If worse lying down, consider vascular origin, such as small vessel peripheral vascular disease. If worse lying on one side, consider greater trochanteric pain syndrome. — Pain unaffected by posture is activity-related. • Is the pain related to walking? — No: Determine the offending activity (e.g. joint movement with arthritis). — Yes: If immediate onset, consider local cause at site of pain (e.g. stress fracture). If delayed onset, consider vascular claudication or neurogenic claudication.

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Pain in the leg • Is the site of pain the same as the site of trauma? — If not, the pain in the leg is referred. Important considerations include lesions in the spine, abdomen or hip and entrapment neuropathy. • Is the pain arising from the bone? — If so, the patient will point to the specific site and indicate a ‘deep’ bone pain (consider tumour, fracture or, rarely, infection) compared with the more superficial muscular or fascial pain. • Is the pain arising from the joint? — If so, the clinical examination will determine whether it arises from the joint or juxtaposed tissue.

Examination The first step is to watch the patient walk and assess the nature of any limp. Note the posture of the back and examine the lumbar spine. Have both legs well exposed for the inspection. Inspect the patient’s stance and note any asymmetry and other abnormalities, such as swellings, bruising, discolouration, or ulcers and rashes. Note the size and symmetry of the legs and the venous pattern. Look for evidence of ischaemic changes, especially of the foot. Palpate for local causes of pain and if no cause is evident examine the spine, blood vessels (arteries and veins) and bone. Areas to palpate specifically are the ischial tuberosity, trochanteric area, hamstrings and tendon insertions. Palpate the superficial lymph nodes. Note the temperature of the feet and legs. Perform a vascular examination, including the peripheral pulses and the state of the veins if appropriate. If evidence of peripheral vascular disease (PVD), remember to auscultate the abdomen and adductor hiatus, and the iliac, femoral and popliteal vessels. A neurological examination may be appropriate, particularly to test nerve root lesions or entrapment neuropathies. Examination of the joints, especially the hip and SIJs, is very important.

Investigations A checklist of investigations that may be necessary to make the diagnosis is as follows: • FBE and ESR

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• radiology: — leg X-rays, especially knee, hip — plain X-ray of lumbosacral spine — CT scan of lumbosacral spine — ultrasound or MRI of greater trochanteric area — MRI scan of lumbosacral spine — bone scan • electromyography • vascular: — arteriography — duplex ultrasound scan — ankle brachial index — venous pool radionuclide scan — contrast venography — air plethysmograph (varicose veins) — D-dimer test

Leg pain in children Aches and pains in the legs are a common complaint in children. The most common cause is soreness and muscular strains due to trauma or unaccustomed exercise. One cause of bilateral leg pain in children is leukaemia. Consider osteomyelitis (refer CHAPTER 69). It is important to consider child abuse, especially if bruising is noted on the back of the legs.

‘Growing pains’ So-called ‘growing pains’, or idiopathic leg pain, is thought to be responsible for up to 20% of leg pain in children.2 Such a diagnosis is vague and often made when a specific cause is excluded. It is usually not due to ‘growth’ but related to excessive exercise or trauma from sport and recreation, and probably emotional factors. The pains are typically intermittent and symmetrical and deep in the legs, usually in the anterior thighs or calves. Although they may occur at any time of the day or night, typically they occur at night, usually when the child has settled in bed. The pains usually last for 30 to 60 minutes and tend to respond to attention such as massage with an analgesic balm or simple analgesics (refer to CHAPTER 91).

Serious problems It is important to exclude fractures (hence the value of X-rays if in doubt), malignancy (such as osteogenic sarcoma, Ewing tumour or infiltration from leukaemia or lymphoma), osteoid osteoma, osteomyelitis, scurvy and beriberi (rare disorders in

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developed countries) and congenital disorders such as sickle-cell anaemia, Gaucher disease and Ehlers– Danlos syndrome.

Leg pain in the elderly The older the patient, the more likely it is that arterial disease with intermittent claudication and neurogenic claudication due to spinal canal stenosis will develop. Other important problems of the elderly include degenerative joint disease, such as osteoarthritis of the hips and knees, muscle cramps, herpes zoster, Paget disease, polymyalgia rheumatica (affecting the upper thighs) and sciatica.

SPINAL CAUSES OF LEG PAIN Problems originating from the spine are an important, yet at times complex, cause of pain in the leg. Important causes are: • nerve root (radicular) pain from direct pressure • referred pain from: — disc pressure on tissues in front of the spinal cord — apophyseal joints — SIJs • spinal canal stenosis causing claudication Various pain patterns are presented in FIGURES 66.3 and 66.4.

Nerve root pain

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Nerve root pain from a prolapsed disc is a common cause of leg pain. A knowledge of the dermatomes of the lower limb (see FIG. 66.1) provides a pointer to the involved nerve root, which is usually L5 or S1 or both. The L5 root is invariably caused by an L4–5 disc prolapse and the S1 root by an L5–S1 disc prolapse. The nerve root syndromes are summarised in TABLE 66.3. A summary of the physical examination findings for the most commonly involved nerve roots is presented in TABLE 66.3.

Sciatica See CHAPTER 38. Sciatica is defined as pain in the distribution of the sciatic nerve or its branches (L4, L5, S1, S2, S3) that is caused by nerve pressure or irritation. Most problems are due to entrapment neuropathy of a nerve root, in either the spinal canal (as outlined above) or the intervertebral foramen. It should be noted that back pain may be absent and peripheral symptoms only will be present.

Treatment

Acute sciatica A protracted course can be anticipated, in the order of 12 weeks (see CHAPTER 38). The patient should be reassured that spontaneous recovery can be expected. A trial of conservative treatment would be recommended thus: • back care education • relative bed rest if very painful only (2 days is optimal)—a firm base is ideal • return to activities of daily living ASAP • analgesics (avoid narcotic analgesics if possible) • NSAIDs (2 weeks is recommended) • basic exercise program, including swimming • traction can help, even intermittent manual Referral to a therapist of your choice (e.g. physiotherapist) might be advisable. Conventional spinal manipulation is usually contraindicated for radicular sciatica. If the patient is not responding or the circumstances demand more active treatment, an epidural anaesthetic injection is appropriate. Surgical intervention may be necessary.

Chronic sciatica If a trial of NSAIDs, rest and physiotherapy has not brought significant relief, an epidural anaesthetic (lumbar or caudal) using half-strength local anaesthetic (e.g. 0.25% bupivacaine HCl) and a depot corticosteroid (e.g. triamcinolone) is advisable. The lumbar route under image intensification is preferred.

REFERRED PAIN Referred pain in the leg can arise from disorders of the SIJs or from spondylogenic disorders. It is typically dull, heavy and diffuse. The patient uses the hand to describe its distribution compared with the use of fingers to point to radicular pain.

Spondylogenic pain Non-radicular or spondylogenic pain is that which originates from any of the components of the vertebrae (spondyles), including joints, the intervertebral disc, ligaments and muscle attachments. An important example is distal referred pain from disorders of the apophyseal joints, where the pain can be referred to any part of the limb as far as the calf and ankle but most commonly to the gluteal region and proximal thigh (see FIG. 66.4). Another source of referred pain is that caused by compression of a bulging disc against the posterior

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Pain in the leg

Table 66.3

795

747

Comparison of neurological findings of the neurological levels L3, L4, L5 and S1

Nerve root

Pain distribution (see FIG. 67.1)

L3

Front of thigh, inner aspect of thigh, knee and leg

Sensory loss

Motor function

Reflex

Anterior aspect of thigh

Extension of knee

Knee jerk

Flexion, adduction of knee, inversion of foot

Knee jerk

L3

L4

Anterior thigh to front of knee

Lower outer aspect of thigh and knee, inner great toe

tibialis anterior

L4

L5

Lateral aspect of leg, dorsum of foot and great toe

Dorsum of foot, great toe, 2nd, 3rd and 4th toes, anterolateral aspect of lower leg

Dorsiflexion of great toe

Tibialis posterior (clinically impractical)

extensor hallucis longus none L5

S1

Buttock to back of thigh and leg, central calf, lateral aspect of ankle and sole of foot

Lateral aspect of ankle, foot (4th and 5th toes)

Plantar flexion of ankle and toes, eversion of foot

Ankle jerk

S1 peroneus longus + brevis

Source: Reproduced in part with permission from S Hoppenfeld. Physical Examination of the Spine and Extremities. Norwalk, CT: Appleton & Lange

66

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longitudinal ligament and dura. The pain is typically dull, deep and poorly localised. The dura has no specific dermatomal localisation, and so the pain is usually experienced in the low back, sacroiliac area and buttocks. Less commonly it can be referred to the coccyx, groin and both legs to the calves. It is not referred to the ankle or the foot.

Sacroiliac dysfunction This causes typically a dull ache in the buttock but it can be referred to the iliac fossa, groin or posterior aspects of the thighs (see CHAPTER 65). It rarely radiates to or below the knee. It may be caused by inflammation (sacroiliitis) or mechanical dysfunction. The latter must be considered in a postpartum woman presenting with severe aching pain present in both buttocks and thighs.

NERVE ENTRAPMENT SYNDROMES Entrapment neuropathy can result from direct axonal compression or can be secondary to vascular problems, but the main common factor is a nerve passing through a narrow rigid compartment where movement or stretching of that nerve occurs under pressure.

66

Clinical features • Pain at rest (often worse at night) • Variable effect with activity • Sharp, burning pain • Radiating and retrograde pain • Clearly demarcated distribution of pain • Paraesthesia may be present • Tenderness over nerve • May be positive Tinel sign

Meralgia paraesthetica This is the commonest lower limb entrapment and is due to the lateral femoral cutaneous nerve of the thigh being trapped under the lateral end of the inguinal ligament, 1 cm medial to the ASIS.3 The nerve is a sensory nerve from L2 and L3. It occurs mostly in middle-aged people, due mainly to thickening of the fibrous tunnel beneath the inguinal ligament, and is associated with obesity, pregnancy, ascites or local trauma such as belts, trusses and corsets. Its entrapment causes a burning pain with associated numbness and tingling (see FIG. 66.3). The distribution of pain is confined to a localised area of the lateral thigh and does not cross the midline of the thigh.

Differential diagnosis • L2 or L3 nerve root pain (L2 causes buttock pain also) • Femoral neuropathy (extends medial to midline) Treatment • Injection of corticosteroid medial to the ASIS, under the inguinal ligament • Surgical release (neurolysis) if refractory • Treat the cause (e.g. weight reduction, constricting belt, corset) Note: Meralgia paraesthetica often resolves spontaneously.

Peroneal nerve entrapment The common peroneal (lateral popliteal) nerve can be entrapped where it winds around the neck of the fibula or as it divides and passes through the origin of the peroneus longus muscle 2.5 cm below the neck of the fibula. It is usually injured, however, by trauma or pressure at the neck of the fibula. Symptoms and signs • Pain in the lateral shin area and dorsum of the foot • Sensory symptoms in the same area • Weakness of eversion and dorsiflexion of the foot (described by patients as ‘a weak ankle’) Differential diagnosis • L5 nerve root (similar symptoms) Treatment • Shoe wedging or other orthotics to maintain eversion • Neurolysis is the most effective treatment

Tarsal tunnel syndrome This is an entrapment neuropathy of the posterior tibial nerve in the tarsal tunnel beneath the flexor retinaculum on the medial side of the ankle. The condition is due to dislocation or fracture around the ankle or tenosynovitis of tendons in the tunnel from injury, rheumatoid arthritis, and other inflammations. Symptoms and signs • A burning or tingling pain in the toes and sole of the foot, occasionally the heel

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Pain in the leg • Retrograde radiation to calf, perhaps as high as the buttock • Numbness is a late symptom • Discomfort often in bed at night and worse after standing • Removal of shoe may give relief • Sensory nerve loss variable, may be no loss • Tinel test (finger or reflex hammer tap over nerve below and behind medial malleolus) may be positive • Tourniquet applied above ankle may reproduce symptoms The diagnosis is confirmed by electrodiagnosis. Treatment • Relief of abnormal foot posture with orthotics • Corticosteroid injection into tunnel • Decompression surgery if other measures fail

797

749

‘saddle’ embolus iliac common femoral (most common site)

superficial femoral

popliteal

tibial

VASCULAR CAUSES OF LEG PAIN

Occlusive arterial disease Risk factors for peripheral vascular disease (for development and deterioration): • • • • • •

smoking diabetes mellitus hypertension hypercholesterolaemia family history atrial fibrillation (embolism)

FIGURE 66.5 Common sites of acute arterial occlusion

Aggravating factors: • beta-blocking drugs • anaemia

Acute lower limb ischaemia Sudden occlusion is a dramatic event that requires immediate diagnosis and management to save the limb. Causes • Embolism—peripheral arteries • Thrombosis: major artery, popliteal aneurysm • Traumatic contusion (e.g. postarterial puncture) The symptoms and signs of acute embolism and thrombosis are similar, although thrombosis of an area of atherosclerosis is often preceded by symptoms of chronic disease (e.g. claudication). The commonest site of acute occlusion is the common femoral artery (see FIG. 66.5).

Signs and symptoms—the 6 Ps • Pain • Pallor • Paraesthesia or numbness • Pulselessness • Paralysis • ‘Perishing’ cold The pain is usually sudden and severe and any improvement may be misleading. Sensory changes initially affect light touch, not pinprick. Paralysis (paresis or weakness) and muscle compartment pain or tenderness is a most important and ominous sign. Other signs include mottling of the legs, collapsed superficial veins, and no capillary return. If the foot becomes dusky purple and fails to blanch on pressure, irreversible necrosis has occurred. Note: Look for evidence of atrial fibrillation.

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Examination of arterial circulation This applies to chronic ischaemia and also to acute ischaemia.

Skin and trophic changes Note colour changes, hair distribution and wasting. Note the temperature of the legs and feet with the backs of your fingers.

Palpation of pulses It is important to assess four pulses carefully (see FIG. 66.6). Note that the popliteal and posterior tibial pulses are difficult to feel, especially in obese subjects. Femoral artery. Palpate deeply just below the inguinal ligament, midway between the ASIS and the symphysis pubis. If absent or diminished, palpate over abdomen for aortic aneurysm. Popliteal artery. Flex the leg to relax the hamstrings. Place fingertips of both hands to meet in the midline. Press them deeply into the popliteal fossa to compress artery against the upper end of the tibia (i.e. just below the level of the knee crease). Check for a popliteal aneurysm (very prominent popliteal pulsation).

Posterior tibial artery. Palpate, with curved fingers, just behind and below the tip of the medial malleolus of the ankle. Dorsalis pedis artery. Feel at the proximal end of the first metatarsal space just lateral to the extensor tendon of the big toe.

Oedema Look for evidence of oedema: pitting oedema is tested by pressing firmly with your thumb for at least 5 seconds over the dorsum of each foot, behind each medial malleolus and over the shins.

Postural colour changes (Buerger test) Raise both legs to about 60° for about 1 minute, when maximal pallor of the feet will develop. Then get the patient to sit up on the couch and hang both legs down.4 Note, comparing both feet, the time required for return of pinkness to the skin (normally less than 10  seconds) and filling of the veins of the feet and ankles (normally about 15 seconds). Look for any unusual rubor (dusky redness) that takes a minute or more in the dependent foot. A positive Buerger test is pallor on elevation and rubor on dependency and indicates severe chronic ischaemia.

Auscultation for bruits after exercise Listen over abdomen and femoral area for bruits. Note: Neurological examination (motor, sensory, reflexes) is normal unless there is associated diabetic peripheral neuropathy.

femoral

66

popliteal

posterior tibial

dorsalis pedis

FIGURE 66.6 Sites of palpation of peripheral pulses in the leg

Treatment Golden rules. Occlusion is usually reversible if treated within 4 hours (i.e. limb salvage). It is often irreversible if treated after 6 hours (i.e. limb amputation). • Intravenous heparin (immediately) 5000 U • Emergency embolectomy (ideally within 4 hours): — under general or local anaesthesia — through an arteriotomy site in the common femoral artery — embolus extracted with Fogarty balloon or catheter or • Stenting of vessels (a good modern option)—discuss this with an interventional cardiovascular physician • Arterial bypass if acute thrombosis in chronically diseased artery • In selected cases thrombolysis with streptokinase or urokinase appropriate

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Pain in the leg • Amputation (early) if irreversible ischaemic changes • Lifetime anticoagulation with warfarin will be required Note: An acutely ischaemic limb is rarely life threatening in the short term. Thus, even in the extremely aged, demented or infirm, a simple embolectomy not only is worthwhile but also is usually the most expedient treatment option.

Chronic lower limb ischaemia Chronic ischaemia caused by gradual arterial occlusion can manifest as intermittent claudication, rest pain in the foot, or overt tissue loss—ulceration, gangrene (see FIG. 66.7).

FIGURE 66.7 Gangrene of the lateral aspect of the foot following attempted amputation of an ischaemic toe. A below-knee amputation was eventually required.

Intermittent claudication is a pain or tightness in the muscle on exercise (Latin claudicare, to limp), relieved by rest. Rest pain is a constant severe burning-type pain or discomfort in the forefoot at rest, typically occurring at night when the blood flow slows down. The main features are compared in TABLE 66.4. Intermittent claudication The level of obstruction determines which muscle belly is affected (see FIGS 66.2 and 66.6). Proximal obstruction (e.g. aortoiliac) • Pain in the buttock, thigh and calf, especially when walking up hills and stairs • Persistent fatigue over whole lower limb • Impotence is possible (Leriche syndrome)

Table 66.4

799

751

Comparison between intermittent claudication and ischaemic rest pain Intermittent claudication

Ischaemic rest pain

Quality of pain

Tightness/ cramping

Constant ache

Timing of pain (typical)

Daytime; walking, other exercise

Night-time; rest

Tissue affected

Muscle

Skin

Site

Calf > thigh > buttock

Forefoot, toes, heels

Aggravation

Walking, exercise

Recumbent, walking

Relief

Rest

Hanging foot out of bed; dependency

Associations

Beta blockers Anaemia

Night cramps Swelling of feet

Obstruction in the thigh • Superficial femoral (the commonest) causes pain in the calf (e.g. 200–500 m), depending on collateral circulation • profunda femoris →  claudication at about 100 m • multiple segment involvement →  claudication at 40–50 m Causes • Atherosclerosis (mainly men over 50, smokers) • Embolisation (with recovery) • Buerger disease: affects small arteries, causes rest pain and cyanosis (claudication uncommon) • Popliteal entrapment syndrome (15° in men and >19° in women there is a predisposition to patellofemoral pain and instability.9

Q

long axis of femur

Q angle midpoint of patella

line from midpoint of tibial tuberosity to midpoint of patella

FIGURE 67.10 The Q angle of the knee gives a measure of patellar alignment

813

765

Investigations Investigation for the diagnosis of knee pain can be selected from: • blood tests: — RA factor tests; ANA; HLA–B27 — ESR — blood culture (suspected septic arthritis) • radiology9: — plain X-ray — special views: intercondylar (osteochondritis dissecans, loose bodies); tangential (or skyline view for suspected patella pathology); oblique (to define condyles and patella); weightbearing views looking for degenerative arthritis — bone scan: for suspected tumour, stress fracture, osteonecrosis, osteochondritis dissecans — MRI: excellent for diagnosing cartilage and menisci disorders and ligament damage; the investigation of choice for internal ‘derangement’ — arthrography (generally superseded by arthroscopy) or MRI — ultrasound: good for assessment of patellar tendon, soft tissue mass, fluid collection, Baker cyst and bursae • CT: useful for complex fractures of tibial plateau and patellofemoral joint special dysfunction • special: — examination under anaesthesia — arthroscopy — knee aspiration: culture or crystal examination Fractures that may be missed on plain films10 • Patellar fracture • Tibial plateau fracture • Tibial spine fracture • Epiphyseal injuries in children • Osteochondral fracture: — patella — femoral condyle • Stress fracture upper tibia • Avulsion fracture (e.g. Segond fracture of upper lateral tibia, with ACL tear)

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Knee pain in children Children may present with unique conditions that are usually related to growth, including epiphyseal problems. Their tendency towards muscle tightness, especially in the growth spurt, predisposes them to overuse injuries such as patellar tendonopathy and patellofemoral pain syndrome.

First decade A painful knee during the first decade of life (0–10 years) in non-athletes is an uncommon presenting symptom, but suppurative infection and juvenile chronic arthritis have to be considered. Genu valgum or varum is a common presentation but usually not a source of discomfort for the child. However, genu valgum, which is often seen around 4–6 years, may predispose to abnormal biomechanical stresses, which contribute to overuse-type injuries if the child is involved in sport.

Second decade Pain in the knee presents most frequently in this decade and is most often due to the patellofemoral syndrome,11 which is related to the retropatellar and peripatellar regions and usually anterior to the knee. It occurs in the late teenage years of both sexes. An important problem is subluxation of the patella, typically found in teenage girls. It is caused by maltracking of the patellofemoral mechanism without complete dislocation of the patella (see FIG. 67.11).

On examination, the patella is usually in a high and lateral position. Surgery may be required if symptoms persist. OSD is common in pre-pubertal adolescent boys but can occur in those aged 10–16 years. Other conditions found typically in this age group include: • slipped upper femoral epiphysis—usually in middle teenage years after a growth spurt • anserinus (‘goose foot’) bursitis • osteochondritis dissecans Age-related causes of the painful knee are presented in TABLE 67.3.11 Table 67.3

Age-related causes of painful knee

First decade (0–10 years) Infection Juvenile chronic arthritis Second decade (10–20 years) Patellofemoral syndrome Subluxation/dislocation of patella Slipped femoral epiphysis (referred) ‘Hamstrung’ knee Osteochondritis dissecans Osgood–Schlatter disorder Anserinus tendonopathy Third decade (20–30 years) Bursitis Mechanical disorders Fourth and fifth decades (30–50 years) Cleavage tear of medial meniscus Radial tear of lateral meniscus Sixth decade and older (50 years and over) Osteoarthritis Osteonecrosis Paget disease (femur, tibia or patella) Anserinus bursitis Chondrocalcinosis and gout Osteoarthritis of hip (referred pain)

67

The little athlete

FIGURE 67.11 Lateral subluxation of the patella

Children competing in sporting activities, especially running and jumping, are prone to overuse injuries such as the patellofemoral pain syndrome, traumatic synovitis of the knee joint and OSD. Haemarthrosis can occur with injuries, sometimes due to a synovial tear without major joint disruption. If knee pain persists, especially in the presence of an effusion, X-rays should be performed to exclude osteochondritis of the femoral condyle.12

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The painful knee The Ottawa knee rules A knee X-ray series is only required for children with any of the findings in the Ottawa knee rules (see earlier in this chapter).

Osgood–Schlatter disorder Osgood–Schlatter disorder (OSD) is a traction apophysitis resulting from repetitive traction stresses at the insertion of the patellar tendon into the tibial tubercle, which is vulnerable to repeated traction in early adolescence. Clinical features • Commonest in ages 10–14 years • Boys:girls = 3:1 • Bilateral in about one-third of cases • Common in sports involving running, kicking and jumping • Localised pain in region of tibial tubercle during and after activity • Aggravated by kneeling down and going up and downstairs • Development of lump in area • Localised swelling and tenderness at affected tubercle • Pain reproduced by attempts to straighten flexed knee against resistance

815

767

• If acute, use ice packs and analgesics. • The main approach is to abstain from or modify active sports. • Localised treatments such as electrotherapy are unnecessary. • Corticosteroid injections should be avoided.13 • Plaster cast immobilisation should also be avoided. • Surgery may be used (rarely) if an irritating ossicle persists14 after ossification. • Gentle quadriceps stretching. • Graded return to full activity. Prevention • Promote awareness and early recognition of OSD. • Program of stretching exercises for quadriceps mechanism in children in sport.

Osteochondritis dissecans: juvenile form7 This commonly occurs in adolescent boys aged 5–15 years whereby a segment of articular cartilage of the femoral condyle (85%) undergoes necrosis and may eventually separate to form an intra-articular loose body (see FIG. 67.13). It usually presents as pain and effusion and locking. If the fragment has separated, surgery to reattach it can be contemplated.

X-ray to confirm diagnosis (widening of the apophysis and possible fragmentation of bone) and exclude tumour or fracture (see FIG. 67.12).

typical site of OSD

67

tibial tubercle (X-ray appearance)

FIGURE 67.13 Osteochondritis dissecans: on X-ray, sclerosis of the lateral aspect of the medial condyle FIGURE 67.12 Features of Osgood–Schlatter disorder

Management Treatment is conservative as it is a self-limiting condition (6–18 months: average 12 months).

Knee pain in the elderly Rheumatic disorders are very common and responsible for considerable pain or discomfort, disability and loss of independence in the elderly.

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Osteoarthritis is the most common cause and excellent results are now being obtained using total knee replacement in those severely affected. The elderly are particularly prone to crystalassociated joint diseases, including monosodium urate (gout), CPPD (pseudogout) and hydroxyapatite (acute calcific periarthritis).

Chondrocalcinosis of knee (pseudogout) The main target of CPPD is the knee, where it causes chondrocalcinosis. Unlike gout, chondrocalcinosis of the knee is typically a disorder of the elderly with about 50% of the population having evidence of involvement of the knee by the ninth decade.15 Most cases remain asymptomatic but patients (usually aged 60 or older) can present with an acutely hot, red, swollen joint resembling septic arthritis. Investigations include aspiration of the knee to search for CPPD crystals, and X-ray. If positive, consider an associated metabolic disorder such as haemochromatosis, hyperparathyroidism or diabetes mellitus. The treatment is similar to acute gout although colchicine is less effective. Acute episodes respond well to NSAIDs or intra-articular corticosteroid injection.

Osteonecrosis7,16

67

Spontaneous osteonecrosis of the knee (SONK) is more common after the age of 60, especially in females; it can occur in either the femoral (more commonly) or tibial condyles. The aetiology is unknown. The sudden onset of pain in the knee, with a normal joint X-ray, is diagnostic of osteonecrosis. However, the X-ray (especially later) will demonstrate an area of osteonecrosis. The pain is usually persistent, with swelling and stiffness, and worse at night. It can take three months for the necrotic area to show radiologically although a bone scan or MRI may be positive at an early stage (see FIG. 67.14). The condition may resolve in time with reduction of weight-bearing. Surgery in the form of subchondral drilling may be required for persistent pain in the early stages.

Osteochondritis dissecans: adult form7 The adult form occurs more often in males and may be the result of cysts of osteoarthritis fracturing into the joint. Up to 30% are bilateral. Symptoms depend on whether the osteochondral fragment becomes

FIGURE 67.14 Osteonecrosis: necrosis in the medial femoral condyle can take three months to show radiologically

separated. A loose fragment may produce locking or collapse of the knee.

Loose bodies7 The large knee joint is a ‘haven’ for intra-articular loose bodies, which may be formed from bone, cartilage or osteochondral fragments following injury (‘chip’ fragment), osteochondritis dissecans, osteoarthritis, synovial chondromatosis or other conditions. They may be asymptomatic but usually cause clicking or locking with swelling. Diagnosis is by X-ray and surgical removal is necessary for recurrent problems.

The knee ‘mouse’ This common complaint is usually a result of a pedunculated fibrous lump in the prepatellar bursa, often secondary to trauma, such as falls onto the knee.

ACUTE INJURIES

Meniscal tears Medial and lateral meniscal tears are usually caused by abduction and adduction forces causing the meniscus to be compressed between the tibial and femoral condyles and then subjected to a twisting force or a rotatory movement on a semi-flexed weightbearing knee. The medial meniscus is three times more likely to be torn than the lateral. These injuries are common in contact sports and are often associated with ligamentous injuries. Suspect these injuries when there is a history of injury with a twisting movement with the foot firmly fixed on the ground.

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The painful knee However, pain in the knee can present in the patient aged 30–50 years as the menisci degenerate, with resultant cleavage tears from the posterior horn of the medial meniscus and ‘parrot beak’ tears of the mid-section of the lateral meniscus. These problems cause pain because these particular deformities create tension on the joint capsule and stretch the nerve ends. X-rays are not specifically useful but an MRI scan should confirm diagnosis. Clinical features • General symptoms:9 — joint line pain (49%) — locking (17%) — swelling (14%) — loss of movement: restricted flexion, loss of last 5–10° extension • Parrot beak tear of lateral meniscus: — pain in the lateral joint line — pain radiating up and down the thigh — pain worse with activity — a palpable and visible lump when the knee is examined at 45° Arthroscopic partial meniscectomy offers relief. The peripheral meniscus is vascular and can be repaired within 6–12 weeks of injury.17 • Cleavage tear of medial meniscus: — pain in medial joint line — pain aggravated by slight twisting of the joint Table 67.4

817

769

— pain provoked by patient lying on the side and pulling the knees together — pain worse with activity Arthroscopic meniscectomy is appropriate treatment, but some do settle with a trial of physiotherapy.

A diagnostic memoire is a useful aid in the diagnosis of these injuries. There is a similarity in the clinical signs between the opposite menisci, but the localisation of pain in the medial or lateral joint lines helps to differentiate between the medial and lateral menisci. Note: The diagnosis of a meniscal injury is made if three or more of the five examination findings (‘signs’ in TABLE 67.4) are present.

TABLE  67.4

LIGAMENT INJURIES Tears of varying degrees may occur in the: • • • •

anterior cruciate ligament posterior cruciate ligament medial collateral ligament lateral collateral ligament

Anterior cruciate ligament rupture This is a very serious and disabling injury that may result in chronic instability. Chronic instability can result in degenerative joint changes if not dealt with

Typical symptoms and signs of meniscal injuries Medial meniscus tear

Lateral meniscus tear

Abduction (valgus) force Internal rotation of femur on tibia

Adduction (varus) force External rotation of femur on tibia

1 Knee pain during and after activity

Medial side of knee

Lateral side of knee

2 Locking

Yes

Yes

3 Effusion

+ or –

+ or –

1 Localised tenderness over joint line (with bucket handle tear)

Medial joint line

Lateral joint line (may be cyst)

2 Pain on hyperextension of knee

Medial joint line

Lateral joint line

3 Pain on hyperflexion of knee joint

Medial joint line

Lateral joint line

4 Pain on rotation of lower leg (knee at 90°)

On external rotation

On internal rotation

5 Weakened or atrophied quadriceps

May be present

May be present

Mechanism Twisting force on a weight-loaded flexed knee

Symptoms

Signs

67

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• Problem solving in general practice • Immediate effusion of blood, usually within 30 minutes • Common sports: contact sports—rugby, football and soccer, basketball, volleyball, skiing • Differential diagnosis is a subluxed or dislocated patella • Subsequent history of pain and ‘giving way’ of the knee Examination • Gross effusion • Diffuse joint line tenderness • Joint may be locked due to effusion, anterior cruciate tag or associated meniscal (usually medial) tear • Ligament tests: — anterior drawer: negative or positive — pivot shift test: positive (only if instability) — Lachman test: lacking an end point Note: It may be necessary to examine the knee under anaesthesia, with or without arthroscopy, to assess the extent of injury.

The Lachman test This test is emphasised because it is a sensitive and reliable test for the integrity of the ACL. It is an anterior draw test with the knee at 15–20° of flexion. At 90° of flexion, the draw may be negative but the anterior cruciate torn.

FIGURE 67.15 Sites of rupture of the anterior cruciate ligament

adequately. Early diagnosis is essential but there is a high misdiagnosis rate. Sites of ACL rupture are shown in FIGURE 67.15.

67

Mechanisms • Sudden change in direction with leg in momentum • Internal tibial rotation on a flexed knee (commonest) (e.g. during pivoting) • Marked valgus force (e.g. a rugby tackle) • May be associated with collateral ligament tears and meniscus injuries. The so-called ‘unhappy triad’ is a ruptured ACL, medial meniscus tear and medial collateral ligament tear. Clinical features • Onset of severe pain after a sporting injury, such as landing from a jump, or a forced valgus rotational strain of the knee when another player falls across the abducted leg

Method—Lachman test 1

2

3

4

5

The examiner should be positioned on the same side of the examination couch as the knee to be tested. The knee is held at 15–20° of flexion by placing a hand under the distal thigh and lifting the knee into 15–20° of flexion. The patient is asked to relax, allowing the knee to ‘fall back’ into the steadying hand and roll slightly into external rotation. The anterior draw is performed with the second hand grasping the proximal tibia from the medial side (see FIG. 67.16) while the thigh is held steady by the other hand. The examiner’s knee can be used to steady the thigh. The feel of the end point of the draw is carefully noted. Normally there is an obvious jar felt as the anterior cruciate tightens. In an anterior cruciate deficient knee there is excess movement and no firm end point. The amount of draw is compared with the opposite knee. Movement greater than 5 mm is usually considered abnormal.

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The painful knee

sharp ‘draw’

Head steadies femur supporting knee under patient’s thigh (optional)

FIGURE 67.16 The Lachman test

Functional instability due to anterior cruciate deficiency is best elicited with the pivot shift test. This is more difficult to perform than the Lachman test.

Pivot shift test This is an important test for anterolateral rotatory instability. It is positive when anterior cruciate injuries are sufficient to produce a functional instability.

Method—Pivot shift test 1 2

3

4

The tibia is held in internal rotation by grasping the ankle firmly, with the knee in full extension. A valgus force is applied to the knee with the hand placed on the lateral aspect of the knee just below it (this maximises subluxation in the presence of an ACL tear). The knee is then flexed from 0–90°, listening for a ‘clunk’ of reduction. The test is positive when there is a sudden change of rhythm during flexion which corresponds to relocation of the subluxed knee. This usually occurs between 30° and 45° of flexion. From this flexed position the knee is extended, seeking a click into subluxation. This is called a positive jerk test.

Management17 The management depends on the finding by the surgeon. Surgical repair is reserved for complete ligament tears. This usually involves reconstruction

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of the ligament using patellar or preferably hamstring tendons. Early reconstruction is appropriate in younger patients who participate in high levels of sporting activity for whom it can be predicted that functional instability will be a problem. In less active people, a conservative approach is appropriate. The ACL may be trimmed. Cruciate reconstruction can then be undertaken if the knee becomes clinically unstable. The presence of an ACL injury with a significant medial ligament injury will necessitate reconstructive surgery but this is probably best delayed for some weeks as the subsequent incidence of knee stiffness is high.

Posterior cruciate ligament rupture Mechanisms • Direct blow to the anterior tibia in flexed knee • Severe hyperextension injury • Ligament fatigue plus extra stress on knee Clinical features • Posterior (popliteal) pain, radiating to calf • Usually no or minimal swelling • Minimal disability apart from limitation of running or jumping • Pain running downhill • Recurvatum • Posterior sag or draw Management • Usually managed conservatively with immobilisation and protection for 6 weeks • Graduated weight-bearing and exercises

Medial collateral ligament rupture Mechanisms • Direct valgus force to knee—lateral side knee (e.g. rugby tackle from side) • External tibial rotation (e.g. two soccer players kicking ball simultaneously) Clinical features These depend on the degree of tear (1st, 2nd or 3rd degree): • • • • • •

pain on medial knee aggravated by twisting or valgus stress localised swelling over medial aspect pseudo-locking—hamstring strain ± effusion no end point on valgus stress testing (3rd degree) (see FIG. 67.9a)

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Note: Check lateral meniscus if MCL tear. Pellegrini– Stieda syndrome—calcification in haematoma at upper (femoral) origin of MCL—may follow. Management If an isolated injury, this common injury responds to conservative treatment with early limited motion bracing to prevent opening of the medial joint line. Six weeks of limited motion brace at 20–70° followed by knee rehabilitation usually returns the athlete to full sporting activity within 12 weeks. Note: The same principles of diagnosis and management apply to the less common rupture of the lateral collateral ligament, which is caused by a direct varus force to the medial side of the knee. However, lateral ligament injuries tend to involve the cruciate ligament and reconstruction of both ligaments is usually necessary.16

It is amazing how often palpation identifies localised areas of inflammation (tendonopathy or bursitis) around the knee, especially from overuse in athletes and in the obese elderly (see FIG. 67.17). (a) quadriceps tendonitis or rupture iliotibial band friction syndrome anserinus bursitis/ tendonopathy

Osgood–Schlatter disorder

Complex regional pain syndrome I

patellar tendonopathy biceps femoris tendonopathy

A localised complex regional pain syndrome I (also known as reflex sympathetic dystrophy) can follow a direct fall onto the knee. (See CHAPTER 12.) Symptoms • Hypersensitivity • Full extension, loss of flexion • Possible increasing sweating • Tenderness of the joint

OVERUSE SYNDROMES

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The knee is very prone to overuse disorders. The pain develops gradually without swelling, is aggravated by activity and relieved with rest. It can usually be traced back to a change in the sportsperson’s training schedule, footwear or technique, or to related factors. It may also be related to biomechanical abnormalities ranging from hip disorders to feet disorders. Overuse injuries include: • patellofemoral pain syndrome (‘jogger’s knee’, ‘runner’s knee’) • patellar tendonopathy (‘jumper’s knee’) • anserinus tendonopathy/bursitis • semimembranous tendonopathy/bursitis • biceps femoris tendonopathy • quadriceps tendonopathy/rupture • popliteus tendonopathy • iliotibial band friction syndrome (‘runner’s knee’) • the hamstrung knee • synovial plica syndrome • infrapatellar fat-pad inflammation

(b) quadriceps tendonitis or rupture patella patellofemoral joint pain syndrome patellar tendonopathy

medial collateral ligament semimembranous tendonitis/bursitis

anserinus tendonitis/bursitis

FIGURE 67.17 Typical painful areas around the knee for overuse syndromes: (a) anterior aspect, (b) medial aspect

Patellofemoral pain syndrome This syndrome, also known as chondromalacia patellae or anterior knee pain syndrome and referred to as ‘jogger’s knee’, ‘runner’s knee’ or ‘cyclist’s knee’, is the most common overuse injury of the knee. There is usually no specific history of trauma. It may be related to biomechanical abnormalities and abnormal position and tracking of the patella (e.g. patella alta).

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The painful knee It usually presents in females aged 13–15 years with faulty knee mechanisms or in people aged 50–70 years with osteoarthritis of the patellofemoral joint.18 Clinical features • Pain behind or adjacent to the patella or deep in knee • Pain aggravated during activities that require flexion of knee under loading: — climbing stairs — walking down slopes or stairs — squatting — prolonged sitting • The ‘movie theatre’ sign: using aisle seat to stretch knee • Crepitus around patella may be present Signs (chondromalacia patellae) Patellofemoral crepitation during knee flexion and extension is often palpable, and pain may be reproduced by compression of the patella onto the femur as it is pushed from side to side with the knee straight or flexed (Perkins test).

Method for special sign See FIGURE 67.18. • Have the patient supine with the knee extended. • Grasp the superior pole of the patella and displace it inferiorly. • Maintain this position and apply patellofemoral compression. • Ask the patient to contract the quadriceps (it is a good idea to get the patient to practise quadriceps contraction before applying the test). • A positive sign is reproduction of the pain under the patella and hesitancy in contracting the muscle.

FIGURE 67.18 Special sign of the patellofemoral pain syndrome

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Treatment • Give reassurance and supportive therapy. • Reduce any aggravating activity. • Refer to a physiotherapist. • Correct any underlying biomechanical abnormalities such as pes planus (flat feet) by use of orthotics and correct footwear. • Employ quadriceps (especially) and hamstring exercises. • Consider course (trial) of NSAIDs.

Patellar tendonopathy (‘jumper’s knee’) ‘Jumper’s knee’, or patellar tendonopathy (see FIG. 67.2, earlier in this chapter), is a common disorder of athletes involved in repetitive jumping sports, such as high jumping, basketball, netball, volleyball and soccer. It probably starts as an inflammatory response around a small tear. Clinical features • Gradual onset of anterior pain • Pain localised to below knee (in patellar tendon) • Pain eased by rest, returns with activity • Pain with jumping The diagnosis is often missed because of the difficulty of localising signs. The condition is best diagnosed by eliciting localised tenderness at the inferior pole of the patella with the patella tilted. There may be localised swelling.

Method • Lay the patient supine in a relaxed manner with the head on a pillow, arms by the side and quadriceps relaxed (a must). • The knee should be fully extended. • Tilt the patella by exerting pressure over its superior pole. This lifts the inferior pole. • Now palpate the surface under the inferior pole. This allows palpation of the deeper fibres of the patellar tendon (see FIG. 67.19). • Compare with the normal side. • Very sharp pain is usually produced in the patient with patellar tendonopathy. Management Early conservative treatment including rest from the offending stresses is effective. Referral to a physiotherapist for exercise-based rehabilitation is appropriate. This includes adequate warm-up and warm-down. Training modification includes

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patella

Popliteus tendonopathy Tenosynovitis of the popliteus tendon may cause localised pain in the posterior or the posterolateral aspect of the knee. Tenderness to palpation is elicited with the knee flexed to 90°.

Iliotibial band syndrome

FIGURE 67.19 Patellar tendonopathy: method of palpation

calf, hamstring and quadriceps muscle stretching. Modified footwear and a patellar tendon strap may be helpful in some cases. The use of NSAIDs and corticosteroid injections is disappointing. Chronic cases may require surgery.

Anserinus tendonopathy/bursitis Localised tenderness is found over the medial tibial condyle where the tendons of the sartorius, gracilis and semitendinosus insert into the bone. It is distal to the joint line. It is a common cause of knee pain in the middle aged or elderly, especially the overweight woman. Pain is aggravated by resisted knee flexion.

Semimembranous tendonopathy/ bursitis

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This inflamed area is sited either at the tendon insertion or in the bursa between the tendon and the medial head of the gastrocnemius. It is an uncommon problem. The bursa occurs on the medial side of the popliteal fossa between the medial head of gastrocnemius and the semimembranous tendon. It often communicates with the knee joint and, if so, treat knee joint pathology. If not, one can give an injection of depot triamcinolone or betamethasone.

Biceps femoris tendonopathy/ bursitis The tendon and/or the bursa that lies between the tendon insertion and the fibular collateral ligament at the head of the fibula may become inflamed due to overuse. It is usually encountered in sprinters.

Inflammation develops over the lateral aspect of the knee where the iliotibial band passes over the lateral femoral condyle. An inflamed bursa can occur deep to the band. The problem, which is caused by friction of the iliotibial band on the bone, is common in long-distance runners, especially when running up and down hills, and cyclists. It presents with well-localised lateral knee pain of gradual onset. Palpation reveals tenderness over the lateral condyle 1–2 cm above the joint line. Treatment of tendonopathy and bursitis (small area) Generally (apart from patellar tendonopathy), the treatment is an injection of local anaesthetic and long-acting corticosteroids into and deep to the localised area of tenderness. In addition it is important to restrict the offending activity and refer for physiotherapy for stretching exercises. Attention to biomechanical factors and footwear is important. If conservative methods fail for iliotibial tract tendonopathy, surgical excision of the affected fibres may cure the problem.

Prepatellar bursitis Repetitive low-grade direct trauma, such as frequent kneeling, can cause inflammation with swelling of the bursa, which lies between the anterior surface of the patella and the skin. ‘Housemaid’s knee’, or ‘carpet layer’s knee’, can be difficult to treat if rest from the trauma does not allow it to subside. If persistent, drain the fluid with a 23 gauge needle and then introduce 0.5–1 mL of long-acting corticosteroid. The presence of a bursa ‘mouse’ and persistent bursitis usually mean that surgical intervention is required. Acute bursitis may also be caused by acute infection, or one of the inflammatory arthropathies (e.g. gout, seronegative spondyloarthropathies).

Infrapatellar bursitis ‘Clergyman’s knee’ is produced by the same mechanisms as prepatellar bursitis and can be involved with inflammatory disorders or infection. Treatment is also the same.

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The painful knee

The hamstrung knee Cross describes this condition in young active sportspeople (second decade)9 as one that causes bilateral knee pain and possibly a limp. It is caused by a failure to warm up properly and stretch the hamstring muscles, which become tender and tight during the growth spurt. A 6-week program of straight leg raising and hamstring stretching will alleviate the pain completely.

Synovial plica syndrome This syndrome results from a synovial fold (an embryological remnant) being caught between the patella and the femur during walking or running. It causes an acute ‘catching’ knee pain of the medial patellofemoral joint (see FIG.  67.2, earlier in this chapter) and sometimes a small effusion. It generally settles without treatment.

Infrapatellar fat-pad inflammation Acute compression of the fat-pad, which extends across the lower patella deep to the patellar tendon and into the knee joint (see FIG.  67.2, earlier in this chapter), during a jump or other similar trauma, produces local pain and tenderness similar to the sensation of kneeling on a drawing pin.19 The pain usually settles without therapy over a period of days or weeks. There is localised tenderness and it can be confused with patellar tendonopathy.

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• Pain may occur after rest, especially prolonged flexion • Minimal effusion and variable crepitus • Restricted flexion but usually full extension • Often quadriceps wasting and tender over medial joint line • Diagnosis confirmed by X-ray (weight-bearing view) Management options • Relative rest • Weight loss • Analgesics and/or judicious use of NSAIDs • Glucosamine: a Cochrane review showed that it is both safe and modestly effective (see CHAPTER 35) • Walking aids and other supports • Physiotherapy (e.g. hydrotherapy, quadriceps exercises, mobilisation and stretching techniques) • Viscosupplementation: intra-articular injection of hylans • Intra-articular injections of corticosteroids are generally not recommended but a single injection for severe pain can be very effective • Surgery is indicated for severe pain and stiffness and includes arthroscopic debridement and wash out, osteotomy, arthrodesis and total joint replacement (see FIG. 67.20) or hemiarthroplasty, especially for the medial compartment with focal arthritis and varus deformity

ARTHRITIC CONDITIONS

Osteoarthritis Osteoarthritis is a very common problem of the knee joint. Symptoms usually appear in middle life or later. It is more common in women, the obese, and in those with knee deformities (e.g. genu varum) or previous trauma, especially meniscal tears. The degenerative changes may involve either the lateral or the medial tibiofemoral compartment, the patellofemoral joint or any combination of these sites. Clinical features • Slowly increasing joint pain and stiffness • Aggravated by activities such as prolonged walking, standing or squatting • Descending stairs is usually more painful than ascending stairs (suggestive of patellofemoral osteoarthritis)

bone

67 plastic bearing surface

metal component acrylic cement

FIGURE 67.20 Total joint replacement of knee

acrylic cement

plastic bearing surface

bone

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Rheumatoid arthritis The knee is frequently affected by rheumatoid arthritis (RA) although it rarely presents as monoarticular knee pain. RA shows the typical features of inflammation—pain and stiffness that is worse after resting. Morning stiffness is a feature. Note: The spondyloarthropathies have a similar clinical pattern to RA. Synovectomy is a useful option with persistent boggy thickening of synovial membrane but without destruction of the articular cartilage.2

Baker cyst A popliteal cyst (Baker cyst) is a herniation of a chronic knee effusion between the heads of the gastrocnemius muscle and usually is associated with osteoarthritis (most common), rheumatoid arthritis or internal derangement of the knee. It presents as a mass behind the knee and may or may not be tender or painful. It tends to fluctuate in size. A Baker cyst indicates intra-articular pathology and indicates a full assessment of the knee joint. Rupture may result in pain and swelling in the calf, mimicking DVT. Treat underlying knee inflammation (synovitis). Surgical removal of the cyst is advisable for persistent problems.

Septic arthritis

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This tends to be more common in the knee than other joints. Septic (pyogenic) arthritis should be suspected when the patient complains of intense joint pain, malaise and fever. In the presence of acute pyogenic infection the joint is held rigidly. The differential diagnosis includes gout and pseudogout (chondrocalcinosis).

• Adequate support for ligament sprains— supportive elastic tubular (Tubigrip) bandage or a firm elastic bandage over Velband. • Simple analgesics—paracetamol (acetaminophen). • Judicious use of NSAIDs and corticosteroid injections. • Physiotherapy to achieve strength and stability. • Attend to biomechanical abnormalities, inappropriate footwear and athletic techniques. • Orthotics and braces to suit the individual patient. • Specialised exercise techniques (e.g. the McConnell technique).2 • Quadriceps exercises: these simple exercises are amazingly effective.

Quadriceps exercises (examples) • Instruct the patient to tighten the muscles in front of the thighs (as though about to lift the leg at the hip and bend the foot back but keeping the leg straight). The patient should hold the hand over the lower quadriceps to ensure it is felt to tighten. This tightening and relaxing exercise should be performed at least 6 times every 2 hours or so until it becomes a habit. It can be done sitting, standing or lying (see FIG. 67.21). • Sitting on a chair the patient places a weight of 2–5 kg around the ankle (e.g. a plastic bag with sand or coins in a sock) and lifts the leg to the horizontal and then gently lowers it (avoid in patellofemoral problems).

(a)

(b)

Principles of management Most painful knee conditions are not serious and, providing a firm diagnosis is made and internal knee disruption or other serious illness discounted, a simple management plan as outlined leads to steady relief. For more serious injuries the primary goal is to minimise the adverse consequences of forced inactivity. • First aid: RICE (avoid heat in first 48 hours). • Lose weight if overweight.

FIGURE 67.21 A quadriceps exercise: with outstretched legs the quadriceps muscle is slowly and deliberately tightened by straightening the knee to position (a) from the relaxed position (b)

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The painful knee

When to refer • Early referral is required for knees ‘at risk’ following acute injuries where one or more of the following are present: — locked knee — haemarthrosis — instability • Clinical evidence of a torn cruciate ligament, third degree tear of the collateral ligaments or torn meniscus • Undiagnosed acute or chronic knee pain • Recurrent subluxation or dislocation of the patella • Suspected septic arthritis • Presence of troublesome intra-articular loose body

•

•

•

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Reserve intra-articular corticosteroid injections for inflammatory conditions such as rheumatoid arthritis or a crystal arthropathy: regular injections for osteoarthritis are to be avoided. Do not give the injections when the inflammation is acute and diffuse or in the early stages of injury. Many inflammatory conditions around the knee joint, such as bursitis or tendonopathy, respond to a local injection of local anaesthetic and corticosteroid but avoid giving injections into the tendon, especially the patellar tendon. Keep in mind the technique of autologous cartilage transplantation: in this technique cartilage cells (chondrocytes) are taken from the patient, multiplied in a laboratory and eventually implanted into the damaged area. It can be used for damage in any major joint, especially the knee, being ideal for osteochondritis dissecans.

Practice tips • •

•

•

•

•

•

•

•

• •

The absence of an effusion does not rule out the presence of severe knee injury. Examine the hip and lumbosacral spine if examination of the knee is normal but knee pain is the complaint. Always think of an osteoid osteoma in a young boy with severe bone pain in a leg (especially at night) that responds nicely to aspirin or paracetamol or other NSAID. Tears of the meniscus can occur, especially in middle age, without a history of significant preceding trauma. If a patient presents with a history of an audible ‘pop’ or ‘crack’ in the knee with an immediate effusion (in association with trauma) he or she has an ACL tear until proved otherwise. Haemarthrosis following an injury should be regarded as an anterior cruciate tear until proved otherwise. The ‘movie theatre’ sign, whereby the patient seeks an aisle seat to stretch the knee, is usually due to patellofemoral pain syndrome. The ‘bed’ sign, when pain is experienced when the knees touch while in bed, is suggestive of a medial meniscal cleavage tear. A positive squat test (medial pain on full squatting) indicates a tear of the posterior horn of the medial meniscus. Joint aspiration should not be performed on the young athlete with an acute knee injury. If an older female patient presents with the sudden onset of severe knee pain think of osteonecrosis.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Baker cyst • Exercises for your knee • Knee: anterior knee pain • Osgood–Schlatter disorder

References 1 Knox JDE. Knee problems. In: Practice. London: KluwerHarrap Handbooks, 1982; 3.66: 1–5. 2 Selecki Y, Helman T. Knee pain: how to treat. Australian Doctor, 22 April 1993: i–viii. 3 McLean I. Assessment of the acute knee injury. Aust Fam Physician, 1984; 13: 575–80. 4 Cyriax J. Textbook of Orthopaedic Medicine, Vol. 1 (6th edn). London: Bailliere Tindall, 1976: 594. 5 Moulds R (Chair). Therapeutic Guidelines: Rheumatology. Melbourne: Therapeutic Guidelines Ltd, 2010: 155. 6 Noyes FR. Arthroscopy in acute traumatic haemarthrosis of the knee. J Bone Joint Surg, 1980: 624–87. 7 Corrigan B, Maitland GD. Practical Orthopaedic Medicine. Sydney: Butterworths, 1986: 126–61. 8 Brukner P, Khan K. Clinical Sports Medicine (3rd edn). Sydney: McGraw-Hill, 2007: 506–37. 9 Cross MJ, Crichton KJ. Clinical Examination of the Injured Knee. London: Harper & Row, 1987: 21–46. 10 Lau L (ed.). Imaging Guidelines (4th edn). Melbourne: RAZNC Radiologists, 2001: 200–1. 11 Jackson JL, O’Malley PG et al. Evaluation of acute knee pain in primary care. Ann Intern Med, 2003; 139 (7): 575–88. 12 Larkins P. The little athlete. Aust Fam Physician, 1991; 20: 973–8.

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13 Rostrom PKM, Calver RF. Subcutaneous atrophy following methyl prednisolone injection in Osgood–Schlatter epiphysitis. J Bone Joint Surg, 1979; 61A: 627–8. 14 Mital MA, Matza RA, Cohen J. The so-called unresolved Osgood–Schlatter’s lesion. J Bone Joint Surg, 1980; 62A: 732–9. 15 Wilkins E et al. Osteoarthritis and articular chondrocalcinosis in the elderly. Ann Rheum Dis, 1983; 42 (3): 280–4.

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16 Rush J. Spontaneous osteonecrosis of the knee. Current Orthopaedics, 1999; 13: 309–14. 17 Edwards E, Miller R. Management of acute knee injuries. Medical Observer, 17 March 2000: 67–9. 18 Moulds R (Chair). Therapeutic Guidelines: Rheumatology (Version 2). Melbourne: Therapeutic Guidelines Ltd, 2010: 230. 19 Fricker P. Anterior knee pain. Aust Fam Physician, 1988; 17: 1055–6.

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Pain in the foot and ankle

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The victim goes to bed and sleeps in good health. About two o’clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep . . . The part affected cannot bear the weight of the bed clothes nor the jar of a person walking in the room. The night is spent in torture. Thomas Sydenham (–) on gout Pain in the foot (podalgia) and ankle problems are a common occurrence in general practice. Various characteristics of the pain can give an indication of its cause, such as the description of gout by Thomas Sydenham. There are many traumatic causes of podalgia and ankle dysfunction, especially fractures and torn ligaments, but this chapter will focus mainly on everyday problems that develop spontaneously or through overuse. Forefoot pain is common especially in the elderly. The forefoot comprises the toes to the middle of the metatarsals and all of the supporting structures. Metatarsalgia is a term used to describe pain in the distal aspect of one or more of the metatarsal bones during weight-bearing.1

Key facts and checkpoints • • • • • • • • •

•

Foot deformities such as flat feet (pes planus) are often painless. Foot strain is probably the commonest cause of podalgia.2 A common deformity of the toes is hallux valgus, with or without bunion formation. Osteoarthritis is a common sequel to hallux valgus. Osteoarthritis affecting the ankle is relatively uncommon. All the distal joints of the foot may be involved in arthritic disorders. Many foot and ankle problems are caused by unsuitable footwear and lack of foot care. Ankle sprains are the most common injury in sport, representing about 25% of injuries. Severe sprains of the lateral ligaments of the ankle due to an inversion force may be associated with various fractures. Bunions and hammer toes are generally best treated by surgery.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 68.1.

Probability diagnosis Common causes include osteoarthritis, especially of the first metatarsophalangeal (MTP) joint, acute or chronic foot strain, plantar fasciitis, plantar skin conditions such as warts, corns and calluses and various toenail problems.

Serious disorders not to be missed The very important serious disorders to consider include: • • • • •

vascular disease—affecting small vessels diabetic neuropathy osteoid osteoma rheumatoid arthritis complex regional pain syndrome I

Vascular causes The main problem is ischaemic pain that occurs only in the foot. The commonest cause is atheroma. Vascular causes include: • • • •

acute arterial obstruction chilblains atherosclerosis, especially small vessel disease functional vasospasm (Raynaud)—rare

Symptoms: • claudication (rare in isolation) • sensory disturbances, especially numbness at rest or on walking • rest pain—at night, interfering with sleep, precipitated by elevation, relieved by dependency For treatment refer to CHAPTER 67. Complex regional pain syndrome I Also known as reflex sympathetic dystrophy or Sudeck atrophy, regional pain syndrome is characterised by severe pain, swelling and disability of the feet. It is a neurovascular disorder resulting in hyperaemia and osteoporosis that may be a sequela of trauma (often

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trivial) and prolonged immobilisation. Complex regional pain syndrome I usually lasts 2 years and recovery to normality usually follows. The clinical features include sudden onset in middle-aged patients, pain worse at night, stiff joints and skin warm and red. X-rays that show patchy decalcification of bone are diagnostic. Treatment includes reassurance, analgesics, mobility in preference to rest, and physiotherapy. Osteoid osteoma Osteoid osteomas are rare but important little ‘brain teasers’ of benign tumours that typically occur in older children and adolescents. Males are affected twice as often as females. Any bone (except those of the skull) can be affected but the tibia and femur are the main sites. Nocturnal pain is a prominent symptom with pain relief by aspirin being a feature. Diagnosis is dependent on clinical suspicion and then X-ray, which shows a small sclerotic lesion with a radiolucent centre. Treatment is by surgical excision.

Pitfalls There are many traps in the diagnosis and management of problems presenting with a painful foot. Common problems require consideration—these include gouty arthritis, chilblains, a stress fracture and a foreign body in the foot, especially in children. Nerve entrapment, as outlined in CHAPTER 66, is uncommon but Morton neuroma is reasonably common. Less common disorders include complex regional pain syndrome, which is often misdiagnosed, the spondyloarthropathies (psoriasis, reactive arthritis, ankylosing spondylitis and the inflammatory bowel disorders) and osteochondritis of the calcaneus, navicular bone and metatarsal head. If there is an exquisitely tender small purple–red spot beneath a toenail, a glomus tumour (a benign hamartoma) is the diagnosis. It is worth noting that most of these conditions are diagnosed by X-rays.

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General pitfalls • Failing to order X-rays of the foot. • Failing to order X-rays of the ankle following injury. • Failing to appreciate the potential for painful problems caused by diabetes—neuropathy and small vessel disease. • Neglecting the fact that most of the arthritides can manifest in joints in the foot, especially the forefoot.

Table 68.1

The painful foot and ankle: diagnostic strategy model

Q. Probability diagnosis A. Acute or chronic foot strain Sprained ankle Osteoarthritis (esp. great toe) Plantar fasciitis Achilles tendonopathy Tibialis posterior tendonopathy Wart, corn or callus Ingrowing toenail/paronychia Q. Serious disorders not to be missed A. Vascular insufficiency: • small vessel disease Neoplasia: • osteoid osteoma • osteosarcoma • synovial sarcoma Severe infections (rare): • septic arthritis • actinomycosis • osteomyelitis Rheumatoid arthritis Peripheral neuropathy Complex regional pain syndromes Ruptured Achilles tendon Ruptured tibialis posterior tendon Q. Pitfalls (often missed) A. Foreign body (especially children) Gout Morton neuroma Tarsal tunnel syndrome Deep peroneal nerve entrapment Chilblains Stress fracture (e.g. navicular) Erythema nodosum Rarities: • spondyloarthropathies • osteochondritis: navicular (Köhler), metatarsal head (Freiberg), calcaneum (Sever) • glomus tumour (under nail) • Paget disease Q. Seven masquerades checklist A. Depression (?) Diabetes Drugs Spinal dysfunction Q. Is the patient trying to tell me something? A. A non-organic cause warrants consideration with any painful condition.

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Pain in the foot and ankle • Regarding the sprained ankle in adults and children as an innocuous injury: associated injuries include chondral fractures to the dome of the talus, impaction fractures around the medial recess of the ankle, avulsion fractures of the lateral malleolus and base of fifth metatarsal. • Misdiagnosing a stress fracture of the navicular which, like the scaphoid fracture, causes delayed union and non-union. Cast immobilisation for 8 weeks initially may prevent the need for surgery. • Misdiagnosing a complete rupture of the Achilles tendon because the patient can plantar flex the foot. • Overlooking tibialis posterior tendonopathy as a cause of ankle pain.

Seven masquerades checklist The checklist has four conditions that should be considered, especially diabetes and spinal dysfunction. Diabetes may be responsible for a simple type of atherosclerotic pattern, possibly complicated by infection and ulceration. The neuropathy of diabetes can cause a burning pain with paraesthesia. It has a ‘sock’-type pattern as opposed to the dermatome pattern of nerve root pressure arising from the lumbosacral spine. The common S1 pain is experienced on the outer border of the foot, into the fifth toe and on the outer sole and heel of the foot. Drugs and anaemia could indirectly cause pain through vascular insufficiency. The drugs that could cause vasospasm include beta blockers and ergotamine. An alcoholic neuropathy also has to be considered.

Red flag pointers for foot pain • • • •

Pain in forefoot disturbing sleep Fever and systemic illness with bone pain Localised tenderness away from heel in child ‘Burning’ feet

Psychogenic considerations Any painful condition can be closely associated with psychogenic disorders, including depression.

The clinical approach History This is very important, as always, since various characteristics of the pain can give an indication of its cause. Questions should address the quality of the pain, its distribution, mode of onset, periodicity,

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relation to weight-bearing, and associated features such as swelling or colour change. It is relevant to enquire about pain in other joints such as the hand and spine, including the sacroiliac joints, which might indicate that the foot pain is part of a polyarthritis. A history of diarrhoea, psoriasis, urethritis or iritis may suggest that one of the spondyloarthropathies has to be excluded. Key questions The practitioner should address the following questions: • Does the pain arise from a local condition or is it part of a generalised disease? • Is there a history of psoriasis, chronic diarrhoea or colitis, urethritis or iritis? • Is pain also present in other joints, thus indicating the foot pain is part of a polyarthritis, such as rheumatoid arthritis? • Is the problem related to unsuitable footwear? • Does the nature of the pain point to the cause? — throbbing pain → inflammation — burning pain → nerve entrapment, diabetic neuropathy or regional pain syndrome — severe episodic pain → gout — pain worse at night → ischaemia (small vessel disease), regional pain syndrome, cramps or osteoid osteoma — pain worse at night, relieved by aspirin → osteoid osteoma — pain worse on standing after sitting and getting out of bed → plantar fasciitis For ankle injuries it is important to ask about the nature of the injury: • Did the foot twist in (invert) or twist out (evert)? • Was the foot pointing down or up at the time of injury? • Point with one finger to where it hurts (the finger-pointing sign). • What happened immediately after the injury? • Were you able to walk straight away? • What happened when you cooled off? If there has been a fall onto the foot from a height, consider the possibility of a fracture of the calcaneus or talus or disruption of the syndesmosis between the tibia and fibula.

Examination Inspection Inspect the feet with the patient standing, sitting, walking (in shoes and barefooted) and lying down (note

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plantar surfaces). Inspect the footwear (normally, a shoe wears first on the outer posterior margin of the heel). Note: • any gait abnormalities, including limping and abnormal toe in or toe out • deformities, such as hammer toes, bunions— medial (hallux valgus) and lateral (Tailor bunion)—and claw toes • swellings, including callosities • muscle wasting • skin changes and signs of ischaemia Palpation Systematic palpation is very useful as most structures in the foot are accessible to palpation. Movements (active and passive) The joints to test are: • ankle (talar) joint • hindfoot (subtalar) joint • midfoot (midtarsal) joint Movements • Plantar flexion (normal—50°) and dorsiflexion (20°) of foot (see FIG. 68.1) • Inversion and eversion of hindfoot (mainly subtalar joint)—hold heel and abduct and adduct (see FIG. 68.2) • Inversion and eversion of forefoot (midtarsal joint)—hold heel in one hand to fix hindfoot, hold forefoot in the other and abduct and adduct (rotation movement) (see FIG. 68.3) • Test other joints individually (e.g. MTP, midtarsal)

dorsiflexion (extension)

plantar flexion

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FIGURE 68.1 Dorsiflexion and plantar flexion of the ankle joint

FIGURE 68.2 Testing inversion and eversion of the hindfoot

Special tests • Achilles tendon, including calf squeeze (Thompson or Simmond test) (see FIG. 136.17 in CHAPTER 136) • Compress MTP joints from above and below • Compress metatarsals mediolaterally between thumb and forefinger • Press upwards from sole of foot just proximal to third and fourth MTP joints—Morton test • Check circulation—test dorsalis pedis and posterior tibial pulses • Neurological examination, including tests for L4, L5 and S1 nerve root function

Investigations The choice of investigations depends on the clinical features elicited by the history and examination. Select from the following list: • for systemic diseases: — blood glucose — RA tests — ESR/C-reactive protein — HLA-B27 • serum uric acid • radiology: — X-ray ± stress and weight-bearing views — radionuclide scans (for bone or joint pathology) — CT or MRI (especially helpful) scans — ultrasound (operator dependent) • nerve conduction studies Note: High-resolution ultrasound is used to diagnose disorders of the Achilles and posterior tibialis tendons and to locate foreign bodies such as splinters of wood and glass. Radionuclide scanning may detect avascular necrosis in bones, stress fractures, osteoid osteomas, inflammatory osteoarthritis and similar lesions.3

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of the tendoachilles. It is diagnosed by X-ray. The only treatment is to ensure that the child avoids wearing flat-heeled shoes and wears a slightly raised heel. Strenuous sporting activities should be restricted for 12 weeks and then reviewed.

Köhler disorder of the navicular

FIGURE 68.3 Testing eversion and inversion of the forefoot

Foot and ankle pain in children Apart from the common problem of trauma, special problems in children include: • foreign bodies in the foot • tumours (e.g. osteoid osteoma, osteosarcoma, Ewing tumour) • plantar warts • osteomyelitis/septic arthritis • ingrowing toenails • osteochondritis/aseptic necrosis • osteochondritis dissecans of talus (in adolescents) • pitted keratolysis and juvenile plantar dermatosis (adolescents) • stress fractures Think of osteoid osteoma in children with night pain.

OSTEOCHONDRITIS/ASEPTIC NECROSIS Three important bones to keep in mind are: • the calcaneum—Sever disorder • the navicular—Köhler disorder • the head of the second metatarsal—Freiberg disorder Sever disorder is traction osteochondritis while the other disorders are a ‘crushing’ osteochondritis with avascular necrosis.

Sever disorder of the heel This is calcaneal apophysitis, which presents in a child (usually a boy) aged 7–15 years (average of 10 years) with a painful tender heel at the insertion

This disorder causes a painful limp (usually mild) with some swelling and tenderness around the navicular in a child (usually a boy) aged 3–6 years, although it is seen sometimes in older children. Complete recovery occurs with temporary resting. Sometimes a supportive strapping is helpful.

Freiberg disorder This problem affects the head of the second metatarsal (rarely the third), which feels tender and swollen on palpation. It is more common in girls aged 12–16 years and can present in young adults as pain aggravated by standing on the forefoot. Plain X-ray shows the characteristic collapse of the metatarsal head. The treatment is restriction of activity, protective footwear and protective padding.

Sprained ankle in a child Children rarely sprain ligaments so it is important to assess apparent strains carefully, including an X-ray.

The little athlete The ‘little athlete’ can suffer a variety of injuries from accidents and overuse. Diffuse heel pain, which is common, is most often related to Sever apophysitis of the calcaneum. Occasionally, a juvenile-type plantar fasciitis may occur. Little athletes can develop tendonitis around the ankle, either on the lateral side (peroneals) or medially (tibialis posterior). Occasionally, a stress fracture of the metatarsals or other bones can occur.4 Special attention must be paid to any developmental structural abnormalities and to footwear.

Foot and ankle problems in the elderly Foot problems are more prevalent in old age. Some are due to a generalised disease, such as diabetes or peripheral vascular disease, while others, such as bunions, hammer toes, calluses and corns, atrophy of the heel fat-pad and Morton neuroma, increase with ageing. The transverse arch may flatten out and the protective pads under the metatarsals may atrophy, resulting in painful callosities.

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Unfortunately, many elderly people regard foot problems as a normal process but these problems actually require considerable care and attention, especially in the presence of peripheral vascular disease, diabetes or rheumatoid arthritis. Deformed toenails (onychogryphosis) are also common albeit not a painful condition. Flat foot occurring in middle age is usually due to stretching or rupture of the tibialis posterior tendon.5

Sprained ankle There are two main ankle ligaments that are subject to heavy inversion or eversion stresses, namely the lateral ligaments and the medial ligaments respectively. Most of the ankle ‘sprains’ or tears involve the lateral ligaments (up to 90%) while the stronger, tauter medial (deltoid) ligament is less prone to injury. It is important not to misdiagnose a complete rupture of the lateral ligaments. Most sprains occur when the ankle is plantar flexed and inverted, such as when landing awkwardly after jumping or stepping on uneven ground. It is a very common sporting injury and is presented in more detail in CHAPTER 136. Note the Ottawa rules for taking an X-ray of the ankle in CHAPTER 136). Clinical features (sprained lateral ligaments) • Ankle ‘gives way’ • Difficulty in weight-bearing • Discomfort varies from mild to severe • Bruising (may take 12–24 hours) indicates more severe injury • May have functional instability: ankle gives way on uneven ground Physical examination Perform as soon as possible:

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• note swelling and bruising • palpate over bony landmarks and three lateral ligaments (see FIG. 136.12, CHAPTER 136) • test general joint laxity and range of motion • a common finding is a rounded swelling in front of the lateral malleolus (the ‘signe de la coquille d’oeuf’) • test stability in AP plane (anterior draw sign) Is there an underlying fracture? For a severe injury the possibility of a fracture— usually of the lateral malleolus or base of fifth metatarsal—must be considered. If the patient is able to walk without much discomfort straight after

the injury a fracture is unlikely. However, as a rule, ankle injuries should be X-rayed. See the Ottawa rules in CHAPTER 136.

HEEL PAIN Important causes of heel pain in adults (see FIG. 68.4)6 include: • Achilles tendon disorders: — tendonopathy/peritendonitis (see CHAPTER 136) — bursitis: postcalcaneal, retrocalcaneal — tendon tearing (see CHAPTER 136): partial, complete • bruised heel • tender heel pad: — usually atrophy — also inflammation • neuropathies (e.g. diabetic, alcoholic) • tenosynovitis (FHL, FDL) • ‘pump bumps’ • plantar fasciitis • periostitis • calcaneal apophysitis • peroneal tendon dislocation • nerve entrapments — tarsal tunnel — medial calcaneal nerve — nerve to abductor digiti minimi Ultrasound examination is useful to differentiate the causes of Achilles tendon disorders.

Achilles tendonopathy6 The pathology is a combination of degenerative and inflammatory changes due to overuse and may occur either in the tendon itself or in the surrounding paratendon. It presents with tendon pain during and after weight-bearing activities with a tender local swelling of the tendon. The latter is called peritendonitis rather than tenosynovitis because there is no synovial sheath. Management • Relative rest • Course of NSAIDs for acute pain • Heel padding • Consider heel ‘raisers’ • Consider continuous topical glyceryl trinitrate as patches • Physiotherapy for stretching and an eccentric exercise program6 • Physiotherapy

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Achilles tendon bursitis Bursitis can occur at two sites: • posterior and superficial—between skin and tendon • deep (retrocalcaneal)—between calcaneus and tendon (see FIG. 68.4) The former occurs mainly in young women from shoe friction and is readily palpated. Tenderness from the deep bursitis is elicited by squeezing in front of the tendon with the thumb and index finger: a swelling may be seen bulging on either side of the tendon. Treatment • Avoid shoe pressure (e.g. wear sandals) • 1–2 cm heel raise inside the shoe • Apply local heat and ultrasound • NSAIDs • Inject corticosteroid into bursa with a 25 gauge needle

Fat-pad disorders A tender heel pad or cushion causes a dull throbbing pain under the heel. It is localised more proximal to that of plantar fasciitis. Once established, it is very difficult to treat. The fat-pad, which consists of globules of fat encapsulated in multiple U-shaped scepti, acts as a hydraulic shock absorber on heel strike. It also

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contains significant nerve endings.7 It can undergo atrophy, especially in the elderly, and also become inflamed. Treatment • Reduction of aggravating activity • Weight loss (if applicable) • Simple analgesics • Orthotic (cushioning heel cup) ± foam insert • Good footwear Problems are treated with an orthotic or an insert and good footwear. Corticosteroids should be avoided as they can accelerate the atrophy.8

Plantar fasciitis This common condition (also known as ‘policeman’s heel’) is characterised by pain on the plantar aspect of the heel, especially on the medial side; it usually occurs about 5 cm from the posterior end of the heel although it can be experienced over a wide area beneath the heel. The pain radiates into the sole. Clinical features • Pain: — under the heel — first steps out of bed — relieved after walking — increasing towards the end of the day — worse after sitting

peroneal tendon dislocation or tendonitis

peritendonitis

tendonitis arthritis subtalar joint ruptured tendoachilles partial tear

retrocalcaneal bursitis disease of calcaneus plantar fasciitis

postcalcaneal bursitis

calcaneal apophysitis (Sever disorder) tender heel pad

FIGURE 68.4 Important causes of the painful heel

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May be bilateral—usually worse on one side Typically over 40 years Both sexes Sometimes history of injury or overuse No constant relationship to footwear

Signs8 • Tenderness: — localised to medial tuberosity — may be more posterior — may be lateral — may be widespread — not altered by tensing fascia (but this action may cause pain) • Heel pad may bulge or appear atrophic • Crepitus may be felt • No abnormality of gait, heel strike, or foot alignment • Patient often obese

‘Cracked’ heels • Soak feet for 30 minutes in warm water containing an oil such as Alpha-Keri or Derma Oil. • Pat dry, then apply a cream such as Nutraplus (10% urea) or Eulactol heel balm. Use hydrocortisone 0.5% cream for resistant cases. • For severe cases use sorbolene cream with 20% glycerol and 30% urea (test skin sensitivity first).

ARTHRITIC CONDITIONS Arthritis of the foot or ankle is a rather meaningless diagnosis and specificity is required. Typical sites of arthritic targets are shown in FIGURE 68.5. spondyloarthropathies rheumatoid arthritis

Treatment Plantar fasciitis tends to heal spontaneously in 12–24 months. It has a variable response to treatment with NSAIDs, injections, ultrasound and insoles. Rest from long walks and from running is important. Systematic reviews to date indicate that taping is effective for short-term relief. Plantar fascia stretching exercises, when combined with prefabricated insoles and a short course of NSAIDs, are effective for shortterm and long-term pain relief. For patients with chronic symptoms, newer extracorporeal shockwave therapy devices are effective.9 Another systematic review supports a conservative approach based on maximising comfort during the 3-month period of considerable discomfort.10

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Protection Symptomatic relief is obtained by protecting the heel with an orthotic pad to include the heel and arch of the foot (e.g. Rose insole). Otherwise, a pad made from sponge or sorbo rubber that raises the heel about 1 cm is suitable. A hole corresponding to the tender area should be cut out of the pad to avoid direct contact with the sole. The aim is to get all of the foot to take the stress. Injection technique Disabling plantar fasciitis can be treated by injecting local anaesthetic and long-acting corticosteroid into the site of maximal tenderness in the heel. An alternative is to inject the corticosteroid into the anaesthetised heel and this is usually for temporary relief.

gout

Osteoarthritis (including hallux rigidus)

Osteoarthritis talonavicular joint subtalar joint

FIGURE 68.5 Typical sites of arthritic causes of podalgia on skeleton of right foot (plantar aspect)

Osteoarthritis Osteoarthritis may occur in any of the joints of the foot but it commonly involves the first MTP joint, leading to hallux rigidus. It can affect the subtalar joint, but the ankle joint proper is usually not affected by osteoarthritis.

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Hallux rigidus Osteoarthritis of the first MTP joint can lead to gradual loss of motion of the toe and considerable discomfort. Roomy protective footwear and relative rest is the basis of treatment, coupled with daily self-mobilisation (stretching toe into plantar flexion morning and night). Other measures include manipulation under general anaesthesia or surgery (arthrodesis or arthroplasty) for severe cases.

Rheumatoid arthritis Rheumatoid arthritis is typically a symmetrical polyarthritis presenting with pain in the MTP joints. It may also affect the ankle, mid-tarsal and tarsometatarsal joints. The interphalangeal joints are seldom affected primarily. It causes pain and stiffness under the balls of the feet, especially first thing in the morning.

Gout Gout typically affects the first MTP and should be considered with the sudden onset of pain, especially in the presence of redness, swelling and tenderness. It can affect any synovial joint and occasionally may be polyarticular. Gout is often dismissed by the patient as a ‘sprain’. A history of alcohol consumption or diuretic treatment is relevant.

Spondyloarthropathies This group of arthritic disorders (reactive arthritis, ankylosing spondylitis, psoriatic arthritis and arthritides associated with chronic bowel disorders) may involve peripheral joints. Other foot involvement includes plantar fasciitis, Achilles tendonitis and sausage-shaped toes due to tenosynovitis, and arthritis of the proximal interphalangeal joints.

‘Burning’ feet

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• complex regional pain syndrome I or II • Morton neuroma (localised pain between toes) • psychogenic, especially anxiety It is worth considering tarsal tunnel syndrome if there is anterior burning pain in the forefoot with associated aching in the calf. It is usually present in menopausal women and worse at night. It is caused by entrapment of the posterior tibial nerve near the medial malleolus, and may be associated with rheumatoid arthritis. Treat with physiotherapy, a medial arch support and a corticosteroid injection before contemplating surgery.

FOOT STRAIN Foot strain is probably the commonest cause of podalgia. A foot may be strained by abnormal stress, or by normal stress for which it is not prepared. In foot strain the supporting ligaments become stretched, irritated and inflamed. It is commonly encountered in athletes who are relatively unfit or have a disorder such as flat feet, or in obese adults. Symptoms and signs • Aching pain in foot and calf during or after prolonged walking or standing • Initial deep tenderness felt on medial border of plantar fascia (see FIG. 68.6) • Worse with new shoes, especially a change to high heels

Acute foot strain Acute ligamentous strain, such as occurs to the occasional athlete or to the person taking long unaccustomed walks, is usually self-limiting. It recovers rapidly with rest.

Chronic foot strain

It is not uncommon for people, especially the elderly, to present with the complaint of ‘burning’ feet. A careful history is needed to elicit exactly what they mean by ‘burning’—is it real pain, a cold sensation or paraesthesia? A checklist of causes is as follow:

Foot strain will become chronic with repeated excessive stress or with repeated normal stress on a mechanical abnormality. A common consequence is an everted foot, leading to flattening of the longitudinal arch on weight-bearing. It is important to establish whether the symptoms commenced after the patient began wearing a different type of footwear.

• vascular: ischaemic rest pain from small vessel disease, chilblains or other cold reaction, functional vasospasm (Raynaud phenomenon) • diabetic neuropathy • tarsal tunnel syndrome

Treatment The treatment is basically the same as that of the adult flat foot. Acute strain is treated with rest and by reducing walking to a minimum. Try the application of cold initially and then heat. The management of chronic

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Freiberg disorder

tendonitis of FHL tendon

Morton neuroma

bunion stress (march) fracture

fractured tubercle 5th metatarsal

Köhler disorder

foot strain

plantar fasciitis

FHL: flexor hallucis longus

FIGURE 68.6 Typical sites of important causes of podalgia (other than arthritis)—right foot

strain is based on an exercise program and orthotics, including arch supports, to correct any deformity.

Aching feet • • • •

Avoid wearing high heels. Wear insoles to support the foot arch. Perform foot exercises. Soak the feet in a basin of warm water containing therapeutic salts (Epsom salts is suitable). • Massage feet with baby oil followed by a special ribbed wooden foot massager.

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Flat feet (pes planus) Flat feet are normal in young children. No treatment is required in flat feet in which the arch is restored by standing on tiptoe (see CHAPTER 92). If painful, treat with exercises and insoles. Refer if concerned. Hind foot fusion can be performed for severe pain.

Claw foot (pes cavus) High foot arch is usually of congenital origin. It may be secondary to polio or various neurological conditions.

The foot is inflexible and the toes may be ‘hammer’ or clawed. Treatment includes special orthotics with good shock-absorbing properties, appropriate footwear, foot exercises and padding under the metatarsal heads. Operative treatment involves soft tissue release or arthrodesis to strengthen toes.

DISORDERS OF THE ANKLE TENDONS Inflammation of a tendon sheath about the ankle may result from repetitive overuse, trauma such as a sprained ankle or unaccustomed stress, including sporting injuries. Tenosynovitis commonly involves the tibialis posterior tendon over the medial compartment or the peroneal tendons over the lateral compartment. It may also affect the tibialis anterior and extensor digitorium longus tendons. Friction at the point where the tendons become angulated at the ankle causes the inflammation. The patient presents with pain, swelling and restricted movement. On examination there is swelling and tenderness where the tendon bulges out from behind and below the malleolus. If necessary the diagnosis can be confirmed by ultrasound or MRI imaging. Complications include tenovaginitis, weakness, ganglion formation, subluxation or dislocation and rupture. Treatment of tendonitis includes partial immobilisation (rarely in a cast) or an orthotic device to support the arch of the foot. A carefully directed injection of corticosteroid into the tendon sheath can be very effective.

Peroneal tendonitis This occurs along the course of the tendon from behind the lateral malleolus to the outer side of the foot and is common in athletes and ballet dancers. Pain is reproduced on palpation, on stretching the tendons by passive inversion of the foot or by resisting eversion of the foot.

Peroneal tendon dislocation It is most commonly a dislocated leg tendon as a result of forceful dorsiflexion. An audible painless snapping sensation may be experienced. Surgical repair is necessary.

Tibialis posterior tendonopathy This is a common problem, especially in middleaged females, in ballet dancers and in those with pes planus with a valgus deformity. The tendon (see

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Pain in the foot and ankle FIG. 68.7), which is an invertor of the foot, is attached to the navicular tuberosity.11

tibialis anterior tendonopathy

tibialis posterior tendonopathy

FIGURE 68.7 Medial aspect of the foot illustrating tendon disorders: tendonopathy of tibialis anterior and tibialis posterior

Clinical features6,11 • Pain and a feeling of weakness in the medial ankle and foot • Pain aggravated by standing and walking • Standing on toes is painful and difficult • Pain on palpation anterior and inferior to the medial malleolus • Pain on stretching into eversion • Painful resisted active inversion • May cause tarsal tunnel syndrome Diagnosis Ultrasound examination—but MRI is the gold standard for delineating tendon tears and inflammation.12

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Tibialis posterior tendon rupture Rupture of the tibialis posterior tendon after inflammation, degeneration or trauma13 is a relatively common and misdiagnosed disorder, especially in middle-aged females. It causes collapse of the longitudinal arch of the foot, leading to a flat foot.5 It is uncommon for patients to feel obvious discomfort at the moment of rupture. They may subsequently present with the sudden appearance of an ‘abnormal’ flat foot. There is gross eversion of the foot. A simple test is the ‘too many toes’ test whereby more toes are seen on the affected side when the feet are viewed from about 3 m behind the patient (see 5 FIG. 68.8). The single heel raise test is also diagnostic. The most useful investigation is an ultrasound examination. Minor cases can be treated conservatively with orthotics, but severe problems respond well to surgical correction.

Sesamoiditis1 The two sesamoids that lie beneath the head of the first metatarsal may develop painful conditions such as chondromalacia, osteoarthritis and stress fractures. A special ‘sesamoid’ X-ray assists diagnosis. Painful callus can develop over here in the elderly. Well-designed insoles are usually effective as is surgical excision for persistent problems.

Treatment This is basically conservative with a good outcome in 12–24 months. • Orthotic correction (bilateral) with semi-rigid orthosis to support faulty arch • Exercises under physiotherapist guidance • Remedial massage Consider ultrasonic guided injection of corticosteroids into tendon sheath (but best avoided) and a surgical opinion for failed conservative management.

Tibialis posterior tendon dislocation This can occur with forceful ankle dorsiflexion and inversion. The patient usually experiences pain and cannot weight-bear. The dislocated tendon may be seen overlying the medial malleolus. Immediate surgical repair is recommended.

68 FIGURE 68.8 Tibialis posterior tendon rupture (right foot): the ‘too many toes’ posterior view

Metatarsalgia1 Metatarsalgia is a symptom rather than a disease and refers to pain and tenderness over the plantar heads of the metatarsals (the forefoot). Causes include

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foot deformities (especially with depression of the transverse arch), leading to painful strain, arthritis of the MTP joints, trauma, Morton neuroma, Freiberg disorder and entrapment neuropathy. However it can occur in normal feet after prolonged standing. Depression of the transverse arch results in abnormal pressure on the second, third and fourth metatarsal heads with possible callus formation. Repetitive foot strain, pes cavus and high heels may cause a maldistribution of weight to the forefoot. Treatment involves treating any known cause, advising proper footwear and perhaps a metatarsal bar. Flat-heeled shoes with ample width seldom cause problems in the metatarsal region.

Stress fractures14 Clinical features • The aches or pains may be slow in onset or sudden • Common in dancers, especially classical ballet, and in unfit people taking up exercise • Examination is often unhelpful: swelling uncommon12 • Routine X-rays often unhelpful • A bone scan is the only way to confirm the suspected diagnosis • Basis of treatment is absolute rest for 6 or more weeks with strong supportive footwear • A walking plaster is not recommended

the advent of nuclear bone scans and CT scans. A protracted course of treatment can be expected.

Calcaneum Stress fractures of the os calcis usually have an insidious onset. Osteoporosis is a predisposing factor, as is an increased training program.14

Morton neuroma12 Morton interdigital neuroma is probably misdiagnosed more often than any other painful condition of the forefoot. It is not a true neuroma but a fibrous enlargement of an interdigital nerve, and its aetiology is still uncertain. It is related to overuse and inappropriate footwear. The diagnosis is made on clinical grounds. An ultrasound examination may detect a neuroma. Clinical features • Usually presents in adults 1000 U/L). A result >125 U/L suggests active disease.6 Note: calcium and phosphate normal. arthritis Bone problems pain deformities pathological fractures osteogenic sarcoma

bowed (legs) tibia

69 FIGURE 69.1 Paget disease of the left leg showing deformity of the tibia with a ‘sabre’ tibia due to its enlargement of length and bulk

FIGURE 69.2 Paget disease: possible clinical features

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Walking difficulty and leg swelling Localised and asymptomatic disease requires no treatment. Three groups of drugs are currently available: • the calcitonins • the bisphosphonates—e.g. etidronate, pamidronate disodium (APD), alendronate, risedronate • various antineoplastic agents (e.g. mithramycin) Bisphosphonates have become the preferred drugs for first-line therapy and include:6 • alendronate 40 mg (o) daily for 6 months (oesophagitis can be problematic) • pamidronate disodium 30–60 mg IV infused over 2–4 hours (usually the preferred option) • risedronate 30 mg (o) daily for 2 months • tiludronate 400 mg (o) daily for 3 months • zoledronic acid 5 mg IV over at least 15 minutes, once yearly All oral agents should be taken on an empty stomach. Repeated doses may rarely be required in severe cases as judged by symptoms and disease activity (e.g. monitoring with serum ALP).

Leg swelling Diagnostic features and pitfalls • Not all swollen legs require investigation and treatment. • The significance of leg swelling varies according to the age group, whether it is bilateral or unilateral, and whether the onset is sudden or gradual (see TABLE 69.2). • If the onset of oedema is acute (often 40 years presenting with painless unilateral leg oedema. • A drug history is essential as several drugs can cause oedema. • Pitting oedema is a feature of venous thrombosis or insufficiency, not lymphatic obstruction.

Investigations Select from these first-line tests: • urinalysis (? albumin) • FBE and ESR

Table 69.2

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Leg and ankle swelling: diagnostic strategy

Q. Probability diagnosis A. Physiological: • dependency/gravitational • prolonged sitting, standing, walking • hot weather • pregnancy • mechanical (e.g. constricting clothing) Chronic venous insufficiency (varicose veins) Congestive cardiac failure Drugs (e.g. calcium antagonists, NSAIDs, steroids, glitazones, beta blockers) Local trauma Obesity Q. Serious disorders not to be missed A. Vascular: • deep venous thrombosis (DVT) • inferior vena cava thrombosis • thrombophlebitis Infection: • cellulitis • tropical infections (e.g. filariasis, hookworm) Cancer: • obstruction from pelvic cancer • localised malignancy Other: • kidney disease (e.g. nephrotic syndrome) • liver disease (e.g. cirrhosis) • skin allergy (e.g. angioneurotic oedema) Q. Pitfalls (often missed) A. Idiopathic (periodic or cyclic) oedema Protein-losing enteropathy (e.g. Crohn) Lipoedema (fat and fluids) of legs Lipidema (fat) of legs Rarities: • malnutrition • lymphoedema: primary or secondary Q. Seven masquerades checklist A. Diabetes Drugs (multiple) Thyroid/endocrine (hypothyroidism, Cushing syndrome) Anaemia

• • • • • •

serum electrolytes, urea and creatinine blood sugar serum albumin/LFTs TSH level ultrasound (DVT screen) other radiographs (e.g. CT scan, venogram)

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Calf swelling of sudden onset Causes to consider: • • • • • •

acute arterial occlusion ruptured Baker cyst ruptured medial head of gastrocnemius DVT (usually gradual) cellulitis/erysipelas compartment syndrome

Pain accompanies most of these conditions but the absence of pain does not exclude DVT or thrombophlebitis. Refer to CHAPTER 66.

Lipoedema and lipidemia Lipoedema is the development of bilateral leg swelling that does not involve the feet (in lymphoedema the swelling develops in the most distal part of the foot). Lipoedema is fat and fluid while lipidemia is fat only. Clinical features • Exclusive to obese women • Spares the feet • Bilateral and symmetrical distribution of fat • The legs are often painful and bruise easily • The Stemmer sign (the ability to pick up a fold of skin at the base of the large toe) is usually negative8

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Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Deep venous thrombosis • Paget disease of bone • Parkinson disease

References 1 Horne M. Gait and postural disorders. Monash University Neurology Notes, 1996: 1–4. 2 Kincaid-Smith P, Larkins R, Whelan G. Problems in Clinical Medicine. Sydney: MacLennan & Petty, 1990: 190–4. 3 Paxton G, Munro J (eds). Paediatric Handbook (7th edn). Melbourne: Blackwell Science, 2003: 550–4. 4 Moulds R (Chair). Therapeutic Guidelines: Antibiotic (Version 14). Melbourne: Therapeutic Guidelines Ltd, 2010: 41–9. 5 Ralson D, Langston AL, Reid IR. Pathogenesis and management of Paget disease of bone. Lancet, 2008; 372 (9633): 155–63. 6 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 121–6. 7 Diu P, Juergens C. Clinical approach to the patient with peripheral oedema. Medicine Today, October 2009; 10 (10): 37–42. 8 Piller N, Birrell S. Lymphoedema: how to treat. Australian Doctor, 6 June 2003: I–VIII.

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The most important requirement of the art of healing is that no mistakes or neglect occur. There should be no doubt or confusion as to the application of the meaning of complexion and pulse. These are the maxims of the art of healing. Huang Ti (The Yellow Emperor) (– BC) Palpitations are an unpleasant awareness of the beating of the heart. By definition it does not always imply ‘racing’ of the heart but any sensation in the chest, such as ‘pounding’, ‘flopping’, ‘skipping’, ‘jumping’, ‘thumping’ or ‘fluttering’ of the heart. The problem requires careful attention and reassurance (if appropriate) because heartbeat is regarded as synonymous with life. To the practitioner it may simply represent anxiety or it could be a prelude to a cardiac arrest. In many circumstances prompt referral to a cardiologist is imperative.

Key facts and checkpoints • • •

•

•

• •

•

• •

The symptom of palpitations is suggestive of cardiac arrhythmia but may have a non-cardiac cause. Palpitations not related to emotion, fever or exercise suggest an arrhythmia. Perhaps the commonest arrhythmia causing a patient to visit the family doctor is the symptomatic premature ventricular beat/complex (ventricular ectopic). The commonest cause of an apparent pause on the ECG is a blocked premature atrial beat/complex (atrial ectopic). A 12-lead electrocardiographic diagnosis is mandatory. If the cause is not documented, an ambulatory electrographic monitor (e.g. Holter) may be used. Consider myocardial ischaemia as a cause of the arrhythmia. Consider drugs as a cause, including prescribed drugs and non-prescribed drugs such as alcohol, caffeine and cigarettes. Common triggers of paroxysmal supraventricular tachycardia (PSVT) include anxiety and cigarette smoking. The commonest mechanism of any arrhythmia is re-entry. Get patients to tap out the rate and rhythm of their abnormal beat.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE  70.1, which includes significant causes of palpitations.

Probability diagnosis If the palpitations are not caused by anxiety or fever, the common causes are sinus tachycardia and premature complexes/ectopics (atrial or ventricular). Sinus tachycardia, which by definition is a rate of 100–160/min, may be precipitated by emotion, stress, fever or exercise. PSVT and atrial fibrillation are also quite common arrhythmias. Some cardiologists claim that the commonest arrhythmia causing a patient to visit the family doctor is the symptomatic ventricular ectopic beat.1 Sinus tachycardia can be differentiated clinically from PSVT in that it starts and stops more gradually than PSVT (abrupt) and has a lower rate of 100–150 compared with 160–220. Important causes of tachyarrhythmias are: • ischaemic heart disease, especially acute coronary syndrome • hypertension • heart failure • mitral disease • thyrotoxicosis • atrial septal deficit

Serious disorders not to be missed It is vital not to overlook acute coronary syndromes as a cause of the arrhythmia manifesting as palpitations. About 25% of infarcts are either silent or unrecognised. Sinister life-threatening arrhythmias are: • • • •

ventricular tachycardia atypical ventricular tachycardia (torsade de pointes) sick sinus syndrome (SSS) complete heart block

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Table 70.1

• Problem solving in general practice

Palpitations: diagnostic strategy model

Q. Probability diagnosis A. Anxiety Premature beats (ectopics) Sinus tachycardia Drugs (e.g. stimulants) Supraventricular tachycardia Q. Serious disorders not to be missed A. Myocardial infarction/angina Arrhythmias: • atrial fibrillation/flutter • ventricular tachycardia • bradycardia • sick sinus syndrome • torsade de pointes Long QT syndrome Wolff–Parkinson–White (WPW) syndrome Electrolyte disturbances: • hypokalaemia • hypomagnesaemia • hypoglycaemia (type 1 diabetes) Q. Pitfalls (often missed) A. Fever/infection Pregnancy Menopause (sudden vasodilatation) Drugs (e.g. caffeine, cocaine) Mitral valve disease Aortic incompetence Hypoxia/hypercapnia Rarities: • tick bites (T1–5) • phaeochromocytoma Q. Seven masquerades checklist A. Depression Diabetes (indirect) Drugs Anaemia Thyroid disorder (hyperthyroidism) Spinal dysfunction UTI (possible) Q. Is the patient trying to tell me something? A. Quite likely. Consider cardiac neurosis, anxiety.

It is also important not to miss: • hypokalaemia • hypomagnesaemia

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Pitfalls There are many pitfalls in the diagnosis and management of arrhythmias, especially in the

elderly, where symptoms of infection may be masked. Palpitations associated with the menopause can be overlooked. Valvular lesions, usually associated with rheumatic heart disease, such as mitral stenosis, and aortic incompetence may cause palpitations. The rare tumour, phaeochromocytoma, presents with palpitations and the interesting characteristic of postural tachycardia (a change of more than 20 beats/ min). The toxin from tick bites in dermatomes T1–5 can cause palpitations. General pitfalls • Misdiagnosing PSVT as an anxiety state • Overlooking a cardiac arrhythmia as a cause of syncope or dizziness • Overlooking atrial fibrillation (AF) in the presence of a slow heartbeat • Overlooking mitral valve prolapse in a patient, especially a middle-aged woman presenting with unusual chest pains and palpitations (auscultate in standing position to accentuate click(s) ± murmurs)

Seven masquerades checklist Surprisingly, all the masquerades have to be considered, either as direct or indirect causes: depression, especially with anxiety and in the postpartum period; diabetes, perhaps as an arrhythmia associated with a silent myocardial infarction or with hypoglycaemia; drugs as a very common cause (see TABLE 70.2); anaemia, causing a haemodynamic effect; hyperthyroidism; spinal dysfunction of the upper thoracic vertebrae T1–5; and urinary tract infection, especially in the elderly. PSVT has been described as resulting from injury or dysfunction of the upper thoracic spine (especially T4 and T5) in the absence of organic heart disease.2 The author has personally encountered several cases of PSVT alleviated by normalising function of the spine.

Psychogenic considerations Emotional factors can precipitate a tachycardia, which in turn can exaggerate the problem in an anxious person. Some people have a cardiac neurosis, often related to identification with a relative or friend. A family history of cardiac disease can engender this particular anxiety. Evidence of anxiety and depression should be sought in patients presenting with palpitations without clinical evidence of cardiovascular disease.

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Palpitations

Table 70.2

Some drugs that cause palpitations

Alcohol Alendronate Aminophylline/theophylline Amphetamines Antipsychotics (e.g. CPZ, haloperidol, olanzapine) Antiarrhythmic drugs Antidepressants: • tricyclics • MAO inhibitors Atropine, hyoscine, hyoscyomine Caffeine Cocaine Class 1a and 1c drugs Digitalis Diuretics → K ↓, Mg ↓ Glyceryl trinitrate Sympathomimetics: • in decongestants (e.g. pseudoephedrine, ephedrine) • β-agonists (e.g. salbutamol, terbutaline) Thyroxine

The clinical approach Careful attention to basic detail in the history and examination can point the way clearly to the clinical diagnosis.

History Ask the patient to describe the onset and offset of the palpitations, the duration of each episode and any associated features. Then ask the patient to tap out on the desk the rhythm and rate of the heartbeat experienced during the ‘attack’. If the patient is unable to do this, tap out the cadence of the various arrhythmias to find a matching beat. An irregular tapping ‘all over the place’ suggests atrial fibrillation, while an isolated thump or jump followed by a definite pause on a background of a regular pattern indicates premature beats (ectopics/ extrasystoles) usually of ventricular origin. The thump is not the abnormal beat but the huge stroke volume of the beat following the compensatory pause.

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Key questions • Do the palpitations start suddenly? How long do they last? • What do you think brings them on? • Are they related to stress or worry or excitement? • What symptoms do you notice during an attack? • Do you have pain in the chest or breathlessness during the attack? • Do you feel dizzy or faint during the attack? • What medications do you take? • How much coffee, tea, Coke do you drink? • Have you been using nasal decongestants? • Did you eat Chinese food before the attack? • Do you smoke cigarettes, and how many? • Do you take any of the social drugs, such as cocaine or marijuana? • Have you ever had rheumatic fever? • Have you lost weight recently or do you sweat a lot? Chest pain may indicate myocardial ischaemia or aortic stenosis; breathlessness indicates anxiety with hyperventilation, mitral stenosis or cardiac failure; dizziness or syncope suggests severe arrhythmias such as SSS and complete heart block, aortic stenosis and associated cerebrovascular disease.

Examination The ideal time to examine the patient is while the palpitations are being experienced. Often this is not possible and the physical examination is normal. Measurement of the heart rate may provide a clue to the problem. As a working guide, a rate estimated to be about 150 beats/minute suggests PSVT, atrial flutter/ fibrillation or ventricular tachycardia (see FIG.  70.1). A rate less than 150 beats per minute is more likely to be sinus tachycardia, which may be associated with exercise, fever, drugs or thyrotoxicosis.3 Assess whether the pulse is regular or irregular. If irregular, the possible causes are ectopic beats, atrial fibrillation and atrial flutter with varying degrees of block. The nature of the pulse, especially the pulse pressure and rhythm, should be carefully evaluated (see FIG. 70.2). Look for evidence of fever and infection and features of an anxiety state or depressive illness. Have the patient hyperventilate for 3 minutes to determine whether the arrhythmia is induced. Evidence of underlying disease such as anaemia, thyroid disorder, alcohol abuse or cardiac disease including the JVP and pulmonary congestion should be sought. Also look for evidence of a mitral valve

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60

100

150

anxiety

atrial flutter

sinus bradycardia

atrial fibrillation anaemia supraventricular tachycardia ventricular tachycardia

thyrotoxicosis

complete heart block

valvular disease aortic incompetence mitral stenosis

60

sinus tachycardia

100

150

Pulse rate per minute

FIGURE 70.1 Heart rate guide to causes of various arrhythmias

Form

Significance

Normal

Weak, small volume

Large volume, bounding

Collapsing

Plateau

Pulsus alternans

Pulsus bigeminus

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FIGURE 70.2 Various pulse forms

‘shock’ mitral stenosis constrictive pericarditis pericardial effusion hypertension aortic incompetence high output states e.g. anaemia fever A-V fistula aortic stenosis

severe myocardial dysfunction premature ectopic complex following every sinus beat —consider digoxin toxicity

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Palpitations

bright eyes ‘thyroid glitter’ ocular fundal changes

senile arcus

exophthalmos of hyperthyroidism

goitre

Cannon waves in jugular vein (CHB) hypertension

855

807

malar flush

signs of: aortic stenosis aortic incompetence mitral incompetence mitral stenosis others cardiac enlargement lung—basal crackles

collapsing pulse

thickened atherosclerotic radial artery palm signs: sweaty (hyperthyroidism) pallor of anaemia

peripheral vascular disease

ankle oedema

FIGURE 70.3 Signs to consider in a patient with palpitations

prolapse (mid-systolic click; late systolic murmur). Possible signs in the patient presenting with palpitations are shown in FIGURE 70.3.4

Investigations The number and complexity of investigations should be selected according to the problem and test availability. A checklist would include: • blood tests (for underlying disease): — haemoglobin and film — thyroid function tests — serum electrolytes and magnesium — serum digoxin ? digitalis toxicity — virus antibodies ? myocarditis • chest X-ray

• cardiac (ischaemia and function): — ECG (12 lead) — ambulatory 24-hour ECG monitoring — echocardiography (to look for valvular heart disease and assess left ventricular function) — electrophysiology studies — exercise stress test (? underlying CAD) — event monitor (can record up to 2 weeks) — implantable monitor (may last 1 year)

Palpitations in children Children may complain of palpitations which may be associated with exercise, fever or anxiety. Various arrhythmias can occur with three requiring

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special consideration—PSVT, heart block and ventricular arrhythmias.5 PSVT is characterised by beats at 200–300 per minute, the fastest rates occurring in infants. The cause is often not found but some children have ECG abnormalities compatible with the Wolff–Parkinson– White (WPW) syndrome. The recommended firstline treatment of PSVT is vagal stimulation via the application of ice packs to the upper face (forehead, eyes and nose) of the affected infant. Intravenous adenosine will usually terminate the episode. A particular concern is these children who have the familial long QT syndrome. They are prone to develop ventricular tachyarrhythmias, which may lead to sudden death. Consider it in children developing syncope on exertion.

Palpitations in the elderly The older the patient, the more likely is the onset of palpitations due to cardiac disease such as myocardial infarction/ischaemia, hypertension, arrhythmias and drugs, especially digoxin. Occasional atrial and ventricular arrhythmias, especially premature complexes (ectopics), occur in 40% of old people6 and treatment is rarely required. Atrial fibrillation occurs in 5–10% of patients over 65 years of age, 30% of whom have no clinical evidence of cardiovascular disease. A rapid ventricular rate with symptoms is the only indication for digoxin in the elderly but beware of SSS, especially if dizziness or syncope accompanies the fibrillation. In the elderly, thyrotoxicosis may present as sinus tachycardia or atrial fibrillation with only minimal signs—the so-called ‘masked thyrotoxicosis’—so it is easy to overlook it. The only clue may be bright eyes (‘thyroid glitter’) due to conjunctival oedema (see CHAPTER 23).

Arrhythmias Facts and figures

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• See FIGURE 70.4 for tracings of important arrhythmias. • Cardiac arrhythmias account for about 25% of management decisions in cardiology (see TABLE 70.3). • Commonest are premature (ectopic) ventricular beats and atrial fibrillation. • PSVT is next most common—6 per 1000 of population. • The commonest mechanism of paroxysmal tachycardias is re-entry (see FIG. 70.5).

Table 70.3

Types of arrhythmias

Non-pathological sinus rhythms Sinus arrhythmia Sinus bradycardia Sinus tachycardia Pathological bradyarrhythmias Sinus node disease (sick sinus syndrome) Atrioventricular (AV) block: • first degree AV block • second degree AV block • third degree (complete) AV block Pathological tachyarrhythmias 1 Atrial: • atrial premature (ectopic) complexes • PSVT • atrial flutter • atrial fibrillation (AF) 2 Ventricular: • ventricular premature (ectopic) complexes • ventricular tachycardia • ventricular fibrillation • torsade de pointes (twisting of points)

• Electrophysiological studies are the gold standard investigation for tachycardias but are rarely needed for diagnosing most arrhythmias. • Almost all antiarrhythmic drugs have a proarrhythmic potential (i.e. they may worsen existing arrhythmias or provoke new arrhythmias in some patients) (see TABLE 70.4). Always consider the no-treatment option. • Avoid digoxin in cases with an accessory pathway. • If ‘quinidine syncope’ occurs, consider torsade de pointes as the cause. • Any patient commencing antiarrhythmic therapy should have a 12-lead ECG 1–2 weeks later to check the QT interval. If prolonged, treatment should usually be ceased. • The two main indications for permanent pacemaking are SSS (only if symptomatic) and complete heart block.

Management strategies • • • •

Treat the underlying cause. Give appropriate reassurance. Provide clear patient education. Explain about the problems of fatigue, stress and emotion.

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809

normal sinus rhythm

sinus bradycardia and sinus arrhythmia—rate approx. 55 per minute

sinus tachycardia—rate approx. 100 per minute

complete heart block

atrial flutter

atrial fibrillation

FIGURE 70.4 Tracings of important arrhythmias

continued

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atrial premature complexes

ventricular premature complexes

supraventricular tachycardia

ventricular tachycardia

ventricular fibrillation

FIGURE 70.4 Tracings of important arrhythmias continued

• Advise moderation in consumption of tea, coffee, caffeine-containing soft drinks and alcohol. • Advise about cessation of smoking and other drugs.

Sinus bradycardia

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Look for causation (e.g. hypothyroidism and drugs). Correct the cause. Treatment is required only if symptomatic, which is uncommon at rates >40–45 beats/min. Use IV atropine if acute treatment is

required. However, mild or transient bradyarrhythmias may be asymptomatic or even physiological, such as in a healthy athlete. Palpitations are not a feature but they can cause dizziness, fatigue or syncope (e.g. Stokes–Adams attack—transient bradycardia due to complete heart block). Stokes–Adams attack • Sudden onset without warning • Patient falls to ground

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• Collapse with loss of consciousness • Pallor and still as if dead with slow or absent pulse • Recovery—in seconds back to normal • Patient flushes as pulse increases • Refer for management as attacks may be recurrent

abnormal conducting tissue blocked

PREMATURE (ECTOPIC) COMPLEXES

re-entry

Premature (ectopic) atrial complexes • These are usually asymptomatic. • Management is based on reassurance. • Check lifestyle factors such as excess alcohol, caffeine, stress and smoking; avoid precipitating factors. • Treatment is rarely required and should be avoided if possible. • At present there is no ideal anti-ectopic agent. • They may be a forerunner of other arrhythmias (e.g. PSVT, atrial fibrillation). • For intolerable symptoms give:6

impulse

FIGURE 70.5 Diagrammatic mechanism of re-entry tachycardia

Table 70.4

atenolol or metoprolol 25–100 mg (o) daily or verapamil SR 160–480 mg (o) daily

Electrophysiological classification of common antiarrhythmic drugs (after Vaughan Williams)

Class

Drug

Usual dosage

Common side effects

I

Membrane depressant drugs (sodium-channel blockers) Disopyramide Procainamide Quinidine

100–200 mg qid 1 g qid IV use 2–3 SR tabs (0.25 g) bd

Lignocaine Mexiletine Flecainide β-blockers

IV use 200 mg tid 100 mg bd various

Blurred vision, dry mouth, urinary problems in males (avoid in men >50) Anorexia, nausea, urticaria Diarrhoea, headache, tinnitus Nausea, dizziness, tremor Nausea, vomiting, tremor, dizziness Nausea, dizziness, rash Fatigue, insomnia, nightmares, hypotension, bronchospasm Avoid in asthmatics

Prolong action potential Amiodarone Sotalol

SVT: 200 mg daily VT: 400 mg daily 80–160 mg bd

Rash, pulmonary fibrosis, thyroid, hepatic and CNS effects As for β-blockers

Calcium channel blockers Verapamil Diltiazem

(SR) 160–480 mg daily (CR) 180–360 mg daily

Constipation, dizziness, hypotension Hypotension, headache

Ia

Ib Ic II

III

IV

Note: Sotalol is a β-blocker and thus is a class II and III agent. All drugs are taken orally unless IV indicated. Adenosine and digoxin are not classified.

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Premature (ectopic) ventricular complexes • These are also usually asymptomatic (90%). • They occur in 20% of people with ‘normal’ hearts. • Symptoms are usually noticed at rest in bed at night. • Check lifestyle factors as for atrial premature beats. • Drugs that can cause both types of premature beats include digoxin and sympathomimetics. • Look for evidence of ischaemic heart disease, mitral valve prolapse (especially women), thyrotoxicosis and left ventricular failure. • Ventricular premature complexes may be a forerunner of other arrhythmias (e.g. ventricular tachycardia). • If symptomatic but otherwise well with a normal chest X-ray and ECG, reassure the patient. • Drug therapy. Never commence drug therapy without performing an echocardiograph. This will help to guide the choice of agent. Class 1 agents can make the arrhythmia worse or even life-threatening if there is reduced ventricular function. If this is the case, the patient should be referred to a cardiologist. • For troublesome symptoms the β-blockers, atenolol or metoprolol, can be used e.g. atenolol 25–100 mg (o) daily.

Supraventricular tachycardia7 • SVT can be paroxysmal or sustained. • Rate is 150–220/min. • There are at least eight different types of SVT with differing risks and responses to treatment. • PSVT commonly presents with a sudden onset in otherwise healthy young people. • Passing copious urine after an attack is characteristic of PSVT. • Look for predisposing factors such as an accessory pathway and thyrotoxicosis. • Approximately 60% are due to atrioventricular (AV) node re-entry and 35% due to accessory pathway tachycardia (e.g. WPW).8 • Look for evidence of accessory pathways after reversion because accessory pathways can lead to sudden death (avoid digoxin in WPW). • Consider SSS in a patient with SVT and dizziness.

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Wolff–Parkinson–White syndrome The structural basis for the arrhythmia of SVT in WPW syndrome is an accessory pathway that

bypasses the AV node. A typical ECG shows a short PR interval and slurred upstroke of the QRS complex (delta wave). Patients are prone to sudden attacks of SVT. Up to 30% of patients will develop atrial fibrillation or flutter. Even one episode of PSVT requires consideration for radiofrequency ablation.9

Management of PSVT 1 Vagal stimulation can be attempted. Carotid sinus massage is the first treatment of choice. Other methods of vagal stimulation include: • Valsalva manoeuvre (easiest for patient) • self-induced vomiting • ocular pressure (avoid) • cold (ice) water to face or swallowing ice • immersion of the face in water 2 If vagal stimulation fails give adenosine IV (try 6 mg first over 5–10 seconds, then 12 mg in 2 minutes if unsuccessful, then 18 mg in 2 minutes if necessary and well tolerated). Second-line treatment is verapamil IV 1 mg/min up to 10–15 mg (provided patient is not taking a beta blocker).8 Precautions • Adenosine causes less hypotension than verapamil but may cause bronchospasm in asthmatics • Use only if narrow QRS and BP >80 mm Hg • Carefully monitor blood pressure • AVOID verapamil if taking β-blockers and persistent tachycardia with QRS complexes >0.14 s (suggests ventricular tachycardia) 3 In the rare event of failure of medical treatment, consider DC cardioversion or overdrive pacing. Prevention To prevent recurrences (frequent episodes) use atenolol or metoprolol, flecainide (only if no structural heart damage) or sotalol. If these agents fail, consider amiodarone. Do an echocardiograph first to exclude structural heart disease. Radiofrequency catheter ablation, which is usually curative, is indicated for frequent attacks not responding to medical therapy.

Carotid sinus massage1 Carotid sinus massage causes vagal stimulation and its effect on SVT is all or nothing. It has no effect on ventricular tachycardia. It slows the sinus rate and breaks the SVT by blocking AV nodal conduction.

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Palpitations Method • Locate the carotid pulse in front of the sternomastoid muscle just below the angle of the jaw (see FIG. 70.6). • Ensure that no bruit is present. • Rub the carotid with a circular motion for 5–10 seconds. • Rub each carotid in turn if the SVT is not ‘broken’, but never both together. In general, right carotid pressure tends to slow the sinus rate and left carotid pressure tends to impair AV nodal conduction. Precautions Avoid in the elderly (risk of embolism or bradycardia).

sternomastoid muscle

site for carotid sinus massage

FIGURE 70.6 Carotid sinus massage

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— persistent AF: abrupt onset, lasts >7 days — permanent (chronic) AF: cannot be converted to normal rhythm All types appear to have a similar risk for thromboembolism. • Remember to look for the underlying cause: myocardial ischaemia (15% of cases), mitral valve disease, thyrotoxicosis, hypertension, pericarditis, cardiomyopathy including chronic alcohol dependence, alcohol binge. • No cause is found in 12%—isolated9,10 atrial fibrillation. • All patients should have thyroid function tests and an echocardiograph to help find a cause. • With sustained atrial fibrillation there is a 5% chance per annum of embolic episodes. There is a fivefold risk of CVA overall. • The risk of CVA is greater in those with previous CVA, valvular heart disease, prosthetic mitral valve and cardiac failure. • For reversion anticoagulate with warfarin for 4 weeks beforehand and maintain for 4 weeks afterwards. • Digoxin controls the ventricular rate but does not terminate or prevent attacks. • Sotalol, flecainide and amiodarone are used for conversion of atrial fibrillation and maintenance of sinus rhythm. Flecainide should never be prescribed in patients with reduced LV function. • Evidence basis: RCTs showed that digoxin was beneficial for lowering the ventricular rate in the short term but no better than placebo in restoring rhythm. Beta blockers and calciumchannel antagonists benefited rate control but verapamil was much less effective than amiodarone at restoring cardiac rhythm.11

Atrial flutter Atrial fibrillation Facts and figures • A common problem (9% incidence in the over-70 age group). • It usually presents with an irregular ventricular rate of about 160–180 beats/minute in untreated patients with a normal AV node. • Apart from acute AF (new onset 38˚C, tender neck glands and white spots in the throat, antibiotics are indicated.8 Treatment should be with penicillin or an alternative antibiotic (see TABLE 73.3).4 Antibiotic treatment has a variable effect on the resolution of symptoms. It does not protect against glomerulonephritis but does protect against rheumatic fever.7 Amoxycillin should be avoided in tonsillitis because of confusion caused should mononucleosis be present. Frequent fluids are advisable.

Quinsy Quinsy is a peritonsillar abscess characterised by marked swelling of the peritonsillar area with medial displacement of tonsillar tissue (see FIG.  73.6). It is usually caused by GABHS or anaerobes, occasionally Haemophilus sp. and Staphylococcus aureus. A typical picture of tonsillitis is followed by increasing difficulty in swallowing and trismus. Treatment Antibiotics (e.g. procaine penicillin IM or clindamycin) plus aspiration or drainage in hospital under local anaesthetic if it is pointing. Oral penicillin treatment is likely to fail. Subsequent tonsillectomy may, but not always, be necessary. The cover can be broadened by adding metronidazole.4

Treat with prophylactic penicillin for patients with more than five episodes of presumptive bacterial tonsillitis in a year. The decision should be based on the severity of the episode, time lost from work or school, infectivity and response to antibiotics.

displaced uvula tonsils abscess

site of incision

Treatment for streptococcal throat (proven or suspected)4

Children phenoxymethyl penicillin 50 mg/kg/day (o) in 2 divided doses for 10 days (to max. 1 g/day) or (if hypersensitive to penicillin) roxithromycin 4 mg/kg up to 150 mg (o) bd for 10 days Adults phenoxymethyl penicillin 500 mg (o) 12 hourly for 10 days (can initiate treatment with one injection of procaine penicillin) or (if hypersensitive to penicillin) roxithromycin 300 mg (o) daily for 10 days In poorly compliant patients: benzathine penicillin 900 mg IM as a single dose in adults In severe cases: procaine penicillin 1–1.5 mg IM daily for 3–5 days plus phenoxymethyl penicillin (as above) for 10 days Note: Although symptoms and most evidence will disappear within 1–2 days of treatment, a full course of 10 days should be given to provide an optimal chance of eradicating S. pyogenes from the nasopharynx and thus minimising the risk of recurrence or complications such as rheumatic fever.4 Some studies indicate that 7 days may be sufficient.

843

Tonsillectomy in children results in only a modest reduction in the number of subsequent sore throats.9

Recurrent tonsillitis4,7

Table 73.3

891

FIGURE 73.6 Peritonsillar abscess (quinsy): a tense red bulging mass is noted and the uvula is displaced from the mid-line; a site of incision for drainage is indicated

Acute epiglottitis In children this is a life-threatening infection. It may be overlooked in adults where, unlike children, the airway is usually not obstructed and the patient presents with a severe sore throat, dysphagia, drooling of saliva and a tender neck. Examination of the throat may appear quite normal. However, it is a severe infection requiring hospitalisation and parenteral antibiotics (e.g. cefotaxime).

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Diphtheria Due to the bacterium Corynebacterium diphtheriae, the potentially fatal form of this disease almost always occurs in non-immunised people. The clinical presentation may be modified by previous immunisation or by antibiotic treatment.

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Clinical features • Insidious onset • Mild to moderate fever • Mild sore throat and dysphagia • Patient looks pale and ill • Enlarged tonsils • Pharynx inflamed and oedematous • Pseudomembrane (any colour but usually grey– green) can spread beyond tonsils to fauces, soft palate, lateral pharyngeal wall and downwards to involve larynx (see FIG. 73.7) • Enlarged cervical lymph nodes • Soft tissue swelling of neck → ‘bull neck’ appearance spreading membranous exudate

Clinical features • Sore throat • Prodromal fever, malaise, lethargy • Anorexia, myalgia • Nasal quality to voice • Skin rash Examination • Petechiae on palate (not pathognomonic) • Enlarged tonsils with or without white exudates (looks, but isn’t, purulent) • Peri-orbital oedema • Lymphadenopathy, especially posterior cervical • Splenomegaly (50%) • Jaundice ± hepatomegaly (5–10%)

The rash • Primary rash (5%) • Secondary rash: with ampicillin, amoxycillin (90–100%) with penicillin (50%) Note: This rash is not synonymous with penicillin hypersensitivity. Diagnosis • Blood film—atypical lymphocytes • White cell count—absolute lymphocytosis • Heterophil antibodies or Monospot test or • EBV IgM test (more specific)

FIGURE 73.7 Diphtheria: tonsils and pharynx are red and swollen; a thick grey-green exudate forms on the tonsils as a spreading membrane

Management • Throat swabs • Antitoxin • Penicillin or erythromycin 500 mg qid for 10 days • Isolate patient

Viral causes of sore throat Epstein–Barr mononucleosis The angiose form of EBM is a real trap and must be considered in patients aged 15–25 years (peak incidence) with a painful throat that takes about 7 days to reach its peak. Refer to CHAPTER 28.

Treatment4 Symptomatic e.g. paracetamol for pain. Parenteral corticosteroids only in most severe cases.

Herpangina An uncommon infection caused by the Coxsackie virus. Presents as small vesicles on soft palate, uvula and anterior fauces. These ulcerate to form small ulcers. The problem is benign and rapidly self-limiting.

Herpes simplex pharyngitis In adults primary infection is similar to severe streptococcal pharyngitis but ulcers extend beyond the tonsils.

Other viral pharyngitis Typically, the signs are fewer than with other causes. The typical case has mild redness without exudate and

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Sore throat prominent (sometimes pale) lymphoid patches on the posterior pharynx (see FIG.  73.1). Tonsillar lymph nodes are usually not enlarged or tender. This picture is the commonest encountered in general practice.

Candida pharyngitis Oral candidiasis typically presents as milky-white growths on the palate, buccal and gingival mucosae, pharynx and dorsum of the tongue (see FIG. 73.2). If scraped away, a bleeding ulcerated surface remains. A bad (metallic) taste is a feature but the patient may  complain of a sore throat and tongue and dysphagia. Causes or predisposing factors to consider: • • • • • •

HIV infection diabetes mellitus broad-spectrum antibiotics corticosteroids, including inhalers dentures debility

Management • Determine underlying cause. Nystatin suspension, rinse and swallow qid or amphotericin 10 mg lozenge dissolved slowly in oral cavity, 6 hourly, for 7–14 days

Practice tips • •

•

• • • •

Consider severe tonsillitis with a covering membrane as EBM. If an adult presents with an intensely painful throat with a heavy exudate and seems toxic, consider primary herpes simplex as well as streptococcal throat. Reserve swabs of the throat for verification of a streptococcal throat where it is important to do so, for suspected diphtheria and for suspicion of other serious infections such as tuberculosis. Be aware of possible complications, such as febrile convulsions in children and abscess formation. Do not misdiagnose unusual causes of a sore throat, such as cancer (see FIG. 73.8). The triad: hoarseness, pain on swallowing and referred ear pain = pharyngeal cancer. The two major considerations in managing the acute sore throat are: — Can diphtheria be excluded? — Should the patient be treated with an antibiotic?

trauma

carcinoma: palate tonsil tongue

glossopharyngeal neuralgia

aphthous ulcers tonsils: tonsillitis quinsy pharyngitis

FIGURE 73.8 General causes of a sore throat: note the importance of excluding cancer

Guidelines for tonsillectomy10 • Repeated attacks of acute tonsillitis • Enlarged tonsils and/or adenoids causing airway obstruction, including OSA • Chronic tonsillitis • More than one attack of peritonsillar abscess • Biopsy excision for suspected new growth

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Antibiotic treatment is aimed primarily at streptococcal pharyngitis and this is often based on clinical judgment.

When to refer • Acute epiglottitis in children (a medical emergency) • Inaccessible foreign body • Abscess: peritonsillar or retropharyngeal • Recurrent attacks of tonsillitis and adenoid hypertrophy for an opinion about tonsillectomy and/or adenoidectomy • Suspicion or evidence of HIV infection or diphtheria • Patients not responding to treatment • Patients with more generalised disorders that are not yet diagnosed9

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References

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1 Office of Population Censuses and Surveys. Morbidity Statistics from General Practice Studies on Medical and Population Subjects. No 26. London: HMSO, 1974: 33–40. 2 Cormack J, Marinker M, Morrell D. Practice: A Handbook of Primary Medical Care. London: Kluwer-Harrap, 1980: 3 (25): 1–7. 3 Del Mar CB, Glasziou PO, Spinks AB. Antibiotics for Sore Throat (Cochrane review). In: The Cochrane Library, Issue 1. Oxford: Update Software, 2002. 4 Moulds R (Chair). Therapeutic Guidelines: Antibiotics (14th edn). Melbourne: Therapeutic Guidelines Ltd, 2010: 263–6. 5 Yung AP, McDonald MI et al. Infectious diseases: a clinical approach. Melbourne: A Yung, 2001: 66–74.

6 Brook I, Gober AE. Persistence of group A β-hemolytic streptococci in toothbrushes and removable orthodontic appliances following treatment of pharyngotonsillitis. Arch Otolaryngol Head Neck Surg, 1998; 124: 993–5. 7 Cooper RJ, Hoffman JR et al. Principles of appropriate antibiotic use for acute pharyngitis in adults. Ann Intern Med, 2001; 134: 509–17. 8 Rosser W, Shafir MS. Evidence-Based Family Medicine. Hamilton: BC Decker Inc, 1998: 108–10. 9 Burton MJ, Glasziou PP. Tonsillectomy or adeno-tonsillectomy versus non-surgical treatment for chronic/recurrent acute tonsillitis. Cochrane Database Syst Rev 2009; (1): CD001802. 10 Jacobson I. Choosing the appropriate patients for tonsillectomy. Medicine Today, October 2012; 13 (10): 39–42.

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Tiredness/fatigue

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Chronic fatigue syndrome is not tiredness: there is a difference between feeling tired and ‘fatiguey’. Fatigue involves a heaviness in the limbs, a sense of inability to think or move, pain in muscles and joints, nausea etc. Please understand the difference. CFS patient to author, January  Tiredness, which basically means ‘a desire to rest’, or chronic fatigue is not a diagnosis but rather a symptom of illness: it may occur as either a presenting or a supporting symptom. Tiredness is interchangeable with terms such as weariness, lethargy, loss of energy, listlessness and exhaustion. It is a common and difficult presenting symptom often known by the acronym TATT—‘tired all the time’. The symptom of tiredness is likely to be ‘hidden’ behind the request for a tonic or a physical check-up.1 Tiredness can be a symptom of a great variety of serious and uncommon diseases, including malignant disease. The challenge for the family doctor is to diagnose such disorders quickly without extravagant investigation.

•

•

•

•

Key facts and checkpoints •

• •

•

•

The commonest cause of tiredness is psychological distress, including anxiety states, depression and somatisation disorder. An Australian study showed that fatigue presents at a rate of 1.4 per 100 encounters.2 The study by Hickie et al3 showed that 25% of a sample of attendees visiting general practices had chronic fatigue. Of these, 70% had psychological distress. The others were more likely to have a current depressive disorder. In Jerrett’s study4 no organic cause was found in 62.3% of patients presenting with lethargy; the constant factors were sleep disturbance and the presence of stress in their lives. Many of them turned out to be suffering from psychological problems or psychiatric illnesses, including depression, anxiety state or bereavement. An important cause of daytime tiredness is a sleep disorder such as obstructive sleep apnoea, which results in periodic hypoventilation during sleep. It occurs in 2% of the general population in all age groups and in about 10% of middle-aged men.4 A history of snoring is a pointer to the problem. See CHAPTER 71.

Underlying disorders that need to be considered as possible causes of chronic fatigue are endocrine and metabolic disorders, malignancy, chronic infection, autoimmune disorders, primary psychiatric disorders, neuromuscular disorders, anaemia, drugs and cardiovascular disorders. Prolonged or chronic tiredness is characterised clinically by disabling tiredness, typically lasting more than 2 weeks, associated with nonrestorative sleep, headaches and a range of other musculoskeletal and neuropsychiatric symptoms.3 Sociodemographic correlates are concurrent psychological distress, female sex, lower socioeconomic status and fewer total years of education.3 Chronic fatigue syndrome (CFS) is defined as debilitating fatigue, persisting or relapsing over 6 months, associated with a significant reduction in activity levels of at least 50%, and for which no other cause can be found.

Causes of tiredness Analysing the symptom and reaching a diagnosis demands considerable skill, since tiredness may indicate the first subtle manifestation of a serious physical disease or, more commonly, may represent a patient’s inability to deal with the problems of everyday life. Chronic tiredness or fatigue is a feature of the ‘high pressure’ nature of many people’s lifestyles. Careful consideration must be given to the differentiation of physiological tiredness, as a result of excessive physical activity, from psychological tiredness. Furthermore, before diagnosing tiredness as psychological, pathological as well as physical causes must be excluded. A summary of causes of chronic tiredness is presented in TABLE 74.1.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 74.2.

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Table 74.1

• Problem solving in general practice

Causes of chronic tiredness/fatigue

Psychogenic/non-organic Psychiatric disorders: • anxiety states • depression/dysthymia • other primary disorders • bereavement • somatisation disorder

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Lifestyle factors: • workaholic tendencies and ‘burnout’ • lack of exercise/sedentary lifestyle • mental stress and emotional demands • exposure to irritants (e.g. carbon monoxide, ‘lead’ fumes) • inappropriate diet • obesity • sleep deprivation Organic Congestive cardiac failure Anaemia Malignancy HIV/AIDS Subacute to chronic infection (e.g. hepatitis, malaria, Lyme disease) Endocrine: various, especially thyroid (hyper and hypo), Addison disease and diabetes mellitus Nutritional deficiency Kidney failure Liver disorders: chronic liver failure, chronic active hepatitis Respiratory conditions (e.g. asthma, COPD) Neuromuscular (e.g. MS, myasthenia gravis, Parkinson disease) Metabolic (e.g. hypokalaemia, hypomagnesaemia Drug toxicity, addiction or side effects (see TABLE 74.3) Autoimmune disorders Sleep-related disorders Postinfectious fatigue syndrome (e.g. influenza, mononucleosis) Unknown Fibromyalgia Chronic fatigue syndrome Somatisation disorder Irritable bowel syndrome

Table 74.2

Tiredness/chronic fatigue: diagnostic strategy model

Q. Probability diagnosis A. Stress and anxiety Depression Inappropriate lifestyle and psychosocial factors

Viral/postviral infection Sleep-related disorders (e.g. sleep apnoea) Q. Serious disorders not to be missed A. Vascular: • cardiac arrhythmias • cardiomyopathy • incipient CCF Infection: • hidden abscess • HIV/AIDS • hepatitis B and C (others) Cancer Other: • anaemia • haemochromatosis Q. Pitfalls (often missed) A. ‘Masked’ depression Food intolerance Coeliac disease Chronic infection (e.g. Lyme disease) Incipient CCF Fibromyalgia Lack of fitness Drugs: alcohol, prescribed, withdrawal Menopause syndrome Pregnancy Neurological disorders: • post-head-injury • CVA • Parkinson disease Kidney failure Metabolic (e.g. hypokalaemia, hypomagnesaemia) Chemical exposure (e.g. occupational) Rarities: • hyperparathyroidism • Addison disease (see CHAPTER 23) • Cushing syndrome • narcolepsy • multiple sclerosis • autoimmune disorders Q. Seven masquerades checklist A. Depression Diabetes Drugs Anaemia Thyroid disease (other endocrine) Spinal dysfunction UTI Q. Is the patient trying to tell me something? A. Highly likely.

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Tiredness/fatigue

Probability diagnosis The most probable diagnoses to consider are: • • • • •

tension, stress and anxiety depression inappropriate lifestyle and psychosocial factors viral or postviral infection sleep-related disorders

Research studies have reported that over 50% (and in some cases as many as 80%) of reported cases of fatigue have been of psychological causation.3 Overwork is a common cause of fatigue and is often obvious to everyone but the patient. The modern approach to sleep-related disorders has revealed several important factors causing excessive tiredness.

Serious disorders not to be missed Many serious disorders such as anaemia, malignant disease and subacute or chronic infections (e.g. hepatitis, bacterial endocarditis and tuberculosis) can be ‘hidden’ or masked in the initial stages or not readily apparent. Neuromuscular diseases such as myasthenia gravis and multiple sclerosis, connective tissue disorders and HIV infection also have to be excluded.

Pitfalls The symptom of tiredness is fraught with pitfalls. Common ones include depression and other psychoneurotic disorders, and incipient congestive cardiac failure. Drug intake is a very common pitfall, whether it be by self-administration (including alcohol) or iatrogenic. Tiredness is a feature of pregnancy in many women, so this association is worth keeping in mind, especially in the early stages when a change in menstrual history is not given or a young single woman will attempt to conceal the fact. It is also a presenting symptom of the menopause syndrome, which should not be misdiagnosed. Two classic causes of tiredness are haemochromatosis and coeliac disease.

Seven masquerades checklist All these important problems are capable of being responsible for tiredness, especially depression, diabetes, drugs, anaemia and urinary infection. Thyroid disorder could certainly be responsible. Spinal pain can indirectly cause tiredness. Drugs that commonly cause tiredness are listed in TABLE 74.3. Antihypertensives require special consideration. Drug withdrawal, especially for illicit drugs such as amphetamines, marijuana, cocaine and heroin, has to be considered.

Table 74.3

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Drugs that can cause tiredness

Alcohol Analgesics Antibiotics Anticonvulsants Antidepressants Anti-emetics Antihistamines Antihypertensives e.g. β-blockers Anxiolytics Corticosteroids Digoxin Ergot alkaloids Hormones (e.g. oral contraceptives) Hypnotics Nicotine NSAIDs Vitamins A and D (early toxic symptoms) Note: Most drugs have a considerable capacity to cause tiredness.

Psychogenic considerations Tiredness is a symptom that may represent a ‘ticket of entry’: a plea for help in a stressed, anxious or depressed patient. Any of the primary psychiatric disorders can present as tiredness.

Red flag pointers for tiredness • • • • •

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Unexplained weight loss Sleep disturbance Symptoms of depression Drug and alcohol abuse Persistent fever

The clinical approach—key history In routine history taking, it is mandatory that questions be asked about the following if the information is not volunteered by the patient: • sleep pattern (it is not uncommon for patients to say they sleep well and yet on questioning it is found they have initial insomnia, or middle insomnia, or both, with or without early morning waking). It is most relevant to talk to any sleeping partners to obtain a history of sleep disturbance • weight fluctuations • energy—performance—ability to cope

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• sexual activity/sexual problems • suicidal ideas • self-medication—OTC preparations (e.g. bromides, stimulants, analgesics, alcohol, cigarettes, other drugs); this is particularly important in the drug addiction-prone group: doctors, chemists, nurses, workers in the liquor industry, truck drivers • fears (including phobic symptoms, hypochondriasis) • precipitating factors (present in over 50% of patients with depressive illness): — postpartum — postoperative — associated with chronic physical illness — bereavement — pain—chronic pain conditions — retirement — medication — post trauma (e.g. motor vehicle accident) — postviral infections, especially hepatitis, mononucleosis, influenza • work history—determine whether the patient is a workaholic; ask about bullying at work • dietary history—determine pattern, including fad diets or skipped meals • psychological history—stress, anxieties, phobias, depression • menstrual history and symptoms related to the menopause syndrome • final questions: ‘Is there anything else you feel you should tell me?’ ‘Do you have any explanation for your tiredness?’ • self-question: ‘Is this patient depressed?’

Physical examination—key features • General inspection noting facial features, skin appearance and colour, hyperpigmentation, conjunctivae • Vital signs • Anthropometric measurements • Basic respiratory and cardiovascular • Abdominal examination with focus on masses and inguinal lymphadenopathy • Urinalysis

Key investigations (screening) guidelines5 • • • •

FBE ESR/CRP Blood sugar Serum electrolytes, calcium, magnesium

• • • • • • • •

Kidney function tests Liver function tests Iron studies Gluten sensitivity screening blood tests Faecal occult blood Thyroid function tests CXR Urine—dipstick/MCU

Consider others according to clinical features e.g. chronic infection and HIV screening, autoimmune disorders, cancer markers and sleep disorder studies. The diagnosis of CFS can be made only when the minimum investigations have been shown to be normal or to demonstrate minor abnormalities in liver function or blood film (atypical lymphocytes).

Tiredness in children Tiredness in children is caused by a range of predictable conditions, such as physiological factors (excessive exercise, lack of sleep, poor diet), infections, allergies including asthma, drugs, depression and various illnesses in general. Overweight children are likely to fatigue more rapidly than children of normal weight.6 Any bacterial, viral or other infection may be associated with tiredness, with EBV being very significant in adolescents. Chronic EBV infection causing recurrent episodes of fever, pharyngitis, malaise and adenopathy can occur, especially in teenagers, who present with chronic exhaustion that is frequently mistaken for malignancy.6 Tiredness is a presenting feature of depression in adolescents, a serious problem that often goes unrecognised. Tonsillar–adenoidal hypertrophy may be large enough to compromise air exchange, particularly during sleep. Snoring may be a feature plus tiredness and lethargy in the waking state.

Tiredness in the elderly Elderly people tend to tire more quickly and recover more slowly and incompletely than younger ones. Sleep in older people is generally shorter in duration and of lesser depth, and they feel less refreshed and sometimes irritable on awakening. Fatigue may be present as a result of emotional frustration. Whenever the prospect of gratification is small, a person tends to tire quickly and to remain so until something stimulating appears. Since the prospects for gratifying experience wane with the years, easy ‘fatigueability’ or tiredness is common in this age group.

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Tiredness/fatigue

Bereavement Although a bereavement reaction is common and a normal human response that occurs at all ages, it is more frequently encountered in the elderly, with the loss of a spouse or a child (young or middle-aged!). Fatigue that occurs during the initial mourning period is striking and might represent a protective mechanism against intense emotional stress. With time, usually around 6 to 12 months, a compensated stage is reached, fatigue gradually abates, and the patient resumes normal activities as the conflicts of grief are gradually resolved. Freud pointed out the complexities of mourning as the bereaved person slowly adjusts to the loss of the loved one. In others, various symptoms persist as an ‘abnormal grief reaction’, including persistence of fatigue. Some factors that may lead to this include: • unexpected death • high dependence upon the dead person • guilt feelings, especially in a love/hate relationship Studies in general practice have shown that widows see their family doctors for psychiatric symptoms at three times the usual rate in the first 6 months after bereavement. The consultation rate for nonpsychiatric symptoms also increases, by almost 50%.

Role of the family doctor Following bereavement it is important to watch for evidence of depression, drug dependency, especially on alcohol, and suicidal tendencies. In cases of expected death, management should, if possible, start before the bereavement. Supportive care and ongoing counselling are very important.

Burnout Definition Burnout is a clinical syndrome with three components: • long-term emotional exhaustion • depersonalisation of others and • lack of personal accomplishment7 It is similar to stress-related depression but mood lowering is temporary and work-specific. Burnout is not a recognised disorder in the DSM-5 criteria, although the ICD-10 classifies it under ‘problems related to life management’ as a ‘state of vital exhaustion’.8 Patients sometimes claim that they feel ‘burnout’. Burnout can mean many things and include a

whole constellation of psychogenic symptoms, such as exhaustion, boredom and cynicism, paranoia, detachment, heightened irritability and impatience, depression and psychosomatic complaints, such as headache and tiredness. Ellard9 defines burnout as the syndrome that arises when a person who has a strong neurotic need to succeed in a particular task becomes confronted with the impossibility of success in that task. This seems a realistic explanation, but the important factor is to clarify the nature of the problem with care and determine whether the patient has a psychoneurotic disorder, such as hypomania, anxiety state or depression, or a personality disorder or simply unrealistic goals. Another viewpoint is that it is caused by chronic emotional stress resulting from prolonged intensive involvement with people.10 Burnout can be work related. Those who tend to be prone to it are musicians, authors, health professionals, teachers, athletes, engineers, emergency service workers, soldiers, reporters and high-technology professionals. Management involves appropriate counselling, which aims to help the patient to identify life stressors, set realistic personal goals and develop good support mechanisms.

Chronic fatigue syndrome This complex syndrome, which causes profound and persistent tiredness, is also referred to as myalgic encephalomyelitis, chronic neuromuscular viral syndrome,10 postviral syndrome, chronic EBV syndrome, viral fatigue state, epidemic neuromyasthenia, neurasthenia, Icelandic disease, Royal Free disease and Tapanui disease. CFS is not to be confused with the tiredness and depression that follow a viral infection such as infectious mononucleosis, hepatitis or influenza. These postviral tiredness states are certainly common but resolve within 6 months or so. Typical features of CFS (see FIG. 74.1):11 • • • • • • • • • • •

extreme exhaustion (with minimal physical effort) headache or a vague ‘fuzzy’ feeling in the head aching in the muscles and legs poor concentration and memory hypersomnia or other sleep disturbance waking feeling tired emotional lability/anxiety depressive-type illness, mood swings arthralgia (without joint swelling) sore throat subjective feeling of fever (with a normal temperature)

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cognitive dysfunction

arthralgia (without arthritis)

headache sleep disturbance mild pharyngitis tender cervical or axillary lymph nodes fatigue myalgia

Table 74.4

Criteria for the diagnosis of chronic fatigue syndrome12

Fatigue Clinically evaluated, unexplained, persistent or relapsing fatigue persistent for 6 months or more, that: • is of new or definite onset • is not the result of ongoing exertion • is not substantially alleviated by rest • results in substantial reduction in previous levels of occupational, educational, social or personal activities and

74 FIGURE 74.1 Chronic fatigue syndrome: characteristic symptoms

• shortness of breath • tender, swollen lymph nodes • usually occurs between 20 and 40 years of age Epidemiologically it has been related to Coxsackie B virus infections. The responsible organism is referred to as a slow virus infection by some authorities.8 In approximately two-thirds of patients the illness follows a clearly defined viral illness. However, no single virus has been consistently associated with the development of the syndrome, which is known to develop following a wide range of viral and non-viral infective illness. Immune system dysfunction with chronic overproduction of cytokines (e.g. interferon) is a possible pathogenetic mechanism. Every family doctor probably has patients with this disorder and the syndrome has been observed in isolated endemics from time to time. Hickie et al3 found that only 0.3% of those with prolonged fatigue had been diagnosed with CFS by their family doctor. There is no doubt that the syndrome is real in these patients. One of the major problems confronting clinicians is that there is no diagnostic test for this illness, so it remains a clinical diagnosis backed up by normal baseline investigations. Diagnostic criteria for CFS have been published12 (see TABLE 74.4), which emphasise the positive clinical features of the syndrome and the chronicity of symptoms (greater than 6 months), in addition to the need for careful exclusion of alternative diagnoses by history, physical examination and laboratory investigation.

Other symptoms Four or more of the following symptoms that are concurrent, persistent for 6 months or more and which did not predate the fatigue: • impaired short-term memory or concentration • sore throat • tender cervical or axillary lymph nodes • muscle pain • multi-joint pain without arthritis • headaches of a new type, pattern, or severity • unrefreshing sleep • post-exertional malaise lasting more than 24 hours

Examination and investigation Apart from mild pharyngeal infection, cervical lymphadenopathy or localised muscle tenderness, the physical examination is normal. Investigations should be directed towards excluding possible diagnoses for that patient, such as chronic infection, autoimmune disorders, endocrine and metabolic disorders, primary neuromuscular disorders, malignancy and primary psychiatric disorders. The last mentioned is the most difficult of the differential diagnoses and psychiatric referral will often need to be considered. Management Patients who have CFS are really suffering and unhappy people, similar to those with fibromyalgia (see CHAPTER 37). They require considerable understanding and support. Multidisciplinary intervention is recommended. Symptoms last approximately 2½ years. Management strategies include:11 • CFS recognition—explain that the illness is real but the cause unknown and tests are likely to be normal • explanation and reassurance that the illness is usually self-limiting with no permanent

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Tiredness/fatigue complications; and that a slow, steady improvement can be anticipated, with most CFS patients returning to normal health provide continued psychological support review for diagnostic reappraisal (examine at least every 4 months) avoid telling patients they are depressed treat symptomatically—pain relief, consider NSAIDs and antidepressants if significant depression refer to counselling and support groups provide a realistic, regular, graduated exercise program reduce relevant stress factors (map a realistic living program) psychiatric referral if appropriate ask the patient to keep a diary of exercise/stress and symptom severity, in particular avoid long-distance travel, which is poorly tolerated

• • • • • • • • • •

Cognitive behaviour therapy appears to help some patients, as do relaxation therapy, meditation, stress management and psychotherapy, where indicated. The emphasis should be placed on caring, rather than curing, until a scientific solution is found. A systematic review has found that cognitive behaviour therapy administered by skilled therapists and exercise are beneficial. There is insufficient data or evidence to support the use of antidepressants, corticosteroids, complementary therapies and dietary supplements, including vitamins B12 and C and co-enzyme Q10.5 Prolonged rest and immunotherapy was unlikely to be beneficial.13

Fibromyalgia The fibromyalgia syndrome (see CHAPTER 37) bears a clinical resemblance to CFS. Musculoskeletal pain

Practice tips • • • • • •

Always consider underlying psychological distress, especially a depressive disorder. Do not overlook a sleep disorder. Believe the patient’s symptoms. Ask the patient what he or she believes may be the cause of the tiredness. Be careful of labelling a patient as having CFS. Restrict investigations to those which are more likely to be relevant, therapeutic and reassuring.

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is more prominent although tiredness (fatigue) and sleep disturbance are features. According to Schwenk,14 fibromyalgia affects 5% of the American population with a peak age of 35 years (range 20–60) and a female:male ratio of 10:1. The management is similar to CFS but the prognosis less optimistic.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Chronic fatigue syndrome

References 1 Marinker M, Watter CAH. The patient complaining of tiredness. In: Cormack J, Marinker M, Morrell D (eds). Practice. London: Kluwer Medical, 1982: Section 3.1. 2 Britt H, Henderson J, Charles J et al. General practice activity in Australia 2011–12. General Practice Series no. 31. Sydney: Sydney University Press, 2012. 3 Hickie IB et al. Sociodemographic and psychiatric correlates of fatigue in selected primary care settings. Med J Aust, 1996; 164: 585–8. 4 Jerrett WA. Lethargy in general practice. Practitioner, 1981; 225: 731–7. 5 National Institute for Health and Care Excellence. Chronic fatigue syndrome/myalgic encephalitis. London: NICE, 2007. Available at . 6 Tennessen WW. Signs and Symptoms in Paediatrics. Philadelphia: Lippincott, 1988: 37–40. 7 Kirwan M, Armstrong D. Investigation of burnout in a sample of British general practitioners. Br J Gen Pract, 1995; 45: 259–60. 8 Sartorius N (Chair). International Classification of Mental and Behavioural Disorders. Problems related to life management. Burnout. Geneva, 2007; 273: 24v. 9 Ellard J. A note on burnout. Modern Medicine Australia, 1987; January: 32–5. 10 Freudenberger HJ. Burn-Out: The High Cost of High Achievement. New York: Anchor Press, 1980. 11 Loblay R, Stewart G (Convenors). Chronic fatigue syndrome: clinical practice guidelines 2002. RACGP/Med J Aust, 2002; 176: Supplement. 12 Fukuda K, Straus SE, Hickie I et al. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med, 1994; 121: 953–9. 13 Barton S. Chronic fatigue syndrome. In: Clinical Evidence. London: BMJ Publishing Group, 2001: 729–33. 14 Schwenk TL. Fibromyalgia and chronic fatigue syndrome: solving diagnostic and therapeutic dilemmas. Modern Medicine (US), 1992; 60: 50–60.

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The unconscious patient

In whatever disease sleep is laborious, it is a deadly symptom; but if sleep does good, it is not deadly. Hippocrates The state of arousal is determined by the function of the central reticular formation, which extends from the brain stem to the thalamus. Coma occurs when this centre is damaged by a metabolic abnormality or by an invasive lesion that compresses this centre. Coma is also caused by damage to the cerebral cortex.1 The word ‘coma’ is derived from the Greek koma, which is deep sleep. The deeply unconscious patient is not in deep sleep. Coma is best defined as ‘lack of self-awareness’.2 The various levels of consciousness are summarised in TABLE  75.1; the levels vary from consciousness, which means awareness of oneself and the surroundings in a state of wakefulness,3 to coma, which is a state of unrousable unresponsiveness. Rather than using these broad terms in clinical practice it is preferable to describe the actual state of the patient in a sentence.

Key facts and checkpoints •

Always consider hypoglycaemia or opioid overdose in any unconscious patient, especially of unknown background.

Table 75.1

•

•

•

•

If a patient is unconscious and cyanosed consider upper airway obstruction until proved otherwise. The commonest causes of unconsciousness encountered in general practice are reflex syncope, especially postural hypotension, concussion and cerebrovascular accidents (CVAs). The main causes are presented in TABLE 75.2. Do not allow the person who accompanies the unconscious patient to leave until all relevant details have been obtained. Record the degree of coma as a baseline to determine improvement or deterioration.

Urgent attention The initial contact with the unconscious patient is invariably sudden and dramatic and demands immediate action, which should take only seconds to minutes. The primary objective is to keep the patient alive until the cause is determined and possible remedial action taken.3

The five conscious levels State

Clinical features

Simplified classification

1 Consciousness 2 Clouded consciousness

Aware and wakeful Reduced awareness and wakefulness ‘Alcohol effect’ Confusion Drowsiness Unconscious Deep-sleep-like state Arousal with vigorous stimuli Unconscious (deeper) Responds only to painful stimuli (sternal rubbing with knuckles)without arousing Deeply unconscious Unrousable and unresponsive

Awake Confused

Degree of consciousness 3 Stupor

4 Semicomatose

5 Coma

Responds to shake and shout

Responds to pain

Unresponsive coma

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The unconscious patient

Table 75.2

Main causes of loss of consciousness

Episodic causes—blackouts Epilepsy Orthostatic intolerance and syncope Drop attacks Cardiac arrhythmias (e.g. Stokes–Adams attacks) Vertebrobasilar insufficiency Psychogenic disorders, including hyperventilation Breath-holding (children) Silent myocardial infarction Hypoxia Coma (COMA provides a useful mnemonic for four major groups1 of causes of unconsciousness) C = CO2 narcosis: respiratory failure O = Overdose of drugs: • alcohol • opioids • tranquillisers and antidepressants • carbon monoxide • analgesics • others M = Metabolic: • diabetes: — hypoglycaemia — ketoacidosis • hypothyroidism • hypopituitarism • hepatic failure • Addison disease • kidney failure (uraemia) • others A = Apoplexy: • intracerebral haemorrhage • haematoma: subdural or extradural • head injury • cerebral tumour • cerebral abscess Infratentorial (posterior fossa): • pressure from above • cerebellar tumour • brain-stem infarct/haemorrhage • Wernicke encephalopathy Meningismus (neck stiffness): • subarachnoid haemorrhage • meningitis Other: • encephalitis • overwhelming infection Trauma

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History A history can be obtained from relatives, friends, witnesses, ambulance officers or others. The setting in which the patient is found is important. Evidence of discs or cards identifying an illness such as diabetes or epilepsy should be searched for. Is there a known history of hypertension, heart disease, respiratory disease or psychiatric illness?

Questions to be considered4 • Is the patient diabetic? Does the patient have insulin injections? Has the patient had an infection? Has the patient been eating properly? • Is drug overdose possible? Has the patient been depressed? Has the patient experienced recent stress or personal ‘mishaps’? Has the patient been on any medications? • Is opioid usage possible in this patient? Are the presenting circumstances unusual? • Is epilepsy possible? Was twitching in the limbs observed? Did the patient pass urine or faeces? • Is head injury possible? Has the patient been in a recent accident? Has the patient complained of headache? • Has a stroke or subarachnoid haemorrhage occurred? Has the patient a history of hypertension? Did the patient complain of a severe headache? Has the patient complained of weakness of the limbs?

Examination General features requiring assessment: • breathing pattern: — Cheyne–Stokes respiration (periodic respiration) = cerebral dysfunction — ataxic respiration: shallow irregular respiration = brain-stem lesion — Kussmaul respiration: deep rapid hyperventilation = metabolic acidosis • breath: characteristic odours may be a feature of alcohol, diabetes, uraemia and hepatic coma • level of consciousness: degree of coma (see TABLE 75.1); the Glasgow coma scale (see

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TABLE 75.3) is frequently used as a guide to the

•

• • • •

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conscious state skin features: look for evidence of injection sites (drug addicts, diabetics) and snake bite marks, colour (cyanosis, purpura, jaundice, rashes, hyperpigmentation) and texture circulation pulse oximetry temperature: consider infection such as meningitis and hyperpyrexia if raised and hypothermia (e.g. hypothyroidism) if low hydration: dehydration may signify conditions such as a high fever with infections, uraemia, hyperglycaemic coma

Examination

Action

Is the patient breathing?

If not, clear airway and ventilate.

Note chest wall movement. Check pulse and pupils.

Perform cardiopulmonary resuscitation if necessary. Consider naloxone.

Is there evidence of trauma?

Consider extradural haematoma.

Is the patient hypoglycaemic?

Consider glucometer estimation of blood sugar.

Evidence of diabetes (discs, etc.) Are vital functions present yet immediate correctable causes eliminated?

Table 75.3

Glasgow coma scale Score

Eye opening (E) Spontaneous opening To verbal command To pain No response Verbal response (V) Orientated and converses Disoriented and converses Inappropriate words Incomprehensible sounds No response Motor response (M) Obeys verbal command Response to painful stimuli Localises pain Withdraws from pain stimuli Abnormal flexion Extensor response No response Coma score = E + V + M Minimum 3 Maximum 15 If 8–10: take care—monitor the airway

4 3 2 1 5 4 3 2 1 6 5 4 3 2 1

Place in coma position.

Examination of the head and neck3,4 The following should be considered: • facial asymmetry • the skull and neck: palpate for evidence of trauma and neck rigidity • eyes, pupils and ocular fundi: look for constricted pupils in opioid overdose • tongue • nostrils and ears • auscultation of the skull

Examination of the limbs Consider: • injection marks (drug addicts, diabetics) • tone of the limbs by lifting and dropping (e.g. flaccid limbs with early hemiplegia) • reaction of limbs to painful stimuli • reflexes—tendon reflexes and plantar response

General examination of the body This should include assessment of the pulses and blood pressure.

Urine examination Catheterisation of the bladder may be necessary to obtain urine. Check the urine for protein, sugar and ketones.

Diagnosing the hysterical ‘unconscious’ patient One of the most puzzling problems in emergency medicine is how to diagnose the unconscious patient caused by a conversion reaction (hysteria). These patients really experience their symptoms (as opposed to the pretending patient) and resist most normal stimuli, including painful stimuli. Method • Hold the patient’s eye or eyes open with your fingers and note the reaction to light.

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The unconscious patient • Now hold a mirror over the eye and watch closely for pupillary reaction. The pupil should constrict with accommodation from the patient looking at his or her own image.

The clinical features of various types of blackouts are summarised in TABLE 75.4.

Investigations

Epilepsy is the commonest cause of blackouts. There are various types, the most dramatic being the tonic– clonic seizure in which patients have sudden loss of consciousness without warning. See CHAPTERS 54 and 84. The typical features (in order) of a tonic–clonic convulsion are:

Appropriate investigations depend on the clinical assessment. The following is a checklist. • Blood tests: — All patients:

• •

• • •

• •

blood sugar urea and electrolytes

— Selected patients: FBE blood gases liver function tests blood alcohol serum cortisol thyroid function tests serum digoxin Pulse oximetry Urine tests: — a urine specimen is obtained by catheterisation — test for glucose and albumin — keep the specimen for drug screening Stomach contents: aspiration of stomach contents for analysis Radiology: CT or MRI scan are the investigations of choice (if available). If unavailable, X-ray of the skull may be helpful. Cerebrospinal fluid: lumbar puncture, necessary with neck stiffness, has risks in the comatose patient. A preliminary CT scan is necessary to search for coning of the cerebellum. If clear, the lumbar puncture should be safe and will help to diagnose subarachnoid haemorrhage and meningitis. Electroencephalograph ECG; look for ↑ QT interval, etc.

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• • • •

aura (sensory or psychological feelings) initial rigid tonic phase (up to 60 seconds) convulsion (clonic phase) (seconds to minutes) mild coma or drowsiness (15 minutes to several hours)—postictal confusion Associated features:

• • • •

cyanosis, then heavy ‘snoring’ breathing eyes rolling ‘back into head’ ± tongue biting ± incontinence of urine or faeces

It should be noted that sphincter incontinence is not firmly diagnostic of epilepsy. In less severe episodes the patient may fall without observable twitching of the limbs.5 In atonic epilepsy, which occurs in those with tonic–clonic epilepsy, the patient falls to the ground and is unconscious for only a brief period.

Orthostatic intolerance and syncope In syncope there is a transient loss of consciousness but with warning symptoms and rapid return of alertness following a brief period of unconsciousness (seconds to 3 minutes). The three main syndromes that are outlined in CHAPTER 54 are reflex syncope, postural orthostatic tachycardia syndrome and autonomic failure.

Reflex syncope

Blackouts—episodic loss of consciousness

Relevant features of reflex syncope or vasovagal or common faint (see TABLE 75.4):

Episodic or transient loss of consciousness is a common problem. The important causes of blackout are presented in TABLE 75.4. The history is important to determine whether the patient is describing a true blackout or episodes of dizziness, weakness or some other sensation.

• occurs with standing or, less commonly, sitting • warning feelings of dizziness, faintness or true vertigo • nausea, hot and cold skin sensations • fading hearing or blurred vision • sliding to ground (rather than heavy full-length fall)

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Clinical features of blackouts

Cause

Precipitants

Subjective onset

Observation

Recovery

Reflex syncope

Posture Stress Haemorrhage Micturition

Warning of feeling ‘faint’, ‘distant’, ‘clammy, sweaty’

Very pale Sweating

Gradual Feels ‘terrible’ Fatigue Nausea

Cardiac syncope including POTS syndrome

Various

May be palpitations

Pale

Rapid May be flushing

Autonomic syncope

Postural change orthostasis, food alcohol

Warning (feels faint)

Pale

Rapid

Respiratory syncope

Cough Weight-lifting ‘Trumpet playing’

Warning (feels faint)

Pale

Rapid

Carotid sinus syncope

Carotid pressure (e.g. tight collar + turning neck) Postendarterectomy

Warning (feels faint)

Pale

Rapid

Migrainous syncope

Foods Stress Sleep deprivation

Scotomas

Pale

Nausea and vomiting Throbbing headache

Epilepsy

Stress Sleep deprivation Alcohol withdrawal Infection Menstruation Drug non-compliance

Aura with complex partial seizures (CPS)

Automatism (e.g. fidgeting, lip smacking) with CPS

Slow Confused

• rapid return of consciousness • pallor and sweating and bradycardia • often trigger factors (e.g. emotional upset, pain) The patient invariably remembers the onset of fainting. Most syncope is of the benign vasomotor type and tends to occur in young people, especially when standing still (e.g. choir boys). It is the main cause of repeated fainting attacks. The treatment is to avoid precipitating causes (e.g. prolonged standing, especially in the sun) and bend forwards with the head down or lie down with premonitory signs. ‘Smelling salts’ (ammonium carbonate) can be carried and used in these circumstances.

Other forms of syncope Micturition syncope This uncommon event may occur after micturition in older men, especially during the night when they leave a warm bed and stand to void. The cause appears to be peripheral vasodilatation associated with reduction of venous return from straining. Cough syncope Severe coughing can result in obstruction of venous return with subsequent blackout. This is also the mechanism of blackouts with breath-holding attacks.

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The unconscious patient Carotid sinus syncope This problem is caused by pressure on a hypersensitive carotid sinus (e.g. in some elderly patients who lose consciousness when their neck is touched).

Patients with aortic stenosis are prone to have exercise-induced blackouts. Consider the prolonged QT interval syndrome in all age groups when the person presents with dizziness or blackouts.

Effort syncope Syncope on exertion is due to obstructive cardiac disorders, such as aortic stenosis and hypertrophic obstructive cardiomyopathy.

Vertebrobasilar insufficiency

Choking Sudden collapse can follow choking. Examples include the so-called ‘cafe coronary’ or ‘barbecue coronary’ when the patient, while eating meat, suddenly becomes cyanosed, is speechless and grasps the throat. This is caused by inhaling a large bolus of meat that obstructs the larynx. To avoid death, immediate relief of obstruction is necessary. An emergency treatment is the Heimlich manoeuvre, whereby the patient is grasped from behind around the abdomen and a forceful squeeze applied to try to eject the food. If this fails, the foreign body may have to be manually removed from the throat.

Drop attacks Drop attacks are episodes of ‘blackouts’ in which the patient suddenly falls to the ground and then immediately gets up again. They involve sudden attacks of weakness in the legs. Although there is some doubt about whether loss of consciousness has occurred, most patients cannot remember the process of falling. Drop attacks occur typically in middleaged women and are considered to be brain-stem disturbances producing sudden changes in tone in the lower limbs. Other causes of drop attacks include vertebrobasilar insufficiency, Parkinson disease and epilepsy.5

Cardiac arrhythmias Stokes–Adams attacks (see CHAPTER 70) and cardiac syncope are manifestations of recurrent episodes of loss of consciousness, especially in the elderly, caused by cardiac arrhythmias. These arrhythmias include complete heart block, sick sinus syndrome and ventricular tachycardia. The blackout is sudden with the patient falling straight to the ground without warning and without convulsive movements. The patient goes pale at first and then flushed. Twenty-four-hour ambulatory cardiac monitoring may be necessary to confirm the diagnosis.

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Loss of consciousness can occur rarely with vertebrobasilar insufficiency (VBI) transient ischaemic attack. Typical preceding symptoms of VBI include dyspnoea, vertigo, vomiting, hemisensory loss, ataxia and transient global amnesia.

Hypoglycaemia Hypoglycaemia can be difficult to recognise but must be considered as it can vary from a feeling of malaise and lightheadedness to loss of consciousness, sometimes with a convulsion. There are usually preliminary symptoms of hunger, sweating, shaking or altered behaviour. Hypoglycaemic attacks are usually related to diabetes and can occur with oral hypoglycaemics as well as insulin. Causes of hypoglycaemia are presented in TABLE  75.5. Refer to CHAPTER 130. Table 75.5

Causes of hypoglycaemia (adults)

Diabetes-related including insulin and oral hypoglycaemics Drugs (e.g quinine, salicylates, pentamidine) Alcohol Fasting Tumours (e.g. insulinomas) Addison disease Hypopituitarism Liver disease Post-gastrectomy Gastric ‘dumping’ syndrome Autoimmune: antibodies to insulin or insulin receptors

Head injuries and unconsciousness Some non-life-threatening head injuries are sufficiently serious to cause significant loss of consciousness and retrograde amnesia. The clinical terms used to describe brain injury of concussion, contusion and laceration simply indicate minor to major degrees of a similar injury. Severe individual cases of the above can certainly result in fatal outcomes.

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Concussion6

extradural subdural

Concussion is a transient disturbance of neurological function induced by head injury and resulting in no persistent abnormal neurological signs. There may or may not be brief loss of consciousness. The old definition of loss of consciousness with eventual recovery applies only to more severe forms of concussion. The features of the various grades of concussion are shown in TABLE 75.6. Note: There is no such thing as delayed concussion or progressive deterioration due to concussion. Table 75.6

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bruise

dura skull bone

Classification of concussion

Grade

Clinical features

Mild (grade 1)

Stunned or dazed Sensorium clears in 60 seconds Headache Amnesia 60 seconds Irritable Persistent headache Unsteady gait ± Loss of consciousness

Moderate (grade 2)

Severe (grade 3)

Post-concussion syndrome Occasionally a person who has an episode of concussion has persistence of headaches and dizziness for a number of weeks. Poor memory and concentration and sluggish decision-making indicate impaired mental capacity. Patients with this problem should be investigated with neuropsychological testing and CT scanning or MRI of the brain.

FIGURE 75.1 Illustration of sites of subdural and extradural haematomas in relation to the dura, skull and brain

Injury

Lucid interval

Alert Lucid Confused

Diagnosis of haematoma

Unconscious

FIGURE 75.2 Classic conscious states leading to extradural haematoma after injury

Extradural haematoma This life-threatening head injury is caused by arterial bleeding between the skull bone and dura mater (see FIG. 75.1). Following injury there may be a short lucid interval followed by loss of consciousness. The patient is restless, confused, irritable (see FIG. 75.2), has severe headaches and develops neurological signs such as seizures, ipsilateral pupil dilatation and facial weakness. A skull X-ray and CT scan should demonstrate the haematoma. Lumbar puncture is contraindicated. Urgent decompression of the haematoma is required.

Subdural haematoma This is due to a venous bleed between the dura and the arachnoid. It follows injury, which may be seemingly trivial, especially in the elderly, and may be acute, subacute and chronic. Consider it in a person with personality change, slowness and unsteadiness of movement, headache, irritability and fluctuating conscious level. A CT scan or MRI should reveal the haematoma and/or a midline shift. Neurological referral is urgent.

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The unconscious patient

Psychogenic factors Psychogenic factors leading to blackouts represent a diagnostic dilemma, especially if occurring in patients with tonic–clonic epilepsy. If the attacks are witnessed by the practitioner then the possibility of functional origin can be determined. Hysterical blackouts or fits are not uncommon and have to be differentiated from hyperventilation. It is unusual for hyperventilation to cause unconsciousness but it is possible to get clouding of consciousness, especially if the patient is administered oxygen. Other features that suggest psychogenic rather than organic factors are: • • • •

labile affect rapidly changing levels of consciousness well-articulated speech bizarre thought control

The patient found unconscious7 Most likely causes to consider • • • • • • •

drug overdose, including alcohol head injury postictal state (epilepsy or CVA) hypoglycaemia or ketoacidosis subarachnoid haemorrhage respiratory failure hypotension, including cardiac arrhythmias or myocardial infarction • infection e.g. meningitis • psychogenic

Basic investigations • • • • • • •

oxygen saturation blood glucose urine or blood drug profile brain CT scan lumbar puncture (CT scan permitting) routine blood chemistry ECG

Initial management of the unconscious patient The first principle of management of a person found unconscious is to keep the patient alive by maintaining the airway and the circulation. The basic management essentials are summarised in TABLE 75.7.

Table 75.7

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Basic management essentials

Keep patient alive (maintain airway and circulation) Get history from witnesses Examine patient Give ‘coma cocktail’ (TONG) Take blood (for investigations) CT scan (if diagnosis doubtful)

Before embarking on a secondary survey always consider giving the ‘coma cocktail’ (also called TONG2), which refers to the combination of: T O N G

= = = =

Thiamine Oxygenation Naloxone Glucose

100 mg IM or IV 0.1–0.2 mg IV i.e. 50 mL, 50% dextrose

The rapid administration of these agents should be considered for any patient3,8 with an altered level of consciousness because they may lessen or reverse metabolic insult to the brain. Some emergency physicians recommend adding flumazenil to the cocktail. In the presence of hypoventilation, constricted pupils9 or circumstantial evidence of opioid use, naloxone (the specific opiate antagonist) should be given intravenously. If there is no response the patient should be intubated before further naloxone is given. Use a nasogastric tube to prevent acute gastric dilatation. Catheterise to relieve urinary distension, send a urine sample for micro and culture, pregnancy test and drug screen.

Use of flumazenil Flumazenil is a specific benzodiazepine antagonist and may have an important use in the assessment of the unconscious patient. It can have a dramatic effect on benzodiazepine overdosage. After an initial dose of 0.2 mg IV, 0.3–0.5 mg boluses should be given every 1–2 minutes with caution until a response is observed.9

Opioid (heroin) overdose A known overdose patient should be treated initially with both IV and IM naloxone: • naloxone 0.4 mg IV (repeat in 3 minutes if necessary) • naloxone 0.4 mg IM (to maintain cover)

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Practice tips2 • • • • •

•

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The hypotensive patient is bleeding until proved otherwise. The presence of a head injury should not prevent rigorous resuscitation of the hypotensive patient. Always suspect cervical injury in the presence of patients who are victims of time-critical trauma. Tachypnoea is a sign of inadequate oxygenation and not a sign of central nerve damage. Always suspect opioid overdosage in the ‘unknown’ patient brought in with an altered conscious state. Consider administration of TONG—the ‘coma cocktail’.

References 1 Talley N, O’Connor S. Clinical Examination (3rd edn). Sydney: MacLennan & Petty, 1996: 414. 2 Wassertheil J. Management of neurological emergencies. Melbourne: Monash University, Update for GPs: Course notes, 1996: 1–10. 3 Kumar PJ, Clark ML. Clinical Medicine (5th edn). London: Bailliere Tindall, 2003: 1161–2. 4 Davis A, Bolin T, Ham J. Symptom Analysis and Physical Diagnosis (2nd edn). Sydney: Pergamon Press, 1990: 276–9. 5 Kincaid-Smith P, Larkins R, Whelan G. Problems in Clinical Medicine. Sydney: MacLennan & Petty, 1990: 340–7. 6 Brukner P, Khan K. Clinical Sports Medicine (4th edn). Sydney: McGraw-Hill, 2012: 272–87. 7 Brown FT. Emergency Medicine: Diagnosis and Management. Oxford: Butterworth Heinemann, 2004: 43–6. 8 McGirr J, McDonagh T. Management of acute poisoning. Current Therapeutics, 1995; 36 (5): 51–9. 9 Webster V. Trauma. Melbourne: RACGP Check Program 293, 1996: 3–14.

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Urinary disorders

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As men draw near the common goal, Can anything be sadder Than he who, master of his soul, Is servant to his bladder? Anonymous Speculum,  Disturbances of micturition are a common problem in general practice, with an annual incidence of about 20 per 1000 patients at risk.1 Such disturbances include dysuria, frequency of micturition, difficulty or inability to initiate micturition, stress incontinence and haematuria. These symptoms are three times as common in women as in men.1 The combination of dysuria and frequency is the most common of the symptoms with an incidence of about 14 per 1000 patients and a female:male ratio of 5:1.1 Among children and the elderly, the patient may complain of urinary incontinence unassociated with stress. However, with the exception of enuresis (CHAPTER  91), disturbances of micturition are uncommon in children.

Dysuria and frequency Dysuria, or difficult and/or painful micturition, which is characterised mainly by urethral and suprapubic discomfort, indicates mucosal inflammation of the lower genitourinary tract (i.e. the urethra, bladder or prostate). The passage of urine across inflamed mucosa causes pain. Frequency can vary from being negligible to extreme. It can be ‘habit frequency’ or associated with anxiety, which is typically long term and worse with stress and cold weather. In these conditions urinalysis is normal. Sometimes haematuria and systemic symptoms can accompany dysuria and frequency. A summary of the diagnostic strategy model for dysuria is presented in TABLE 76.1.

Key facts and checkpoints1,2 • •

Strangury = difficult and painful micturition with associated spasm. Inflammation usually results in the frequent passage of small amounts of urine and a sense of urgency.

• • • •

• • • •

• •

Urethritis usually causes pain at the onset of micturition. Cystitis usually causes pain at the end of micturition. Suprapubic discomfort is a feature of bladder infection (cystitis). Vesicocolonic fistulas (e.g. prostatic cancer) cause severe dysuria, pneumaturia and foul-smelling urine. Dysuria and frequency are most common in women aged 15 to 44 years. They are four times more common in sexually active women. Vaginitis is an important cause and must be considered. Dysuria and discomfort is a common feature of postmenopausal syndrome, due to atrophic urethritis. The urethra and lower bladder are oestrogen-dependent. Unexplained dysuria could be a pointer to Chlamydia urethritis. Urinary infection and other disorders can be quite asymptomatic.

Is it really a urinary tract infection? Although UTIs account for the majority of cases of dysuria in women it must be remembered that vaginitis and postmenopausal atrophic vaginitis can cause dysuria (see FIG. 76.1). Vaginitis is the most common cause of dysuria in the adolescent age group and is a relatively common cause of dysuria in family practice, estimated at around 15%. Postmenopausal oestrogen deficiency is estimated at 5–10%.3 In the latter it is worthwhile prescribing oestrogen, either topically or systemically. Acute bacterial cystitis accounts for about 40% of causes of dysuria. The dysuria associated with vaginitis may be described as burning ‘on the outside’ with the discomfort usually felt at the beginning or end of micturition. If

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Q. Probability diagnosis A. UTI esp. cystitis (female) Urethritis Urethral syndrome (female) Vaginitis Q. Serious disorders not to be missed A. Neoplasia: • bladder • prostate • urethra Severe infections: • gonorrhoea • NSU • genital herpes Reactive arthritis Calculi (e.g. bladder)

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Other causes: sexual abuse trauma/foreign bodies poor perineal hygiene allergic reactions chemical irritants: – deodorant sanitary pads – contraceptive foams, etc. – vaginal lubricants – vaginal cosmetics – bubble baths, soaps, etc.

Dysuria: diagnostic strategy model

Q. Pitfalls (often missed) A. Menopause syndrome Adenovirus urethritis Prostatitis Foreign bodies in lower urinary tract (LUT) Acidic urine Acute fever Interstitial cystitis Urethral caruncle/diverticuli Vaginal prolapse Obstruction: • benign prostatic hyperplasia • urethral stricture • phimosis • meatal stenosis Q. Seven masquerades checklist A. Depression Diabetes Drugs UTI Q. Is the patient trying to tell me something? A. Consider psychosexual problems, anxiety and hypochondriasis.

vaginitis is suspected, a pelvic examination should be carried out to inspect the genitalia and obtain swabs.3

Urethral syndrome Also known as chronic sterile inflammatory disorder and abacterial cystitis, it presents with lower urinary tract symptoms (LUTS) or symptoms of urethritis. Others refer to it as ‘painful bladder syndrome’ or interstitial cystitis. It affects 20–30% of adults, mainly female. Management, which is difficult, is supportive.

urethral syndrome (including urethritis)

acute cystitis

vaginitis

postmenopausal atrophic vaginitis

FIGURE 76.1 Relative causes of dysuria in women

The clinical approach History It is important to determine whether dysuria is really genitourinary in origin and not attributable to functional disorders, such as psychosexual problems. Disturbances of micturition are uncommon in the young male and if present suggest venereal infection. Key questions • Could you describe the discomfort? • What colour is your urine? • Does it have a particular odour? • Have you noticed a discharge? • If so, could it be sexually acquired? • Do you find intercourse painful or uncomfortable (women)? • Have you any fever, sweats or chills? Examination The general inspection and examination should include measurement of the basic parameters of pulse, temperature and blood pressure. The possibility of underlying kidney disease, especially in the presence of an obstructive component, should be kept in mind. Abdominal palpation is important with a focus on the loins and suprapubic areas. The possibility of sexually transmitted diseases should also be considered and vaginal examination of the female and rectal and genital examination in the male may be appropriate. In the menopausal female, a dry atrophic urethral opening, a urethral caruncle or

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Urinary disorders urethral prolapse may give the clue to this important and neglected cause of dysuria. Investigations Basic investigations include: • dipstick testing of urine • microscopy and culture (midstream specimen of urine, or suprapubic puncture in children), and possibly urethral swabs or first pass urine for sexually transmitted infections Further investigations depend on initial findings and referral for detailed investigation will be necessary if the primary cause cannot be found.

• • •

•

•

Haematuria Haematuria is the presence of blood in the urine and can vary from frank bleeding (macroscopic) to the microscopic detection of red cells. Haematuria can occur in a wide variety of disorders but a careful history and examination can often lead to the source of the bleeding and help with the selection of investigations. It is often a sign of a serious underlying disorder.

Key facts and checkpoints •

• •

•

•

•

Macroscopic haematuria is the presence of blood visible to the naked eye. It is always abnormal except in menstruating women. Small amounts of blood (1 mL/1000 mL urine) can produce macroscopic haematuria. Microscopic haematuria is the presence of blood in the urine that can only be detected by microscopic or chemical methods. Microscopic haematuria includes the presence of red blood cells (RBC) >8000 per mL of urine (phase contrast microscopy) or >2000 per mL of urine (light microscopy) representing the occasional RBC on microscopic examination. Joggers and athletes engaged in very vigorous exercise can develop transient microscopic haematuria. Microscopic (asymptomatic haematuria) can be classified as either: — glomerular (from kidney parenchyma): common causes are IgA nephropathy and thin membrane disease4 or — non-glomerular (urological): the common causes are bladder cancer, benign prostate hyperplasia and urinary calculi

•

Common sources of macroscopic haematuria are the bladder, urethra, prostate and kidney.5 Macroscopic haematuria occurs in 70% of people with bladder cancer and 40% with kidney cancer.5 Common urological cancers that cause haematuria are the bladder (70%), kidney (17%), kidney pelvis or ureter (7%) and prostate (5%).6 It is important to exclude kidney damage, so patients should have blood pressure, urinary protein and plasma creatinine levels measured as a baseline. All patients presenting with macroscopic haematuria or recurrent microscopic haematuria require judicious investigation, which may involve both radiological investigation of the upper urinary system and visualisation of the lower urinary system to detect or exclude pathology. The key radiological investigation is the intravenous urogram (pyelogram), unless there is a history of iodine allergy, severe asthma or other contraindications, when ultrasound is the next choice.

The clinical approach History Is it really haematuria? In many patients the underlying disorder may be suspected from a detailed enquiry about associated urinary symptoms. The presence of blood can be verified rapidly by microscopy so that red discolouration due to haemolysis or red food dye can be discounted. The time relationship of bleeding is useful because, as a general rule, haematuria occurring in the first part of the stream suggests a urethral or prostatic lesion, while terminal haematuria suggests bleeding from the bladder. Uniform haematuria has no localising features. The possibility of sexually acquired urethritis should be kept in mind. It is most unusual for haematuria to cause anaemia unless it is massive. Massive haematuria is a feature of radiation cystitis. Painful haematuria is suggestive of infection, urethral caruncle, calculi or kidney infarction, while painless haematuria is commonly associated with infection, trauma, tumours or polycystic kidneys. Loin pain can occur as a manifestation of nephritis and may be a feature of bleeding in cancer of the kidney or polycystic kidney. A drug history is relevant, especially with anticoagulants and cyclophosphamide. A diet history should also be considered.

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It is worth noting that large prostatic veins, secondary to prostatic enlargement located at the bladder neck, may rupture when a man strains to urinate. A summary of the diagnostic strategy model for haematuria is presented in TABLE 76.2.

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Key questions • Have you had an injury such as a blow to the loin, pelvis or genital area? • Have you noticed whether the redness is at the start or end of your stream or throughout the stream? • Have you noticed any bleeding elsewhere, such as bruising of the skin or nose bleed? • Have you experienced any pain in the loin or abdomen? • Have you noticed any burning or frequency of your urine? • Have you had any problems with the flow of your urine? • Have you been having large amounts of beetroot, red lollies or berries in your diet? • Could your problem have been sexually acquired? • Have you been overseas recently? • What is your general health like? • Have you been aware of any other symptoms? • Do you engage in strenuous sports such as jogging? • Have you had any kidney problems in the past? Examination The general examination should include looking for signs of a bleeding tendency and anaemia, and recording the parameters of temperature, blood pressure and the pulse (see FIG. 76.2). The heart should be assessed to exclude atrial fibrillation or infective endocarditis with emboli to the kidney, and the chest should be examined for a possible pleural effusion associated with perinephric or kidney infections. The abdomen should be examined for evidence of a palpable enlarged kidney or spleen. The different clinical findings for an enlarged left kidney and spleen are shown in TABLE 76.3. Kidney enlargement may be due to kidney tumour, hydronephrosis, or polycystic disease. Splenomegaly suggests the possibility of a bleeding disorder. The suprapubic region should be examined for evidence of bladder tenderness or enlargement. In men the prostate should be examined rectally to detect benign or malignant enlargement or tenderness from prostatitis.

Table 76.2

Haematuria: diagnostic strategy model

Q. Probability diagnosis A. Infection: • cystitis/urethrotrigonitis (female) • urethritis (male) • prostatitis (male) Calculi—kidney, ureteric, bladder Q. Serious disorders not to be missed A. Cardiovascular: • kidney infarction • kidney vein thrombosis • prostatic varices Neoplasia: • kidney tumour • urothelial: bladder, kidney, pelvis, ureter • prostate cancer Severe infections: • infective endocarditis • kidney tuberculosis • acute glomerulonephritis • Blackwater fever IgA nephropathy Kidney papillary necrosis Other kidney disease e.g. polycystic kidneys Q. Pitfalls (often missed) A. Urethral prolapse/caruncle Pseudohaematuria (e.g. beetroot, porphyria) Haemorrhagic cystitis Benign prostatic hyperplasia Trauma: blunt or penetrating Foreign bodies Bleeding disorders Exercise Radiation cystitis Menstrual contamination Rarities: • hydronephrosis • Henoch–Schönlein purpura • bilharzia • polycystic kidneys • kidney cysts • endometriosis (bladder) • systemic vasculitides Q. Seven masquerades checklist A. Drugs (cytotoxics, anticoagulants) UTI Q. Is the patient trying to tell me something? A. Consider artefactual haematuria.

In women a vaginal examination should be performed to search for possible pelvic masses. The urethral meatus should be inspected to exclude a

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General fever anaemia purpura Cardiovascular heart murmurs evidence SBE atrial fibrillation pleural effusion (kidney infections) hypertension

Urinary tract kidney mass

splenomegaly

bladder: palpable tenderness urethra: caruncle blood

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prostate: inflammation mass

FIGURE 76.2 Features to consider in the physical examination of the patient with haematuria

Table 76.3

Differences between spleen and left kidney on abdominal examination Spleen

Left kidney

Palpable upper border

Impalpable

Palpable

Movement with inspiration

Inferomedial

Inferior

Notch

Yes

No

Ballotable

No

Yes

Percussion

Dull

Resonant (usually)

Friction rub

Possible

Not possible

urethral caruncle (‘raspberry tumour’) or urethral prolapse.

Investigations It is important to identify the cause, especially if a possible sequel is impaired kidney function. • Urinalysis by dipstick testing (e.g. Hemastixaffected derivatives—affected by vitamin C intake).

• Urine microscopy: — formed RBCs in true haematuria — red cell casts indicate glomerular bleeding — deformed (dysmorphic) red cells indicate glomerular bleeding • Urinary culture: early culture is important because of the common association with infection and consideration of early treatment with antibiotics. If tuberculosis is suspected, three early morning urines should be cultured for tubercle bacilli. • Urinary cytology: this test, performed on a urine sample, may be useful to detect malignancies of the bladder and lower tract but is usually negative with kidney cancer. • Blood tests: appropriate screening tests include a full blood count, ESR and basic kidney function tests (urea and creatinine). If glomerulonephritis is suspected, antistreptolysin O titres and serum complement levels should be measured. • Radiological techniques—available tests include: — intravenous urography (IVU); intravenous pyelogram (IVP)—the key investigation — ultrasound (less sensitive at detecting LUT abnormalities) — CT scanning

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— kidney angiography — retrograde pyelography • Direct imaging techniques: these include urethroscopy, cystoscopy and ureteroscopy. In all patients, regardless of the IVU findings, cystoscopy is advisable. • Kidney biopsy: indicated if glomerular disease is suspected, especially in the presence of dysmorphic red cells on microscopic examination.

Treatment includes warm salt baths and oestrogen creams. Otherwise obliteration by laser vaporisation, cryotherapy or cautery or even surgical excision is used.

Pseudohaematuria

Clinical features • Haematuria/microhaematuria • Irritative symptoms: frequency, urgency, nocturia • Dysuria

Pseudohaematuria is red urine caused by pigments other than red blood cells that simply stain the culture red. Causes include:

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• • • • • •

anthocyanins in food (e.g. beetroot, berries) red-coloured confectionery porphyrins free haemoglobin (e.g. haemoglobinuria) myoglobin (red-black colour) drugs (e.g. pyridium, phenolphthalein—alkaline urine)

Exercise haematuria Exercise or sports haematuria is the passage of a significant number of red cells in the urine during or immediately after heavy exercise. It has been recorded in a wide variety of athletes, including swimmers and rowers. Dipstick testing is usually positive in these athletes. Despite the theory that it is largely caused by the posterior wall of the bladder impacting repetitively on the base of the bladder during running, there are other possible factors and glomerular disease must be excluded in the athlete with regular haematuria, especially if dysmorphic red cells are found on microscopy.

Artefactual haematuria Macroscopic haematuria is a common presenting ploy of people with Munchausen syndrome and pethidine addicts simulating kidney colic. If suspected, it is wise to get these people to pass urine in the presence of an appropriate witness before examining the urine.

Bladder cancer7 Bladder cancer is the seventh most common malignancy, with 90% being transitional cell carcinomas. Other forms include squamous cell carcinoma and adenocarcinoma. Smoking is the most common association.

Diagnosis • Urine cytology: three specimens • Cystoscopy and biopsy • Imaging of upper tracts: IVU, ultrasound, but CT IVU is the gold standard • Differential diagnosis is haemorrhagic cystitis Management • Cease smoking (if applicable) • Lifestyle attention • Drink ample purified (no chlorine) water Treatment depends on the staging and grading. • The common carcinoma in situ is treated with intravesical BCG immunotherapy. This 6-week course and follow-up if necessary leads to 60–75% remission • Other intravesical agents used include various cytotoxics (e.g. mitomycin C) • Other treatments include surgery such as tumour resection plus intravesical agents, bladder resection (partial or total) and radio– chemotherapy. Regular patient surveillance, which may be lifelong, is essential.

Glomerulonephritis8

Urethral caruncle

Glomerulonephritis means kidney inflammation involving the glomeruli. It can be simply classified into:

This is a benign granulomatous tumour about the size of a pea in the distal urethra. Almost exclusive to post-menopausal women, it is very tender and bleeds easily. The main symptom is haematuria. It may require cystoscopy and biopsy for diagnosis.

• nephritic syndrome: oedema + hypertension + haematuria • nephrotic syndrome: oedema + hypoalbuminaemia + proteinuria • asymptomatic kidney disease

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Urinary disorders The main causes of glomerulonephritis–nephritic syndrome are: • IgA nephropathy (commonest) • thin glomerular basement membrane disease (has an AD genetic link) • post-streptococcal glomerulonephritis • systemic vasculitis • others

IgA nephropathy Typically presents as haematuria in a young male adult at the time of or within 1–2 days of a mucosal infection (usually throat, influenza or URTI) and persists for several days. Other presentations are as incidentally found microscopic haematuria or as previously unsuspected chronic kidney failure. Due to deposition of IgA antibody complexes in the glomeruli, it runs a variable course. There is no specific treatment to date but immune suppression may be used. Refer suspected cases immediately. Diagnosis is by biopsy.

Acute post-streptococcal glomerulonephritis Typically seen in children (>5 years), especially in Indigenous communities following GABHS throat infection or impetigo. Presents after a gap of 7–10 days or so. Clinical features • Irritable, lethargic, sick child • Haematuria: discoloured urine (‘Coke’ urine) • Peri-orbital oedema (may be legs, scrotum) • Rapid weight gain (from oedema) • Scanty urine output (oliguria) • Hypertension → may be complications Usual course • Oliguria 2 days • Oedema and hypertension 2–4 days • Invariably resolves • Good long-term prognosis Diagnosis • GABHS antigens • Blood urea, creatinine, C3&4 (complement), ASOT, DNase B Treatment • Hospital admission • Bed rest

• • • • • •

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Strict fluid balance chart Daily weighing Penicillin (if GABHS +ve) Fluid restriction Low protein, high carbohydrate, low salt diet Antihypertensives and diuretics (as necessary)

Follow-up: monitor BP and kidney function. Regular urinalysis (microscopic haematuria may last for years). DxT discoloured urine + peri-orbital oedema + oliguria post-streptococcal glomerulonephritis

Proteinuria Proteinuria is an important and common sign of kidney disease. The protein can originate from the glomeruli, the tubules or the LUT. Healthy people, however, do excrete some protein in the urine, which can vary from day to day and hour to hour; hence the value of collecting it over 24 hours. While proteinuria can be benign, it always requires further investigation. Important causes of proteinuria are presented in TABLE 76.4.

Key facts and checkpoints9 • • • • • •

•

The amount of protein in the urine is normally less than 100 mg/24 hours. Greater than 150 mg protein/24 hours is abnormal in adults. Greater than 300 mg/24 hours is abnormal for children and adults. Proteinuria >1 g/24 hours indicates a serious underlying disorder. If accompanied by dysmorphic haematuria or red cell casts, this tends to confirm glomerular origin. Routine dipstick testing will only detect levels greater than 300 mg/24 hours and thus has limitations. In diabetics, microalbuminuria is predictive of nephropathy and an indication for early blood pressure treatment.

Predictive levels • • •

Proteinuria Microalbuminuria Macroalbuminuria

>150–300 mg/day 30–300 mg/day >300 mg/day

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Table 76.4

• Problem solving in general practice

Important causes of proteinuria

Transient Contamination from vaginal secretions Urinary tract infection Pre-eclampsia These all require exclusion and follow-up.

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Kidney disease Glomerulonephritis Nephrotic syndrome Congenital tubular disease, e.g. • polycystic kidney • kidney dysplasia Acute tubular damage Kidney papillary necrosis, e.g. • analgesic nephropathy • diabetic papillary necrosis Overflow proteinuria, e.g. • multiple myeloma Systemic diseases affecting the glomeruli: • diabetes mellitus • hypertension • SLE • malignancy • drugs (e.g. penicillamine, gold salts) • amyloid • vasculitides No kidney disease Orthostatic proteinuria Exercise Emotional stress Fever Cold exposure Postoperative Acute medical illness (e.g. heart failure)

If proteinuria is confirmed on repeated dipstick testing it should be measured more accurately by measuring daily albumin excretion with a 24-hour urine or the albumin creatinine ratio (ACR), which is preferred. High values require referral for investigation. The minimum investigations are microurine and assessment of kidney function (eGFR). Nephrotic range proteinuria (>3 g/24 hours) is due to one or other form of glomerulonephritis in over 90% of patients.8 Possible contamination from vaginal secretions or from a low UTI needs to be excluded.

Orthostatic proteinuria Orthostatic proteinuria is the presence of significant proteinuria after the patient has been standing but is absent from specimens obtained following

recumbency for several hours, such as an early morning specimen. It occurs in 5–10% of people,6 especially during their adolescent years. In the majority it is of no significance and eventually disappears without the development of significant kidney disease. However, in a small number the proteinuria can foreshadow serious kidney disease.

Diabetic microalbuminuria The presence of protein in the urine is a sensitive marker of diabetic nephropathy, so regular screening for microalbuminuria in diabetics is regarded as an important predictor of nephropathy and other possible complications of diabetes. Dipstick testing for microalbuminuria is now available but more accurate measurement can be performed with radioimmunoassay techniques. The use of ACE inhibitors at the microalbuminuria stage may slow the development of overt nephropathy. The gold standard is a 24-hour collection.

Consequences of proteinuria While proteinuria is usually simply a marker of kidney disease, heavy proteinuria in excess of 3 g/24 hours may have severe clinical consequences, including oedema, intravascular volume depletion, venous thromboembolism, hyperlipidaemia and malnutrition. Minimal change glomerulonephritis is the commonest cause of the nephrotic syndrome in childhood and accounts for about 30% of adult nephrotic syndrome.7 It is steroid responsive.

Nephrotic syndrome8,9 DxT proteinuria + generalised oedema + hypoalbuminaemia  nephrotic syndrome

Clinical features • Proteinuria >3 g/day (3–41 on dipstick) • Swelling of eyelids and face • Generalised oedema, especially peripheral oedema • Hypoalbuminaemia 4.5 mmol/L • Waxy pallor • Normal BP • Dyspnoea • Frothy urine

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Urinary disorders Predisposes to sepsis (e.g. pyelonephritis, thromboembolism).

peritonitis,

Causes • 1 in 3 (approx.): — systemic kidney disease (e.g. diabetes, SLE, amyloid) • 2 in 3 (approx.): — idiopathic nephrotic syndrome (based on kidney biopsy) — minimal change disease (commonest) — focal glomerular sclerosis — membranous nephropathy — membranoproliferative glomerulonephritis • Others: drugs, malignancy, infection e.g. malaria Treatment • Referral to renal physician or unit • Bed rest • Diet: low fluid, high protein, low salt • Diuretics • Prednisolone • Phenoxymethylpenicillin • Aspirin

URINARY INCONTINENCE

Definitions Functional incontinence Loss of urine secondary to factors extrinsic to the urinary tract. Nocturnal enuresis (or bed-wetting) Involuntary urine loss during sleep. Overactive bladder (detrusor instability) The commonest cause of urge incontinence; synonymous with an irritable or unstable bladder; characterised by involuntary bladder contractions, resulting in a sudden urge to urinate. Overflow incontinence Escape of urine following poor bladder emptying. Stress incontinence The involuntary loss of urine on coughing, sneezing, straining or lifting, or any factor that suddenly increases intra-abdominal pressure. Urge incontinence An urgent desire to void followed by involuntary loss of urine. Urinary incontinence The involuntary loss of urine during the day or night. Voiding dysfunction Includes urinary difficulties, detrusor instability and overflow incontinence.

A summary of the types of incontinence and their causes is presented in TABLE 76.5.

Table 76.5

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Types of incontinence and their implied causes

Type of incontinence

Likely cause

Simple stress incontinence (with cough/sneeze)

Sphincter incompetence

Urge incontinence Giggle incontinence Stress and urge incontinence Enuresis Complex stress incontinence (with exercise)

Unstable bladder, with or without sphincter weakness

Quiet dribble incontinence

Sphincter incompetence and unstable bladder or overflow

Continuous leakage

Fistula, ectopic ureter, patulous urethra

Reflex incontinence

Neuropathic bladder

The basic requirements for continence are: • adequate central and peripheral nervous function • an intact urinary tract • a compliant stable bladder • a competent urethral sphincter • efficient bladder emptying

Female urinary incontinence Urinary leakage affects at least 37% of women in Australia.11 Successful treatment depends on accurate assessment of the LUT storage and emptying functions. The most common contributing factor is weakness of the pelvic floor muscles. Assessment The basic assessment of the incontinent patient requires a careful history and examination, exclusion of infection and keeping of a micturition or bladder chart. Use of a severity index questionnaire is very helpful. Drugs that adversely affect urinary function are presented in TABLE 76.6. Investigations may be required to dispel doubt about the diagnosis or to exclude intravesical or kidney disorders: these include cystometry, uroflowmetry, cystourethroscopy, micturating cystourethrogram, IVU and also residual volume (>100 mL is abnormal).

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Table 76.6 • • • •

• Problem solving in general practice

Drugs that can cause or aggravate incontinence

ACE inhibitors phenoxybenzamine (Dibenyline) prazosin labetalol

Bladder relaxants → overflow incontinence: • anticholinergic agents • tricyclic antidepressants Bladder stimulants → urge incontinence: • cholinergic agents • caffeine Sedatives → urge incontinence: • antidepressants • antihistamines • antipsychotics • hypnotics • tranquillisers

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Others → urge incontinence: • alcohol • loop diuretics (e.g. frusemide), other diuretics • lithium

Causes of incontinence (a mnemonic)10,11 D I A P P E E R S S

= = = = = = = = = =

Delirium Infection of urinary tract Atrophic urethritis Pharmacological (e.g. diuretics) Psychological (e.g. acute distress) Endocrine (e.g. hypercalcaemia) Environmental (e.g. unfamiliar surrounds) Restricted mobility Stool impaction Sphincter damage or weakness

The severity index questionnaire •

•

How often do you experience urine leakage? 0 = never 1 = less than once a month 2 = one or several times a month 3 = one or several times a week 4 = every day and/or night How much urine do you lose each time? 1 = drops or little 2 = more

The total score is the score for the first question multiplied by the score for the second question. 0 = dry, 1–2 = slight, 3–4 = moderate, 6–8 = severe

Management 1 Exclude UTI and drug causes. 2 Is it stress incontinence? • key symptoms: involuntary loss with coughing, jumping, etc. • demonstrable (e.g. patient coughs when standing with full bladder—check for leakage) Treatment • Weak pelvic floor—exercises • Obesity—weight reduction • Menopause—HRT/vaginal oestrogen creams • Chronic cough—physiotherapy If urodynamic studies of LUT function show genuine stress incontinence (GSI) due to urethral sphincter weakness, consider surgery (e.g. suprapubic urethral suspension—better than vaginal repair) 3 Is it urge incontinence? • urge symptoms prominent • no residual urine • urodynamic studies to confirm GSI Treatment • neurological signs →  neurologist • abnormal voiding pattern →  bladder retraining (e.g. void more urine less frequently) • surgery (e.g. Burch procedure) 4 Is it voiding dysfunction? • symptoms of voiding difficulty (e.g. frequency, urgency, nocturia, incomplete emptying) • large residual urine Treatment • Neurological signs →  neurologist • Gynaecological cause (e.g. pelvic mass) →  gynaecologist • If bladder atony →  anticholinergic drugs • Intravesical treatment: — oxybutynin — botulinum toxin — others, e.g. capsaicin • May require catheterisation

Anticholinergic/antispasmodic drugs12 These may be worth a trial for bladder instability or voiding dysfunction: • solifenacin 5–10 mg (o) daily • propantheline 15 mg (o) bd or tds • oxybutynin 2.5–5 mg (o) bd or tds • tolterodine 2 mg (o) bd • imipramine 10–75 mg (o) nocte The future: • neuromodulation (e.g. sacral nerve)

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Pelvic floor muscle training13 • The mainstay of treatment of most problems, especially GSI (e.g. 40 ‘squeezes’ daily). • 75% improved and 25% cured. • Best in motivated young women with bladder GSI. • At least 3 months trial with supervision (physiotherapist or continence nurse adviser).

enterocele

Basic techniques: • Advise the patient to pull up her pelvic muscles to imagine herself stopping passing urine (or controlling diarrhoea) and hold the ‘squeeze’ for a count of 10. Repeat many times daily. Refer to Patient Education. • Bladder retraining includes getting the patient to delay micturition for 10–15 minutes whenever she wishes to void.

Bladder dysfunction (in women during night) Women with urethral syndrome constantly wake at night with urge to micturate but produce only a small dribble of urine. • Instruct patient to perform a pelvic tilt exercise by balancing on upper back, lifting her pelvis with knees flexed and holding position for 30 seconds • Squeeze pelvic floor inwards (as though holding back urine or faeces) • Repeat a few times

Uterovaginal prolapse14 Uterovaginal prolapse is very common, affecting 50% of parous women. The main complaint is of ‘heaviness’ in the vagina and a sensation of ‘something coming down’. Relevant symptoms that are of considerable distress for the patient and, depending on the type of prolapse, include voiding difficulties, urinary stress incontinence, faecal incontinence, incomplete rectal emptying and recurrent cystitis. Backache is a common associated symptom, usually relieved by lying down. Classification of prolapse See FIGURE 76.3. • • • •

Cystocele—bladder descends into vagina Urethrocele—urethra bulges into vagina Rectocele—rectum protrudes into vagina Enterocele—loop of small intestine bulges into vagina (usually posterior wall)

cystocele

rectocele

FIGURE 76.3 Uterovaginal prolapse

• Uterine—uterus and cervix descend toward vaginal introitus: — first degree—cervix remains in vagina — second degree—cervix protrudes on coughing/straining — third degree (procidentia)—uterus lies outside vagina Examination This is best performed with women in the left lateral position using a Sims speculum or posterior blade of the Graves speculum. Ask the patient to cough or bear down (several times)—observe anterior, posterior and lateral vaginal walls and descent of cervix. Management As a rule asymptomatic prolapse does not need invasive treatment, just basic reassurance and education, including pelvic floor exercises (see earlier in this chapter). Consider referral to a physiotherapist. Lifestyle measures include optimal nutrition, weight loss if obese, smoking cessation and exercise. Aggravating comorbidities such as constipation, menopause/atrophic vaginitis and COPD require optimal treatment. Consider topical oestrogens. Prevention Promote optimal obstetric management, especially postpartum exercises, lifelong pelvic floor exercises, ideal weight and sensible bladder and bowel function. Ring pessaries Pessaries are an option for those who are poor anaesthetic risks, too frail for surgery, don’t want surgery, are young and have not completed their family or are awaiting surgery. Each patient needs

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to be fitted individually with the correct-sized pessary. Topical oestrogens will improve comfort. The pessary needs to be cleaned or changed every 4–6 months. Surgery Refer to a gynaecological surgeon if the patient who is fit for surgery has symptomatic prolapse that warrants surgery especially with associated incontinence and recurrent UTIs. The principles of reconstructive pelvic surgery are to: • reposition pelvic structures to normal anatomical relationships • restore and maintain urinary and/or faecal continence • maintain coital function • correct coexisting pelvic pathology

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Options include repair procedures (vaginally, sometimes abdominally, per laparoscopy), colpo/ vaginal suspension, hysteroscopy and hysterectomy (vaginal or abdominal).

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Incontinence of urine

References 1 Cormack J, Marinker M, Morrell D. Practice. A Handbook of Primary Medical Care. London: Kluwer-Harrap Handbooks, 1980: 3.51: 1–10. 2 Kincaid-Smith P, Larkins R, Whelan G. Problems in Clinical Medicine. Sydney: MacLennan & Petty, 1990: 105–8. 3 Sloane PD, Slatt PD, Baker RM. Essentials of Family Medicine. Baltimore: Williams & Wilkins, 1988: 169–74. 4 Mathew T. Microscopic haematuria: how to treat. Australian Doctor, 27 April 2007: 27–34. 5 Walsh D. Symptom Control. Boston: Blackwell Scientific Publications, 1989: 229–33. 6 George C. Haematuria and proteinuria: how to treat. Australian Doctor, 15 March 1991: I–VIII. 7 Gray S, Frydenberg M. Bladder cancer: how to treat. Australian Doctor, 21 November 2008: 29–36. 8 Faull R. Glomerulonephritis: how to treat. Australian Doctor, 8 February 2002: I–VIII. 9 Thomson N. Managing the patient with proteinuria. Current Therapeutics, 1996; 9: 7–28. 10 Jayasuriya P. Urinary incontinence: how to treat. Australian Doctor, 11 May 2001: I–VIII. 11 Whishaw DMK. Urinary incontinence in the frail female: how to treat. Australian Doctor, 25 July 2008: 29–36. 12 Haylen B. Advances in incontinence treatment. Australian Doctor, 10 September 1999: 66–70. 13 Mazza D. Women’s Health in General Practice (2nd edition). Sydney: Elsevier Australia, 2011: 288–94. 14 Haylen B. Pelvic organ prolapse. Australian Doctor, 21 February 2014: 23–30.

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All those, therefore, who have cataract see the light more or less, and by this we distinguish cataract from amaurosis and glaucoma, for persons affected with these complaints do not perceive the light at all. Paul of Aegina (–) The commonest cause of visual dysfunction is a simple refractive error. However, there are many causes of visual failure, including the emergency of sudden blindness, a problem that requires a sound management strategy. Apart from migraine, virtually all cases of sudden loss of vision require urgent treatment. The ‘white’ eye or uninflamed eye presents a different clinical problem from the red or inflamed eye.1 The ‘white’ eye is painless and usually presents with visual symptoms and it is in the ‘white’ eye that the majority of blinding conditions occur.

•

•

• •

The presence of floaters or ‘blobs’ in the visual fields indicates pigment in the vitreous: causes include vitreous haemorrhage and vitreous detachment. Posterior vitreous detachment is the commonest cause of the acute onset of floaters, especially with advancing age. Retinal detachment has a tendency to occur in short-sighted (myopic) people. Suspect a macular abnormality where objects look smaller or straight lines are bent or distorted.

Criteria for blindness and driving This varies from country to country. The WHO defines blindness as ‘best visual acuity less than 3/60’, while in Australia eligibility for the blind pension is ‘bilateral corrected visual acuity less than 6/60 or significant visual field loss’ (e.g. a patient can have 6/6 vision but severely restricted fields caused by chronic open-angle glaucoma). The minimum standard for driving is 6/12 (Snellen system).

Key facts and checkpoints •

•

•

•

The commonest cause of blindness in the world is trachoma. The other major causes of gradual blindness are cataracts, onchocerciasis and vitamin A deficiency.2 In Western countries the commonest causes are senile cataract, glaucoma, age-related macular degeneration, trauma and the retinopathy of diabetes mellitus.2 The commonest causes of sudden visual loss are transient occlusion of the retinal artery (amaurosis fugax) and migraine.3 ‘Flashing lights’ are caused by traction on the retina and may have a serious connotation: the commonest cause is vitreoretinal traction, which is a classic cause of retinal detachment.

The clinical approach History The history should carefully define the onset, progress, duration, offset and the extent of visual loss. An accurate history is important because a longstanding visual defect may only just have been noticed by the patient, especially if it is unilateral. Two questions need to be answered: • Is the loss unilateral or bilateral? • Is the onset acute, or gradual and progressive? The distinction between central and peripheral visual loss is useful. Central visual loss presents as impairment of visual acuity and implies defective retinal image formation (through refractive error or opacity in the ocular media) or macular or optic nerve dysfunction. Peripheral field loss is more subtle, especially when the onset is gradual, and implies extramacular retinal disease or a defect in the visual pathway. It is important to differentiate the central field loss of macular degeneration from the hemianopia of a CVA. A drug history is very important (see TABLE 77.1). Treatment for tuberculosis with ethambutol or

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Table 77.1

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Visual disorders associated with drugs

Disorder

Drug

Corneal opacities

Amiodarone Hydroxychloroquine Chlorpromazine Vitamin D Indomethacin Chlorpropamide

Precipitating of acute narrow angle glaucoma

Mydriatic drops Tricyclics Antihistamines

Refractive changes

Thiazides

Lens opacities

Corticosteroids Phenothiazines

Retinopathy

Hydroxychloroquine Chloroquine Thioridazine (other phenothiazines less commonly) Tamoxifen

Papilloedema (secondary to benign intracranial hypertension)

Oral contraceptives Corticosteroids Tetracyclines Nalidixic acid Vitamin A

Optic neuropathy

Ethanol Tobacco Ethambutol Disulfiram

Source: Reprinted from Central Nervous System: Clinical Algorithms, published by the BMJ, with permission

treatment with quinine/chloroquine has to be considered as these drugs are oculotoxic. The family history is relevant for diabetes, migraine, Leber hereditary optic atrophy, Tay–Sachs disease and retinitis pigmentosa. Questions directed to specific symptoms • Presence of floaters → normal ageing (especially ≥55 years) with posterior vitreous detachment or may indicate haemorrhages or choroiditis • Flashing lights → normal ageing with posterior vitreous detachment or indicates traction on the retina (? retinal detachment) • Coloured haloes around lights → glaucoma, cataract • Zigzag lines → migraine • Vision worse at night or in dim light → retinitis pigmentosa, hysteria, syphilitic retinitis • Headache → temporal arteritis, migraine, benign intracranial hypertension

• Central scotomata → macular disease, optic neuritis • Pain on moving eye → retrobulbar neuritis • Distortion, micropsia (smaller), macropsia (larger) → macular degeneration • Visual field loss: — central loss—macular disorder — total loss—arterial occlusion — peripheral loss It is worth noting that if a patient repeatedly knocks into people and objects on a particular side (including traffic accidents), a bitemporal or homonymous hemianopia should be suspected. Diseases/disorders to exclude or consider • Diabetes mellitus • Giant cell (temporal) arteritis • Hypopituitarism (pituitary adenoma) • Cerebrovascular ischaemia/carotid artery stenosis (emboli) • Multiple sclerosis • Cardiac disease (e.g. arrhythmias, and SBE— emboli) • Anaemia (if severe can cause retinal haemorrhage and exudate) • Marfan syndrome (subluxated lenses) • Malignancy (the commonest cause of eye malignancy is melanoma of the choroid)

Examination The same principles of examination should apply as for the red eye. Testing should include: • visual acuity (Snellen chart)—with pinhole testing • pupil reactions, to test afferent (sensory) responses to light • confrontation fields (using a red pin) • colour vision • Amsler grid (or graph paper) • fundus examination with dilated pupil (ophthalmoscope), noting: — the red reflex — appearance of the retina, macula and optic nerve • tonometry General examination General examination should focus on the general features of the patient, the nervous system, endocrine system and cardiovascular system.

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Causes of sudden blindness vitreous haemorrhage retinal detachment Typical defects in visual fields L

disciform macular degeneration papilloedema

R 1

unilateral blindness

central retinal artery occlusion 1

central retinal vein occlusion

optic nerve

optic neuritis

optic chiasma 2

2 3

bitemporal hemianopia

optic tract

3 R homonymous hemianopia

4

geniculate body optic radiation

4 quadrantic field defect

5

5 R homonymous hemianopia

77 occipital cortex

FIGURE 77.1 Diagrammatic representation of important causes of sudden painless loss of vision (right side) and typical defects in the visual fields (left side)

Perimetry Various defects in the visual fields are depicted in FIGURE 77.1.

Investigations Depending on the clinical examination the following tests can be selected to confirm the diagnosis: • blood tests: — full blood (? anaemia, lead poisoning, leukaemia) — ESR (? temporal arteritis) — blood sugar (? diabetes mellitus) • temporal artery biopsy (? temporal arteritis) • CT/MRI scan (? CVA, optic nerve lesions, spaceoccupying lesions) • formal perimetry and Bjerrum screen • fluorescein angiography (? retinal vascular obstruction, diabetic retinopathy) • visual evoked responses (? demyelinating disorders) • carotid Doppler ultrasound

Visual failure in children There are long lists of causes for visual failure or blindness in children. An approximate order of frequency of causes of blindness in children is cortical blindness, optic atrophy, choroidoretinal degeneration, cataract and retinopathy of prematurity. Almost half the causes of blindness are genetically determined, in contrast to the nutritional and infective causes that predominate in third world countries.4 About 3% of children will fail to develop proper vision in at least one eye. The eyes of all babies should be examined at birth and at 6 weeks.

Amblyopia Amblyopia is defined as a reduction in visual acuity due to abnormal visual experience in early childhood. It is the main reason for poor unilateral eyesight until middle age and is usually caused by interference with visual development during the early months and years of life.

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The common causes are: • strabismus • large refractive defect, especially hypermetropia • congenital cataract Principles of management5 • Most cases are treatable. • Early diagnosis and intervention is fundamental to achieving useful vision. • No child is too young to have the visual system assessed. • The good eye should be patched in order to utilise the affected eye. • Remove a remedial cause such as strabismus. • Correct any refractive error, usually by prescription of glasses.

Some important guidelines in children

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Referral Refer if any of the following are present in infants: • nystagmus • a wandering eye • a lack of fixation or following of movements • photophobia • opacities (seen with ophthalmoscope set on +3, held 30 cm from baby’s eye) • delayed development Strabismus • The two serious squints are the constant and alternating ones, which require early referral. Transient squint and latent squint (occurs under stress e.g. fatigue) usually are not a problem. • Always refer children with strabismus (squint) when first seen to exclude ocular pathology such as retinoblastoma, congenital cataract and glaucoma, which would require emergency surgery. • Children with strabismus (even if the ocular examination is normal) need specialist management because the deviating eye will become amblyopic (a lazy eye with reduced vision i.e. ‘blind’ if not functioning by 7 years of age). The younger the child, the easier it is to treat amblyopia; it may be irreversible if first detected later than school age. Surgical correction of a true squint is preferred at 1–2 years of age. (See also CHAPTER 92.) Cataracts Children with suspected cataracts must be referred immediately; the problem is very serious as the

development of vision may be permanently impaired (amblyopia).2 Cataracts are diagnosed by looking at the red reflex and this should be a routine part of the examination of a young child. Common conditions causing cataracts are genetic disorders and rubella but most causes are unknown. Rarer conditions, such as galactosaemia, need to be considered. Refractive errors Refractive errors, with the error greater in one eye, can cause amblyopia. Detection of refractive errors is an important objective of screening. Retinoblastoma Retinoblastoma, although rare, is the commonest intraocular tumour in childhood. It must be excluded in any child presenting with a white pupil. Such children also have the so-called ‘cat’s eye reflex’. In 30% of patients the condition is bilateral with an autosomal dominant gene being responsible.

Visual failure in the elderly Most patients with visual complaints are elderly and their failing vision affects their perception of the environment and their ability to communicate effectively. Typical problems are cataracts, vascular disease, macular degeneration, chronic simple glaucoma and retinal detachment. Retinal detachment and diabetic retinopathy can occur at any age, although they are more likely with increasing age. Macular degeneration in its various forms is the commonest cause of visual deterioration in the elderly. For the elderly with cataracts the decision to operate depends on the patients’ vision and their ability to cope. Most patients with a vision of 6/18 or worse in both eyes usually benefit from cataract extraction, but some can cope with this level of vision and rely on a good, well-placed (above and behind) reading light.6 Sudden loss of vision in the elderly is suggestive of temporal arteritis or vascular embolism, so this problem should be checked.

Floaters and flashes When the vitreous gel shrinks as part of the normal ageing process, it tugs on the retina (rods and cones), causing flashing lights. When the gel separates from the retina, floaters (which may appear as dots, spots or cobwebs) are seen. Floaters are more commonly seen with age, but are also more common in people

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Visual failure who are myopic or who have had eye surgery such as removal of cataracts. It is important to consider retinal detachment but if floaters remain constant there is little cause for concern. The appearance of a fresh onset of flashes or floaters is of concern.

Refractive errors Indistinct or blurred vision is most commonly caused by errors of refraction. In the normal eye (emmetropia) light rays from infinity are brought to a focus on the retina by the cornea (contributing about two-thirds of the eye’s refractive power) and the lens (one-third). Thus, the cornea is very important in refraction and abnormalities such as keratoconus may cause severe refractive problems.6 The process of accommodation is required for focusing closer objects. This process, which relies on the action of ciliary muscles and lens elasticity, is usually affected by ageing, so that from the age of 45 close work becomes gradually more difficult (presbyopia).6 The important clinical feature is that the use of a simple ‘pinhole’ in a card will usually improve blurred vision or reduced acuity where there is a refractive error only.1

Myopia (short-sightedness) This is usually progressive in the teens. Highly myopic eyes may develop retinal detachment or macular degeneration. Management • Glasses with a concave lens • Contact lenses • Consider radial keratotomy or excimer laser surgery

Hypermetropia (long-sightedness) This condition is more susceptible to closed angle glaucoma. In early childhood it may be associated with convergent strabismus (squint). The spectacle correction alone may straighten the eyes. It is mostly overcome by the accommodative power of the eye, though it may cause reading difficulty. Typically, the long-sighted person needs reading glasses at about 30 years.

Presbyopia There is a need for near correction with loss of accommodative power of the eye in the 40s.

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Astigmatism This creates the need for a corrective lens that is more curved in one meridian than another because the cornea does not have even curvature. If uncorrected, this may cause headaches of ocular origin. Conical cornea is one cause of astigmatism.

Pinhole test The pinhole reduces the size of the blur circle on the retina in the uncorrected eye. A pinhole acts as a universal correcting lens. If visual acuity is not normalised by looking through a card with a 1 mm pinhole, then the defective vision is not solely due to a refractive error. The pinhole test may actually help to improve visual acuity with some cataracts. Further investigation is mandatory.

Cataract The term ‘cataract’ describes any lens opacity. The symptoms depend on the degree and the site of opacity. Cataract causes gradual visual loss with normal direct pupillary light reflex. The prevalence of cataracts increases with age: 65% at age 50 to 59, and all people aged over 80 have opacities.3 Significant causes of cataracts are presented in TABLE 77.2 and causes of progressive visual loss in TABLE 77.3. Typical symptoms: • • • • • •

reading difficulty difficulty in recognising faces problems with driving, especially at night difficulty with television viewing reduced ability to see in bright light may see haloes around lights

Table 77.2

Causes of cataracts

Advancing age Diabetes mellitus Steroids (topical or oral) Radiation: long exposure to UV light TORCH organisms → congenital cataracts Trauma Uveitis Dystrophia myotonica Galactosaemia

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• Problem solving in general practice

Progressive bilateral visual loss

Globe

Chronic glaucoma Senile cataracts

Retina

Macular degeneration Retinal disease: • diabetic retinopathy • retinitis pigmentosa • choroidoretinitis

Optic nerve

Optic neuropathies

The red reflex and ophthalmoscopy The ‘red reflex’ is a reflection of the fundus when the eye is viewed from a distance of about 60 cm (2 feet) with the ophthalmoscope using a zero lens. This reflex is easier to see if the pupil is dilated. Commencing with the plus 15 or 20 lens, reduce the power gradually and, at plus 12, lens opacities will be seen against the red reflex, which may be totally obscured by a very dense cataract. The setting up of the ophthalmoscope to examine intraocular structures is illustrated in FIGURE 77.3.

Optic nerve compression (e.g. aneurysm, glioma) Toxic damage to optic nerves Optic chiasma

Chiasmal compression: pituitary adenoma, craniopharyngioma, etc.

Occipital cortex

Tumours

red reflex

zero lens

Degenerative conditions Note: Unilateral causes (e.g. cataract, refractive errors, uveitis, glaucoma, progressive optic atrophy and tumours) can affect the second eye.

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0 retina

+8 vitreous

+ 12 + 15 lens cornea

FIGURE 77.3 Settings of the ophthalmoscope used to examine intraocular structures

FIGURE 77.2 Blurred vision: appearance of a subject through the eyes of a person with cataracts. Photo courtesy Allergan Pharmaceuticals

The type of visual distortion seen by patients is illustrated in FIGURE 77.2. Examination • Reduced visual acuity (sometimes improved with pinhole) • Diminished red reflex on ophthalmoscopy • A change in the appearance of the lens

Management Advise extraction when the patient cannot cope. Contraindications for extraction include intraocular inflammation and severe diabetic retinopathy. There is no effective medical treatment for established cataracts. The removal of the cataractous lens requires optical correction to restore vision and this is usually performed with an intraocular lens implant. Full visual recovery may take 2–3 months. Complications are uncommon yet many patients may require YAG laser capsulotomy to clear any opacities that may develop behind the lens implant.

Postoperative advice to the patient • Avoid bending for a few weeks. • Avoid strenuous exercise. • The following drops may be prescribed: — steroids (to reduce inflammation) — antibiotics (to avoid infection) — dilators (to prevent adhesions) Prevention Sunglasses, particularly those that wrap around and filter UV light, may offer protection against cataract formation.

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• Medication (for life) usually selected from: — timolol or betaxolol drops bd Note: These beta blockers can cause systemic complications, e.g. asthma — latanoprost drops, once daily — pilocarpine drops qid — dipivefrine drops bd — acetazolamide (oral diuretics) • Surgery or laser therapy for failed medication

Retinitis pigmentosa Primary degeneration of the retina is a hereditary condition characterised by a degeneration of rods and cones associated with displacement of melanincontaining cells from the pigment epithelium into the more superficial parts of the retina. FIGURE 77.4 Typical visual field loss for chronic simple glaucoma; a similar pattern occurs with retinitis pigmentosa and hysteria

Glaucoma Chronic simple glaucoma is the commonest cause of irreversible blindness in middle age.1 At a very late stage it presents as difficulty in seeing because of loss of the outer fields of vision due to optic atrophy (see FIG. 77.4). Acute glaucoma, on the other hand, has a relatively rapid onset over a few days.

Typical features • Begins as night blindness in childhood • Visual fields become concentrically narrowed (periphery to centre) • Blind by adolescence (sometimes up to middle age) • Irreversible course—may be delayed by vitamin A Examination (ophthalmoscopic) • Irregular patches of dark pigment, especially at periphery • Optic atrophy

Clinical features (chronic glaucoma) • Familial tendency • No early signs or symptoms • Central vision usually normal • Progressive restriction of visual field

Trauma

Investigations

A small metal chip may penetrate the eye with minimal pain and the patient may not present with an ocular problem until the history of injury is long forgotten. If infection does not supervene, presentation may be delayed for months or years until vision deteriorates due to metal degradation. The iris becomes rust-brown. It is important to X-ray the eye if it has been struck by a hammered fragment or if in any doubt at all about the mechanism of the injury.1

Tonometry • Upper limit of normal is 22 mmHg

Ophthalmoscopy • Optic disc cupping >30% of total disc area Screening • Adults 40 years and over: 2–5 yearly (at least 2 yearly over 60) • Start about 30 years, then 2 yearly if family history Management • Treatment can prevent visual field loss

Trauma to the eye may cause only a little discomfort so it is important to keep this in mind.

Intraocular foreign body

Chronic uveitis Pain and redness may be minimal with this chronic inflammation. If untreated, visual loss often develops from secondary glaucoma and cataract. The pupil is bound to the lens by synechiae and is distorted.

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HIV infection

Amaurosis fugax

AIDS may have serious ocular complications, including Kaposi sarcoma of the conjunctivae, retinal haemorrhage and vasculitis.3 Another problem is ocular cytomegalovirus infection, which presents as areas of opacification with haemorrhage and exudates.

Sudden loss of vision It is important to remember that the problem is alarming and distressing to the patient; considerable empathy is needed and care must be taken not to diagnose seemingly inappropriate behaviour as of psychogenic origin. A comparison of bilateral and unilateral causes of sudden loss of vision is presented in TABLE 77.4, and the diagnostic strategy model in TABLE 77.5. A simplified classification is:

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unilateral: retinal detachment retinal artery occlusion retinal vein thrombosis temporal arteritis optic neuritis migraine bilateral: bilateral optic nerve lesion hysteria

Transient ocular ischaemia Unilateral loss of vision provoked by activities such as walking, bending or looking upwards is suggestive of ocular ischaemia.7 It occurs in the presence of severe extracranial vascular disease and may be triggered by postural hypotension and stealing blood from the retinal circulation.

Retinal detachment8

A flow chart for the diagnosis of painless loss of vision is presented in FIGURE 77.5. Table 77.4

Amaurosis fugax is transient loss of vision (partial or complete) in one eye due to transient occlusion of a retinal artery. It is painless and lasts less than 60 minutes. It is usually caused by an embolus from an atheromatous carotid artery in the neck. The most common emboli are cholesterol emboli, which usually arise from an ulcerated plaque.7 Other causes include emboli from the heart, temporal arteritis and benign intracranial hypertension. Other symptoms or signs of cerebral ischaemia, such as transient hemiparesis, may accompany the symptom. The source of the problem should be investigated. The risk of stroke after an episode of amaurosis fugax appears to be about 2% per year.7

Retinal detachment may be caused by trauma, thin retina (myopic people), previous surgery (e.g. cataract operation), choroidal tumours, vitreous degeneration or diabetic retinopathy.

Causes of sudden loss of vision7 Unilateral Bilateral

Transient

Permanent

Vascular causes

Occipital cortex ischaemia Pituitary apoplexy Homonymous hemianopia— vascular

Amaurosis fugax Transient ocular ischaemia Retinal emboli Malignant hypertension

Central retinal artery occlusion Central retinal vein occlusion Vitreous haemorrhage Ischaemic optic neuropathy

Other causes

Bilateral optic neuritis Toxic damage to optic nerve: • methanol • ethanol • tobacco • lead Leber optic atrophy Quinine poisoning of retina Cerebral oedema Occipital lobe trauma Craniopharyngioma Hysteria

Acute angle closure glaucoma Uhthoff phenomenon Papilloedema Posterior vitreous detachment

Optic neuritis Retinal detachment Optic nerve compression Carcinomatous optic neuropathy Intraocular tumour

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Visual failure

Table 77.5

Acute or subacute painless loss of vision: diagnostic strategy model

Q. Probability diagnosis A. Amaurosis fugax Migraine Retinal detachment Q. Serious disorders not to be missed A. Cardiovascular: • central retinal artery occlusion • central retinal vein occlusion • hypertension (complications) • CVA Neoplasia: • intracranial tumour • intraocular tumour: — primary melanoma — retinoblastoma — metastases Vitreous haemorrhage AIDS Temporal arteritis Acute glaucoma Benign intracranial hypertension Q. Pitfalls (often missed) A. Acute glaucoma Papilloedema Optic neuritis Intraocular foreign body Posterior uveitis Q. Seven masquerades checklist A. Diabetes (diabetic retinopathy) Drugs (quinine) Thyroid disorder (hyperthyroidism) Q. Is this patient trying to tell me something? A. Consider ‘hysterical’ blindness, although it is uncommon.

Clinical features • Sudden onset of floaters or flashes or black spots • Blurred vision in one eye becoming worse • ‘A curtain came down over the eye’, grey cloud or black spot • Partial or total loss of visual field (total if macula detached)

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• Pneumatic retinopexy is an option • True detachments usually require surgery

Vitreous haemorrhage Haemorrhage may occur from spontaneous rupture of vessels, avulsion of vessels during retinal traction or bleeding from abnormal new vessels.6 Associations include ocular trauma, diabetic retinopathy, tumour and retinal detachment. Clinical features • Sudden onset of floaters or ‘blobs’ in vision • May be sudden loss of vision • Visual acuity depends on the extent of the haemorrhage; if small, visual acuity may be normal Ophthalmoscopy may show reduced light reflex: there may be clots of blood that move with the vitreous (a black swirling cloud). Management • Urgent referral to exclude retinal detachment • Exclude underlying causes such as diabetes • Ultrasound helps diagnosis • May resolve spontaneously • Bed rest encourages resolution • Surgical vitrectomy for persistent haemorrhage

Central retinal artery occlusion The cause is usually arterial obstruction by atherosclerosis, thrombi or emboli. There may be a history of TIAs. Exclude temporal arteritis (perform immediate ESR). Clinical features • Sudden loss of vision like a ‘curtain descending’ in one eye • Vision not improved with 1 mm pinhole • Usually no light perception Ophthalmoscopy • Initially normal • May see retinal emboli • Classic ‘red cherry spot’ at macula

Ophthalmoscopy may show detached retinal fold as large grey shadow in vitreous cavity.

Management If seen early, use this procedure within 30 minutes:

Management • Immediate referral for sealing of retinal tears • Small holes treated with laser or freezing probe

• massage globe digitally through closed eyelids (use rhythmic direct digital pressure)—may dislodge embolus

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Painless loss of vision

Is vision normal through pinhole?

no

Was onset sudden?

yes

yes

refractive error

Was visual loss transient?

no, prolonged

no

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no, gradual

Is red reflex normal?

yes

Is direct pupil response normal?

? associated headache

yes

yes

retinal detachment vitreous haemorrhage central retinal vein occlusion cerebrovascular accident posterior vitreous detachment

migraine (without headache)

no

yes

no

chronic simple glaucoma diabetic retinopathy macular degeneration optic atrophy

amaurosis fugax cataract malignant melanoma

temporal arteritis central retinal artery occlusion optic neuritis

FIGURE 77.5 Diagnosis of painless loss of vision Source: Reproduced with permission of Dr J Reich and Dr J Colvin

• rebreathe carbon dioxide (paper bag) or inhale special CO2 mixture (carbogen) • intravenous acetazolamide (Diamox) 500 mg • refer urgently (less than 6 hours)—exclude temporal arteritis Prognosis is poor. Significant recovery is unlikely unless treated immediately (within 30 minutes).

Central retinal vein thrombosis Thrombosis is associated with several possible factors, such as hypertension, diabetes, anaemia, glaucoma and hyperlipidaemia. It usually occurs in elderly patients.

Clinical features • Sudden loss of central vision in one eye (if macula involved): can be gradual over days • Vision not improved with 1 mm pinhole Ophthalmoscopy shows swollen disc and multiple retinal haemorrhages, ‘stormy sunset’ appearance. Management No immediate treatment is effective. The cause needs to be found first and treated accordingly. Some cases respond to fibrinolysin treatment. Laser photocoagulation may be necessary in later stages if neovascularisation develops to prevent thrombotic glaucoma.

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Macular degeneration There are two types: exudative or ‘wet’ (acute), and pigmentary or ‘dry’ (slow onset). • ‘Wet’ MD is caused by choroidal neovascular membranes that develop under the retina of the macular area and leak fluid or bleed. It is a serious disorder. • ‘Dry’ MD (9 out of 10 cases of MD) develops slowly and is always painless. • More common with increasing age (usually over 60), when it is termed ‘age-related MD’, and in those with myopia (relatively common). • May be familial. Clinical features • Sudden fading of central vision (see FIG 77.6) • Distortion of vision • Straight lines may seem wavy and objects distorted • Use a grid pattern (Amsler chart): shows distorted lines • Central vision eventually completely lost • Peripheral fields normal

Temporal arteritis With temporal arteritis (giant cell arteritis) there is a risk of sudden and often bilateral occlusion of the short ciliary arteries supplying the optic nerves, with or without central retinal artery involvement.11 Clinical features • Usually older person: over 65 years • Sudden loss of central vision in one eye (central scotoma) • Can rapidly become bilateral • Associated temporal headache (not invariable) • Temporal arteries tender, thickened and nonpulsatile (but often normal) • Visual acuity severely impaired • Afferent pupil defect on affected side • Usually elevated ESR >40 mm

Management • Other eye must be tested • Immediate corticosteroids (60–100 mg prednisolone daily for at least 1 week) • Biopsy temporal artery (if there is a localised tender area)

Retinal migraine Photo courtesy Allergan Pharmaceuticals

Ophthalmoscopy • White exudates, haemorrhage in retina • Macula may look normal or raised Management No treatment is available to stop or reverse MD. For ‘wet’ MD refer urgently for treatment, which is currently based on injection of antivascular endothelial growth factor drugs (ranibizumab or bevacizumab) into the vitreous humour.9 The

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Age-Related Eye Disease Study provided confirmatory evidence that the chronic pigmentation type responds to free-radical treatment with the antioxidants vitamins A, C, E, and zinc using betacarotene, 15 mg; vitamin C, 500 mg; vitamin E, 400 IU; and 80 mg zinc oxide.10 Advise patient to cease smoking if applicable.

Ophthalmoscopy shows optic disc swollen at first, then atrophic. The disc may appear quite normal.

FIGURE 77.6 Appearance of a subject through the eyes of a person with age-related macular degeneration.

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Migraine may present with symptoms of visual loss. Associated headache and nausea may not be present. Clinical features • Zigzag lines or lights • Multicoloured flashing lights • Unilateral or bilateral field deficit • Resolution within a few hours

Posterior vitreous detachment The vitreous body collapses and detaches from the retina. It may lead to retinal detachment. Clinical features • Sudden onset of floaters

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• Visual acuity usually normal • Flashing lights indicate traction on the retina Management • Refer to an ophthalmologist urgently. • An associated retinal hole or detachment needs exclusion.

Optic (retrobulbar) neuritis Causes include multiple sclerosis, neurosyphilis and toxins. A significant number of cases eventually develop multiple sclerosis. Clinical features • Usually a woman 20–40 years • Loss of vision in one eye over a few days • Retro-ocular discomfort with eye movements • Variable visual acuity • Usually a central field loss (central scotoma) • Afferent pupil defect on affected side

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Ophthalmoscopy • Optic disc swollen if ‘inflammation’ anterior in nerve • Optic atrophy appears later • Disc pallor is an invariable sequel Management • Test visual field of other eye • Consider MRI • Most patients recover spontaneously but are left with diminished acuity • Intravenous steroids hasten recovery and have a protective effect against the development of further demyelinating episodes

Corneal disorders Patients with corneal conditions typically suffer from ocular pain or discomfort and reduced vision. The common condition of dry eye may involve the cornea while contact lens disorders, abrasions/ulcers and infections are common serious problems that threaten eye sight. Inflammation of the cornea—keratitis—is caused by factors such as ultraviolet light e.g. ‘arc eye’, herpes simplex, herpes zoster ophthalmicus and the dangerous ‘microbial keratitis’. Bacterial keratitis is an ophthalmological emergency that should be considered in the contact lens wearer presenting with pain and reduced vision. Topical corticosteroids should be avoided in the undiagnosed red eye. Refer to CHAPTER 51 for corneal lesions.

Pitfalls • Mistaking the coloured haloes of glaucoma for migraine. • Failing to appreciate the presence of retinal detachment in the presence of minimal visual impairment. • Omitting to consider temporal arteritis as a cause of sudden visual failure in the elderly. • Using eyedrops to dilate the pupil (for fundal examination) in the presence of glaucoma.

When to refer • Most problems outlined need urgent referral to an ophthalmologist. • Acute visual disturbance of unknown cause requires urgent referral. • Any blurred vision—sudden or gradual, painful or painless—especially if 1 mm pinhole fails to alter visual acuity. • Refer all suspicious optic discs.

Practice tips •

• •

• • • • • • •

•

Tonometry is advised routinely for all people over 40 years; those over 60 years should have tests every 2 years. Any family history of glaucoma requires tonometry at earliest age. Sudden loss of vision in the elderly suggests temporal arteritis (check the ESR and temporal arteries). It requires immediate institution of highdose steroids to prevent blindness in the other eye. A time-scale guide showing the rate of visual loss is presented in TABLE 77.6. Temporal arteritis is an important cause of retinal artery occlusion. Suspect field defect due to chiasmal compression if people are misjudging when driving. Pupillary reactions are normal in cortical blindness. Central retinal artery occlusion may be overcome by early rapid lowering of intraocular pressure. Retinal detachment and vitreous haemorrhage may require early surgical repair. Keep in mind antioxidant therapy (vitamins and minerals) for chronic macular degeneration. Consider multiple sclerosis foremost if there is a past history of transient visual failure, especially with eye pain. If the patient has been using a hammer, always X-ray if a fragment of metal has hit the eye but nothing can be seen.

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Visual failure

Table 77.6 Time-scale guide for rate of visual loss3,7

Hand-out sheets from Murtagh’s Patient Education 6th edition: • Cataracts • Floaters and flashes • Glaucoma • Macular degeneration

Within 24 hours Central retinal vein occlusion Hysteria

1 Colvin J, Reich J. Check Program 219–220. Melbourne: RACGP, 1990: 1–32. 2 Hopcroft K, Forte V. Symptom Sorter (4th edn). Oxford: Ratcliffe Publishing, 2010: 138. 3 Enoch B. Painless loss of vision in adults. Update, 1987; 5 June: 22–30. 4 Robinson MJ, Roberton, DM. Practical Paediatrics (5th edn). Melbourne: Churchill Livingstone, 2003: 756–70. 5 Cole GA. Amblyopia and strabismus. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 20–4. 6 Elkington AR, Khaw PT. ABC of Eyes. London: British Medical Association, 1990: 20–38. 7 King J. Loss of vision. Mod Med Aust, 1990; May: 52–61. 8 Hodge C, Ng D. Eye emergencies. Check Program 400. Melbourne: RACGP, 2005: 1–34. 9 Bunting R, Guymer R. Treatment of age-related macular degeneration. Aust Prescr, 2012; 35: 90-3. 10 Age-Related Eye Disease Study Research Group. A randomised, placebo-controlled, clinical trial of high dose supplementation with vitamins C and E, beta-carotene, and zinc for age-related macular degeneration and vision loss. Arch Ophthalmol, 2001; 119: 1417–36. 11 Warne R, Prinsley D. A Manual of Geriatric Care. Sydney: Williams & Wilkins, 1988: 191–5.

Up to several weeks (variable) Choroiditis Malignant hypertension Gradual Compression of visual pathways Chronic glaucoma Cataracts Diabetic maculopathy Retinitis pigmentosa Macular degeneration Refractive errors

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Sudden: less than 1 hour Amaurosis fugax Central retinal artery occlusion Hemianopias from ischaemia (emboli) Migraine Vitreous haemorrhage Acute angle glaucoma Papilloedema

Less than 7 days Retinal detachment Optic neuritis Acute macular problems

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Weight gain

Persons who are naturally very fat are apt to die earlier than those who are slender. Hippocrates Obesity is the most common nutrition-related disorder in the Western world; as Tunnessen puts it, ‘Obesity is the most common form of malnutrition in the United States’.1 Most overweight adults and children who are obese have exogenous obesity, which tends to imply that ‘they ate too much’, but the problem is more complex than relative food input. Physical activity and environmental and genetic influences must also be taken into account. However, only a small percentage (4–6%) of human obesity is thought to be due to a single gene mutation.2 There is still a persisting tendency of affected families to blame ‘glandular’ problems as a cause of obesity. It is now considered that there is a strong genetic basis to obesity and that attributing it to overeating and lack of exercise is an overly simplistic viewpoint.

Key facts and figures • Two-thirds of the Australian population are overweight or obese and only 2–4% underweight.3 • Abdominal obesity gives a higher cardiovascular risk at any weight. • The onset of obesity can occur at any age. • Secondary or pathologic causes are rare. • Less than 1% of obese patients have an identifiable secondary cause of obesity.2 • Two conditions causing unexplained weight gain that can be diagnosed by the physical examination are Cushing syndrome and hypothyroidism. • After pregnancy, obesity may result from a failure to return to prepartum energy requirements. • Even small weight losses are effective in preventing diabetes and improving the cardiovascular risk profile.4

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 78.1. Table 78.1

Weight gain: diagnostic strategy model

Q. Probability diagnosis A. Exogenous obesity Alcohol excess Drugs Q. Serious disorders not to be missed A. Cardiovascular: • cardiac failure Hypothalamic disorders (hyperphagia): • craniopharyngiomas • optic gliomas Liver failure Nephrotic syndrome Q. Pitfalls (often missed) A. Pregnancy (early) Endocrine disorders: • hypothyroidism • Cushing syndrome • insulinoma • acromegaly • hypogonadism • hyperprolactinaemia • polycystic ovarian syndrome Idiopathic oedema syndrome Klinefelter syndrome Congenital disorders: • Prader–Willi syndrome • Laurence–Moon–Biedl syndrome Q. Seven masquerades checklist A. Depression Drugs Thyroid disorder (hypothyroidism) Q. Is the patient trying to tell me something? A. Yes: the reasons for obesity should be explored.

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Probability diagnosis The outstanding cause of weight gain in exogenous obesity is excessive calorie intake coupled with lack of exercise. This is determined largely by environmental influences. Overweight people often deny overeating but the true situation can be determined by recording actual food intake and energy expenditure, and by interviewing reliable witnesses.

Serious causes not to be missed It is important not to misdiagnose hypothalamic disorders, which may result in hyperphagia and obesity. Injury to the hypothalamus may occur following trauma and encephalitis and with a variety of tumours, including craniopharyngiomas, optic gliomas and pituitary neoplasms. Some of these tumours may cause headaches and visual disturbances. It is also important not to overlook major organ failure and kidney disorders as a cause of increased body weight, especially cardiac failure, liver failure and the nephrotic syndrome. The associated increase in body water needs to be distinguished from increased body fat.

Pitfalls Endocrine disorders The endocrine disorders that cause obesity include Cushing syndrome, hypothyroidism, insulinsecreting tumours and hypogonadism. They should not represent difficult diagnostic problems. An insulin-secreting tumour (insulinoma) is a very rare adenoma of the B cells of the islets of Langerhans. The main features are symptoms of hypoglycaemia and obesity. Congenital disorders The rare congenital disorders that cause obesity, such as Prader–Willi and Laurence–Moon–Biedl syndromes, should be easy to recognise in children (see CHAPTER 18 and later in this chapter). Chromosomal abnormalities An important abnormality to bear in mind is Klinefelter syndrome (XXY karyotype), which affects one out of every 400–500 males. The boys show excessive growth of long bones and are tall and slim. Without testosterone treatment they become obese as adults. Some girls with Turner syndrome (XO karyotype) may be short and overweight.

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Some gender pointers Consider polycystic ovarian syndrome in women and obstructive sleep apnoea in obese men.

Seven masquerades checklist The important masquerades include hypothyroidism and drug ingestion. Hypothyroidism is usually not associated with marked obesity. Drugs that can be an important contributing factor include tricyclic antidepressants, mirtazapine, corticosteroids, pizotifen, thioridazine, haloperidol, Depo-Provera and the contraceptive pill. Obesity (overeating) may be a feature of depression, especially in the early stages. Prescribed tricyclic antidepressants may compound the problem.

Psychogenic considerations An underlying emotional crisis may be the reason for the overweight patient to seek medical advice. It is important to explore diplomatically any hidden agenda and help the patient to resolve any conflict.

The clinical approach A careful history is very valuable in ascertaining food and beverage intake and perhaps giving patients insight into their calorie intake, since some deny overeating or will underestimate their food intake.4 Enquire about gynaecological and family history e.g. diabetes, cardiac disease.

Relevant questions • • • •

Do you feel that you have an excessive appetite? Tell me in detail what you ate yesterday. Give me an outline of a typical daily meal. Tell me about snacks, soft drink and alcohol that you have. • What exercise do you get? • Do you have any special problems, such as getting bored, tense and upset or depressed? • What drugs are you taking?

Examination In the physical examination it is very important to measure body weight and height and calculate the BMI, and assess the degree and distribution of body fat and the overall nutritional status. Record the blood pressure and test the urine with dipsticks. Keep in mind that a standard blood pressure cuff on a large arm may give falsely elevated values. Remember the rare possibilities of Cushing syndrome, acromegaly and hypothyroidism. Search for evidence of atherosclerosis and diabetes and for signs of alcohol abuse.

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An extensive working up of the CNS is not indicated in obesity without the presence of suspicious symptoms such as visual difficulties.

BMI

Investigations

Classification of obesity (based on WHO guidelines)6 Grading

Suggested therapy Diet and counselling

35

≥40

Grade III: severely obese

Important investigations • Cholesterol/triglycerides • Glucose (fasting) • Liver function tests • Electrolytes and urea Investigations to consider • Thyroid function tests • Cortisol (if hypertensive) • Testosterone (suspected sleep apnoea) • ECG and chest X-ray (older than 40) 5

Anthropometric measurements

Useful measuring instruments include:

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Table 78.2

• BMI: ‘healthy’ range is between 20 and 25 • Waist circumference: increased risk of comorbidities — in men >94 cm (>102—high risk) — in women >80 cm (>88—high risk) Measure waist halfway between inferior margin of last rib and crest of ilium in mid-axillary line over bare skin. • waist–hip circumference ratio (W/H ratio): healthy range 25 mm suggests increased body fat) • upper arm circumference • 4 skinfold thickness (sum of suprailiac, subscapular, triceps and biceps skinfolds)—for calculation of percentage body fat Abdominal fatness, which is defined as a W/H  ratio of >0.85 in women and >0.95 in men, is a more accurate indicator of the complications of diabetes. Body mass index The easiest and possibly most accurate assessment of obesity is the BMI (refer to Appendix V): BMI = weight (kg) height (m2)

Combined program plus medical therapy Consider gastric surgery

Garrow6 has produced a simple classification of the BMI associated with the relative degree of risk increase and suggested therapy (see TABLE 78.2). The BMI has limitations. It doesn’t distinguish between men and women or between body types and it doesn’t work for children.

Weight gain in children Various studies have found that approximately 10% of prepubertal and 15% of adolescent age groups are obese.1 Obesity in children is a BMI for age >95th percentile while overweight is >85th percentile. There is a risk of obesity associated diseases and carrying the problem into adulthood. Raising the issue with parents and child requires sensitivity and discretion. Parents often blame obesity in children on their ‘glands’, but endocrine or metabolic causes are rare and can be readily differentiated from exogenous obesity by a simple physical examination and an assessment of linear growth. Children with exogenous obesity tend to have an accelerated linear growth whereas children with secondary causes are usually short.

Congenital or inherited disorders associated with obesity Prader–Willi syndrome The characteristic features are bizarre eating habits (e.g. binge eating), obesity, hypotonia, hypogonadism, intellectual disability, small hands and feet and a

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Weight gain characteristic facial appearance (narrow bifrontal diameter, ‘almond-shaped’ eyes and a ‘tented’ upper lip). Progressive obesity results from excessive intake in addition to decreased caloric requirements (see CHAPTER 18). Laurence–Moon–Biedl syndrome The characteristic features are obesity, intellectual disability, polydactyly and syndactyly, retinitis pigmentosa and hypogonadism. Beckwith–Wiedemann syndrome Characteristics include excessive growth, macrosomia, macroglossia, umbilical hernia and neonatal hypoglycaemia. Children appear obese as they are above the 95th percentile by 18 months of age. Intelligence is usually in the normal range.

Endocrine disorders Endocrine disorders in children that can rarely cause obesity include hypothyroidism (often blamed as the cause but seldom is), Cushing syndrome, insulinomas, hypothalamic lesions, Fröhlich syndrome (adiposogenital dystrophy) and Stein– Leventhal syndrome (PCOS) in girls.

Managing obesity in children Childhood obesity usually reflects an underlying problem in the family system. It can be a very difficult emotional problem in adolescents, who develop a poor body image. An important strategy is to meet with family members, determine whether they perceive the child’s obesity as a problem and whether they are prepared to solve the problem. The family dynamics will have to be assessed and strategies outlined. This may involve referral for expert counselling. It is worth pointing out that children eat between one-third and two-thirds of their meals at school so schools should be approached to promote special programs for children who need weight reduction. Conventional therapy by dietary modification, increasing energy expenditure by increasing activity, reducing sedentary behaviour, behaviour modification and family involvement is recommended. Some authorities emphasise that weight maintenance rather than weight loss is appropriate since many children will ‘grow into their weight’.7

Cushing syndrome Cushing syndrome is the term used to describe the chemical features of increased free circulating glucocorticoid. The most common cause is iatrogenic  with the prescribing of synthetic

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corticosteroids. The spontaneous primary forms such as Cushing disease (pituitary dependent hyperadrenalism) are rare. As the disorder progresses the body contour tends to assume the often quoted configuration of a lemon with matchsticks (see CHAPTER 23). Clinical features • Change in appearance • Central weight gain (truncal obesity) • Hair growth and acne in females • Muscle weakness • Amenorrhoea/oligomenorrhoea (females) • Thin skin/spontaneous bruising • Polymyalgia/polydipsia (diabetes mellitus) • Insomnia • Depression Signs • Moon face • ‘Buffalo hump’ • Purple striae • Large trunk and thin limbs: the ‘lemon with matchsticks’ sign The patient should be referred for diagnostic evaluation, including plasma cortisol and overnight dexamethasone suppression tests. Untreated Cushing syndrome has a very poor prognosis, with premature death from myocardial infarction, cardiac failure and infection; hence early diagnosis and referral is essential.

Obesity Obesity and overweight are the most common pathological conditions in our society and are caused by an accumulation of adipose tissue (see TABLE 78.3). It is not the extra weight per se that causes problems but excess fat. The calculation of the BMI gives a better estimate of adiposity and it is convenient and preferable to use this index when assessing the overweight and obese. However, recent data suggest that the distribution of body fat is as important a risk factor as its total amount. Abdominal fat (upper body segment obesity, or ‘apple’ obesity) is considered a greater health hazard than fat in the thighs and buttocks (lower body segment obesity, or ‘pear’ obesity) (see FIG. 78.1). Obese patients with high waist–hip ratios (>1.0 in men and >0.9 in women) have a significantly greater risk of diabetes mellitus, stroke, coronary artery disease and early death than equally obese people with lower waist–hip ratios.2

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Table 78.3

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300

Factors predisposing to primary obesity

Genetic

Familial tendency

Sex

Women more susceptible

Activity

Lack of physical activity

Psychogenic

Emotional deprivation, depression

Socioeconomic status

Lower

Alcohol

Problem drinking

Smoking

Cessation of smoking

Prescribed drugs

Tricyclic derivatives

200 Mortality index

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100 underweight

healthy

overweight

obese

0 1

20

25

30

35

40

Body mass index (BMI)

FIGURE 78.2 Body mass index (BMI) reference scale

FIGURE 78.1 Comparison of two types of obesity according to distribution of body fat

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In regard to the BMI reference scale it is worth noting that the risks follow a J-shaped curve (see FIG. 78.2) and are only slightly increased in the overweight range but increase with obesity so that a BMI of >40 carries a threefold increase in mortality. The consequences of obesity include: • cardiovascular: — increased mortality (stroke, ischaemic heart disease, etc.) — hypertension — varicose veins • metabolic: — dyslipidaemia — type 2 diabetes — insulin resistance — hyperuricaemia/gout — infertility — PCOS • mechanical: — osteoarthritis — obstructive sleep apnoea — restrictive pulmonary disease — spinal dysfunction — low back pain

• other: — hiatus hernia — gall bladder disease — fatty liver — cancer (various) — kidney disease (check microalbuminuria) — excessive daytime sleepiness — erectile dysfunction — psychological problems/depression Management An imperative of treatment is to address the serious comorbidities of type 2 diabetes and insulin resistance. Treatment is based on four major interventions, the choice of which depends on the degree of obesity, the associated health problems and the health risk posed: 1 2 3 4

reduction in energy intake change in diet composition increased physical activity behavioural therapy

Pharmacological agents are not used for firstline therapy although they may have a place in management, especially at grade III level of obesity. Surgery is an option for the treatment of morbid obesity. There is no single effective method for the treatment of obesity, which is a difficult and frustrating problem. A continuing close therapist/ patient contact has a better chance of success than any single treatment regimen.

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Weight gain Goals

A doctor–patient strategy A close therapeutic supportive relationship with a patient can be effective using the following methods:8 1 Promote realistic goals. Lose weight at the same rate that it was gained (i.e. slowly)—for example, 5–10 kg a year. A graph can be used for this purpose with an ‘exaggerated’ scale on the vertical axis so that small variations appear highly significant and encouraging (see FIG. 78.3). Promote the equation: Energy In = Energy Out + Energy Stored The appropriate way to reduce the stored energy (fat) is either to reduce energy in (eat less) or increase energy out (exercise). 2 Dietary advice. It is important to be realistic and allow patients to eat their normal foods but advise them about quantity and frequency. Give advice on simple substitutions (e.g. fortified skim milk in place of whole milk, high-fibre wholemeal bread instead of white bread, and fruit and vegetables instead of biscuits and cakes as in-between snacks).8 A strategy that seems to work effectively is to advise patients, especially those who are overweight (and grade I obesity), to eat one-third less than they usually do and discipline themselves not to ‘pick’ and to avoid second helpings. 3 Counselling is simple and commonsense. It involves being supportive, interested and encouraging. A list of tips on coping is provided (see below ‘A practical plan’ for grade II and III obesity) and the patient advised to keep a food, exercise and behaviour diary.

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1 no further weight gain 2 loss of 5–10% initial body weight 3 improve activity

ex

pe

cte

d

ra

te

Weight

Most successful programs involve a multidisciplinary approach to weight loss, embracing the four major interventions. The first goal should be no further weight gain. Emphasis must be on maintenance of weight loss. Behaviour modification is important and the most valuable strategy is to emphasise planning and record keeping with a continuous weekly diary of menus, exercise and actual behaviour. Social support is essential for a successful weight  loss program. A better result is likely if close family members, especially the chief cook, are involved in the program, preferably striving for the same goals.2

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igh

t lo

ss

goal weight

Time

FIGURE 78.3 Weight loss chart to encourage patient Source: After Kaczmarczyk8

4 Review. ‘Review is the most vital part of the weight loss programme as it stimulates and revitalises motivation and enables assessment of progress.’8 It should be frequent initially (e.g. fortnightly), then monthly until the goal weight has been achieved and then 3-monthly. It is important never to be judgmental or critical if progress is unsatisfactory. A practical plan The following patient education sheet to be handed to patients represents useful advice to offer the obese patient.8 The emphasis is on a healthy lifestyle program.

Physical activity • A brisk walk for at least 20–30 minutes each day is the most practical exercise. • Other activities such as tennis, swimming, golf and cycling are a bonus.

Dietary advice Provide patients with a glycaemic index guide (see TABLE 10.1 in CHAPTER 10). Breakfast: • oatmeal (soaked overnight in water); after cooking, add fresh or dried fruit; serve with fatreduced milk or yoghurt or • muesli (homemade or from a health food store)—medium serve with fat-reduced milk, perhaps add extra fruit (fresh or dried)

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• slice of wholemeal toast with a thin scraping of margarine, spread with Vegemite, Marmite or sugar-free marmalade • fresh orange juice or herbal tea or black tea/ coffee Morning and afternoon tea: • piece of fruit or vegetable (e.g. carrot or celery) • freshly squeezed juice or chilled water with fresh lemon Midday meal: • salad sandwich with wholemeal or multigrain bread and thin scraping of margarine (for variety use egg, salmon, chicken or cheese fillings) • drink as for breakfast Evening meal: • Summer (cold)—lean meat cuts (grilled, hot or cold), poultry (skin removed) or fish; fresh garden salad; slices of fresh fruit • Winter (hot)—lean meat cuts (grilled), poultry (skin removed) or fish; plenty of green, red and yellow vegetables and small potato; fruit for sweets

Weight-losing tips9

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• Have sensible goals; do not ‘crash’ diet but have a 6–12 month plan to achieve your ideal weight. • Go for natural foods; avoid junk foods. • Select fish, poultry and lean meats. • Trim excess fat from meat and skin from poultry. • Eat more breads (wholemeal), cereals, fruit and vegetables. • Increase intake of complex carbohydrates that contain starch and fibre. • Plant food is good for you; have it as part of breakfast. • Eat less sugar; avoid lollies and syrups. • Avoid alcohol, sugary soft drinks and high-calorie fruit juices. • Strict dieting without exercise fails. • If you are mildly overweight, eat one-third less than you usually do. • Do not eat biscuits, cakes, buns, etc. between meals (preferably at no time). • Limit the intake of full-cream products, fried foods and fatty take-away meals. • Limit the amount of butter or margarine on vegetables and bread. • Reduce calorie intake; reduce fat intake to 30 and failed well-supervised lifestyle measures. The agents are:4,5,9,10 • Local, acting on GIT: — bulking agents (e.g. methylcellulose) — lipase inhibitor—orlistat (Xenical) 120 mg (o) tds ac (used with a low-fat eating program) • Centrally acting agents: — amphetamine derivatives (reduce hunger): — phentermine 15–40 mg (o) daily (limited use) — serotonin analogues (enhance satiety): — fluoxetine 20–40 mg (o) daily — sibutramine 10–15 mg (o) daily (monitor BP) — sertraline A summary of systemic reviews to date indicates that the effectiveness of serotonin analogues is unknown or, with sibutramine and phentermine, of some benefit, which has to be weighed against adverse effects, including the potentially fatal serotonin syndrome. The same applies to orlistat, which, together with a low-fat eating program, does produce extra weight loss over placebo.11 Drugs should not be expected to have a continuing effect after therapy ceases.

Meal replacements Food replacement agents such as Optifast have been promoted but there is insufficient evidence so far to evaluate their effectiveness and the reduced intake of key vitamins. Surgery (bariatric surgery)5,7 Surgery is the most effective treatment for obesity but is associated with risks such as malabsorption.4 In those with morbid obesity (about 2% of the population) unresponsive to behaviour modification therapy and a course of pharmacological agents for 3 months or so, gastric banding has a place. It is recommended in those with a BMI >40 or >35

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Weight gain with severe comorbidities such as poorly controlled diabetes or severe OSA. One example is Lap-Band, which is inserted laparoscopically and can be adjusted and eventually removed with minimal significant residual adverse defect left in the stomach. It appears to be effective for 10 years.5,12 Sleeve gastrectomy gastric bypass such as Roux-en-Y bypass and other techniques to consider.

Oedema Oedema (dropsy) is an excessive accumulation of fluid in tissue spaces. It may be generalised or localised— periorbital, peripheral or an arm (lymphoedema, refer CHAPTER 69).

Generalised oedema The site of generalised oedema is largely determined by gravity. It is due to an abnormal excess of sodium in the body, which leads to accumulation of water. The causes can be generally divided into two groups— oedema associated with a decreased plasma volume and oedema associated with an increased plasma volume (see TABLE 78.4). Table 78.4

Causes of generalised oedema

Decreased plasma volume Hypoalbuminaemia (e.g. nephrotic syndrome, chronic liver disease, malnutrition) Increased plasma volume Congestive cardiac failure Chronic kidney failure Drugs (e.g. corticosteroids, NSAIDs, certain antihypertensives, oestrogens, lithium, others) Idiopathic oedema

Diagnosis Clinical examination, including urinalysis, is usually sufficient to establish the cause of the oedema. In other cases, investigation of kidney or liver function may be required. Treatment • Treat the cause where known • Salt (sodium) restriction • Diuretics: — a loop diuretic (e.g. frusemide) — a potassium-sparing diuretic (e.g. spironolactone)

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Idiopathic oedema Idiopathic oedema, also known as cyclical or periodic oedema, is a common problem and the diagnosis is made on a characteristic history: • • • • • • • •

exclusive to women may be cyclical or persistent usually unrelated to menstrual cycle excessive diurnal weight gain (worse on prolonged standing) abdominal bloating may affect hands and face as well as feet often made worse by diuretics may be associated with headache, depression, tension

Treatment of this condition is difficult. Most diuretics can aggravate the problem. Supportive stockings and a nutritious diet (with restricted sodium intake) is recommended as first-line treatment. A trial of spironolactone is often recommended.

Swelling (puffiness) of the face and eyelids The causes are similar to those for generalised oedema. Important specific causes to consider are: • kidney disease (e.g. nephrotic syndrome, acute nephritis) • hypothyroidism • Cushing syndrome and corticosteroid treatment • mediastinal obstruction • angio-oedema • skin sensitivity (e.g. drugs, cosmetics, hair dryers)

Swelling of the legs Refer to CHAPTER 69.

‘Cellulite’ ‘Cellulite’ refers to a characteristic form of dimpling seen in the subcutaneous tissues of hips, buttocks and thighs of females. The dimpling pattern is related to the manner of attachment of fibrous septae that contain the fat. Many patients seek advice about ‘cellulite’ in the buttocks and thighs in particular. Explain that the best way to overcome it is to maintain an ideal weight. If overweight, lose it slowly and exercise to improve the muscle tone in the buttocks and thighs.

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When to refer

Patient education resources

• Patients with grade II or III obesity (BMI >35) who are resistant to simple weight control measures.5 • Patients with associated medical problems such as angina or severe osteoarthritis who require relatively rapid weight reduction. • Possibility of endocrine cause of obesity. • Suspicion of congenital or inherited disorder in children.

Hand-out sheets from Murtagh’s Patient Education 6th edition: • Obesity: how to lose weight wisely

Practice tips • • •

•

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•

Avoid a critical or judgmental attitude to the overweight patient. Diplomatically seek independent information from a spouse or parent about food and beverage intake. Obtain a chronological history of the patient’s weight from infancy onwards and attempt to correlate any significant changes to stressful life events. Central or visceral obesity carries a large risk factor for medical complications. People are advised to keep the waist circumference to less than 100 cm, and ideally less than 80 cm in women and 94 cm in men. The best approach is to focus on fitness, with dietary advice on fresh vegetables and fewer ‘empty’ calories (soft drinks, snack foods). It is much better to be overweight and fit than normal weight and unfit.3

References 1 Tunnessen WW Jr. Signs and Symptoms in Paediatrics (2nd edn). Philadelphia: JB Lippincott, 1988: 33–41. 2 Papdakis MA, McPhee SJ. Current Medical Diagnosis and Treatment (52nd edn). New York: McGraw-Hill Lange, 2013: 1259. 3 Funder J. Weighing it up. RACGP: Good Practice. Issue 4, 2014: 13. 4 Caterson ID. Weight management. Australian Prescriber, 2006; 29: 43–7. 5 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 49–58. 6 WHO Technical Report Series Number 894. Geneva: WHO, 2000. 7 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013: 513-4. 8 Kaczmarczyk W. The obese patient. In: How I manage my difficult problems. Aust Fam Physician, 1991; 20: 417–21. 9 RACGP. Guidelines for Preventive Activities in General Practice (8th edn). Melbourne, 2013: 43-5. 10 Padwal R, Li SK, Lau DC et al. Long term pharmacotherapy for obesity and overweight. (Cochrane Review). Cochrane Database, Sept. Rev. 2008; (1): CD 004094. 11 Arterburn D, Noel P. Obesity. In: Barton S (ed.). Clinical Evidence (issue 5). London: BMJ Publishing Group, 2001: 412–19. 12 Dixon J, O’Brien P et al. Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomised controlled trial. JAMA, 2008; 299 (3): 316–22.

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Among young women dieters in modern society about 1 in 20 will become preoccupied with their appearance and progress to the eating disorders of anorexia nervosa and bulimia. Professor Doris Young  In family practice complaints of loss of weight are more frequent than complaints about being too thin. Of great significance is the problem of recent loss of weight. A very analytical history is required to determine the patient’s perception of weight loss. The equivalent problem in children is failure to gain weight or thrive. Weight loss is an important symptom because it usually implies a serious underlying disorder, either organic or functional. It may or may not be associated with anorexia and thus diminished food intake.

Key facts and checkpoints • • •

•

•

•

Any loss of more than 5% of normal body weight is significant. The most common cause in adults of recent weight loss is stress and anxiety.1 Serious organic diseases to consider are: — malignant disease — diabetes mellitus — chronic infections (e.g. tuberculosis) — thyrotoxicosis The most important variable to consider in evaluating weight loss is appetite. Eating and weight go hand in glove. Two conditions commonly associated with weight loss are anaemia and fever; they must be excluded. Early detection of eating disorders improves outcome.

A diagnostic approach A summary of the diagnostic strategy model is presented in TABLE 79.1.

Probability diagnosis Excluding planned dietary restriction, psychological factors are the most common cause, particularly

recent stress and anxiety.1 Elderly people with adverse psychological factors, neglect and possibly drug effects can present with wasting.

Serious disorders not to be missed Many of the problems causing weight loss are very serious, especially malignant disease. Malignant disease Weight loss may be a manifestation of any malignancy. With cancer of the stomach, pancreas and caecum, malignant lymphomas and myeloma, weight loss may be the only symptom. Occult malignancy must be regarded as the most common cause of weight loss in the absence of major symptoms and signs. The mechanisms may be multiple, with anorexia and increased metabolism being important factors. Chronic infections These are now less common but tuberculosis must be considered, especially in people from less developed countries. Some cases of infective endocarditis may progress only very slowly with general debility, weight loss and fever as major features.2 Other infections to consider are brucellosis, and protozoal and systemic fungal infection. Infection with HIV virus must be considered, especially in highrisk groups.

Pitfalls Drug dependency, including alcohol and narcotic drugs, must be considered, especially when the problem may result in inappropriate nutrition. Apart from malignant disease there is a whole variety of gastrointestinal disorders that require consideration—these include malabsorption states, gastric ulceration, and intestinal infestations that should be considered, especially in people returning from a significant stay in tropical and underdeveloped countries. Addison disease (CHAPTER 23) can be very difficult to diagnose. Symptoms include excessive

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Weight loss: diagnostic strategy model (other than deliberate dieting or malnutrition)

Q. Probability diagnosis A. Stress and anxiety (e.g. redundancy, divorce) Depressive illness Non-coping elderly/dementia Eating disorders: anorexia nervosa/bulimia Q. Serious disorders not to be missed A. Chronic heart failure Malignant disease, including: • stomach • pancreas • lung • myeloma • caecum • lymphoma Chronic infection: • HIV infections (AIDS, AIRC) • tuberculosis • hidden abscess • infective endocarditis • brucellosis • others e.g. overseas acquired infection

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Q. Pitfalls (often missed) A. Drug dependence esp. alcohol Malabsorption states: • ? intestinal parasites/infestations • coeliac disease Other GIT problems Chronic kidney failure Connective tissue disorders (e.g. SLE, RA) Dementia Rarities: • Malnutrition • Addison disease • hypopituitarism Q. Seven masquerades checklist A. Depression Diabetes Drugs Anaemia Thyroid disorder (hyperthyroidism) UTI Q. Is the patient trying to tell me something? A. A possibility. Consider stress, anxiety and depression. Anorexia nervosa and bulimia are special considerations.

fatigue, anorexia, nausea and postural dizziness. Hyperpigmentation is a late sign.

Seven masquerades checklist Depression and the endocrine disorders, diabetes mellitus and hyperthyroidism, are important causes. Diabetes The diabetic who presents with weight loss will be young and insulin-dependent. The initial presentation may be ketoacidosis. The triad of symptoms is thirst + polyuria + weight loss. Hyperthyroidism This is usually associated with weight loss although in some, such as an elderly male, it may not be obvious. An important clue will be weight loss in the presence of an excellent appetite and this helps to distinguish it from a psychoneurotic disturbance. Depression Weight loss is a common feature of depression and is usually proportional to the severity of the disease. In the early stages of depression, weight gain may be present but when the classic loss of the four basic drives (appetite, energy, sleep and sex) becomes manifest, weight loss is a feature. Drugs Any prescribed drugs causing anorexia can cause weight loss. Important drugs include digoxin, narcotics, cytotoxics, NSAIDs, some antihypertensives and theophylline.

Red flag pointers for weight loss • • • • •

Weight loss per se is a big red flag Rapid weight loss with malaise Acid dental erosion on surfaces of upper teeth: think bulimia Weakness and malaise in young females: consider eating disorder and hypokalaemia Evidence of abuse in a child

Psychogenic considerations Weight loss is a feature of anxiety as well as depression. Some patients with psychotic disturbances, including schizophrenia and mania, may present with weight loss.

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Weight loss Anorexia nervosa is quite common and is almost entirely confined to females between the ages of 12 and 20 years. The main differential diagnosis is hypopituitarism, although anorexia nervosa can cause endocrine disturbances through the hypothalamic pituitary axis.

The clinical approach History It is important to document the weight loss carefully and evaluate the patient’s recordings. The same set of scales should be used. It is also important to determine the food intake. However, in the absence of an independent witness such as a spouse or parent, this can be difficult. Food intake may be diminished with psychogenic disorders and cancer but increased or steady with endocrine disorders, such as diabetes and hyperthyroidism, and with steatorrhoea. FIGURE 79.1 shows the possible causes of weight loss.

Malignancy lymphoma

stress and anxiety depression eating disorders drugs hyperthyroidism

lung congestive cardiac failure tuberculosis

pancreas

colon caecum ovary others

FIGURE 79.1 Weight loss: causes to consider

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General questions • Exactly how much weight have you lost and over how long? • Have you changed your diet in any way? • Has your appetite changed? Do you feel like eating? • Have your clothes become looser? • What is your general health like? • How do you feel in yourself? • Do you feel uptight (tense), worried or anxious? • Do you get very irritable or tremulous? • Do you feel depressed? • Do you ever force yourself to vomit? • Are you thirsty? • Do you pass a lot of urine? • Do you have excessive sweating? • Do you experience a lot of night sweats? • What are your motions like? • Are they difficult to flush down the toilet? • Do you have a cough or bring up sputum?

melanoma

stomach kidney

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chronic kidney failure diabetes (type 1) GIT disorders: malabsorption post surgery

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Do you get short of breath? Do you have any abdominal pain? Are your periods normal (for females)? What drugs are you taking? How many cigarettes do you smoke?

Examination A careful general examination is essential with special attention to: • vital parameters e.g. BMI, temperature, BP • the thyroid and signs of hyperthyroidism • the abdomen (check liver, any masses and tenderness) • rectal examination (test stool for occult blood) • reflexes • look for acid dental erosion on surface of upper teeth (bulimia)

Investigations Basic investigations include: • • • • • • • • •

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haemoglobin, red cell indices and film white cell count ESR/CRP thyroid function test random blood sugar urea and electrolytes chest X-ray urine analysis faecal occult blood Others to consider:

• upper GIT (endoscopy or barium meal) • HIV serology • ultrasound of abdomen (or CT if suspected abnormality not found) • colonoscopy • LFTs • tumour markers e.g. CA-125, CEA

Weight loss in children Weight loss in children can be considered as: 1 failure to thrive (FTT): the child up to 2 years below 3rd percentile (refer to CHAPTER 91) 2 weight loss in a child after normal development

Loss of weight in the older child Acute or chronic infections are the most common causes of weight loss in children beyond infancy.3 In acute infections the weight loss is transient, and

once the infection clears the child generally regains the lost weight. In chronic infections signs may be more difficult to detect (e.g. urinary tract infection, pulmonary infection, osteomyelitis, chronic hepatitis). In common with the younger child who fails to thrive, the older child may be suffering from malabsorption syndrome, chronic infection of the urinary tract or a rare chromosomal or metabolic disorder.4 Tuberculosis, diabetes and malignant disease may present as weight loss and it is necessary to exclude organic disease before considering the more common emotional disorders.

Eating disorders in the adolescent Concerns about body image and dieting are very common among young women in modern society. Among these dieters 5–10% become abnormally preoccupied with dieting and slimness and progress to the eating disorders of anorexia nervosa and bulimia. Sufferers often have extremely low self-esteem and feel ineffective. They tend to be perfectionists with obsessive–compulsive traits. A history of childhood sexual abuse may be relevant. Media images alone do not cause eating disorders but have a role—genetic vulnerability, temperament, psychological and environmental factors also mediate these illnesses: ‘Genes load the gun—the environment pulls the trigger’.5 The DSM-5 criteria for diagnosing these disorders, which have serious physical and psychological consequences, are presented in TABLE  79.2. The differential diagnosis of anorexia nervosa includes most of the problems listed in TABLE 79.1.

Anorexia nervosa See FIGURE 79.2. Anorexia nervosa is a syndrome characterised by the obsessive pursuit of thinness through dieting with extreme weight loss and disturbance of body image.6 The main symptoms are anorexia and weight loss. The mortality rate may be as high as 18%. It has the highest mortality and suicide rate of any psychiatric disorder.5 Typical features • Adolescent and young adult females • Up to 1% incidence among schoolgirls aged 167 • Bimodal age of onset: 13–14 and 17–18 years6 • Unknown cause • Poor insight • Severe emaciation

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Weight loss

Table 79.2

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DSM-5 criteria for diagnosing anorexia nervosa and bulimia

Anorexia nervosa A Restriction of energy intake relative to requirements leading to significantly low body weight in context of age, sex and physical health. That weight is less than minimally normal or expected B Intense fear of gaining weight or becoming fat, despite current underweight status C Disturbance of body image (body size or shape) or persistent lack of recognition of seriousness of low body weight Types restricting type—no binge eating or purging binge eating/purging type Bulimia nervosa A Recurrent episodes of binge eating, that is: 1 eating in a discrete period of time an abnormal quantity of food compared with the average person 2 a sense of lack of control during the binge B Recurrent inappropriate compensatory behaviour to prevent weight gain (e.g. self-induced vomiting; misuse of laxatives, diuretics, enemas etc.); fasting or excessive exercise C A and B both occur, on average, at least twice a week for 3 months D Self-evaluation is unduly influenced by body shape and weight E Does not occur exclusively during periods of anorexia nervosa Types purging non-purging (e.g. fasting, excessive exercise)

FIGURE 79.2 18-year-old adolescent with severe anorexia nervosa (BMI 8.7). This patient survived after care by her GP. Photo and history courtesy Dr MM O’Brien

• • • • • •

Amenorrhoea Loss of body fat Sallow, dry and scaly skin, hair loss Increased lanugo body hair BMI 90% of people with agoraphobia develop it as a result of recurrent panic attacks.10 Management Reassurance, explanation and support (as for generalised anxiety). This is the mainstay of treatment. A patient who is experiencing a panic attack should be taught breathing techniques to help control hyperventilation (e.g. timing breaths, breathing through nose, slow inspiration, measured medium-sized breaths). Relaxation techniques can also be employed, such as progressive muscle relaxation, and patients can teach themselves these techniques via online resources (see TABLES  81.2 and 81.3). Rebreathing into a paper bag is rarely indicated in a general practice setting9,10 as the hyperventilation has usually settled by the time the patient presents. The above breathing techniques can be used by the patient anywhere and are more socially acceptable than breathing noisily into a paper bag when an attack is feared.

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The danger in a panic attack is the danger to the self by the self 8(e.g. fleeing into danger, non-intentional overdose).

Cognitive behaviour therapy (CBT) (See CHAPTER 5.) CBT aims to reduce anxiety by teaching patients how to identify, evaluate, control and modify their negative, fearful thoughts and behaviour. If simple psychotherapy and stress management fail then patients should be referred for CBT. Patients’ fears, especially if irrational, need to be clearly explained by the therapist, examined rationally and challenged, then replaced by positive calming thoughts.

Pharmacological treatment Pharmacological treatment is rarely of benefit in the acute attack, as the attacks occur too quickly for their effect to be of use. Antidepressants can be useful in reducing panic attacks and agoraphobia (see 9 TABLE 81.4) with the response rate being 60–90%.

Table 81.4

Dosage recommendations for SSRIs in anxiety disorders10

Drug

Initial dose

Maximum dose

citalopram

10 mg

40 mg

escitalopram

5 mg

20 mg

fluoxetine

10 mg

80 mg

fluvoxamine

50 mg

300 mg (split dose to bd over 150 mg)

paroxetine

10 mg

60 mg

sertraline

25 mg

200 mg

81 Continual use of benzodiazepines (BDZs, e.g. alprazolam or clonazepam) has previously been utilised in panic and other anxiety disorders but is now no longer recommended.10 Problems associated with benzodiazepine use include: • • • • • • •

impaired alertness, oversedation dependence increased risk of accidents adverse effects on mood and behaviour interaction with alcohol and other drugs potential for abuse and overdose risks during pregnancy and lactation

• • • • •

muscle weakness sexual dysfunction diminished motivation lowered sense of competency lower self-esteem

Some principles of using BDZs in anxiety disorders10 are: • always check for a history of problem alcohol or drug use • be wary of prescribing to unfamiliar patients, especially if asking for a particular drug by name (may indicate drug-seeking behaviour) • carefully discuss the potential for addiction with the patient • avoid using short-acting drugs as they are the most highly addictive • prescribe only small quantities of medication at a time • use only as short-term treatment • ensure regular review of the patient and continuity of care If already being used, BDZs should be tapered very slowly (this may take 6–12 months or longer). A benzodiazepine withdrawal syndrome, which can include rebound anxiety, depression, confusion, insomnia and seizures, may occur. Specialist drug and alcohol advice should be sought in such situations.

Phobic disorders In phobic states, the anxiety is related to specific situations or objects. Phobic disorders include agoraphobia, social anxiety disorder (otherwise known as social phobia) and specific phobias. Patients avoid these objects or situations, become anxious when they anticipate having to meet them and/or endure them with intense distress. A list of specific phobias is presented in TABLE 81.5. Common phobias are spiders, people and social situations, flying, open spaces, confined spaces, heights, cancer, thunderstorms, death and heart disease. The problem is seldom encountered in practice and there is usually no call for drug therapy.

Agoraphobia Avoidance includes staying away from many situations where there are issues of distance from home, crowding or confinement. Typical examples are travel on public transport, crowded shops and confined places. Patients fear they may lose control, faint and suffer embarrassment.

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Anxiety disorders

Table 81.5

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Social anxiety disorder

Phobias

Name of phobia

Fear of or aversion to

Acrophobia

Heights

Aerophobia

Draughts

Agoraphobia

Open spaces

Aichmophobia

Sharp objects

Ailurophobia

Cats

Algophobia

Pain

Androphobia

Men

Anthophobia

Flowers

Anthropophobia

People

Apiphobia

Bees

Aquaphobia

Water

Arachnophobia

Spiders

Astraphobia

Lightning

Aviatophobia

Flying

Bacteriophobia

Bacteria

Bathophobia

Depth

Belonephobia

Needles

Brontophobia

Thunder

Cancerophobia

Cancer

Cardiophobia

Heart disease

Claustrophobia

Closed spaces

Cynophobia

Dogs

Demonophobia

Demons

Dromophobia

Crossing streets

Equinophobia

Horses

Genophobia

Sex

Gynophobia

Women

Haptephobia

Being touched

Herpetophobia

Creeping, crawling things

Homophobia

Homosexuals

Hypsophobia

Falling

Hypnophobia

Going to sleep

Iatrophobia

Doctors

Social anxiety disorder is experienced in anxietyprovoking social situations in which the person feels subject to critical public scrutiny (e.g. canteens, restaurants, staff meetings, speaking engagements). It can either be generalised (fear of numerous social situations, including both performance and interactional situations) or non-generalised (fear of one or just a few situations of performance type). The treatments for the two subtypes are quite different (see TABLE  81.6). The sufferer may be a shy, selfconscious, premorbid personality. Social phobias, including performance anxiety and symptoms, are often related to sympathetic overactivity.

Table 81.6

First-line medication options for anxiety disorders10

Condition

Medication options

Generalised anxiety disorder

SSRI, duloxetine (30–120 mg), venlafaxine controlled release (75–225 mg)

Panic disorder

SSRI, venlafaxine controlled release (75–225 mg)

Obsessive-compulsive disorder

SSRI

Agoraphobia (without panic)

none

Social anxiety disorder (generalised)

SSRI, venlafaxine controlled release (75–225 mg)

Social anxiety disorder (non-generalised)

propranolol 10–40 mg orally, 30–60 minutes before the social event or performance

Specific phobias

none

Post-traumatic stress disorder

SSRI

Musophobia

Mice

Mysophobia

Dirt, germs, contamination

Necrophobia

Death

Neophobia

Anything new

Noctiphobia

Night

Numerophobia

Numbers

Nyctophobia

Darkness

Ochlophobia

Crowds

Management

Ophidiphobia

Snakes

Pyrophobia

Fire

Scotophobia

Blindness

Sociophobia

Social situations

The basis of treatment for all phobias is psychotherapy that involves behaviour therapy (e.g. graduated exposure therapy) and cognitive therapy.

Taphophobia

Being buried alive

Theophobia

God

Trypanophobia

Injections

Xenophobia

Strangers

Zoophobia

Animals

Obsessive–compulsive disorder (OCD) Anxiety is associated with obsessive thoughts and compulsive rituals.

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The obsessions are recurrent and persistent intrusive ideas, thoughts, impulses or images that are usually resisted by the patient. Compulsions are repetitive, purposeful and intentional behaviours conducted in response to an obsession to prevent a bad outcome for the person (e.g. excessive washing of the genitals). Mild obsessional or compulsive behaviour can be regarded as normal in response to stress. Management Optimal management is a combination of psychotherapeutic— particularly CBT—and pharmacological treatment, namely: • cognitive behaviour therapy for obsessions • exposure and response prevention for compulsions

Body dysmorphic disorder The person with this disorder has an exaggerated preoccupation with an imagined defect in appearance (see CHAPTER 45). Patients may be helped by counselling and psychotherapy.

Typical distressing recurrent symptoms: • intrusive features—recollections, nightmares, flashbacks • avoidance of events that symbolise or resemble the trauma • persistent negative alterations in cognitions and mood • hyperarousal phenomena: exaggerated startle response, irritability, anger, difficulty with sleeping and concentrating, hypervigilance, reckless or self-destructive behaviour

Treatment This is difficult and involves counselling, the basis of which is facilitating abreaction of the experience by individual or group therapy. The aim is to allow the patient to face up openly to his or her memories. Persistent symptoms are an indication for referral.

Pharmacological treatment SSRIs have limited evidence of some benefit, but response is slower than for their use in depression (trial for 8–12 weeks) and they should be used for at least 12 months.10

Hyperventilation

Acute stress disorder

81

This is defined as a constellation of abnormal anxiety-related symptoms lasting at least 3 days and occurring within 4 weeks of a traumatic event. The symptoms can include a sense of numbing, altered sense of reality, amnesia of the event, intrusive memories or dreams of the event, dissociative reactions, physiological reactions to triggers, avoidance of reminders, sleep disturbance, hypervigilance, anger and aggression, exaggerated startle response and agitation. It is appropriate to provide people with an acute stress reaction with debriefing and counselling (if agreeable); pharmacological intervention is rarely indicated.

Post-traumatic stress disorder (PTSD) PTSD is defined somewhat differently, in terms of time lapses from the traumatic event. It refers to a similar constellation of symptoms that persist for 1 month after exposure: • acute PTSD: duration of symptoms 15% in FEV1 and PEFR. • Inhalation challenge tests: airway reactivity is tested in a respiratory laboratory to inhaled histamine, methacholine or hypertonic saline. Sometimes useful to confirm diagnosis. • Mannitol inhalation test.

symptoms recurrent or seasonal worse at night or early morning history of allergies family history of asthma or allergies widespread audible wheeze on chest auscultation • symptoms rapidly relieved by a short-acting β-agonist bronchodilator (SAβA) Note: Asthma should be suspected in children with recurrent nocturnal cough and in people with intermittent dyspnoea or chest tightness, especially after exercise.

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Asthma • An exercise challenge may also be helpful. • Allergy testing may be appropriate. • Chest X-ray: not routine but useful if complications suspected or symptoms not explained by asthma.

Significant advances in the management of asthma 1

2 3 4 5

The realisation that asthma is an inflammatory disease. Therefore the appropriate first- or secondline treatment in moderate to severe asthma is inhaled sodium cromoglycate (especially in children) or inhaled corticosteroids (ICS). The regular use of spirometry. The use of spacers attached to inhalers/puffers. Improved and more efficient inhalers. Combined long-acting relievers and preventers including combinations of long-acting β-agonists (LAβA) and ICS—the fixed-dose inhalers.

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inhaled corticosteroids for the management of patients with moderately severe asthma.

Measurement of peak expiratory flow rate Patients with moderate to severe chronic asthma require regular measurement of PEFR, which is more useful than subjective symptoms in assessing asthma control. This allows the establishment of a baseline of the ‘patient’s best’, monitors changes, and allows the assessment of asthma severity and response to treatment. Spirometry including FEV1 is the gold standard (see CHAPTER 49). Peak flow meters are not a substitute for spirometry. There is considerable variation between users and instruments. However, they have a place in helping patients self-manage their asthma by serially recording their PEFR and comparing this with the best peak flow.

Spacers3 Reasons for suboptimal asthma control are presented in TABLE 82.1. Table 82.1

Reasons for suboptimal asthma control2,4

Poor compliance Inefficient use of inhaler devices Procrastination in introducing optimal therapy Failure to prescribe preventive medications, particularly inhaled corticosteroids for chronic asthma Using bronchodilators alone and repeating these drugs without proper evaluation Reliance on inappropriate alternate therapies Patient fears: • inhaled or oral corticosteroids • concern about aerosols and the ozone layer • overdosage • developing tolerance • embarrassment • peer group condemnation Doctor’s reluctance to: • use corticosteroids • recommend obtaining a mini peak flow meter • recommend obtaining a spacer

Large volume spaces Some people who have trouble using metered dose inhalers (MDIs) can have a special ‘spacer’ fitted onto the mouthpiece of the inhaler. One puff of the MDI is put in the spacer. The patient breathes in from its mouthpiece, taking one deep inhalation, then 1–2 very deep breaths, or 4–6 normal breaths (especially in children). This method is useful for adults having trouble with the MDI and for younger children (older than 3 years). Spacers are very efficient, overcome poor technique and cause less irritation of the mouth and throat (see FIG. 82.2). They allow increased airway deposition of inhalant and less oropharyngeal deposition.

82 inhaler (puffer)

Treating inflammatory airways disease If inflammatory airways disease is undertreated there is the risk of fixed irreversible airways obstruction from submucosal fibrosis. One of the most common mistakes in medical practice is to fail to introduce

spacer

FIGURE 82.2 Using a spacer device. Rules: children— single puff, then 4–5 breaths; adults—single puff, 1–4 breaths

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Note: It is recommended to dip plastic spacers into ordinary household detergent and dry in sunlight (no rinsing, no wiping) every 10 days or at least monthly.

Pharmacological agents to treat asthma Simple classification

Small volume spacers Children under 5–6 years and/or 20 kg can use an MDI and a small volume valved spacer (AeroChamber, Breath-A-Tech) with a face mask.

Management principles Starting treatment1 • Confirm the diagnosis. • Assess recent asthma control and risk factors (see TABLE 82.2). • Choose initial treatment appropriate to the above. • Document evidence—patient’s notes. • Identify management goals in collaboration. • Provide clear written patient information. • Educate and review regularly. Goals of management: • absent or minimal daytime symptoms and no nocturnal symptoms; restore normal airway function (>80% of predicted) • maintain best possible lung function at all times—keep asthma under control • reduce morbidity • control asthma with the use of regular antiinflammatory medication and relieving doses of β2-agonist when necessary Long-term goals: • achieve use of the least drugs, least doses and least side effects • reduce risk of fatal attacks • reduce risk of developing irreversible abnormal lung function

82

Definition of good asthma control • • • • • •

Minimal symptoms day and night No nocturnal waking due to asthma No limitation of normal or physical activity Minimal need for reliever medication No exacerbation Normal lung function (FEV1 and/or PEFR >80% predicted or best) • No side effects of medication • Near or near-normal lung function (i.e. >80% predicted)

• • •

Reliever = bronchodilator Preventer = anti-inflammatory Symptom controller = long-acting β2-agonist (LAβA)

It is useful to teach patients the concept of the ‘preventer’ and the ‘reliever’ for their asthma treatment. The pharmacological treatment of asthma is summarised in TABLE 82.3.

‘Preventer’ drugs or anti-inflammatory agents These medications are directed towards the underlying abnormalities—bronchial hyperreactivity and associated airway inflammation. Treatment with a ‘preventer’ is recommended if asthma episodes  are  >3/week or those who use SAβA >3 times a week. Corticosteroids

Inhaled (ICS) Types: • • • •

beclomethasone budesonide ciclesonide (single daily dose) fluticasone Dose range:

• 400–1600 mcg (adults); aim to keep below 500 mcg children and 1000 mcg (adults) Availability: • • • •

MDI Turbuhaler Autohaler Accuhaler Frequency:

• once or twice daily (helps compliance) Side effects: • oropharyngeal candidiasis, dysphonia (hoarse voice)—less risk with once daily ciclesonide • bronchial irritation: cough • adrenal suppression (doses of 2000 mcg/daily; sometimes as low as 800 mcg) Note: Rinse mouth out with water and spit out after using inhaled steroids.

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Asthma

Table 82.2

Severity/grade

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Asthma severity classification for an untreated newly diagnosed adult asthma patient5

Status before treatment

Lung function FEV1 or PEFR (% predicted)

Recommended β-agonist

Estimated starting daily dose range of ICS required to achieve good control

Intermittent

Episodic Symptoms 2 per month Symptoms regularly with exercise

≥ 80%

SAβA prn

500 mcg fluticasone >320 mcg ciclesonide

ICSs have a flat dose–response curve so it may not be necessary to prescribe above ICS doses considered high—beclomethasone or budesonide 1000 mcg/ day or fluticasone 500 mcg/day. For newly diagnosed patients with mild-to-moderate asthma ‘start low and step up prn’ (e.g. 250–400 mcg/day).4

Oral Prednisolone is used mainly for exacerbations. It is given with the usual inhaled corticosteroids and bronchodilators. Dose: • up to 1 mg/kg/day for 1–2 weeks Side effects: • these are minimal if drug is used for short periods

• long-term use: osteoporosis, glucose intolerance, adrenal suppression, thinning of skin and easy bruising Oral corticosteroids can be ceased abruptly.

82 Cromolyns These are sodium cromoglycate (SCG) and nedocromil sodium. SCG is available as dry capsules for inhalation, metered dose aerosols and a nebuliser solution. The availability of the metered aerosol and spacer has helped the use of SCG in the management of asthma in children. Adverse effects are uncommon; local irritation may be caused by the dry powder. Systemic effects do not occur.

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• Chronic disorders: continuing management

Pharmacological treatment of bronchial asthma5 Vehicle of administration

Generic types

Examples

Nebulising solution

Oral

Aerosol (metered dose inhalation)

Salbutamol

Ventolin









Salmeterol

Serevent





Terbutaline

Bricanyl

Eformoterol

Foradile, Oxis

Dry powder (inhalation)

Injection



Bronchodilators 1 β2-adrenoceptor agonists











Adrenaline



2 Anticholinergics

Ipratropium bromide

Atrovent

3 Methylxanthines

Theophylline

Nuelin



 

Aminophylline



Mast cell stabilisers Sodium cromoglycate

Intal Intal Forte

Nedocromil sodium

Tilade



Beclomethasone

QVAR (50, 100)





Budesonide

Pulmicort





Ciclesonide

Alvesco

Fluticasone

Flixotide



 



Corticosteroids—for inhalation



 





Leucotriene antagonists Combination reliever (LAβA) + preventer (LACS)—fixed combination MDI

82

Salmeterol + fluticasone (Seretide)



Eformoterol + fluticasone (Flutiform)



Eformoterol + budesonide (Symibort)







Vilanterol + fluticasone (Breoellipta)

Nedocromil is used for frequent episodic asthma in children over 2 years of age for the prevention of exercise-induced asthma and the treatment of mildto-moderate asthma in some adults. The initial dose is 2 inhalations qid. Adverse effects are uncommon.

Leucotriene antagonists These drugs, which include montelukast and zafirlukast, are very useful for seasonal asthma and aspirin-sensitive asthma and reduce the need for inhaled steroids or offer an alternative for those

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Asthma who cannot tolerate ICSs or have trouble using an inhaler. Favourable evidence is based on a small number of trials only, mostly in children but some adults benefit.6 Montelukast is taken as a 5 or 10 mg chewable tablet once daily.

Omalizumab This anti-IgE agent is marketed for SC injection in patients >12 years with moderate to severe allergic asthma treated by ICS and who have raised serum IgE levels.

Indications for preventive therapy7

Starting treatment Current treatment supports the initial treatment (summarised in TABLE  82.2) of a SAβA with low to moderate doses of ICS with estimated equivalent doses shown in the table. Initiate therapy sufficient to achieve best lung function promptly. Wean inhaled corticosteroids to the minimum dose needed to maintain adequate asthma control.

Guidelines for introducing preventive asthma therapy in adults and children include any of the following: • requirement of β2-agonist >3–4 times each week or >1 canister every 3 months (excluding preexercise) • symptoms (non-exercise) >3–4 times per week between attacks • spirometry showing reversible airflow obstruction during asymptomatic phases • asthma significantly interfering with physical activity despite appropriate pre-treatment • asthma attacks >every 6–8 weeks • infrequent asthma attacks but severe or lifethreatening

‘Reliever’ drugs or bronchodilators The three groups of bronchodilators are: • the β2-adrenoceptor agonists (β2-agonists)— short acting (SAβA) and long acting (LAβA) • methylxanthines—theophylline derivatives • anticholinergics β2-agonists These drugs ‘stimulate’ the β2 adrenoreceptors and thus relax bronchial smooth muscle. The inhaled route of delivery is the preferred route and the vehicles of administration include metered dose inhalation, a dry powder, and nebulisation where the solution is converted to a mist of small droplets by a flow of oxygen or air through the solution. Oral administration of β2-agonists is rarely required. The inhaled drugs produce measurable bronchodilation in 1–2 minutes and peak effects by 10–20 minutes. The traditional agents such as salbutamol and terbutaline are short-acting preparations. The new longer acting agents (LAβA) include salmeterol, eformoterol and vilanterol. These are to be used in combination, not as monotherapy.8 Theophylline derivatives These oral drugs may have complementary value to the inhaled agents but tend to be limited by side effects and efficacy.

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Prophylactic agents This term is reserved for those medications that are taken prior to known trigger factors, particularly for exercise-induced asthma. Exercise-induced asthma (options) • β2-agonist inhaler (puffer): two puffs 5 minutes immediately before exercise last 1–2 hours. LAβA such as salmeterol and eformoterol are more effective. • SCG or nedocromil, two puffs. • Combination β2-agonist + SCG (5–10 minutes beforehand). • Montelukast 10 mg (less in children ≥ 2 years) (o) daily or 1–2 hours beforehand. • Paediatricians often recommend a nondrug warm-up program as an alternative to medication.

Ongoing management The three-step asthma control plan9,10 The National Asthma Council of Australia has developed the following follow-up plan, summarised in FIGURE 82.3. Step 1: Assess asthma symptom control and identify the patient’s risk factors. • Assess asthma symptom control over the previous 4 weeks. • Assess the patient’s risk factors. • Exclude factors contributing to poor control before intensifying preventer treatment: — check adherence — check inhaler technique — check inhaler device is appropriate — consider that symptoms may be due to alternative or comorbid diagnoses

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Step 1 Assess asthma symptom control and risk factors for poor outcomes

1 2

Refe

rral

Step 2 Treat and adjust to achieve control

High e ICS/ r-dose LAβ A*

3 Step 3 Review response and monitor to maintain control

Few nts patie

Few nts patie

Low ICS/ -dose LAβ A*

Continue as-needed reliever*

930

e Som nts patie

FIGURE 82.3 Asthma: ongoing management steps Low

Source: Reprinted with permission from NPS Medicine Wise

-dos

e IC

S

Step 2: Treat and adjust to achieve good control. • All patients should have a reliever inhaler for asneeded use. • Most patients can achieve well-controlled asthma with low-dose ICS. • Trial low-dose ICS before ICA/LAβA fixed combination therapy11 • Reserve ICS/LAβA as a later option. • Where appropriate, step down treatment. • Schedule follow-up visit. See TABLE 82.3. Step 3: Review response and monitor to maintain control. • Review diagnosis and treatment regularly. • Monitor to maintain control. A general management plan for chronic asthma is summarised in FIGURE 82.4.

As-n

eed

ed S

AβA

t Mos nts e ti a p

All nts patie

FIGURE 82.4 Stepped approach to adjusting asthma medication in adults10 Source: Reprinted with permission from NPS Medicine Wise

The two main techniques The open-mouth technique and the closed-mouth technique are the main methods, and both are effective but the closed-mouth technique is preferred. Both techniques are suitable for most adults. Most children from the age of 7 can learn to use puffers quite well.

The closed-mouth technique

Practice tip •

82

See FIGURE 82.5.

For breakthrough asthma or persistent poorly controlled asthma with poor compliance switch to combined medication (e.g. Seretide MDI Accuhaler, or Symbicort).

Correct use of the asthma MDI (puffer) Did you know that: • faulty inhaler technique occurs in at least onethird of users? • 90% of the medication sticks to the mouth and does not reach the lungs? • it is the inhalation effort—not the pressure from the aerosol—that gets the medication to the lungs? • it is important to instruct patients properly and check their technique regularly?

FIGURE 82.5 Using the metered dose inhaler: the closedmouth technique

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Asthma Instructions for patients: 1 Remove the cap. Shake the puffer vigorously for 1–2 seconds. Hold it upright (canister on top) to use it (as shown). 2 Place the mouthpiece between your teeth but do not bite it and close your lips around it. 3 Breathe out slowly and gently to a comfortable level. 4 Tilt your head back slightly with your chin up. 5 Just as you then start to breathe in (slowly) through your mouth, press the puffer firmly, once. Breathe in and hold as far as you can over 3–5 seconds. (Do not breathe in through your nose.) 6 Remove the puffer from your mouth and hold your breath for about 10 seconds; then breathe out gently. 7 Breathe normally for about 1 minute, and then repeat the inhalation if you need to.

Extra points • The usual dose of standard MDI is one or two puffs (adult) every 3–4 hours for an attack (four puffs in children). • If you do not get adequate relief from your normal dose, you should contact your doctor. • It is quite safe to increase the dose, such as to 4–6 puffs. • If you are using your inhaler very often, it usually means your other asthma medication is not being used properly. Discuss this with your doctor.

Autohaler The Autohaler is a breath-activated MDI which can improve lung deposition in patients with poor inhaler technique.

The Turbuhaler The Turbuhaler is a dry powder delivery system that is widely used as an alternative to the MDI. It is a breath-activated device. Other dry powder devices are the Accuhaler and Diskhaler.

Spacers versus nebulisers Both MDIs via a spacer and dry powder inhalers are at least as effective as a nebuliser for treating acute exacerbations in both adults and children.12

Summary of devices •

Breath-activated MDIs: Autohaler

•

• •

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Breath-activated dry powder inhalers: Accuhaler, Aerolizer, Diskhaler, Rotahaler, Spinhaler, Turbuhaler Large-volume spacer: Nebuhaler, Volumatic Small-volume spacer: Aerochamber, Breath-A-Tech

Dangerous asthma Failure to recognise the development of a severe attack has cost the lives of many asthmatics. The severe attacks can start suddenly (even in mild asthmatics) and catch people by surprise.

High-risk patients People who have experienced one or more of the following are more likely to have severe attacks: • previous severe asthma attack • previous hospital admission, especially admission to intensive care • hospital attendance in the past 12 months • long-term oral steroid treatment • carelessness with taking medication • night-time attacks, especially with severe chest tightness • recent emotional problems • frequent SAβA use Early warning signs of severe asthma or an asthma attack: • symptoms persisting or getting worse despite adequate medication • increased coughing and chest tightness • poor response to two inhalations • benefit from inhalations not lasting 2 hours • increasing medication requirements • sleep being disturbed by coughing, wheezing or breathlessness • chest tightness on waking in the morning • low PEFR readings

Dangerous signs • Marked breathlessness, especially at rest • Sleep being greatly disturbed by asthma • Asthma getting worse quickly rather than slowly, despite medication • Feeling frightened • Difficulty in speaking; unable to say more than a few words • Pulsus paradoxus • Exhaustion and sleep deprivation

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• Drowsiness or confusion • Chest becoming ‘silent’ with a quiet wheeze, yet breathing still laboured • Cyanosis • Chest retraction • Respiratory rate greater than 25 (adults) or 50 (children) • Pulse rate >120 beats/min • Peak flow 65 years Smoking Diabetes mellitus Dyslipidaemia (total cholesterol >6.5 mmol/L, >250 mg/dL or LDL-cholesterol >4.0 mmol/L, >155 mg/dL or HDL-cholesterol M 1 g/day (with or without diabetes)

300 mg/day) • stroke/TIA

90 mmHg on several occasions

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Start lifestyle changes. Assess 5-year absolute cardiovascular risk.

low risk (10%)

moderate risk (10–15%)

Maintain lifestyle changes for 6–12 months. Consider drug treatment if BP remains > 150/95 mmHg.

Maintain lifestyle changes for 3>6 months. Consider drug treatment if BP remains > 140/90 mmHg.

High risk (> 15%) or associated clinical conditions or target organ disease or high-risk ethnic groups

Maintain lifestyle changes, begin drug treatment immediately.

FIGURE 86.7 Decision tree for managing hypertension As recommended by the National Heart Foundation

The upper limits of normal BP for children in different age groups are:1 Age (in years)

Arterial pressure (mmHg)

14–18

135/90

10–13

125/85

6–9

120/80

5 or less

110/75

The proper cuff size is very important to avoid inaccurate readings and a larger rather than a smaller cuff is recommended. The width of the bladder should cover 75% of the upper arm. In infants and toddlers, use of an electronic unit may be necessary. Although cessation of sound (phase 5) is the better reflection of true diastolic pressure, there is often no disappearance of sound in children and so estimation of the point of muffling has to be recorded. Diagnostic evaluation and drug treatment for children are similar to those for adults. When a child is obese, reduction in weight may adequately lower BP. ACE inhibitors or calcium-channel blocking agents are preferable in the young hypertensive, with diuretics a second agent. ACE inhibitors should be avoided in postpubertal girls.

Guidelines for treatment • Isolated systolic hypertension is worth treating.17 • Older patients may respond to nonpharmacological treatment. • Reducing dietary sodium is more beneficial than with younger patients. • If drug treatment is necessary, commence with half the normal recommended adult dosage— ‘start low and go slow’. • Patients over 70 years and in good health should be treated the same as younger patients. • A gradual reduction in BP is recommended. • Drug reactions are a limiting factor. • Drug interactions are also a problem: these include NSAIDs, antiparkinson drugs and phenothiazines. Specific treatment • First-line choice: indapamide (preferred) or thiazide diuretic (low dose);1 check electrolytes in 2–4 weeks: if hypokalaemia develops add a K-sparing diuretic rather than K supplements. Use a combination thiazide and K-sparing diuretic. Diuretics may aggravate bladder difficulties (e.g. incontinence). • Second line choice: ACE (or ARB) inhibitors (especially with heart failure)

Hypertension in the elderly

Other effective drugs (especially for isolated systolic hypertension):

BP shows a gradual increasing linear relationship with age.

• β-blockers (low dose) where diuretic cannot be prescribed or if angina

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• calcium-channel blockers

When to refer4

Both these groups are generally well tolerated but constipation may be a problem with verapamil. Kidney function and electrolytes should be monitored when ACE inhibitors are started.

• Refractory hypertension—adequate control not possible and cause not obvious • Suspected ‘white coat’ hypertension—for ambulatory BP monitoring • Severe hypertension—diastolic BP >115 mmHg • Hypertensive emergency • If there is evidence of ongoing target organ impairment • If there is significant kidney impairment eGFR 140 mmHg or diastolic pressures >90 mmHg are required for the diagnosis.

Choice of drugs in patients with coexisting conditions Diuretic

ACE inhibitors ARBs

Calcium-channel blockers  β-blockers

Asthma/COPD







 Caution

Bowel disease/constipation









Bradycardia/heart block





Care



Cardiac failure

*

*

Care



Depression





 Care



Diabetes



*



 Care

Dyslipidaemia









Hyperuricaemia/gout



*

*



Impotence









Ischaemic heart disease





*

*

Peripheral vascular disease





*



Pregnancy







 Not in late term

Raynaud phenomenon





*



Kidney artery stenosis





* Care

* Care

Kidney failure



Care





Tachycardia (resting)





Care

*

*Drugs of choice. Calcium-channel blockers need to be selected with care—some are suitable, others not.

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Hypertension

• • • •

•

• •

Beware of using β-blockers in a patient with a history of wheezing. Add only one agent at a time and wait about 4 weeks between dosage adjustments. Excessive intake of alcohol can cause hypertension and hypertension refractory to treatment. If hypertension fails to respond to therapy, an underlying kidney or adrenal lesion may have been missed. The low-pitched bruits of kidney artery stenosis are best heard by placing the diaphragm of the stethoscope firmly in the epigastric area. Older patients may respond better to diuretics, calcium-channel blockers and ACE inhibitors. Younger patients may respond better to β-blockers or ACE inhibitors.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Hypertension

References 1 Sandler G. High blood pressure. In: Common Medical Problems. London: Adis Press, 1984: 61–106. 2 Guidelines Subcommittee 1999. WHO–ISH guidelines for the management of hypertension. J Hypertens, 1999; 17: 151–83. 3 Practice guidelines for primary care physicians: 2003 ESH/ ESC Hypertension Guidelines. J Hypertens, 2003; 21 (10): 1779–86. 4 Stokes G. Essential hypertension. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 252–4.

5 Royal Australian College of General Practitioners. Guidelines for Preventive Activities in General Practice (8th edn). Melbourne: RACGP, 2013: 51–3. 6 Bates B. A Guide to Physical Examination and History Taking (5th edn). Philadelphia: Lippincott, 1991: 284. 7 National Heart Foundation of Australia. Guide to Management of Hypertension. Canberra: National Heart Foundation of Australia, 2008 (updated 2012). 8 Hovell MF. The experimental evidence for weight loss treatment of essential hypertension: a critical review. Am J Public Health, 1982; April 72 (4): 359–68. 9 Blair SN, Goodyear NN, Gibbons LW et al. Physical fitness and incidence of hypertension in healthy normotensive men and women. JAMA, 1984; 252 (4): 487–90. 10 Rouse IL, Beilin LJ. Vegetarian diet and blood pressure. Editorial review. J Hypertens, 1984; 2: 231–40. 11 Jennings G, Sudhir K. Initial therapy of primary hypertension. Med J Aust, 1990; 152: 198–202. 12 Moulds R (Chair). Therapeutic Guidelines: Cardiovascular (Version 6). Melbourne: Therapeutic Guidelines Ltd, 2012. 13 Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in prevention of cardiovascular disease: meta analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies. BMJ, 2009 May 19; 338: b1665. 14 Kjeldsen SE, Jamerson KA, Bakris GL et al. Avoiding Cardiovascular events through COMbination therapy in Patients LIving with Systolic Hypertension investigators. Predictors of blood pressure response to intensified and fixed combination treatment of hypertension: the ACCOMPLISH study. Blood Press, 2008; 17: 7–17. 15 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013. 16 Yusef S et al. Effects of an angiotensin-converting inhibitor, ramipril, on cardiovascular events in high risk patients. The Heart Outcomes Prevention Evaluation Investigations. N Engl J Med, 2000; 342: 145. 17 SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA, 1991; 265: 3255–64.

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Dyslipidaemia

The landmark Scandinavian Simvastatin Survival Study (4S) published in 1994, may well be remembered as the study that finally put to rest many of the apprehensions and misconceptions regarding lipid-lowering therapy. Duffy and Meredith  Dyslipidaemia is the presence of an abnormal lipid/lipoprotein profile in the serum and can be classified as: • predominant hypertriglyceridaemia • predominant hypercholesterolaemia • mixed pattern with elevation of both cholesterol and triglyceride (TG) Modern epidemiological studies have established the facts that elevated plasma cholesterol causes pathological changes in the arterial wall leading to CAD, and that lipid-lowering therapy results in reduction of coronary and cerebrovascular events with improved survival. These studies, which can be summarised by their acronyms—4S,2 PLACI,3 PLACII,4 ACAPS,5 KAPS6 and REGRESS7—all reinforce the benefits of lipidlowering therapy for dyslipidaemia and the primary prevention of coronary heart disease (CDH). One systematic review showed that statins and n-3 fatty acids are the most favourable lipid-lowering interventions, with reduced risks of overall and cardiac mortality.8 The main focus of treatment will be on primary dyslipidaemia but secondary causes (see TABLE  87.1) also need to be addressed. LDL-C is the lipid with the highest correlation with CHD. 9,10,11

Established facts

• Major risk factors for CAD include: — increased LDL cholesterol + reduced HDL cholesterol — ratio LDL-C:HDL-C >4 • Risk increases with increasing cholesterol levels (90% if >7.8 mmol/L) • TG levels >10 mmol/L increases risk of pancreatitis • Management should be correlated with risk factors • 10% reduction of total cholesterol gives 20% reduction in CAD after 3 years

• LDL-C reduction with statin therapy reduces heart attacks, stroke, the need for revascularisation and death Table 87.1

Common causes of secondary dyslipidaemia

Hypothyroidism Nephrotic syndrome Type 2 diabetes Cholestasis Anorexia nervosa Obesity Kidney impairment Alcohol excess Obstructive liver disease

Investigations10 The following fasting tests are recommended in all adult patients 18 years and over: • serum triglyceride level • serum cholesterol level and HDL-C and LDL-C levels if cholesterol ≥5.5 mmol/L • TFTs if overweight elderly female Confirm an initial high result with a second test at 6–8 weeks. Patients requiring treatment are summarised in TABLE  87.2. Testing should occur at least every 5 years.

Recommended treatment goals • • • • •

Total cholesterol for updates.

9

and 13 years • boys >14 years Significant causes include: • constitutional delay of growth and puberty (CDGP) is usually familial and the commonest cause. It is associated with delayed growth and bone age • chronic illness (e.g. severe asthma, cystic fibrosis, kidney failure) • poor nutrition and exercise • anorexia nervosa Other less common causes include chromosomal abnormalities (e.g. Turner syndrome) and gonadal hormone deficiency (e.g. Kallman syndrome, postchemotherapy). Consider referral to a paediatric endocrinologist for investigation and management, which can include testosterone for boys and oestrogen for girls.

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Precocious puberty10 Puberty is trending earlier than in previous generations, known as the ‘secular trend’, and is presumed to be due to improved nutrition and absence of chronic disease. True precocious puberty is considered to be: • girls 12 months

• inguinal hernia

ASAP, especially infants and irreducible hernias Reducible hernias: the ‘6–2’ rule Birth–6 weeks: surgery within 2 days 6 weeks–6 months: surgery within 2 weeks Over 6 months: surgery within 2 months

• femoral hernia

ASAP

• torsion of testicle

Surgery within 4 hours (absolutely 6 hours)

• hydrocele

Leave to 12 months, then review (often resolve; if not, repair by 2 years)

• varicocele

Leave and review

Other hernias: • umbilical hernia

Leave to age 4 Surgery after 4 if persistent (tend to strangulate) Never tape down

• para-umbilical hernia

Any age—best after 6 months

• epigastric hernia

Any age—best after 6 months

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Leg and foot development problems: • developmental dysplasia hip

Most treated successfully by abductor splinting (e.g. Pavlik harness)

• bow legs (genu varum)

Normal up to 3 years Usually improve with age: refer if ICS> 6 cm

• knock knees

Normal 3–8 years, then refer if IMS> 8 cm

• flat feet

No treatment unless stiff and painful

• internal tibial torsion

Refer 6 months after presentation if unresolved

• medial femoral torsion

Leave to 8 years, then refer if unresolved

• metatarsus varus

Refer 3 months after presentation if unresolved

• Exomphalos (intestinal contents in a sac) Action: nasogastric tube, IV dextrose drip, temperature control, refer • Gastroschisis (exposed bowel contents through anterior wall defect) Action: as for exomphalos; cover with plastic wrap • Pierre–Robin syndrome: micrognathia + cleft palate + respiratory obstruction from tongue

Action: early referral • Tension pneumothorax Action: intercostal needle/catheter with aspiration • Myelomeningocele and meningocele Action: early neurosurgical referral Note the importance of plain X-rays as urgent firstline investigations and early surgical referral.

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Surgical problems in children

Other important childhood emergencies • Pyloric stenosis: projectile vomiting weeks 2–6, epigastric ‘tumour’ • Torsion of testis: severe groin/low abdominal pain + vomiting • Intussusception: pallor + abdominal pain (severe and intermittent) + inactivity • Acute appendicitis: abdominal pain + a/n/v + guarding • Peritonitis • Intestinal obstruction: colicky pain + vomiting + distension • Irreducible inguinal hernia • Paraphimosis • Cerebral abscess • Meckel diverticulum—diverticulitis or haemorrhage • Various neoplasias

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References 1 MacGill KA. Paediatric plastic surgery. Australian Doctor, 9 September 2005: 32. 2 Hutson JM, Woodward A, Beasley SW. Jones Clinical Paediatric Surgery. Oxford: Blackwell Publishing, 2003: 18–72. 3 Lalakea ML, Messner AH. Ankyloglossia: does it matter? Pediatr Clin North Am, 2003; 50: 381–97. 4 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 3). Melbourne: Therapeutic Guidelines Ltd, 2009: 209. 5 Kerr G, Barnett P. Orthopaedic conditions. In: Smart J (ed), Paediatric Handbook (6th edn). Melbourne: Blackwell Science, 2000; 454–9. 6 Jones PG. Clinical Paediatric Surgery. Sydney: Ure Smith, 1970: 16–19. 7 Thomson K, Tey D, Mark M. Paediatric Handbook (7th edn). Oxford: Wiley-Blackwell, 2009: 532–42.

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Common childhood infectious diseases (including skin eruptions)

The physical signs of measles are nearly the same as those of smallpox, but nausea and inflammation is more severe. The rash of measles usually appears at once, but the rash of smallpox spot after spot . . . Avicenna (–)

Chickenpox (varicella) Epidemiology Chickenpox has become much less common since the introduction of the varicella vaccine in 2000 and its inclusion on the National Immunisation Program in 2005, because of both individual and herd immunity.1 Prior to this, nearly all children acquired it (15 minutes • face-to-face contact • household contact The results are interpreted as:

possible lymphadenopathy

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erythematous ‘slapped’ cheek appearance in well child

erythematous rash, mainly on forearms and thighs

• IgG alone detected—immune • IgM detected—false positive or early infection. Repeat in 2 weeks to see if rising IgG levels • IgM and IgG not present—susceptible. If susceptible and becomes unwell, repeat test If infection occurs in the first half of pregnancy, the fetus may become anaemic (the virus replicates in erythroid progenitor cells) and hydrops fetalis and miscarriage can occur. Women in this situation should be reassured that 15 mm diameter, usually unilateral, single, non-purulent and painful) circumoral pallor strawberry tongue

background erythema with tiny fine superimposed puncta (scarlet spots) Pastia lines

FIGURE 93.10 Scarlet fever: typical presentation of rash

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Treatment Phenoxymethylpenicillin (dose according to age) for 10 days with rapid resolution of symptoms. Children can return to school 24 hours after taking antibiotics and feeling well.

Kawasaki disease5,6 This is an uncommon but important systemic vasculitis, usually in children under 5 years of age, likely caused by an infection, though the presumed agent remains unknown. It is characterised by an acute onset of fever >39°C of 5 days or more and accompanied by 4 out of 5 of the following features: • polymorphous rash • bilateral (non-purulent) conjunctival infection • mucous membrane changes, e.g. reddened or dry cracked lips, strawberry tongue, diffuse redness of oral or pharyngeal mucosa • peripheral changes, e.g. erythema of the palms or soles, oedema of the hands or feet (and in convalescence desquamation)

Other diseases with similar signs should be excluded (e.g. staph or strep infections, measles, viral exanthems, drug reactions or JRA). Kawasaki disease can be elusive as there are variations with atypical or incomplete manifestations. Think of it in a miserable child with a high fever ≥5 days and arrange for paediatric review if suspicious. Blood results will also help contribute to the diagnosis and management decisions (e.g. ESR and CRP usually raised, thrombocytosis often raised in second week, neutrophilia, normochromic normocytic anaemia, hypoalbuminuria, abnormal LFTs). The disease is generally benign and self-limiting but it is important to make an early diagnosis because early treatment may prevent complications (which also occur in the atypical cases). The major complication is vasculitis, which causes coronary aneurysms and ectasia in 15–25% of untreated cases, and which can lead to ischaemic heart disease and sudden death either at the time or years later. The aneurysms usually develop between the second week and the second month of the illness. Early treatment with immunoglobulin and aspirin has been shown to be effective in reducing the prevalence of coronary artery abnormalities. Echocardiography is used to detect the aneurysms and determine prognosis.

Mumps1 Mumps is an acute infectious disease caused by a paramyxovirus with an affinity for the salivary glands and meninges. It is usually transmitted by respiratory secretions or saliva. A third of infections are asymptomatic, and most of the others have nonspecific symptoms, such as fever, headache, malaise, myalgia and anorexia. The classic parotitis occurs in only two-thirds of clinical cases and is usually bilateral. The submandibular and sublingual glands are less commonly involved. About 6% of patients will have presternal oedema resembling cellulitis of the neck. Mumps can result in spontaneous abortion if contracted in the first trimester of pregnancy. Maternal infection is not associated with an increased risk of congenital malformations. Prior to vaccination, cases peaked in the 5–9year age group; however, since 2000 it is now most commonly seen in adolescents and young adults. Recent outbreaks have occurred in the developed world in areas of declining vaccination rates.

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Common childhood infectious diseases (including skin eruptions) Clinical diagnosis Enlargement of the cervical lymph glands can be mistaken for parotitis but the correct diagnosis is indicated by the anatomy of this area. Lymph nodes are posteroinferior to the ear lobe; the parotid gland is anterior and, when enlarged, obscures the angle of the mandible. Bacterial (suppurative) parotitis is associated with toxaemia and results in a high leucocyte count. The skin over the parotid gland is tense and shiny and the Stensen duct might discharge pus. Rare disorders such as Sjögren syndrome can be misdiagnosed as mumps. Complications The complications are summarised in TABLE 93.6. Orchitis, usually unilateral, occurs in 15–30% of postpubertal males, developing 3–4 days after parotitis. Subsequent sterility is rare, even if both testes are affected. Aseptic meningitis is common but benign. Many patients suffer transient abdominal pain and vomiting. Table 93.6

Complications of mumps

Common Orchitis Meningeal symptoms (10%) Abdominal pain (transient) Rare Oophoritis Encephalitis Arthritis (one or several joints) Deafness (usually transient) Pancreatitis

Management Treatment is symptomatic. Paracetamol may be prescribed for fever, meningitis and orchitis. The patient with orchitis should use supportive underwear. Children should be excluded until 9 days after the onset of the parotitis.

Epstein–Barr mononucleosis Although glandular fever is more common in adolescents and young adults, it can occur in young children but is often asymptomatic or atypical. The differential diagnosis includes cytomegalovirus

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infection and acute lymphatic leukaemia. Diagnosis is confirmed by specific antibody tests. Refer to CHAPTER 28.

Pertussis1,7 Pertussis (whooping cough) is a respiratory infection (a bronchitis) caused by Bordetella pertussis and occurs worldwide. Other organisms (Bordetella parapertussis, Mycoplasma pneumoniae, Chlamydia pneumoniae) can cause a pertussis-like syndrome. Despite vaccination, pertussis remains prevalent in Australia, and is the least well-controlled vaccine-preventable disease. Between 2000 and 2010 multiple epidemics caused over 139 000 confirmed cases. The greatest risk of severe infection and complications is to infants with their soft and easily damaged airways, especially before the first 2 vaccine doses are administered. Adolescents and adults with waning immunity (both from vaccination and previous infection) are often the source of infection, in particular the parents (>50% of identified primary cases). Clinical features Pertussis is highly infectious, with B. pertussis spreading to >90% of household contacts. The incubation period is 7 to 20 days. The classical paroxysmal cough followed by an inspiratory whoop is less common in older children and adults, or children who have partial immunity from vaccination. A prolonged cough may be the only presenting feature, and in local epidemics every cough needs to be approached with a suspicion for pertussis. B. pertussis accounts for 7% of cough illnesses in adults, and given that each year 25% of adults have a cough ≥5 days duration, many cases go undiagnosed. The primary goal of preventing complications and deaths is centred on protecting children, particularly infants (see Prevention below). The fatality rate in unvaccinated infants less than 6 months is 8 per 1000 cases. The most common cause of death is pertussis pneumonia, sometimes complicated by seizures and hypoxic encephalopathy. Apnoea and cyanosis from coughing spasms are also common in the very young. Even in adults the cough can be very distressing and prolonged. Pertussis is also referred to as the ‘100 day cough’. This can lead to issues with sleep disturbance, work performance (especially when dealing with machinery or driving) and rarely rib fractures. Classic whooping cough is characterised by cough and coryza for 1 week (catarrhal phase) followed by

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paroxysms of a more pronounced cough (paroxysmal phase). Fever is uncommon, there are often no other clinical signs, and children are well between coughing paroxysms. Vomiting may follow a coughing spasm (a ‘cough-vomit’). Diagnosis As well has having a high index of suspicion with coughing patients (both immunised and nonimmunised), particularly in outbreaks, any suspicion should lead to PCR testing of nasopharyngeal aspirate/swab. Complications • Neurological: asphyxia, hypoxia, seizures, cerebral haemorrhages • Pulmonary: atelectasis, pneumonia, pneumothorax, bronchiectasis Treatment7,8 Treatment during the catarrhal phase or early in the paroxysmal stage may ameliorate symptoms. Treatment early in the disease will help reduce infectiousness; however, once the cough has been present for 3 weeks there is little risk of infectiousness. Options include:

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• azithromycin — 6 months: 10 mg/kg on day 1 (up to 500 mg) then 5 mg/kg (up to 250 mg) for a further 4 days • clarithromycin — >1 month: 7.5 mg/kg (up to 500 mg) bd for 7 days • erythromycin — >1 month: 10 mg/kg (up to 250 mg, or 400 mg if ethyl succinate) qid for 7 days Cough mixtures are ineffective. Good ventilation is important: avoid dust and smoke, and also emotional excitement and overfeeding during the paroxysmal phase. All infants under 6 months and older children with complications (e.g. apnoea, cyanosis, pneumonia, encephalopathy) require admission to hospital. Treatment of contacts8 High-risk contacts of a pertussis case (those with close/household contact and who may be vulnerable to complications, or transmit to others who are vulnerable) should be treated with the same medications, dosage and duration as above. There is

little evidence that prophylactic antibiotic treatment of contacts reduces secondary transmission outside of household settings (i.e. not in child-care centres, preschools, schools or workplaces). State public health officers should be contacted to determine which contacts require prophylaxis. Prevention8 Other strategies to reduce the incidence of pertussis and its complications, particularly in infants, include: • a ‘cocoon’ strategy of vaccinating any adults who are or will be in close contact with an infant. Fathers and other adult contacts can be vaccinated before the birth • mothers should be vaccinated in pre-pregnancy planning or straight after delivery. Alternatively, if more than 5 years has elapsed since their last previous dose, a pertussis vaccine should be given in their third trimester (which will boost maternal antibodies that are transmitted in utero to the about-to-be-newborn) • a single booster dose of pertussis-containing vaccine is recommended in health care workers and other adults in regular contact with young children (booster required after 10 years)

Herpes simplex9 Herpes simplex virus (HSV) infection is common and widespread. Primary HSV infection is usually a disease of childhood readily transmitted through direct contact, with the majority of the population being infected in early childhood. Many cases are asymptomatic or non-specific. The specific gingivostomatitis occurs in 25–30% of cases and can be severe and acute. Clinical features Typical clinical features of the primary infection: • • • • • •

children 1–3 years fever and refusal to feed ulcers on gums, tongue and palate prone to dehydration may be lesions on face and conjunctivae resolution over 7–14 days

Pushing fluids and monitoring for dehydration is important. Topical lignocaine preparations can help. Paracetamol is often not useful, though if the child is very distressed codeine-containing compounds (Painstop) can be considered. Topical antivirals usually do not contribute and are not recommended.

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Common childhood infectious diseases (including skin eruptions) Serious complications (seek specialist advice): • encephalitis can develop in otherwise healthy children (see CHAPTER 30) • eczema herpeticum—children with eczema can get widespread severe herpetic lesions • disseminated HSV infection in neonates (avoid contact until recovered) • HSV can be a serious issue in the immunocompromised patient

Impetigo10 Impetigo (school sores) is a contagious superficial bacterial skin infection caused by Streptococcus pyogenes or Staphylococcus aureus or a combination of these two virulent organisms. There are two common forms: 1 vesiculopustular with honey-coloured crusts (either strep or staph) 2 bullous type, usually S. aureus

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Head lice10 Head lice is an infestation caused by the louse Pediculus humanus capitis (see FIG. 93.11). The head louse is about 1–3 mm in length, white to grey, wingless and has a flat elongated body. They spread through close contact, and do not jump or fly. The female louse lays eggs (or ‘nits’), which are glued to the hairs a few millimeters from the scalp. The nit moves away from the scalp as the hair grows. They hatch at around 8 days, mature into adults in about 10 days and live for about a month. Head lice spread from person to person by direct contact, such as sitting and working very close to one another. They can also spread by the sharing of combs, brushes and headwear, especially within the family. Children are the ones usually affected, but people of all ages and from all walks of life can be infested. It is more common in overcrowded living conditions but is not a reflection of poor hygiene. Resistance to the usual agents is becoming a problem.

Treatment If mild with small lesions and a limited area: • soak a clean cloth in a mixture of ½ cup white vinegar and 1 L of tepid water. Apply the compress to moist areas for 10 minutes several times a day then wipe off crusts (alternatively just use soap and water) • antiseptic (povidone iodine, chlorhexadine) or mupirocin (Bactroban), a small amount tds for 10 days. Topical antibiotics other than mupirocin 2% (Bactroban) are not recommended • general measures while still oozing or crusted: — cover the sores — avoid close contact with others (especially touch and bathing contact) — regular hand washing — use separate towels and cloths — change and launder clothes and linen daily If extensive and causing systemic symptoms: flucloxacillin/dicloxacillin 12.5 mg/kg up to 500 mg) 6 hourly for 10 days or cephalexin 25 mg/kg up to 1 g 12 hourly for 10 days Boils (furunculosis) and carbuncles can use the same treatment as impetigo. The child should be excluded from child-care settings until antibiotic treatment has commenced. Any sores on exposed skin should be covered with a watertight dressing.2

louse (enlarged)

FIGURE 93.11 Louse (enlarged)

Clinical features Infestations can vary from a few dozen to hundreds of lice and eggs. • • • • •

Asymptomatic or itching of scalp White spots of nits can be mistaken for dandruff Unlike dandruff, the nits cannot be brushed off Diagnosis by finding lice (or ‘nits’) Occasionally the eyelashes can be affected (use physical removal methods outlined below) • ‘Wet combing’ (see below) improves detection rate Treatment Treatment can be based on physical methods, chemical methods or both (the most effective). Physical methods Wet combing: • Inspection—look for both lice and nits behind and above the ears and at the back of the scalp. • Treat all members of family at the same time.

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• Have ready a metal nit comb (available at pharmacies), a good light, some paper towels or tissues and lots of cheap hair conditioner. Sitting a child in front of the TV will help them keep still (it takes around 30 minutes). • Wet the hair with a handful or two of conditioner. • Work through the hair in sections, removing resistant nits by combing down the hair towards the shaft. • Wipe the conditioner onto tissues or paper towels, where the lice and nits will be visible. Repeat the combing routine for at least 2 more consecutive nights. Repeat weekly until no lice are found on 3 consecutive nights (nits may persist but do not necessarily mean active infection—they may be empty or dead eggs). Other physical measures include: • machine wash bed-linen, clothes, towels in hot water • items that can’t be washed such as soft toys/ helmets should be placed in an airtight plastic bag for two weeks • vacuum pillows • spray hairbrushes and combs with fly spray Chemical treatments Insecticides used to treat head lice include:

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• malathion • permethrin • phenothrin These applications can be irritating to the scalp, so use caution in children prone to atopic dermatitis; following the manufacturer’s instructions carefully is important. A second application 7 days after the first may be required. Many other methods are used and recommended for head lice, both commercially available or ‘home remedies’, which may or may not be useful. These include suffocating agents (e.g. mayonnaise, olive oil, petroleum jelly), natural oils and cutting the hair short (especially in boys e.g. a No. 1 cut). Treatment failure and/or reinfestation is common. The former can be from inappropriately applied treatments, resistance to chemical treatments or misdiagnosis of old nits as active infection.

Community or school-wide education programs can also keep infestation rates down.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Chickenpox (varicella) • Hand, foot and mouth disease • Head lice • Herpes simplex (cold sores) • Impetigo • Measles • Mumps • Roseola • Rubella • Slapped cheek disease • Whooping cough (pertussis)

References 1 National Health and Medical Research Council. The Australian Immunisation Handbook (10th edn, updated January 2014). 2 National Health and Medical Research Council. Staying Healthy in Child Care—Preventing Infectious Diseases in Child Care (4th edn), December 2005. 3 The Center for Disease Control. Measles (home page), July 2014 (accessed 27/7/2014). 4 The Center for Disease Control. Pregnancy and fifth disease, February 2012 (accessed 27/7/2014). 5 The Royal Children’s Hospital Melbourne. Clinical Practice Guidelines: Kawasaki Disease, December 2012 (accessed 28/7/2014). 6 American Academy of Pediatrics. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals. Pediatrics, 2004; 114 (6): 1708–33. 7 The Royal Children’s Hospital Melbourne. Clinical Practice Guidelines: Whooping cough (Pertussis), May 2014 (accessed 28/7/2014). 8 Therapeutic Guidelines: Pertussis, June 2011 (eTG 4, accessed 29/7/2014). 9 The Royal Children’s Hospital Melbourne. Clinical Practice Guidelines: HSV Gingivostomatitis, November 2013 (accessed 29/7/2014). 10 DermNet NZ: the dermatology resource (accessed 30/7/2014). 11 Therapeutic Guidelines: Impetigo, March 2014 (eTG 4, accessed 30/7/2014).

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Behavioural and developmental issues and disorders in children Although the world is full of suffering, it is also of the overcoming of it.

Helen Keller  Many behavioural issues in children arise because of (and in the context of) factors such as the child’s temperament, parental schema and child–parent attachment. These factors determine, in the beginning, how the parent–child relationship will evolve, and also strongly affect the psychological development of the child.

Temperament Temperament refers to the personality characteristics you are born with—what is innate rather than learned. An awareness of the fact that children are born with characteristics over which parents have no control can be liberating, especially for parents of children with challenging temperaments. The best-known description of temperament is based on the work of Thomas and Chess from the 1970s.1 They found that about two-thirds of children can be classified into one of three categories: easy, difficult and slow to warm up. Of these, about 15% were considered easy, 70% slow to warm up and 15% difficult. A child with a difficult temperament will be emotionally labile and have difficulty coping with new experiences. A child with a slow-to-settle temperament will have some difficulty coping with new experiences, but will eventually manage after repeated exposures. A child with an easy temperament will cope easily with new experiences and will have a calm nature. Easy doesn’t mean good, and difficult doesn’t mean bad. These children may just require more patience and a thoughtful and paced approach to parenting. Further, the characteristics that can make a child ‘difficult’ can be the flipside of other characteristics that lead them to achieve success (if appropriately nurtured and guided). A stubborn child may have good persistence, and a distractible child may be artistic and expressive. Of course, most children will have a few ‘difficult’ characteristics, but some will have more than others.

Table 94.1

Easy and difficult temperament characteristics

Easy temperament characteristic

Difficult temperament characteristic

Generally happy

Generally serious

Goes with the flow

Inflexible

Laid-back

In-your-face

Patient

Impulsive

Flexible

Stubborn

Friendly

Shy

Calm body movements

Restless

Persistent

Gives up easily

Calm nature

Hot-tempered

Expressive

Reserved

‘Even’ mood

Up and down mood

Thick-skinned

Over-sensitive

Good concentration

Distractible

Regular body clock

Chaotic body clock

Tolerates sensations well

‘Sensory defensiveness’ (light, sounds, tastes, textures)

Raising parents’ awareness of this, getting them to think about the innate characteristics of their child (which may or may not be similar to their siblings or one or both of the biological parents) and to adjust their parenting style accordingly will help them deal more effectively with the challenges of raising their child.

Parental schema Schema is the view you have of the world based on your own experiences; it is the ‘soup in your head’. Parental schema is how parents view how they should parent, and is often based on how they were brought up themselves. Parental schemas may not match, and

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this can cause relationship issues. Parental attitudes to issues such as communication, emotion sharing and discipline can fundamentally affect the behaviour and psychological health of a child. Parental schema can also commonly be influenced by cultural factors.

Child–parent attachment

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Rather than nature versus nurture, for human beings, nurture is nature. While we do not start with a blank slate (we have our innate temperament), the most essential nutrient for a child’s mind, the thing that makes it grow, is a meaningful connection with other minds, particularly those of their parents. The way we end up is not predetermined, like Michelangelo ‘finding’ the David within the marble; we, as human beings, are built up, constructed out of the clay that comes largely from the relationship between parent and child. However, an infant first has to learn how to connect with other minds. A child does this in their first relationship, usually with their mother. This is attachment. If we were a tree, our attachment would be our trunk. Just like a tree trunk’s fastening to the ground, everything else flows from it. It is how a child orientates to the rest of the social world. It’s important to note that attachment is an ongoing phenomenon, even into adulthood. Children attach not only to their mother, but to other people from whom they can ‘gather strength’. Children’s attachment to their two parents may differ and can also change over time. A secure attachment is achieved if a parent responds to a child’s cries promptly, consistently and appropriately. The three main ways in which attachment can go wrong are: • Carer not responding—this can result in a lack of emotional depth in the child. People who are raised in this way can even develop what is called ‘learnt unresponsiveness’ and be emotionally barren. They are also more likely to parent this way themselves (so it can become ‘heritable’). • Carer responding inconsistently—this can lead to uncertainty and anxiety in the child. • Carer responding inappropriately—such as with aggression or anger. This is obviously very damaging, and happens in situations of emotional abuse, particularly with mental health or drug and alcohol issues in the carer. It creates a terrible and unsolvable paradox for children, where the person on whom they are completely reliant to teach them how to relate to the world is also a threat.

Observing how carers, particularly mothers, respond and interact to their child can give the family doctor insight into this relationship. Gently advising and encouraging appropriate responses to the child’s needs can be beneficial, particularly in a mother with poor parenting capabilities and/ or difficult circumstances (e.g. very young mothers, socially isolated, postnatal depression, drug using or alcoholic parents, violence in the household). In highrisk situations, further referral to support services or even protective agencies may be required (see CHAPTER 95).

Child behaviour and discipline2,3 Issues around child behaviour and how to deal with unwanted behaviours commonly arise and are often a source of conflict and angst. It is normal for children, especially toddlers, to have resistant and oppositional behaviour. The word ‘discipline’ comes from the Latin disciplina, which means ‘to teach’. The purpose of disciplining a child is to guide and teach, so they know what is allowed and what is not allowed, what ‘works’ in the world and what will not. Parents can teach children in a variety of ways. The most effective forms of discipline are actually praise and encouragement—of wanted behaviours. However, when children are doing something that they should not—an unwanted behaviour—they need to learn that this is the case. The challenge for parents is to get this message across to them clearly and effectively. A simple equation sums up the best way to deliver this message: unwanted behaviour = unwanted (by your child) outcome Educating parents to recognise that the thing a child desires most in the world is the attention (this is a survival instinct) and approval of their parents will help them understand how to reinforce desired behaviours, and extinguish unwanted behaviours. That is, pay attention to when the child is behaving, and even praise particularly wanted behaviours, and ignore unwanted behaviours.

Consequences3 Consequences work only with children >3  years of age, and should be used solely in response to a small fraction of a child’s behaviour, regardless of the child’s temperament. If consequences are overused, their effectiveness diminishes and family relationships can be damaged.

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Behavioural and developmental issues and disorders in children There are three types of consequences that work (in decreasing order of usefulness): • Natural consequences: where there is a natural flow from the misdemeanour to the consequence. For example, if a child refuses to have dinner, he or she goes to bed hungry. Natural consequences have a momentum of their own and, assuming they do not result in harm, can provide many valuable lessons. • Related consequences: where there is some link between the unwanted behaviour and the result. This is also sometimes called a ‘logical consequence’. For example, if a child makes a mess, he or she must clean it up. Or, if two children are fighting over a toy, the toy gets taken away for a while. Related and natural consequences allow a child to link the unwanted behaviour with the consequence. • Losing a privilege: This can be a very powerful technique as it focuses the child’s attention but is more punitive than natural and related consequences. Also, there is no logical link between behaviour and consequence. Parents should only withdraw a privilege with care as it can cause resentment, and the child should be warned beforehand that he or she is going to lose a particular privilege for a particular unwanted behaviour. 4

Time-outs are another response to unwanted behaviours. Time-outs are useful from 2–3 years of age, and can take the heat out of a situation, for both the parent and child. Time-outs should be consistent, enforced promptly and calmly, even with empathy, and short—a good rule of thumb is a minute per year of age. Responses that don’t work when disciplining children include: screaming, constantly explaining, repeatedly warning, threatening, pleading, arguing, bribing and giving in, as well as smacking.5 Most parents who are struggling with behaviour and discipline issues respond with relief when provided with a set of alternative responses for disciplining children, though care needs to be used when raising these issues, as they can be highly emotional and confronting topics for parents.

Tantrums6 Tantrums are when we lose control of our feelings and behaviour. Everyone, including adults, is capable of tantrums. Tantrums are what we use to deal with an emotionally confronting situation when we have no

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other option—the emotional response of last resort. They are more common in toddlers (particularly between 18 months and 3 years of age) because they have not learned any or many other emotional responses to challenging situations, such as ignoring, negotiating, reconsidering or reframing a situation. There is a lot of misinformation about tantrums, frequently over-emphasising control rather than guidance. Diverting a child from predictable tantrum triggers, ‘scaffolding’ (giving necessary support) to handle the event (e.g. a 5-minute warning), distraction or active listening in the build-up to a tantrum can be useful strategies to employ. Once a child is mid-tantrum, any attempts at negotiation will be ineffective. Afterwards, an unemotional and calm response from the parent will tell the child that tantrums don’t work (though, of course, this can be difficult for a stressed parent). Skill-building toddlers in how to handle emotionally challenging situations (i.e. expanding their repertoire beyond tantrums) is best done either before or after (‘What else could you have done?’). Rousing at a child is counter-productive; they are still learning to control their emotions, and this will just increase the risk of them becoming demoralised and losing self-esteem.

Breath-holding attacks7 Breath-holding is common (around 5% of children do so at some stage), and occurs between 6 months and 6 years (peak at age 2). While frightening to watch, such attacks are harmless, and no treatment or action is required. There are two types: • blue spells (more common)—these happen in response to being upset or angry. The child cries loudly then holds his or her breath at the end of expiration • pale spells—these happen in response to pain or a fright They can last from 10–60 seconds, and can cause the child to faint or, rarely, fit. They cause no harm, and parents should be reassured. Approaches to discipline should not change because of them. There is no need to blow air or splash water in the child’s face, and the child should be treated as if they have not occurred (i.e. no discussion or punishment).

Head banging and rocking8 Head banging and rocking, which usually occur before the child goes to sleep, are common. Head banging occurs in up to 30% of normal infants and toddlers,

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and rocking is even more prevalent. They are more frequent in children with developmental disability and autism, where these behaviours may be more pervasive through the day. Features • Usually starts after 8–9 months, and is rare after 2 years of age • Usually prior to going to sleep • Child usually not distressed and rarely selfinjurious Management There is no need to try to stop the behaviour, and attempting to do so is often not successful. • Reassure parents that it’s a self-limiting behaviour and usually settles by 2 years. • Avoid reinforcing behaviour by excessive attention or punishment. • Ignore the behaviour. • Place the bed or cot in the middle of the room away from a wall (reduces disruption from noise). • Monitor the condition of the cot, to ensure screws and hinges are not being loosened.

Sibling rivalry Sibling rivalry is very common and can cause a lot of disruption in the family. A toddler may pinch, prod and even attempt to smother a new baby, so providing the toddler with attention from the mother and encouraging the child to see that it is his or her baby too can ease the jealousy. In school-age children the following tips are useful:9

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• Be fair. • Avoid making comparisons between your children. • Encourage the children to work out their own differences. • Avoid taking sides in sibling conflicts. Set guidelines on how children can disagree and resolve conflicts. • Discourage telling tales on each other. • When it is necessary to punish or reprimand, do it with the child alone in a quiet, private place. • Use regular family meetings to establish family rules and negotiating conflicts.

Stutters Stuttering10 usually begins at age 2–4 years, as children start to use more words and longer sentences.

It can start suddenly or develop slowly. Up to 12% of children will stutter by the age of 4. Stutters can be repetitions (of a sound, word or phrase), prolongations of a sound (e.g. ‘aaaand’), a block (where no sounds comes out) or combinations of these. There is no known cause, though it can run in families. Stutters are not associated with other disabilities, though they may cause psychological distress for the child. They are not caused by anxiety or stress, but can be more prominent when the child is excited. A child developing a stutter should see a speech pathologist as soon as possible, as early treatment is more successful. The most common program used in Australia to treat stuttering is the Lidcombe Program, which is often successful and can even sometimes stop the stutter.

Habit cough This is a common problem usually affecting schoolage children and occurs in the absence of underlying disease. It occurs only when the child is awake—not during sleep. There are two common types of habit cough: 1 A honking-type cough (heard from the waiting room) in teenage girls. There is no dyspnoea or sputum production. 2 A throat-clearing cough commonly seen in boys aged 7–10. This is related to a transient tic disorder. Habit cough is a diagnosis of exclusion and there should be a careful assessment to exclude other causes such as respiratory disorders or pertussis. Underlying triggers include inter-family problems and bullying or other perceived stress or anxiety. Management includes explanation, reassurance and CBT. Referral for resistant cases is appropriate. Other functional respiratory problems: • hyperventilation • sighing dyspnoea • vocal cord dysfunction (see CHAPTER 57)

Sleep disorders in children See CHAPTER 71.

Bullying11,12 There are varying figures on how common bullying is, but most suggest more than a quarter of children are significantly bullied at some stage. It is more common

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Behavioural and developmental issues and disorders in children in the early school years, but can happen at any age. Bullying differs from conflict, in that there is an imbalance of power between the perpetrator and the victim. It is a deliberate behaviour repeatedly done and intended to harm the victim. It is a power play, constructed on contempt, not anger, and this is what can make it so damaging. Types of bullying include physical harm, verbal assaults, hidden bullying (e.g. exclusion or spreading rumours) and cyberbullying (now the most common form of bullying). The latter is particularly insidious as it is difficult to detect and follows the victim home and even into their bedroom via social media or phones. Bullying can lead to physical, psychological and social consequences, and in extreme cases depression and even suicide. Despite this, less than half of bullying is reported (with boys reporting less than girls) due to fear of retaliation or not being believed. Bullies themselves tend to be assertive, impulsive and aggressive, with little empathy for their victims or remorse for their actions. They often come from dysfunctional backgrounds, and their bullying tendency may have been learned from being modelled by parents or peers. If bullying is raised, the child should be believed, and a history carefully, gently and non-judgmentally extracted. Parents should be encouraged to stay calm, involve other adults in the environment (e.g. teachers at school) and to formally address the issue after educating themselves on the best approach. There are many good resources available for this, such as the National Centre Against Bullying at . A vigilant approach to this common and serious problem by GPs and parents should be employed, especially in those particularly vulnerable to bullying, such as children who are shy, lacking in confidence, children with disabilities or who physically or socially stand out in some way (e.g. children with speech disorders). Indicative signs to watch out for include: • • • • • • •

school phobia: sham sickness and other excuses being tense, tearful and miserable after school reluctance to talk about happenings at school poor appetite functional symptoms (e.g. habit cough) repeated abdominal pains/headache unexplained bruises, injuries, torn clothing, damaged books • lack of a close friend; not bringing peers home • crying during sleep • restless sleep with bad dreams

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• appearing unhappy or depressed • unexpected irritability and moods; temper outbursts Referral to a psychologist should be considered in severe cases, in those that fail to be resolved, or if there are other psychological or family issues. If child abuse is suspected, appropriate action should be taken (see CHAPTER 95).

BEHAVIOURAL AND DEVELOPMENTAL DISORDERS

Developmental disability and delay The family doctor is in an ideal position to recognise and initiate evaluation of the child with a developmental disability, whether it is a physical disability or delay, an intellectual disability or a learning disability. All children with a suspected developmental delay should be promptly evaluated by a paediatrician or a multidisciplinary developmental assessment team, and the family doctor should remain a key player in the long-term management both of the child and the family. Many developmental problems will be obvious but others are subtle. Several disabilities may evade a diagnosis. Transient developmental delay may be associated with factors such as prematurity, family stress, physical illness and learning opportunities, while persistent delay can be caused by intellectual disability, cerebral palsy, autism and hearing and visual impairment. Many rare dysmorphic syndromes are becoming more recognised and defined with the rapid advances in genetics, and referral to genetic disorder units will help in getting an appropriate evaluation.

Evaluation An appropriate history includes a careful look at developmental milestones, social and behavioural issues, and family history (see CHAPTER 9). A new diagnosis of developmental delay of any sort can have a massive impact on family members, especially parents, and the family doctor should keep a watchful eye on how they are coping and reacting to the diagnostic process. The physical examination includes growth parameters, assessment of all developmental domains, looking for dysmorphic features, testing of hearing and vision, examining for neurocutaneous stigmata (e.g. café-au-lait spots, neurofibromas, hypopigmented macules) and careful systems examination, including cardiac and neurological

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examination. Eyes, ears, mouths (including teeth), hands and feet, and genitals should all be examined. Investigations are usually coordinated via specialist services, but often include bloods (including karyotyping and genetic tests), urinary metabolic screening, and imaging such as cerebral MRI (which may require a general anaesthetic).

Intellectual disability Intellectual disability (ID) is a neurodevelopmental disorder characterised by deficits in intellectual and adaptive functioning that present before 18 years of age.13 The term replaces and improves upon the older term ‘mental retardation’. The term ‘global developmental delay’ (GDD) is usually used to describe children 3/week for >12 months • Conduct disorder—where there is behaviour that violates the rights of others or societal norms, such as aggression directed towards people, animals or property, often with a callous manner and lack of empathy

Tic disorders22 Tics are sudden, rapid, recurrent involuntary vocalisations or movements usually appearing in bouts that wax and wane in intensity, frequency and type of tic. They include behaviours such as grunting, blinking, shrugging shoulders, humming, yelling out a word or phrase or clearing the throat. Tic disorders are classified into:13 • Tourette syndrome—motor and vocal tics for >1 year • persistent motor or vocal tic disorder—motor or vocal tics for >1 year • provisional tic disorder—motor and/or vocal tics for 2 siblings low infant birth weight unmarried mother poverty significant life stressors in parents caregiver role conflicts living in house with unrelated adult (50 times more likely to die from inflicted injuries)

Physical abuse indicators Accidental injuries such as bruises or fractures are common in children, but tend to follow certain patterns. A GP should be aware of cases where the injury or injuries suggest a non-accidental cause is possible, when the history doesn’t match up with the injury or developmental age of the child, or when the behaviour of the parent and/or child is suggestive of non-accidental injury.

Bruises Bruises are commonly found on the front of the body over bony prominences (e.g. forehead in toddlers, knees and shins in older children). Suspicious bruises include: • finger-shaped bruises (e.g. thumb grip marks) • multiple bruises/welts of different ages (the colour of a bruise doesn’t reliably indicate when it occurred) • bruises in premobile children • bruises away from bony prominences—face, scalp, neck, buttocks (see FIG. 95.2), genitalia, earlobes, behind the ears

FIGURE 95.2 Physical abuse: imprint of a boot on the buttock of a child

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Child abuse • abdominal bruising (consider damage to internal organs, including organ rupture) • multiple bruises of uniform shape • multiple bruises in clusters

Scalds and burns Beware of: • a scald of uniform depth, sparing flexures, uniform burn line demarcation, bilateral and no splash marks (suggests forced immersion) • unusual position (e.g. back of hand, genitals) • cigarette butt-type burns

Fractures Look out for: • metaphyseal fractures of the proximal humerus and proximal or distal tibia are highly suggestive • other fractures commonly non-accidental: rib (especially posterior), clavicle, vertebral body, sternum, scapula • multiple, especially bilateral • complex or multiple skull fractures

Shaking and brain injury Shaking a baby is a critically dangerous thing to do, a danger often underestimated by perpetrators. The relatively large head size and weak neck muscles can easily lead to serious injury. Suspicion of traumatic brain injury should be raised when there is: • • • • •

unexplained encephalopathy unexplained vomiting, irritability and apnoeas altered states of consciousness neurological symptoms and signs torn frenulum or retinal damage

History • Unexplained injury • Different explanations offered • Vague or changing history • Injury unlikely to have occurred in manner stated • Unreasonable delays between injury and presentation • Presentation inconsistent with child’s developmental capabilities • Evidence of neglect (clues include failure to thrive, dental caries, severe nappy rash, poor wound care) Remember Munchausen syndrome by proxy. Behavioural indicators • Wariness of adult contacts • Inappropriate clothing (e.g. long sleeves on a hot day)

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• • • • •

Apprehension when other children cry or shout Behavioural extremes Fear of parents Afraid to go home Child reports injury by parents or gives inappropriate explanation of injury • Excessive compliance • Extreme wariness • Attaches too readily to strangers Management If suspected or disclosed, a thorough assessment, with detailed documentation (including measurement and photography of bruises/other injuries) of findings should be undertaken. A detailed history and thorough examination of all areas of the body is required. In a general practice setting, getting help with this difficult situation would often be useful. Discussing (immediately) with colleagues or child protection authorities is advisable, with the safety of the child (and other cohabiting children) being ensured at all stages. Verbatim comments should be written down and, if possible, information gathered from other sources or witnesses. The family doctor should diplomatically confront the parents and/or carers and always act in the best interests of the child. Offer to help the family. An approach would be to say, ‘I am very concerned about your child’s injuries as they don’t add up—these injuries are not usually caused by what I’m told has been the cause. I will therefore seek assistance—it is my legal obligation. My duty is to help you and, especially, your child.’

Acquiring essential help • Psychosocial assessment of child and family: involves social worker and multidisciplinary assessment • Admission to hospital: for moderate and severe injuries • Investigations done in conjunction with specialists • Case conference (where appropriate) • Mandatory reporting: notify child protection authorities

Emotional abuse Physical indicators • There are few physical indicators, but emotional abuse can cause delay in physical, emotional and mental development.

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Behavioural indicators • Extremely low self-esteem. • Compliant, passive, withdrawn, tearful and/or apathetic behaviour. • Aggressive or demanding behaviour. • Anxiety. • Serious difficulties with peers and/or adult relations. • Delayed or distorted speech. • Regressive behaviour (e.g. soiling).

Sexual abuse presents in three main ways: • • •

Allegations by the child or an adult Injuries to the genitalia or anus Suspicious presentations, especially: — genital infection (see FIG. 95.3) — recurrent urinary infection — unexplained behavioural changes/ psychological disorders

Neglect Physical indicators • Consistent hunger. • Failure to thrive, or malnutrition. • Poor hygiene. • Inappropriate clothing. • Consistent lack of supervision. • Unattended physical problems or medical needs. • Abandonment. • Dangerous health or dietary practices. Behavioural indicators • Stealing food. • Extending stays at school. • Consistent fatigue, listlessness or falling asleep in class. • Alcohol or drug abuse. • Child states there is no caregiver. • Aggressive or inappropriate behaviour. • Isolation from peer group.

Sexual abuse3,5

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• Only 6% of child sexual abuse is by strangers. Most are known by parents and child; that is, familiar people in familiar environments, especially within the family. • A child may disclose up to 12 times before they are believed (listen for hints). • Most (but not all) of the adults who sexually abuse are men. • Boys are assaulted less commonly than girls, but are less likely to disclose if they are assaulted. • Adolescents are perpetrators in at least 20% of cases. • Child sexual abuse is usually about power rather than sexual gratification.

FIGURE 95.3 Genital human papillomavirus infection—a sign of sexual abuse in a child

Clinical indicators that may suggest child sexual abuse are presented in TABLE 95.1. Clinical approach Ideally, the child should be assessed by experienced medical officers at the regional sexual assault service, so the temptation for the inexperienced GP to have a quick look should be resisted. For the practitioner having to assess the problem, a complete medical and social history, including a behavioural history, should be obtained prior to examination. The child’s history must be obtained carefully, honestly, patiently and objectively, without leading the child. The history is more important than the physical findings as there are no abnormal physical findings in many confessed cases. Examination A parent or legal guardian must give informed consent before the child is physically examined. It is

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Child abuse

Table 95.1

Clinical indicators that may suggest child sexual abuse

Child disclosing abuse (rarely invented, and the majority of presentations) Parent or adult disclosing abuse allegation Vaginal discharge Sexually transmitted infections (acquired in 5% of sexually abused children) Urinary tract infection

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recommended that the physical examination of any child suspected of being sexually abused is performed by a paediatrician or forensic physician experienced in the area of sexual abuse.

Point of caution: Perianal erythema due to streptococcal infection (GABHS) (see FIG 95.4) or threadworms and nonspecific vulvovaginitis (see CHAPTER 107) can be misinterpreted as sexual abuse.

Unexplained genital trauma Unexplained perianal trauma Overt sexual play Pregnancy in an adolescent Deterioration in school work Family disruption Indiscriminate attachment Abnormal sexualised behaviour (many abused children do not do this) Poor self-esteem Psychological disorders: • behaviour disturbances • regression in behaviour • sleep disturbances • abnormal fears/reactions to specific places or persons • psychosomatic symptoms • anxiety • lack of trust • overcompliance • aggressive behaviour Depression: • self-destructive behaviour • substance abuse • suicidal tendencies Non-specific physical problems: • abdominal pain • enuresis (especially secondary) • encopresis

FIGURE 95.4 Perianal dermatitis with erythema caused by group A beta-haemolytic streptococcal infection

The crisis situation It is important to realise that the child will be in crisis. Children are trapped into the secrecy of sexual abuse, often by a trusted adult, through powerful threats of the consequences of disclosure. They are given the great responsibility of keeping the secret and holding the family together or disclosing the secret and disrupting the family. A crisis occurs when these threats become reality.

Vaginal discharge

Management It is important to act responsibly in the best interests of the child. When we encounter real or suspected child abuse, immediate action is necessary. The child needs an advocate to act on its behalf and our intervention actions may have to override our relationship with the family. Some golden rules are:

Look for semen and STIs

• Never attempt to solve the problem alone.

Examination (abnormal findings uncommon) Genital trauma Perforated hymen/lax vagina Perianal trauma

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• Do not attempt confrontation and counselling in isolation (unless under exceptional circumstances). • Seek advice from experts (only a telephone call away). • Avoid telling the alleged perpetrator what the child has said. • Refer to a child sexual assault centre or Protective Services Unit where an experienced team can take the serious responsibility for the problem.

Supporting the child • • • • •

Acknowledge the child’s fear and perhaps guilt. Assure the child it is not his or her fault. Tell the child you will help. Obtain the child’s trust. Tell the child it has happened to other children and you have helped them.

Prevention of child abuse Prevention of abuse, particularly self-perpetuating abuse, can be helped by creating awareness through media attention, programs in schools and the community in general, and increased knowledge and surveillance by all professionals involved with children. Clear guidelines on reporting and the accessibility of child abuse clinics are important for the strategies to be effective. Teaching children how to protect themselves offers the greatest potential for prevention.5

Counselling the secondary victims

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Non-offending parents, who are the secondary victims of the abused child, will require help and guidance from their family doctor on how to manage the crisis at home.3 Parents should be advised to reassure the child of support and safety and to maintain usual routines. The child should be allowed to set the pace, without overattention and pressure from the parents. Siblings should be informed that something has happened but that the child is safe. Ensure that the child will inform if the perpetrator attempts further abuse. Parents need substantial support, including alleviation of any guilt. An unhappy consequence of the crisis is the problem of broken relationships, which may involve the separation of the child from the family. At least one hitherto unsuspecting parent will be devastated if a parent is responsible for the abuse. The sexually abused child needs to be living with a protective parent or carer, with the abusive parent living separately.

Support for doctors The attending doctor also requires support, and sharing the problem with colleagues, mentors and family is recommended. Some helpful guidelines are as follows. • Carefully record all examination findings (take copious notes). • Always keep to the facts and be objective. • Do not become emotionally involved. • Work with (not for) the authorities. • Avoid making inappropriate judgments to the authorities (e.g. do not state ‘incest was committed’, but rather say ‘there is evidence (or no evidence) to support penetration of . . .’). • If called to court, be well prepared; rehearse presentation; be authoritative and keep calm without allowing yourself to be upset by personal affronts. The main difficulty in diagnosing child abuse is denial that it could be possible.

Adult survivors of child abuse10 All forms of child abuse can result in PTSD (from a single incident) or complex trauma (cumulative). Because of the high rate of child abuse, much of it unreported and hidden away for many years, adult survivors of child abuse are likely to be presenting to GPs on a frequent basis, often unknowingly. Childhood trauma, especially in the first few years during formative brain development, can lead to lifelong problems with dealing with stress. Unresolved trauma restricts the capacity to respond flexibly to life challenges. Patients may present with diverse and puzzling symptoms, including medically unexplained symptoms. Substance abuse, mood disorders and other psychological impairments may result. A GP should be aware of this possibility, and screen for trauma from child abuse in patients presenting with such issues. Take particular care with physical examination, particularly in sensitive areas or involving internal examination, and realise that many patients on whom we are doing Pap tests or rectal examinations may be survivors of child abuse. Procedures can also cause pain, and may retraumatise such a patient. Practising in a ‘trauma informed’ manner involves paying attention to the way we perform a service or procedure, as well as what it comprises, and being sensitive to the context of what may have come before. Trauma from previous child abuse can often be helped by appropriately targeted psychological therapies.

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Child abuse

Basic rules

When to refer

• Suspect child abuse. • Recognise child abuse. • Consult the child protection authorities.

Unless there are exceptional circumstances, referral to an appropriate child abuse centre where an expert team is available is recommended. If doubtful, relatively urgent referral to a paediatrician is an alternative.

Mandatory reporting In most states of Australia and in many areas throughout the world it is mandatory to notify the relevant statutory authorities about suspected child abuse. All family doctors should become familiar with the appropriate local legislation.

Practice tips and guidelines • A child’s statement alleging abuse should be accepted as true until proved otherwise. • Children rarely lie about sexual abuse. • False allegations, however, are a sign of family disharmony and an indication that the child may need help. • Do not insist that the child has ‘got it wrong’, even if you find the actions by the alleged perpetrator unbelievable. • Do not procrastinate—move swiftly to solve the problem. • The genitalia are normal in the majority of sexually abused children. • Be supportive to the child by listening, believing, being kind and caring.

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References 1 Australian Institute of Family Studies. Child abuse and neglect statistics, May 2013 (accessed 18/8/2014). 2 Australian Institute of Family Studies. The prevalence of child abuse, March 2013 (accessed 18/8/201). 3 Kellogg N. The evaluation of sexual abuse in children. Pediatrics, 2005; 116: 506–12. 4 Australian Institute of Health and Welfare. Child Protection Australia 2011–2012, March 2013 (accessed 18/8/2014). 5 Briggs F. Smart Parenting for Safer Kids. Melbourne: JoJo Publishing, 2011. 6 Australian Institute of Family Studies. Child abuse and neglect statistics, May 2013 (accessed 18/8/2014). 7 Bird S. Child abuse: mandatory reporting requirements. Aust Fam Physician, 2011; 40 (11): 921–6. 8 Kellogg N. Evaluation of suspected child physical abuse. Pediatrics, 2007; 119: 1232–41. 9 Smith A. Nonaccidental injury in childhood. Aust Fam Physician, 2011; 40 (11): 858–61. 10 Adults surviving child abuse (ASCA). ASCA factsheet for general practitioners: understanding complex trauma, 2014

(accessed 25/8/2014).

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Emergencies in children

We can say with some assurance that, although children may be the victims of fate, they will not be the victims of our neglect. John F Kennedy (–) Important serious emergencies in children include: • trauma, especially head injuries and intraabdominal injuries • painful conditions • swallowed foreign bodies (FB) • respiratory problems: — bronchial asthma — epiglottitis — croup — inhaled FB — acute bronchiolitis • severe gastroenteritis • septicaemia (e.g. meningococcal septicaemia) • myocarditis • immersion • poisoning • bites and stings • seizures • febrile convulsions • sudden infant death syndrome (SIDS) and apparent life-threatening episode (ALTE) • child abuse: — emotional — physical — sexual — neglect — potential • psychogenic disturbances • anxiety/hyperventilation • suicide/parasuicide

Survey by age group The author’s study analysed emergencies into three groups:1 preschool (0–5 years), primary school (6–12), adolescence (13–17). The commonest emergency calls in the 0–5 years group were poisoning, accidents and violence, dyspnoea, fever/rigors, convulsions, abdominal pain, earache, vomiting. In the 6–12 years age group: accidents and violence, dyspnoea, abdominal pain, vomiting, acute allergy, bites and stings, earache.

In the 13–17 years age group: accidents and violence, abdominal pain, psychogenic disorders, acute allergy, bites and stings, epistaxis.

The signs and symptoms of a serious illness Babies who are febrile, drowsy and pale are at very high risk and require hospital admission.

The busy GP will see many sick children in a day’s work, especially in the winter months with the epidemic of URTIs. It is vital to be able to recognise the very sick child who requires special attention, including admission to hospital. It is unlikely that the commonplace robust, lustily crying, hot, red-faced child is seriously ill but the pale, quiet, whimpering child spells danger. These rules are particularly helpful in the assessment of babies under six months of age.2,3 The presence of a fever in itself is not necessarily an indication of serious illness but rather that the baby has an infection.2

The features of a very sick infant include: • • • •

• • • • • •

inactive, lying quietly, uninterested increased respiratory rate increased work of breathing noisy breathing: — chest wall or sternal retraction — wheezes, grunting, stridor tachycardia sunken eyes cold, pale skin cold extremities drowsiness poor perfusion (reduced capillary refill time)

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Emergencies in children A Melbourne study4 of the sensitivity of clinical signs in detecting serious illness in infants identified five key signs or markers: Marker

Risk to baby

Drowsiness

58%

Pallor

49%

Chest wall retraction

41%

Temperature >38.9°C or 2 cm

42%

If sepsis suspected, investigate with: • • • • •

blood culture FBE/ESR/CRP lumbar puncture urine culture chest X-ray Serious infectious illnesses to consider include:

• Haemophilus influenza type B (Hib) infection: — acute epiglottitis — meningitis (now uncommon since Hib immunisation) • acute bacterial meningitis • septicaemia: — meningococcaemia — toxic shock syndrome — other bacterial sepsis • acute viral encephalitis • acute myocarditis • asthma/bronchitis/bronchiolitis • pneumonia • intussusception/bowel obstruction/appendicitis • severe gastroenteritis

Strategic approach5 It is useful to have a systematic mnemonic for appraisal of the sick child. One general pattern (ABCDEFG) for the primary survey is: • • • • • • •

Airway Breathing Circulation Disability (neurological assessment) Exposure Fluids: in and out Glucose Another is the ABCD assessment (see below). Blood glucose should not be overlooked: • normal random range — children 3.5–5.5 mmol/L — neonates 2.9–7 mmol/L

• hyperglycaemia >12 mmol/L • hypoglycaemia 2 cm other than hydrocele or umbilical hernia, significant faecal blood • CNS: convulsions • Skin: petechial rash

Airway and breathing5 Assessment of the airway and breathing is an important barometer of life-threatening illness and impending cardiac arrest due to hypoxia. The effort and efficacy of breathing must be assessed in the sick infant and child.

Important signs to observe with indicators • Inspiratory noises with obstruction — bubbly noises—partial obstruction with fluid — snoring—decreased level of consciousness — stridor—partial obstruction to larynx or trachea • Apnoea—no respiratory effort for >20 seconds • Bradypnoea—respiratory rate < normal for age • Tachypnoea—rate > normal for age (indicates need to ↑ O2 and ↓ CO2) • Chest recession—on inspiration • Tracheal tug—downward pull on inspiration • Accessory muscle use • Nasal flaring • Gasping—severe hypoxia; impending arrest

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• Child and adolescent health

• Grunting—expiration against obstructed glottis • Oxygen saturation—efficacy of breathing; use oximetry only as an adjunct to clinical assessment • Cyanosis

Secondary signs of worsening obstruction • • • • •

Increased respiratory rate or effort Decreased oxygen saturation Increasing tachycardia Deterioration of colour Development of agitation or decreased level of consciousness

Indications for investigations are presented in TABLE 96.1.

Table 96.1

Indications for investigations in the sick child2

There is only a 2-minute reserve once cerebral blood flow stops. Bacterial meningitis should be considered as a cause. Important causes of collapse are presented in TABLE  96.2. Keep in mind child abuse as a cause of collapse.

Table 96.2

Collapse in children: causes to consider

Anaphylaxis

Penicillin injection Stings

Asphyxia

Near drowning Strangulation

Airways obstruction

Asthma Epiglottitis Croup Inhaled foreign body

CNS disorders

Convulsions Meningitis Encephalitis Head injury

Urine microscopy, culture and sensitivity

All with fever

Full blood examination

All 30 minutes)

Poisoning

Drug ingestion Envenomation

SIDS

Near miss

Functional

Breath-holding attacks Conversion reaction Vasovagal

Collapse in children Collapse in children is a very dramatic emergency and often represents a life-threatening event. It is important to remember that the child’s brain requires two vital factors: oxygen and glucose.

Note: Consider child abuse.

Initial basic management6 1 2 3 4 5 6

Lay child on side. Suck out mouth and nasopharynx. Rescue breaths. Intubate or ventilate (if necessary). Give oxygen 8–10 L/min by mask. Pass a nasogastric tube: 0–3 years 12 FG 4–10 years 14 FG

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Emergencies in children 7 Attend to circulation: IV access ? give blood, Haemaccel or N saline. 8 Take blood for appropriate investigations. 9 Consider ‘blind’ administration of IV glucose. 10 A pulse oximeter is ideal. Cardiopulmonary resuscitation6 Sudden primary cardiac arrest is rare in children. Mostly due to hypoxia. Asystole or severe bradycardia is the usual rhythm at the time of arrest. The following basic life support plan should be followed: • Check breathing and pulse. • Inspect oropharynx and clear any debris. • Basic life support outside the hospital setting is 30:2 compression ventilation ratio, including two initial rescue breaths. The ratio of 30:2 is recommended for all ages regardless of the number of revivers present . • Tilt head backwards, lift chin and thrust jaw forwards (the sniffing position). • Ventilate lungs at about 20 inflations/min with bag-valve-mask or mouth to mask or mouth to mouth. An Air-viva using 8–10 L/min of oxygen is ideal if available. • Intubate via mouth and secure, if necessary (must pre-oxygenate). • If intubation not possible, use a needle cricothyroidotomy as an emergency. • Start external cardiac compression if pulseless or 4 cm in diameter — axillary node involvement of >3 nodes — the presence of positive or close tumour margins • Intraoperative radiotherapy following tumour excision is one of several techniques for partial breast irradiation.15 • Cytotoxic chemotherapy has an important place in management, especially in young healthy women who are E receptor negative and have visceral spread.16 Newer regimens containing anthracyclines (e.g. epirubicin) and a taxane (e.g. docetaxel) have largely replaced the traditional CMF (cyclophosphamide, methotrexate and fluorouracil) regimen.15 • Adjuvant hormonal therapy by the anti-oestrogen agent tamoxifen 20 mg (o) daily if E receptor +ve, which is a specific modulating agent, is widely used and is most suitable in postmenopausal women. The usual course is 5 years.

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Adjunct agents available for treatment include:17,18

101

• anti-oestrogens (E receptor blockers or SERMS): tamoxifen, toremifene • aromatase inhibitors (for hormone receptor +ve cancer in postmenopausal women): anastrozole, letrozole, exemestane • monoclonal antibodies: trastuzumab (Herceptin) • bisphosphonates: recommended for women with bony metastases since evidence indicates reversal of bone density loss and cancer recurrence16,17 • progesterones (e.g. medroxyprogesterone acetate) Guidelines for adjuvant treatments can be accessed at .

Fibrocystic disease Synonyms: fibroadenosis, chronic mastitis, mammary dysplasia, cystic hyperplasia. Clinical features • Most common in women between 30 and 50 years • Hormone-related (between menarche and menopause) • Pain and tenderness and swelling • Premenstrual discomfort or pain and increased swelling • Fluctuation in the size of the mass • Usually settles after the period • Unilateral or bilateral • Nodularity ± a discrete mass • Ache may extend down inner aspect of upper arm • Nipple discharge may occur (various colours, mainly green–grey) • Most cysts are premenopausal (final 5 years before menopause) Examination. Look for lumpiness in one or both breasts, usually upper outer quadrant. Management • Consider mammography if diffuse lumpiness is present in patient >40 years. • Perform needle biopsy if a discrete lump is present and aspirate palpable cysts. • Reassure patient that there is no cancer. • Give advice to alleviate mastalgia (see treatment for cyclical mastalgia in CHAPTER 100). • Use analgesics as necessary. • Surgically remove undiagnosed mass lesions.

Breast cyst • Common in women aged 40–50 years (perimenopausal) • Rare under 30 years • Associated with mammary dysplasia • Tends to regress after the menopause • Pain and tenderness variable, most asymptomatic • Has a 1 in 1000 incidence of cancer • Usually lined by duct epithelium Examination. Look for a discrete mass, firm, relatively mobile, that is rarely fluctuant. Diagnosis • Mammography • Ultrasound (investigation of choice) • Cytology of aspirate Management • Drainage with a fine needle Surgery is rarely required.

Localised nodularity Usually: • • • •

in upper outer quadrant of breast a physiological change to breast managed with clinical surveillance investigate with imaging in older women if asymmetric or perceived change

Lactation cysts (galactoceles) • These milk-containing cysts arise during pregnancy and present postpartum with similar signs to perimenopausal cysts. • They vary from 1–5 cm in diameter. • Treat by aspiration: fluid may be clear or milky.

Fibroadenoma Clinical features • A discrete, asymptomatic lump • Usually in 20s (range: second to sixth decade, commonly 15–35 years) • Firm, smooth and mobile (the ‘breast mouse’) • Usually rounded • Usually in upper outer quadrant • They double in size about every 12 months7 Management Ultrasound and fine-needle aspiration or core biopsy with cytology is recommended plus mammography

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Lumps in the breast in older women. If needle aspiration or core biopsy is negative the patient can be reassured and left unless there is some concern by both patient and surgeon about size or subsequent change. Excision biopsy if large (>3–4 cm), continues to enlarge, suspicious biopsy or woman >40 years.

Phyllodes tumour19 These are giant fibroadenoma-like tumours that are usually benign but 25% are malignant and metastasise. They are completely excised with a rim of normal breast tissue.

Fat necrosis Fat necrosis is usually the end result of a large bruise or trauma that may be subtle, such as protracted breastfeeding. The mass that results is often accompanied by skin or nipple retraction and thus closely resembles cancer. If untreated it usually disappears but the diagnosis can only be made on excision biopsy. The full triple test is required.

Duct papillomas These are benign hyperplastic lesions within large mammary ducts and are not premalignant (nor usually palpable). They present with nipple bleeding or a bloodstained discharge and must be differentiated from infiltrating carcinoma. Mammography and ductography are usually of limited value. The involved duct and affected breast segment should be excised.19

Mammary duct ectasia Synonyms: plasma cell mastitis, periductal mastitis. In this benign condition a whole breast quadrant may be indurated and tender. The larger breast ducts are dilated. The lump is usually located near the margin of the areola and is a firm or hard, tender, poorly defined swelling. There may be a toothpaste-like nipple discharge. It is a troublesome condition with a tendency to repeated episodes of periareolar inflammation with recurrent abscesses and fistula formation. Many cases settle but sometimes surgical intervention is necessary to make the diagnosis. The condition is most common in the decade around the menopause.

The problem of mammary prostheses8 Clinical examination is still necessary and fortunately the residual mammary tissue is usually spread over the prosthesis in a thin, easily palpable

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layer. The areas of clinical difficulty lie at the margin of the prosthesis, especially in the upper outer quadrant where most of the breast tissue is displaced. It should be noted that mammography may be of limited value in the presence of prostheses, especially if a fibrous capsule exists around the prosthesis. Ultrasound examination may be helpful.

Lymphoedema of arm This is a long-term complication of surgery plus irradiation for breast cancer treatment when there is a failure of the lymphatic system to adequately drain extracellular fluid. The limb feels tight and heavy with decreased mobility. Exclude obstruction of the deep venous system by Doppler ultrasound. Skin changes can occur from long-term lymphoedema without treatment, and cellulitis from abrasions and wounds is a concern. Management • Encourage movement; elevation of the arm on a pillow at night; avoid slings • Physiotherapy: a reduction phase with nonelasticised bandages then maintenance with graduated pressure support sleeves • Elastic sleeves worn all day but not at night • Lymphoedema massage at home • Skin hygiene: regular use of non-perfumed emollients, prevention of infection and injury. Avoid sunburn and insect bites • Avoid BP measurement, venesection and IV therapy in that arm • Consider diuretics to relieve pressure

Breast lumps in children There are several benign conditions that can cause a breast lump in children, although the commonest presentation is a diffuse breast enlargement.

Neonatal enlargement20 Newborn babies of either sex can present with breast hyperplasia and secretion of breast milk (see CHAPTER  91). This is due to transplacental passage of lactogenic hormones. The swelling usually lasts 7–10 days if left alone. Any attempts to manipulate the breasts to facilitate emptying will prolong the problem.

Premature hyperplasia20 The usual presentation is the development of one breast in girls commonly 7–9 years of age but

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sometimes younger. The feature is a firm discoid lump 1–2 cm in diameter, situated deep to the nipple. The same change may follow in the other breast within 3–12 months. Reassurance and explanation is the management and biopsy must be avoided at all costs.

Management program for women at high risk of breast cancer9

Monthly breast self-examination At least an annual consultation with GP—if aged 40 or older Aspiration of cysts

Counselling of patients 8

101

Table 101.5

‘Treat the whole woman, not merely her breasts.’ Extreme anxiety is generated by the discovery of a breast lump and it is important that women are encouraged to visit their doctor early, especially as they can learn that there is a 90% chance of their lump being benign. It is possible that denial may be a factor or there is a hidden agenda to the consultation. The decision to perform a lumpectomy or a mastectomy should take the patient’s feelings into consideration—many do fear that a breast remnant may be a focus for cancer. Long-standing doctor–patient relationships are the ideal basis for coping with the difficulties.

Screening Screening mammography should be encouraged for women between 50 and 70 years, and performed at least every 2 years (see CHAPTER 9). Technically it is a better diagnostic tool in older women because of the less dense and glandular breast tissue. It has a specificity of around 90%. A management program for women at high risk of breast cancer is presented in TABLE 101.5. Breast self-examination is a controversial issue and has no proven benefit in reducing morbidity and mortality. The false positive rate is high, especially in those under 40 years. However, regular BSE is recommended for all women 35 years and over.

Mammography, ultrasound and/or fine-needle biopsy to diagnose any localised mass Ultrasound alone for further assessment of young, dense breasts Regular screening mammography after 50 years of age—every 2 years Source: After Barraclough9

Table 101.6

A stony, hard lump or area, regardless of size, history or position A new palpable ‘anything’ in a postmenopausal woman A persisting painless asymmetrical thickening An enlarging mass—cyclic or not A ‘slow-to-resolve’ or recurrent inflammation A bloodstained or serous nipple discharge Skin dimpling, of even a minor degree, or retraction of the nipple A new thickening or mass in the vicinity of a scar Source: After Hirst8

Practice tips

When to refer

• •

• Patients with a solitary breast mass • Following cyst aspiration: — blood in aspirate — palpable residual lump — recurrence of the cyst • Patients given antineoplastic drugs, whether for adjuvant therapy or for advanced disease, require skilled supervision

•

Lumps that require investigation and referral are presented in TABLE 101.6.

Lumps that require investigation and referral8

•

•

Any doubtful breast lump should be removed. Fibroadenomas commonly occur in women in their late teens and 20s, benign breast cysts between 35 years and the menopause, and cancer is the most common cause of a lump in women over 50 years.6 Never assume a palpable mass is a fibroadenoma in any woman over 30 years of age.8 Gentle palpation is required. Squeezing breast tissue between finger and thumb tends to produce ‘pseudolumps’. Any eczematous rash appearing on the nipple or areola indicates underlying breast cancer.

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Lumps in the breast

• • • •

• • • • • •

Mammary duct ectasia and fat necrosis can be clinically indistinguishable from breast cancer. Nine out of 10 women who get breast cancer do not have a strong family history. The oral contraceptive pill has been generally shown not to alter the risk of breast cancer. Never assume that a lump is due to trauma unless you have seen the bruising and can observe the lump decrease in size.8 Never assume a lesion is a cyst—prove it with ultrasound or successful aspiration.8 Never ignore skin dimpling even if no underlying mass is palpable.8 Never ignore a woman’s insistence that an area of her breast is different or has changed.8 Mammography can detect breast cancers which are too small to feel. Mammography is not a diagnostic tool. Recommended mammography screening for women 50–69 years and those aged 40–49 who request it.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Breast cancer • Breast lumps • Breast self-examination

References 1 Green M. Breast cancer. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 83–5. 2 Australian Cancer Incidence and Mortality (ACIM) books. Breast Cancer for Australia (ICD-IO C50) (accessed March 2014).

3 Australian Institute of Health and Welfare & Australasian Association of Cancer Registries 2012. Cancer in Australia: an overview, 2012. Cancer Series No. 74, Cat. No. CAN 70. Canberra: AIHW. 4 Dixon JM, Mansel RE. Congenital problems and aberrations of normal breast development. In: Dixon JM (ed.), ABC of Breast Diseases. London: British Medical Journal Publishing Group, 1995. 5 Mazza D. Women’s Health in General Practice (2nd edn). Sydney: Elsevier, 2011: 185. 6 Fox J. Breast problems. In: Smith JA et al (eds), Hunt and Marshall’s Clinical Problems in General Surgery (2nd edn), Sydney: Elsevier, 2010: 67–76. 7 Talley N, O’Connor S. Clinical Examination (7th edn). Sydney: Elsevier, 2010: 435–7. 8 Hirst C. Managing the breast lump. Solving the dilemma— reassurance versus investigation. Aust Fam Physician, 1989; 18: 121–6. 9 Barraclough B. The fibrocystic breast—clinical assessment, diagnosis and treatment. Modern Medicine Australia, 1990; April: 16–25. 10 Crea P. Benign breast diseases: a management guide for GPs. Modern Medicine Australia, 1995; 38 (8): 74–88. 11 National Health and Medical Research Council. Management of Advanced Breast Cancer: Clinical Practice Guidelines. NHMRC Clinical Practice Guidelines 2001. Canberra: NHMRC, 2001. 12 Stuart K, Boyages J, Brennan, M et al. Ductal carcinoma in situ. Aust Fam Physician, 2005: 949–53. 13 Coates A. Breast Cancer Consensus report. Med J Aust, 1994; 161: 510–13. 14 Wetzig NR. Breast cancer: how to treat. Australian Doctor, 19 October 2001: I–VIII. 15 Buglar L, James T et al. Breast cancer for GPs. Australian Doctor (Suppl), March 2008: 10–13. 16 Crea P, Segelov E, Yeo B. Breast cancer—part 2: how to treat. Australian Doctor, 20 Nov 2010: 23–9. 17 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013: 559–63. 18 Boyages J, Prassar G. Adjuvant hormonal treatment of breast cancer. Medical Observer, 3 August 2012: 27–9. 19 Burkitt H, Quick C, Gatt D. Essential Surgery (2nd edn). Edinburgh: Churchill Livingstone, 1996: 542. 20 Hutson JM, Beasley SW, Woodward AA. Jones Clinical Paediatric Surgery. Melbourne: Blackwell Scientific Publications, 1992: 266–7.

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102 Abnormal uterine bleeding It is advisable that menstruation begin before the individual ceases to be a virgin. Soramus of Ephesus (nd century), text on diseases of women Abnormal uterine bleeding is a common problem encountered in general practice. Heavy menstrual bleeding is the commonest cause of iron-deficiency anaemia in the Western world. A classification of abnormal uterine bleeding is presented in TABLE 102.1.

Table Classification of abnormal uterine 102.1 bleeding Abnormal rhythm Irregularity of cycle

• • •

• •

•

The mean blood loss in a menstrual cycle is 30–40 mL. Blood loss is normally less than 80 mL. Heavy menstrual bleeding (menorrhagia)— HMB—is a menstrual loss of more than 80 mL per menstruation. HMB disposes women to iron-deficiency anaemia. Two common organic causes of HMB are fibroids and adenomyosis (presence of endometrium in the uterine myometrium).3 Various drugs can alter menstrual bleeding (e.g. anticoagulants, cannabis, steroids).

Intermenstrual bleeding (metrorrhagia) Postcoital bleeding Postmenopausal bleeding Abnormal amount Increased amount = menorrhagia Decreased amount = hypomenorrhoea Combination (rhythm and amount) Irregular and heavy periods = metromenorrhagia Irregular and light periods = oligomenorrhoea

Key facts and checkpoints • • •

•

•

Up to 20% of women in the reproductive age group complain of increased menstrual loss.1 At least 4% of consultations in general practice deal with abnormal uterine bleeding. Up to 50% of patients who present with perceived menorrhagia (or excessive blood loss) have a normal blood loss when investigated.1 Their perception is unreliable. The possibility of pregnancy and its complications, such as ectopic pregnancy, abortion (threatened, complete or incomplete), hydatidiform mole or choriocarcinoma should be kept in mind.2 A menstrual record is a useful way to calculate blood loss.

Defining what is normal and what is abnormal This feature is based on a meticulous history, an understanding of the physiology and physiopathology of the menstrual cycle and a clear understanding of what is normal. Most girls reach menarche by the age of 13 (range 10–16 years).1 Dysfunctional bleeding is common in the first 2–3 years after menarche due to many anovulatory cycles resulting in irregular periods, heavy menses and probably dysmenorrhoea. Once ovulation and regular menstruation are established the cycle usually follows a predictable pattern and any deviation can be considered as abnormal uterine bleeding (see TABLE 102.2). It is abnormal if the cycle is less than 21 days, the duration of loss is more than 7 days, or the volume of loss is

Table 102.2

Normal menstruation in the reproductive age group Mean

Range

Length of cycle

26–28 days

21–35 days

Menstrual flow

3–4 days

2–7 days

30–40 mL

20–80 mL

Normal blood loss Source: After Fung1

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Abnormal uterine bleeding such that menstrual pads of adequate absorbency cannot cope with the flow or clots.4 A normal endometrial thickness, as measured by ultrasound, is between 6 and 12 mm. The menstrual cycle is confirmed as being ovulatory (biochemically) if the serum progesterone (produced by the corpus luteum) is >20 nmol/L during the mid-luteal phase (5–10 days before menses).2

Relationship of bleeding to age Dysfunctional uterine bleeding (DUB) is more common at the extremes of the reproductive era (see 2,3 FIG. 102.1). The incidence of malignant disease as a cause of bleeding increases with age, being greatest after the age of 45, while endometrial cancer is predicted to be less than 1 in 100 000 in women under the age of 35.1

Frequency

dysfunctional uterine bleeding (DUB) organic disease (non-cancer, e.g. fibroids) organic disease (cancer)

0

20

Age

40

60

FIGURE 102.1 The relationship between age and various causes of abnormal uterine bleeding. Dysfunctional uterine bleeding is more common in the extremes of the reproductive era, while the incidence of cancer as a cause of bleeding is greatest in the perimenopausal and postmenopausal phases. Source: After Mackay et al2

Heavy menstrual bleeding Heavy menstrual bleeding is: • • •

blood loss >80 mL per menstrual cycle bleeding that persists >7 days bleeding that is unacceptable to the woman

Menorrhagia4 is essentially caused by excessive local production of prostaglandins in the endometrium and myometrium and/or excessive local fibrinolytic activity. Heavy bleeding, possibly with clots, is the

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major symptom of menorrhagia. Dysmenorrhoea may accompany the bleeding and, if it does, endometriosis or PID should be suspected. With care a 60–80% accuracy can be achieved in clinical assessment.4 A summary of the diagnostic strategy model is presented in TABLE 102.3. By far the most common single ‘cause’ of menorrhagia is ovulatory dysfunctional uterine bleeding (DUB). Anovulatory DUB occurs at the extremes of the reproductive period—around menarche and perimenopausally. The most common organic causes are fibromyomatas (fibroids), Table 102.3

HMB: diagnostic strategy model

Q. Probability diagnosis A. Dysfunctional uterine bleeding—ovulatory Fibroids Complications of hormone therapy Adenomyosis Q. Serious disorders not to be missed (see TABLE 101.4) A. Disorders of pregnancy: • ectopic pregnancy • abortion or miscarriage Neoplasia: • cervical cancer • endometrial cancer • oestrogen-producing ovarian tumour (cancer) • leukaemia • benign tumours (polyps, etc.) Endometrial hyperplasia Severe infections: • PID Q. Pitfalls (often missed) A. Genital tract trauma IUCD Adenomyosis/endometriosis Pelvic congestion syndrome SLE Rarities: • endocrine disorders (e.g. thyroid disease) • bleeding disorder (e.g. von Willebrand disease) • liver disease Q. Seven masquerades checklist A. Depression (association) Diabetes Drugs Anaemia (association) Thyroid disorder (hypothyroidism) Q. Is the patient trying to tell me something? A. Consider exaggerated perception. Note association with anxiety and depression.

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Table Important ‘not to miss’ causes of irregular 102.4 bleeding5 15–20

20–30

30–45

Chlamydia/PID

45–55

55 + (years)

Endometrial/ovarian cancer

Pregnancy and pregnancy complications Endometrial polyps Endometrial hyperplasia

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Cervical cancer

5

endometriosis, adenomyosis (‘endometriosis’ of the myometrium), endometrial polyps and PID.2 Acute heavy bleeding or ‘flooding’ most often occurs in pubertal girls before regular ovulation is established. History Bearing in mind that abnormal uterine bleeding is a subjective complaint, and a detailed history is the key initial step in management. The patient’s perception of abnormal bleeding may be quite misleading and education about normality is all that is necessary in her management. A meticulous history should include details of the number of tampons or pads used and their degree of saturation. A menstrual calendar (over 3+ months) can be a very useful guide. A history of smoking and other psychosocial factors should be checked. For unknown reasons, cigarette smokers are five times more likely to have abnormal menstrual function.1 Questions need to be directed to rule out:1 • pregnancy or pregnancy complications (e.g. ectopic pregnancy) • trauma of the genital tract • medical disorders (e.g. bleeding disorder) • endocrine disorders • cancer of the genital tract • complications of the pill Examination1 A general physical examination should aim at ruling out anaemia, evidence of a bleeding disorder and any other stigmata of relevant medical or endocrine disease. Specific examinations include: • speculum examination: ? ulcers (cervical cancer) or polyps

• Pap test (ensure up to date) • bimanual pelvic examination: ? uterine or adnexal tenderness, size and regularity of uterus It is prudent to avoid vaginal examination in selected patients, such as a young virgin girl, as the procedure is unhelpful and unnecessarily traumatic. Investigations Investigations, especially vaginal ultrasound scans, should be selected very carefully and only when really indicated. Abnormal pelvic examination findings, persistent symptoms, older patients and other suspicions of disease indicate further investigation to confirm symptoms of menorrhagia and exclude pelvic or systemic pathology. Consider foremost: • full blood count (to exclude anaemia and thrombocytopenia) • iron studies: serum ferritin Special investigations (only if indicated): • pregnancy testing (SBHG) • laparoscopy where endometriosis, PID or other pelvic pathology is suspected • serum biochemical screen • coagulation profile screen • thyroid function tests, especially TSH • tests for SLE: antinuclear antibodies • transvaginal ultrasound Ultrasound: reserved for women who fail conservative treatment or who are at increased risk of endometrial cancer (see later in this chapter). US is an initial screening tool for identifying risk—high and low. It is best performed in the first half of the menstrual cycle when endometrial thickness should be requested. If it is >12 mm for premenopausal women or >5  mm for perimenopausal women, endometrial biopsy (with or without hysteroscopy) is indicated. Note: Hysteroscopy and D&C remain the gold standard for abnormal uterine bleeding. In some women, a transvaginal ultrasound, Pipelle endometrial sampling or hysteroscopy and D&C will be indicated.6

Dysfunctional uterine bleeding DUB, which is a diagnosis of exclusion, is defined as ‘excessive bleeding, whether heavy, prolonged or frequent, of uterine origin, which is not associated with recognisable pelvic disease, complications of pregnancy or systemic disease’.2

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Abnormal uterine bleeding Clinical features • It is a working clinical diagnosis based on the initial detailed history, normal physical examination and normal initial investigation. • Very common: 10–20% incidence of women at some stage. It is more common in ovulatory (regular) rather than anovulatory (irregular) cycles. • Peak incidence of ovulatory DUB in late 30s and 40s (35–45 years). • Anovulatory DUB has two peaks: 12–16 years and 45–55 years. The bleeding is typically irregular with spotting and variable menorrhagia. • The majority complain of menorrhagia. • The serum progesterone and the pituitary hormones (LH and FSH) will confirm anovulation. • Up to 40% with the initial diagnosis of DUB will have other pathology (e.g. fibroids, endometrial polyps) if detailed pelvic endoscopic investigations are undertaken.

• Provide reassurance about the absence of pathology, especially cancer, and give counselling to maximise compliance with treatment. • Consider surgical management if fertility is no longer important and symptoms cannot be controlled by at least 3–4 months of hormone therapy.

Symptoms • Heavy bleeding: saturated pads, frequent changing, ‘accidents’, ‘flooding’, ‘clots’ • Prolonged bleeding: — menstruation >7–8 days or — heavy bleeding >4 days • Frequent bleeding—periods occur more than once every 21 days • Pelvic pain and tenderness are not usually prominent features

Ovulatory cycle: • medroxyprogesterone 10 mg (o), 1–3 times daily on days 1–21 (of 28-day cycle)— up to 6 months or • norethisterone 5 mg (o) 2–3 times daily on days 1–21 of cycle—up to 6 months

Principles of management7 • Establish diagnosis by confirming symptoms and exclude other pathology. • If no evidence of iron deficiency or anaemia, and significant pathology has been excluded, prospective assessment of the menstrual pattern is indicated using a menstrual calendar. • Conservative management is usually employed if the uterus is of normal size and there is no evidence of anaemia. • Drug therapy is indicated if symptoms are persistently troublesome and surgery is contraindicated or not desired by the patient and D&C doesn’t alleviate.

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Medical and surgical management4,7 Medical Treatment regimens are presented in TABLES 102.5 and 102.6. First-line treatment is with fibrinolytic Table 102.5

Regimens used in management of HMB4 (includes options)

Therapy

Mean reduction12 in blood loss 80 mL/cycle %

Levonorgestrel (IUD) Mirena 52 mg—replace every 5 years

94

Oral progestogen

87

Anovulatory cycle: • medroxyprogesterone 10 mg, once daily for the same 12 days of each calendar month or • norethisterone 5 mg (o), once daily for the same 12 days of each calendar month Tranexamic acid 1 g (o) 6 hourly on days 1–4 of menstruation

47

Combined oral contraceptive pill

43

NSAIDs (oral): • ibuprofen 400 mg 3–4 times daily • naproxen 500 mg statim then 250 mg every 6–8 hours • mefenamic acid 500 mg tds

29

*Effectiveness supported by EBM7

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Table 102.6

• Women’s health

Typical treatment options for acute and chronic heavy bleeding4,10

Acute heavy bleeding Curettage/hysteroscopy • oral high-dose progestogens (e.g. norethisterone 5–10 mg 4 hourly until bleeding stops then 5 mg bd or tds for 14 days3) Chronic bleeding

102

For anovulatory women: • cyclical oral progestogens for 12 days • tranexamic acid For ovulatory women: • cyclical prostaglandin inhibitor (e.g. mefenamic acid) or (one of) • oral contraceptive • antifibrinolytic agent (e.g. tranexamic acid 1 g (o) qid, days 1–4) • progesterone-releasing IUDs (e.g. Mirena)

inhibitors or antiprostaglandin agents, given as soon as possible and throughout the menses. These agents are simple to use, generally very safe and can be used over long periods of time. About 60–80% of patients with ovulatory menorrhagia will respond if compliance is good.4 Such agents include tranexamic acid, mefenamic acid, naproxen, ibuprofen and indomethacin. The agent of first choice is usually mefenamic acid, which reduces blood loss by 20–25% as well as helping dysmenorrhoea. Treatment needs to start just before or with the onset of menstrual bleeding and continue for up to 5 days. Evidence-based reviews confirm the benefit of NSAIDs and tranexamic acid for menorrhagia over the other agents.6 Hormonal agents include progestogens, combined oestrogen–progestogen oral contraceptives and danazol.8,9 The COC constitutes important first-line therapy in both ovulatory and anovulatory patients, but at least 20% of patients do not respond. Progestogens can be given via several routes. Oral use is usually of no benefit in ovulatory DUB. In the adolescent with anovulatory DUB, cyclical oral progestogens may be required for 6 months until spontaneous regular ovulation eventuates.8 Intramuscular medroxyprogesterone acetate (DepoProvera) will induce amenorrhoea in 50% of users in 1 year. The most effective agent for both ovulatory and anovulatory DUB is tranexamic acid, which inhibits endometrial plasminogen activation. The dose is 1 g (up to 1.5 g if necessary) orally qid for the first 4 days

of the menstrual cycle commencing at the onset of visible bleeding.4,10 The intra-uterine progesterone implant system (Mirena) releasing 20 mcg of levonorgestrel/day has shown considerable effectiveness.11 It is regarded as the most efficacious of the hormone treatments with a mean blood loss of 94% of women with menorrhagia.7 Surgical treatment This is indicated if menorrhagia interferes with lifestyle despite medical (drug) treatment. The surgical options are: • endometrial ablation or electrodiathermy excision—to produce amenorrhoea • hysterectomy; this requires a very carefully planned approach. It is preferred to drug therapy for women with endometrial hyperplasia with atypia—endometrial ablation is not appropriate

Practice tip Emergency menorrhagia (acute flooding)4 First line: • tranexamic acid 10 mg/kg IV, every 8 hours until bleeding stops or • tranexamic acid 1–1.5 g (o) 6 to 8 hourly until bleeding stops If above unavailable or not tolerated, other options are: • norethisterone 5–10 mg 4 hourly (o) till bleeding stops, then 5 mg bd or tds (or 10 mg daily) for 14 days or • medroxyprogesterone acetate 10 mg (o) 4 hourly until bleeding stops for 7 days then 20 mg daily for 21 days or • COCP e.g. until bleeding stops then re-evaluate after 48 hours

General guidelines for surgical intervention Women who:4 • • • • •

no longer wish to be able to conceive are perimenopausal have poorly controlled symptoms have adverse effects from the drugs have significant uterine pathology

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Abnormal uterine bleeding

Cycle irregularity13 For practical purposes patients with irregular menstrual cycles can be divided into those under 35 and those over 35 years. Patients under 35 years: • the cause is usually hormonal, rarely organic, but keep malignancy in mind • management options:1 — explanation and reassurance (if slight irregularity) — COC pill for better cycle control—any pill can be used — progestogen-only pill (especially anovulatory cycles) norethisterone (Primolut N) 5–15 mg/day from day 5–25 of cycle Patients over 35 years should be referred for investigation for organic pathology, usually by endometrial sampling and/or hysteroscopy. If normal, the above regimens can be instituted.

Intermenstrual bleeding and postcoital bleeding These bleeding problems are due to factors such as cervical ectropion (often termed cervical erosion), cervical polyps, the presence of an IUCD and the oral contraceptive pill. Cervical cancer and intra-uterine cancer must be ruled out, hence the importance of a Pap test in all age groups and endometrial sampling, especially in the over-35 age group. Mismanagement of these presentations is a legal minefield. A Pap smear should be taken, using the speculum carefully so as not to provoke bleeding, if one has not been taken within the previous 3 months, and sent to a laboratory that uses appropriate quality control procedures with notation of the bleeding on the smear request form. Remember that it is only a screening test. Refer women with these bleeding problems with an abnormal smear or even without any unusual features. Those with a friable ectropion that is causing persistent symptoms should also be referred.14 Thus, intermenstrual bleeding (IMB) should always be investigated. Order a pregnancy test if appropriate. Cervical ectropion, which is commonly found in women on the pill and postpartum, can be left untreated unless intolerable discharge or moderate postcoital bleeding (PCB)1 is present. An IUCD should be removed if causing significant symptoms and the causative pill should be changed.

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Uterine fibroids (leiomyoma) Fibroids are benign tumours of smooth muscle of the myometrium. They are classified according to their location: subserosal, intramural, subendometrial or intra-uterine. They are oestrogen-dependent and shrink with onset of menopause. Clinical features • Present in 30% of women >35 • Only 1 in 800 develop malignancy • Usually asymptomatic Symptoms (especially if large) • Menorrhagia • Dysmenorrhoea • Pelvic discomfort ±  pain (pressure) • Bladder dysfunction • Pain with torsion of pedunculated fibroid • Pain with ‘red degeneration’—only in pregnancy (pain, fever, local tenderness)

Other features • Infertility (acts like IUCD if submucosal) • Calcification Examination • Bulky uterus Investigations • Pelvic ultrasound (investigation of choice). Endometrial thickening >4 mm demands endometrial sampling. If >7 mm, endometrial cancer should be excluded. CT scan and plain X-ray of limited value but MRI is accurate • FBE ? anaemia • Uterine biopsy (malignancy suspected) Management • Consider COCP (30 mcg oestrogen can reduce bleeding) • GnRH analogues—especially if >42 years can shrink fibroids (maximum 6 months)—use only immediately pre-operative • Surgical options: — myomectomy (remove fibroids only, esp. child-bearing years) — hysteroscopic resection/endometrial ablation — hysterectomy • Other option: uterine embolisation

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Cervical cancer This should be the diagnosis until proved otherwise for postcoital, intermenstrual or postmenopausal bleeding. Clinical features • Peak incidence in sixth decade • 80% due to squamous cell carcinoma • Risk factors (refer CHAPTER 98)

102

Symptoms • Postcoital bleeding • Intermenstrual bleeding • Vaginal discharge—may be offensive Mainly diagnosed on routine screening. Examination • Ulceration or mass on cervix • Bleeds readily on contact—may be friable Management • Urgent gynaecological referral

Endometrial cancer This is the diagnosis until proved otherwise in any woman presenting with postmenopausal bleeding. Clinical features • Peak incidence 50–70 years • Risk factors: — age — obesity — nulliparity — late menopause — diabetes mellitus — history of chronic anovulatory bleeding — polycystic ovarian syndrome — drugs (e.g. unopposed oestrogen, tamoxifen) — family history—breast, ovarian, endometrial or colon cancer (Lynch syndrome) Symptoms Ninety per cent present with abnormal bleeding, especially postmenopausal bleeding.3 Note: intermenstrual bleeding or prolonged bleeding in postmenopausal women should be treated with suspicion. Examination • Uterus usually feels normal, but may be bulky.

Investigations • Smear (after pregnancy excluded)—detects some cases. Endometrial cancer is not excluded by a normal cervical smear • Transvaginal ultrasound/endometrial biopsy Management • Urgent gynaecological referral

Endometriosis Refer to CHAPTER 103.

Amenorrhoea and oligomenorrhoea Amenorrhoea is classified as primary or secondary. Primary amenorrhoea is the failure of the menses to start by 16 years of age.2 Secondary amenorrhoea is the absence of menses for over 6 months in a woman who has had established menstruation.15 The main approach in the patient with primary amenorrhoea is to differentiate it from delayed puberty, in which there are no signs of sexual maturation by age 13. It is important to keep in mind the possibility of an imperforate hymen and also excessive exercise, which can suppress hypothalamic GnRH production. A good rule is to note the presence of secondary sex characteristics.2 If absent it implies that the ovaries are non-functional. Causes of primary amenorrhoea include genital malformations, ovarian disease, pituitary tumours, hypothalamic disorder and Turner syndrome. Diagnostic tests include serum FSH, LH, prolactin, oestradiol and also chromosome analysis. Early referral is appropriate. In secondary amenorrhoea, consider a physiological cause such as pregnancy or the menopause, failure of some part of the hypothalamic– pituitary–ovarian–uterine axis (e.g. PCOS) or a metabolic disturbance. Important causes to consider are emotional, psychiatric and constitutional causes such as anorexia nervosa, hyperprolactinaemia, strenuous exercise, weight loss below 75% of ideal, and drugs/hormone therapy (e.g. oral contraceptives). Oligomenorrhoea is the term for infrequent and usually irregular periods, where the cycles are between 6 weeks and 6 months. Gynaecological intervention is appropriate for women with prolonged amenorrhoea due to the increased risk of endometrial cancer.

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Abnormal uterine bleeding

Premature ovarian failure

Hand-out sheets from Murtagh’s Patient Education 6th edition: • Fibroids • Menorrhagia (heavy periods) • Understanding your menstrual cycle

Postmenopausal bleeding

References

Postmenopausal bleeding is vaginal bleeding of any amount occurring 6 months or more after the menopause.2 It suggests cervical or uterine body cancer (up to 25%).2 Other causes include polyps, atrophic vaginitis, endometrial hyperplasia and urethral caruncle. Care has to be taken with women on HRT who have irregular bleeding—they require investigation. Early referral is usually indicated with a view to a diagnostic procedure (hysteroscopy and D&C). If bleeding recurs despite curettage, hysterectomy should be performed since early cancer of the uterus may be missed.

1 Fung P. Abnormal uterine bleeding. Modern Medicine Australia, 1992; May: 58–66. 2 Mackay EV, Beischer NA, Pepperell RJ et al. Illustrated Textbook of Gynaecology (2nd edn). Sydney: WB Saunders, 1992: 77–107. 3 O’Connor V, Kovacs G. Obstetrics, Gynaecology and Women’s Health. Cambridge: Cambridge University Press, 2003: 466–8. 4 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2013 (CD-ROM and TG complete). 5 Read C, May T, Stellingwerff M. Irregular vaginal bleeding: how to treat. Australian Doctor, 18 May 2007: 27–32. 6 Barton S (ed.). Clinical Evidence. London: BMJ Publishing Group, 2001: 1311–16. 7 Quinlivan J, Petersen RW. Menorrhagia. Medical Observer, 16 April 2004: 31–4. 8 Knight D, Robson S, Scott P. Menorrhagia: how to treat. Australian Doctor, 6 March 2009: 31–8. 9 Farquhar C, Brown J. Oral contraceptive pill for heavy menstrual bleeding. Cochrane Database Syst Rev. 2009; (4): CD00154. 10 Bonnar J, Sheppard BL. Treatment of menorrhagia during menstruation: randomised controlled trial of ethamsylate, mefenamic acid and tranexamic acid. BMJ, 1996; 313: 579–82. 11 Gupta J, Kai J, Middleton L et al. Levonorgestrel intrauterine system verus medical therapy for menorrhagia. N Eng J Med, 2013; 268 (2): 128–31. 12 National Advisory Committee on Health and Disability. Guidelines for the Management of Heavy Menstrual Bleeding. New Zealand: NACHP, 1998. 13 Hewson A. Menstrual disorders. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 307–10. 14 Royal Australian and New Zealand College of Obstetricians and Gynaecologists and Royal Australian College of General Practice. Joint Guidelines for Referral for Investigation of Intermenstrual and Postcoital Bleeding. Melbourne: RANZCOG & RACGP, 1996. 15 Warton B. Gynaecology. Check Program 240. Melbourne: RACGP, 1992: 2–20.

• As indicated by investigation results • Women with persistent IMB and/or PCB without any unusual features • Women with IMB/PCB and an abnormal smear14 • Women with a friable ectropion • To exclude intra-uterine pathology • The patient does not respond to initial therapy • There is evidence of underlying disease (e.g. endometriosis, SLE) • Surgery is indicated (minor or major)

Practice tips • •

•

Remember that mental dysfunction can obscure the organic causes of menorrhagia. Non-menstrual bleeding suggests cancer until proved otherwise: it may be postcoital (cervical cancer); intermenstrual (common with progestogenonly pill); postmenopausal (endometrial cancer). Hysteroscopy is more effective than the traditional curettage. Studies have shown that usually less than 50% of the uterine cavity is sampled by curettage.15

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Apart from iatrogenic causes this may be caused by idiopathic early menopause and autoimmune ovarian failure. It can be treated with mid- to high-dose oestrogens plus corresponding cyclical progestogen or cyclical combined preparations.4

When to refer

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Resources Mazza D. Women’s Health in General Practice (2nd edn). Sydney: Elsevier, 2011: 16–21. Mazza D, Drillich A. Women’s Health. Check Program 471. Melbourne: RACGP, 2011.

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103 Lower abdominal and pelvic pain in women Man endures pain as an undeserved punishment, woman accepts it as a natural heritage. Anonymous Pain in the lower abdomen and pelvis is one of the most frequent symptoms experienced by women. The diagnostic approach requires a wide variety of consultative skills, especially when the pain is chronic. The examination of acute abdominal pain has been simplified by the advent of sensitive serum pregnancy tests, ultrasound investigation and the increasing use of laparoscopy. However, an accurate history and examination for all types of pain will generally pinpoint the diagnosis. The ever-present problem of PID, the leading cause of infertility in women, demands an early diagnosis and appropriate management.

Key facts and checkpoints • •

•

• • •

•

A distinction has to be made between acute, chronic and recurrent pain. Ectopic pregnancy remains a potentially lethal condition and its diagnosis still requires a high index of suspicion. Sudden sharp pain in the pelvis that becomes more generalised indicates rupture of an ectopic pregnancy or an ovarian cyst. Recurrent sharp self-limiting pain indicates a ruptured Graafian follicle (mittelschmerz). Recurrent pain related to menstruation is typical of dysmenorrhoea or endometriosis. A UK study1 of chronic lower abdominal pain in women showed the causes were adhesions (36%), no diagnosis (19%), endometriosis (14%), constipation (13%), ovarian cysts (11%) and PID (7%). An Australian study found that endometriosis accounted for 30% and adhesions 20%.2 The principal afferent pathways of the pelvic viscera arise from T10–12, L1 and S2–4. Thus disorders of the bladder, rectum, lower uterus, cervix and upper vagina can refer pain to the low back, buttocks and posterior thigh.3

Table 103.1

Lower abdominal and pelvic pain in women: diagnostic strategy model

Q. Probability diagnosis A. Primary dysmenorrhoea Mittelschmerz Pelvic/abdominal adhesions Endometriosis Q. Serious disorders not to be missed A. Ectopic pregnancy Neoplasia: • ovary • uterus • other pelvic structures Severe infections: • PID • pelvic abscess Acute appendicitis Internal iliac claudication Q. Pitfalls (often missed) A. Endometriosis/adenomyosis Torsion of ovary or pedunculated fibroid Constipation/faecal impaction Irritable bowel syndrome Misplaced IUCD Nerve entrapment Referred pain (to pelvis): • appendicitis • cholecystitis • diverticulitis • urinary tract disorders Q. Seven masquerades checklist A. Depression Drugs Spinal dysfunction (referred pain) UTI Q. Is the patient trying to tell me something? A. May be relevant

A diagnostic approach

Probability diagnosis

A summary of the diagnostic strategy model is presented in TABLE 103.1.

The commonest causes are primary dysmenorrhoea, the pain of a ruptured Graafian follicle (mittelschmerz),

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Lower abdominal and pelvic pain in women endometriosis and adhesions. In many instances of pain no diagnosis is made as no pathological cause can be found.

Serious disorders not to be missed The potentially lethal problem of a ruptured ectopic pregnancy must not be missed, hence the axiom ‘be ectopic minded’. PID can be overlooked, especially if chronic, and requires early diagnosis and aggressive treatment. Neoplasia must be considered, especially malignancy of pelvic structures, including the ‘silent’ ovarian cancer.

Pitfalls Several disorders are very difficult to diagnose and these include haemorrhage into the ovary or a cyst, torsion of the ovary or pedunculated fibroid. Endometriosis may be missed so it is important to be familiar with its symptoms. Chronic constipation may be a trap.

Seven masquerades checklist Two important conditions to consider are urinary tract infection and spinal dysfunction. Just as disorders of the pelvic organs, such as endometriosis and PID, can refer pain to the low back and buttocks, so can disorders of the lumbosacral spine cause referred pain to the lower abdomen and groin.

The clinical approach History The pain should be linked with the menstrual history, coitus and the possibility of an early pregnancy. For recurrent and chronic pain, it is advisable to instruct the patient to keep a diary over two menstrual cycles. The severity of the pain can be assessed as follows:2 • does not interfere with daily activity • results in days off work • results in confinement to bed In this way the pain can be classified objectively as mild, moderate or severe. Risk factors in the past history should be assessed, for example: • IUCD (salpingitis, ectopic pregnancy) • infertility (endometriosis, salpingitis) • tubal surgery (ectopic) The typical pain patterns in relation to menstruation are shown in FIGURE 103.1.

Examination

These can be extremely relevant. Problems in the patient’s social, marital or sexual relationships should be evaluated, especially in the assessment of chronic

One objective is to correlate any palpable tenderness with the patient’s statement of the severity of the pain. Use the traditional abdominal and pelvic

endometriosis

secondary dysmenorrhoea (other than endometriosis) primary dysmenorrhoea distension of ovarian capsule pain mittelschmerz

menses

5

ovulation

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pain. Many patients with undiagnosed chronic pain exhibit psychoneurotic traits and this renders management very complex. Some appear to have the ‘pelvic congestion syndrome’ and need to be handled with sensitivity and tact, especially if the help of a psychiatrist or psychologist is sought.

Psychogenic considerations

0

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FIGURE 103.1 Typical pain patterns for menstrual cycle related gynaecological pain

menses

5

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examination to identify the site of tenderness and rebound tenderness, and any abdominal or pelvic masses. The pelvis should be examined by speculum (preferably bivalve type) and bimanual palpation. Proper assessment can be difficult if the patient cannot relax or overreacts, if there is abdominal scarring or obesity, or if extreme tenderness is present. It is therefore important, especially in the younger and apprehensive patient, to conduct a gentle, caring vaginal examination with appropriate explanation and reassurance. Explanation of the procedure during vaginal examination, preferably using eye contact with the patient, can help her relax and be more confident in the procedure.

Investigations 103

Investigations may be selected from: • haemoglobin level • white blood cell count (limited value) • haematocrit • ESR/CRP • microbiology (limited value): — urine for microscopy and culture ±  Chlamydia PCR — endocervical, urethral, cervical and vaginal swabs • serum β-hCG assay • urinary hCG tests (can be negative in the presence of an ectopic pregnancy) Diagnostic imaging: • vaginal ultrasound—to define a gestation sac • pelvic ultrasound—to differentiate a cystic from a solid pelvic mass Indicated for: — pelvic pain — a palpable pelvic mass — a palpable lower abdominal mass — ascites Laparoscopy is indicated if the history and examination are suggestive of ectopic pregnancy and ultrasound fails to confirm an intra-uterine pregnancy.

Acute pain The causes of acute pain are summarised in TABLE 103.2. The patient is usually young (20–30 years old), sexually active and distressed by the pain, and should be considered foremost to have a bleeding ectopic pregnancy. Important differential diagnoses include acute PID, rupture or torsion of an ovarian cyst and acute appendicitis. Cases of acute ruptured ectopics are obviously easier to diagnose in the presence of circulatory collapse.

Table 103.2

Causes of acute lower abdominal and pelvic pain in women3

Genital Acute salpingitis Pelvic peritonitis Bleeding Rupture or torsion of ovarian cyst Threatened or incomplete abortion Rupture or aborting tubal ectopic pregnancy Rupture or bleeding endometrioma Non-genital Acute appendicitis Bowel obstruction Urinary tract infection (cystitis) Ureteric colic (calculus) Functional Primary dysmenorrhoea Retrograde menstruation Source: After Soo Keat Khoo3

Chronic pain Chronic pelvic pain is constant or recurrent pain of at least 6 months’ duration.

Features • Incidence 15% in 18–50-year-olds • Endometriosis causes 33%, adhesions 24% • It is the reason for up to 40% of gynaecological laparoscopies • Reason for 15% hysterectomies The pain can be cyclical (e.g. endometriosis, mittelschmerz) or continuous. The common causes of chronic pain are listed in TABLE 103.3. Chronic pain is more difficult to diagnose and it is often difficult to differentiate between problems such as endometriosis, PID, an ovarian neoplasm and the irritable bowel syndrome. A comparison of the clinical features of endometriosis and PID is presented in TABLE 103.4. Furthermore it is difficult to distinguish clinically between endometriosis of the uterus (adenomyosis) and pelvic congestion syndrome. Both conditions are associated with dysmenorrhoea and a tender normal-sized uterus.

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Lower abdominal and pelvic pain in women

Table 103.3

Causes of chronic lower abdominal and pelvic pain in women3

Genital Endometriosis/adenomyosis Pelvic inflammatory disease (chronic; adhesions) Ovarian neoplasm Fibromyomata (rarely) Non-genital Diverticulitis Bowel adhesions Irritable bowel syndrome Urinary disorders e.g. urethral syndrome Functional Secondary dysmenorrhoea—IUCD, polyp Irritable bowel, chronic bowel spasm

Table 103.4

Ectopic pregnancy occurs approximately once in every 100 clinically recognised pregnancies. If ruptured it can be a rapid, fatal condition so we have to be ‘ectopic minded’. It is the commonest cause of intraperitoneal haemorrhage. There is usually a history of a missed period but a normal menstrual history may be obtained in some instances. Clinical features of a ruptured ectopic pregnancy • Average patient in mid-20s • First pregnancy in one-third of patients • Patient at risk — previous ectopic pregnancy — previous PID — previous abdominal or pelvic surgery, especially sterilisation reversal

Feature

Chronic PID

Endometriosis

History

Acute pelvic infection (e.g. ruptured appendix)

Dysmenorrhoea

IUCD usage

Dyspareunia

Infertility Pelvic pain

Backache

+ to ++ (mild to moderate)

++ to +++ (moderate to severe)

Premenstrual

Premenstrual and menstrual

Lower abdominal location

Acute pain if rupture of endometrioma

+ mild

++ moderate Low sacral pain with menstruation

Secondary dysmenorrhoea

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Ectopic pregnancy

Comparison of clinical features of PID and pelvic endometriosis

Pelvic pain

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Moderate to severe

Moderate to severe

From onset of acute PID

Gradual onset increases in severity throughout menstruation

Decreases with menstruation Menstruation

Irregular and heavy

Heavy

Dyspareunia

Moderate

Often severe

Infertility

+++

++

Urinary symptoms

—

Frequency, dysuria and haematuria if bladder wall involved

Bowel symptoms

—

Painful defecation if rectal wall involved

Vaginal symptoms

May be chronic purulent discharge or leucorrhoea

—

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— IUCD use — in-vitro fertilisation/GIFT DxT amenorrhoea (65–80%) + lower abdominal pain (95 + %) + abnormal vaginal bleeding (65–85%) ectopic pregnancy

• Pre-rupture symptoms (many cases): — abnormal pregnancy — cramping pains in one or other iliac fossa — vaginal bleeding • Rupture: — excruciating pain (see FIG. 103.2) — circulatory collapse

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Note: In 10–15% there is no abnormal bleeding. • Pain may radiate to rectum (lavatory sign), vagina or leg • Signs of pregnancy (e.g. enlarged breasts and uterus) usually not present Examination • Deep tenderness in iliac fossa • Vaginal examination: — tenderness on bimanual pelvic examination (pain on cervical provocation i.e. cervical motion tenderness)

— palpable adenxal mass — soft cervix • Bleeding (prune juice appearance) • Temperature and pulse usually normal early Diagnosis4 It is possible to diagnose ectopic pregnancy at a very early stage of pregnancy. • Urine pregnancy test (positive in 1500 IU/L (invariably positive if a significant amount of viable trophoblastic tissue present)—may need serial quantitative tests to distinguish an ectopic from a normal intra-uterine pregnancy (IUP). If it is 1.0 mg/dL

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6 Isolation of N. gonorrhoeae and/or C. trachomatis

most common causative organism) and Neisseria gonorrhoeae. This usually leads to salpingitis. 2 Endogenous infections: these are normal commensals of the lower genital tract, especially Escherichia coli and Bacteroides fragilis. They become pathogenic under conditions that interrupt the normal cervical barrier, such as recent genital tract manipulation or trauma (e.g. abortion, presence of an IUCD, recent pregnancy or a dilatation and curettage). The commonest portals of entry are cervical lacerations and the placental site. These organisms cause an ascending infection and can spread direct or via lymphatics to the broad ligament, causing pelvic cellulitis (see FIG. 103.6). 3 Actinomycosis: due to prolonged IUCD use. Look for Actinomyces israelii on culture. Investigations A definitive diagnosis is difficult since routine specimen collection has limitations in assessing the organisms. Definitive diagnosis is by laparoscopy but this is not practical in all cases of suspected PID.

7 Histological evidence of infection (e.g. plasma cells)

Causative agents These can be subdivided into three broad groups: 1 Exogenous organisms: those which are community acquired and initiated by sexual activity. They include the classic STIs, Chlamydia trachomatis (the

• Cervical swab for Gram stain and culture, PCR (N. gonorrhoeae) • Cervical swab and special techniques (e.g. PCR for C. trachomatis) Polymicrobial

Mono-aetiology

pyosalpinx pelvic abscess tubo-ovarian abscesses

tubal damage

salpingitis

broad ligament

salpingitis

cervicitis

+ genital manipulation

Sexually transmitted pathogens

Vaginal flora Streptococci Bacteroides fragilis Enterobacteriaceae

C. trachomatis N. gonorrhoeae Mycoplasma hominis IUCD actinomycosis

FIGURE 103.6 The pathogenesis of PID

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Lower abdominal and pelvic pain in women

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When to refer

• Blood culture • Pelvic ultrasound Treatment Note: Any IUCD or retained products of contraception should be removed at or before the start of treatment. Sex partners of women with PID should be treated with agents effective against C. trachomatis and N. gonorrhoeae.

Sexually acquired infection10 Mild to moderate outpatient):

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infection

(treated

as

an

ceftriaxone 500 mg (in 2 ml 1% lignocaine) IM or 500 mg IV, as a single dose (for gonorrhoea) plus azithromycin 1 g (o), as 1 dose plus metronidazole 400 mg (o) 12 hourly for 14 days Severe infection (treated in hospital): ceftriaxone 1 g IV daily plus azithromycin 500 mg IV daily plus metronidazole 500 mg IV 12 hourly until there is substantial clinical improvement, when the oral regimen above can be used for the remainder of the 14 days

Infection non-sexually acquired (related to genital manipulation) Mild to moderate infection: amoxycillin + clavulanate (875 mg/125 mg) (o) 12 hourly for 14 days plus azithromycin 1 g (o) as single dose Severe infection (including septicaemia): amoxy/ampicillin 2 g IV 6 hourly plus gentamicin 4–6 mg/kg IV for 1 dose, then 1 or 2 further doses based on renal function plus metronidazole 500 mg IV 12 hourly

Actinomycosis amoxycillin 500 mg tds + metronidazole 400 mg bd for 14 days. Ensure IUCD is removed

• All cases of ‘unexplained infertility’ • All teenagers with dysmenorrhoea sufficient to interfere with normal school, work or recreational activities, and not responding to prostaglandin inhibitors • Patients with dysmenorrhoea reaching a crescendo mid-menses • Patients with dysmenorrhoea and unexplained bowel or bladder symptoms • Patients with positional dyspareunia • Patients with cyclic pain or bleeding in unusual sites Note: Pelvic disease that can be treated by advanced laparoscopy surgery includes ectopic pregnancy, ovarian cysts, endometriosis and endometriomas, fibromyomata, pelvic adhesions and hydrosalpinx.

Practice tips • •

•

• •

Think of endometriosis and ovarian cysts in any woman with lower abdominal pain. In any woman whose normal activities are disturbed by dysmenorrhoea unrelieved by NSAIDs, endometriosis should be suspected. If an ectopic pregnancy is suspected and there are no facilities for resuscitation, digital vaginal examination should be deferred for it may provoke rupture.2 Acute abdominal and pelvic pain in the presence of a negative β-hCG is most often due to an ovarian cyst. A positive β-hCG plus an empty uterus and an adnexal mass are the classic diagnostic features of ectopic pregnancy.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Dysmenorrhoea • Endometriosis • Pelvic inflammatory disease

References 1 Foy A, Brown R. Chronic lower abdominal pain in gynaecological practice. Update, 1987; 27 March: 19–25. 2 Forbes KL. Lower abdominal and pelvic pain in the female: a gynaecological approach. Modern Medicine Australia, 1991; September: 24–31.

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3 Soo Keat Khoo. Lower abdominal pain in women. Patient Management (Suppl), 1990; August: 13–23. 4 O’Connor V, Kovacs G. Obstetrics, Gynaecology and Women’s Health. Cambridge: Cambridge University Press, 2003: 325–7. 5 Wong CL, Fraquhar C, Roberts H et al. Oral contraceptive pill for primary dysmenorrhoea. Cochrane Database Syst Rev. 2009; (4): CD002120. 6 Barton S (ed.). Clinical Evidence. London: BMJ Publishing Group, 2001: 1255–63. 7 Johnson NP, Hummelshoj L, The World Endometriosis Society Montpellier Consortium. Consensus on current

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management of endometriosis. Hum Reprod, 2013; 28 (6): 1552–68. 8 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2014 (eTG, accessed 1/9/2014). 9 O’Connor V, Kovacs G. Obstetrics, Gynaecology and Women’s Health. Cambridge: Cambridge University Press, 2003: 476–97. 10 Moulds R (Chair). Therapeutic Guidelines: Antibiotic (Version 14). Melbourne: Therapeutic Guidelines Ltd, 2010: 105-7.

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Premenstrual syndrome

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I’m tired of all this nonsense about beauty being only skin deep. That’s deep enough. What do you want—an adorable pancreas? Jean Kerr  Premenstrual syndrome (PMS) is defined as a group  of  physical, psychological and behavioural changes that  begin 2–14 days before menstruation and are relieved immediately the menstrual flow begins.1 These symptoms occur in the luteal phase of the menstrual cycle yet the pathogenesis of PMS is still uncertain. Among the proposed causes are pyridoxine deficiency, excess prostaglandin production and increased aldosterone production in the luteal phase.1 However, PMS is most probably related to enhanced sensitivity to progestogen with an underlying serotonin deficiency.2

Aetiology Various aetiological factors have been identified as contributing to PMS.1 Predisposing factors: • • • • •

Precipitating factors: • hysterectomy • tubal ligation • cessation of the OCP

Key facts and checkpoints • •

• •

•

PMS increases in incidence after 30 years, with a peak incidence in the 30–40 years age group. PMS also occurs in the 45–50 years age group, when it may alternate with menopausal symptoms, causing clinical confusion.3 The symptoms of PMS decrease in severity just before and during menstruation. The symptoms cannot be explained by the presence of various psychological or psychiatric disorders. The severe form of PMS is classified in the Diagnostic and Statistical Manual of Mental Disorders (4th and 5th edns) as premenstrual dysphoric disorder (PMDD).

mental illness alcoholism sexual abuse family history stress

Sustaining factors: • • • •

diet containing caffeine, alcohol, sugar smoking stress sedentary lifestyle

Symptoms Various symptoms from among the 150 reported are summarised in FIGURE 104.1. The most common symptoms are depression 71%, irritability 56%, tiredness 35%, headache 33%, bloatedness 31%, breast tenderness 21%, tension 19% and aggression/violence 13%.6 Other important symptoms include weight gain, lowered performance, decreased libido and feeling out of control.

Incidence Up to 90% of women may experience premenstrual symptoms, which can vary from moderately severe in 20–40% of women to disabling in 2%.4 Interestingly, up to 15% of women can feel better premenstrually.5 Statistics from countries such as Sweden, the US and the UK indicate that up to 40% of women are significantly affected.5 About 5–10% of women experience such severe symptoms that PMS disrupts their quality of life.

Classification of PMS It is convenient to classify PMS in terms of severity of symptoms.3 1 Mild: symptoms signal onset of menstruation. No medical advice sought or needed. 2 Moderate: symptoms annoying but insufficient to interfere with function at home or work. Medical advice sought in about one-third.

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Psychological symptoms insomnia moodiness irritability anxiety tension depression confusion food cravings

Physical symptoms nausea headache dizziness hot flushes acne

Table 104.1 A

B

breast swelling and tenderness

bloated abdomen

C

constipation

swelling of ankles

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D FIGURE 104.1 Symptoms of premenstrual syndrome

E F

3 Severe: symptoms are such that functions at work or home are disrupted. Medical advice is usually sought. This disruptive form is labelled PMDD (see TABLE 104.1).

Differential diagnosis3 • Menopause syndrome • Mastalgia • Other causes of fluid retention—kidney or adrenal • Thyroid disorder (hyper- or hypo-activity) • Polycystic ovarian syndrome (PMS may be a feature of oestrogen excess) • Psychiatric disorders: depression, mania

Diagnosis • Thorough history—including diet, exercise habits, psychosocial background, emotional influences and family history • Menstrual calendar—for 3 months, showing timing of the three main symptoms3 • Physical examination to exclude gynaecological, endocrine or other systemic disease; and also include: — breast examination — vaginal examination and Pap test

G

Summary of PMDD criteria*7

Symptoms must occur during the week before menses and start to improve within a few days after onset of menses. One (or more) of the following symptoms must be present and marked: 1 Affective lability 2 Irritability or anger 3 Depressed mood or dysphoria 4 Anxiety, tension or feelings of being on edge One or more of the following to reach a total of 5 symptoms when combined with those from criterion B above: 1 Decreased interest in usual activities 2 Concentration difficulties 3 Marked lack of energy; lethargy 4 Marked change in appetite, overeating, or food cravings 5 Hypersomnia or insomnia 6 Feeling overwhelmed or out of control 7 Other physical symptoms (e.g. breast tenderness, bloating) Symptoms must interfere with work, school, productivity, usual activities or relationships Symptoms must not merely be an exacerbation of another disorder such as major depression Criteria for A must be confirmed by prospective daily ratings for at least two cycles The symptoms are not attributable to the physiological effects of a substance or other medical condition

*Adapted from DSM-5-TR

• Investigations (if considered appropriate, perform one or more serological tests): — thyroid function tests — serum progesterone and oestradiol in midluteal phase of three representative cycles — electrolytes and creatinine — prolactin—if galactorrhoea or oligomenorrhoea present

Management2,4 The basic aim of management is to reassure and treat the woman in such a way that she makes changes in her lifestyle to cope with the hormonal dysfunction rather than rely on medication. The management strategies include the following, with the emphasis on lifestyle factors. Explanation, reassurance and insight4 Cognitive-based therapy, which has been shown to have a positive effect in several RCTs,4,8 is very helpful for the patient to understand the nature of

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Premenstrual syndrome her symptoms and to receive appropriate support and rapport. Advise her to be open about her problem and inform her family and close friends about her symptoms. This is the prime treatment strategy. Keeping a diary3 Advise the patient to keep a daily diary of all her symptoms and when they occur over a 2–3 month period. This information should help her to plan around her symptoms: for example, avoid too many social events and demanding business appointments at the time when PMS symptoms are worst. Dietary advice3 Advise the patient to eat regularly and sensibly; eat small rather than large meals and aim for ideal weight (if necessary). Increase amount of complex carbohydrates (whole grains, vegetables and fruit), leafy green vegetables and legumes. Decrease or avoid: refined sugar, salt, alcohol, caffeine (tea, coffee, chocolate), tobacco, red meat and excessive fluid intake during premenstrual phase. Decrease total protein to 1 g/kg/day; decrease fats.9 Exercise Recommend a program of regular exercise such as swimming, aerobics, jogging or tennis. Such exercise has been proven to decrease depression, anxiety and fluid retention premenstrually.9 Relaxation Advise patients to plan activities that they find relaxing and enjoyable at the appropriate time. Consider stress reduction therapy, including appropriate counselling. Appropriate dress Advise sensible dressing to cope with breast tenderness and a bloated abdomen, such as a firmfitting brassiere and loose-fitting clothes around the abdomen. Medication Pharmaceutical agents that have been used with success in some patients and little or no relief in others include diuretics (e.g. spironolactone), vitamins and minerals (e.g. pyridoxine and evening primrose oil), antiprostaglandin preparations (e.g. mefenamic acid, indomethacin), bromocriptine,

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danazol (suppresses ovulation), GnRH agonists and hormone preparations such as the OCP, progestogens and oestradiol implants. A combination of agents may have to be used. The evidence base for symptom relief so far is as follows:2,10 • nil or negative—evening primrose oil,11 gingko biloba, progesterone/progestogens, OCP, bromocriptine, massage, homeopathy, reflexology, multivitamins • weak—magnesium, calcium, vitamin E, vitex angus castus (chaste tree) • moderate—vitamin B6,12 St John’s wort, spironolactone • strong (for PMDD)—SSRI agents and clomipramine, GnRH agonists, danazol

Oral contraception4 If contraception is required it is appropriate to use a COC-containing ethinyloestradiol and drospirenone since a meta-analysis of drospirenone, which is a progestogen derivative of spironolactone, concluded that it was effective in reducing the severe symptoms of PMDD. ethinyloestradiol 20 mgm + drospirenone 3 mg (o) once daily on days 1 to 24 of a 28-day cycle

Mild to moderate symptoms A trial of pyridoxine (vitamin B6) 50–100 mg daily.

Moderate to severe symptoms4,13 A trial of an SSRI is warranted in women with incapacitating PMDD who are unresponsive to CBT. fluoxetine 20 mg mane for 14 days before the anticipated onset of menstruation4 or sertraline 50 mg daily for 14 days before the anticipated onset of menstruation

Individualised therapy14 • PMS + fluid retention—use spironolactone 100 mg daily 3 days before expected onset of symptoms to day 1 of menstruation • PMS + severe mastalgia—consider danazol 200 mg (o) daily from onset of symptoms to onset of menses No matter what medication is taken, up to 70% of women will report an improvement in the early months of treatment, suggesting that a strong placebo factor is involved in management.15

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Practice tip Moderate to severe PMDD • Fluoxetine 20 mg (o) or sertraline 50 mg (o) daily in morning for 14 days before anticipated onset of menstruation and through to the first full day of menses of each cycle.

When to refer3

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• If the recommended approach of support, education, reassurance and stress management is still not effective. • Refer to a gynaecologist if underlying disease is suspected or proven (e.g. polycystic ovarian syndrome, endometriosis) • Consider referral if prescribing of danazol is contemplated • Refer to an endocrinologist if an endocrine disorder such as adrenal, pituitary or thyroid is suspected or proven • Consider referral if depression or psychosis worsens or is not cyclical

Practice tips • • • •

•

•

Keeping a daily diary of symptoms is very helpful for both patient and clinician. Aim for lifestyle changes and commonsense nonpharmacological management. Allow at least three cycles of treatment to provide a reasonable time for a particular medication. Drugs such as danazol are second-line drugs with significant side effects and should be used with caution. High doses of pyridoxine, such as 500 mg a day, are associated with peripheral neuropathy so the dosage should be kept at or below 100 mg/day. Be careful of overdiagnosing PMS and overlooking disorders such as depression, which may be exacerbated in the premenstrual phase.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Premenstrual syndrome

References 1 Smith MA, Yong Kin EQ. Managing the premenstrual syndrome. Clin Pharmacokinet, 1986; 5: 788–97. 2 Mazza D. Women’s Health in General Practice (2nd edn). Sydney: Elsevier, 2011: 16–21. 3 Smith M. Premenstrual syndrome. In: MIMS Disease Index. Sydney: IMS Publishing, 1991–92: 439–41. 4 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2014. 5 Farrell E. Menstrual disorders: how to treat. Australian Doctor, 25 May 1990: IV–VI. 6 Dalton K. The Premenstrual Syndrome and Progesterone Therapy. London: Heinemann, 1984: 3. 7 Premenstrual dysphoric disorder. In: Diagnostic and Statistical Manual of Mental Disorders (5th edn). Arlington: American Psychiatric Association, 2013: 191–4. 8 Blake F, Salkovskis P et al. Cognition therapy for premenstrual syndrome—a controlled trial. J Psychosom Res, 1998; 45 (4): 307–18. 9 Papadakis MA, McPhee SJ. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013: 749–50. 10 Wyatt K et al. Premenstrual syndrome. Clinical Evidence, 2000; 4: 1121. 11 Budeiri DJ et al. Is evening primrose oil of value in the treatment of premenstrual syndrome? Controlled Clinical Trials, 1996; 17: 60–8 (eTG 4, accessed 2/9/2014). 12 Wyatt K et al. Efficacy of vitamin B6 in the treatment of premenstrual syndrome: systemic review. BMJ, 1999; 318: 1375. 13 Brown J et al. Selective serotonin reuptake inhibitors for premenstrual syndrome. Cochrane Database Syst Rev. 2009 Apr 15; (2): CD006586 (PMID 193706 44). 14 Roughan P. Premenstrual syndrome. Current Therapeutics, 1995; 36 (11): 53–9. 15 Abraham S. The premenstrual syndrome. Modern Medicine Australia, 1992; September: 80–6.

Resource National Association of Premenstrual Syndrome

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The menopause

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Every woman should use what Mother Nature gave her before Father Time takes it away. L aurence J Peter 

Definitions

Physiology of the menopause

The menopause is the permanent cessation of menstruation in a non-hysterectomised woman. In most Western women it occurs between the ages of 45 and 55 years, with an average age of 51.5 years.1 Premature menopause is menopause occurring before age 40. The WHO has defined the menopause as signifying the permanent cessation of menstruation, resulting from the loss of ovarian follicular activity.2 However, the term is used in a broader sense to include the perimenopausal phase when ovarian function waxes and wanes and the periods become irregular. This may last 2–5 years and sometimes longer and involves the premenopausal and menopausal phases. The postmenopause is the period following the menopause but cannot be defined until after 12 months of spontaneous amenorrhoea, except in women who have had an oophorectomy. Surgical menopause is known as bilateral oophorectomy.

FIGURE 105.1 provides an overview of how menopausal symptoms are related to ovarian follicular activity and hormonal activity. The number of ovarian primary follicles declines rapidly as the menopause approaches, with few if any being identifiable following the cessation of menstruation. In the postmenopause phase, FSH rises to levels 10–15 times that of the follicular phase of the cycle while LH levels rise about threefold. The ovary secretes minimal oestrogen but continues to secrete significant amounts of androgens. An uncomfortable effect of oestrogen withdrawal, often not appreciated by medical practitioners, involves urogenital problems where the epithelium of the vagina, vulva, urethra and the base of the bladder becomes thin and dry, leading possibly to dysuria and frequency, itching, dyspareunia and atrophic bleeding. Hormone replacement therapy (HRT) can ameliorate these urogenital symptoms.

Summary The climacteric can be subdivided into four phases: Phase 1 Premenopausal: up to 5 years before the last menstrual period. Phase 2 Perimenopausal: the presence of early menopausal symptoms with vaginal bleeding (usually irregular). Phase 3 Menopausal: the last menstrual period. Phase 4 Postmenopausal: the phase beginning 12 months after the last menstrual cycle.

Osteoporosis Osteoporosis, which literally means porous bone, is reduced bone mass per unit volume. Osteoporosis is usually addressed in the context of the menopause because it is found mainly in postmenopausal middleaged and elderly women and can be largely prevented by correcting oestrogen deficiency.

Clinical features Because small amounts of oestrogen are still being produced in the adrenal glands, symptoms other than cessation of periods may be mild or absent. Up to 80% of women experience vasomotor symptoms for an average duration of 5 years.3

Symptoms Vasomotor:1 • • • • •

hot flushes (80%) night sweats (70%) palpitations (30%) lightheadedness/dizziness migraine

Psychological: • irritability • depression • anxiety/tension

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• Women’s health • formication (17%) • new facial hair • breast glandular tissue atrophy

tearfulness loss of concentration poor short-term memory unloved feelings sleep disturbances mood changes loss of self-confidence

Other: • unusual tiredness • headache

Urogenital (60%): • • • • • •

Clinical approach

atrophic vaginitis vaginal dryness (45%); itching; burning dyspareunia decline in libido bladder dysfunction (e.g. frequency dysuria) stress incontinence/prolapse

A thorough evaluation of the patient is important, including a good history. History Enquire about any symptoms related to oestrogen deficiency and other related symptoms, with an emphasis on the menstrual history and hot flushes. Enquire about mental state symptoms, such as anger, irritability, depression, moodiness, loss of selfesteem and other such problems. Ask about sexual history, contraception, micturition and social history, including relationships.

Musculoskeletal: • non-specific muscular aches • non-specific joint aches and pains Skin and other tissue changes: • dry skin

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Cessation of menses Years before (–) or after (+) the menopause

–3

–2

–1

+1

+2

+3

periods (menses) follicle number oestradiol progesterone FSH LH fertility hot flushes dry vagina psychological symptoms osteoporosis

FIGURE 105.1 Schematic representation of some clinical, biological and endocrinological features of the perimenopausal and postmenopausal phases Source: After Burger3

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The menopause Consider all women at the menopause to be at risk for cardiovascular disease, cancer (especially breast, ovary and cervix), diabetes and osteoporosis.2 Information on family history of osteoporosis, cancer and cardiovascular disease should be sought. Physical examination The general examination should include measurement of blood pressure, weight and height, breast palpation, abdominal palpation, vaginal examination and Pap test. Note the texture of the vaginal epithelium. Investigations2 Apart from a Pap test, the following tests should be considered:

Sexual activity Advise that it is normal to continue sexual relations, using a vaginal lubricant for a dry vagina. Contraception is advisable for 12 months after the last period for women over 50 years and two years for those under 50 years. The OCP can be used up to 50–51 years if there are no risk factors.

Hormone replacement therapy

urinalysis full blood count, lipids including HDL liver function tests thyroid stimulating hormone (TSH) mammography (all women, preferably before or after 3 months on HRT) • diagnostic hysteroscopy and endometrial biopsy only if undiagnosed vaginal bleeding • bone density study (if risk factors) If diagnosis is in doubt (e.g. perimenopause, younger patient 12 months HBV and HCV serology HIV serology (after counselling) Syphilis serology (TPHA) MSU and dipstick urine Discuss: First trimester combined screening test + NF test Ultrasound—18–20 weeks Subsequent visits Oral glucose challenge test or OGTT (now preferred to OGC because more accurate)—28 weeks

• 18-week morphology scan

Rubella anti—D immunoglobulin 28 and 34 weeks (Rh-negative mother) FBC—36 weeks Group B Streptococcus (GBS) swab—36 weeks

• • • •

Initial in first trimester: 8–10 weeks Up to 28 weeks: every 4–6 weeks Up to 36 weeks: every 2 weeks 36 weeks–delivery: weekly

Guidelines for OGTT • • •

First visit—if previous gestational diabetes or strong family history About 20 weeks—as above + normal initial test About 26 weeks—for all other patients

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The average number of visits is 12 but the need for this number is being questioned, with some authorities recommending as few as six visits. A systematic review of seven RCTs found no difference in the detection of pre-eclampsia, urinary tract infection, low birthweight or maternal mortality when a schedule of reduced antenatal visits was compared with the traditional routine.5,8 However, a sensible approach would be to plan visits according to need and circumstances in a flexible way. For each visit record: • weight (to calculate gain) • blood pressure • urinalysis (protein and sugar)—many clinics repeat at each visit only if there is proteinuria at the first visit or if signs of hypertension, kidney disease or pre-eclampsia develop. See TABLE 108.2 • uterine size/fundal height • fetal heart (usually audible with stethoscope at 25 weeks and definitely by 28 weeks): detected by Sonicaid (or similar) from 18–20 weeks3 • fetal movements (if present) • lie, presentation and position of fetus (third trimester) • presence of any oedema Record day of first fetal movements (i.e. ‘quickening’) (ask patient to write down the dates): • primigravida: 17–20 weeks • multigravida: 16–18 weeks Table 108.2

Causes of proteinuria in pregnancy

Urinary tract infection Contamination from vaginal discharge

A common routine schedule (if all appears normal)

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Pre-eclampsia toxaemia Underlying chronic kidney disease

Fundal height The relative heights of the uterus fundus are shown in FIGURE 108.2. The uterus is a pelvic organ until the twelfth week of pregnancy. After this time it can be palpated abdominally. At about 20–22 weeks it has reached the level of the umbilicus and reaches the xiphisternum between 36 and 40 weeks. If the symphysis fundal height is more than 2 cm different from that expected for the gestation, the cause of this should be evaluated by ultrasound examination. Palpation of the fundal height is affected by obesity and tenseness of the abdominal wall.

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Multigravida

Primigravida

40

36

36

32

32 28

28

24

24

20

16 12

20

16 12

FIGURE 108.2 Fundal height in normal pregnancy (in weeks); the height of the fundus is a guide to the period of gestation. Nulliparas experience lightening at about 36 weeks when the fundal height usually reverts to the 34-week level.

Management of specific issues Nutrition advice A healthy diet is very important and should contain at least the following daily allowances:

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1 Eat most: • fruit and vegetables (at least 4 serves) • cereals and bread (4–6 serves) 2 Eat moderately: • dairy products—3 cups (600 mL) of milk or equivalent in yoghurt or cheese • lean meat, poultry or fish—1 or 2 serves (at least 2 serves of red meat per week) 3 Eat least: • sugar and refined carbohydrates (e.g. sweets, cakes, biscuits, soft drinks) • polyunsaturated margarine, butter, oil and cream Bran with cereal helps prevent constipation of pregnancy. If the ideal diet is followed, iron, vitamin and calcium supplements should not be necessary, although most patients prefer to take OTC vitamin and mineral preparations (e.g. iron, folic acid, multivitamins, iodine). Do not diet to lose weight. It is usual to gain about 12 kg during pregnancy.

Less weight gain is recommended for women who are overweight pre-conception.

Smoking, alcohol and other drugs Encourage patients to avoid all street drugs, alcohol, tobacco and caffeine (ideally). If they find this impossible, encourage the following daily limitations: • 1 standard drink of alcohol • 1 cup of coffee or 2 cups of tea Other household members should also stop smoking as passive smoking may be harmful to mother and child. There is convincing evidence that promotion of smoking cessation programs during pregnancy is effective, with improved outcomes, including reduction in preterm birth rates and low birthweight rate.10 The fetal alcohol syndrome is a leading cause of mental impairment, so it is best to abstain. Mothers taking illicit drugs, especially opioids and amphetamines, require identification, counselling, treatment and surveillance for the neonatal abstinence syndrome in the newborn child.

Breastfeeding Mothers-to-be should be encouraged to breastfeed. Give advice and relevant literature. They can be directed to a local nursing mothers’ group for support and guidance if necessary.

Antenatal classes Referral to therapists conducting such classes can provide advice and supervision on antenatal exercises, back care, posture, relaxation skills, pain relief in labour, general exercises and swimming. Enrolment with the partner is recommended.

Normal activities Mothers should be reassured that pregnancy is a normal event in the life cycle and that normal activities should be continued. Housework and other activities should be performed to just short of getting tired. The importance of getting sufficient rest and sleep should be emphasised.

Sex in pregnancy11 Coitus should be encouraged during pregnancy but with appropriate care, especially in the 4 weeks before delivery. Restriction would only seem necessary if there has been an adverse obstetric history or there are major complications in the current pregnancy such as antepartum haemorrhage.

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Basic antenatal care The couple should be encouraged to be loving to each other and communicate their feelings freely, as the need for affection and physical contact is important. Coital techniques can be modified as the pregnancy progresses—posterior entry and the female superior position are quite suitable.

Travel Pregnant women should avoid standing in trains. They should avoid international air travel after 28 weeks and travel after 34 weeks is usually not permitted. Patients should be counselled to wear a seat belt during car travel. Refer to CHAPTER 14 for travel sickness in pregnancy.

Psychosocial and emotional stress Antenatal visits provide an ideal opportunity to become acquainted with the ‘real’ person and explore issues that help the patient. Provide whole person understanding with appropriate help and reassurance where necessary. Areas to be explored include support systems, attitudes of patient and partner to the pregnancy, sexuality, expectation of labour and delivery, financial issues, and attitudes of parents and in-laws.

Weight gain in pregnancy Although a standard weight gain is given as 12 kg over 40 weeks of pregnancy, it is common for some women in Australia to gain up to 20 kg without adverse effects.4 Encourage sensible weight control. Normal weight gain is minimal in the first 20 weeks, resulting in a 3 kg weight gain in the first half of pregnancy. From 20 weeks onwards there is an average weight gain of 0.5 kg per week. From 36 weeks the weight gain usually levels off.4

Fetal movement chart If daily fetal movements exceed 10 and the regular pattern has not changed significantly, then usually the fetus is at no risk. However, if the movements drop to fewer than 10 per day, the patient should be referred to hospital for fetal monitoring.

Possible exposure to rubella When contact with a possible case of rubella occurs during pregnancy it is essential to establish the immune status of the patient. If she is already immune no further action is necessary. If her immune status is unknown, perform a rubella IgG titre and IgM and repeat the IgG and IgM titres in 2–3 weeks.

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Vaginal bleeding in early pregnancy12 This is a common problem in the first trimester in particular. At least 10% of normal pregnancies will have an episode and about 15% of recognised pregnancies will miscarry. If the bleeding is light to moderate and the pain mild or absent the question is ‘Can a viable pregnancy continue or is there an ectopic pregnancy or a threatened miscarriage?’ • 1500 IU/L transvaginal ultrasound should be arranged as, if the pregnancy is progressing normally and within the uterine cavity, it will usually be seen. • 6–8 weeks: Ultrasound will define an intrauterine pregnancy and exclude an ectopic. • >8 weeks: Normal ultrasound is reassuring since miscarriage rate is only 3% unless the amount of intrauterine blood is large. Note: Rest is not necessary for threatened miscarriage. A small bleed between 18–24 weeks indicates possible cervical ‘weakness’ and warrants a speculum or vaginal examination plus fetal assessment. Be aware that an incomplete abortion can cause cervical shock (pelvic pain and fainting). Products of conception must be removed from the cervical os. Consider the antiphospholipid syndrome for recurrent miscarriage and arrange antibody testing (see CHAPTER 32). Refer to a specialist for full assessment if 3 consecutive miscarriages have occurred. Threatened miscarriage If a threatened miscarriage occurs, check the blood group and test for rhesus antibodies in maternal serum. If the mother is Rh-negative and no antibodies are detected, give one ampoule of anti-D gammaglobulin intramuscularly if the woman actually miscarries (not for threatened abortion). Assess her pelvis to rule out an ectopic pregnancy and, if indicated and the β-hCG is >1500 IU/L, perform pelvic scanning to confirm viability of the fetus or the presence of an extra-uterine gestation.

Pregnancy sickness13 • Nausea and vomiting occur in more than 50% of women

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• Almost always disappears by the end of first trimester • Mild cases can be dealt with by explanation and reassurance; it is preferable to avoid drug therapy if possible • Simple measures: — small, frequent meals including ginger up to 1 g daily — a fizzy soft drink, especially ginger drinks, may help — ensure adequate hydration, including sucking ice chips and drinking small amounts of fluid — avoid stimuli such as cooking smells — take care with teeth cleaning — avoid oral iron • Medication (for severe cases): — pyridoxine 25–50 mg bd or tds — if still ineffective add metoclopramide 10 mg tds

Hyperemesis gravidarum This is severe vomiting in pregnancy, which may result in severe fluid and electrolyte depletion. It occurs in about 1 in 100 pregnancies. Associations • Normal complication • Hydatidiform mole • Multiple pregnancy • Urinary infection

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Management • Test urine—MCU (micro-culture of urine); ketones: if +ve, admit to hospital • Ultrasound examination • Test electrolytes, urea, LFTs • Bed rest • Nil orally • Fluid and electrolyte replacement • Pyridoxine 50–100 mg daily IV/oral • Metoclopramide 10 mg IV → 10 mg (o) tds (if necessary); if ineffective, ondansetron 4–8 mg IV 8–12 hourly • Return to oral intake

Heartburn Gastro-oesophageal reflux is a major source of discomfort to women in the latter half of pregnancy. Non-pharmacological treatment such as frequent small meals, avoidance of bending over and elevation of the head of the bed are the mainstays of treatment. Smoking, alcohol and caffeine (coffee, chocolate, tea) intake should be avoided. Regular use of antacids is

effective (e.g. alginate/antacid liquid—Gaviscon, Mylanta Plus—10–20 mL) before meals and at bedtime. H2-receptor antagonists or PPIs may be necessary.

Cramps Pregnant women are more prone to cramp. If it develops they should be advised simply to place a pillow at the foot of the bed so that plantar flexion of the feet is avoided during sleep. Prolonged plantar flexion is the basis of the cramps. Quinine, including tonic water, should be avoided. There is no evidence that calcium supplements help cramps during pregnancy.14

Varicose veins These can be troublesome as well as embarrassing. Wearing special supportive pantyhose (not elastic bandages) is the most comfortable and practical way to cope, in addition to adequate rest.

Haemorrhoids Haemorrhoids in the later stages of pregnancy can be very troublesome. Emphasising the importance of a high-fibre diet to ensure regular bowel habit is the best management. Painful haemorrhoids may be eased by the application of packs soaked in warm saline or perhaps haemorrhoidal ointments containing local anaesthetic.

Dental hygiene Dental problems can worsen during pregnancy so special care of teeth and gums, including a visit to the dentist, is appropriate. Continuation of cleaning with a softer brush is recommended.

Back pain Back pain, especially low back pain, is common during pregnancy and special back care advice can help women cope with this problem, which can become debilitating. Advice about lifting, sitting and resting using a firm mattress, and avoiding high-heeled shoes, will help. Physical therapy administered by a skilled therapist can be extremely effective for pregnant patients but certain safety rules should be followed: • First trimester: use normal physical therapy and advise exercises. • Second trimester: use supine side lying rotation and sitting techniques only; advise exercises. • Third trimester: avoid physical therapy (if possible); encourage exercises.

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Basic antenatal care Guidelines for treatment • Keep mobilisation and manipulation to a minimum. • Use stretching and mobilisation in preference to manipulation. • Safeguard the SIJs in the last trimester. • Encourage active exercises as much as possible. • Avoid medications wherever possible. • Give trigger point injections (5–8 mL 1% lignocaine) around the SIJs if necessary.

Exercise guidelines Advise the patient that walking is an excellent exercise. For additional exercise activity: • exercise at a mild to moderate level only • avoid overheating and dehydration • allow for a long warm-up before exercise and a long cool-down • choose low-impact or water exercise • stop if there are adverse symptoms (e.g. any pain, bleeding, faintness, undue distress) • avoid scuba diving and sky diving

Carpal tunnel syndrome Splinting of the hand and forearm at night might be beneficial. If desperate, an injection of corticosteroid into the carpal tunnel can be very effective (check drug category for risk relative to dates). Sometimes operative division of the volar carpal ligament is necessary. Most problems subside following delivery.

Hypotension This is due to increased peripheral circulation and venous pooling. If bleeding is eliminated, advise to avoid standing suddenly and hot baths. It may cause syncope. Fainting may occur when the woman lies on her back in the latter half of pregnancy (supine hypotension). Avoid lying on the back—lie on the left side.

Pruritus Generalised itching (pruritus gravidarum) is usually associated with cholestasis due to oestrogen sensitivity in the third trimester. Order LFTs and, if not serious, reassure and prescribe a soothing skin preparation (e.g. aqueous cream ± glycerol). If LFTs markedly abnormal or if pruritus is severe, the risk of fetal death is increased and special care and assessment is required.

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Obesity15 Obesity is associated with increased obstetric morbidity, including difficult labour and potential anaesthetic risks. Encourage weight loss diet with the aid of a dietitian.

Breathlessness of pregnancy16 Consider physiological breathlessness of pregnancy in a woman with unexplained dyspnoea. It starts in the second trimester, is constant and aggravated by exercise and emotional stress. No special treatment is needed or helpful. The breathlessness usually settles 6–8 weeks after delivery.

Mineral supplements in pregnancy Iron Iron is not routinely recommended for pregnant women who are healthy, following an optimal diet and have a normal blood test. Those at risk (e.g. with poor nutrition, vegan diet) will require supplementation. Folic acid Folic acid is advised for all women contemplating pregnancy, starting about 3 months prior to conception and continuing until 12 weeks after conception. Dose: 0.5 mg (o) daily.12 In those at risk (e.g. previous neural tube defect and history of epilepsy), the dose is 5 mg per day.15 Vitamin B12 Vitamin B12 is essential for the developing fetus and if deficiency is known or suspected (e.g. vegetarian/ vegan diet), test and give injections of B12 if deficient. Iodine It is recommended, for pregnant and lactating women and those planning a pregnancy, to take 150 mcg of supplementary iodine as soon as possible by using iodised salt for cooking and a multivitamin that includes iodine. Vitamin D There may be a case for routine testing but it is advisable to test women who are dark-skinned, veiled and at risk.17,18 If deficient (70 nmol/L with cholecalciferol 1000–2000 IU daily.19

Advice on when to seek medical help • If contractions, unusual pain or bleeding occur before term • If the baby is less active than usual: fetal movements should not decrease close to term

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• If the membranes rupture (with fluid loss) • The onset of regular contractions 5–10 minutes apart if >34 weeks gestation but earlier if possible premature labour occurring between 22 and 34 weeks gestation

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • About your pregnancy • Miscarriage • Pregnancy planning

References 1 Barker JH. General Practice Medicine. Edinburgh: Churchill Livingstone, 1984: 76–89. 2 Harris M (Chair) Guidelines for Preventive Activities in General Practice (7th edn). Melbourne: RACGP, 2009: 11–14. 3 The Royal Women’s Hospital (Victoria). Clinical Practice Guidelines (Professional). 4 Fung P, Morrison J. Obstetric share-care. Aust Fam Physician, 1989; 18: 479–84. 5 Oats JJN. Routine antenatal screening: a need to evaluate Australian practice (editorial). Med J Aust, 2000; 172: 311–12. 6 Hunt JM, Lumley J. Are recommendations about routine antenatal care in Australia consistent and evidence-based? Med J Aust, 2002; 176: 255–61. 7 Hyett J. Non-invasive prenatal testing for Down syndrome. Aust Prescr, 2014; 37: 51–5. 8 Carroli G, Villar J, Piaggio G et al. WHO systematic review of randomised controlled trials of routine antenatal care. Lancet, 2001; 357: 1565–70.

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9 The Royal Women’s Hospital (Victoria). Clinical Practice Guidelines. Antenatal care schedule—routine low risk.

10 Lumley J, Oliver S, Waters E. Interventions for promoting smoking cessation during pregnancy (Cochrane review). In: the Cochrane Library, Issue 1, Oxford: Update Software, 2001. 11 Beischer NA, Mackay EV. Obstetrics and the Newborn. Sydney: Saunders, 1986. 12 Peat B. Antenatal care: common issues facing GPs in shared care. Med Today, 2001; June: 81–5. 13 Humphrey M. Common conditions in an otherwise normal pregnancy. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 116–20. 14 Hammer I et al. Calcium treatment of leg cramps in pregnancy. Acta Obstet Gynaecol Scand, 1981; 60: 345–7. 15 Public Affairs Committee of the Teratology Society. Teratology Public Affairs Committee Position Paper: Maternal obesity and pregnancy. Birth Defects Research (Part A), 2006; 76: 73–7. 16 Burdon J. Respiratory medicine. Check Program 395. Melbourne: RACGP, 2005: 17–8. 17 MRC Vitamin Study Research Group. Prevention of neural tube defects. Lancet, 1991; 338: 131–7. 18 Grover SR, Morley R. Vitamin D deficiency in veiled or darkskinned pregnant women. Med J Aust, 2001: 151–2, 175. 19 Ebeling PR. Routine screening for vitamin D in pregnancy: past its due date? Med J Aust, 2011; 194 (7): 234–7.

Resources NICE NHS Fetal Anomaly Screening Programme The Royal Women’s Hospital

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Infections in pregnancy

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After autopsies I concluded that the newborn died of childbed fever, or in other words, they died from the same disease as the maternity patients . . . from hands contaminated with cadaverous particles brought into contact with the genitals of delivering maternity patients. If those particles are destroyed chemically, so that in examinations patients are touched by fingers but not by these particles, the disease must be reduced. To destroy cadaverous matter adhering to hands I used chlorine liquida . . . starting in May 1847 . . . When I look back upon the past, I can only dispel the sadness which falls upon me by gazing into the happy future when the infection will be banished. Ignaz Semmelweis (–), Autobiographical Introduction Semmelweis discovered the infectious nature of puerperal fever and how physicians transmitted it, but was not believed at the time. He died in a mental institution.

Urinary tract infection Urinary tract infection includes pyelonephritis, cystitis and asymptomatic cases (see CHAPTER 25).

Acute pyelonephritis This infection, usually due to Escherichia coli, is one of the most common infective complications of pregnancy. Symptoms include fever, chills, vomiting and loin pain. Bladder symptoms such as frequency and dysuria are commonly absent. The patient should be hospitalised and usually requires intravenous antibiotic therapy and possibly rehydration. Treatment amoxycillin 1 g IV 6 hourly for 48 hours, then 500 mg (o) 8 hourly (if bacteria sensitive) for 14 days1, 2 • Alternatives: cephalosporins (e.g. ceftriaxone 1 g IV and cephalexin 500 mg (o))

Acute cystitis Patients with acute cystitis typically have dysuria and frequency. Treat for 10–14 days. Treatment cephalexin 250 mg (o) 6 hourly2 or amoxycillin/potassium clavulanate (500/125 mg) (o) 12 hourly or nitrofurantoin 50 mg (o) 6 hourly, if a betalactam antibiotic is contraindicated

Note: Nitrofurantoin is contraindicated in the third trimester of pregnancy as it may lead to haemolytic diseases in the newborn. Cotrimoxazole and sulphonamides should be avoided. Amoxycillin is recommended only if susceptibility of the organism is proven. • A high fluid intake should be maintained during treatment

Asymptomatic bacteriuria1 • 5–10% of pregnant asymptomatic women have positive cultures during pregnancy. • Approximately 5% of such women subsequently develop pyelonephritis during pregnancy with an increased risk of preterm labour, mid-trimester abortion and pregnancy-induced hypertension. • Ideally all women should be screened for bacteriuria at their first visit. • Less than 1% will subsequently develop bacteraemia. Treatment Treatment is recommended according to culture sensitivities. It is preferable to delay it until the first trimester has passed (see CHAPTER 25).2

Puerperal infection Puerperal infection is defined as a wound infection of the genital tract arising as a complication of childbirth. It especially involves the placental site in the uterus and laceration or incisions of the birth canal. Chorioamnionitis is infection of the placenta

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and membranes usually from normal vaginal flora (e.g. Group B Streptococcus (GBS), E. coli). It is worth recalling that Lancefield group A Streptococcus infection was the outstanding cause of septic maternal death before the introduction of penicillin. GBS has only recently been identified as a human pathogen.3 It is carried by 15–20% of pregnant women in the vagina, usually without causing maternal problems or symptoms. Routine testing for GBS is recommended at 36 weeks because:

Vaginal candidiasis

• if antibiotics are not given to carriers (the 15–20% who carry GBS) in labour, 50% of babies become colonised and 1% of these are severely affected and often die4 • the onset can be early or late in the neonate with a severe clinical presentation of rapid deterioration with septic shock. High-risk situations are premature rupture of the membranes, especially preterm, early labour and maternal intrapartum fever and also vaginal delivery • if antibiotics are given in labour (at least 2 hours prior to delivery) fetal colonisation and infection almost never occurs

TRANSMISSIBLE VIRAL INFECTIONS

Intrapartum GBS prophylaxis3 Indicated for GBS carrier in current pregnancy and previous baby with early onset disease. During labour: benzylpenicillin 1.2 g IV statim then 600 mg IV 4 hourly until delivery (clindamycin 600 mg IV 8 hourly if hypersensitive to penicillin)

Intra-uterine sepsis (overt or suspected)3 Maternal puerperal GBS infection usually has the following features:

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• • • •

high fever >38°C on any 2 days from days 1 to 14 tachycardia (maternal and fetal) endometritis—offensive or purulent discharge maybe abdominal pain, collapse or delirium if severe (indicates chorioamnionitis)

Swab the genital tract and culture and order FBE (neutrophilia + leucocytosis). If the woman is febrile but not clinically ill, treat with amoxycillin  +  clavulanate 875/125 (o) bd for 5–7 days. If septic treat with: amoxycillin 2 g IV 6 hourly plus gentamicin 4–6 mg/kg IV daily plus metronidazole 500 mg IV 12 hourly

Candida (thrush) is common in pregnancy since pregnancy is a predisposing factor to the growth of the fungus. Treatment follows conventional lines with topical creams and vaginal tablets as described in CHAPTER 106. Clotrimazole is a first-line treatment. Oral medication with fluconazole or itraconazole should be avoided.

Rubella Key facts and checkpoints • Fewer than 5% of women are not immune (IgG negative) and many are immigrants. • Take blood for IgG antibodies—no concerns if negative. • Rubella IgM indicates recent infection, rises 7–10 days after infection, and a real risk if pregnant. • Reinfection can occur even after vaccination so test all pregnant contacts. • Congenital rubella features are described in CHAPTER 93. • Effects on fetus:5 —  41 weeks) Multiple pregnancy Polyhydramnios Need for amniocentesis: • genetic concerns • abnormal AFP • other General factors

Age >35 years; 30 at first visit Pre-pregnancy weight 18 h

Malpresentation Placental insufficiency Inadequate antenatal care

Late presentation (after 20 weeks) No antenatal care Failed or poor attendance

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High-risk pregnancy Risk factors The following are risk factors for pregnancy-induced hypertension: • • • • • • • • • • • •

nulliparity/primigravida family history of hypertension/pre-eclampsia chronic essential hypertension diabetes complicating pregnancy obesity donor sperm or oocyte pregnancy multiple pregnancy hydatidiform mole hydrops fetalis hydramnios kidney disease autoimmune disease (e.g. SLE)

Clinical features of superimposed pre-eclampsia include hypertension, excessive weight gain, generalised oedema and proteinuria (urinary protein >0.3 g/24 hours). Late symptoms include headache (related to severe hypertension), epigastric pain and visual disturbances. Risks of severe pre-eclampsia/ hypertension7

Maternal risks (poor control) • • • •

Kidney failure Cerebrovascular accident Cardiac failure Coagulation failure

Risks to baby • Hypoxia • Placental separation • Premature delivery Management The optimal treatment is delivery, and induction of labour needs to be timed appropriately—based on parameters such as the BP level and the development of proteinuria. The BP level should be kept below 160/100 mmHg because at this level intra-uterine fetal death is likely to occur and there is a risk of maternal stroke. 6

Antihypertensive drugs

Contraindicated drugs are ACE inhibitors and diuretics. There is no place for the use of diuretics alone unless cardiac failure is present. Commonly used medications: • beta blockers (e.g. labetalol, oxprenolol and atenolol) (used under close supervision and after 20 weeks gestation)

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• methyldopa: good for sustained BP control • nifedipine Labetalol, hydralazine and diazoxide are useful for rapid control of BP in hypertensive crises (e.g. hydralazine 5 mg IV bolus every 20–30 minutes or continuous infusion). Guidelines for urgent referral/admission to hospital

Maternal factors • Progressing pre-eclampsia including development of proteinuria • Inability to control BP • Deteriorating liver, blood (platelets), kidney function • Neurological symptoms and signs (e.g. headache, drowsy and confused, twitching, rolling eyes, vomiting, visual disturbances, hyper-reflexia, clonus) — i.e. imminent eclampsia

Fetal factors • Abnormal cardiotocograph (CTG) indicating fetal distress • Intra-uterine growth retardation Refer to eclampsia ward under specialist care. Treatment of severe pre-eclampsia: prevention of convulsions • Control BP: use IV hydralazine or diazoxide—don’t suppress to 5.5 mmol/L or 2-hour level >8.5 mmol/L The same risks to mother and fetus such as macrosomia, IUFD, congenital malformations, hyaline membrane disease and neonatal hypoglycaemia as for pre-existing diabetes are applicable.11 Note: Glycosuria in pregnancy is unhelpful for screening because it is common in pregnancy and lacks specificity. Principles of management These are the same as for pre-existing diabetes (above). If insulin is required antenatally, cease insulin postpartum. Aim to deliver vaginally at term at the latest, unless earlier delivery is indicated by obstetric complications.

Post delivery Follow up GTT at 6 weeks and then every 5 years. Gestational diabetes is likely in subsequent pregnancies and there is a 30% risk of developing diabetes in later life—even 0.25 mmol/L).

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• Pregnancy uncommon in dialysis patients. If so, there can be many problems requiring increased use of dialysis. • Refer these patients and admit if hypertension becomes poorly controlled or marked proteinuria (>2 g/24 hours) is present. • Aim for delivery at 38–40 weeks at the latest. Delivery is usually required before this time. • In kidney transplant patients the risk of early miscarriage is ↑ —surviving pregnancies have >90% success. ↑  risk hypertension and pre-eclampsia but low chance of kidney rejection. Pelvic site of transplant is not a problem.

Systemic lupus erythematosus Key facts and checkpoints • Pregnancy does not seem to cause exacerbations of SLE. • SLE can adversely affect pregnancy according to disease severity. • Increased incidence of spontaneous abortions and stillbirths—related to lupus anticoagulant and anticardiolipin antibodies (see CHAPTER 32). • ↑  risk pre-eclampsia, prematurity, IUGR, perinatal mortality. • Neonatal lupus syndrome includes blood disorders and cardiac abnormalities in the neonate. • Increased maternal morbidity—kidney complications, pre-eclampsia.

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Management • Careful preconception counselling—plan pregnancy in remission phase. • Refer for review of drugs. • Many investigations required under specialist supervision including lupus antibodies, APTT, FBE, kidney function, ultrasound scans. • Corticosteroids (e.g. prednisone) are mainstay of therapy. • Low dose aspirin (100 mg daily) if anticardiolipin antibodies present, to prevent onset of preeclampsia or IUGR. • Low molecular weight heparin may be used as alternative to aspirin and in presence of prolonged APTT. • Timing of delivery according to assessment of progress and status of fetus. • Watch for flare-up postpartum (may require increased prednisolone).

Thrombocytopenia in pregnancy The two most common causes of significant thrombocytopenia (TCP) in an otherwise normal pregnancy blood film are gestational thrombocytopenia and immune thrombocytopenia. Other causes that need to be considered are SLE, anti-phospholipid syndrome (APS), drug-induced thrombocytopenia and HIV infection.

Gestational thrombocytopenia In up to 4% of pregnancies, mild TCP in the range 75–150 nL develops, usually in the third trimester. Because of the increasing hazard of epidural anaesthesia in platelet counts under 75/nL, a 2-week course of prednisolone is often prescribed at 37–38 weeks gestation, aiming for a platelet count in excess of 100/nL at the time of delivery. It is prone to recur in subsequent pregnancies.

Immune TCP Although less common than gestational ITP, it is clinically more significant since it is typically severe and arises earlier in pregnancy. ANA factor and other antibody studies are necessary to exclude SLE and APS. Platelet-specific antibodies are found in at least 50% of ITP patients. Life-threatening cases (1L), 3 small bleeds (1000 mL blood loss. Causes • Uterine atony • Retained placenta/placental fragments • Soft tissue laceration of genital tract (e.g. episiotomy, cervical tear) • Ruptured or inverted uterus • Coagulation disorder Principles of management • Rub up the uterine fundus and give oxytoxic agents. • Resuscitate. • Stop the bleeding. • Make the diagnosis—inspect placenta/speculum examination of genital tract. • Catheterise (a full bladder can aggravate the problem). • An urgent examination and exploration under general anaesthetic may be necessary. Treatment13 • IV access—commence crystalloid IV fluids • Tests: FBE, cross-match blood, coagulation profile • High-flow oxygen by mask • IV oxytocin (Syntocinon) 10 IU followed by 40 IU in IV infusion of Hartman solution • If continuing heavy bleeding ergometrine 0.25–0.5 mg IM or IV + 10 mg metoclopramide IV • Consider 1 mg (5 tablets) of misoprostol per rectum • If retained placenta—deliver with cord traction or manual removal • If continuing heavy bleeding—bimanual compression for 3 minutes • Treat any coagulation disorder (e.g. fresh plasma/ platelet transfusion) If a persistent atonic uterus is not controlled by oxytocics, 1–2.5 mg doses of intramyometrial prostaglandin F2-α can be injected through the abdominal wall. Life-saving measures can include insertion of a Bakri balloon for tamponade,14 uterine artery ligation, internal iliac artery ligation (usually bilateral) or hysterectomy.

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High-risk pregnancy

Blood group isoimmunisation Blood group or red cell isoimmunisation is primarily related to Rhesus D (RhD) isoimmunisation leading to haemolytic disease of the newborn from the effect of the development of anti-D antibodies.10 These antibodies develop from feto-maternal haemorrhage/ transfusion in RhD-negative women carrying an RhD-positive fetus. Effects of haemolytic disease on the fetus includes hydrops (oedema), FDIU. Effects on the neonate include anaemia, heart failure, jaundice and hepatosplenomegaly. Screening Rh negative mothers: at presentation, 28 weeks, and 34–36 weeks. Do not perform screening if anti-D has been given.

Rhesus immunoprophylaxis Indications for giving anti-D Ig to the RhD-negative mother free of immune anti-D: • after spontaneous miscarriage at any stage of pregnancy • after threatened miscarriage • after delivery of an RhD-positive baby • following termination of pregnancy or ectopic pregnancy • following any sensitising event during pregnancy that may provoke a transplacental haemorrhage (e.g. amniocentesis or CVS, APH, external cephalic version, significant closed abdominal trauma) • prophylactically at 28 and 34 weeks in an apparently normal pregnancy Kleihauer test This is a test on maternal blood after a sensitising event to detect the degree of feto-maternal transfusion and whether increased anti-D Ig is required.

ABO incompatibility This usually occurs when the mother is group O and the baby A or B and can occur in the first pregnancy without a tendency to become increasingly severe in subsequent pregnancies. A small number of babies have mild jaundice while severe haemolytic consequences are rare.

Thromboembolism in pregnancy Pregnancy is associated with an increased risk of thromboembolism with an incidence of about 1% of deep venous thrombosis (DVT). Untreated DVT carries about 15% risk of pulmonary embolism.

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DVT or pulmonary embolism should be suspected in a woman in the antenatal or postpartum period who complains of pain or swelling in the leg, mild unexplained fever, dyspnoea or chest pain (see CHAPTER 133). Risk factors include past history of DVT, prolonged bed rest, operative delivery, multiparity, postpartum surgical procedure, anaemia, inherited thrombophilia disorders or antiphospholipid antibodies. If a DVT is suspected, low molecular weight heparin is recommended until investigation and specialist advice are obtained.

Hydatidiform mole10 Hydatidiform mole is an overgrowth of gestational trophoblastic tissue. The moles may be complete (no fetal tissue) or partial (some fetal tissue). Incidence 1:1400 pregnancies. There is a risk that some persistent gestational trophoblastic may become invasive and penetrate the uterus and metastasise to the lungs. One in 20 progress to develop choriocarcinoma. Presentation • Bleeding in early pregnancy ± passage of grapelike debris • May be exaggerated symptoms of pregnancy (e.g. hyperemesis) • Uterus large for dates Management • Investigations: FBC, blood group and crossmatch, hCG level (very high), ultrasound pelvis (typical ‘snow-storm’ appearance), chest X-ray • Suction curette with oxytocin drip • Consider hysterectomy if patient has completed family planning • Register in the trophoblastic registry Follow-up • Chest X-ray: ? metastatic disease • Weekly serum (or urine) hCG until zero (usually takes 8–12 weeks), then monthly for 12 months • Avoid pregnancy for 12 months after hCG levels normal • The oral contraceptive pill is appropriate • Later a putrid vaginal discharge indicates malignancy • Refer for possible cytotoxic therapy (e.g. methotrexate and folinic acid) if hCG does not become normal or the process is >3 months, or it becomes elevated again and a new pregnancy has been excluded

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Multiple pregnancy This is associated with increased risks to mother and children. Facts • Spontaneous incidence9,11: twins 1:80; triplets 1:802 (1:6400); quads 1:804 • Increased incidence with clomiphene-induced ovulation and IVF • Twins: monozygotic (identical) 30%, dizygotic 70% • Conjoint twins are a special problem • Predisposing factors: family history, previous twins, infertility treatment, race esp. black Africans, age • Diagnosis: hyperemesis, ultrasound, polyhydramnios, large for dates, palpation two fetal heads/three poles ± many limbs, two different hearts heard • Presentation twins: first twin cephalic 70%, both cephalic 40%, cephalic + breech 30% Complications • Maternal: increased risk anaemia; symptoms of pregnancy (e.g. morning sickness, varicose veins); pre-eclampsia × 3; antepartum and postpartum haemorrhage; malpresentation; cord prolapse; CS • Fetal/neonatal: increased risk abnormalities, preterm delivery (premature labour, premature rupture membranes); intra-uterine growth restriction of one fetus; twin–twin transfusion; perinatal mortality × 5; prematurity; malformations × 2–4; (also those of mother)

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Principles of management • Increased supplements (iron/folic acid), nutrition requirements and rest • Increased frequency of antenatal visits and associated care (e.g. weekly visits from 28 weeks) • Education and counselling about increased incidence of above (e.g. preterm birth) • Early referral to self-help groups • Ultrasound examination at 28 weeks, then serial scans to check fetal growth of both babies. Monozygotic twins need a scan every 2–3 weeks from 16 weeks until delivery to recognise evidence of twin-to-twin transfusion syndrome (TTTS) • Intensive fetal monitoring • If threatened premature delivery admit to hospital for rest; consideration of tocolytics to gain time and antenatal corticosteroids for fetal lung maturation

• Aim to deliver at 38 weeks if possible either by vaginal delivery (if favourable conditions such as normal growth and double cephalic presentations) or CS (e.g. malpresentation first twin, conjoint twins) • As a rule, elective CS is favoured at 37 or 38 weeks • Careful attention to third stage—risk of haemorrhage

Preterm labour Preterm or premature labour is confirmed labour after 20 weeks and before 37 weeks gestation. The incidence is 5–10% (average 7%) of all deliveries and is associated with 85% of neonatal deaths, especially if delivery occurs before 26 weeks. There is often a past history. Causes of spontaneous preterm labour: • • • • • •

unknown (approx. 40%) multiple pregnancy cervical incompetence polyhydramnios uterine abnormality maternal medical conditions (e.g. diabetes, drug abuse, infection) • antepartum haemorrhage The patient may present with regular contractions or premature rupture of the membranes. Management • Admit to an obstetric unit. • Consider tocolysis (inhibition of uterine contractions) with atosiban, nifedipine (preferred) or β-sympathomimetic agents (salbutamol, ritodrine, fenoterol). • Give corticosteroid (e.g. betamethasone, hydrocortisone) for ↑  fetal lung maturity (maximum benefit 26–32 weeks).

Premature rupture of membranes Premature rupture of the membranes (PROM) is rupture of the membranes with amniorrhoea before labour commences. Preterm PROM (PPROM) is rupture of the membranes at 24 hours or patient is unwell obtain breast milk culture and commence antibiotics.5 • Antibiotics: resolution without progression to an abscess will usually be prevented by antibiotics: dicloxacillin 500 mg (o) qid for 7–10 days

or flucloxacillin 500 mg (o) qid for 7–10 days or cephalexin 500 mg (o) qid for 7–10 days If severe cellulitis: flucloxacillin/dicloxacillin 2 g IV 6 hourly • Ibuprofen or paracetamol for pain

Instructions to patients • Keep the affected breast well drained. • Continue breastfeeding: do it frequently and start with the sore side or begin feeding from the normal side until the milk comes and then switch to the sore side. • Heat the sore breast before feeding (e.g. hot shower or hot face washer). • Cool the breast after feeding: use a cold face washer from the freezer. • Massage any breast lumps gently towards the nipple while feeding. • Empty the breast well: hand express if necessary. • Get sufficient rest. • Keep to a nutritious diet and drink ample fluids.

Candida mastitis Clinical features • Painful breasts—often exquisite pain especially during and after feeding • No fever • Nipple pain and sensitivity • Usually but not always bilateral • Nipples can be pink and shiny • ± Pink haloes around the base of the nipple • Breasts usually normal: no heat, lumps or tender points Note: May follow a course of antibiotics. Swabs are of limited value. Treatment fluconazole 150 mg (o) every second day for 3 doses5 then oral nystatin (o) tds for 10 days miconazole gel qid to nipple after feeds Treat the baby with oral nystatin drops or miconazole oral gel.

Maternal diet • Remove refined carbohydrates especially sugarand yeast-containing foods for at least 6 weeks.

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Postnatal care

Breast abscess If tenderness and redness persist beyond 48 hours and an area of tense induration develops, then a breast abscess may have formed. It can be treated with needle aspiration or may require surgical drainage under general anaesthesia. For a description of surgical and other management refer to CHAPTER 100.

Secondary postpartum haemorrhage2,6 Primary PPH is presented in CHAPTER 110. Secondary postpartum haemorrhage is any bright bleeding from the birth canal 24 hours or more after delivery. It may vary from very slight to torrential and may occur at any time up to 6 weeks postpartum. It tends to peak at 5–10 days. Causes • Retained products of conception (PoC) • Infection, especially at placental site • Laceration of any part of the birth canal • Coagulation disorder No cause is found in one-third of cases (i.e. idiopathic subinvolution). Treatment Rule: An empty and contracted uterus will not bleed. • Investigation: — ultrasound (? retained PoC) — cervical swab for smear and culture — FBE • IV oxytocin 10 IU followed by infusion of 40 IU in Hartman solution • Ergometrine 250 mcg IM or 25–50 mcg slowly IV (if continuing heavy bleeding) • Consider misoprostol, 4 or 5 × 200 mcg tablets per rectum or otherwise by intramyometrial injection of prostaglandin F2 alpha (caution: specialist supervision) • Exploration under general anaesthetic if blood loss >250 mL: — gentle blunt curettage required in the postpartum uterus (aim to prevent uterine adhesions—Asherman syndrome) • Arrange blood transfusion if Hb is 3 months, anti-epileptics e.g. phenytoin). Other risk factors for osteoporosis and fractures include a family history of osteoporosis, malabsorption, hypothyroidism, hyperparathyroidism, being underweight and being at risk of falls. Men with risk factors should be screened using BMD testing. Other indications for screening include height loss, kyphosis or back pain suggesting possible vertebral fractures, low-impact fractures and possibly even high-impact fractures.12 Investigations can include bone densitometry, FBE, LFTs, testosterone and vitamin D. When identified, osteoporotic men should be encouraged to have adequate dietary calcium, be educated on fallprevention strategies and encouraged to do weightbearing exercise. Medication management options include oral bisphosphonates (first-line treatment) and calcium, vitamin D or testosterone if deficient.

Gynaecomastia This is a ‘true’ enlargement of the male breasts, not to be confused with false enlargement of obese men. Gynaecomastia occurs in up to 50% of adolescent boys. Virtually no breast tissue is palpable in normal men. If present in adult men, look for evidence of testosterone deficiency. Other causes include drugs (e.g. anabolic steroids, oestrogen, digoxin, calcium antagonists, marijuana, spironolactone, amiodarone, tricyclic antidepressants, cimetidine), liver failure, testicular feminisation syndrome and oestrogensecreting tumours, such as adrenal carcinoma and Leydig cell tumour.

Sex-linked inherited disorders

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Males bear the burden of X-linked recessive gene disorders, which always manifest as there is no normal gene on the additional X chromosome (as there is in the female) to counteract the action of the abnormal gene. Occasionally a gene can be carried on an autosome but manifests only in one sex. An example is malepattern baldness, manifesting as an autosomal dominant disorder in males but as a recessive disorder in females.

Examples of X-linked disorders significantly affecting males include: • • • • • •

haemophilia A and B glucose-6-phosphate dehydrogenase deficiency Duchenne muscular dystrophy retinitis pigmentosa Hunter syndrome ocular albinism

Summary There is an increasing emphasis on and interest in men’s health. In 2008, in response to the growing awareness of men’s health issues, the first Australian National Male Health Policy13 was developed. Initiatives that have emerged from and been enhanced by this policy include programs and campaigns that focus on male mental health, work safety, male health in particular risk groups and prevention of chronic disease and injury. Examples include the Men’s Sheds, Man Health and Strong Father Strong Family programs. Also available are information sources and links, resources and research on male health issues. Many of these programs, especially those concerning mental health and psychosocial aspects such as family relationships and risk behaviour, focus on issues such as what it means to be male. Topics explored include the positives of maleness, the behaviours males should be avoiding and personal responsibility. The GP is in an ideal position to identify, assess and manage significant health problems in males. Men’s reluctance to access health services when they need them makes the GP’s role all the more important. Opportunities should be grasped to discuss health issues with male patients and foster preventive issues where appropriate.

References 1 Pattison A. The M Factor (2nd edn). Sydney: Simon & Schuster, 2001. 2 AIHW 2013. Australia’s Health 2014. Cat. No. AUS 178. Canberra: AIHW. 3 AIHW 2011. The Health of Australia’s Males. Cat. No. PHE 141. Canberra: AIHW. 4 Pawlowski B, Atwal R. Sex differences in everyday risk-taking behavior in humans. Evolutionary Psychology, 2008; 6 (1): 29–42. 5 Australian Bureau of Statistics. Causes of Death. Canberra: ABS, 2010. 6 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 253–8.

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Male health: an overview 7 Andrology Australia. Clinical Summary Guideline 4: Androgen Deficiency, May 2010 (accessed 27/1/2014). 8 Andrology Australia. The Andrology Australia orchidometer (accessed 27/1/2014). 9 RACGP. Clinical Guideline for the Prevention and Management of Osteoporosis in Women and Older Men, February 2010 (accessed 27/1/2014).

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10 Eisman J, Clapham S, Kehoe L. Osteoporosis prevalence and levels of treatment in primary care: The Australian Bone Care Study. J Bone Miner Res, 2004; 19 (12): 1969–75. 11 Ewald DP et al. Population rates of bone densitometry use in Australia, 2001–2005, by sex and rural versus urban location. Med J Aust, 2009; 190 (3): 126–8. 12 Mackey D et al. High-trauma fractures and low bone mineral density in older women and men. JAMA, 2007; 298 (20): 2381–8. 13 The Department of Health. National Male Health Policy, 2008 (accessed 27/1/2014).

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113 Scrotal pain Acute scrotal pain in infancy and adolescence should be regarded as torsion of the testis until proved otherwise. Text, page  Scrotal pain in males can occur in all age groups but the child or adolescent with acute scrotal pain often poses a diagnostic challenge. Serious problems include testicular torsion, strangulation of an inguinoscrotal hernia, a testicular tumour and a haematocele, all of which require surgical intervention.

Key facts and checkpoints •

• • •

•

•

•

•

•

•

•

Torsion of the testis is not the most common cause of acute scrotal pain in childhood and adolescence, but it is the most important.1 Torsion is also a feature of young men younger than 25 years. Testicular pain can be referred to the abdomen. Torsion of the testis should form part of the differential diagnosis in a boy or young man who is vomiting and has intense pain in the lower abdominal quadrant inguinal region. The loss of a testicle from torsion, an avoidable problem, is a real ‘time bomb’ and a common reason for litigation for medical negligence. The clinical picture of epididymo-orchitis can mimic torsion of the testis so closely that in most boys and young men the diagnosis should be made only at surgical exploration.1 An abnormality predisposing to torsion of the testis is usually present bilaterally; the opposite testis should also be fixed to prevent torsion (orchidopexy). Torsion must be corrected as soon as possible to reduce the chance of gangrene and loss of the testis. Suspect self-correcting testicular torsion in repeated episodes of severe spontaneously resolving pain. Refer for possible orchidopexy. Suspect abscess formation if epididymo-orchitis does not settle with a reasonable course of antibiotics. Surgical drainage may be necessary. A varicocele can cause testicular discomfort— examine the patient in the standing position.

The clinical approach History It is important to determine whether there were any pre-existing predisposing factors or history of trauma.

Key questions • Have you noticed any burning of urine or penile discharge? • Have you had an injury to your scrotal region such as being struck by a baseball, cricket ball or falling astride something? • Have you travelled overseas recently? • Have you been aware of a lump in your testicle or groin? • Have you had an illness lately and have you noticed swelling of the glands in your neck or near your ear (i.e. screening for mumps)? • Do you have back pain or have you injured your back?

Examination Both sides of the scrotum must be examined and contrasted. Inguinal and femoral hernial orifices, the spermatic cord, testis and epididymis must be checked on both sides. The size, lie and elevation in the scrotum of the testis should be assessed, as should the cremasteric reflex. This is done by stroking or pinching the medial thigh, and considered positive if the testicle moves at least 0.5 cm. An absence of the ipsilateral cremasteric reflex is the most sensitive physical finding in testicular torsion but the reflex is often absent in small boys (under 2½ years) without torsion.2 The patient should be examined standing and supine. The scrotum and its contents are examined systematically starting with the skin, which may include sebaceous cysts or other dermatological

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Scrotal pain conditions. A painful testis should be elevated gently to determine if the pain improves.

spermatic cord

Investigations

hydatids of Morgagni

Investigations that may help diagnose the painful testis in particular include: • • • • •

blood cell count urine analysis: microscopy and culture Chlamydia antigen detection tests ultrasound technetium-99m scan

Acute scrotal pain in children and adolescents—‘the acute scrotum’ This problem is more likely to be encountered in the adolescent, especially after the testis enlarges at puberty (13–16 year olds).1 A list of causes is presented in TABLE  113.1. Infants, however, can also have torsion of a testis or a testicular appendage. Table 113.1

Causes of scrotal pain or swelling

Torsion of the testis Torsion of a testicular appendage Epididymo-orchitis Mumps orchitis Acute hydrocele Idiopathic scrotal oedema Haematoma/haematocele Testicular neoplasm Henoch–Schönlein purpura Strangulated inguinoscrotal hernia Scrotal skin conditions Varicocele Referred pain (e.g. spine, ureteric colic, abdominal aorta)

Clinical problem A 15-year-old teenager presents with relatively acute onset of pain in his lower right abdomen and scrotum. He has vomited several times. On examination the right testicle is tender, red and swollen. Discussion The three main differential diagnoses of the acute scrotum in an adolescent are torsion of the testis, torsion of a testicular appendage and acute epididymoorchitis (see FIG. 113.1). Less commonly the problem would be a haematoma or an acute hydrocele mimicking testicular torsion. This patient, however, must be regarded as having torsion of the testis until proven otherwise. Early operation with torsion is

paradidymis

testicular torsion

appendages

epididymis testis

FIGURE 113.1 Illustration of torsion of the testis and an appendage: the ‘black’ hydatid of Morgagni is the one most likely to undergo torsion

imperative because if the testis is deprived of its blood supply, infarction is inevitable and excision becomes necessary. Excluding mumps, no pre- or peripubertal youth should be diagnosed as suffering from acute epididymo-orchitis until the testis has been exposed at operation and torsion excluded.

Torsion of the testis Torsion usually occurs because of an abnormally narrow anchoring of the testis by the testicular mesorchium posteriorly1 and the tunica vaginalis (which normally covers only the testicle and epididymis) also covering the bottom end of the spermatic cord. This allows the testicle to have a more mobile and transverse lie, referred to as a ‘bell clapper deformity’, and makes it easier for the testicle to twist around upon its cord. This deformity is almost invariably present on the other testicle, so when surgical correction of the torted testis is done, orchidopexy should always be done on the other side also. When a testicle torts, time is of the essence. One study suggests that the testicular salvage rate is 90% if detorsion occurs less than 6 hours after the onset of symptoms, but this drops to 50% after 12 hours and 3 months after surgery). Chronic pain is the most serious longterm complication of hernia repair and may persist for several years. It may be severe in up to 3% of patients1 and can require referral to pain clinics or further surgery. An increase in infertility risk and testicular atrophy on the side of the surgery has been noted but is not common. Most patients return to work after hernia repairs in around 7 days, or 14 days for those doing strenuous work.1

Conservative Asymptomatic inguinal hernias in patients with associated medical conditions, and who pose a

Umbilical hernias Clinical features • Soft, round, skin-coloured lump in umbilicus, occurring in around 15% of infants.6 • May increase in size in first few months • Not painful, not tender to palpate, easily reducible • Swelling disappears when child asleep • Usually gradually disappears • Most disappear by age of 12 months6 • Larger ones usually disappear by age of 4 years6 • Consider hypothyroidism Management • Explanation and reassurance • No treatment required • Do not tape or strap (may cause strangulation and does not help) • Refer for repair if still present at age 4 years

Inguinal hernia Clinical features • More common in premature infants and boys • Present with groin lumps—may be intermittent sightings (e.g. when crying) • May cause intermittent pain or discomfort • If irreducible, consider possibility of strangulation Note: Bowel strangulation is a possibility. Management Rules for surgical intervention: • general rule is ASAP, especially in infants and for irreducible ones • reducible herniae—the ‘6–2’ rule: — birth–6 weeks: surgery within 2 days — 6 weeks–6 months: surgery within 2 weeks — over 6 months: surgery within 2 months

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Scrotal lumps

114

The scrotum contains the testes and distal parts of the spermatic cords, covered by layers of fascia and the dartos muscle. The testes are invested with tunica vaginalis derived from the peritoneal cavity during their descent.1 Disorders of the scrotum may be acute or chronic and bilateral or unilateral. Lumps may be cystic, solid or otherwise, such as a varicocele, oedema or hernia. Solid lumps include a testicular tumour, epididymoorchitis, and torsion of the testes. Cystic lumps include hydroceles, epididymal cysts and spermatoceles. A comparison of scrotal lumps appears in FIGURE 114.6 and TABLE 114.3. Lumps in the scrotum usually develop from deeper structures, particularly the testes and their coverings, rather than scrotal skin. The cardinal sign of a true scrotal mass is that it is possible to palpate it from above (i.e. get above the lump) (see FIG. 114.7). The patient usually presents with pain or a lump.

Examination of the scrotum The scrotum should be examined with the patient supine and then standing. The left testis usually

hangs lower than the right. On inspection note any sebaceous cysts in the scrotal skin (common); scabies if there are very pruritic nodules; and scrotal oedema, which causes taut pitting skin. Careful palpation will elicit the relevant structures in the scrotum. Gently palpate each testis and epididymis between the thumb and the first two fingers. The spermatic cord is palpable as it enters the scrotum after passing through the superficial ring and the testis and epididymis are readily palpable. After palpation, test for translucency of any swelling in a darkened room by shining the beam of a strong torch from behind the scrotum through the swelling. Transilluminable swellings that light up with a red glow (referred to as a ‘Chinese lantern sign’) include hydroceles and cysts of the epididymis. Swellings that contain blood or other tissue, such as testicular tumours and most hernias, do not transilluminate.

Unilateral scrotal swelling It is important to determine whether the lump is inguinoscrotal or scrotal. It is scrotal if it is possible to get above the lump. If it is not possible to get above the lump then it is a large inguinal hernia or

vas deferens

epididymis testis scrotum Normal

? secondary hydrocele

firm mass Testicular tumour

Swelling of the epididymis (separate from testis) (e.g. chronic epididymitis or cyst)

dilated veins

blood

serous fluid Haematocele

FIGURE 114.6 Basic comparison of scrotal lumps

Varicocele

Hydrocele

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Inguinoscrotal lumps

possible to palpate above and feel the swelling

not possible to palpate above and feel the swelling

Inguinoscrotal swelling

True scrotal swelling

FIGURE 114.7 Difference between a true scrotal swelling and an inguinoscrotal swelling

a combined hernia and hydrocele (see FIG.  114.7). This palpation should be coordinated with the cough impulse. The next feature to determine is whether the testis and/or epididymis can be palpated or whether they are obscured by a swelling.5 Table 114.3

Small testes Normal testicular size in children and adolescents is 4–14 mL or 15–35 mL in adults (this can be assessed with an orchidometer).7,8 Small firm testes less than 10 mL are a feature of Klinefelter syndrome. Small

Features of scrotal lumps Possible clinical setting

Position

Palpation

Trans-illumination

Hydrocele

Any age Primary or secondary: • tumour • infection • torsion

Confined to scrotum Anterior: surrounds testis except posteriorly

Smooth, pear-shaped Lax or tense Testis impalpable, non-tender

Yes

Cyst of epididymis Epididymal cysts and spermatoceles clinically similar

Asymptomatic or dragging sensation

Behind and above testis

Smooth and tense Multilocular swelling Testis easily palpable Appears separate from testis

Yes

Chronic epididymoorchitis

Non-specific Tuberculosis Chlamydia (Occasional associated small hydrocele)

Behind and above testis

Firm swelling Hard and craggy Normal testis

No

Varicocele

Dragging discomfort

Usually left-sided Along line of spermatic cord Above testis

Soft, like bunch of worms or grapes Collapses when patient supine and testis elevated Testis often smaller

No

Cancer

Young men 20–40 Painless lump Loss of testicular sensation

In body of testis Usually felt anteriorly May be hydrocele

Enlarged firm testis Feels heavy if large Normal epididymis (palpable)

No

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soft testes indicate atrophy, which may follow mumps orchitis, oestrogen therapy, androgen deficiency or anti-androgen therapy, hypopituitarism, cirrhosis and other related conditions.

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Hydrocele A hydrocele is a collection of clear amber fluid in the tunica vaginalis and can be primary or secondary. If a hydrocele develops it is important to rule out intrascrotal disease, such as a tumour or infection. Ultrasound examination of the scrotum is helpful in assessing the state of the testis in the presence of a hydrocele. Hydroceles may be symptomless or cause dragging discomfort in the scrotum and groin.

Hydroceles in the neonate5,9 Hydroceles present at birth are communicating (failed closure of the processus vaginalis) or (less commonly) non-communicating, where the tunica vaginalis contains fluid, which can sometimes be loculated or cystic. Transillumination will prove that it is cystic but if the diagnosis is in doubt perform an ultrasound. Hydroceles may vary in size from day to day and can appear quite large. They do not extend proximal to the external inguinal ring so it is possible to palpate above them. There is no impulse on crying or straining. Of the 5% of those born with a hydrocele, most will resolve spontaneously within 12 months. If the hydrocele is very large or persists beyond 12 months, surgical intervention should be considered. Treatment of a primary hydrocele in adults If underlying pathology has been excluded, hydroceles can be managed conservatively with reassurance and scrotal support.10 If the hydrocele is large and uncomfortable, simple aspiration with or without the injection of sclerosing agents can be attempted, but the fluid usually reaccumulates and there is a risk of bleeding or infection with repeated procedures. However, aspiration can prevent fluid accumulation and after two or three times can often cure the problem. This sclerotherapy may be complicated by pain and inflammatory reaction to the sclerosant. Surgery is generally considered a second-line procedure after observation with or without aspiration.

Practice tip Consider testicular cancer in a young man presenting with a hydrocele. Perform an ultrasound examination.

Encysted hydrocele of the cord This is a localised fluid-filled segment of the processus vaginalis within the spermatic cord. It is palpable as a cystic lump in the upper scrotum above the testis. It characteristically moves down with traction on the testis. Treatment is not usually needed.

Epididymal cysts These are common, often multiple, and are usually found in middle-aged/elderly men. The majority of epididymal cysts are about the size of a pea and contain a clear colourless fluid. If the cysts communicate with the vasa efferentia, a spermatocele filled with whitish fluid containing spermatozoa may form. Epididymal cysts may be asymptomatic or they may cause discomfort and cosmetic embarrassment and if so can be excised. Fertility may be impaired in patients undergoing bilateral cyst excision. Aspiration and injection of sclerosant agents can also be used for epididymal cysts.

Varicoceles A varicocele is a varicosity of the veins of the pampiniform plexus (see FIG.  114.6). It is seen in 8–10% of normal males and occurs on the left side in 98% of affected patients, due to a mechanical problem in drainage of the left kidney vein. A relationship with infertility has been observed but its nature is controversial, as is whether repairing varicoceles in subfertile men improves fertility chances.10 Most varicoceles are asymptomatic and incidental findings. They can cause a dragging discomfort in the scrotum. Investigation is usually not necessary but an ultrasound is useful where the diagnosis is doubtful or a neoplasm is suspected. Treatment is indicated if it is symptomatic or for infertility. Firmfitting underpants may relieve discomfort. Surgical treatment is by venous ligation, above the deep inguinal ring. Ligation is indicated if there is any reduction in the size of the left testis.

Haematoceles These can be either acute, resulting from trauma such as a fall astride, sports injury or tapping of a hydrocele, or chronic, where there is no obvious history of injury. Haematoceles are anterior to the testis and not transilluminable. Surgical drainage is required with acute injury where there is a possibility of testicular rupture (associated urethral injury has to be considered); and a tumour has to be excluded with

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the chronic type. Pressure atrophy of the testis can occur with injury and is much more common if early drainage is not instigated.

Sperm granulomas • Firm tender lumps • Post-vasectomy—at cut end of vas

Testicular tumours11,12 A mass that is part of the testis, and solid, is likely to be a cancer. Malignant testicular tumours account for about 1–1.5% of malignant tumours in men. They mainly affect fit young men and represent the commonest cancer in men aged 20–40 years in Australia (see TABLE 114.4). Some 90–95% of testicular tumours arise from the germ cells, and for practical purposes are classified into: • seminomas 40% • non-seminoma germ cell tumours (NSGCT) 60% Table 114.4

Inguinoscrotal lumps

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• Associated presentations (may mask tumour): — hydrocele — varicocele — epididymo-orchitis — swollen testis with trivial injury — gynaecomastia (teratoma) — back and flank pain

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Risk factors Those at high risk include those men with:

Treatment • Leave to resolve. • Consider NSAIDs. • Refer for excision if symptomatic and enlarging.

• cryptorchidism/orchidopexy (testicular dysgenesis syndrome) • previous testicular cancer • family history of testicular cancer (brother/ father) • Klinefelter syndrome • infertility Golden rules • All solid scrotal lumps are malignant until proved otherwise and must be surgically explored. • Beware of hydroceles in young adults. • Tumours can mimic acute epididymo-orchitis— the so-called ‘inflammatory’ or ‘flash fire’ presentation. If a man has a testicular lump he should visit his GP and have ultrasound screening and baseline tumour markers. If it is cancer, he should:

Testicular tumours

Tumour

Incidence (%)

Peak incidence (years)

Seminoma

40

25–40

Teratoma

32

20–35

Mixed seminoma/teratoma

14

20–40

Lymphoma

7

60+

Other tumours (e.g. interstitial—Leydig, gonadoblastoma)

uncommon

variable

Clinical features • Young men aged 20–40 years (NSGCTs peak in the third decade of life, seminomas peak in the fourth decade) • Most common presentation is a painless lump in the body of one testis (only 1–2% present with bilateral tumours) • Up to a quarter of men have pain at presentation • Loss of testicular sensation

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• be treated in a specialist centre • undergo careful staging • have an orchidectomy and adjunct therapy Metastases Testicular tumours spread by direct infiltration via the lymphatics and the bloodstream. Metastases typically occur in the para-aortic nodes and so may not be detected by abdominal palpation. They are best detected by a CT scan of the abdomen and chest. Metastases also occur in the neck, brain, liver, chest and bones. Investigations Investigations to aid diagnosis include: • ultrasound of the testis should always be done as it can detect and diagnose with considerable precision underlying testicular lumps plus any invasion of the tunica • tumour markers: α-fetoprotein and β-hCG— indicates teratomas

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Investigations for staging include:

114

• chest X-ray • CT scanning of abdomen, pelvis and chest for node involvement (any spread is usually direct to the para-aortic nodes) • lactate dehydrogenase—monitors secondary spread and indicates tumour mass Note: Avoid scrotal needling biopsy because of the potential risk of tumour implantation in the scrotal wall. Avoid scrotal incisions for surgery. Treatment The initial treatment is orchidectomy through an inguinal incision with inguinal division of the spermatic cord. Further treatment then depends on the type and staging of the tumour. Early seminomas are given radiation to the ipsilateral lymph nodes or a single dose of chemotherapy. Early NSGCTs undergo active surveillance (tumour markers, CXR, CT scans) but no further treatment. More advanced disease may have further chemotherapy or radiotherapy. The results for NSGCTs in general are not as satisfactory as for seminoma, though prognosis is good for both, with current 5-year relative survival rates of 99% for localised disease (majority of presentations), 96% for regional disease and 74% for distant disease.13 A comparison of the testicular tumours is summarised in TABLE 114.5. Surgery should not affect the remaining testis but production of motile and functional sperm may be reduced. However, sperm production can be temporarily or permanently reduced following radiotherapy and chemotherapy. Pretreatment sperm storage may be discussed with the patient, and the psychological implications of testicular cancer need to be carefully monitored. The GP may also play a role in coordinating appropriate active surveillance investigations. Screening and testicular self-examination Studies of testicular cancer have shown the benefits of early detection. However, studies to date indicate that there is insufficient evidence to screen routinely for testicular cancer in asymptomatic patients. It is recommended for those at high risk. This screening includes colour Doppler ultrasound and tumour markers. Evidence also indicates that, to date, there is little evidence to show that those performing testicular self-examination are more likely to detect early stage tumours or have better survival than those who do not.14

Table 114.5

Comparison of the common testicular cancers Seminoma

Non-seminoma (NSGCT)

Typical age

30–40 years

20–30 years

Incidence

40%

60%

Growth rate

Slow

Rapid

Nature

Solid

Mixed—solid + cystic

Stage at presentation

90%—stage 1

60%—stage 1

α-FP

Never

Common

β-hCG

Occasional

Common

Treatment

Inguinal orchidectomy + radiotherapy

Stage 1: orchidectomy

Sensitive to chemotherapy

+ + +

+ + +

Sensitive to radiotherapy

+ + +

±

Tumour markers:

Relapse: chemotherapy

Undescended testes (cryptorchidism)15 An undescended testis is one that fails to reach the bottom of the scrotum by 3 months of age. It has stopped in the normal path of descent and can occupy the intra-abdominal, inguinal canal, emergent (just outside the external ring), high scrotal and mid-scrotal positions (see FIG.  114.8). The cause of maldescent is most probably mechanical. After the indirect inguinal hernia, it is the most common problem in paediatric surgery. The incidence at birth is 4–5% but this falls to 1–2% in the first 3 months of life as testicular descent can continue, though further descent after 3 months is rare. More than two-thirds of undescended testes are located in the superficial inguinal pouch; that is, they are palpable in the groin. The testis is usually normal at birth but may become secondarily dysplastic if left outside the scrotum.

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Inguinoscrotal lumps

abdominal

inguinal

high scrotal

Examination12 The examination of the testes should take place in a warm room and relaxed environment. Begin by placing one finger on each side of the neck of the scrotum to prevent a retractile testis from being retracted when palpation is commenced with the other hand. The scrotum is then carefully palpated for a testis. If impalpable the fingertips of one hand are placed just medial to the anterior superior iliac spine and moved firmly towards the pubic tubercle where the other hand waits to entrap the testis should it appear. The diagnosis then depends on carefully determining the range of movement.

mid scrotal

normal position

FIGURE 114.8 Undescended testis: arrested in the line of descent

superficial inguinal

thigh

Retractile testis A retractile testis is one that can be manipulated into the scrotum irrespective of the position in which it is first located. It is a common condition and requires no further investigation or treatment. The testis can be present in the scrotum under circumstances such as a warm bath but retracted out of the scrotum when cold. Cremasteric contraction is absent in the first few months after birth and is maximal between 2 and 8 years.

Ectopic testis An ectopic testis is one that has left the normal path of descent and cannot be manipulated into the scrotum. It can be found in the perineum, upper thigh (femoral), base of the penis (prepubic), anterior abdominal wall or in the superficial inguinal pouch (see FIG.  114.9). True ectopic testes form only about 2.5% of all undescended testes.

normal

FIGURE 114.9 Undescended testis: ectopic

Practice tip If the testis is not palpable at birth, review in 3 months. Refer for specialist evaluation if it still cannot be palpated.

The problem of non-descent

Ascending testis

• Testicular dysplasia • Susceptible to direct trauma (if in inguinal region) • Risk of malignant change (seminoma) is 5–10 times greater than normal

An ‘ascending’ testis is one that was in the scrotum in infancy but subsequently moved back to the groin because the spermatic cord failed to elongate at the same rate of body growth.

Optimal time for surgery The optimal time for orchidopexy is 6–12 months of age. It is considered to be satisfactory as long as the

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testis is in the scrotum by 2 years. The production of spermatozoa is adversely affected in undescended testes from the age of 2 years onwards. Exploration for the uncommon impalpable testis is worthwhile: 50% salvage rate, while in the other 50% either there is no testis or an abnormal and potentially neoplastic testis is removed. The advantages of early orchidopexy are summarised in TABLE 114.6. Hormone injections Injections of chorionic gonadotrophic hormones are generally not recommended. They are ineffective except for cases of borderline retractile testes. Table 114.6

Advantages of early orchidopexy (1 year)

Provides optimal chance of fertility Corrects indirect inguinal hernias (coexists in 90%) Reduces risk of trauma Reduces risk of torsion Reduces psychological consequences Probably lessens the risk of malignancy (seminoma)

Vasectomy Dangerous features (beware) • • • • •

Unmarried Young 3.0 • there is insufficient evidence to recommend screening in men aged >70 • men should not be tested if they are not expected to live for another 7 years • digital rectal examination (DRE) is no longer recommended in asymptomatic men presenting in general practice

• 28 men will experience a side effect from the biopsy they consider a moderate/major problem • 28 men will be diagnosed with prostate cancer, many of whom would have remained asymptomatic • 25 men will undergo cancer treatment, many of whom would have remained asymptomatic • 7–10 men will develop persistent impotence and/or urinary incontinence, and some will develop persistent bowel problems due to the treatments

Core biopsy A urologist will consider biopsy guided by transrectal ultrasound if the DRE is positive or if the PSA is elevated, depending on the man’s individual risk profile, clinical findings and PSA levels. A biopsy is the only certain measure of diagnosis. Grading and staging A good way of explaining to patients about grading and staging is to say ‘the grade is how aggressive the cancer is, and the stage is how much there is and how far it has spread’. From the biopsy, the pathologist determines the grading using the Gleason score (see TABLE 116.2 and FIG. 116.4). The score is based on the addition of the grading of the 2 most common types of cells found in the samples (graded from 1, being well differentiated, to 5, most dysplastic). Therefore the lowest score possible is 2 and the highest 10. Prognosis is also determined by the ratio of the higher of the two histological scores (e.g. Gleason 7 with 80% stage 4/20% stage 3 will be worse than Gleason 7 with only 20% stage 4/80% stage 3). Table 116.2

Gleason score and risk of cancer

Gleason score

Threat from cancer

2–4

Low

Fully counselling a man can be challenging. A useful guide23 on the outcomes of screening 1000 men aged 60 (with no significant family history and screened annually for 10 years) would result in the following:

5–6

Moderate

7

Intermediate

8–10

High

• 2 men will avoid death from prostate cancer before the age of 85 • 2 men will avoid metastatic prostate cancer before the age of 85 • 85 men who do not have prostate cancer will have a biopsy

Staging24,25 Clinical staging is based on 5 sources of information: • the extent of the primary tumour (T category) • whether the cancer has spread to nearby lymph nodes (N category)

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Disorders of the prostate

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FIGURE 116.4 Gleason pattern (grading) scale of prostate cancer 26

• the absence or presence of distant metastasis (M category) • the PSA level at the time of diagnosis • the Gleason score, based on the prostate biopsy (or surgery) Local prostate gland disease (T1–T2) is based on the DRE and transrectal ultrasound (TRUS) with T3 to T4 indicating spread beyond the capsule. Stages T1 and T2 have a good prognosis, and some T3 tumours can be cured. Whole-body radionucleide bone scanning, CT, MRI scanning and surgical pathology results also assist staging. Axial skeleton metastases are involved in 85% of patients who die of prostate cancer.27 After the TNM status is determined, this information is combined with the PSA and Gleason scores in what is termed stage grouping, from I (the least advanced) to IV (the most advanced). This will help determine treatment options and prognosis. This information can also be put into nomograms by either the doctor or patient to clarify the patient’s status and options. Treatment28,29,30 Deciding on treatment options for prostate cancer needs to take into account not only the grade and stage, but also the age and general health/life expectancy of the patient, available treatments and, importantly, patient preferences. Psychosocial support (both at the time of diagnosis and subsequently) and

appropriate patient education will help make these patient preferences more clear. Options for localised prostate cancer include radical prostatectomy, radiotherapy and no active treatment. The latter is now referred to as ‘active surveillance’, which means actively monitoring for changes such as a rising PSA or deteriorating biopsy results. Previously the term ‘watchful waiting’ was used, which was a more palliative approach used in the pre-PSA era (before 1990), which involved awaiting the appearance of symptoms or signs of local or systemic progression and then treating these as needed. Most of the evidence points to there being little difference (when the reduction in cancer risk is offset against the potential negative consequences of the interventions) in long-term outcomes between the three different approaches. This, however, needs to be put into the context of the individual patient’s situation, his clinical presentation and his preferences, so active interventions may well be warranted. Radical prostatectomy is most likely to benefit the patient with a relatively long life expectancy (>10 years), no significant surgical risk factors, a low volume stage and a low PSA and who, after being informed of the risks and benefits, prefers surgery. Approaches include radical perineal, laparoscopic and robot-assisted prostatectomy. Major complication issues include incontinence and impotence, and the risk of these will vary depending on the surgical approach and the patient’s age and health.

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Radiotherapy is also likely to benefit those with a long life expectancy and low-volume low PSA, who have a moderately (or worse) differentiated tumour and who, after being informed of the risks and benefits, prefer external beam or interstitial radiotherapy (brachytherapy). The main adverse reactions from external radiotherapy are faecal urgency and diarrhoea together with urine frequency. Impotence is common for up to 2 years after external beam radiotherapy. Active surveillance is often used for those with a low life expectancy, or those who prefer to avoid the possible complications of surgery or radiotherapy. PSA monitoring is done for surveillance, or for followup after treatment with curative intent. For locally advanced or metastatic disease, androgen deprivation is the cornerstone of treatment, the options being: bilateral orchidectomy or daily anti-androgenic tablets, for example: — cyproterone acetate (Androcur) — flutamide (Eulexin) — bicalutamide (Cosudex) — abiraterone (Zytiga) or luteinising hormone releasing hormone (LHRH) agonists: depot injections of LHRH analogues, for example: — goserelin (Zoladex) — leuprorelin acetate (Lucrin, Eligard) Treatment combinations for small volume metastatic prostate cancer may prolong life, for example: • orchidectomy plus flutamide • LHRH agonists plus flutamide or bicalutamide— LHRH agonists cause an initial surge of testosterone so a preliminary anti-androgenic agent is advised to prevent a flare in the cancer. As well as androgen deprivation, radiotherapy to bony metastases or local disease and other adjuvant therapy options can be considered. Complementary medicine Among the disorders most widely promoted as benefiting from natural remedies are those of the prostate, though none has enough evidence to warrant its recommendation.6 Herbal remedies that have been widely used include saw palmetto (Serenoa repens), stinging nettle (Urtica dioica), African prune

(Pygeum africanum, syn. prunus africana), willowherb (Epilobium) and cernilton. Saw palmetto has been used widely, especially in Germany, with initial studies suggesting efficacy in LUTS consistent with BPH. However, a recent Cochrane review concludes it is not more effective than placebo.31 BPH has been treated with isoflavone phytoestrogens. A weak oestrogen agonist effect in males may antagonise the growth-promoting effects of androgens on the prostate. Epidemiological data indicate that in countries such as Japan where isoflavone diets are prevalent, prostatic enlargement occurs less with ageing. The most widely used source of phytoestrogens is soy protein. It is also present in lentils, chickpeas, some variations of beans and alfalfa sprouts. A variety of nutrients may play a role in the development and progression of prostate cancer. There is evidence from some epidemiological studies that selenium, leucopenes (from tomato and tomato products), vitamin D, vitamin E, calcium and green tea in the diet protect against cancer of the prostate, though their true role remains largely unclear.32

References 1 Andrology Australia. Clinical Summary Guide 7: prostate disease (BPH and prostatitis—diagnosis and management), May 2010 (accessed 20/3/2014). 2 Therapeutic Guidelines. Prostatitis, 2013 (eTG 4, accessed 20/3/2014). 3 European Association of Urology. Guidelines on Chronic Pelvic Pain, 2010 (accessed 20/3/2014). 4 Nickel J et al. Alfuzosin and symptoms of chronic prostatitis—chronic pelvic pain syndrome. N Eng J Med, 2008; 359: 2663–73. 5 Litwin M et al. The National Institute of Health chronic prostatitis symptom index: development and validation of a new outcome measure. Chronic Prostatitis Collaborative Research Network. J Urol, 1999; 162: 369–75 (accessed 20/3/2014). 6 American Urological Association. Management of benign prostatic hyperplasia, revised 2010 (accessed 20/3/2014). 7 Barry M et al. The American Urological Association symptom index for benign prostatic hyperplasia. The Measurement Committee of the American Urological Association. J Urol, 1992; 148: 1549. 8 Abrams P et al. Evaluation and treatment of lower urinary tract symptoms in older men. J Urol, 2009; 181: 1779.

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Disorders of the prostate 9 Abdel-Azis S, Mamalis N. Intraoperative floppy iris syndrome. Curr Opin Opthalmol, 2009; 20: 37. 10 McConnell J et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Eng J Med, 2003; 349: 2387. 11 Roehrborn C et al. The effect of dutasteride, tamsulosin and combination therapy on lower urinary tract symptoms in men with benign prostatic hyperplasia and prostatic enlargement: 2-year results from the CombAT study. J Urol, 2008; 179: 616. 12 Wasson J et al. A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia: The Veterans Affairs Cooperative Study Group on Transurethral Resection of the Prostate. N Eng J Med, 1995; 332: 75. 13 Australian Institute of Health and Welfare. Cancer in Australia: key facts (accessed 23/4/2014). 14 Kumar P, Clark M. Clinical Medicine (7th edn). London: Saunders, 2009: 674–6. 15 Baade P et al. Communicating prostate cancer risk: what should we be telling our patients? Med J Aust, 2005; 182 (9): 472–5. 16 Johns L, Heuston R. A systematic review and meta-analysis of familial prostate cancer risk. BJU Int, 2003; 91 (9): 789–94. 17 Royal Australian College of General Practitioners. Guidelines for Preventative Activities in General Practice (the red book) (accessed 23/4/2014). 18 Gronberg H. Prostate cancer epidemiology. Lancet, 2003; 361: 859–64. 19 Barton S (ed.). Clinical Evidence. London: BMJ Publishing Group, 2001: 588–98. 20 Sikaris K. Prostate specific antigen. Aust Prescr, 2011; 34 (6): 186–8. 21 US Preventive Services Task Force. Screening for prostate cancer: US Preventive Services Task Force Recommendation Statement. Ann Intern Med, 2008; 149 (3): 185–91. 22 National Health and Medical Research Council. PSA testing for prostate cancer in asymptomatic men, information for

23

24

25

26

27 28

29

30

31

32

health practitioners (accessed 23/4/2014). Prostate Cancer Foundation of Australia and Cancer Council Australia PSA Testing Guidelines Expert Advisory Panel. Draft Clinical Practice Guidelines PSA Testing and Early Management of Test-Detected Prostate Cancer. Sydney: Cancer Council Australia (accessed 13/12/2014). Prostate Cancer Foundation of Australia. How is prostate cancer graded and staged? (accessed 13/12/2014). American Cancer Society. How is prostate cancer staged? (accessed 23/4/2014). Gleason DF. Histologic grading and clinical staging of prostatic carcinoma. In Tannenbaum M. Urologic Pathology: The Prostate. Philadelphia, PA: Lea and Febiger; 1977: 171–97. Whitmore W. Natural history and staging of prostate cancer. Urol Clin North Am, 1984; 11 (2): 205–20. National Health and Medical Research Council Clinical Practice Guidelines: Evidence-based Information and Recommendations for the Management of Localised Prostate Cancer (accessed 23/4/2014). Cancer Council Australia Advanced Prostate Cancer Guidelines Working Party. Management of locally advanced and metastatic prostate cancer. (accessed 23/4/2014). European Association of Urology. Guidelines on Prostate Cancer, 2013 (accessed 24/4/2014). Tacklind J et al. Serenoa repens for benign prostatic hyperplasia. Cochrane Database Syst Rev. 2012 Dec 12; (12): CD001423. Sonn G et al. Impact of diet on prostate cancer: a review. Prostate Cancer and Prostatic Dis, 2005; 8: 304–10.

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117 The subfertile couple You notice that the tabetic has the power of holding water for an indefinite period. He is also impotent—in fact, two excellent properties to possess for a quiet day on the river. Dr Dunlop, Teaching at Charing Cross Hospital,  Subfertility is defined as the absence of conception after a period of 12 months of normal unprotected sexual intercourse.1 Interestingly, normal fertility is defined as ‘achieving a pregnancy within 2 years of regular sexual intercourse’ and applies to about 95% of couples.2 The inability to conceive can be a very distressing and emotional problem for a couple, who need considerable care, empathy and relatively rapid investigation of their problem. In assessing a couple with the problem of subfertility (this term is a preferable way of describing the condition to the patients), it is appropriate to involve both partners in the consultation. In determining the cause of the subfertility, three basic fertility parameters should be investigated.3 • The right number of sperm have to be placed in the right place at the right time. • The woman must be ovulating. • The tubes must be patent and the pelvis sufficiently healthy to enable fertilisation and implantation. As a general rule, the major factors limiting fertility are one-third female, one-third male and one-third combined male and female.4 In addition, there are couples who fulfil the three primary fertility factors (egg, sperm and tubes) but do not conceive. This is known as unexplained (idiopathic) subfertility.

Key facts and checkpoints • • • •

•

Infertility affects about 10–15% (1 in 7) of all cohabitating couples.4 This incidence increases with age. After the age of 32 fertility decreases by 1.5% per year. About 15% of couples who do not use contraception fail to achieve a pregnancy within 12 months.5 More than 5% remain unsuccessful after 2 years.5

• • • •

•

•

•

• •

•

About 50% of couples will seek medical assistance.5 The main factors to be assessed are ovulation, tubal patency and semen analysis. About 40% of couples have an identifiable male factor. Treatable causes are rare. The main identifiable causes of male infertility are failure of spermatogenesis, failure of sperm delivery and sperm autoimmunity.4 The technique of intracytoplasmic sperm injection (ICSI) has revolutionised the treatment of male infertility. Female factors account for about 40%: tubal problems account for about half and ovulatory disorders for roughly the other half.4 Polycystic ovarian syndrome (PCOS) is the most common cause of ovulatory dysfunction.6 Treatable factors are the big three causes—tube disease, anovulation and endometriosis. The initial investigation for the man is semen analysis on two occasions. The initial investigation for the woman is a basal body temperature chart, associated with midluteal progesterone measurement. In about 20% of couples, no apparent cause is identified (idiopathic).4 Sperm autoantibodies (IgG and IgA) can be detected in the blood and/or seminal plasma of 10% of infertile men (a special problem with vasectomy reversal). Current specialised treatment helps the majority of subfertile couples to achieve pregnancy.

Physiological factors3,7 Male fertility Fertility in the male requires: • normal hypothalamic function producing gonadotrophin-releasing hormone (GnRH) • normal pituitary function producing the gonadotrophin hormones—follicle stimulating hormone (FSH) and luteinising hormone (LH)

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The subfertile couple

Significant causes of infertility are summarised in TABLE 117.1 and illustrated in FIGURE 117.2.

Facts about sperm viability: • the maximum number of viable sperm is found in the ejaculate after a 48-hour abstinence • after entering receptive cervical mucus, sperm are capable of fertilising an egg for at least 48 hours • sperm survive for less than 30 minutes in the vagina due to an acidic environment

A diagnostic approach

Female fertility

The man • Sexual function • Previous testicular problems/injury (e.g. orchitis, trauma, undescended testes) • Medical problems: diabetes, epilepsy, tuberculosis, kidney disorders • Past history (PH) of STIs • PH of mumps • PH of urethral problems • Genitourinary surgery (e.g. hernia) • Recent severe febrile illness • Occupational history (exposure to heat, pesticides, herbicides) • Drug intake (possible adverse effects from): — alcohol — chemotherapy — anabolic steroids — aminoglycoside antibiotics — sulphasalazine — cimetidine/ranitidine — colchicine — spironolactone — antihypertensive agents

Fertility in the female requires: • normal function of the ovulatory cycle, which requires: — normal hypothalamic–pituitary function producing the hormones GnRH, FSH and LH — normal ovarian function with follicular response to FSH and LH (see FIG. 117.1) — appropriate prolactin levels (which are normally low); excessive prolactin secretion (hyperprolactinaemia) causes anovulation • normal tubal transport and access of the ovum to incoming sperm • receptive cervical mucus • normal uterus to permit implantation of the fertilised ovum

Probabilities of pregnancy About 50% of normal couples, having unprotected intercourse at least twice a week, will probably achieve pregnancy in 6 months, 85% in 1 year and 95% in 2 years.3 (a) Follicular phase

0

It is important to see both partners, not just the woman.

History The following basic facts should be ascertained.

(b) Luteal phase

midcycle peak

progesterone oestradiol

ovulation

7

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Causes of infertility

• normal seminiferous tubule and Leydig cell function • normal sperm transport and delivery

menstruation

1299

14

21

28

luteinising hormone (LH)

Days

FIGURE 117.1 The normal ovulatory cycle: the midcycle peak of LH and FSH is at 14 days and ovulation occurs shortly afterwards

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— — — — —

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• Sexual health

narcotics phenytoin nitrofurantoin nicotine marijuana

The woman • Evidence of previous fertility • Onset of menarche • Menstrual history • Symptoms of ovulation • Symptoms of endometriosis • PH of STIs and pelvic infection • Previous IUCD use • PH of intra-abdominal surgery (e.g. appendicitis, ovarian cyst) • PH of genitourinary surgery, including abortions • Obstetric history • Body weight: eating disorders (anorexia, obesity) • Drug intake: — alcohol — smoking, especially >20/day — oral contraception — anabolic steroids — major tranquillisers Combined history • Frequency and timing of intercourse • Adequate penetration with intercourse, and ejaculation • Use of lubricants • Attitudes to pregnancy and subfertility • Expectations for the future

Examination A general assessment of body habitus, general health, including diabetes mellitus, and secondary sexual characteristics should be noted in both man and woman. Urinalysis should be performed on both partners. The man • Secondary sexual characteristics; note any gynaecomastia • Genitalia — size and consistency of the testes—can compare to an orchidometer: normal range 15–35 mL (average 18 mL); small in Klinefelter syndrome (approx. 7–8 mL) — palpate epididymis and vas (present and nontender is normal)

Table 117.1

Significant causes of subfertility

Female factors Ovulation disorders: • hypothalamic/pituitary disorders • hyperprolactinaemia • other endocrine disorders • ovarian failure (e.g. oocyte ageing) • stress • PCOS • weight-related ovulation disorders Tubal disease: • PID • endometriosis • previous ectopic pregnancy • previous tubal ligation • previous peritonitis Uterine and cervical abnormalities: • congenital • acquired Endometriosis Male factors Reduced sperm production: • idiopathic • congenital cryptorchidism (maldescent) • inflammation (e.g. mumps orchitis) • antispermatogenic agents: — chemotherapy — drugs — irradiation — heat • Klinefelter syndrome (46 XXY) • Sperm autoimmunity Hypothalamic pituitary disease: • hypogonadotropic disorder • hypoprolactinaemia Disorders of coitus: • erectile dysfunction • psychosexual ejaculatory failure • retrograde ejaculation: — genitourinary surgery — autonomic disorders (e.g. diabetes) — congenital abnormalities Ductal obstruction Couple factors Joint subfertility Psychosexual dysfunction

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The subfertile couple

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GnRH hypothalamus

anterior pituitary

FSH LH

prolactin FSH LH

FSH

LH

117 excess prolactin inhibits ovulation

ovum

oestrogens progesterone ovulation

testosterone

tubal disorders

uterine disorders

cervicalvaginal factors

Female factors

X

potencysperm dysfunction

vas blockage

testicular dysfunction

Male factors

? adequate coitus

Combined factors

indicates possible disorder causing infertility

FIGURE 117.2 The major factors involved in subfertility. Source: Adapted from Kumar and Clarke1

— evidence of varicocele (controversial role) — PR: check prostate — note penis and location of urethra (always retract the foreskin for examination) The woman • Secondary sexual characteristics • Thyroid status • Genitalia and breasts • Vaginal and pelvic examination: — assess uterus and ovaries (normal—present, mobile and non-tender) — the adnexae (any masses)

Investigations These are usually performed after referral but the family doctor should organise initial investigations

to assess where to refer (e.g. endocrinologist, gynaecologist).

andrologist,

Initial investigations

Male—semen analysis It is advisable to obtain two samples at least 80–90 days apart as the cycle of production of sperm is about 80 days. It requires a complete ejaculation, preferably by masturbation, after at least 3 days sexual abstinence. Use a clean, dry widemouthed bottle; condoms should not be used. Semen should be kept at body temperature and examined within 1 hour of collection.2,7 • Normal values: — volume >2 mL (average 2–6 mL) — concentration >15 million sperm/mL — motility >40% after 2 hours

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— normal forms >4% — velocity >30 microns/s

(Other investigations may be necessary.)

Female—ovulation status

117

• Educate about temperature chart and cervical mucus diary, noting time of intercourse (take temperature with thermometer under tongue before getting out of bed in the morning)—now considered to be of low value. • Midluteal hormone assessment (21st day of cycle)—i.e. serum progesterone. This is the most common first-line test for ovulation (see TABLE 117.2). • Early ultrasound (day 5–9 of cycle). • Anti-Mullerian hormone—a predictor of ovarian function.

Table 117.2

WHO classification of ovulatory dysfunction6

• • • • • • •

Thyroid function tests: ? hypothyroidism Serum prolactin, FSH, LH androgen levels Sonohysterogram Endometrial biopsy Transvaginal ultrasound Hysteroscopy/laparoscopy CT of the pituitary fossa—if prolactin significantly elevated • Chlamydia (cervical culture) Note: Ovulation or its absence is best demonstrated by luteal progesterone. Essential investigations are outlined in TABLE 117.3. Table 117.3

Essential first-line investigations of the subfertile couple2

Basal body temperature chart and cervical mucus diary

Group 1

Hypothalamic– pituitary failure

Low FSH, LH (e.g. anorexia nervosa)

Semen analysis

Group 2

Hypothalamic– pituitary dysfunction

Normal FSH (e.g. PCOS)

Transvaginal ultrasound

Group 3

Ovarian failure

High FSH (e.g. ovarian failure)

Serum progesterone (mid-luteal—day 21) in female Rubella immune status (female)

Management principles5 Subsequent investigations Diagnostic laparoscopy—direct visualisation of corpus luteum, tubes; check tubal patency by insufflating blue dye from the cervix through the tubes to the peritoneal cavity. Further investigations (if necessary)

Male

• Both partners should be involved in management decisions since fertility is a couple’s problem. • Infertility can cause considerable emotional stress, including the taking or placing of blame by one partner or the other, and subsequent guilt feelings; hence sensitive and empathetic support is essential. This may include marital counselling. • Since recent advances have helped this problem so much, there is no place for guesswork or for empirical therapy and early referral is necessary.

If azoospermia or severe oligospermia: • serum FSH level (if 2.5 times normal, indicates irreversible testicular failure)—this is the most important endocrine test in the assessment of male infertility • LH • antisperm antibodies (in semen or serum) • sperm function tests • chromosome analysis: 46 XXY or 46 XXY/46 XY or microdeletion • testosterone • testicular ultrasound

Fertility awareness This education is helpful for couples: • women always ovulate about 12–14 days before the period • fertile mucus is copious, slippery and has the appearance of egg white (ovulation occurs within 24 hours) • ova can survive up to 24 hours and sperm up to 5 days within the female genital tract • the chance of fertilisation is best during days 10–16 of a 28-day cycle

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The subfertile couple

Polycystic ovarian syndrome PCOS is an ultrasound diagnosis—10 to 12 small cysts around the periphery of at least one ovary. About 50% of women have no other signs or symptoms. PCOS is the above plus clinical symptoms— one of: • • • •

oligomenorrhoea hirsuitism acne obesity

PCOS has a strong hereditary basis and can begin in the pubertal years. There are variations of the syndrome, including normal menstruation (20%) and abnormal uterine bleeding (50%). General features8 Patients have some of the following (it is rare to have all): • ovarian dysfunction—infertility, oligomenorrhoea, anovulation, tendency to miscarry, endometrial cancer • androgen excess—hirsutism and acne • obesity • metabolic (insulin resistance) syndrome—upper truncal obesity, impaired glucose tolerance, hyperlipidaemia, hypertension, tendency towards type 2 diabetes • ovarian abnormalities—multiple small follicles, stromal expansion Aetiology The exact cause is unknown. There is a hereditary factor, and hormonal dysfunction resulting from several follicles failing to mature and release eggs, instead dying out on the ovarian surface. Some experts claim that the principal underlying disorder is insulin resistance with hyperinsulinaemia. Diagnosis/investigations • Raised LH level with normal FSH levels (LH/FSH ratio >2) • Raised serum testosterone level (not always) • Transvaginal ultrasound (usually at least 12 follicles, small in size in an enlarged ovary) • Possible endometrial biopsy Suggested screening for all women with PCOS8 • Smoking history • Blood pressure

• • • •

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Blood glucose levels Oral glucose tolerance test Fasting plasma insulin Fasting serum HDL and LDL levels

Management strategies8

First-line4 • Lifestyle modification: weight reduction and exercise (the key—this alone may restore normal ovarian function) • PCOS support group

Potential • Screening and treat if necessary: — glucose intolerance and diabetes mellitus — hyperlipidaemia — hypertension • Primary treatment of insulin resistance: — metformin — thiazolidinediones (glitazones) • Ovulation induction—clomiphene/ gonadotrophins • Laparoscopic ovarian diathermy (failed medical treatment) • Assisted conception

Counselling the subfertile couple9 The counselling of subfertile couples has to be adapted to the level reached by the couple along the infertility pathway. The needs of each couple may be very different depending on their emotional nature, their lifestyle, and their moral, religious and ethical beliefs. However, their suffering can run very deep and deserves attention, time and opportunities for free expression of feelings and concerns. The medical counselling model developed by Colagiuri and Craig9 (see FIG. 5.1 in CHAPTER 5) is very useful as it empowers patients to make their own decision through facilitation as opposed to the directive and advisory medical model. The couple are provided initially with accurate and appropriate information. Anxiety is alleviated by reassurance and by dispelling myths such as their problem being caused by an unfavourable position for intercourse, leakage of excess semen from the vagina or previous use of the pill. The facilitation process enables the couple to ventilate any feelings of guilt, anxiety, fear, anger and sexuality. The style of questioning should aim to explore the influence that the problem has had on the

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couple and then the influence they have over it. These processes then lead to decision making by the couple about further management strategies. A graph of emotional responses to the infertility (see FIG. 117.3) can be used to help the couple explore their current and past emotional responses to their problem. Apart from helping them realise that their problem is not unique, it provides opportunities for ventilation of important feelings that can act as a basis for counselling.

•

Treatment

Assisted conception10

If the problem has been identified, specific treatment needs to be prescribed by the consultant. Treatable factors in female subfertility are tubular diseases, anovulation and endometriosis. In males the treatable causes are rare but include gonadotrophin deficiency, inherited congenital adrenal hyperplasia and simple occlusion of the vas deferens.

This is the only option for subfertility/infertility due to azoospermia, anovulation and complete fallopian tube exclusion. The main techniques are: • assisted insemination (intra-uterine) • ovulation • IVF

• Anovulation can be treated with ovulation induction drugs such as clomiphene, bromocriptine, gonadotrophins or GnRH. • Endometriosis can be treated medically or surgically (peritubal adhesions). • Male problems—little can be done (including testosterone and vitamins) to enhance semen quality. Corticosteroids may help if sperm antibodies are present. Consider in vitro

New NICE guidelines for fertility treatment • NHS-funded IVF should be offered up to age 42 (in certain circumstances). • Couples having conception difficulties should be offered treatment after 2 years of regular unprotected intercourse, instead of the current 3 years.

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Anxiety

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• • •

fertilisation (IVF) and related technology for male factor infertility, particularly intracytoplasmic sperm injection (ICSI) into the oocyte. Artificial insemination. Donor insemination. Severe tubal disease—use IVF and embryo transfer (IVF-ET). Unexplained subfertility—consider IVF, which depends on the woman's age and the couple's attitudes.

Years 0.5 Surprise Denial Fear

2–3

1 Anger Frustration Resentment Depression Guilt Loss of self-esteem Loss of libido

FIGURE 117.3 Emotional responses to infertility Source: Reproduced with permission from Craig.9

Adjustment Resolution Control

4–5 Reawakening of fears and doubts Christenings Friends falling pregnant New treatment Adoption Donor insemination (DI), IVF

10 Control: but their infertility never leaves them completely

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The subfertile couple • Those women under 40 also with 2 years of failure or 12 cycles of artificial insemination should be offered 3 full cycles of IVF with or without ICSI. • Women aged 40–42 should be offered one full cycle of IVF with or without ICSI (with certain qualifications). • Women with idiopathic subfertility should not be offered ovarian stimulation drugs such as clomifene, since they are considered ineffective. Other guidelines can be accessed via the NICE website .

Evidence-based RCTs The conclusion as published in Clinical Evidence11 has summarised known benefits of infertility treatment (to date) as follows: • ovarian disorders—clomiphene, laparoscopic ovarian ‘drilling’ • tubal infertility—IVF • endometriosis—intra-uterine insemination with ovarian stimulation

When to refer A family doctor should perform the initial investigations of a couple with infertility, including

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temperature chart, semen analysis and hormone levels, to determine whether it is a male or female problem and then organise the appropriate referral.

References 1 Kumar PJ, Clark ML. Clinical Medicine (5th edn). London: Elsevier Saunders, 2003: 1028–30. 2 Stern K. Infertility: how to treat. Australian Doctor, 12 July 2002: I–VIII. 3 O'Connor V, Kovacs G. Obstetrics, Gynaecology and Women's Health. Cambridge: Cambridge University Press, 2003: 454–66. 4 Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2013. 5 Jequier AM. Infertility. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 273–8. 6 Illingworth P, Lahoud R. Investigation of the infertile couple 1. Medical Observer, 21 April 2006: 27–30. 7 DeKrester D. Female infertility. Modern Medicine Australia, 1990; July: 98–109. 8 Norman RJ et al. Metformin and intervention in polycystic ovary syndrome. Med J Aust, 2001; 174: 580–3. 9 Craig S. A medical model for infertility counselling. Aust Fam Physician, 1990; 19: 491–500. 10 Liberman D. Infertility. Medical Observer, 1 March 2013: 25–7. 11 Duckitt K. Infertility and subfertility. In: Barton S (ed.). Clinical Evidence. London: BMJ Publishing Group, 2001, issue 5: 1279–94.

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118 Sexual health The functional form of impotence fills the coffers of the quacks, and swells the list of suicides. Rutherford Morrison (–) Drink, sir, provokes the desire, but it takes away the performance. William Shakespeare (–), Macbeth, Act , Scene  Family doctors are often asked to provide advice and help for sexual concerns and are continually challenged to detect such problems presenting in some other guise. Since we deal with so much illness, including debilitating problems, and prescribe so many drugs, we must be aware of and sensitive to the possible implications of their various effects on sexual health. Sexual disorders can be considered in three major groups: sexual dysfunction, sexual deviation and gender role disorders. This chapter largely confines itself to a discussion of sexual dysfunction.

Sexual dysfunction Sexual dysfunction in men refers to persistent inability to achieve normal sexual intercourse while in women it refers to a persistent lack of sexual satisfaction.1 Several studies have demonstrated that sexual concerns and problems are common, with a prevalence ranging from 10–70% of the population.2 Difficult problems are summarised in TABLE  118.1. These studies have also indicated that patients are certainly willing to discuss their sexuality and wish their family doctors to become involved in counselling and management of their problems. Between 25% and 30% of sexual difficulties have an organic cause, while the remainder are emotional or psychogenic in origin.3 The unique place of general practice and the family doctor provides ideal opportunities to address the sexual concerns of patients as the family doctor often has considerable insight into the family dynamics and first-hand perspective of the individuals involved. The most common problem influencing an effective outcome is difficulty in communication between doctor and patient, which prejudices effective history taking and counselling. The problem is not contentrelated, much of which is based on commonsense, but the ubiquitous problem of communication.

Table 118.1

Sexual dysfunction: difficult problems

Sexual desire: • low libido Sexual arousal: • erectile impotence • failure of arousal in women Sexual orientation/activity: • homosexuality • fetishism Orgasm: • premature ejaculation • retarded ejaculation • orgasmic dysfunction in women Male problems: • low libido • erectile difficulties • premature ejaculation • failure to ejaculate, or retarded ejaculation Female problems: • low libido • failure of arousal • vaginismus • orgasmic difficulties • dyspareunia

If, as a practitioner, you counsel on the assumption that astounding ignorance about sexuality still exists in our society, you will be amazed at the results and at how relatively simple it is to help so many confused people who often have unrealistic expectations of their partners and themselves.

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Sexual health

Opportunistic sexuality education The family doctor has many opportunities to provide education in sexuality throughout the lifelong care of the patient and it is wise to have a strategy that matter of factly incorporates enquiries and information about sexual health. Examples include: • • • • • •

antenatal and postnatal care contraceptive requests parents concerned about their children’s sex play serious illness—medical and surgical adolescent problems menopause problems

Presentation of sexual concerns Although some patients may present directly with a complaint of sexual dysfunction, many will be less direct and use some other pretext or complaint as a ‘ticket of entry’ for their sexual concerns (see TABLE  118.2). Despite a seemingly terse approach the issue must be recognised and treated with considerable importance. This may mean scheduling an appropriate time to discuss the concerns. Table 118.2

How sexual issues may present in family practice2

Minor non-sexual complaint—‘entry ticket’ Specific sexual concern Marital or relationship problem Non-sexual problem (as perceived by the patient) Sexual enquiry and counselling as part of illness management Sexual enquiry as part of total health check-up Infertility Menopausal problems

Sometimes patients are unaware of an association between their medical problem and underlying sexual issues.2 Doctors may recognise such an association and initiate a tactful psychosocial history that includes questions about sexuality. Examples are chronic backache, pelvic pain, vaginal discharge, tiredness, insomnia and tension headache.

The effect of illness on sexual function Doctors seldom enquire about the impact of an illness on the sexual function of patients and their

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partners and tend to be unaware of the sexual needs of elderly people (see TABLE  118.3). It is most appropriate to enquire about these issues in our patients—e.g. the postmyocardial infarction patient, Table 118.3

Medical conditions affecting sexual performance

Cardiovascular: • previous myocardial infarction • angina pectoris • peripheral vascular disease • hypertension and its treatment Respiratory: • asthma • COPD Endocrine: • diabetes mellitus • hypothyroidism • hyperthyroidism • Cushing syndrome Neurological: • multiple sclerosis • neuropathy • spinal cord lesions • Parkinson disease Musculoskeletal: • arthritis Depression Kidney: • kidney failure Urological problems: • prostatectomy • phimosis • Peyronie disorder • priapism Hepatobiliary: • cirrhosis Surgical: • vaginal repair • hysterectomy • others Trauma: • motor vehicle accidents Cancer Other: • Klinefelter syndrome

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• Sexual health

the postprostatectomy patient, the patient taking antihypertensives or other drugs (see TABLE 118.4), and the post-mastectomy or post-hysterectomy patient. Diabetes deserves special attention as 27–55% of diabetic men reported some erectile difficulties.2 Table 118.4

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Drugs affecting sexual arousal and function

• Are you sexually active? • What is the physical side of your marriage/ relationship like? • Do you have any pain or discomfort during intercourse? • Is your relationship good? • Do you communicate well? Generally? Sexually? • Do you have any difficulties in your sexual relationships? • What is your sexual preference? • Are you attracted to men, women or both? • Have you experienced the ‘coming out’ process? • What drugs are you taking? • Do you take recreational drugs (e.g. alcohol, nicotine, marijuana, other illicit drugs)?

Male

Female

Alcohol

Alcohol

Anticholinergics

Anti-androgens

Anti-epileptics

Antidepressants (selected) e.g. SSRIs

Antihistamines

Anti-epileptics

Specific questions about sexuality

Antihypertensives

Antihypertensives (selected)

Benzodiazepines

CNS depressants

Cytotoxic drugs

Hormone contraception e.g. combined oral contraceptive

Disulfiram

Marijuana

Marijuana

Narcotics

• Do you get aroused/turned on? What turns you on? • Do you look forward to making love? • Do you spend much time on love play? • Does lovemaking make you feel happy and relaxed? • Do you worry about getting pregnant (women)? • What do you do about contraception? • Do you worry about getting an STI? • Do you worry about getting AIDS? • How often do you reach a climax during lovemaking? • How often do you have intercourse, or sexual activity without intercourse? • Do you ‘come’ together?

Narcotics Oestrogens Psychotherapeutic drugs

Taking a sexual history It is important to be alert for psychiatric disorders and situational factors and not to predict a person’s sexual disposition. Avoid being too formal or too familiar but aim to display a wise, matter-of-fact, empathic, commonsense rapport. Tactfully explore the patient’s attitude to sexuality and examine the relationship. Ideally, it is best to see a couple together if the problem is occurring within a steady relationship. As a practitioner, you have to be comfortable with your own sexuality and learn to be relaxed, confident and understanding when dealing with sexual concerns. Enquiry about possible child sexual abuse is an important part of the history.

Probing questions for a suspected sexual problem • Do you have any trouble passing urine or any vaginal discharge (women)?

Female • Do you have enough lubrication? Are you wet enough? • Do you find intercourse uncomfortable or painful? Male • Do you have trouble getting a full erection? • How long does it take you to ‘come’ after you insert your penis? • Do you ‘come’ too quickly?

Background history for an admitted problem • Can you think of any reasons why you have this problem? • What sex education did you have as a child? At home or at school? • Were your parents happily married?

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Sexual health • Were sexual matters something that could be discussed in the home? • Did you come from a religious family? • Did you receive warnings or prohibitions as a child? • What was the family attitude to masturbation, extramarital sex, menstruation, contraception, etc.? • What is your attitude to masturbation? • Were you fondled or sexually abused by an adult, especially a member of the family? • Were there healthy shows of affection such as touching or hugging between family members? • Did you have any upsetting sexual experiences during childhood and adolescence? • What was your first sexual experience like?

Sexual myths in the male4

Examination

Basic sexual counselling

The routine medical examination should include the basics such as urinalysis, BP measurement, genital examination and neurological where indicated. A careful vaginal and pelvic examination should be an opportune educational experience for the patient and an exercise in preventive medicine.

The family doctor can learn to be an effective sex counsellor. Sex counselling can be emotionally demanding and, while good interviewing skills, interest, support and basic advice are important, additional skills are needed to be an effective counsellor. The fundamental methods involve:5

Investigations No particular routine tests are recommended. Tests for male erectile dysfunction (impotence) are outlined later in this chapter. Tests that may help exclude significant causes of low libido are those for diabetes, liver dysfunction, thyroid dysfunction and endocrine dysfunction. Endocrine dysfunction tests include prolactin, free testosterone, FSH, LH and oestradiol estimations. Other investigations may include pelvic ultrasonography, colposcopy or laparoscopy.

Exploring sexual myths The acceptance in part or in total of many sexual myths that have prevailed in our society may have affected the relationship of a couple, especially in the context of the modern trend towards openness in discussing sexuality. It is worthwhile to help patients identify whether any of these myths have influenced their concerns by exploring common myths and their significant consequences to the individual or couple. Sexual myths that could be explored include:2 • • • • • •

men need sex, women need love men need more sex than women men must be the instigators men know all about it sex = intercourse in this enlightened age everyone understands sexual issues

• • • • • • • • •

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A hard erection is essential for good sex. A man should not show his feelings. A real man is always horny and ready for sex. As a person gets older there is no change in sexual interest, response or performance. As a person gets older there is a loss of interest in sex. Sexual performance is what really counts. Men are responsible for their partner’s sexual pleasure. Sex must lead to orgasm. A man and his partner must reach orgasm simultaneously.

• good communication and allowing a ‘comfortable’ exchange of information • giving the patient ‘permission’ to talk openly about sexual matters • providing basic ‘facts of life’ information • dispelling sexual myths, correcting other misunderstandings • gentle guidance for appropriate insight • de-emphasising the modern-day obsession with performance and orgasm and emphasising the value of alternative forms of sexual expression (e.g. caressing, kissing, and manual and oral stimulation) • reducing the patient’s anxiety • bolstering self-images affected by feelings of rejection, avoidance, guilt, resentment or incompetence • reassuring the patient that he or she is normal (where appropriate) Inappropriate doctor behaviour is presented in TABLE 118.5.

An interesting realisation after counselling families in sexuality is that most of the problems are not difficult and often spring from basic ignorance of normal sexual function; it’s simply a matter of setting the record straight. The greatest hurdle is ‘getting started’ with delineating the problem. Once that barrier is crossed, satisfactory results appear to follow.

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Table 118.5

• Sexual health

Sexual counselling: inappropriate doctor behaviour

Overfamiliarity Being too formal Being too talkative Blunt questioning Being judgmental Making assumptions about the other’s sexuality Imposing one’s own beliefs and standards Dogmatism Tackling problems beyond one’s experience

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Another significant realisation is that sexual problems can be grossly underestimated. Human beings generally have a basic craving for intimacy, touching, stroking and loving sex. Apparently ‘good’ harmonious relationships can lack this type of intimacy, which may lead to various psychosomatic manifestations. Ideally the family doctor should undertake a course in sexual counselling to promote confidence in the counselling process. Patients can be taught basic methods (where appropriate) such as sensate focus, squeeze or stop–start techniques for premature ejaculation, self-exploration using Kegel pelvic floor exercises, fantasy conditioning with DVDs, and behaviour modification. Complex problems, especially those involving erectile dysfunction, infertility and sexual deviations or perversions, demand referral to an expert.

Most medically trained people can probably provide the limited information required about sexual physiology and behavioural patterns.3 ‘Specific suggestion’ provides ideas for self-help and may include key reference books, and relevant audiotapes or VHS/DVDs (see box titled Further reading). DVDs can certainly arouse interest, ideas and motivation for a renewal of sexual activity. With a little support and permission, the patient can take simple action to remedy or improve a problem. Intensive therapy, whether psychiatric or emotional, calls for deeper involvement and can be a dangerous area for the inexperienced. Referral to the appropriate practitioner is usually advisable.3

Further reading Recommended books • Comfort A. The Joy of Sex. London: Mitchell Beazley, 1987 (revised edition); ebook: 1/2013; paperback 12/2009. • Fisch Harry. The New Naked: The Ultimate Sex Education for Grown-ups. Illinois: Source Books, 2014. • Zilbergeld B. Men and Sex. A Guide to Sexual Fulfilment. Harper Collins (reissue) 1995. • Rickard-Bell R. Loving Sex: Happiness in Mateship. Sydney: Wypikaninkie Publications, 2002. • Heiman J, Lo Piccolo J. Becoming Orgasmic: a Sexual Growth Program for Women. Sydney: Simon & Schuster, 1987. Recommended DVDs • The Lovers’ Guide I and II. Andrew Stanway. • The Language of Love.

The PLISSIT counselling model The PLISSIT counselling model developed by Annon5 can be used to build the skills needed to deal with sexual problems, especially if there is a psychological element.3 The mnemonic PLISSIT stands for: P LI SS IT

= = = =

Permission giving Limited Information Specific Suggestion Intensive Therapy

‘Permission giving’ allows patients to talk about sex, ask questions, feel guilty and so on. Their problems are shared with a reflective listening confidant.

Analogous roles of the penis and clitoris An explanation of the analogous roles of the penis and clitoris (proposed by Cohen and Cohen) is a very useful strategy for educating patients and helping them to understand the relationship of intercourse and penile and clitoris stimulation with orgasm. The simple model (see FIG. 118.1) can be shown to patients to explain, for example, why some women are unable to achieve orgasm by intercourse alone, especially using the conventional missionary position.2,6 It can readily be explained that clitoral stimulation in women is analogous to penile stimulation in men. Such information is very helpful for women and also

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Sexual health

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clitoral shaft

penile shaft

hood

prepuce

clitoral glans

penile glans

urethral opening

minor lips major lips scrotum vagina

anus

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FIGURE 118.1 Analogous structures in male and female genitalia Source: Reproduced with permission from G and M Cohen, Canadian Family Physician, 852, 31: 767–712

to men who may perceive themselves as inadequate lovers. The use of such explanatory aids greatly facilitates the educational process and makes it more ‘comfortable’ for all concerned.

Female orgasmic difficulties It is necessary to determine whether the woman has been anorgasmic or can experience orgasms from other activities such as masturbation, manual or oral stimulation, even though she is non-orgasmic during intercourse. The use of the Cohen model (see FIG. 118.1) is very helpful in emphasising the importance of clitoral stimulation. Therapy includes: • sensate focus exercises7 • advice on the most appropriate positions for intercourse • permission to use: — sexual aids: books, magazines — visual tapes — self-stimulation

Dyspareunia Painful intercourse is a source of considerable distress both physically and psychologically for the sufferer

and also for her partner. It may be one of the ‘hidden agenda’ presentations with a vague complaint such as ‘I am uncomfortable down below’. Tact and sensitivity is very important in management. The patient needs to be encouraged to talk freely during history taking with an opportunity to express what they believe is the basic problem. Montgomery claims that most cases (about 80%) of dyspareunia have a physical cause and careful physical examination is mandatory. In particular it is helpful to keep in mind vulval vestibular syndrome, which has subtle physical signs (see CHAPTER 107). Important causes are listed in TABLE 118.6. A common problem encountered is the presence of painful scar tissue following an episiotomy, especially after the first vaginal delivery, so it is worth asking about this potential problem because some women are reluctant to raise the issue. Management of dyspareunia involves treating the organic cause and giving appropriate advice about the use of lubricants, including oestrogen creams.

Vaginismus Vaginismus is the involuntary contraction of muscles around the introitus (outer third of vagina) in response to and preventing the possibility of penetration. It can be classified as primary or secondary. In primary

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Table 118.6

• Sexual health

Important causes of dyspareunia

Pain worse on insertion Physiological—inadequate lubrication Provoked vestibulodynia syndrome Vaginitis in chronic candidiasis Vulvar dermatoses Postnatal perineal scarring Incompletely ruptured hymen Vulvovaginal atrophy (e.g. postmenopausal) Vaginismus Pain worse on deep penetration Endometriosis PID Pelvic adhesions

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Ovarian and uterine tumours Postnatal

vaginismus tampons will probably never have been inserted. It is often related to provoked vestibulodynia (vestibular hypersensitivity—see CHAPTER 107). In some instances vaginismus may be voluntary. It is not an uncommon cause of unconsummated marriages, usually associated with fears of internal damage, pregnancy, learned negative attitudes to sex and past sexual trauma. The problem usually responds well to brief therapy. This includes explanation of the anatomy and physiology with the use of a hand-held mirror during examination. The patient or couple can use a lubricant such as baby oil, KY gel, Vaseline or oestrogen cream to make intercourse comfortable. The couple will benefit from a sensate focus program, which includes the most comfortable position for intercourse, controlled by the woman usually in a superior position. Otherwise, progressive vaginal dilation can be practised using lubricated fingers or graduated dilators.

Erectile dysfunction Erectile dysfunction (impotence) is the inability to achieve or maintain an erection of sufficient quality for satisfactory intercourse. It doesn’t refer to ejaculation, fertility or libido. Patients often use the term to refer to a problem of premature ejaculation, hence careful questioning is important. Erectile dysfunction is a common problem. US data shows the prevalence to be 39% of males at 40 years and 67% of males aged 70.8

The most effective and practical approach to the man with erectile dysfunction is to determine the response to an intrapenile injection, where prostaglandin E1 is preferred to papaverine. Causes9 • Psychogenic: related to stress, interpersonal or intrapsychic factors (e.g. depression, marital disharmony, performance anxiety) • Neurogenic: disorders affecting the parasympathetic sacral spinal cord (e.g. multiple sclerosis); it usually develops gradually • Vascular • Diabetes • Hypertension • Chronic kidney disease • Urological problems (e.g. Peyronie disorder, pelvic trauma and surgery) • Hormone disorder — androgen deficiency (e.g. testicular disease) — hypothyroidism — hyperprolactinaemia (rare) → impotence and loss of libido due to secondary testosterone deficiency • Drug-induced: — alcohol — cocaine, cannabis — nicotine (four times the risk by age 50) — antihypertensive agents — pharmaceutical preparations • Ageing • Unknown

Practice tip Erectile dysfunction may be the first symptom of atherosclerotic disease (e.g. CAD).

History The nature of the onset of erectile dysfunction is very important and this includes the nature of the relationship. Of particular importance is a drug history, including alcohol, nicotine, street drugs and pharmaceutical agents, particularly antihypertensives (beta blockers and thiazide diuretics), hypolipidaemic agents, antiandrogens (prostate cancer treatment), antidepressants, antipsychotics and H2-receptor antagonists. Ask about nocturnal and early morning erections. Examination Genitourinary, cardiovascular and neurological examinations are important. This should include a

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Sexual health rectal examination and examination of the vascular and neurological status of the lower limbs and the genitalia, especially the testicles and penis. Check the cremasteric and bulbocavernosus reflexes. Investigations First-line blood tests: • free testosterone ? androgen deficiency • thyroxine ? hypothyroidism • prolactin ? hyperprolactinaemia • luteinising hormone • glucose Other blood tests to consider: • LFTs, especially GGT (alcohol effect) • kidney function tests

Nocturnal penile tumescence This is an electronic computerised test used to detect and measure penile erections during REM sleep. Normally, there are 3–5 spontaneous erections lasting 20–35 minutes. The test helps to differentiate between psychogenic (normal studies) and organic (poor function). A very simple screening test is to use the snap gauge device.

Dynamic tests of penile function7 These tests include injections of drugs into the corpus cavernosum (which is the simplest method) to assess function. If the patient does not have overt psychogenic erectile dysfunction and the diagnosis is uncertain, the response to intracavernosal injections of prostaglandin E (PGE) can be tested. A good response to PGE indicates that the patient has psychogenic or neurogenic impotence (e.g. due to pelvic nerve division during colon resection). Responses at higher doses indicate an incomplete organic disorder (e.g. partial arterial occlusion, venous leak, or diabetic neuropathy—early). Total failure to respond suggests arterial occlusion or an idiopathic disorder of the corpora cavernosa. Management Address modifiable risk factors, including medications (if feasible), psychosocial issues and lifestyle (see NEAT, CHAPTER 7). Management should comprise appropriate patient education including a DVD of the specific recommended treatment and technique. The partner should be included in the discussions and general management process with an emphasis on bolstering the couple’s self-image, which may have been affected by feelings of rejection or avoidance.

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Psychogenic disorders These will involve psychotherapy and sex behavioural modification as outlined earlier in the chapter under Basic sexual counselling. Referral to a consultant may be appropriate.

Hormonal disorders • Testosterone for androgen deficiency: primary testicular disease (e.g. Klinefelter syndrome) or gonadotrophin deficiency Stepwise trial 1 Oral: testosterone undecanoate (Andriol) 2 IM: testosterone enanthate (Primoteston Depot) or testosterone esters (Sustanon) 3 Subcutaneous implantation: testosterone implants (last 5–6 months) • Thyroxine for hypothyroidism • Bromocriptine for hyperprolactinaemia

Oral medication PDE-5 inhibitors: the phosphodiesterase type 5 (PDE5) inhibitors are the first-line oral medication (see TABLE  118.7). They are about 70% effective but not very effective for neurogenic ED. They do not initiate an erection but enhance whatever erection the man is capable of having. Sexual stimulation is necessary. They are contraindicated if the patient has unstable angina, recent stroke or myocardial infarction. Use with nitrates should be avoided and a nitrate should never be taken within 24 hours of use. The interaction with nitrates can result in a severe and potentially fatal hypotensive response. PDE-5 inhibitors have the potential for side effects, especially headache. Treatment is not considered a failure until a full dose has been trialled 7–8 times.9 In some cases combining them with alcohol or fatty foods can delay their onset of action.10 • • • •

Four basic rules: sexual stimulation is necessary avoid fatty foods minimal or no alcohol no nitrates

Intrapenile injection • Alprostadil intracavernosal injections: — self-administered after supervised teaching (use a penile model if available) — start with a lower dose, 2.5–5 mcg — maximum of three a week — spontaneous erection in 5 minutes — if prolonged erection >2 hours take 120 mg pseudoephedrine orally—repeat at 3½ hours if necessary (provided not hypertensive)

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Phosphodiesterase type 5 inhibitors10

Table 118.7

Sildenafil (Viagra)

Tadalafil (Cialis)

Vardenafil (Levitra)

Dosage (mg)

25, 50, 100

5, 10, 20

5, 10, 20

Usual starting dose (1 hour pre i/c)

50 mg

10 mg

10 mg

Onset of action

30–60 min

1–2 hours

30–60 min

Alcohol effect

Possibly

Possibly

Possibly

Nitrate contraindication

Yes

Yes

Yes

Class side effects

Headache, nasal stuffiness, facial flushing, dyspepsia

Specific side effects

Blue vision, diarrhoea

Myalgia, back pain

Visual disturbance

The cooperation of the partner is essential and urological back-up must be arranged.

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Transurethral alprostadil (Muse) Urethral pellet: initial dose 250 mcg

Vacuum constriction Vacuum constriction devices may have a place in management, especially in men in long-term relationships and where pharmacological therapies are inappropriate. About 80% effective.9

Surgery • Malleable penile prosthesis • Inflatable penile prosthesis (see FIG. 118.2) • Vascular surgery where appropriate

Premature ejaculation Premature ejaculation is defined as ‘ejaculation that occurs sooner than desired’ or, more precisely, as ‘persistent or recurrent ejaculation, before, on or shortly after penetration and associated with significant personal distress’. For the latter the intravaginal ejaculatory time is 2 months of age. Apply to whole body from jawline down (include every flexure and area), leave overnight, then wash off. Wash clothing and linen after treatment and hang them in sun. or benzyl benzoate 25% emulsion left for 24 hours before washing off; repeat after 7 days The whole family and close contacts must be treated, regardless of symptoms, which can take weeks to develop. One treatment is usually sufficient. It can be repeated in a week if necessary. Note: Persistence of the itch after treatment is common. If the itch has not abated after 7 days, re-treat. After this, reassurance is usually all that is required. Also prescribe a topical antipruritic (e.g. crotamiton cream for 3–5 days or a topical corticosteroid or an oral antihistamine for the itch).

Pubic lice

119

permethrin 1% lotion: apply to pubic hair and surrounding area, leave for 20 minutes and then wash off or pyrethrins 0.165% with piperonyl butoxide 2% in foam base; apply as above Shaving pubic hair is also effective. Bed clothes and underwear should be washed normally in hot water after treatment and hung in the sun to dry. Repeat the treatment after 7 days. Sometimes a third treatment is necessary. Sexual contacts and the family must be treated (young children can be infested from heavily infested parents). Where the lice or the nits are attached to eyelashes, insecticides should not be used: apply white soft paraffin (e.g. Vaseline) liberally to the lashes bd for 8 days. Then remove the nits with forceps.

Candidiasis topical imidazole (e.g. clotrimazole 1% applied 2–3 times daily)

Extragenital STIs Viral hepatitis Sexual activity is a factor in the transmission of hepatitis B (in particular), hepatitis A (where faecal– oral contact is involved), hepatitis C (probably occasionally) and hepatitis D.1

Hepatitis B In Western societies, sexual transmission of HBV is a common mode of spread and there is a higher prevalence in homosexual men and prostitutes. HBV prevalence in homosexual men is correlated with insertive and receptive anogenital contact and oro– anal contact. There is no specific therapy for hepatitis B, so prevention is important. Interferon α-2 and lamivudine or tenofir can be used for complications such as chronic active hepatitis. Prevention4 Several prevention strategies are available; they include: • immunisation • prevention of infection in health care establishments • management of exposure (needle stick injuries, etc.) • management of infants of mothers who are hepatitis B carriers • condoms, which offer some reduction of risk of sexual transmission • personal hygiene Immunisation Immunisation should be encouraged in hepatitis B marker-free people at risk of acquiring this infection. At-risk groups include sexual partners of carriers, institutional individuals, MSM, sex workers and drug addicts. Some health workers are exposed to risk. Management of exposure Sexual partners of acute cases and chronic carriers who are negative for surface antigen (HBsAg) and antibody can be offered hepatitis B immunoglobin, and routine hepatitis B immunisation should be commenced.

Hepatitis C Although there have been doubts about the potential for sexual transmission of hepatitis C, Tedder et al. in 199111 demonstrated evidence for the sexual transmission of HCV but the epidemiological evidence is not strong.

HIV infection HIV infection (colloquially called AIDS, although this represents only the severe end of the disease

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Sexually transmitted infections spectrum) is predominantly transmitted by IV drug use in the community. In Australia about 80% of HIV cases are related to IV drug use and the rest are mainly sexually transmitted.12 The important risk factors in infected men are receptive anal intercourse and multiple sexual partners. Sexual transmission to women4 Although the heterosexual partners of infected men are at risk of infection, spread to and from women has been relatively uncommon in developed countries, but now appears to be increasing significantly. In central Africa, heterosexual spread is an important means of transmission. Genital ulcerative diseases such as syphilis and genital herpes may be associated with an increased risk of heterosexual transmission. HIV infection is considered in more detail in CHAPTER 27.

When to refer13 • Syphilis: — probably all suspected or confirmed cases but certainly for suspected tertiary syphilis — HIV-positive patients, and — suspected treatment failure • Pubic lice and scabies: — unresolved rash or itch despite apparently appropriate treatment • Genital warts: — urethral or cervical warts — associated cervical HPV changes on cytology — refractory warts • Gonorrhoea or non-specific urethritis: — if complications, pelvic spread or extragenital problems develop, or if symptoms persist after two courses of antibiotics

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Practice tips • •

•

• • •

Do not presume that the patient or his/her partner has acquired an STI outside their relationship. The itch of scabies or pubic lice can be distressing: prescribe the topical antipruritic (crotamiton cream) and/or an oral antihistamine. Reassure the patient that the itch will gradually subside over a few weeks (especially with scabies). This allays anxiety that may lead to overzealous self-medication. Make every attempt to confirm or exclude genital herpes, using the appropriate investigations. Use aciclovir or similar antivirals for first episodes of genital herpes and for all recurrences. Twelve golden rules of management are presented in TABLE 119.4.

Table 119.4

STIs: Twelve golden rules of management (Sexual Health Society of Victoria)

1

An STI can only be diagnosed if the possibility is considered.

2

An adequate sexual history is paramount.

3

A proper history and careful examination must precede laboratory investigations.

4

Remember the sexual partner(s)!

5

Treatment consists of the appropriate antibiotic in correct dosage for an adequate period of time.

6

A patient concerned about STIs is probably an ‘at risk’ patient.

7

Counselling and education are fundamental to STI management.

8

Penicillin will not cure NSU.

9

Not all vaginal discharges are thrush.

10

Multiple, painful genital ulcers are most often due to herpes simplex.

Contact tracing

11

Prompt, accurate treatment of PID is necessary to preserve fertility.

It is important to contact partners of those presenting with more serious STIs. Government guidelines recommend that for patients with asymptomatic infection (e.g. Chlamydia, gonorrhoea), partners in the previous 12 months should be contacted and they should refer sexual contact partners within 30 days of the onset of symptoms. A discreet letter sent to the contact is advisable.14 There are several helpful websites including , which assist with sending anonymous emails or text messages to contacts.

12

Remember the three Cs—Consent, Confidentiality and Counselling—of HIV antibody testing.

Good communication Note: Tests for STIs, including the HIV antibody test, should only be performed with the patient’s knowledge and consent and after adequate counselling. An appointment should be made to give  results person  to person, irrespective of the results.

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• Sexual health

Acknowledgment Professor John Turnidge has given permission to adopt his categories of presenting conditions.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Chlamydial urethritis • Gonorrhoea • Hepatitis B • Herpes: genital herpes • HIV infection and AIDS • Lice: pubic lice • Pelvic inflammatory disease • Warts: genital warts

References

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1 Turnidge J. Sexually Transmitted Diseases. Check Program 210/211. Melbourne: RACGP, 1989. 2 Sexual Health Society of Victoria. National Management Guidelines for Sexually Transmissible Infections. Melbourne: Sexual Health Society of Victoria, 2008 (accessed 13/12/2014). 3 Royal Australian College of General Practitioners. Guidelines for Preventive Activities in General Practice (8th edn). East Melbourne: Royal Australian College of General Practitioners, 2013.

4 Collins K, Coorey W, Couldwell D et al. Sexually Transmissible Infections. Check Program 447. Melbourne: RACGP, 2009: 3–17. 5 Waddell R. Sexually Transmitted Diseases. Check Program 363. Melbourne: RACGP, 2002. 6 Department of Health and Ageing. Communicable Diseases Intelligence 2005, 29: 417–33. 7 Moulds R (Chair). Therapeutic Guidelines: Antibiotic (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2010 (eTG Complete). 8 Donovan B. Management of sexually transmissible infections. Medicine Today, 2006; 7 (1): 63–5. 9 Zhu, Frank. Australian Anti-infection Handbook (2nd edn). Sydney: Palmer Higgs Books, 2010. 10 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 136–46. 11 Tedder RS, Gilson RJC, Briggs M et al. Hepatitis C virus: evidence for sexual transmission. BMJ, 1991; 302: 1299–302. 12 National Centre in HIV Epidemiology and Clinical Research. HIV/AIDS and Related Diseases in Australia. Annual Surveillance Report, 1997. 13 Bradford D. Sexually Transmitted Disease. Check Program 252/253. Melbourne: RACGP, 1993: 7–8. 14 Wines N, Daylan L. Nongonococcal urethritis management in general practice. Medicine Today, 2000; November: 33–6.

Resources National Management Guidelines for Sexually Transmissible Infections. Melbourne: Sexual Health Society of Victoria, 2008.

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120

The root of Solomons seale when applied, taketh away in one or two nights, any bruise, blacke or blue spots gotton by falls or womens wilfulnesse, in stumbling upon their hasty husbands fists, or such like. John Gerard (–) Intimate partner (or domestic) violence is defined by the World Health Organization as ‘any behaviour within an intimate relationship that causes physical, psychological or sexual harm to those in the relationship’. On the other hand, abuse can be of an elderly parent by the children or of some other member of the household to another member. It usually results from abuse and/or imbalance of power in close relationships. One person in the relationship consistently dominates or threatens with power and the abused victim gradually gives over more power. A major problem in dealing with intimate partner violence (IPV) is that it is hidden and the victims are reluctant to divulge the cause of their injuries when visiting medical practitioners.

Key facts and checkpoints1 • • • • •

•

• •

•

Between one-quarter and one-third of relationships experience violence at some time. In 90–95% of cases the victims are women. Ten per cent of women have been violently assaulted in the last year. Twenty-two per cent of homicides in Queensland in 1982–87 were spouse murders. In violent families with children, 90% of children witness the violence and 50% of children are victims of violence. Four per cent of relationships will experience chronic domestic violence (in 20% this occurs before marriage). Less than 20% of those who abuse their spouse abuse some other person.2 Alcohol is a factor in 50% of IPV incidents (i.e. not the sole cause; it does make violence easier, and is used as an excuse). Other factors include work stress/pressure, financial stress and illness. However, there are no excuses for domestic violence. Pregnancy is a high-risk time for victims of domestic battering.

•

•

•

Fifty per cent of people know someone affected by IPV, but one-third refuse to speak about it or get involved in any way because they regard it as a ‘private matter’. It is estimated that between 65% and 75% of women killed by abusive partners are killed while leaving or after leaving the relationship.3 One in five people think that domestic violence is acceptable in certain circumstances.

We usually think of domestic violence in terms of physical violence but it can take many forms.4 These include: • • • • •

physical abuse psychological abuse economic abuse social abuse (e.g. isolation) sexual abuse

Possible presentations3 • Physical injuries: usually bruising caused by punching, kicking or biting; also fractures, burns, genital trauma • Physical symptoms (e.g. back pain, headache, abdominal pain, chronic diarrhoea, vague symptoms, sexual dysfunction, anxiety) • Sleeping and eating disorders • Psychological problems (in both the woman and her children, e.g. depression, somatiform disorders, anxiety disorders, stress syndrome, including panic attacks) • Pregnancy and childbirth (e.g. unwanted pregnancy, miscarriages, antepartum haemorrhage, poor prenatal care) • Suicide attempts The physical injuries are rarely overlooked but the other symptoms are frequently overlooked.

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• Sexual health

A study by Stark et al.5 defines a three-stage sequence to the battering syndrome: • Stage 1: woman presents with injuries in the central anterior regions of the body (face, head and torso). • Stage 2: multiple visits to clinics, often with vague complaints. • Stage 3: development of psychological sequelae (alcohol, drug addiction, suicide attempts, depression).

Diagnosis It is important to have a high index of suspicion and recognise and manage the problem to prevent further violence. Diagnosing the problem, which is usually ‘hidden’, can be a challenge to the skill of the GP. If you suspect domestic violence—ASK! Talk to the woman alone: • How are things at home? • How are things with your spouse/children? • Did anything unusual happen to bring about these injuries? • Has there been any violence towards you? • You seem to be having a hard time.

120

It is vital to believe the woman’s story. Women are most likely to seek help from their family doctor in preference to any other agency.6 The doctor has to take the initiative because patients rarely complain about the violence.3 They may present up to 30 times before they take action to end the violence.4

Barriers to communication about abuse7 • •

• • • •

Concerns about confidentiality Perceptions about doctors: — do not ask directly — have no time — are not interested Embarrassment Fear of involving police/courts Fear of shaming family Fear of partner hurting or killing them

Assessment • Delineate the problem: pattern of violence; effect on the woman and her children; resources available to women; social/cultural environment. • Examine and investigate presenting symptoms.

• Check for coexisting injuries (common target areas are breast, chest, abdomen and buttocks). Inspect the ears, teeth and jaw. • Check the patient’s general health status. • Look for signs of alcohol or drug abuse. • Keep accurate records and consider taking photographs. • X-rays are helpful and may show old fractures.

Victims The victims come from all socioeconomic and cultural groups. As a rule they enter the relationship as normal, independent, competent women but gradually lose their coping ability and self-esteem and may become compliant victims.1 This has been demonstrated by Hazelwood and colleagues in their investigations of sexual sadists.2 Unfortunately, many victims believe that somehow they deserve their punishment. Many would like to leave home but the move is not so simple. Some do love their husbands and live in hope that the marriage will eventually work. They may feel that they cannot cope with living alone or with the guilt and perceived failure of moving out. The victim may be at various stages of change in terms of taking action in accordance with Prochaska and Di Clemente’s model of change (see CHAPTER 21, FIG. 21.4) and the counsellor should be aware of this process.

Perpetrators Perpetrators come from all walks of life and from all social and ethnic groups. They generally have inner drives to be strong, protective and powerful but can only achieve this at home through an inappropriate show of strength. However, they are basically insecure with poor self-esteem, poor communication skills, learned violence from family origins and an inability to express appropriate emotions, which tend to manifest as anger and violence.1 Although they usually control their violence outside the home, there is evidence that some perpetrators are guilty of violent behaviour in the community.

Cycle of violence A predictable pattern that is referred to as the ‘cycle of violence’ has been identified in many marriages. It is controlled by the perpetrator while the victim feels confused and helpless. The cycle repeats itself with a tendency for the violence to increase in severity (see FIG. 120.1).

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Honeymoon phase denial togetherness clinging intimacy Wooing phase denial gifts and promises retribution

Remorse phase guilt denial justification

Table 120.1

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Management strategy for domestic violence

Treat the physical injury and suspect domestic violence Tension build-up phase

↓ Establish the diagnosis ↓

EXPLOSION Violence/ abuse self-righteous anger

Initiate crisis intervention: • organise admission to a refuge • ensure informed consent for all actions • consider notifying police ↓ Establish an empathic, trusting relationship ↓ Build the victim’s coping skills and self-esteem

FIGURE 120.1 The cycle of IPV

↓

Management

Make effective use of community resources: • support services • women’s support group • domestic violence resource centre (in each capital city) • social services/police • social workers • private counsellors and psychologists

The key to successful management is initial recognition of the problem and establishment of empathic caring and support for the victim and family. Do not try to fit the victims into the disease model. It must be emphasised that the perpetrators (as in most criminal activity) do not readily change their behavioural pattern and thus there is minimal prospect of the violence decreasing unless there is a dramatic reason to change. As with an alcohol problem, the person has to admit that he has a problem before effective counselling can begin. A management strategy is presented in TABLE  120.1. The safety of women and children is always the prime working rule.

Useful strategies Do believe her. • Talk openly and explicitly about it. • Express concern for her safety. • Give information (i.e. about the course of action available to her, contacts for legal advice). • Respect her right to make her own decisions.

Harmful strategies Don’t: • deny domestic violence • minimise the importance of domestic violence • blame the victim

• treat with tranquillisers • refer to a psychiatrist • refer to marriage guidance if the husband isn’t interested, but refer to specialist counsellors • set explicit criteria/rules (takes away her power yet again) It is uncommon to get the cooperation of the perpetrator in the management process. If they do seek help they require counselling by a skilled and experienced practitioner, as treatment will be prolonged and complex. If an abusive incident develops or is imminent, the victim should have safety planning. One such plan is: • Be aware of all exit routes and safety areas • Have a plan that includes: — calling emergency services (000 or other) — safely exiting the house — seeking help — accessing a safety refuge • Ask neighbours to call police of the hear any disturbance8 As a general rule the most effective intervention in arresting the violence is to arrest the violent person.3

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Sexual assault Medical practitioners dealing with the difficult and distressing problem of alleged sexual assault should be trained in the subject and familiar with the laws applicable to sexual assault in their own state. Sexual assault is defined broadly as any unwanted sexual contact that occurs without a person’s consent. The sexual act can range from touching to the penetration of an orifice. Rape involves considerable violence and physical injury in 5–10% of cases,9 in which the victims fear for their lives. Apart from the inevitable psychological consequences, particularly acute stress disorder and PTSD, the possibility of pregnancy (overall rate is 5% per assault)9,10 or acquired STI should be considered. The inexperienced practitioner should refer the patient to the nearest available resource but continue a caring involvement as the patient’s GP.  Survivors of sexual assault should be allowed to accept or decline various treatment options offered by the practitioner.

Management of the victim8,10

120

What you should do for the patients first is to offer and provide privacy, safety, confidentiality and emotional support. Believe them, listen to them and be non-judgmental. Five important things to say initially to any victim: • • • • •

You are safe now. I am sorry this happened to you. This is a crime—it was not your fault. It’s good that you are seeing me. I will do what I can to help you

Initial advice to the victim If victim reporting to police: 1 Notify the police at once. 2 Take along a witness to the alleged assault (if there was a witness). 3 Do not wash or tidy yourself or change your clothing. 4 Do not take any alcohol or drugs. 5 Don’t drink or wash out your mouth if there was oral assault. 6 Take a change of warm clothing. If not reporting to police or unsure, contact any of the following: 1 a friend or other responsible person 2 Lifeline or Lifelink or a similar service

3 sexual assault referral/resource/forensic centre 4 a doctor 5 a counselling service Obtaining information—examining doctor 1 Obtain consent from the patient to record and release information. 2 Take a careful history and copious relevant notes. 3 Keep a record, have a protocol. 4 Obtain a kit for examination. 5 Have someone present during the examination (especially in the case of male doctors examining women). 6 Air-dry swabs (media destroy spermatozoa). 7 Hand specimens to police immediately.

Examination If possible the patient should be clothed when seen. Have the patient undress while standing on a white sheet to collect debris, and note any injuries as each  item is removed. Each part of the body should be examined, under good illumination, and all injuries measured and recorded carefully on a diagram. Injuries should be photographed professionally. Examine the body and genital area with a Wood’s light to identify semen, which fluoresces. Perform a careful speculum examination. Palpate the scalp for hidden trauma. Collect appropriate swabs. Making reports Remember that as a doctor you are impartial. Never make inappropriate judgments to authorities (e.g. ‘This patient was raped’ or ‘Incest was committed’). Rather say: ‘There is evidence (or no evidence) to support penetration of the vagina/anus’ or ‘There is evidence of trauma to _______________.’ Post-examination After the medical examination a discussion of medical problems should take place with the patient. This should be done in private and kept totally confidential. A management plan for physical injuries and emotional problems is discussed. Consider the possibility of STI and possible referral. Consider also the possibility of pregnancy and the need for postcoital hormone tablets. Organise follow-up counselling and STI screening.

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Intimate partner violence and sexual assault

Table 120.2

STI prophylaxis (consider)11

Chlamydia

— 1 g azithromycin (o)

Gonorrhoea

— ceftriaxone 500 mg IM if high risk or azithromycin 1 g (o)

Hepatitis B

— Hepatitis B vaccine (dose 1) — immune globulin IM (if high risk)

Syphilis

— benzathine penicillin 1.8 g IM

Trichomonas

— metronidazole 1 g (o)

HIV

— consult appropriate physician

Management issues • Take swabs and/or first-void specimen for testing gonococcus and chlamydia (PCR). • Take blood for HIV, syphilis, hepatitis B. • Collect specimens—swab, aspirate of any fluid and keep for DNA analysis. • Give prophylactic antibiotics (see TABLE 120.2)— depends on type of assault and assailant. • Emergency contraception. • Review in 3 weeks—check tests. • Screen for HBV, HCV, syphilis and HIV in about 3 months. • Refer to Rape Crisis centre.

Drug-assisted sexual assault Consider this when patient has no memory of events and time or other suspicious circumstances. Urine or blood testing may be appropriate.

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References 1 Kerr A. Domestic violence. Treat it seriously. Aust Fam Physician, 1989; 18: 1362–9. 2 Hazelwood R, Warren J, Dietz P. Compliant victims of the sexual sadist. Aust Fam Physician, 1993; 22: 474–9. 3 Hegarty K. Domestic violence: how to treat. Australian Doctor, 20 February 2009: 29–36. 4 Knowlden S, Helman T. How to treat domestic violence. Australian Doctor, 21 April 1989: I–VIII. 5 Stark E et al. Wife Abusing in the Medical Setting—an Introduction for Health Personnel. Rockville, MA: National Clearing House for Domestic Violence, 1981: 7. 6 Western Australian Domestic Violence Task Force. Break the Silence. Report to the Western Australian Government. Perth: Government Printer, 1986: 26–35, 162–3. 7 Rodriguez MA et al. The factors associated with disclosure of intimate partner abuse to clinicians. J Fam Pract, 2001; 50 (4): 338–44. 8 Boyle J, Buist A et al. Women’s Health. Melbourne RACGP: Check Unit 509, September 2014. 9 Papadakis MA, McPhee SJ. Current Medical Diagnosis and Treatment (49th edn). New York: The McGraw-Hill Companies, 2013: 777–8. 10 Parekh V, McCoy R. Adult sexual assault: how to treat. Australian Doctor, 25 May 2007: 33–40. 11 Mein JK, Palmer CM, Shand M et al. Management of acute adult sexual assault. Med J Aust, 2003; 178: 226–30.

Resources Hindmarsh E, Roberts G (eds). RACGP Manual: Abuse & Violence, Working with Our Patients in General Practice (The White Book) (PDFIMB). Victorian Government Department of Justice. What is Interpersonal Abuse and Violence?: Guidelines for Primary Care Physicians, 2006

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121 A diagnostic and management approach to skin problems The skilful doctor knows by observation, the mediocre doctor by interrogation, the ordinary doctor by palpation. Chang Chung-ching (c. AD –) The diagnosis of skin problems depends on astute clinical skills based on a systematic history and examination and, of course, experience. If the diagnosis is in doubt, it is appropriate to refer the patient to a skilled cooperative consultant, as the referral process is an excellent educational opportunity for the GP. Another opinion from a colleague/s in a group practice is also very educative. At least, cross-referencing the skin lesion with a colour atlas facilitates the learning process.

Terminology of skin lesions Primary lesions • Macule. Circumscribed area of altered skin colour (Latin for stain) without elevation 1 cm diameter (see FIG. 121.1). • Papule. Palpable mass on skin surface 0.5 cm diameter (see FIG. 121.2). • Plaque. A flat-topped palpable mass >1 cm diameter. • Wheal. An area of dermal oedema (can be any size), which is pale and compressible. • Angio-oedema. A diffuse area of oedema extending into subcutaneous tissue. • Vesicle. A fluid-filled blister 0.5 cm diameter (see FIG. 121.3). • Pustule. A visible collection of pus in the skin 1 cm diameter. • Furuncle. A purulent infected hair follicle; includes: — folliculitis (small furuncles) — boils (larger furuncles) • Carbuncle. A cluster of boils discharging through several openings.

• Purpura. Bleeding into the skin (dermis) appearing as multiple haemorrhages. May be macular or papular. • Petechiae. Purpuric lesions 2 mm or less in diameter. • Ecchymosis. Larger purpuric lesion. • Haematoma. A swelling from gross bleeding. • Telangiectasia. Visible dilatation of small cutaneous blood vessels. • Comedo. A plug of keratin and sebum in a dilated pilosebaceous gland. • ‘Blackhead’. An open comedo. • ‘Whitehead’. A closed comedo. • Erythema. Redness of the skin due to increased vascularity. • Milium. Tiny white cyst containing keratin, from occlusion of pilosebaceous gland. • Papilloma. Warty projection above the skin surface.

Secondary lesions • Scales. An accumulation of excess keratin that presents as flaking. • Crusts (scabs). Superficial dried secretions (serum and exudate). macule

patch

epidermis

dermis

FIGURE 121.1 Macule and patch papule

nodule

FIGURE 121.2 Papule and nodule

epidermis

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A diagnostic and management approach to skin problems vesicle

ulcer

bulla

erosion

FIGURE 121.4 Ulcer, erosion and fissure

• Ulcer. A circumscribed deep defect with loss of all the epidermis and part or all of the dermis (see FIG. 121.4); they usually heal with scarring. • Erosion. A skin defect with complete or partial loss of the epidermis; they heal without scarring (see FIG. 121.4). • Fissure. A linear split in the epidermis and dermis (see FIG. 121.4). • Atrophy. Thinning or loss of epidermis and/or dermis with loss of normal skin markings. • Sclerosis. Thickening of the dermis with induration of subcutaneous tissue; resembles a scar but may arise spontaneously (e.g. scleroderma). • Scar. A healed dermal lesion where normal structures are replaced by fibrous tissue. • Hypertrophic scar. Rises above the skin surface. • Atrophic scar. Settles below the skin surface. • Keloid. Overgrowth of dense fibrous tissue extending beyond the original wound. • Excoriation. Scratch marks causing an erosion or an ulcer (loss of epidermis). • Acanthosis. Thickening of skin without accentuation of skin markings. • Lichenification. Thickening secondary to chronic scratching or rubbing (in dermatitis). • Callus. Localised hypertrophy of the stratum corneum. • Exfoliation. Loss of epidermal keratin as large scales or sheets. • Keratoderma. Thickening of skin especially stratum corneum.

presentation of a common condition and probably merits a consultant’s opinion. Note: TABLES  121.1 to 121.6 were prepared by Professor Robin Marks1 and are reproduced with his permission.

1

The diagnostic approach of Robin Marks presented here helps to achieve order in the midst of confusion. He describes the importance of simplifying the diagnostic process by being a ‘lumper’ rather than a ‘splitter’. Most common dermatological problems fall into one of seven categories (see TABLE  121.1). A problem that does not fit into one of these seven groups is either an unusual condition or an unusual

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fissure

FIGURE 121.3 Vesicle and bulla

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Defining terms Terms that are continually referred to in skin disease include the following: Seborrhoeic Yellow-brown and waxy Nummular Coin-like (interchangeable) Discoid Disc-like Annular Ring-like Circinate Circular Arcuate Curved Reticulate Net-like Pityriasis (pityron = bran) Fine, bran-like scaly desquamation or powdery Guttate ‘Dew drop’ Rosea Rose-coloured Morbilliform Like measles Morphoea Circumscribed scleroderma or skin infiltrate Livido Cyanotic discolouration Lichen Any papular skin disorder resembling lichens Verrucous Rough and warty

}

History The three basic questions are:1 1 Where is the rash and where did it start? 2 How long have you had the rash? Note: The split into three time zone groups (see is very useful. This question leads on to the next question regarding itch, as the patient is unlikely to tolerate an itchy eruption.

TABLE  121.2)

3 Is the rash itchy? If so, is it mild, moderate or severe? The nature of the itch is very helpful diagnostically. A severe itch is one that wakes the patient at night and leads to marked excoriation of the skin, while

121

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Table 121.1

• Problems of the skin

Common dermatological conditions

Infections

Table 121.2

How long has the rash been present?

Acute (hours–days)

Urticaria Atopic dermatitis Allergic contact dermatitis Insect bites Drugs Herpes simplex/zoster Viral exanthemata

Acute → chronic (days–weeks)

Atopic dermatitis Impetigo Scabies Pediculosis Drugs Pityriasis rosea Psoriasis Tinea Candida

Chronic (weeks–months)

Psoriasis Atopic dermatitis Tinea Pityriasis versicolor Warts Cancers Skin infiltrations (such as granulomata, xanthomata)

Bacterial: • impetigo Viral: • warts • herpes simplex, herpes zoster • pityriasis rosea • exanthemata Fungal: • tinea • candidiasis • pityriasis versicolor Acne Psoriasis Atopic dermatitis (eczema) Urticaria Acute and chronic Papular: • pediculosis • scabies • insect bites Sun-related skin cancer Drug-related eruptions

Table 121.3

121

a mild itch is one that is only slightly upsetting for the patient and may not be noticeable for significant periods during the day. Three questions the doctor must consider 1 Could this be a drug rash? 2 Has this rash been modified by treatment? 3 Do any contacts have a similar rash?

Very

Urticaria Atopic dermatitis Scabies, pediculosis Insect bites Chickenpox (adults) Dermatitis herpetiformis Grover disease

Mild to moderate

Tinea Psoriasis Drugs Pityriasis rosea Candida Stress itching/lichen simplex

Often not

Warts, tinea Impetigo, psoriasis Cancers Viral exanthemata Seborrhoeic dermatitis

Further questions for the patient • Do you have contact with a person with a similar eruption? • What medicines are you taking or have you taken recently? • Have you worn any new clothing recently? • Have you been exposed to anything different recently? • Do you have a past history of a similar rash or eczema or an allergic tendency (e.g. asthma)? • Is there a family history of skin problems?

The nature of itching1 The characteristics of the itch are very useful in dividing up the diagnoses: an eruption that is not

Is the rash itchy?

itchy is unlikely to be scabies and one that is very itchy is unlikely to be a skin tumour (see TABLE 121.3). However, nothing is absolute and variations to the rule will occur—tinea, psoriasis and pityriasis versicolor are sometimes itchy and sometimes not.

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A diagnostic and management approach to skin problems Chickenpox can vary from being intensely itchy, especially in adults, to virtually no itching. Relieving or aggravating factors of the itch provide useful diagnostic guidelines; for example, Whitfield’s ointment applied to an itchy eruption for a provisional diagnosis of ringworm would make the itch worse if it were due to eczema.

Examination1 Examine the skin in good light, preferably natural light, and ensure that any make-up is removed. There are two basic stages in the physical examination of a rash. The first is an assessment of the characteristics of the individual lesion and the second is the distribution or pattern of the lesions. Characteristics of the individual lesion The single most important discriminating feature is whether it involves the dermis alone or the epidermis as well (see TABLE  121.4). If the lesion involves the epidermis there will be scaling, crusting, weeping, vesiculation or a combination of these (see FIG.  121.5). If the dermis alone is involved, the lesion is by definition a lump, a papule or a nodule (see FIG. 121.6). No lesion ever involves the epidermis without involving the dermis as well. Other characteristics of individual lesions that must be sought are the colour, the shape and the size. It is important to feel the skin during the physical examination and to note the consistency of the lesion. Is it firm or soft? The activity of the lesion may also be useful: does it have a clearing centre and an active edge? Distribution of the lesions The clinician must decide whether the lesions are localised or widespread. If they are widespread, are Table 121.4 Epidermal

Dermal

Urticaria Insect bites, pediculosis, scabies Drugs Skin infiltrations Viral exanthemata

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they distributed centrally, peripherally, or both? (See TABLE  121.5.) Diagnosis is often helped when the skin lesions are in a specific area (see TABLE 121.6 and FIGS  121.7 and 121.8). Itchy papules on the penis associated with a widespread pruritus are likely to be scabies. However, care has to be taken because many misdiagnoses are made instinctively on the distribution (e.g. anything in the flexures is dermatitis or anything on the feet is tinea).

epidermis affected with scaling, crusting and weeping

dermis

subcutaneous fat

FIGURE 121.5 Epidermal skin lesion

FIGURE 121.6 Dermal skin lesion

Table 121.5

Distribution of the rash

Widespread

Atopic dermatitis Psoriasis Scabies Drugs Urticaria

Central trunk (initially at least)

Pityriasis versicolor Herpes zoster Seborrhoeic dermatitis Guttate psoriasis Pityriasis rosea Viral exanthemata

Peripheral

Atopic dermatitis Herpes zoster Tinea Psoriasis Warts Insect bites

Appearance of individual lesions Atopic dermatitis Psoriasis Tinea Pityriasis rosea Impetigo, herpes, warts Cancers Scabies Solar keratoses

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Table 121.6

• Problems of the skin

Specific areas affected

Face

Rosacea Impetigo Atopic dermatitis Psoriasis Photosensitive (e.g. drugs) Herpes simplex Acne vulgaris Cancers Viral exanthemata

Scalp

Psoriasis Seborrhoeic dermatitis Pediculosis Tinea Folliculitis Chickenpox

Flexures

Mouth

Atopic dermatitis Psoriasis Seborrhoeic dermatitis Tinea Candida Pediculosis Aphthous ulcers Herpes simplex Candida Measles

Nails

Psoriasis Tinea Dermatitis

Penis

Scabies Genital herpes and warts Candida Psoriasis

121

Another feature of an eruption, which should be sought on examination, is whether the lesions are all at the same stage of evolution. It is necessary to perform a complete physical examination as well. There is, after all, no such thing as a skin disease but rather disease affecting the skin. The clinician must always bear this in mind when managing patients complaining of a skin eruption. Disease does not affect the skin in isolation and it is unforgivable to look only at the skin and ignore the patient as a whole. Note: In every case examine the mouth, scalp, nails, hands and feet.

• a ‘Maggylamp’, which is a hand-held fluorescent light with an incorporated magnifier; the device allows shadow-free lighting and magnification • a dermatoscope, which is very valuable in the diagnosis of pigmented tumours but it does require skill and familiarity to achieve effective use • Wood’s light • swabs for culture and NAAT test (PCR) • skin biopsy (even with psoriasis, etc.)

Office tests and diagnostic aids Wood’s light Wood’s light examination is an important diagnostic aid for skin problems in general practice. It has other uses, such as examination of the eye after fluorescein staining. (A low-cost, small ultraviolet light unit called ‘the black light’ is also available.)

Method Simply hold the ultraviolet light unit above the area for investigation in a dark room. Limitations of Wood’s light in diagnosis Not all cases of tinea capitis fluoresce because some species that cause the condition do not produce porphyrins as a by-product. See TABLE 121.7 for a list of the skin conditions that do fluoresce. Wood’s light is really only useful for hair-bearing areas. Porphyrins wash off with soap and water, and a negative result may occur in a patient who has shampooed the hair within 20 hours of presentation. Consequently, a negative Wood’s light reading may be misleading. The appropriate way of confirming the clinical diagnosis is to send specimens of hair and skin for microscopy and culture.

Skin scrapings for dermatophyte diagnosis Skin scrapings are an excellent adjunct to diagnosis of fungal infections. Requirements are a scalpel blade, glass slide and cover slip, 20% potassium hydroxide Table 121.7

Skin conditions that produce fluorescence in Wood’s light

Diagnostic tools

Tinea capitis

Appropriate diagnostic tools include:

Erythrasma

Coral pink

Pityriasis versicolor

Pink–gold

• a magnifying lens • a diascope, which is a glass slide or clear plastic spoon that is used to blanch vascular lesions in order to determine their true colour

Green/bright yellow (in hairs)

Pseudomonas spp.

Yellowish-green

Porphyria cutanea tarda

Red (urine)

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Scalp: tinea capitis psoriasis seborrhoeic dermatitis pediculosis

Eyelids: seborrhoeic dermatitis/blepharitis atopic dermatitis xanthelasma allergic contact dermatitis psoriasis

Ears: seborrhoeic dermatitis allergic contact dermatitis solar keratosis

Face: cancers acne rosacea systemic lupus erythematosus atopic dermatitis pityriasis alba impetigo keratoacanthoma solar keratoses seborrhoeic dermatitis leprosy (Hansen disease)

Nasolabial folds: perioral dermatitis seborrhoeic dermatitis Folliculitis: sycosis barbae (S. aureus) tinea barbae Chin: perioral dermatitis seborrhoeic dermatitis rosacea

Lips: herpes simplex Candida chelitis leucoplakia

FIGURE 121.7 Typical sites on the face affected by the skin conditions indicated

Cubital fossa: atopic dermatitis Hands: occupational dermatoses granuloma annularae dyshydrosis contact dermatitis tinea manuum secondary syphilis

Chest seborrhoeic dermatitis acne pityriasis versicolor Grover disease drug exanthem tinea

Knees (dorsum): psoriasis dermatitis herpetiformis Legs: keratitis pilaris dermatofibroma erythema nodosum necrobiosis lipoidica nummular dermatitis stress dermatitis Dorsum of foot: granuloma annularae lichen simplex chronicus contact dermatitis atopic dermatitis

Axillae: hidradenitis erythrasma contact dermatitis seborrhoeic dermatitis tinea psoriasis Nails: tinea candidiasis psoriasis

Groin: tinea cruris candidiasis erythrasma seborrhoeic dermatitis contact dermatitis

Toes: tinea pedis contact dermatitis erythrasma candidiasis

FIGURE 121.8 Typical regional location of various skin conditions *Same conditions apply to chest and trunk

Trunk pityriasis versicolor pityriasis rosea guttate psoriasis drug exanthem scabies

Elbows (dorsum): psoriasis dermatitis herpetiformis Wrists: contact dermatitis (bands) lichen planus solar keratoses

Perianal: psoriasis seborrhoeic dermatitis warts Candida albicans Popliteal fossa: atopic dermatitis Soles of feet: plantar warts tinea hyperhidrosis pitted keratolysis callus corn pustular psoriasis secondary syphilis hand, foot and mouth disease juvenile plantar dermatosis

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(preferably in dimethyl sulphoxide) and a microscope. Skin scrapings can also be sent for microscopy and culture. Clinical indications:

Patch testing

1 tinea (superficial dermatophyte infection) 2 pityriasis versicolor 3 Candida

Biopsies

Method

Hair2

• Scrape skin from the active edge. • Scoop the scrapings onto the glass microscope slide. • Cover the sample with a drop of potassium hydroxide. • Cover this with a cover slip and press down gently. • Warm the slide and wait at least 5 minutes for ‘clearing’. Microscopic examination • Examine at first under low power with reduced light. • When fungal hyphae are located, change to high power. • Use the fine focus to highlight the hyphae (see FIG. 121.9). Note: Some practice is necessary to recognise hyphae.

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Other uses of microscopy Detection of the scabies mite: the burrow of the scabies mite is found (can be difficult!) and the epidermis is decisively scraped with a no. 15 scalpel blade, and transferred to a slide after adding a drop of liquid paraffin. The mite is very distinctive. epidermal cells

fungal hyphae

FIGURE 121.9 Diagrammatic representation of microscopic appearance of fungal hyphae

Patch testing is used to determine allergens in allergic contact dermatitis. Read in 48 hours.

Shave or punch biopsies can be useful (see FIGS 126.26 and 126.27 in CHAPTER 126).

Send hair samples for microscopy and root analysis. There are two main tests: 1 the hair pull test (refer CHAPTER 128) 2 the hair pluck test In the hair pluck test (used for tinea capitis and hair shaft disorder), a tuft of about 20 hairs is drawn out, forceps applied close to the skin of the scalp and rotated slightly prior to sharp extraction. The hair should be collected on a glass slide for counting and analysis.

Traditional chemicals used in extemporaneous preparations3 • Salicylic acid: produces painless destruction of epithelium, thereby facilitating absorption. Consider its use for psoriasis, neurodermatitis, tinea of palms and feet, seborrhoeic dermatitis. • Resorcinol: a topical keratolytic with bactericidal and fungicidal properties. Consider its use for psoriasis, acne, rosacea, seborrhoeic dermatitis. • Coal tar: the two commonly found tar preparations—crude tar and solution: liquor picis carbonis (LPC)—are used for their antiinflammatory, soothing and antimitotic properties. Consider their use for psoriasis, atopic dermatitis, seborrhoeic dermatitis and neurodermatitis. • Menthol and phenol: added to various preparations for their soothing and cooling effects. Consider for use in pruritic problems such as varicella, urticaria and atopic dermatitis. • Sulphur: of benefit in dermatoses, due mainly to its keratolytic properties. The other actions of sulphur are scabicidal, parasiticidal and fungicidal. Consider its use for acne, rosacea, seborrhoeic dermatitis, psoriasis and tinea. • Dithranol: reduces the mitotic activity of a hyperplastic epidermis. Good for thick plaque psoriasis. • Calamine: a mild astringent and antipruritic used as a soothing and protective agent in

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A diagnostic and management approach to skin problems various ‘vehicles’ (bases). It is zinc carbonate or zinc oxide powder mixed with a small amount of iron oxide. Has drying properties so avoid recommending calamine-based preparations for dry skin conditions. • Zinc oxide: a mild astringent used in many preparations and combined with other ingredients. Used for soothing and protective functions.

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• For Candida infection (e.g. complicating seborrhoeic napkin dermatitis), mix 1% hydrocortisone in equal quantities with an antifungal preparation such as nystatin. • Use the weakest strength for chronic dermatoses but treat severe acute dermatoses aggressively. • Steroids not needed if no inflammation present.

Common natural topical preparations4 • Aloe vera: the extract from aloe vera appears to have antiseptic, anaesthetic, anti-inflammatory, antipruritic and moisturising properties. It is used in a variety of products and promotes wound healing including those with mild burns. • Pawpaw: papain extracted from the pawpaw plant is used as a moisturiser and antipruritic. It is used to treat discomfort and itching from bites and stings, minor burns and postsurgical wounds. • Teatree oil: the oil from tea tree (Melaleuca alternifolia) has astringent and mild antibacterial and antifungal properties. It is commonly used as an antiseptic and for prevention of infection in areas prone to folliculitis and tinea (e.g. tinea pedis). • Honey: especially manuka or ‘jelly bush’ unprocessed honey has been used as a non-antibiotic and protective treatment for chronic wound infections and wounds generally. Its properties include antioxidation, absorbance, hygroscopic, hypertonicity, anti-inflammatory and antibacterial. However the scientific evidence to support its use is not convincing and it should be used with care. • Colloidal oatmeal • Wheat grass

Selection of corticosteroid preparations • Class I and class II preparations are appropriate for most problems. • Creams or lotions are used for ‘weeping’ lesions, the face, flexures and hair-bearing areas. • Use ointments for dry and scaly skin. • Use ointments and occlusive vehicles for dry and chronic skin surfaces. • Ointments should not be used on weeping surfaces. • Stubborn dermatoses such as psoriasis respond better to preparations under occlusion, such as plastic wrap applied overnight with appropriate securing in place. • Use a gel or lotion for the scalp.

Terminology of topical skin preparations See also TABLE 121.8. Antipruritic agent One that relieves itching. Examples are: • menthol (0.25%) • phenol (0.5%) • coal tar solution (2–10%) • camphor (1 or 2%) Astringent A topical agent that has styptic or binding properties with an ability to stop secretions from skin or tissues. An example is aluminium acetate solution (Burow’s solution); the aluminium acetate acts as a protein precipitator and is a very effective soothing agent and antipruritic. Base or vehicle A mixture of powders, water and greases (usually obtained from petroleum). The relative blending of these compounds determines the nature of the base (e.g. lotion, cream, ointment, gel or paste). Cream A suspension of a powder in an emulsion of oil and water with the addition of an emulsifying agent. Usually applied to normal or moist skin. Emollient A topical preparation of emulsified oils and fatty acids that is softening or soothing to the skin. It replaces natural oils in the stratum corneum. It also acts as a skin moisturiser and is therefore used on dry skin or dermatoses related to dry skin (e.g. atopic dermatitis). Examples are: • mineral or vegetable oil (e.g. peanut oil 5% cream) • sorbolene cream • aqueous cream Emulsion A mixture of two immiscible liquids, one being dispersed throughout the other in small droplets. Gel A viscous substance with a greaseless, watermiscible base. Humectant A chemical-containing agent that attracts and retains water due to its hygroscopic or osmotic properties. Examples are: • urea 10% cream • glycerol 10% cream continued

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continued Keratolytic An agent that softens or breaks up keratin. Examples are: • urea 10%—for xerosis or keratosis pilaris • urea 20%—cracked palms and soles • salicylic acid 2–10% • benzoic acid alpha-hydroxy acids (e.g. lactic acid, propylene glycol) Lotion A suspension of an insoluble powder in water. Modern lotions use an emulsifying agent, which eliminates the need to shake the lotion. An example is calamine lotion (zinc oxide 5, calamine 15, glycerine 5, water to 100). Moisturiser An agent that increases the water content of the stratum corneum and reduces itching. Classified as: • emollient • humectant, and • occlusive (e.g. white soft paraffin: Vaseline) Ointment A suspension of a substance in an oily vehicle. Generally used for dry skin. Paint and tincture A rapidly drying liquid preparation that is very useful for intertriginous areas, especially between the toes and natal cleft. ‘Tincture’ is the preparation when alcohol is the vehicle. Example: podophyllin in tinct. benz. co. (for genital warts). Paste Similar to ointment in composition but is more viscid. A paste consists of an ointment to which another agent, such as starch, has been added. They dry and protect.

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Table 121.8

Guidelines for choosing a topical vehicle

Disorder

Topical vehicle

Acute inflammation: • erythema, weeping

Wet dressing Solution, lotions

Subacute inflammation: • erythema, scaling

Creams Gels (for hairy areas)

Chronic inflammation: • scaling, dryness, thickening

Ointments Impregnated tapes

Topical corticosteroids for chronic dermatoses Guidelines for long-term use (examples):4 • face—hydrocortisone 1% • flexures—hydrocortisone 1% • trunk —betamethasone valerate 0.2% — triamcinolone acetonide 0.02% • elbows/knees—betamethasone dipropionate 0.05% • palms/soles—methylprednisolone aceponate 0.1%

Cautions • Avoid high-potency preparations on the face, in flexures and on infants. • Corticosteroids can mask or prolong an infection. • Long-term use can cause striae and skin atrophy, peri-oral dermatitis, ‘steroid acne’ and rosacea. • Excessive use of more potent preparations can cause adrenal suppression; predispositions include use >2 weeks, and use on thinner skin such as face, genitalia and intertriginous areas. • Avoid sudden cessation: alternate with an emollient or a milder preparation. The relative clinical potency of topical corticosteroids is given in TABLE 121.9.

Skin tips • Do no harm. Introduce the mildest possible preparation to alleviate the problem. • Creams tend to be drying, lotions even more so. • Ointments tend to reduce dryness and have greater skin penetration. If wet—use a wet dressing (wet soaks and a lotion). If dry—use an ointment (salve). • Occlusive dressings with plastic wraps permit more rapid resolution of stubborn dermatoses. • Most toilet soaps are alkaline and are very drying; they should not be used on dry skin or dermatitis with dry skin. Soap substitutes include neutral soaps (Dove, Neutrogena), superfatted soaps (Oilatum) and non-soap cleanser (Cetaphil). • Soaps should be used only in the axillae and groin and on the feet of people with dry and irritated skin. • Bath additives can be useful for dermatoses such as psoriasis, atopic dermatitis and for pruritus. For some people it may be better not to add it to the bath (diluting effect; accident from slipping) but to massage the oil into the dry itchy skin after the bath. • Always give careful instructions to the patient regarding application of preparations: use a prepared handout if available. • Alter the treatment according to the response. • Explain the costs involved, especially where a preparation is expensive. • Avoid combination creams unless clear evidence of secondary infection proven by culture and sensitivity.

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Table 121.9

Potency ranking of the most commonly used topical corticosteroid preparations in Australia and New Zealand6

Generic name Group I Mild Hydrocortisone Hydrocortisone Hydrocortisone Hydrocortisone

Formulation 0.5% acetate 0.5% 1% acetate 1%

Group II Moderately potent Betamethasone valerate 0.02% Betamethasone valerate 0.05% Clobetasone butyrate 0.05%* Desonide 0.05% Triamcinolone acetonide 0.02% Triamcinolone acetonide 0.05% Group III Potent Betamethasone valerate 0.1% Betamethasone dipropionate 0.05% Methylprednisolone aceponate 0.1% Mometasone furoate 0.1% Triamcinolone acetonide 0.1% Group IV Very potent Betamethasone dipropionate 0.05% (enhanced) Clobetasol propionate 0.05%* Preparations containing other agents Triamcinolone acetonide 0.01% + neomycin, gramicidin, nystatin Betamethasone valerate 0.1% + gentamicin Hydrocortisone 1% + clioquinol 1% Hydrocortisone 1% + clioquinol 3% Hydrocortisone 1% + clotrimazole

4.5%

4.5%

18%

18% 4.5%

4.5%

Cream Cream Cream Cream, ointment

1299

4.5%

4.5%

1% 9%

Cream, Cream, gel Cream, Lotion Cream, Cream,

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9%

9%

9%

ointment ointment, ointment ointment ointment

Cream, ointment, scalp lotion Cream, ointment, lotion Cream, ointment Cream, ointment, lotion Cream, ointment Cream, ointment Cream, ointment, scalp application Cream, ointment Cream, ointment Cream Cream Cream

*Not available in Australia.

Rules for prescribing creams and ointments How much?5 On average, 30 g of cream will cover the body surface area of an adult. Ointments, despite being of thicker consistency, do not penetrate into the deeper skin layers so readily, and the requirements are slightly less. Pastes are applied thickly, and the requirements are at least 3–4 times as great as for creams.

Anterior

Posterior

FIGURE 121.10 ‘Rule of nines’ for body surface area

The ‘rule of nines’, used routinely to determine the percentage of body surface area affected by burns (see FIG. 121.10), may also be used to calculate the amount of a topical preparation that needs to be prescribed. For example: • if 9% of the body surface area is affected by eczema, approximately 3 g of cream is required to cover it • 9 g of cream is used per day if prescribed three times daily • a 50 g tube will last 5–6 days One gram of cream will cover an area approximately 10 cm  ×  10 cm (4 square inches), and this formula may be used for smaller lesions. TABLE  121.10 provides guidelines for approximate weekly quantities of skin preparations required to cover specific areas of the body. Some general rules Remember: • • • •

to use cream or lotions for acute rashes to use ointments for chronic scaling rashes that a thin smear only is necessary that 30 g — will cover the adult body once — will cover hands twice daily for 2 weeks — will cover a patchy rash twice daily for 1 week • that 200 g will cover a quite severe rash twice daily for 2 weeks

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Table 121.10

• Problems of the skin

Suitable quantities of skin preparations for specific body areas7 (twice daily application for 1 week) Creams and ointments

Face and neck Both hands Scalp Both arms Both legs Trunk Groin and genitalia

Corticosteroids

Others

Lotions

15–30 15–30 15–30 30–60 100 g 100 g 15–30

15–30 g 25–50 g 50–100 g 100 g 100–200 g 400 g 15–25 g

100 200 200 200 200 500 100

g g g g

g

References 1 Marks R. A diagnosis in dermatology. Aust Fam Physician, 2001; 30 (11): 1028–32. 2 Marks R, Sinclair R. A Guide to the Performance of Diagnostic Procedures used in the Management of Common Skin Diseases. Melbourne: Skin & Cancer Foundation Publication, 2002: 25–6. 3 Kelly B. Extemporaneous preparations. Aust Fam Physician, 1993; 22: 842–4.

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mL mL mL mL mL mL mL

4 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 3). Melbourne: Therapeutic Guidelines Ltd, 2009: 7–43. 5 Gambrill J. How much cream? Aust Fam Physician, 1982; 11: 350. 6 Buckley N (Chair) Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013: 346. 7 George CF et al. London: British National Formulary, Number 31, 1996; 451–6.

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Pruritus

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It is easy to stand a pain, but difficult to stand an itch. Chang Ch’ao  Pruritus (the Latin word for itch) is defined simply as the desire to scratch. It is one of the most important dermatological symptoms and is usually a symptom of primary skin disease with a visible rash. However, it is a subjective symptom and diagnostic difficulties arise when pruritus is the presenting symptom of a systemic disease with or without a rash—‘pruritus sine materia’. An associated rash may also be a manifestation of the underlying disease. The broad differential diagnoses of pruritus are: • skin disease • systemic disease • psychological and emotional disorders

Physiology1

Table 122.1

Primary skin disorders causing significant pruritus

Atopic dermatitis (eczema) Urticaria Dermatitis herpetiformis Grover disease Scabies Pediculosis Asteatosis (dry skin) Lichen planus Chickenpox Contact dermatitis

Itch arises from the same nerve pathway as pain, but pain and itch are distinct sensations. The difference is in the intensity of the stimulus. Unrelieved chronic itch, like unrelieved pain, can be intolerable and cause suicide. There are many similarities: both are abolished by analgesia and anaesthesia; subdued by counterirritation, cold, heat and vibration; and referred itch occurs just like referred pain. Antihistamines that act on the H1 receptor are often ineffective, suggesting that histamine is not the only mediator of itch.1

Insect bites

Localised pruritus

Generalised pruritus3

Pruritus may be either localised or generalised. Localised itching is generally caused by common skin conditions such as atopic dermatitis (see TABLE 122.1). Scratch marks are generally presented. Pruritus is a feature of dry skin. An intense, localised itch is suggestive of scabies, also known as ‘the itch’. Itching of the scalp, anal or vulval areas is a common presentation in general practice. A careful examination is necessary to exclude primary skin disease; a detailed history and examination should be undertaken to determine if one of the various systemic diseases is responsible. Notalgia paraesthetica is a common localised itch and/or paraesthesia (possibly also pain) in

Pruritus may be a manifestation of systemic disease. It can accompany pregnancy, especially towards the end of the third trimester (beware of cholestasis), and disappear after childbirth. These women are then prone to pruritus if they take the contraceptive pill.4 Systemic causes are summarised in TABLE  122.2 and a summary of the diagnostic strategy model is given in TABLE 122.3. The history may provide a lead to the diagnosis— the itching of polycythaemia may be triggered by a hot bath which can cause an unusual prickling quality that lasts for about an hour.4 On the other hand, the itching may be caused by a primary irritant such as a ‘bubble bath’ preparation.

the interscapular area. It is considered to be due to pressure on spinal nerves from spinal dysfunction. It is usually relieved by physical therapy to the thoracic spine (see CHAPTER 24).2 Pruritic rashes in children commonly include atopic dermatitis, varicella, urticaria (hives), insect bites and scabies.

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Table 122.2

• Problems of the skin

Systemic conditions that can cause pruritus

Xerosis (dry skin, winter itch)

Pregnancy

HIV/AIDS

Chronic kidney failure

Psychological and emotional causes: • anxiety/depression • psychosis • parasitophobia

Liver disorders: • cholestatic jaundice, for example: — cancer of head of pancreas — primary biliary cirrhosis — drugs: chlorpromazine, antibiotics • hepatic failure Malignancy: • lymphoma: Hodgkin lymphoma • leukaemia, esp. chronic lymphatic leukaemia • multiple myeloma • disseminated carcinoma Haematological disorders: • polycythaemia rubra vera (‘bath itch’) • iron-deficiency anaemia • pernicious anaemia (rare) • macroglobulinaemia Endocrine disorders: • diabetes mellitus • hypothyroidism • hyperthyroidism • carcinoid syndrome • hyperparathyroidism Malabsorption syndrome: • gluten sensitivity (rare) Tropical infection/intestinal parasites: • ascariasis • filariasis • hookworm

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Aquagenic pruritus

Drugs: • alkaloids • aspirin/other NSAIDs • diuretics • ACE inhibitors • opiates • cocaine • antibiotics e.g. penicillin, sulfonamides • quinidine • chloroquine • CNS stimulants

Table 122.3

Generalised pruritus: diagnostic strategy model

Q. Probability diagnosis A. Psychological/emotional3 Old, dry skin (senile pruritus) Atopic dermatitis (eczema) Contact (allergic) dermatitis Varicella (chickenpox) Q. Serious disorders not to be missed A. Neoplasia: • lymphoma/Hodgkin • leukaemia: CLL • other cancer • HIV/AIDS Chronic kidney failure Primary biliary cirrhosis Q. Pitfalls (often missed) A. Pregnancy Tropical infection/infestation/scabies Polycythaemia rubra vera Polyarteritis nodosa Lichen planus Generalised sensitivity (e.g. fibreglass, bubble bath) Q. Seven masquerades checklist A. Depression Diabetes Drugs (several) Anaemia (iron deficiency) Thyroid disorders (hyper and hypo) Spinal dysfunction (notalgia paraesthetica) Q. Is the patient trying to tell me something? A. Quite likely: consider anxiety, parasitophobia.

Senile pruritus Autoimmune disorders: • polyarteritis nodosa • sicca syndromes (e.g. Sjögren syndrome) Polyarteritis nodosa Irritants: • fibreglass • others

Guidelines • The prevalence of itching in Hodgkin lymphoma is about 30%. The skin often looks normal but the patient will claim that the itch is unbearable.4 • Pruritus can be the presenting symptoms of primary biliary cirrhosis and may precede other

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Pruritus symptoms by 1–2 years.3 The itch is usually most marked on the palms and soles. • Pruritus can occur in both hyperthyroidism and hypothyroidism, especially in hypothyroidism where it is associated with the dry skin.

Key history Enquire about nature and distribution of itching. Consider pregnancy, liver disease and malignancy of the lymphatic system, particularly Hodgkin lymphoma. A careful review of any drug history is important. Note any associated general symptoms such as fever.

Key examination • General examination of the skin, abdomen and lymphopoietic systems

Key investigations to consider • • • • • • • • • • • • • •

Urinalysis Pregnancy test FBE ESR/CRP Iron studies Kidney function tests Liver function tests Thyroid function tests Random blood sugar Stool examination (ova and cysts) Chest X-ray Skin biopsy Skin testing Lymph node biopsy (if present) Immunological tests for primary biliary cirrhosis

Treatment

1303

— local soothing lotion such as calamine, including menthol or phenol (avoid topical antihistamines) — pine tar preparations (e.g. Pinetarsol) — crotamiton cream — consider topical corticosteroids • sedative antihistamines (not very effective for systemic pruritus) • non-sedating antihistamines during day • antidepressants or tranquillisers (if psychological cause and counselling ineffective)

PRURITIC SKIN CONDITIONS

Scabies Scabies is a highly infectious skin infestation caused by a tiny mite called Sarcoptes scabiei (see FIG. 122.1). It is common in school-aged children, in closed communities such as nursing homes and in some Indigenous communities. The female mite burrows just beneath the skin in order to lay her eggs. She then dies. The eggs hatch into tiny mites that spread out over the skin and live for only about 30 days. The mite antigen, in its excreta, causes a hypersensitivity rash. Diagnosis is by microscopic examination of skin scrapings. A new IgE diagnostic test is available. Clinical features • Intense itching (worse with warmth and at night) • Erythematous papular rash • Usually on hands and wrists • Common on male genitalia (see CHAPTER 119) (see FIG. 122.2) • Also occurs on elbows, axillae, feet and ankles, nipples of females (see FIG. 122.3)

The basic principle of treatment is to determine the cause of the itch and treat it accordingly. Itch of psychogenic origin responds to appropriate therapy, such as amitriptyline for depression.1 If no cause is found: • apply cooling measures (e.g. air-conditioning, cool swims) • avoid rough clothes; wear light clothing • avoid known irritants • avoid overheating • avoid vasodilatation (e.g. alcohol, hot baths/ showers—keep showers short and not too hot) • treat dry skin with appropriate moisturisers (e.g. propylene glycol in aqueous cream) • topical treatment — emollients to lubricate skin

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FIGURE 122.1 Scabies mite (Sarcoptes scabiei)

Spread The mites are spread from person to person through close personal contact (skin to skin), including sexual contact. They may also be spread through contact with infested clothes or bedding, although this is

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• Problems of the skin Crusted (Norwegian) scabies While the majority of cases have a relatively small number of mites (as few as 15), infestation with thousands or millions will cause the crusted condition of Norwegian scabies. Diagnosis is made on a scraping which reveals vast numbers of lesions. It may be encountered in nursing homes. Treatment is with ivermectin 200 mcg/ kg (o) as single dose plus topical treatment.5 Treatment5 For all ages (except children under 6 months):

FIGURE 122.2 Genital scabies causing severe pruritus, showing bruising on the upper thighs from intense scratching

uncommon. Sometimes the whole family can get scabies. The spread is more likely with overcrowding and sexual promiscuity.

permethrin 5% cream (treatment of choice) or benzyl benzoate 25% emulsion (dilute with water if under 10 years) best applied to clean, cool, dry skin • Apply to entire body from jawline down (including under nails, in flexures and genitals). • Leave permethrin overnight, then wash off thoroughly. • Leave benzyl benzoate for 24 hours. • Avoid hot baths or scrubbing before application. • Treat the whole family at the same time even if they do not have the itch. • Wash clothing, any soft toys and bedclothes as usual in hot water and hang in sun. • One treatment is usually sufficient but repeat scabicide treatment in 1 week for moderate and severe infections. • For children less than 2 months use sulphur 5% cream daily for 2–3 days or crotamiton 10% cream daily for 3–5 days.

Dermatitis herpetiformis

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This extremely itchy condition is a chronic subepidermal vesicular condition in which the herpes simplex-like vesicles erupt at the dermo-epidermal junction. The vesicles are so pruritic that it is unusual to see an intact one on presentation. Some consider that it is always caused by a glutensensitive enteropathy. Most patients do have clinical coeliac disease.

FIGURE 122.3 Typical distribution of the scabies rash

Clinical features • Most common in young adults • Vesicles mainly over elbows and knees (extensor surfaces) • Also occurs on trunk, especially buttocks and shoulders (see FIG. 122.4) • Vesicles rarely seen by doctors • Presents as excoriation with eczematous changes

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Pruritus

FIGURE 122.4 Typical distribution of dermatitis herpetiformis

• Masquerades as scabies, excoriated eczema or insect bites • Typically lasts for decades • Associated with gluten-sensitive enteropathy • Skin biopsy shows diagnostic features Treatment • Gluten-free diet, which may suppress the condition • Dapsone 100 mg (o) daily (usually dramatic response)

Lichen planus Lichen planus is an epidermal inflammatory disorder of unknown aetiology characterised by pruritic, violaceous, flat-tipped papules, mainly on the wrists (see FIG.  122.5) and legs. If in doubt, diagnosis is confirmed by biopsy. One differential diagnosis is a lichen planus-like drug eruption (e.g. antihypertensives, anti-malarials). Clinical features • Young and middle-aged adults • 4Ps—papule, purple, polygonal, pruritic • Small, shiny, lichenified plaques • Symmetrical and flat-tipped • Violaceous • Flexor surfaces: wrists, forearms, groin, ankles • Can affect oral mucosa—white streaks or papules or ulcers • Can affect nails and scalp

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FIGURE 122.5 Lichen planus: thick, hypertropic, reddishpurple papules

Management • Explanation and reassurance • Usually resolves over 6–9 months, leaving discoloured marks without scarring • Recurrence rare • Asymptomatic lesions require no treatment • Topical moderate to very potent corticosteroids (may use occlusive dressing) • Oral prednisolone if not successful • Intralesional corticosteroids for hypertrophic lesions

Pruritus ani The generalised disorders causing pruritus may cause pruritus ani. However, various primary skin disorders such as psoriasis, dermatitis, contact dermatitis and lichen planus may also cause it, in addition to local anal conditions. It is covered in more detail in CHAPTER 36.

Pruritus capitis (itchy scalp)6 Scalp pruritus may be caused by several common skin conditions including seborrhoeic dermatitis, atopic dermatitis, psoriasis, tinea capitis, lichen simplex chronicus, contact dermatitis and pediculosis. Look for evidence of these conditions in the scalp and treat accordingly. The less severe form of seborrhoeic dermatitis is known as pityriasis capitis or dandruff.

Pruritus vulvae Refer to CHAPTER 106.

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Tinea cruris Also known as Dhobie itch and jock itch, tinea cruris is a common infection of the groin area in young men (see FIG.  122.6), usually athletes, that is commonly caused by a tinea infection, although there are other causes of a groin rash (see TABLE  122.4). The dermatophytes responsible for tinea cruris (Dhobie itch) are Trichophyton rubrum (60%), Epidermophyton floccosum (30%) and Trichophyton mentagrophytes.7 The organisms thrive in damp, warm, dark sites. The feet should be inspected for evidence of tinea pedis. It is transmitted by towels and other objects, particularly in locker rooms, saunas and communal showers.

• • • •

Usually acute onset More common in hot months—a summer disease More common in physically active people Related to chafing in groin (e.g. tight pants, and especially synthetic jock straps) • Scaling, especially at margin • Well-defined border (see FIG. 122.7) If left untreated, the rash may spread, especially to the inner upper thighs, while the scrotum is usually spared. Spread to the buttocks indicates T. rubrum infection.

FIGURE 122.7 Dermogram for tinea cruris

FIGURE 122.6 Tinea cruris (also known as Dhobie itch and jock itch) in a young man caused by Trichophyton rubrum

Table 122.4

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Common causes of a groin rash (intertrigo)

Simple intertrigo Skin disorders: • psoriasis • seborrhoeic dermatitis • dermatitis/eczema Fungal: • Candida • tinea Erythrasma Contact dermatitis

Clinical features • Itchy rash • More common in young males • Strong association with tinea pedis (athlete’s foot)

Diagnostic aids • Skin scrapings should be taken from the scaly area for preparation for microscopy (see CHAPTER 121). • Wood’s light may help the diagnosis, particularly if erythrasma is suspected. Management • Soak the area in a warm bath and dry thoroughly. • Apply topical terbinafine 1% cream or gel once daily for 7 days or an imidazole topical preparation (e.g. miconazole or clotrimazole cream); rub in a thin layer bd for 3–4 weeks on the rash and 2 cm beyond the border. • Apply tolnaftate dusting powder bd when almost healed to prevent recurrence. • If itch is severe, a mild topical hydrocortisone preparation (additional) can be used.7 • If weeping: Burow’s solution 1 in 40 compresses to dry the area. • For persistent or recurrent eruption, use oral terbinafine for 2–4 weeks or griseofulvin for 6–8 weeks.

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Pruritus

Candida intertrigo Candida albicans superinfects a simple intertrigo and tends to affect obese or bedridden patients, especially if incontinent.8 Clinical features • Occurs equally in men and women • Erythematous scaly rash in groin • Less well-defined margin than tinea (see FIG. 122.8) • Associated satellite lesions • Yeast may be seen on microscopy

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• Coral pink fluorescence with Wood’s light • Common sites: groin, axillae, submammary, toe webs (see FIG. 122.9) Treatment • Topical imidazole e.g. miconazole or erythromycin 2% gel • oral roxithromycin

indefinite border with satellite macular lesions at the edge

FIGURE 122.8 Dermogram for candidiasis of crural area FIGURE 122.9 Typical sites of erythrasma 5,8

Treatment • Treat underlying problem. • Apply an imidazole preparation such as miconazole 2% or clotrimazole 1%. • Continue treatment for 2 weeks after symptoms resolve. • Use Burow’s solution 1 in 40 compresses to dry a weeping area. • Use short-term hydrocortisone cream for itch or inflammation (long-term aggravates the problem).

Erythrasma Erythrasma, a common and widespread chronic superficial skin infection, is caused by the bacterium Corynebacterium minutissimum, which can be diagnosed by coral pink fluorescence on Wood’s light examination. Itch is not a feature. Clinical features • Superficial reddish-brown scaly patches • Enlarges peripherally • Mild infection but tends to chronicity if untreated

Asteatotic eczema (winter itch) This often unrecognised problem, which can be very itchy, is a disorder of the elderly. It is a form of eczema that typically occurs on the legs of the elderly (see FIG.  122.10), especially if they are subjected to considerable scrubbing and bathing. Other predisposing factors include low humidity (winter, central heating) and diuretics. The problem may be associated with a malabsorption state, hypothyroidism or drugs e.g. statins, diuretics. Clinical features • Dry skin • Fine scaling and red superficial cracking • ‘Crazy paving’ appearance • Occurs on legs, especially shins • Also occurs on thighs, arms and trunk Treatment • Avoid scrubbing with soaps • Use aqueous cream and a soap substitute • Apply topical steroid diluted in white soft paraffin

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• Problems of the skin spontaneous resolution occurs. Effective treatments include topical (preferable) or oral corticosteroids and ultraviolet light.3

Lichen simplex Lichenification is a form of dermatitis caused by repeated scratching or rubbing, which results in epidermal thickening. Lichen simplex is the term used when no primary dermatological cause can be found.

Urticaria10 Urticaria is a common condition that mainly affects the dermis. It can be classified as acute (minutes to weeks) or chronic (lasting more than 6 weeks). It can also be classified as diffuse wheal-like or papular (hives). The three characteristic features of diffuse urticaria are: FIGURE 122.10 Asteatotic eczema (winter itch) showing the ‘crazy paving’ pattern with a pruritic scaling erythematous eruption on the legs of a 74-year-old man

‘Golfer’s vasculitis’ (summer leg rash)9 This is a term used to describe an erythematous pruritic rash that appears on the legs after prolonged exercise such as golf or hiking, usually during summer months. The rash is a red, blotchy, flat to slightly raised eruption on the lower leg. It is more common over age 50. It usually clears spontaneously within 3 days.

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Brachioradialis pruritus In this condition, itch and discomfort are limited to the outer surface of the upper limb above and below the elbow. It is often associated with sun damage, xerosis and nerve entrapment, hence the term ‘golfer’s itch’.2

Grover disease Also known as transient acantholytic dermatosis, Grover disease produces small, firm, intensely pruritic, reddish-brown, warty papules with minimal scale, mainly on the upper trunk. It usually occurs in middleaged to elderly men (typically 70–80 years). Trigger factors include heat, sweating, fever and occlusion, especially on photo-damaged skin. Diagnosis is by biopsy. Treatment is to relieve the itch until

• transient erythema • transient oedema • transient itch The most common causes are infections, especially viral URTIs, drug allergies and IgE-mediated food reactions. Classification according to site 1 Superficial: affecting superficial dermis =  urticaria; occurs anywhere on body, especially the limbs and trunk. 2 Deep: affecting subcutaneous tissue = angiooedema; occurs anywhere but especially peri-orbital region, lips and neck. Checklist of causes3 • Infections: viruses (the most common cause in children), bacteria (especially streptococcus infection), parasites, protozoa, yeasts • C1 esterase inhibitor deficiency (hereditary angio-oedema)—recurrent unexplained episodes of angio-oedema • Allergies (acute allergic urticaria is dramatic and potentially very serious): — azo dyes — drugs: penicillin and other antibiotics — foods: eggs, fish, cheese, tomatoes, others • Pharmacological: — drugs: penicillin, aspirin, codeine — foods: fish, shellfish, nuts, strawberries, chocolate, artificial food colourings, wheat, soy beans — plants: nettles, others

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Pruritus • Systemic lupus erythematosus • Physical: — cholinergic: response to sweating induced by exercise and heat (e.g. young athletes) — heat, cold, sunlight • Insect stings: bees, wasps, jellyfish, mosquitoes • Pregnancy (last trimester), other hormonal • Unknown (idiopathic)—80%; possible psychological factors

as Stingose, alcohol, damp soap, anti-itch cream or a mild corticosteroid ointment.

Investigations • Full blood examination—look for eosinophilia of parasites • ANF and DNA binding tests—consider SLE • Challenge tests

FIGURE 122.11 Flea

Treatment5 • Avoid any identifiable causes. • Avoid salicylates and related food preparations (e.g. tartrazine). • Consider elimination diets. • Use oral antihistamines (e.g. cyproheptadine) or a less sedating one (e.g. cetirizine, loratadine, fexofenadine). • Consider adding an H2 antagonist (e.g. ranitidine 150 mg bd). • Give short course of systemic corticosteroids if severe (e.g. prednisolone 50 mg once daily for 3–5 days).11 • For severe urticaria with hypotension and anaphylaxis give IM adrenaline.5 • Use topical soothing preparation if relatively localised (e.g. crotamiton 10%, or phenol 1% in oily calamine or menthol 1% cream). • Lukewarm baths with Pinetarsol or similar soothing bath oil.

Flea bites Fleas (see FIG.  122.11) cause itchy erythematous maculopapular lesions. They are usually multiple or grouped in clusters, occurring typically on the arms, forearms, leg and waist (where clothing is tight). Treat the source of infestation, particularly domestic cats and dogs. The itchy bites can be treated with an application of simple agents such

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Bed bug bites12 The common bed bug (Cimex lectularius, see FIG.  122.12) is now a major problem related to international travel. It travels in baggage and is widely distributed in hotels, motels and backpacker accommodation. The bugs hide in bedding and mattresses. Clinically bites are usually seen in children and teenagers. The presentation is a linear group of three or more bites (along the line of superficial blood vessels), which are extremely itchy. They appear as maculopapular red lesions with possible wheals. The lesions are commonly found on the neck, shoulders, arms, torso and legs. A bed bug infestation can be diagnosed by identification of rust-coloured specimens collected from the infested residence. In hotels and backpacker accommodation look for red specks in mattresses and check luggage.

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Papular urticaria This is a hypersensitivity to insect bites particularly seen in children aged 2–6 years. The lesions are grouped together as very itchy papules. Common urticaria tends to come and go within hours but the lesions of papular urticaria persist.

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FIGURE 122.12 Bed bug

Management • Clean the lesions with antiseptic soap. • Apply a corticosteroid ointment. • A simple antipruritic agent may suffice e.g. calamine lotion. • Call in a licensed pest controller. Control treatment is basically directed towards applying insecticides to the crevices in walls and furniture. Be careful of used furniture and insist that mattresses are delivered in plastic coverings.

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Sandfly bites Refer CHAPTER 130.

When to refer • Lichen planus • Dermatitis herpetiformis • Norwegian scabies

Practice tip An itchy non-specific rash worse at night? Think scabies.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Bed bug bites • Pruritus ani • Scabies • Urticaria

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References 1 Walsh TD. Symptom Control. Oxford: Blackwell Scientific Publications, 1989: 286–94. 2 Wolff K, Johnson RA et al. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology. New York: McGraw-Hill, 2005: 1052–5. 3 Fry L et al. Illustrated Encyclopedia of Dermatology. Lancaster: MTP Press, 1981: 313–15, 485–8. 4 Hunter JAA, Savin JA, Dahl MV. Clinical Dermatology (3rd edn). Oxford: Blackwell Scientific Publications, 2002: 291. 5 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 3). Melbourne: Therapeutic Guidelines Ltd, 2009: 182–5. 6 Ng J, Chong A, Foley P. The itchy scalp. Medicine Today, 2008; 9 (7): 2–9. 7 Gin D. Tinea infection. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 512. 8 Cowen P. Candidiasis, cutaneous. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 89–91. 9 Australas J. Golfers vasculitis: an unusual presentation. Dermatology, 2005; 46: 11–14. 10 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 3). Melbourne: Therapeutic Guidelines Ltd, 2009: 281–5. 11 Levine M, Lexchin J, Pellizzari R. Drugs of Choice: a Formulary for General Practice. Ottawa: Canadian Medical Association, 1995: 15–33. 12 Bed bugs:

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Common skin problems

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The power of making a correct diagnosis is the key to all success in the treatment of skin diseases; without this faculty, the physician can never be a thorough dermatologist, and therapeutics at once cease to hold their proper position, and become empirical. Louis A Duhring (–) Skin disorders are common. They account for 10.8% of all problems1 encountered in general practice, the most common being contact dermatitis, malignant skin neoplasms, solar keratoses/sunburn, lacerations, warts and acne. This chapter focuses on the common dermatoses.

Dermatitis/eczema 1

The terms ‘dermatitis’ and ‘eczema’ are synonymous and denote an inflammatory epidermal rash, acute or chronic, characterised by vesicles (acute stage), redness, weeping, oozing, crusting, scaling and itch. Dermatitis can be divided into exogenous causes (allergic contact, primary irritant contact, photoallergic and phototoxic) and endogenous, which implies all forms of dermatitis not directly related to external causative factors. Endogenous types are atopic, nummular (discoid), vesicular hand/foot (dyshidrotic), pityriasis alba, lichen simplex chronicus and seborrhoeic. Dermatitis is primarily due to an impairment of the barrier function of the skin, making it more susceptible to irritation by soap and other contact irritants, the weather, temperature and non-specific triggers.

The meaning of atopy The term ‘atopic’ refers to a hereditary background or tendency to develop one or more of a group of conditions, such as allergic rhinitis, asthma, eczema, skin sensitivities and urticaria. It is not synonymous with allergy. An estimated 10% of the population are atopics, with allergic rhinitis being the most common manifestation.2

Atopic dermatitis Features of classic atopic dermatitis:3 • itch • usually a family history of atopy

• about 3% of infants are affected, signs appearing between 3 months and 2 years • often known trigger factors (see TABLE 123.1) are evident Table 123.1

Trigger factors for atopic dermatitis

Dust mite (common) Sweating Sand (e.g. in sandpits) Extremes of hot and cold Rapid temperature changes Soap, shampoo and water/frequent washing, especially in winter Chlorinated water Bubble baths Infection (viral, bacterial, fungal) Allergy Stress/emotional factors Skin irritants: • wool (e.g. sheepskin covers) • brushed nylon or silk clothing • rough clothing • chemical disinfectants • detergents • petrochemical products • pollens Scratching and rubbing Perfumes Poor general health Foodstuffs (consider): • cow’s milk • beef • chicken • nuts • eggs • food colourants • oranges and other citrus fruits • tomatoes • wheat Note: The relationship to food is controversial and uncertain. RAST testing is misleading. Consider eliminating the foodstuffs and reintroducing one at a time. If sensitive, the child goes bright red a few minutes after feeding.

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• dust mite allergy is not always obvious, especially for peri-orbital rash • lichenification may occur with chronic atopic dermatitis • flexures are usually involved (see FIG. 123.1) • dryness is usually a feature

(a)

(b)

(c)

FIGURE 123.1 Atopic dermatitis in the flexures of the knees—a typical location

Criteria for diagnosis • • • • •

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Itch Typical morphology and distribution Dry skin History of atopy Chronic relapsing dermatitis

Distribution The typical distribution of atopic dermatitis changes as the patient grows older. In infants the rash appears typically on the cheeks of the face, the folds of the neck and scalp and extensor surfaces of the limbs. It may then spread to the flexures of limbs and groins (see FIG. 91.10 in CHAPTER 91). The change from infancy through to adulthood is presented in FIGURE 123.2. During childhood a drier and thicker rash tends to develop in the cubital and popliteal fossae and on the hands and feet, which may be dry, itchy, fissured and painful. The face often clears. Refer to CHAPTER 91. Prognosis It is generally correct that children tend to ‘grow out of’ the problem as the function of their oil and sweat glands matures. The skin becomes less dry, less overheated and irritable.4 About 60% of patients have virtually normal skin by 6 years and 90% by puberty.4

FIGURE 123.2 Relative distribution of atopic dermatitis in (a) infants, (b) children, and (c) typical distribution of atopic dermatitis in adults

Treatment Advice to parents of affected children: • Avoid soap and perfumed products. Use a bland bath oil in the bath and a cleansing bar (e.g. Cetaphil, DermaVeen) as a soap substitute. Choose cleansers and shampoos with low pH (4.5–6.0) e.g. DermaVeen, Ego or Hamilton body wash and shampoo. • Apply an emollient soon after bathing. • Older children should have short, tepid showers. • Avoid rubbing and scratching—use gauze bandages with hand splints for infants. • Keep fingernails short and clean. • Avoid overheating, particularly at night.

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Common skin problems • Avoid sudden changes of temperature, especially those that cause sweating. • Wear light, soft, loose clothes, preferably made of cotton. Cotton clothing should be worn next to the skin. • Avoid wool next to the skin. • Avoid dusty conditions and sand, especially sandpits. • Avoid contact with people with ‘sores’, especially herpes. • Keep the skin moisturised. Consider dust mite strategies: • dust mite covers (premium grade) for bedding • wash linen in hot water >55°C • consider replacing fabric on chairs and changing carpet

Education and reassurance Explanation, reassurance and support are very important. Emphasise that atopic dermatitis is a superficial disorder and will not scar or disfigure under normal circumstances. The child should be treated normally in every respect. Counselling is indicated where family stress and psychological factors are contributing to the problem. Medication4,5 Note: Corticosteroid creams (for acute phase) and ointments (for chronic phase) in either a step-up or step-down strategy are the basis of treatment. Emollients are the key to preventing flares and steroids are used for the flares. For maintenance, especially if dry, consider coal tar (LPC) 3–6% with salicyclic acid 2–6% in aqueous cream at night.

Mild atopic dermatitis • Soap substitutes • Emollients apply bd to dry skin (choose from): — Ego skin cream — sorbolene alone or with 10% glycerol — paraffin creams (e.g. Dermeze)—good in infants — bath oils (e.g. Alpha Keri) — moisturising lotions (e.g. QV) in summer • 1% hydrocortisone ointment (if not responding to above) once or twice daily: — short term for flares

Moderate atopic dermatitis • As for mild • Topical corticosteroids (twice daily): — vital for active areas

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— moderate strength (e.g. fluorinated) to trunk and limbs, once or twice daily — weaker strength (e.g. 1% hydrocortisone) to face and flexures, once daily increasing to twice daily if inadequate response — use as needed but should not be used for longer than 2 weeks, or use in cyclic fashion for chronic cases (e.g. 10 days on, 4 days off) • Non-steroidal alternative: pimecrolimus (Elidel) cream bd for facial dermatitis; best used when eczema flares—then cease • Oral antihistamines at night for itch

Severe dermatitis • As for mild and moderate eczema • Potent topical corticosteroids to worse areas (consider occlusive dressings) • Consider hospitalisation • Systemic corticosteroids (rarely used) • Allergy assessment if unresponsive • Consider adding UV band therapy as back-up • Systemic immunosuppressants may be used for recalcitrant cases

Weeping dermatitis (an acute phase) This often has crusts due to exudate. Burow’s solution diluted to 1 in 20 or 1 in 10 can be made to soak affected areas. Saline (1 teaspoon to 500 mL water) dressings can also be used: soak old sheets till damp and lay on the areas. Infection is common.

General points of dermatitis management Acute weeping Acute Chronic Lichenified Infection

Moisturising

→ wet dressings (saline or Burow’s) → creams → ointments, with or without occlusion → ointments under occlusion → antibiotics (e.g. mupirocin 2% topical or oral alone if unresponsive to topical) → use lotions not creams

OTHER TYPES OF ATOPIC DERMATITIS

Nummular (discoid) eczema • • • • • • •

Chronic, red, coin-shaped plaques Crusted, scaling and itchy Mainly on the legs, also buttocks and trunk Often symmetrical Common in middle-aged patients May be related to stress Tends to persist for months Treatment as for classic atopic dermatitis.

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Pityriasis alba • These are white patches on the face of children and adolescents • Very common mild condition • More common around the mouth and on cheeks • Can occur on the neck and upper limbs, occasionally on trunk • It is a subacute form of atopic dermatitis • Full repigmentation occurs eventually Treatment • Reassurance • Simple emollients • Restrict use of soap and washing • May prescribe hydrocortisone ointment (rarely necessary)

Lichen simplex chronicus • Circumscribed thick plaques of lichenification • Often a feature of atopic dermatitis • Caused by repeated rubbing and scratching of previously normal skin • Due to chronic itch of unknown cause • At sites within reach of fingers (e.g. neck, forearms, thighs, vulva, heels, fingers) • May arise from habit Treatment • Explanation • Refrain from scratching • Potent fluorinated corticosteroid ointment with plastic occlusion

Dyshidrotic dermatitis (pompholyx)

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• Typically in patients aged 20–40 years • Itching vesicles usually on fingers (pompholyx, see FIG. 123.3) • May be larger vesicles on palms and soles • Commonly affects sides of digits and palms • Lasts a few weeks • Tends to recur • Possibly related to stress • Often triggered by high humidity Treatment • Wet dressings/soaks if severe • As for atopic dermatitis • Potent fluorinated corticosteroids • Topically—use under occlusion (e.g. damp cotton gloves) • Oral corticosteroids (3 weeks) may be necessary

FIGURE 123.3 Pompholyx showing the typical vesicular dermatitis along the borders of the fingers. Look for associated inflammatory tinea of the feet which can precipitate it. Photo courtesy Robin Marks

Asteatotic dermatitis This is the common, very itchy dermatitis that occurs in the elderly, especially in the winter, with a dry ‘crazy paving’ pattern, especially on the legs (see CHAPTER 122). ‘Asteatotic’ means without moisture.

Cracked (fissured) hands/fingers This common cause of disability is usually due to dermatitis of the hands, irritant contact dermatitis or very dry skin. It is usually part of the atopic dermatitis problem and it is important to consider allergic contact dermatitis. Management (hand dermatitis) Hand protection: • avoid domestic or occupational duties that involve contact with irritants and detergents • wear protective work gloves; cotton-lined PVC gloves • avoid perfumed toilet soaps—use a substitute (e.g. Dove, Neutrogena, DermaVeen soap-free cleansing bar) • Cetaphil lotion is a useful soap substitute • apply emollients (e.g. 2% salicylic acid in white soft paraffin at night, or Neutrogena Norwegian Formula hand cream)

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Common skin problems If necessary: hydrocortisone 1% ointment (not cream) or stronger fluorinated preparation (e.g. Advantan fatty ointment)

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(see FIG. 123.4). Contact dermatitis is due to delayed hypersensitivity, sometimes with a long time of days to years. It is common in industrial or occupational situations, where it usually affects the hands and forearms.

Cracked heels Cracked painful heels are a common problem, especially in adult women. It is a manifestation of very dry skin. Treatment • Soak the feet for 15 minutes in warm water containing an oil such as Alpha Keri or Derma Oil. • Pat dry, then apply an emollient foot cream (e.g. Nutraplus—10% urea). • Can use tissue glue (with care) to hold edges together.

CONTACT DERMATITIS Acute contact (exogenous) dermatitis can be either irritant or allergic and it is estimated that at least 70% of patients have an irritant cause. It is difficult to separate these types on clinical or histological grounds. The presence of irritant dermatitis increases the risk of developing a contact allergy. Features: • • • •

itchy, inflamed skin red and swollen papulovesicular may be dry and fissured

Irritant contact dermatitis This is caused by primary irritants such as acids, alkalis, detergents, soaps, oils, solvents. A reaction may result from either a once-only exposure to a very irritant chemical or, more commonly, repeated exposure to weaker irritants. This is irritation, not allergy.

Allergic contact dermatitis Caused by allergens that provoke an allergic reaction in some individuals only—most people can handle the chemicals without undue effect. It is immunologically mediated. This allergic group also includes photo-contact allergens. Approximately 4.5% of the population is allergic to nickel, which is found in jewellery, studs on jeans, keys and coins

FIGURE 123.4 Contact dermatitis due to nickel-containing underwire in brassiere in 17-year-old girl with a history of eczema

Common allergens: • ingredients/fragrances in cosmetics (e.g. perfumes, preservatives) • topical antibiotics (e.g. neomycin) • topical anaesthetics (e.g. benzocaine) • topical antihistamines • plants: Rhus, Grevillea, Primula, poison ivy • metal salts (e.g. nickel sulphate, chromate) • dyes (especially clothing dyes) • perfumes, cosmetics • hairdressing chemicals • rubber/latex • epoxy resins and glues/acrylates • glutaraldehyde (e.g. sterilising agents) • toluene sulfonamide compound resins: nail polish • coral Note: The skin of mangoes cross-reacts with Rhus and Grevillea. Clinical features3 • Dermatitis ranges from faint erythema to ‘water melon’ face oedema • Worse in peri-orbital region, genitalia and hairy skin; least in glabrous skin (e.g. palms and soles) Note: Can be delayed onset. • Think of Rhus, Grevillea or poison ivy allergy if linear blisters on forearms and/or puffy eyes

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Diagnostic hallmarks3 • Site and shape of lesions suggest contact • Linear lesions a feature • Allergic causes may be found by patch testing • Improvement when off work or on holiday Diagnosis • Careful history and examination • Consider occupation, family history, vacation or travel history, clothes (e.g. wetsuits, new clothes, Lycra bras), topical applications (e.g. medicines, cosmetics) • Refer to a dermatologist for patch testing Management • Determine cause with vigour and remove it • Wash with water (only) and pat dry (avoid soap) • If acute with blistering, apply Burow’s compresses • Oral prednisolone for severe cases4 (start with 25–50 mg daily for adults for 1–2 weeks then gradually reduce over 1–2 weeks) • Topical corticosteroid cream • Oral antibiotics for secondary infection

SEBORRHOEIC DERMATITIS Seborrhoeic dermatitis is a very common skin inflammation that usually affects areas abundant in sebaceous glands or intertriginous areas. It is therefore common in hair-bearing areas of the body, especially the scalp and eyebrows. It can also affect the scalp, face, neck, axillae and groins, eyelids (blepharitis), external auditory meatus and nasolabial folds. The presternal area is often involved (see FIG. 123.5).

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FIGURE 123.5 Seborrhoeic dermatitis in an adult showing a typical position on the chest

There are two distinct clinical forms: seborrhoeic dermatitis of infancy, and the adult form, which mainly affects young adults. Studies have indicated that it may be caused by a reaction to the yeast Malassezia sp. It may be associated with HIV infection and Parkinson disease. A feature of seborrhoeic dermatitis is that, unlike atopic dermatitis, it is not itchy. Seborrhoeic scale is greasy and yellowish unlike the silvery scale of psoriasis. Principles of treatment • Topical sulphur, salicylic acid and tar preparations are first-line treatment: they lift the scale while sulphur kills the yeast. • Ketoconazole cream is most effective. • Ketoconazole shampoo for scalp twice weekly for 4 weeks. • Topical corticosteroids are useful for inflammation and pruritus and best used in combination. Avoid corticosteroids if possible.

Seborrhoeic dermatitis of infancy This rash may be known as ‘cradle cap’ if it affects the scalp, or nappy rash/diaper dermatitis if it involves the napkin area. It can be difficult to differentiate the rash from that of atopic dermatitis but seborrhoeic dermatitis tends to appear very early (before atopic dermatitis), even in the first month of life and mostly within the first 3 months, when androgen activity is most prevalent. The different features are summarised in TABLE  123.2 and the distribution is presented in FIGURE 123.6. Seborrhoeic dermatitis usually appears as red patches or blotches with areas of scaling. This becomes redder when the baby cries or gets hot. Cradle cap may appear in the scalp. A flaky, scurf-like dandruff appears first, and then a yellowish, greasy, scaly crust forms. This scurf is usually associated with reddening of the skin. It may resolve spontaneously within a few months (see Cradle cap, CHAPTER 91). The dermatitis can become infected, especially in the napkin area, and this may be difficult to treat. If untreated, it often spreads to many areas of the body. It is said that cradle cap and nappy rash ‘may meet in the middle’. Treatment Simple basic methods are: • keep areas dry and clean

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Common skin problems

Table 123.2

Differential diagnosis of seborrhoeic dermatitis and atopic dermatitis in infancy Seborrhoeic dermatitis

Atopic dermatitis (eczema)

Age of onset

Mainly within first 3 months

Usually after 2 months

Itchiness

Nil or mild

Usually severe

Distribution

Scalp, cheeks, folds of neck, axillae, folds of elbows and knees

Starts on face Elbow and knee flexures

Typical features

Cradle cap Red and yellow greasy scale

Vesicular and weeping Becomes dry and cracked

Napkin rash

Less common Common Prone to infection with Candida

Other features

May become generalised

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Medication4

Scalp Infants: 1–2% sulphur and 1–2% salicylic acid in aqueous cream or same cream with 2% liquor picis carbonis added: — apply overnight to scalp, shampoo off next day with a mild baby shampoo — use 3 times a week until it clears Egozite cradle cap lotion (6% salicylic acid) Older children and adults:

May become generalised

cradle cap eyebrows folds of neck axillae elbows knees

napkin rash

zinc pyrithione 1% or selenium sulphide 2.5% shampoo or ketoconazole 1–2% or miconazole 2% shampoo

Face, flexures and trunk Select from (depending on severity): • ketoconazole 2% cream, once or twice daily • 2% salicylic acid ± 2% sulphur in aqueous or sorbolene cream • if severe, hydrocortisone 1% (irritation on face and flexures) • betamethasone 0.02–0.05% (if severe irritation on trunk) • desonide 0.05% lotion, bd or tds for face/eyelids and for weeping areas

Napkin area • Mix equal parts 1% hydrocortisone with nystatin or ketoconazole 2% or clotrimazole 1% cream (or use Hydrozole Cream) Prognosis Most children are clear by 18 months (rare after 2 years).

FIGURE 123.6 Seborrhoeic dermatitis: typical distribution in infants

• bathe in warm water, pat areas dry with a soft cloth • keep skin exposed to air as much as possible • avoid toilet soaps for washing (use emulsifying ointment or cetaphil lotion) • rub scales of cradle cap gently with baby oil or white soft paraffin then wash away loose scales • change wet or soiled nappies often • for mild areas on body, apply a thin smear of zinc cream

Adult seborrhoeic dermatitis Clinical features • Any age from teenage onwards • The head is a common area: scalp and ears, face, eyebrows, eyelids (blepharitis), nasolabial folds (see FIG. 123.7) • Other areas: centre of chest, centre of back, scapular area, intertriginous areas, especially perianal (see FIG. 123.8) • Red rash with yellow greasy scale • Secondary candidiasis infection common in flexures

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scalp, especially anterior margin

2 ketoconazole shampoo; immediately after using medicated shampoo (leave 5 minutes), twice weekly 3 ciclopirox olamine shampoo, 2 or 3 times weekly 4 betamethasone dipropionate 0.5% lotion to scalp (if very itchy)

eyebrows

Face and body

eyelids (blepharitis)

• Wash regularly using bland soap

wings of nose

salicylic acid 2% + sulphur 2% (± tar) in aqueous cream or ketoconazole 2% cream (very effective); apply once daily for 4 weeks hydrocortisone 1% bd (if inflamed and pruritic) or combination hydrocortisone 1% + clotrimazole 1% cream topically, once or twice daily

nasolabial folds external auditory meatus (otitis externa)

FIGURE 123.7 Seborrhoeic dermatitis: facial distribution in adults external auditory meatus behind ears beard area

axilla

scalp dandruff eyebrows eyelid margins nasolabial folds presternal interscapular submammary intertrigo umbilicus

groin

perianal area (pruritus ani)

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FIGURE 123.8 Seborrhoeic dermatitis: possible distribution in adults

• Dandruff a feature of scalp area • Worse with stress and fatigue • It is a chronic, recurring condition Treatment

Scalp Options: 1 salicylic acid 2% ± sulphur 2% (or LPC 3% plus salicylic acid 3%) in aqueous cream overnight— shampoo off next day using selenium sulphide or zinc pyrithione shampoo (apply 3 times a week)

Note: Oral antifungals are not recommended at all.

PSORIASIS Psoriasis (see FIG.  123.9) is a chronic, immunemediated skin disorder of unknown aetiology which affects 2–4% of the population. It appears most often between the ages of 10 and 30 years, although its onset can occur any time from infancy to old age. It has a familial predisposition although its mode of inheritance is debatable. If one parent is affected there is a 25% chance of developing it; this rises to 65% if both parents are affected.2 Psoriasis is now regarded as a disorder involving activation of helper T cells in the skin. Cytokines are then released and cause skin cells to multiply faster, leading to thickening of the skin and overscaling. The new ‘biological agents’ intervene in this process. Capillary dilatation explains the redness. Be aware of association with cardiovascular disease, particularly heart disease, depressive illness, diabetes, arthritis, inflammatory bowel disease and lymphoma.6

Factors that may worsen or precipitate psoriasis • • • • • •

Infection, especially group A Streptococcus Trauma or other physical stress Emotional stress Sunburn Puberty/menopause Drugs: — antimalarials (e.g. chloroquine) — beta blockers — lithium — NSAIDs — oral contraceptives

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• Rash improves on exposure to sun but worse with sunburn • Worse in winter • Itching not a feature but is present sometimes • Lesions are most unlikely to appear on the face Arthropathy About 5% can develop a painful arthropathy (fingers, toes or a large joint) or a spondyloarthropathy (sacroiliitis).7

The rash The appearance depends on the site affected. The commonest form is plaque psoriasis, which begins with red lesions that enlarge and develop silvery scaling. The commonest sites are the extensor surfaces of the elbows and knees; then the scalp, sacral areas, genitals and nails are affected (see FIG. 123.10).

Diagnosis Psoriasis is a clinical diagnosis but biopsy may be needed for confirmation. No laboratory test (including blood testing) is available.

Principles of management FIGURE 123.9 Psoriasis showing the typically raised pink plaques surmounted with a silvery scale Types of psoriasis

Differential diagnosis

Infantile

Seborrhoeic dermatitis, atopic dermatitis

Plaque (commonest)

Seborrhoeic dermatitis, discoid eczema, solar keratoses, Bowen disorder

Guttate

Pityriasis rosea, secondary syphilis, drug eruption

Flexural

Tinea, candida intertrigo, seborrhoeic dermatitis

Scalp (sebopsoriasis)

Seborrhoeic dermatitis, tinea capitis

Nail

Tinea, idiopathic onycholysis

Pustular (palmoplantar)

Tinea, infected eczema

Exfoliative

Severe seborrhoeic dermatitis

The typical patient • • • •

Older teenager or young adult Possible family history Onset may follow stress, illness or injury Rash may appear on areas of minor trauma—the Koebner phenomenon

While realising there is no cure for psoriasis, the aim of treatment is to relieve discomfort, slow down the rapid skin cell division and work in consultation with a specialist to achieve these aims.7 • Provide education, reassurance and support. • Promote general measures such as rest, and holidays, preferably in the sun. scalp elbows (extensor surface)

sacral area

nails pustular psoriasis

knees (extensor surface) pustular psoriasis

FIGURE 123.10 Psoriasis: typical skin distribution

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• Advise prevention, including avoidance of skin damage and stress if possible. • Tailor treatment (including referral) according to the degree of severity and extent of the disease. • Shared care with a consultant is advisable.

Table 123.3

Treatment options4,7 See TABLE 123.3. Topical agents useful for mild psoriasis include tars, dithranol, salicyclic acid, cacipotriol, corticosteroids and tazarotene (a retinoid).

Psoriasis treatment options

Therapy

Efficacy/notes

1 Topical therapy Dithranol (anthralin): concentrations range from 0.05 to 2% (max.)

Effective on difficult thick patches Facts: • stains light-coloured hair purple so don’t use on scalp • start in low concentration and build up according to tolerance and response • use in strengths 0.05% (children), 0.1%, 0.25%, 0.5% and 2.0% (max.) • can use a higher strength of 0.25% to start but only for short contact therapy (30 minutes before shower) • irritates skin, causing a burning sensation • don’t use it on face, genitalia or flexures

Tar preparations

Effective but messy to use

Corticosteroids

The mainstay of therapy for small plaques; use 1% hydrocortisone on more sensitive areas (genitals, groin, axillae, face) but use stronger types elsewhere (e.g. betamethasone dipropionate) Note: Avoid using corticosteroids alone as they promote instability—best to combine with tar or calcipotriol.

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Calcipotriol 0.005% ointment

Facts: • easy to use • apply twice daily for a minimum of 6 weeks • tends to irritate face and flexures • caution with hypercalcaemia • wash hands after use • used for chronic stable plaques (not for severe extensive rash) • good when combined with a potent corticosteroid (each applied once daily) e.g. Daivobet 50/500

Bland preparations and emollients

These can be used for dryness, scaling and itching—liquor picis carbonis (LPC) and menthol (or salicylic acid) in sorbolene base

2 Systemic therapy Methotrexate

Can have dramatic results in severe cases

Cyclosporin

Hospital use only

Corticosteroids (for erythrodermic psoriasis only)

Oral use may unstabilise psoriasis on withdrawal

Acitretin

A vitamin A derivative effective in severe intractable psoriasis (never use in females of child-bearing age)

3 Biological agents Monoclonal antibodies, anti-TNF agents, other agents

This new class of drugs is directed at the T cell dysfunction (i.e. immune response modifiers) (e.g. efalizumab, infliximab, ustekinumab, alefacept)

4 Physical therapy Phototherapy (ultraviolet light, narrowband or broadband, UV-B):

Needs careful supervision

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UV-B plus coal tar (Goeckerman regimen):

Reserved for severe psoriasis: (a) tar bath (b) UV-B (c) 2–5% crude coal tar

Ingram regime

Also for severe psoriasis (best as inpatient): (a) tar bath (b) UV-B (c) 0.1%–0.5% dithranol in Lassar’s paste

Photochemotherapy (PUVA = psoralen + UV-A)

Reserved for non-responders to UV-B treatment or other therapies.

Intralesional corticosteroids

An excellent and effective treatment for isolated small or moderate-sized plaques that can be readily given by the family doctor

Recommended topical regimens • Combined method for mild to moderate psoriasis (a good starting method): — dithranol 0.1%, salicylic acid 3%, ± LPC (tar) 10% in white soft paraffin (preferable) or sorbolene cream — leave overnight (warn about dithranol stains—use old pyjamas and sheets) — review in 3 weeks then gradually increase strength of dithranol to 0.25%, then 0.5% then 1%. Can cut down frequency to 2–3 times per week — shower in the morning and then apply a topical fluorinated corticosteroid • Short contact anthralin therapy (SCAT method): — apply dithranol 2% in sorbolene cream — wash off in shower after 10–15 minutes • General adjunctive therapy: — tar baths (e.g. Pinetarsol or Polytar) — tar shampoo (e.g. Polytar, Ionil-T) — sunlight (in moderation)

Other practice tips Chronic stable plaque psoriasis apply stronger fluorinated corticosteroid (II–III class) cover with DuoDERM Thin and leave for 7 days (other occlusive dressings can be used) plus tar (as an alternative to dithranol) (e.g. crude coal tar 1–4% plus salicylic acid 3–5% in sorbolene cream)—it can be left on overnight and washed off in the morning or calcipotriol 0.005% ointment or cream, apply bd or calcipotriol once daily + corticosteroids once daily

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Resistant localised plaque intralesional injection with corticosteroid diluted 50:50 with N saline or local anaesthetic

Method of injection Mix equal parts of triamcinolone acetonide 10 mg/ mL, or similar corticosteroid, and plain LA or N saline and, using a 25 gauge or 23 gauge needle, infiltrate the psoriatic plaque intradermally to cover virtually all the plaque. A small plaque can be covered by a single insertion while a larger plaque may require separate insertions (see FIG. 123.11).

long-acting corticosteroid

needle infiltrates all areas of plaque

FIGURE 123.11 Intralesional corticosteroid injection technique for psoriatic plaque (requiring double injection—small plaques need only one infiltration)

Maintenance for milder stabilised plaque psoriasis salicylic acid 3%, LPC 8% in sorbolene Red scale A traditional treatment is tar pomade, which is a preparation of various combinations of LPC (5–10%), salicyclic acid ± dithranol in liquid paraffin. Scalp psoriasis apply 20% urea cream for 4 days then

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tar preparations for the scalp (shampoo with conditioner), steroid lotions or 5–10% salicylic acid in mineral oil; systemic therapy if severe. or intermittent use of mometasone furoate lotion or Daivobet gel Genital psoriasis apply non-fluorinated corticosteroids Flexural psoriasis Note that fissuring (e.g. inframammary, natal cleft) is a feature. It tends to have a silvery scale but is shiny and smooth. apply topical steroids—mild to moderate fluorinated Nail psoriasis Difficult but consider potent topical or intralesional corticosteroids and systemic therapy.

NAPPY RASH4 Nappy rash (or diaper dermatitis) is an inflammatory contact dermatitis occurring in the napkin area and can be a common presentation of mild or moderate underlying skin disease. It is found in children up to 2 years old and has a peak incidence from 9–12 months.8 Most children will develop nappy rash at some stage of infancy with an estimated 50% having it to a significant extent. The commonest type is irritant dermatitis, but consider also: • Candida albicans (invariably present although often not obvious) • seborrhoeic dermatitis • atopic dermatitis • psoriasis

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Irritant dermatitis This is a type of contact dermatitis with the erythema and scaling conforming to the napkin area. The flexures are usually spared. It is related to the activity of faecal proteases and lipases and probably not to the activity of ammonia (from urea) as previously promoted. The problem can vary from mild erythema to a severe blistering eruption with ulceration. Ultrabsorbent disposable nappies appear to be better than cloth nappies.9 Diarrhoea, including spurious diarrhoea with constipation (check rectum) is a causative factor of irritant dermatitis. If the eruption extends further than the points of contact with the nappy an underlying skin disease such as seborrhoeic

or atopic dermatitis must be suspected. Psoriasis always involves the skin folds.

Seborrhoeic dermatitis This affects mainly the flexures of the natal cleft and groin. It is important to look for evidence of seborrhoeic dermatitis elsewhere, such as cradle cap and lesions on the face and axillae.

Atopic dermatitis Atopic dermatitis can involve the napkin area. Pruritus is a feature and the child may be observed scratching the area. There may be evidence of atopic dermatitis elsewhere, such as on the face.

Candidiasis (monilia nappy rash) Superinfection of intertrigo or napkin dermatitis will result in a diffuse, red, raw, shiny rash that will involve the flexures and extend beyond the napkin area as ‘satellite lesions’. Candida tends to invade the skin folds and the foreskin of male babies.

Causes of nappy rash The main predisposing factor in all types is dampness due to urine and faeces. It is far less common since the use of disposable nappies. Other causes or aggravating factors are: • • • • • • • •

a tendency of the baby to eczema a tendency of the baby to seborrhoeic dermatitis infection, especially Candida (thrush) rough-textured nappies detergents and other chemicals in nappies plastic pants (aggravates wetness) excessive washing of the skin with soap too much powder over the nappy area (avoid talcum powders) • teething aggravates (punched out lesions)

Uncommon causes Psoriatic nappy rash This presents as a non-scaling eruption, primarily on the napkin area, but can extend to the flexures, trunk and limbs. The edge of the rash is sharply demarcated. The typical psoriatic scale is absent. It tends to occur in the first weeks of life. There is usually a family history. Infections Bacterial infections to consider include staphylococcal folliculitis, impetigo and perianal

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Common skin problems streptococcal dermatitis. Culture of the lesion will reveal the cause. Impetigo If there is Staphylococcus superinfection, bullae and pus-filled blisters will be present. Histiocytosis X (Letterer–Siwe syndrome) There is a similar rash to seborrhoeic dermatitis but the lesions are purpuric. In this serious syndrome the child is very ill and usually lymphadenopathy and hepatosplenomegaly may be found. Zinc deficiency May be more common than realised.

Management

Medical treatment Some principles follow: • The cornerstone of treatment is prevention. • Emollients should be used to keep skin lubricated (act as a barrier), e.g. zinc oxide (best) or white soft paraffin or a mixture of zinc oxide and castor oil or Vaseline. • A mild topical corticosteroid is the treatment of choice. • It is usual to add an antifungal agent. • Be careful of excessive use of corticosteroids, especially fluorinated steroids.

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• If infection is suspected, confirm by swab or skin scraping. • Consider a combined steroid and antifungal agent e.g. Hydrozole. Treatment: Atopic dermatitis

1% hydrocortisone

Seborrhoeic dermatitis

1% hydrocortisone + ketoconazole cream

Candida

topical nystatin at each nappy change

Widespread (Candida present)

1% hydrocortisone cream mixed in equal quantities with nystatin or clotrimazole cream (apply tds or qid after changes)

Psoriatic dermatitis

tar preparation, or 1% hydrocortisone

Impetigo

topical mupirocin; oral antibiotics if severe

Basic care (instructions to patients): 1 Keep the area dry. Change wet or soiled nappies frequently and as soon as you notice them. Use highly absorbent disposable nappies. 2 After changing, gently remove any urine or moisture with diluted sorbolene cream or warm water. 3 Wash gently with warm water, pat dry (do not rub) and then apply any prescribed cream or ointment to help heal and protect the area. Vaseline or zinc cream applied lightly will do. Stoma adhesive powder is an excellent protector. 4 Expose the bare skin to fresh air wherever possible. Leave the nappy off several times a day, especially if the rash is severe. 5 Do not wash in soap or bathe too often—once or twice a week is enough. 6 Avoid powder and plastic pants. 7 Use special soft nappy liners that help protect the sensitive skin. 8 Thoroughly rinse out any bleach or disinfectants.

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FACIAL RASHES Common facial skin disorders include acne, rosacea, peri-oral dermatitis and seborrhoeic dermatitis. These conditions must be distinguished from lupus erythematosus (discoid LE is more common).

Acne5 Acne is inflammation of the sebaceous (oil) glands of the skin (see FIG.  123.12). At first there is excessive sebum production due to the action of androgen. These glands become blocked (blackheads and whiteheads) due to increased keratinisation of the sebaceous duct. A secondary bacterial infection due to Propionibacterium acnes in the sebum produces lipases with the resultant free fatty acids, thus provoking inflammation characterised by red papules, pustules, nodules and cysts. Consider PCOS as a causative condition. Types10 • Infantile. Occurs in the first few months of life, mainly on the face. Affects mainly boys and is a self-limiting minor problem. Reassurance only is required in most cases. Some are severe and may scar. • Adolescent. The most common type, occurring around puberty. Acne is rare under 10 years; ages 13–16 years are commonest and it is worse in males aged 18–19 years. It is slightly less common in girls and worse around 14 years with premenstrual exacerbations.

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• Problems of the skin their doctor but also of their family. It should not be dismissed as a minor problem.

Education People with acne should understand its pathogenesis and be given leaflets with appropriate explanations. Myths must be dispelled. • It is not a dietary or infectious disorder. • It is not caused by oily hair or hair touching the forehead. • Ordinary chemicals (including chlorine in pools) do not make it worse. • Blackheads are not dirt, and will not dissolve in hot, soapy water. Reassure the patient that acne usually becomes less of a problem after the age of 25 years, although 15% of women and 5% of men continue to have acne as adults.

General factors FIGURE 123.12 Facial acne showing typical nodulocystic acne, a distressing problem which has been improved greatly by the development of isotretinoin

• Cosmetica. In females, associated with the prolonged use of skin care products (e.g. moisturiser, foundation cream and heavy make-up). • Oil. Occurs mainly on the legs of workers exposed to petroleum products. • Drug-induced. Especially steroids.

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History Enquire about use of skin preparations—therapeutic or cosmetic, exposure to oils, possible diet relationships and drug intake. Drugs that aggravate acne:11 • • • • • • •

corticosteroids chloral hydrate iodides or bromides lithium anti-epileptics (e.g. phenytoin) quinine various oral contraceptives

Management

Support and counselling Adolescents hate acne; they find it embarrassing and require the sympathetic care and support not only of

• Diet is considered not to be a causative factor but a healthy diet is encouraged. • Special soaps and overscrubbing are unhelpful. Use a normal soap and wash gently. • Avoid oily or creamy cosmetics and all moisturisers. Use cosmetics sparingly. • Avoid picking and squeezing blackheads. • Exercise, hair washing and shampoos are not of proven value. • Ultraviolet light such as sunlight may help improve acne but avoid overexposure to the sun. Principles of treatment5 1 Comedolysis: unblock the pores (follicular ducts) with keratolytics such as sulphur compounds, salicylic acid (5–10%); with benzoyl peroxide (2.5%, 5% or 10%) or retinoic acid (tretinoin) 0.01% gel, cream (0.025%, 0.05% or 0.1%), lotion or liquid; a tazarotene or adapalene (Differin) cream or gel. 2 Decrease bacteria in the sebum with systemic antibiotics—tetracyclines or erythromycin—or with topical antibiotics such as clindamycin and erythromycin. 3 Decrease sebaceous gland activity with oestrogens, spironolactone, cyproterone acetate, or isotretinoin. Note: Oral isotretinoin is teratogenic. Avoid concomitant use of oral and topical antibiotics.

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Common skin problems Recommended treatment regimens

Other therapies

Topical regimens

Severe cystic or recalcitrant acne (specialist care):

Suitable for mild to moderate acne. • Basic starting regimen is a retinoid (comedolytic) then a benzoyl peroxide (anti-bacterial) combination: — use tretinoin 0.01% gel or 0.05% cream or isotretinoin 0.05% gel cream or gel: apply each night (tretinoins are photosensitive) — if slow response after 6 weeks, add benzoyl peroxide 2.5% or 5% gel or cream once daily (in the morning). That is, maintenance treatment is: — tretinoin or isotretinoin at night — benzoyl peroxide gel mane — maintain for 3 months and review.

• spironolactone • isotretinoin (Roaccutane): outstanding agent • Dapsone

If a large area of mild truncal acne, consider topical salicyclic acid 3% in ethanol 70%, once daily. Alternative or add-on regimens, if persistent: • clindamycin HCl 600 mg in 60 mL of 70% isopropyl alcohol (e.g. ClindaTech). Apply with fingertips twice daily. • alternative bases for clindamycin, especially if the alcohol is too drying or irritating: — Cetaphil lotion 100 mL, or — ClindaTech solution 100 mL Clindamycin is particularly useful for pregnant women and those who cannot tolerate antibiotics or exfoliants.10 In more severe cases, combine with benzoyl peroxide (e.g. Duac). Others: • erythromycin 2% gel, apply bd • azelaic acid, apply bd • adapalene 0.1% cream or gel, apply once nocte • tazarotene 0.1% cream, apply once nocte

Oral antibiotics Use for inflammatory acne: (moderate to severe papulopustular) ± trunk involvement • doxycycline 100 mg per day or minocycline 100 mg per day • use half this dose if mild • reduce dosage according to response (e.g. doxycycline 50 mg per day) or minocycline 50 mg nocte (more adverse effects) • erythromycin or cotrimoxazole are alternatives • give a minimum 12 week trial; 6 months is standard. Avoid using antibiotics alone.

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Females not responding to first-line treatment: • combined oral contraceptive pill with a thirdgeneration progestogen (e.g. ethinyloestradiol/ cyproterone acetate: Diane-35 ED) Avoid higher dose levonorgestrel formulations and progestogen-only preparations. Note: Response to any acne treatment occurs in about 8 weeks or longer.

Common mistakes with acne • • • •

Not treating comedomes with a comedolytic Monotherapy (e.g. antibiotics only) Not using recommended combinations Not using isotretinoin for cystic acne

Rosacea Rosacea is a common persistent eruption of unknown aetiology. It is typically chronic and persistent with a fluctuant course. Clinical features2 • Mainly 30–50 years • Usually females of Celtic origin: ‘the curse of the Celts’ • On forehead, cheeks, nose and chin (see FIG. 123.13 and FIG. 123.14) • ‘Flushing and blushing’ (often precedes the rash) • Fluctuates from day to day • Peri-orbital and peri-oral areas spared • Vascular changes—erythema and telangiectasia • Inflammation—papules and pustules Complications • Blepharitis • Conjunctivitis, rarely keratitis and corneal ulcer • Associated rhinophyma in some cases Management4 • Apply cool packs if severe • Avoid factors that cause facial flushings (e.g. excessive sun exposure, heat, wind, alcohol, excessive exercise, hot baths, spicy foods, hot drinks—tea and coffee)

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• Problems of the skin metronidazole 0.75% gel bd or azelaic acid 15% gel bd or clindamycin 1% solution bd or erythromycin 2% gel bd or brimonidine 0.5% (a vasoconstrictor—helps red flush)

FIGURE 123.13 Rosacea: typical appearance with erythema, papules and pustules

Note: Hydrocortisone 1% cream is effective, but steroids are best avoided and strong topical steroids should not be used because of severe rebound vascular changes.

Laser therapy Telangectasia, erythema and rhinophymas respond to laser therapy.

Rhinophyma This is due to hypertrophy of the nasal sebaceous glands. There is no specific association with alcohol. May be associated with rosacea. Carbon dioxide laser therapy is the treatment of choice. Shave excision is also effective (see CHAPTER 59).

Peri-oral dermatitis

FIGURE 123.14 Rosacea: typical facial distribution

• Sun protection • Use a gentle soap-free cleanser

Clinical features • Acne-like dermatitis of lower face • Usually young women 20–50 years • May be seen in children and adolescents • ‘Muzzle area’ distribution around mouth and on chin, sparing adjacent peri-oral area (see FIG. 123.15 and 123.16); also in peri-orbital skin in men

Systemic antibiotics

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• Minocycline or doxycycline (first choice) 50 mg bd for a total of 8–10 weeks. Repeated for recurrences: avoid maintenance. If using doxycycline, start with 50 mg bd then 50 mg daily, wean slowly. • Erythromycin (second choice) • Metronidazole 200 mg bd for 10 days for resistant cases

Topical agents For mild erythema and inflammatory lesions: 2% sulphur in aqueous cream tds (milder cases) or (for more severe cases)

FIGURE 123.15 Peri-oral dermatitis: typical distribution

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TINEA Tinea (ringworm infections) is caused mainly by three major classes of dermatophytic organisms that have the ability to invade and proliferate in keratin of the skin, nails and hair. It is most useful to perform skin scrapings and microscopy to look for encroaching septate hyphae.12 Confirm the diagnosis by fungal culture. Tinea cruris is presented in CHAPTER 124.

Tinea pedis (athlete’s foot) Tinea pedis is usually caused by Trichophyton rubrum and is the commonest type of fungal infection in humans. Candida intertrigo and interdigital maceration (alone without secondary tinea) in particular and also erythrasma, eczema and psoriasis, are important differential diagnoses. FIGURE 123.16 Peri-oral dermatitis: this eruption (which has been linked with the use of fluorinated steroid creams on the face) frequently begins in the nasolabial fold. Papules and pustules occur on a background of erythema and scaling.

• • • • •

Frequently begins at the nasolabial folds Multiple small red macules and papules On a background of erythema and scaling Burning and irritation May be associated seborrhoeic dermatitis on scalp and head • May be related to pregnancy and oral contraception • Related to the use of creamy cosmetic products • May be related to repeated topical corticosteroid (especially fluorinated) use (may be a rebound on ceasing it) Treatment • Doxycycline or minocycline for 6–8 weeks (e.g. doxycycline or minocycline 100 mg daily). Takes 10–14 days to respond. Use erythromycin if tetracyclines contraindicated. The rash sometimes recurs after the antibiotics are discontinued, even much later, but further courses can be used. • Discontinue any topical corticosteroid therapy (tends to flare initially) and all ‘creamy’ preparations including cleansers, moisturisers and make-up. • Topical: ketoconazole cream and shampoo for 10–14 days or metronidazole 0.75% gel twice daily or clindamycin 1% lotion twice daily.

Symptoms The commonest symptoms are itchiness and foot odour. Sweat and water make the top layer of skin white and soggy. There is scaling, maceration and fissuring of the skin between the fourth and fifth toes and also third and fourth toes. Advice to patients • Keep your feet as clean and dry as possible. • Carefully dry your feet after bathing and showering. • After drying your feet, use an antifungal powder, especially between the toes. • Remove flaky skin from beneath the toes each day with dry tissue paper or gauze. • Wear light socks made of natural absorbent fibres, such as cotton and wool, to allow better circulation of air and to reduce sweating. Avoid synthetic socks. • Change your shoes and socks daily. Spray shoes with an antifungal agent. • If possible, wear open sandals or shoes with porous soles and uppers. • Go barefoot whenever possible. • Use thongs in public showers such as at swimming pools (rather than bare feet). Treatment Clotrimazole 1%, ketoconazole 2%, terbinafine 1% cream or gel, or miconazole 2% cream or lotion or bifonazole 1% (daily), applied after drying, bd or tds for 2–3 weeks. Preferable to use terbinafine 1% daily for 1 week and review. If severe and spreading,

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prescribe oral griseofulvin (see Tinea corporis) or terbinafine for up to 6 weeks after confirming the diagnosis by fungal culture. Castellani paint may be helpful for macerated areas.

Tinea corporis10 Tinea corporis (ringworm infection of the body) is usually caused by Trichophyton rubrum (60%) or Microsporum canis.12 Strongly related to exposure to cats and dogs, while the guinea pig is a potent source of facial tinea (can present as pustular folliculitis). Clinical features • Spreading circular erythematous lesions (see FIG. 123.17) • Slight scaling or vesicles at the advancing edge • Central areas usually normal • Mild itch • May involve hair, feet and nails

palmar aspects of the fingers. It also commonly presents on the dorsum of the hand and is typically unilateral. Differential diagnoses are atopic dermatitis and contact dermatitis of the hands. Clinical features • Usually unilateral • Spreading edge • Erythematous; fine scaling • May be associated with tinea pedis Treatment • Topical clotrimazole 1%, ketoconazole 2% or miconazole 2% cream for 6 weeks or, if resistant, terbinafine 250 mg or griseofulvin 500 mg daily for 6 weeks.

Tinea capitis4 In Australia tinea capitis is usually due to M. canis acquired from cats and dogs. Clinical features • Usually in children (rare after puberty) • Patches of partial alopecia • Scaly patches • Small broken-off hair shafts • Hairs fluoresce yellow-green with Wood’s light (not invariably, e.g. with Trichophyton tonsurans infection)

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FIGURE 123.17 Multiple ringworm (tinea corporis): this 12-year-old boy presented with a two-week history of an increasing number of pruritic scaling erythematous lesions on his face, neck and upper chest. Fungal scrapings confirmed the cause as Microsporum canis. Photo courtesy Robin Marks

Treatment • Clotrimazole 1% or miconazole 2% cream or bifonazole 1% cream or ketoconazole 2% cream, applied bd for 2–4 weeks or terbinafine 1% cream or gel once daily for 1 week • Oral terbinafine or griseofulvin for up to 6 weeks if no response or if widespread

Tinea manuum Tinea manuum is ringworm infection of the hand, usually presenting with scaling of the palms and

Treatment griseofulvin (o): adults 500 mg daily; children 10 mg/kg/day (max. 500 mg) 4–8 week course or ketoconazole (o): adults 200 mg/d, 4–8 weeks; children 5 mg/kg/d (max. 200 mg) or terbinafine: adults 250 mg/d, 4 weeks; children 62.5–125 mg Also take hair plucking and scale for culture. Selsun or ketoconazole shampoo twice weekly.

Kerion Kerion of the scalp and beard area may present like an abscess—tender and fluctuant. Usually occurs on the scalp, face or limbs. A fungal cause is possible if the hairs are plucked out easily and without pain (if painful and stuck, bacterial infection is likely).

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Tinea incognito This is the term used for unrecognised tinea infection due to modification with corticosteroid treatment. The lesions are enlarging and persistent, especially on the groins, hands and face. The sequence is initial symptomatic relief of itching, stopping the ointment or cream and then relapse.

Tinea unguium (toenails and fingernails) Refer to CHAPTER 129.

Pityriasis versicolor (tinea versicolor)12 Pityriasis versicolor is a superficial yeast infection of the skin (usually on the trunk) caused by Malassezia sp.). The old name, tinea versicolor, is inappropriate because the problem is not a dermatophyte infection. It occurs worldwide but is more common in tropical and subtropical climates. There are two distinct presentations: 1 reddish brown, slightly scaly patches on upper trunk 2 hypopigmented area that will not tan, especially in suntanned skin

FIGURE 123.19 Pityriasis versicolor: typical truncal distribution (corresponding area on back)

• Patches may coalesce • May involve neck, upper arms, face and groin • Slight scaling when scratched indicates active infection • Scales removed by scraping show characteristic short stunted hyphae with spores on microscopy • Often recurrent, especially in summer

The term ‘versicolor’ means variable colours. Clinical features • Mainly young and middle-aged adults • Brown on pale skin or white on tanned skin (see FIG. 123.18) • Trunk distribution (see FIG. 123.19)

FIGURE 123.18 Pityriasis versicolor showing the hypopigmented scaly patches on a suntanned skin mainly affecting the trunk

Differential diagnosis Seborrhoeic dermatitis of trunk (more erythematous), pityriasis rosea, vitiligo, pityriasis alba (affects face). Treatment4,12 selenium sulphide (Selsun Yellow shampoo). Wash area, leaving on for 5–10 minutes, then wash off. Do this daily for 2 weeks (at night), then every second day for 2 weeks, then monthly for 12 months. Shampoo scalp twice weekly and/or econazole 1% solution to wet skin, leave overnight, for 3 nights or miconazole or ketoconazole shampoo, once daily for 10 minutes and wash off, for 10 days or terbinafine 1% cream twice daily for 2 weeks or sodium thiosulphate 25% solution bd for 4 weeks (wash off after 10 minutes) or (for persistent or recurrent problems)

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ketoconazole 200 mg (o) daily for 7–10 days or 400 mg (o) single dose12 or itraconazole 200 mg (o) once daily for 5 days or once every 30 to 90 days4 Note: • Ketoconazole may be hepatotoxic. Always perform LFTs first (do not use long-term). Griseofulvin is inappropriate because the rash is not a fungal infection. • Warn patients that the white patches will take a long time to disappear and that cure does not equate with disappearance.

Dry skin Disorders associated with scaling and roughness of the skin include: • atopic dermatitis—all types (e.g. pityriasis alba, nummular eczema, asteatotic dermatitis) • ageing skin • psoriasis • ichthyotic disorders • keratosis pilaris Itching may be a feature of dry skin (but is not inevitable). Aggravating factors: • • • • •

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low humidity (e.g. heaters, air-conditioners) frequent immersion in water heat/hot water toilet soaps swimming in chlorinated pools

Management • Avoid a dry home environment if possible. • Reduce bathing. • Bathe or shower in tepid water. • Use a soap substitute (e.g. Dove or Neutrogena/ Cetaphil lotion). • Pat dry—avoid vigorous towelling. • Rub in baby oil after bathing (better than adding oil to the bath). • Avoid wool next to the skin (wear cotton). • Use emollients/moisturisers (e.g. Alpha-Keri lotion, QV skin lotion, Nutraplus).

Sunburn Sunburn is normally caused by UV-B radiation, which penetrates the epidermis and superficial dermis, releasing substances such as leucotrienes and histamines, which cause redness and pain. Severe

sunburn may develop on relatively dull days because thin clouds filter UV-B poorly. Beware of solariums and the midday sun. Clinical presentations: Minor sunburn:

Mild erythema with minimal discomfort for about 3 days.

Moderate:

Moderate to severe erythema within a few hours; worse the following day—red, hot and moderately painful. Settles in 3–4 days with some desquamation.

Severe:

Classic signs of inflammation— redness, heat, pain and swelling. Skin develops vesicles and bullae. Systemic features develop with very severe burns (e.g. fever, headache, nausea, delirium, hypotension). May require IV fluids.

Differential diagnosis • General photosensitivity: consider drugs (e.g. thiazide diuretics, tetracyclines, sulphonamides, phenothiazines, griseofulvin, NSAIDs, isotretinoin) • Acute systemic lupus erythematosus may present as unexpectedly severe sunburn • Photocontact dermatitis Treatment Hydrocortisone 1% ointment or cream for severe sunburn on face, early. Use hydrocortisone 1% or 0.02% betamethasone valerate for other areas. Repeat in 2–3 hours and then the next day. Hydrocortisone is not useful after 24 hours and should be used for unblistered erythematous skin, not on broken skin. Oral aspirin eases pain. Oil in water baths or bicarbonate of soda paste may help and wet applications such as oily calamine lotions or simply cool compresses may give relief. Prevention Avoid direct exposure to summer sunlight during peak UV periods (10 am to 3 pm). Use natural shade— beware of reflected light from sand or water and light cloud. Use a sunscreen with a minimum of SPF 30. Wear broad-brimmed hats and protective clothing.

Photo-ageing/wrinkles Prevention • Stop smoking. • Avoid cold, dry and windy conditions.

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Common skin problems • • • •

Avoid exposure to the sun. Use an SPF 30 or more sunscreen during the day. Avoid soaps with perfume and alcohol. Wash with a ‘neutral’ mild soap (e.g. Neutrogena, max. twice daily) and pat dry. • Apply a simple moisturiser immediately after the bath. Treatment (options) • Optimal nutrition—diet rich in fruit and vegetables • Alpha hydroxy acid preparations (e.g. Elucent cream) • Tretinoin (Retin-A) cream: apply once daily at bedtime (on dry skin) test for skin irritation by gradual exposure (e.g. 5 minutes at first, wash off, then 15 minutes until it can be left on overnight) • Topical olive oil • Lac-Hydrin (US): 12% solution may be effective alternative; other lactic acid preparations may be useful • Botulinum toxin injections

SWEATING AND ODOUR DISORDERS

Hyperhidrosis (excessive sweating)13 This problem is usually idiopathic and prolonged. Clinical features • Male = female incidence • Affects axilla, groin, soles and palms • Onset usually around puberty • Tends to improve after age 25 years • Family history • ± Bromhidrosis (malodorous perspiration) • Usually independent of climate • Exacerbated by stress and heat; stops during sleep Causes (secondary/pathological) • Fever/sepsis • Thyrotoxicosis • Acromegaly • Diabetes mellitus • Phaeochromocytoma • Drugs: alcohol/narcotics/antidepressants • Some neurological conditions (e.g. Parkinson) • Malignancies especially lymphomas Treatment5 • Reduce caffeine intake

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• Avoid known aggravating factors • First use: an aluminium chlorohydrate-containing antiperspirant deodorant (spray or roll on each morning) in axilla (suitable for palms and soles) or aluminium chloride hexahydrate 20% solution or spray—apply to affected areas at night when the area is dry (best for palms and soles). Irritation is a problem

Additional treatments • Iontophoresis (in specialist centres) to hands and feet • Injection of botulinum toxin into dermis of affected area. Proven effectiveness for axilla and palms • (Trial of) probanthine aluminium chloride 20% in alcohol solution to localised area • Consider oral anticholinergics (e.g. oxybutynin) and beta blockers

Palmar hyperhidrosis Treatment • Aluminium chloride 20% in alcohol solution (Driclor) • Iontophoresis • Consider surgical sympathectomy

Axillary hyperhidrosis14 Treatment • Explanation and reassurance • See treatment of general hyperhidrosis • Aluminium chloride 20% in alcohol solution (Driclor); apply nocte for 1 week, then 1–2 times weekly or as necessary • Botulinum toxin injection

Surgery Wedge resection of a small block of skin and subcutaneous tissue from axillary vault. Define sweat glands with codeine starch powder. The area excised is usually about 4 × 2.5 cm.

Body odour/bromhidrosis Cause: poor hygiene, excessive sweating and active skin bacteria Main focus: axilla and groin Precautions: consider uraemia, vaginitis

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Treatment • Scrub body, especially groins and axillae, with deodorant soap at least morning and night • Try an antibacterial surgical scrub • Keep clothes clean, launder regularly • Choose suitable clothes—natural fibres (e.g. cotton), not synthetics • Use an antiperspirant deodorant • Alternative soap—pine soap • Diet: avoid garlic, fish, asparagus, onions, curry • Reduce caffeine (coffee, tea and cola drinks), which stimulates sweat activity • Consider a sugar-free diet • Shave axillary hair • Axillary wedge resection for excessive perspiration

Foot odour (smelly and sweaty feet) Includes pitted keratolysis secondary to hyperhidrosis (common in teenagers).

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Treatment (with options) • Education and reassurance • Wear cotton or woollen socks • Aluminium chloride 20% in alcohol solution (Driclor, Hydrosol) or Neat Feet—apply nocte for 1 week, then 1–2 times weekly as necessary • Shoe liners (e.g. ‘Odor eaters’), charcoal inner soles • Apply undiluted Burow’s solution after a shower or bath • Formalin 1–5% soaks every second night • Iontophoresis • The teabag treatment (if desperate): — prepare 600 mL of strong hot tea (from two teabags left in water for 15 minutes) — pour the hot tea into a basin with 2 L of cool water — soak the feet in this for 20–30 minutes daily for 10 days, then as often as required

SKIN DISORDERS OF FEET Two conditions commonly seen in teenagers are pitted keratolysis and juvenile plantar dermatosis.

Pitted keratolysis This common malodorous condition known as ‘stinky feet’ or ‘sneakers feet’, usually seen in 10–14 year olds, is related to sweaty feet. It is caused by an overgrowth of the bacterium Kytococcus sedentarius on the feet between the toes. It has a ‘honeycomb’ pitted appearance with maceration between the toes,

resembling tinea. For mild cases no specific treatment is needed other than attending to hyperhidrosis. Otherwise, treatment includes keeping the feet dry and using an ointment such as Whitfield’s (benzoic acid + salicyclic acid) or benzoyl peroxide 5% gel or an imidazole or erythromycin 2% gel or clindamycin 1% lotion to remove the responsible organism. Try oral roxithromycin if topical therapy fails. Change to all-leather shoes with charcoal liners. Use a drying agent to decrease sweating.

Juvenile plantar dermatosis ‘Sweaty sock dermatitis’ is a painful condition of weight-bearing areas of the feet. The affected skin is red, shiny, smooth and often cracked. It is rare in adults. The treatment is to change to leather or open shoes and to cotton socks. A simple emollient cream gives excellent relief.

Prickly heat (miliaria/heat rash) • Avoid sweating as much as possible. • Keep the skin dry and cool (e.g. fan, airconditioner). • Dress in loose-fitting cotton clothing. • Reduce activity. • Avoid frequent bathing and overuse of soap. • Dilute topical steroid cream bd. Treatment lotion: salicylic acid 2%, menthol 1%, chlorhexidine 0.5% in alcohol or calamine lotion or Egozite (infants), Isophyl (adults) If severe: hydrocortisone + clotrimazole cream (brief spells only). Prevention • Ego Prickly Heat powder

CHILBLAINS AND FROSTBITE

Chilblains (perniosis) These are localised inflammatory reactions, caused by prolonged exposure to cold, usually on toes and fingers (see FIG. 123.20) but also on heels, nose, ears and thighs (horse riding). Precautions • Think Raynaud phenomenon. • Protect from trauma and secondary infection. • Do not rub or massage injured tissues.

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Treatment • Elevate affected limb • Rewarm in water just above body temperature 40°C (104°F) or use body heat (e.g. in axillae) • Avoid thawing or refreezing • Surgical debridement • Don’t debride early (wait until dead tissue dried) • Don’t drink alcohol or smoke • For blistering, apply warm water compresses for 15 minutes every 2 hours

Drug treatment • Analgesics FIGURE 123.20 Chilblains (perniosis) showing erythematous purplish swellings on fingers

• Do not apply heat or ice. • Wear warm gloves and socks. Differences between chilblains and Raynaud phenomenon: • • • •

chilblains are intermittent without a pattern itchy at the onset patchy appearance (can be more generalised) Raynaud has two or three phases including a ‘dead white’ phase with line of demarcation • it is significant if it extends to the MCP joints Treatment • Elevate affected part • Warm gradually to room temperature

Drug treatment • Potent topical corticosteroid (see TABLE 121.9 in CHAPTER 121) twice daily • It severe and recurrent, apply glyceryl trinitrate vasodilator spray or 0.2% ointment or patch sparingly once daily (use plastic gloves and wash hands for ointment)

Other treatment • Drink rum at night • Nifedipine CR 30 mg (o) once daily (if very severe) • UVB therapy weekly for 4–6 weeks prior to cold weather

Frostbite Treatment depends on severity. Precautions • Watch for secondary infection, tetanus, gangrene.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Atopic eczema • Body odour • Contact dermatitis • Dry skin • House dust mite management • Nappy rash • Pityriasis rosea • Psoriasis • Ringworm (tinea) • Rosacea and perioral dermatitis • Seborrhoea in infants • Sunburn • Tinea pedis

References 1 Britt H, Miller GC, Charles J. General practice activity in Australia 2009–11. BEACH data. Sydney: Australian Institute of Health and Welfare and the University of Sydney, December 2010. 2 Berger P. Skin Secrets. Sydney: Allen & Unwin, 1991: 93–170. 3 Brown P. Dermatitis/eczema. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 142–4. 4 Moulds R (Chair). Therapeutic Guidelines: Dermatology (Version 4) Melbourne: Therapeutic Guidelines Ltd, 2014 (eTG Complete). 5 Clarke P. Psoriasis. Aust Fam Physician, 2011; 40 (7): 468–73. 6 Tritton SM, Cooper A. Management of psoriasis. Update. Medical Observer, 30 November 2007: 27–30. 7 Howard A, Gamboni S. Psoriasis: how to treat. Australian Doctor, 18 January 2013: 17–24. 8 Gallachio V. Nappy rash. Aust Fam Physician, 1988; 17: 971–2. 9 Aldridge S. Nappy rash. Australian Paediatric Review, 1991; 2 (1): 2. 10 Gin D. Tinea infections. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 511–13. 11 Sullivan J, Preda V. A clinically practical approach to acne. Medicine Today, 2008; 9 (1): 47–56.

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12 Hunter JAA, Savin JA, Dahl MV. Clinical Dermatology (3rd edn). Oxford: Blackwell Scientific Publications, 2002: 171–4. 13 Hunter JAA, Savin JA, Dahl MV. Clinical Dermatology (3rd edn). Oxford: Blackwell Scientific Publications, 2002: 159–60. 14 Perera E, Sinclair M. Hyperhidrosis and bromhidrosis— a guide to assessment and management. Aust Fam Physician, 2013; 42 (5): 266–9.

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Resources DermNet NZ: the dermatology resource Therapeutic Guidelines: eTG Complete

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They say love’s like the measles—all the worse when it comes late in life. Douglas Jerrold (–) The sudden appearance of a rash, which is a common presentation in children (see CHAPTER 93), usually provokes patients and doctors alike to consider an infectious aetiology, commonly of viral origin. However, an important cause to consider is a reaction to a drug. A knowledge of the relative distribution of the various causes of rashes helps with the diagnostic methodology. Many of the eruptions are relatively benign and undergo spontaneous remission. Fortunately, the potentially deadly rash of smallpox is no longer encountered. A list of important causes of acute skin eruptions is presented in TABLE 124.1. Serious eruptions not to be missed and pitfalls are outlined in TABLE 124.2.

A diagnostic approach The diagnostic approach to skin eruptions presupposes a basic knowledge of the causes; a careful history and physical examination should logically follow. The history should include: • • • • • • • • • •

site and mode of onset of the rash mode of progression drug history constitutional disturbance (e.g. pyrexia, pruritus) respiratory symptoms herald patch? diet—unaccustomed food exposure to irritants contacts with infectious disease bleeding or bruising tendency The examination should include:

• skin of whole body • nature and distribution of rash, including lesion characteristics • soles of feet • nails • scalp • mucous membranes

• oropharynx • conjunctivae and the lymphopoietic system (? lymphadenopathy ? splenomegaly) Laboratory investigations may include: • a full blood examination • syphilis serology • Epstein–Barr mononucleosis test • HIV test • rubella haemagglutination tests (x 2) • viral and bacterial cultures

Dermatological manifestations of systemic disease • Painful red nodules — erythema nodosum • Photosensitive rash — dermatomyositis (inflamed muscles + rash)—cause unknown, malignancy known association • Palpable purpura — vasculitis—primary or secondary (e.g. sepsis), various causes • Painful ulceration — pyoderma granulosum Causes — inflammatory bowel disease — rheumatoid arthritis — haematological malignancies

Acute skin eruptions in children The following skin eruptions (some of which may also occur in adults) are outlined in CHAPTER 93. • Measles • Rubella • Viral exanthem (fourth disease) • Erythema infectiosum (fifth disease) • Roseola infantum (sixth disease) • Kawasaki disorder • Varicella • Impetigo

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Important causes of acute skin eruptions

Table 124.2

Acute skin eruptions

Serious disorders not to be missed Maculopapular Measles Rubella Scarlet fever Viral exanthem (fourth disease) Erythema infectiosum (slapped cheek disease or fifth disease)

Vascular: • Henoch–Schönlein purpura • Stevens–Johnson syndrome • other vasculitides Infection: • purpura of meningococcus, typhoid, other sepsis

Roseola infantum (sixth disease)

• primary HIV infection

EBM (primary or secondary to drugs)

• folliculitis (e.g. pseudomonas, staphylococcus)

Primary HIV infection

• secondary syphilis

Secondary syphilis

• scarlet fever

Pityriasis rosea

Other:

Guttate psoriasis

• erythema nodosum

Urticaria

Pifalls (often missed)

Erythema multiforme (may be vesicular)

• guttate psoriasis

Drug reaction

• Epstein-Barr virus (EBV) mononucleosis

Scabies

• arbovirus infection (e.g. dengue, Ross River fever, Barmah Forest virus, Japanese encephalitis)

Ross River and Barmah Forest infection Maculopapular vesicular Varicella

• scabies • Kawasaki disease

Herpes zoster

• eczema herpeticum

Herpes simplex

• zoonoses (e.g. listeriosis, Q fever)

Eczema herpeticum

Rarities:

Impetigo

• filovirus diseases (e.g. Ebola, Marburg virus)

Hand, foot and mouth disease

• erythema multiforme

Drug reaction Maculopapular pustular Pseudomonas folliculitis Staphylococcus aureus folliculitis Impetigo Purpuric (haemorrhagic) eruption

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Purpura (e.g. drug-induced purpura, severe infection) Vasculitis (vascular purpura): • Henoch–Schönlein purpura • polyarteritis nodosa

Pityriasis rosea Pityriasis rosea is a common but mild acute inflammatory skin disorder. Although a viral agent

(possibly human herpes virus 7) is suspected to be the cause, no infective agent has been demonstrated. Clinical features • Any age, mainly young adults (aged 15–30 years) • Preceding oval or round herald patch (1–2 weeks); can have 2–3, but none in 20% (can be mistaken for ringworm) • Oval, salmon-pink or copper-coloured eruption 0.5–2 cm • Coin-shaped patches with scaly margins 1–2 cm • Follows cleavage lines of skin (see FIGS 124.1 and 124.2) with ‘fir tree’ pattern on back • On trunk (‘T-shirt’ distribution) • Occurs also on upper arms, upper legs, lower neck, face (rare) and axillae • Patients not ill

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Differential diagnosis Herald patch: tinea corporis/discoid eczema. Generalised rash: seborrhoeic dermatitis (slower onset), guttate psoriasis, drug eruption (see TABLE 124.3), secondary syphilis.

Table 124.3

Drugs that cause eruptions suggestive of pityriasis rosea1

Main drugs: • captopril • gold salts • penicillamine Others: • arsenicals • barbiturates • bismuth • clonidine • metoprolol • metronidazole

FIGURE 124.1 Pityriasis rosea in a 10-year-old child showing the salmon pink scaly eruption following skin cleavage lines—the ‘Christmas tree’ pattern

widespread and symmetrical, in old ‘bathing trunk’ distribution follows cleavage lines of skin

oval salmon-pink maculopapules herald patch

‘Christmas tree pattern’

FIGURE 124.2 Pityriasis rosea: typical distribution

• Itch varies from nil to severe (typically minor itching) • Scale is on inner aspect of active border

Prognosis A mild, self-limiting disorder with spontaneous remission in 2–10 weeks (average 2–5). It does not appear to be contagious. Recurrence is rare. Management • Explain and reassure with patient education handout.2 • Bathe and shower as usual, using a neutral soap (e.g. Neutrogena). • Use a soothing bath oil (e.g. QV Bath Oil). • For a bothersome itch, apply mild topical corticosteroid ointment or calamine lotion with 1% phenol or menthol 1% in aqueous cream. • For a severe itch, use a potent topical corticosteroid once or twice daily or oral corticosteroids. • UV therapy is good but, like psoriasis, sunburn must be avoided. Expose the rash to sunlight or UV therapy (if florid) three times a week, with care.

Secondary syphilis The generalised skin eruption of secondary syphilis varies and may resemble any type of eruption from

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psoriasiform to rubelliform to roseoliform. The rash usually appears 6–8 weeks after the primary chancre. Clinical features (rash) • Initially faint pink macules • Then becomes maculopapular • Can involve whole body (see FIG. 124.3) • Palms and soles involved • Dull red in colour and round • More prolific on flexor surfaces • Symmetrical and relatively coarse • Asymptomatic

• Can occur on extremities including palms and soles (see FIG. 124.4) • Non-pruritic

face and trunk

lymphadenopathy erythematous maculopapular rash

snail track ulcers? symmetrical, coarse, reddish rash

lymphadenopathy

widespread Note: mimics glandular fever

FIGURE 124.4 Primary HIV infection: typical features

If such a rash accompanied by an illness like glandular fever occurs, HIV infection should be suspected and specific tests ordered.

Guttate psoriasis FIGURE 124.3 Secondary syphilis: typical features

Associations (possible) • Mucosal ulcers: ‘snail track’ • Lymphadenopathy • Patchy hair loss • Condylomata lata Treatment • As for primary syphilis (see CHAPTER 119)

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Primary HIV infection

Guttate psoriasis is the sudden eruption of small (2–10 mm in diameter), very dense, round, red papules of psoriasis on the trunk (see FIGS 124.5 and 124.6). The rash may extend to the proximal limbs. It is usually seen in children and adolescents and often precipitated by a streptococcal throat infection.

? preceding sore throat scaling ‘drop-like’ lesions, mainly on trunk

A common manifestation of the primary HIV infection is an erythematous, maculopapular rash, although other skin manifestations such as a roseolalike rash and urticaria can occur. Clinical features • Symmetrical • May be generalised • Lesions 5–10 mm in diameter • Common on face and/or trunk

FIGURE 124.5 Guttate psoriasis: small, drop-like lesions, mainly on trunk

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rubelliform rash pink to purple maculopapular raised rash extensor surfaces on limbs

FIGURE 124.7 Epstein–Barr mononucleosis: typical rash induced by penicillin, amoxycillin or ampicillin

DRUG ERUPTIONS

FIGURE 124.6 Guttate psoriasis in a child showing the small dense, round erythematous papules of psoriasis on the trunk

The rash soon develops a white can persist for up to 6 months. spontaneous resolution or enlarge which may become chronic. Treatment includes UV light preparations.

silvery scale. It It may undergo to form plaques,

Table 124.4

Most common types of drug eruptions (after Thomas)3 Relative frequency (%)

as well as tar

Epstein–Barr mononucleosis The rash of EBM is almost always related to antibiotics given for tonsillitis (see FIG. 28.3 in CHAPTER 28). The primary rash, most often non-specific, pinkish and maculopapular (similar to that of rubella), occurs in about 5% of cases only. The secondary rash, which can be extensive and sometimes has a purplishbrown tinge, is most often precipitated by one of the penicillins (see FIG. 124.7): • ampicillin 90–100% association • amoxycillin 90–100% association • penicillin up to 50%

A rash is one of the most common side effects of drug therapy, which can precipitate many different types of rash; the most common is toxic erythema (see TABLE  124.4). Most drug-evoked dermatoses have an allergic basis with the eruption appearing approximately 10 days after administration, though much sooner if previously sensitised.3 The most common drugs that cause skin eruptions are summarised in TABLE 124.5.

Toxic erythema Urticaria/angioedema Erythema multiforme Eczematous dermatitis Fixed drug reaction Photosensitivity Others: • acne form • psoriasiform • pigmentation • erythema nodosum • toxic epidermal necrolysis • vasculitis/purpuric • pigmentary • exfoliative Source: After Thomas3

45 25 7 5 3 3

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Table 124.5

• Problems of the skin

The most common drugs that cause skin eruptions

Antimicrobials:

Penicillin/cephalosporins Sulphonamides Tetracyclines Nitrofurantoin Streptomycin Griseofulvin Metronidazole Antiretroviral agents Trimethoprim Dapsone

Diuretics:

Thiazides Frusemide

Anti-epileptics:

Carbamazepine Phenytoin

When taking a history it is appropriate to enquire about medications or chemicals that may be overlooked such as aspirin, vitamins, toxins, laxatives and medicated toothpaste.

Toxic erythema The maculopapular erythematous eruption is either morbilliform or scarlatiniform. It is more pronounced on the trunk than on the limbs and face but may become confluent over the whole body (see FIG. 124.8). Drugs that typically cause toxic erythema include: • antibiotics: — penicillin/cephalosporins — sulphonamides • thiazides • carbamazepine • barbiturates • allopurinol • gold salts

Lamotrigine Tranquillisers:

Phenothiazines Barbiturates Chlordiazepoxide

Anti-inflammatory and analgesics:

Gold salts Aspirin/salicylates Codeine/morphine Pyrazalones (e.g. BTZ) Other NSAIDs

Hormones:

Combined oral contraceptive Stilboestrol Testosterone

Others:

Phenolphthalein Serum Amiodarone Cytotoxic drugs Quinidine/quinine Bromides and iodides

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Sulphonylureas Allopurinol Warfarin Amphetamines

The most important fact to realise about drug reactions is that their appearances are so variable— they may mimic almost any cutaneous disease and, in addition, create unique appearances of their own.

FIGURE 124.8 Toxic erythema: maculopapular erythematous scarlatiniform eruption caused by amoxicillin

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Acute skin eruptions

Photosensitivity Several antibiotics increase the sensitivity of the skin to UV light and may lead to a rash with a distribution according to sunlight exposure. The photosensitive rash may be erythematous, resembling sunburn; eczematous; or vesiculobullous. Typical drugs: • • • • • • • • • •

tetracyclines sulphonamides/sulphonylureas thiazides and frusemide phenothiazines retinoids amiodarone griseofulvin antihistamines, especially promethazine antimalarials psoralens

Table 124.6

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Drugs with the highest skin reaction rates4

Penicillin and derivatives Sulphonamides* Trimethoprim* Thiazide diuretics Allopurinol* Dapsone* NSAIDs, esp. piroxicam* Nevirapine*, abacavir* Barbiturates Quinidine Anti-epileptics (phenytoin, lamotrigine*) Blood products Gold salts

Fixed drug eruption The mechanism of fixed drug eruption is unknown. The most commonly affected areas are the face, hands and genitalia. The lesions, which are usually bright red but can have other characteristics, are fixed in site and appearance within hours of the drug’s administration. Typical drugs: • • • • • • • •

phenolphthalein tetracyclines penicillins sulphonamides salicylates oral contraceptive pill barbiturates quinine

Treatment of any drug reaction The important aspect of management is to recognise the offending agent and withdraw it. The rash should be treated according to its nature. There is a therapeutic impulse to prescribe antihistamines but they should be reserved for the treatment of urticarial drug eruptions. They may actually delay healing in purpuric, erythematous and vesiculobullous reactions. Antihistamines may act as allergens and show cross-sensitivity with phenothiazines, sulphonamides and topical antihistamines. TABLE  124.6 lists drugs with the highest skin reaction rates.

* Severe reactions

ERYTHEMA

Erythema multiforme Erythema multiforme is an acute eruption affecting the skin and mucosal surfaces. Clinical features • Mainly in children, adolescents, young adults • Symmetric • Erythematous papules • Mainly backs of hands, palms and forearms (see FIG. 124.9)

flexor sides of forearms

raised macules of concentric rings usually mouth and extremities

FIGURE 124.9 Erythema multiforme: typical distribution

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• • • • •

• Problems of the skin

Also on feet and toes, mouth Occasionally on trunk and genitalia Polymorphic Vesicles and bullae may develop Self-limiting (up to 2 weeks)

Stevens–Johnson syndrome This is a very severe and often fatal variant. Sudden onset with fever and constitutional symptoms. Causes and associations Erythema multiforme is a vasculitis affecting the skin and mucosa. Herpes simplex virus (usually type 1) is the commonest known association. Associations include: • unknown 50% • herpes simplex virus 33% • other infections: Mycoplasma pneumonia, tuberculosis, Streptococcus, HIV • connective tissue disorders (e.g. SLE) • neoplasia: Hodgkin lymphoma, myeloma, cancer • deep X-ray therapy • drugs: — barbiturates — penicillin — sulphonamides — phenothiazines — anti-epileptics e.g. phenytoin — NSAIDs Treatment • Admit to hospital • Identify and remove cause (e.g. withdraw drugs) • Symptomatic treatment (e.g. antihistamines for itching) • Refer severe cases

Erythema nodosum

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Erythema nodosum is characterised by the relatively sudden onset of bright red, raised, tender nodules on the shins, knees and ankles (see FIG. 29.1, CHAPTER 29). It is an acute, inflammatory, immunological reaction in the subcutaneous fat. The nodules may also appear on the thighs and the arms. Adult females are typically affected. An arthritic reaction can affect the ankles and knees. It is often associated with recent infection and illness. Causes/associations • Sarcoidosis (commonest known cause)

• Infections: — streptococcal infections e.g. strep throat — viral infections (e.g. hepatitis B) — tuberculosis — leprosy — chlamydia infection — fungal infections — bacterial gastroenteritis • Inflammatory bowel disorders (e.g. Crohn) • Drugs: — sulphonamides — tetracyclines — oral contraceptives — bromides and iodides • Malignancy (e.g. lymphoma, leukaemia) • Pregnancy • Unknown (about 40%), perhaps autoimmune Investigations Tests include FBE, ESR/CRP, chest X-ray (the most important), streptococcal serology (e.g. ASOT) and Mantoux test. Treatment Identify the cause if possible. Rest, leg elevation and NSAIDs (e.g. ibuprofen 400 mg (o) bd) for the acute stage. Systemic corticosteroids speed resolution if severe episodes. • prednisolone 0.75 mg/kg (o) once daily for 2 weeks, then reduce Prognosis There is a tendency to settle spontaneously over 3–8 weeks. The lesions may recur.

HERPES ZOSTER Herpes zoster (shingles) is caused by reactivation of varicella zoster virus (acquired from the primary infection of chickenpox) in the dorsal root ganglion. The term comes from the Greek herpes (to creep) and zoster (a belt or girdle). Shingles is from the Latin cingere (to gird) or cingulum (a belt). In most instances the reason for reactivation is unknown, but occasionally it is related to an underlying malignancy, usually leukaemia or a lymphoma, to immunosuppression, or to a local disease or disturbance of the spine or spinal cord, such as a tumour or radiotherapy. The incidence is 3.4 cases per 1000 population per year. A person of any age can get herpes zoster but it is more common in people over 50 years.

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Acute skin eruptions Clinical features The main features are: • the condition is preceded by several days of radicular pain with hyperaesthesia • unilateral patchy rash in one or two contiguous dermatomes (see FIG. 124.10) • intense erythema with papules in affected skin • later crusting and separation of scabs after 10–14 days, often with depigmentation • regional lymphadenopathy

FIGURE 124.10 Herpes zoster (shingles) involving the L2 nerve root in a 63-year-old woman presenting with low back and groin pain. Calamine lotion has been applied to soothe the discomfort.

Distribution Any part of the body may be affected, but thoracic and trigeminal dermatomes are the most common. It follows the distribution of the original varicella rash (worse on the face and trunk).

Cranial nerve involvement The trigeminal nerve—15% of all cases: • ophthalmic branch—50% affects nasociliary branch with lesions on tip of nose and eyes (conjunctivae and cornea) • maxillary and mandibular—oral, palatal and pharyngeal lesions The facial nerve: lower motor neurone facial nerve palsy with vesicles in and around external auditory meatus (notably posterior wall)—the Ramsay–Hunt syndrome.

Complications • Rare: meningoencephalitis • Uncommon: motor paralysis

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• Common: — postherpetic neuralgia; increased incidence with age and debility, with duration greater than 6 months: less than 50 years 1% 50–59 years 7% 60–69 years 21% 70–79 years 30–50% — the neuralgia resolves within 1 year in 70–80% of these patients but in others it may persist for years — eye complications of ophthalmic zoster including keratitis, uveitis and eyelid damage Management • Provide appropriate detailed explanation and reassurance. Dispel myths: namely, that it is not a dangerous disease, the patient will not go insane nor die if the rash spreads from both sides and meets in the middle. • Explain that herpes zoster is only mildly contagious but children can acquire chickenpox after exposure to a person with the disorder. It is advisable to avoid contact with infants and young children who have never had chickenpox and avoid contact with the immunocompromised and those undergoing chemotherapy. Consider giving varicella zoster immunoglobulin to those immunocompromised contacts who have no history of varicella.4 • Treating the rash: Instruct the patient to avoid overtreating the rash, which may become infected. Calamine lotion may be soothing but removal of the calamine can be painful. For a hot, painful rash, to remove crusts and exudate, bathe the lesions with saline three times daily. A drying lotion (e.g. menthol in flexible collodion) is most soothing and suitable. Cover the lesions in a light, non-adherent padded dressing.

Oral medication5 Analgesics such paracetamol with or without codeine should be first-line therapy ± tricyclic antidepressants. Antiviral therapy with a guanine analogue may reduce the duration of the disease in all people. Optimal indications—patients: • treated within 72 hours of onset of vesicles • who are >50 years of age • who are immunocompromised • with acute severe pain • with involvement of special areas (e.g. eye, perineum)

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Dose (e.g. herpes ophthalmicus):5 aciclovir 800 mg (child: 20 mg/kg) (o) 5 times daily for 7 days or famciclovir 250 mg 8 hourly (o) for 7 days or valaciclovir 1000 mg 8 hourly (o) for 7 days Note: increase dose in immunocompromised patients.

Corticosteroids For severe pain, consider prednisolone 50 mg (o) mane for 7 days then taper. Prevention5 • Varicella zoster vaccine (Zostavax).

Postherpetic neuralgia6 This pain, mostly encountered in the elderly, is usually severe, varying in quality from paroxysmal stabbing pain to burning or aching. Spasms of pain upon light brushing of the skin are a feature. Treatment is difficult and a careful ‘trial and error’ approach can be used until appropriate evidence from scientific trials establishes the optimal treatment.

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Treatment options5 • Basic analgesics: paracetamol 1.33 g (o) 6–8 hourly • TENS as often as necessary (e.g. 16 hours/day for 2 weeks)5 plus • Oral medication: — tricyclic antidepressants, for example: amitriptyline 10–25 mg (o) nocte, increasing to a maximum 75–100 mg nocte or — pregabalin (for lancinating pain) 75 mg (o) nocte initially, increasing the dose gradually to maximum tolerated dose (up to 150 mg bd) or — gabapentin 300 mg (o) daily (nocte) initially, increasing as tolerated to maximum 2 400 mg • Topical medication: lignocaine 5% ointment or 10% gel or lignocaine 5% patch to painful area

Evidence-based medicine Systematic reviews confirm that oral antiviral agents (as above) are beneficial for preventing postherpetic

neuralgia while tricyclic antidepressants and gabapentin are beneficial for relieving the established condition.7

Physical treatments • Local corticosteroid and anaesthetic injections. • Nerve blocks (e.g. supraorbital nerve). • Excision of painful skin scar. If the neuralgia of 4 months or more is localised to a favourable area of skin, a most effective treatment is to excise the affected area, bearing in mind that the scar tends to follow a linear strip of skin. This method is clearly unsuitable for a large area.

Herpes simplex6 Herpes simplex is a common infection caused by the large DNA herpes simplex virus (HSV), which can cause a vesicular rash anywhere on the skin or mucous membranes (see FIG.  124.11). There are two major antigenic strains of HSV: • HSV I, which commonly involves the lips and oral mucosa • HSV II, which basically affects the genitalia (common in adolescents and young adults)

FIGURE 124.11 Acute eruption of herpes simplex on the face—a recurrent problem in this person

Epidemiology HSV has a worldwide distribution and is spread orally or genitally by infected secretions. Primary HSV infection is usually a disease of childhood, characteristically causing acute gingivostomatitis in a preschool child (see CHAPTER 72). TABLE 124.7 summarises the major manifestations of HSV and the possible complications.

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Acute skin eruptions

Table 124.7

Herpes simplex virus: manifestations and complications

Examples of manifestations Herpes labialis (synonyms: fever blisters, cold sores) Keratoconjunctivitis, including dendritic ulcer Genital infection Other areas of skin such as buttocks Complications Eczema herpeticum Erythema multiforme (3–14 days postinfection), often recurrent Myeloradiculopathy with genital herpes

idoxuridine 0.5% preparations (e.g. Virasolve) applied hourly or saturated solution of menthol in SVR or povidone–iodine 10% cold sore paint: apply on swab sticks 4 times a day until disappearance or aciclovir 5% cream 5 times daily for 4 days or penciclovir 1% cream for 4 days Note: Corticosteroids are contraindicated.

Oral medication

Encephalitis

For a severe primary attack:

Recurrences range from weeks to months and appear due to reactivation rather than re-infection. The cause is not clear but there are several known precipitating factors. These are fever, sunlight, respiratory infections, menstruation, emotional stress, local trauma and, with genital lesions, sexual intercourse.

Fatalities HSV infections can be potentially fatal. Reactivated HSV can cause a focal destruction encephalitis. The untreated case fatality rate is as high as 70%, but this can be greatly reduced with the use of aciclovir. Neonates exposed to HSV can develop fatal disseminated infection. In compromised patients the infection can be severe.

Diagnosis If the clinical picture is uncertain, immunofluorescence of, or PCR from, vesicle fluid can aid diagnosis.

Genital herpes See CHAPTER 119 and CHAPTER 109.

Herpes labialis (classic cold sores) The objective is to limit the size and intensity of the lesions. Treatment At the first sensation of the development of a cold sore: • apply an ice cube to the site for up to 5 minutes every 60 minutes (for first 12 hours)

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• topical applications include:

Pneumonia

Recurrent infection

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aciclovir 400 mg (child: 10 mg/kg up to 400 mg) 8 hourly for 5 days or until resolution or famciclovir or valaciclovir Prevention If exposure to the sun precipitates the cold sore, use an SPF 30 or more sun protection lip balm, ointment or Solastick. Zinc sulphate solution can be applied once a week for recurrences. Oral aciclovir 200 mg bd (6 months) can be used for severe and frequent recurrences.8 Advice to the patient Herpes simplex is contagious. It is present in saliva and can be spread in a family by the sharing of drinking and eating utensils and toothbrushes, or by kissing. It is most important not to kiss an infant if you have an active cold sore.

FOLLICULITIS9 Folliculitis, which is infection in and around hair follicles, can be superficial or deep. Responsible organisms include bacteria (most common) but consider fungi, dermatophytes and Candida albicans.

Superficial folliculitis This usually presents as mild itchy pustules on an erythematous base on any part of hair-bearing skin, particularly in hot weather in a patient who is often a chronic carrier of S. aureus. A swab supports diagnosis. Management involves removal of the cause and the application of an antiseptic wash, such as triclosan 1%, chlorhexidine or povidone–iodine. Occasionally oral flucloxacillin may also be required.

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Bacterial folliculitis3 A generalised acute erythematous maculopapular rash can be a manifestation of bacterial folliculitis, typically caused by S. aureus, Pseudomonas aeruginosa, or by fungal folliculitis due to Pityrosporum orbiculare or other dermatophytes. Pseudomonas folliculitis can cause confusion, the typical features being: • rapidly spreading rash • mainly on trunk, buttocks and thighs, especially axillae and groin • itchy • small pustules surrounded by circular red–purple halo • follows immersion in a hot spa bath or tub Treatment is based on the sensitivity of the cultured organisms (e.g. ciprofloxacin). Many cases resolve spontaneously in 1–2 weeks.

Folliculitis of trunk from spa baths ‘Hot tub folliculitis’ is caused by P. aeruginosa (usually) in poorly chlorinated water maintained at temperatures 37–40˚C. Treatment is with ciprofloxacin 500 mg (o) bd for 7 days.

Folliculitis of groin (pseudofolliculitis) Folliculitis of the groin area is common in women who shave. It tends to recur.

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Management • Use tea tree (melaleuca) lotion daily for folliculitis. • Prior to shaving apply ‘tea tree wash’. • Change shaving habits: avoid close shaving; shave less often; shave in direction of hair growth and use good quality blades. • If persistent, use povidone–iodine or chlorhexidine (Hibiclens) solution or triclosan 1%. • If severe, use mupirocin 2% (Bactroban) ointment.

Deep folliculitis Deep forms are usually very tender and painful. Examples are styes, boils (furuncles) and carbuncles.

Boil (furuncle)10 This is an S. aureus infection of a hair follicle and may occur in any hair-bearing site. The painful red

nodule enlarges, becomes fluctuant and develops a necrotic centre, which discharges a core of thick yellow pus tinged with blood (with associated relief of pain). Treatment (adults) • (According to swabs) di(flu)cloxacillin 500 mg or cephalexin 500 mg (orally, 6 hourly for 5–7 days) or roxithromycin 300 mg (o) daily or erythromycin 500 mg (o) 12 hourly for 7 days

Boils—recurrent • • • •

Obtain swabs 3% hexachlorophene body wash daily Mupirocin to the lesions and nares Antibiotics (as above)—according to swabs

Carbuncle This is a cluster of small abscesses involving a group of adjoining hair follicles. Common sites are the back of the neck, the shoulders, buttocks or over the hips. Treatment is as for a boil.

Stye of eye • Apply heat with direct steam from a thermos onto the closed eye or by a hot compress (helps spontaneous discharge). • Perform lash epilation to allow drainage (incise with a size 11 blade if epilation doesn’t work). • Only use topical antibiotic ointment (e.g. chloramphenicol) if infection is spreading locally, and systemic antibiotics if distal spread noted by pre-auricular adenitis.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 6th edition: • Herpes simplex (cold sores) • Herpes zoster (shingles) • Pityriasis rosea

References 1 Hunter JAA, Savin JA, Dahl MV. Clinical Dermatology (3rd edn). Oxford: Blackwell Scientific Publications, 2002: 64. 2 Murtagh J. Patient Education (6th edn). Sydney: McGraw-Hill, 2012: 316. 3 Thomas RM. Drug eruptions. Med Int, 1988; 49: 2038–42. 4 Moulds R (Chair). Therapeutic Guidelines: Antibiotic (Version 12). Melbourne: Therapeutic Guidelines Ltd, 2010 (eTG Complete).

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Acute skin eruptions 5 Moulds R (Chair). Therapeutic Guidelines: Neurology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2012 (eTG Complete). 6 Dwyer DE, Cunningham AL. Herpes simplex and varicella zoster virus infection. Med J Aust, 2002; 177: 267–72. 7 Lancaster T, Warehain D, Yaphe J. Postherpetic neuralgia. In: Barton S (ed.), Clinical Evidence (Issue 7). London: BMJ Publishing Group, 2002: 739–45.

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8 Pollack A. Treatment of herpes simplex: a practice tip. Aust Fam Physician, 1982; 11: 952. 9 Marley J (Chair). Therapeutic Guidelines: Dermatology (Version 3). Melbourne: Therapeutic Guidelines Ltd; 2009: 161–3. 10 Russo GJ. Herpes Simplex and Herpes Zoster. Glendale CA: Audio Digest, Family Practice, 1991; 39: 38.

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125 Skin ulcers An ulcer, which occurring at any of the vital parts of the body secretes a copious quantity of pus and blood, and refuses to be healed, even after a course of proper and persistent medical treatment, is sure to have a fatal determination. Sushruta-Samhita (th century BC) An ulcer is a localised break in the epidermal tissue of the surface of the skin or mucous membrane as a result of trauma, pressure, infection; they are associated with an underlying pathology. This applies particularly to leg ulcers. Ulcers are commonly found on the legs and feet, on areas exposed to the sun, and over bony prominences on the sacrum and heels. They may be clean, sloughy or necrotic. The national morbidity survey (UK) showed that 2–3 per 1000 patients per annum consulted their GP with ‘chronic ulcers of the skin’.

•

•

•

•

Key facts and checkpoints1,2 •

•

•

• •

• •

•

The great majority of leg ulcers are vascular in origin due to arterial insufficiency or venous hypertension or to a combination of the two i.e. mixed ulcers. If clinical findings don’t provide the diagnosis, ordering the ankle-brachial index (ABI) is essential if pulses are not palpable to exclude arterial disease. Duplex Doppler ultrasound is the key investigation for both venous and arterial disease. Most ulcers are multifactorial: 1 venous + obesity + immobility (often with osteoarthritis) + poor compliance, or 2 venous + arterial + trauma + infection Identify and treat any intrinsic or extrinsic factors impairing wound healing. High-stretch compression bandages are better than short-stretch compression bandages, which are mainly used in lymphoedema, and multilayer is best. Elastic bandages are better than non-elastic bandages. Venous surgery can improve outcomes—newer methods use non-surgical foam injections and lasers. A moist environment delivered by modern dressings provides a physiological environment for wound healing.

• •

Adequate wound debridement is essential to remove necrotic material and slough, and enable healing to commence and progress. It is important to consider biopsy as hypergranulation that does not respond quickly to topical treatment with hypertonic saline, silver nitrate and compression bandaging may be an SCC. Diabetic ulcers may be either neuropathic, which are mostly caused by pressure damage due to sensory neuropathy, or ischaemic due to loss of peripheral arterial circulation. Autoimmune diseases are the underlying cause of vasculitic wounds. They result from damage caused by circulating antibodies often seen in RA, lupus and scleroderma. They are very painful and difficult to heal without the use of immunosuppressants. Accurate diagnosis of the ulcer is vitally important for management decisions. Bacterial swabs are unhelpful because all chronic ulcers will become colonised with both Grampositive and Gram-negative bacteria.

The clinical approach It is useful to keep in mind the various causes of ulcers (see TABLE  125.1). The commonest causes or types are venous and ischaemic ulcers of the leg, pressure ulcers (decubitus) and trauma. It is important not to misdiagnose malignant ulcers, including ‘Marjolin ulcer’, which is SCC developing in unstable chronic scars or ulcers (e.g. burns, venous ulcers, tropical ulcers) of long-standing duration. Amelanotic melanoma is a specific trap.

History A careful history helps determine the cause of the ulceration. Relevant history includes previous deep venous thrombosis or pulmonary embolism, diabetes, rheumatoid arthritis, inflammatory bowel

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Skin ulcers

Table 125.1

Types and causes of skin ulcers

Traumatic Decubitus (related to trauma—pressure injury) Vascular • Venous: — varicose veins — post thrombophlebitis • Arterial insufficiency • Skin infarction (thrombolytic ulcer) • Vasculitis — rheumatoid arthritis, SLE, scleroderma Infective • Tropical ulcer • Tuberculosis • Mycobacterium ulcerans • Post cellulitis • Chronic infected sinus Malignant • Squamous cell carcinoma • Marjolin ulcer (SCC) in long-standing ulcer • Basal cell carcinoma (rodent ulcer) • Malignant melanoma • Ulcerating metastases

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• • • • •

edge—consider consistency floor base discharge surrounding skin: — colour (? signs of inflammation) — sensitivity • mobility in relation to underlying tissue • regional lymph nodes Site of ulcer Venous ulcers typically occur on the medial side of the leg in relation to incompetent perforating veins in the traditional gaiter area (see FIG. 125.1). Ischaemic ulcers tend to occur on the lateral side and anterior part of the leg and the foot. Trophic ulcers, which are associated with neuropathy, occur on parts subject to repeated pressure and trauma, such as the ball of the foot or the pulps of the fingers.

Neurotrophic • Peripheral neuropathy (e.g. diabetes) • Peripheral nerve injuries (e.g. leprosy) Haematological • Polycythaemia • Spherocytosis • Sickle cell anaemia Miscellaneous • Artefactual • Pyoderma gangrenosum inflammatory ulcer • Insect and spider bites

disease, chronic skin ulcers and arterial insufficiency, including a history of intermittent claudication and ischaemic rest pain. A drug history is important, considering especially beta blockers and ergotamine, which can compromise the arterial circulation, corticosteroids and NSAIDs, which affect healing, and nifedipine, which tends to aggravate ankle oedema. 3

Examination

Any ulcer should be assessed for the following characteristics: • site • shape • size

FIGURE 125.1 Area typically affected by varicose eczema and ulceration (the ‘gaiter’ area)

Postsolar keratoses Solar-induced ulcers, such as SCCs and BCCs, occur on such parts exposed to the sun. It should be noted if the ulcer is related to old scars, including burns and chronic ulcers. Size, shape and edge The classic appearances of various ulcers are presented in FIGURE  125.2. These are general guidelines only. Infective ulcers due to Mycobacterium species and pressure injury tend to have an undermined edge while a trophic ulcer is punched out and typically round in surface shape. A raised firm ulcer edge may indicate malignancy.

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Floor of the ulcer The floor or base of the ulcer provides useful clinical information. A dry or extended base or necrotic eschar in the floor implies ischaemia. Venous ulcers on the other hand are often superficial and tend to have fibrinous exudate and ooze, sometimes purulent fluid. Colour guide: • black—necrosis, ischaemia • yellow—slough • red—granulation • pink—epithelium

Investigations The following should be considered, according to the clinical findings:4 • full blood count • ESR/CRP • random blood sugar/HbAIc (known diabetes) • kidney function tests • rheumatoid factor tests • duplex Doppler ultrasound • swab for specific organisms • biopsy, especially if SCC suspected (be careful of biopsy if melanoma: amelanotic melanomas are a trap); also accurately identify an infective organism

Lower limb ulceration The most common causes of lower limb ulceration are venous disease, arterial disease, mixed venous and arterial, and diabetes. Differentiating between leg ulcers (85%) and foot ulcers (15%) is very important since they present two very different problems.3 According to the survey by Stacey, venous disease is present in two-thirds of leg ulcers, while arterial disease occurs in 28% (see TABLE  125.2). Ulceration on the foot frequently has an arterial aetiology (72%), with many of these patients also having diabetes, whereas venous disease is present in only 6%.5 The differential characteristics are presented in TABLE 125.3. A general examination, including the leg, is very important. This includes examining the venous drainage (CHAPTER 66), the arterial pulses and the sensation of the leg, and checking for the presence of diabetes. Appropriate investigations (if required) include: • full blood count • blood sugar • duplex Doppler ultrasound for arterial circulation

edge

(a)

Table 125.2

Causes of chronic ulceration of the leg and foot5

floor

% The leg base (b)

Edge

Example

punched out

trophic ulcer arterial ulcer

Venous disease

52

Mixed venous and arterial disease

15

Arterial disease

13

Others

20

The foot undermined

125

pressure injury e.g. bed sore

Arterial disease Mixed venous and arterial disease

2

Venous disease

4

everted

squamous cell carcinoma

Others

rolled

basal cell carcinoma

To swab or not to swab

FIGURE 125.2 (a) Parts of an ulcer, (b) types of ulcer. Source: Davis et al. Symptom Analysis and Physical Diagnosis (2nd edn), page 309. Reproduced with permission from Pergamon Press

72

22

A routine ulcer swab is not considered to be of significant value. If specific organisms such as Mycobacterium ulcerans are suspected, then cultures are necessary. Biopsy is considered to be accurate.

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Skin ulcers

Table 125.3

Comparison of typical features of venous and arterial ulceration of the leg Venous

Site

Arterial

Distal to ankle Around ankle and Over pressure points lower third of leg on toes, side of (gaiter area) foot, metatarsal Just above medial and lateral malleoli heads

Pain

Nil to mild

Usually moderate to severe

Oedema

Pitting oedema usually present

Usually absent

Ulcer features

‘Ragged’ edge Often superficial Ooze + + +

‘Punched out’ Often deep, involving deep fascia Dry

Associated limb features

Varicosities Leg warm, red, oedematous Varicose dermatitis Haemosiderin deposits Atrophie blanche

‘Cold’ extremities Ischaemic changes Diminished or absent peripheral pulses Thin, shiny, dry skin Poor perfusion

History

Limb oedema Past DVT Failed graft

Peripheral vascular disease— claudication, rest pain Diabetes Smoker

ABI

>0.9

55 years. Most people have 5–10 melanocytic naevi on average. Multiple dysplastic naevi carry a higher risk of malignant change, which may occur in young adults. Such patients require regular observation (with photography).

Pyogenic granuloma Synonyms: granuloma, granuloma telangiectaticum, acquired haemangioma.

Table 127.1 Classification of pigmented skin lesions Non-melanocytic Pigmented basal cell carcinoma Seborrhoeic keratoses Solar keratoses Dermatofibroma Pyogenic granuloma Foreign body granuloma Talon noir (black heel) Tinea nigra Becker naevus Melanocytic Non-melanoma Freckles Lentigines Naevi: 1 congenital 2 acquired: — junctional → compound → intradermal — halo — blue — Spitz — dysplastic Melanoma 1 Lentigo maligna (Hutchinson melanotic freckle) 2 Superficial spreading melanoma 3 Nodular melanoma 4 Acral lentiginous melanoma

A pyogenic granuloma is a 5–10 mm soft vascular lesion (without pus) due to a proliferation of capillary vessels. It is considered to be an abnormal reaction to minor trauma (see FIG. 127.1). Clinical features • Common in children and young adults • Usually on hands and face • Bright red ‘raspberry’-like lesion • Raised, sometimes pedunculated • Friable—bleeds easily Beware of misdiagnosing pyogenic granuloma for a nodular melanoma.

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Freckles are small, brown flat macules (usually 5 mm (variable size) • Most common on trunk • Irregular and ill-defined border • Irregular pigmentation • Background redness • Variable colours—brown, tan, black, pink, red • Variation of colours within the naevus • Most are stable and do not progress to melanoma

Dysplastic naevus syndrome The presence of multiple, large, irregular pigmented naevi, mainly on the trunk, presents a difficult management problem, especially if there is a family history of melanoma. The lifetime risk of melanoma may approach 100% for such patients.

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Pigmented skin lesions Management Use a follow-up program (similar to excised early melanoma) of 6 monthly review for 2 years (3-monthly if family history of melanoma) and yearly thereafter, provided no lesions become malignant during the first 2 years. During this time the patient and family should become well versed in surveillance. Apart from measurement, good professional-quality photographs of areas of the body including total body photography or specific lesions of concern may also be helpful. Any suspicious lesions should be excised for histological examination. Advice to patients To decrease your chances of getting a melanoma, you should protect yourself from the sun. These rules should be followed. • Try to avoid direct sunlight when the sun is at its strongest (from 10 am to 3 pm). • Always wear a broad-brimmed hat and longsleeved shirt in the sun. • Use an SPF 30 or more sunscreen on exposed skin and renew the sunscreen regularly. • Sunbaking might give you a good tan but it is also going to increase your chances of getting a melanoma, so you should avoid it.

Melanoma Melanomas are malignant tumours derived from melanocytes, with the skin being the most common site. The early diagnosis of melanoma is vital to outcome. Thickness of a melanoma when it is removed is the major factor determining prognosis: it is vital to detect melanomas when they are in the thin stage and look like an unusual freckle. In Australia, only about 30% of melanomas develop in pre-existing melanocytic naevi (moles).2,3 The majority arise in apparently normal skin. Initially the tumour tends to spread laterally in many cases and it should be removed at this stage when it is easily cured. An irregular border or margin is suggestive of the tumour. Risk factors • History of previous melanoma (fivefold) • Presence of many moles (50 or more), especially atypical dysplastic naevi • Family history (one or more members) • History of many sunburns • Sun sensitive skin/fair complexion

• Patient age and sex: increasing age and male • Tanning (including solarium) treatments

Clinical features • Typical age range 30–50 years (average 40 years) • Can occur anywhere on the body—more common: — lower limbs in women — upper back in men • Often asymptomatic • Can bleed or itch Change The sign of major importance is a recent change in a ‘freckle’ or mole: • change in size—at edge or thickening • change in shape • change in colour—brown, blue, black, red, violet, white, including combinations • change in surface • change in the border • bleeding or ulceration • other symptoms (e.g. itching) • development of satellite nodules • lymph node involvement

Red flag pointers for melanoma4 • • • • • •

New or changing lesion (see preceding change list) Rapidly growing nodule of any colour Non-healing lump or ulcer The ‘ugly duckling’ syndrome: a prominent pigment lesion that stands out from any other A lesion that concerns the patient Dermoscopic changes on follow-up or poor dermoscopic–clinical correlation

Types

Lentigo maligna3 Lentigo maligna (Hutchinson melanotic freckle) is a slow-growing form of intra-epidermal melanoma that occurs on areas exposed to light (usually the face), predominantly in the elderly (see FIG.  127.6). If allowed to remain it may become invasive and the prognosis will be similar to that for other invasive melanomas. These lesions have all the variations in size, shape and colour of superficial melanomas. Lentigo maligna should be excised.

Superficial spreading melanoma Like lentigo maligna, the initial growth is in a lateral or radial intra-epidermal manner, rather than in

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FIGURE 127.6 Lentigo maligna in a 72-year-old man. Excision is recommended as it is a form of intra-epidermal melanoma. Photo courtesy Robin Marks

FIGURE 127.8 Nodular melanoma on the back. It has no radial growth phase and because it grows vertically can be readily misdiagnosed. The ABCD rule often does not apply but this lesion shows variable colours and an irregular border. Photo courtesy Robin Marks

FIGURE 127.7 Superficial spreading melanoma with an irregular border which has altered and variable colours. Requires excision. Photo courtesy Robin Marks

an invasive downward or vertical manner (see FIG.  127.7). It exhibits a striking colour variation. It accounts for 70% of melanomas. It can be detected early by biopsy—shave is preferred to punch (less sampling error). Excisional biopsy is preferable.

Nodular melanoma Nodular melanoma, which accounts for 20% of melanomas, has no radial growth phase. It is typically found on the trunk and limbs of young to middle-aged individuals (see FIG. 127.8). It may have a ‘blueberry’like nodule. Prognosis is determined by thickness at the time of excision.

The early nodular melanoma problem4,5 Nodular melanoma can present a diagnostic dilemma since the ABCD rule (see later in this chapter) often does not apply. The mnemonic EFG, standing for

FIGURE 127.9 Acral lentiginous melanoma. A 30-yearold man presented with a ‘mole’ on his toe that had become ‘lumpier’. This type of melanoma, which occurs on the distal areas of the limbs, begins as a spreading pigmented, macule before developing into a nodule surrounded by a pigmented halo (as shown). Photo courtesy Robin Marks

‘Elevated’, ‘Firm’ and ‘Growing for more than 1 month’, is more appropriate. Early melanomas tend to be symmetrical, non-pigmented, even in colour, of small diameter and to grow vertically. They are often mistaken for a haemangioma or a pyogenic granuloma. If one is suspicious, refer early to a specialist/specialist clinic.

Acral lentiginous melanoma These typically occur on palms, soles and distal phalanges (see FIG.  127.9). They have a poorer prognosis than other types. They occur mainly in dark-skinned races.

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Pigmented skin lesions Desmoplastic melanoma4 This is a rare and aggressive subtype of melanoma. They are often subtle clinically and sometimes scarlike. Most are non-pigmented.

Variations Amelanotic melanomas are flesh-coloured papules that increase in size or change shape. These lesions can be extremely difficult to diagnose and the poor prognosis associated with them is due to late diagnosis rather than an increased malignancy. The features and associations of melanoma subtypes are presented in TABLE 127.2.

• thickness (Breslow classification) • level or depth (worse in level IV or V) (see FIG. 127.10) • site (worse on head and neck, trunk) • sex (worse for men)

Vertical growth is associated with invasion and the prognosis worsens with depth. The chance of cure is greater than 90% if a melanoma is removed when it is less than 0.75 mm thick.3 If the lesion is allowed to invade to a thickness of 4 mm or more, the likelihood of a cure is reduced to less than 30%.3 The influence of tumour thickness on 5-year survival rates is shown in TABLE 127.3. Staging is based on the tumour level (depth) shown in FIGURE 127.10:

Features and associations of melanoma subtypes5,6

Melanoma subtype

Frequency %

Radial growth phase

Superficial spreading

70

Nodular

Location

Average age

Occupation profile

+

Trunk (back), limbs (legs)

Middle-aged

Indoor worker

20

-

Trunk, limbs

Middle-aged

Indoor worker

Lentigo maligna

7.5

+

Head, neck

Elderly

Outdoor worker

Acral lentiginous

2.5

+

Palms, soles mucosae

Not known

Not known

Source: Reproduced with permission of J Kelly5,6

Level I

Level II

Level III

Level IV

Level V

epidermis

papillary dermis

reticular dermis

subcutaneous tissue

FIGURE 127.10 Assessment of tumour level: the levels of melanoma invasion

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• level I—confined to the epidermis (in situ) • level II—tumour cells extend into the superficial (papillary) dermis • level III—tumour cells fill up the superficial dermis • level IV—tumour cells extend into the deeper (reticular) layer • level V—invasion of subcutaneous tissue

Prognosis Determinants of prognosis include:3

Table 127.2

• age (worse >50 years) • amelanotic melanoma • ulceration

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Table 127.3

127

• Problems of the skin

The influence of tumour thickness on 5-year survival rates6

Range of tumour thickness (mm)

5-year survival rates %

Level (Clark)

0

I

4.0

V

30–60

Source: Reproduced with permission of J Kelly6

Differential diagnosis There are several common skin lesions that may be mistaken for melanoma.1 They are: • • • • • • • •

haemangioma (thrombosed) dermatofibroma (sclerosing haemangioma) pigmented seborrhoeic keratosis pigmented BCC junctional and compound naevi blue naevi dysplastic naevi lentigines

Facilitating early diagnosis of melanoma An adequate light source without shadows is essential. Refer to CHAPTER 121 for use of the ‘Maggylamp’ and the dermatoscope, which is a very important and useful adjunct to diagnosis.

Clinical examination of the skin1 It is important to examine the entire skin and not just the lesion presented by the patient. Comparison of pigmented skin lesions is very helpful in differentiating between benign and malignant. One satisfactory routine is: • Starting at the head, examine the hairline, backs of ears, neck, back, and backs of the arms. Pull down the underwear to expose the buttocks; examine the backs of the legs. • With the patient facing you, examine the anterior hairline, the front of the ears, the forehead, cheeks and neck, moving downwards to the anterior chest. Move bra straps as required to achieve complete coverage. Then examine the abdomen, pulling down the underwear to examine as far as the pubic hairs.

• Then examine the anterior surfaces of the legs. The ‘Maggylamp’ is very useful for this examination. After scanning the entire skin surface and comparing and contrasting naevi, specific lesions may be examined with the dermatoscope. Compare suspicious lesions with similar lesions elsewhere on the patient’s skin.

Applying the ABCDE system1 A = Asymmetry Melanoma is almost always asymmetrical. Most nonmelanoma lesions are symmetrical, oval or round. B = Border The border of the melanoma is usually well defined, especially in the more malignant, compared with the dysplastic naevus, which is almost always indistinct with a fading-out ‘shoulder’ effect. The border of the melanoma is irregular while most benign lesions have a regular edge. C = Colour The classic blue–black colour is helpful but the variety of colours present in most melanomas is the most helpful. Magnification usually visualises greys, whites, violets, reds, oranges and shades of brown interspersed in the darker blue–black pigmentation. Early melanomas developing in dysplastic naevi tend not to have this deep pigmentation. D = Diameter The majority of melanomas when first seen are at least 7 mm in diameter, especially if arising from a pre-existing naevus. However, it is possible to diagnose small nodular melanomas 1 mm thickness provides accurate prognostic information.

References 1 McCarthy W. The management of melanoma. Aust Fam Physician, 1993; 22: 1177–86. 2 Roberts H, Haskett M, Kelly J. Melanoma: clinical features and early diagnostic techniques. Medicine Today, May 2006; 7 (5): 39–47.

3 Marks R. Skin cancer. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 469–72. 4 Moulds J (Chair). Therapeutic Guidelines (Version 4) Melbourne: Therapeutic Guidelines Ltd, 2014 (eTG Complete). 5 Kelly J. Nodular melanoma—no longer as simple as ABC. Aust Fam Physician, 2003; 32 (9): 702–9. 6 Kelly J. Malignant melanomas—how many have you missed? Med J Aust, 1996; 164: 431–6. 7 Melanoma Guidelines Revision Working Party. Clinical Practice Guidelines for the Management of Cutaneous Melanoma in Australia and New Zealand. Wellington: Cancer Council Australia and Australian Cancer Network, Sydney and New Zealand Guideline Group, 2008. 8 English D et al. Cancer Survival Victoria 2007. Melbourne: Cancer Epidemiology Centre, Cancer Council Victoria, 2007: 40. 9 Thompson JF, Scolyer RA, Kefford RF. Melanoma: a management guide for GPs. Aust Fam Physician, 2012; 41 (7): 470–3.

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Accident and emergency medicine

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Hair disorders

128

Look it’s only death. It’s not like losing your hair. Harold Brodkey upon learning he had AIDS, New Yorker Magazine  The hair of our scalp is referred to as our crowning glory and the threat of hair loss in both sexes provokes extraordinary anxiety bordering on grief in some people. It behoves us as medical practitioners to treat the patient presenting with ‘I’m losing my hair’ with appropriate support and understanding. Likewise, the problem of hirsutism provokes similar anxiety and concerns about body image. Interestingly, women present with hair loss more than men.

Key facts and checkpoints •

• •

•

•

•

• • • •

•

There are two types of hair: terminal hair, which is coarse and well pigmented, and vellus hair, which is fine, soft and relatively unpigmented. Alopecia is a generic term for hair loss. Hair loss (alopecia) generates considerable anxiety and the fear of total hair loss should be addressed with the patient and a realistic prognosis given. Androgenic alopecia is the most common cause of human hair loss, affecting 50% of men by age 40 and up to 50% of women by age 60.2 Other common causes are alopecia areata, seborrhoeic dermatitis and tinea capitis (see TABLE 128.1). In telogen effluvium, the traumatic event has preceded the hair loss by about 2 months (peak loss at 4 months). Although severe stress could precipitate alopecia areata, day-to-day stressors are not considered to be a trigger. Stress seems to be a consequence of alopecia rather than the cause of it.3 Hair loss can be patchy or diffuse where it involves the entire scalp. Patchy loss—alopecia areata and trichotillomania. Generalised loss—telogen effluvium, systemic disease, drugs (see TABLE 128.2). Alopecia areata has a poor prognosis if it begins in childhood, if there are several patches and there is loss of eyebrows or eyelashes. Scarring alopecia can be an indicator of lupus erythematosus or lichen planus.

Table 128.1

Hair loss: diagnostic strategy model

Q. Probability diagnosis A. Androgenetic alopecia (male pattern baldness) Alopecia areata (diffuse type) Telogen effluvium (incl. postpartum) Anagen effluvium (esp. cytotoxic therapy) Seborrhoeic dermatitis Q. Serious disorders not to be missed A. Infection: • tinea capitis • bacterial folliculitis • secondary syphilis • post-febrile state Cancer: • treatment for cancer Other: • systemic disease (e.g. lupus) Q. Pitfalls (often missed) A. Rarities: Heavy metal poisoning Nutritional: • severe dieting • malnutrition • zinc/iron deficiency Q. Masquerades checklist A. Drugs (cytotoxics, anticoagulants, antiepileptics, amphetamines, anti-thyroid agents, various hormones, cessation OCP) Thyroid/other endocrine (hypothyroidism) Q. Is the patient trying to tell me something? A. Emotional stress → telogen effluvium; trichotillomania

The normal hair growth cycle An understanding of the process of normal hair growth is necessary to comprehend and evaluate hair disorders. Each follicle progresses quite independently through regular cycles of growth and shedding (see FIG. 128.1).

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128 telogen club hair

epithelial cells

dermal papilla

Anagen

Catagen

new anagen hair

Telogen

FIGURE 128.1 The normal hair cycle

Table 128.2

Causes of diffuse hair loss

Androgenetic alopecia Telogen effluvium Postpartum telogen effluvium Alopecia areata (diffuse type) Drugs—cytotoxics and others Hypothyroidism Nutritional: • iron deficiency • severe dieting • zinc deficiency • malnutrition Post-febrile state Anagen effluvium

The three phases of follicular activity are:1 1 Anagen phase—the active growth phase of hair production. • The dermal papilla stimulates division of epithelial cells that produce the hair shaft. • The hair shaft grows 1 cm per month. • It lasts for about 2.5–5 years on the scalp (average 1000 days). • It lasts 1–2 months on eyebrows and eyelashes and 6–9 months in the axilla and pubis. • It varies between individuals. 2 Catagen phase—a short transition phase from active growth to inactivity (the involutional stage).

• The base of the hair becomes club-shaped. • It lasts for only about 2 weeks. 3 Telogen phase—the resting (dormant) phase of the cycle at the end of which the club hair with its non-pigmented bulb is shed. • This lasts 2–4 months (average 100 days). • The percentage of hairs in telogen varies from site to site—10% in scalp to 60–80% in pubic hair.2 • The hair is anchored in the follicle but does not grow longer. • The follicle then re-enters anagen. Thus every 3–5 years every hair on the scalp is shed and replaced.

Some facts on hair numbers1 • Hair growth is asynchronous (i.e. continuous production and shedding). • Humans produce 1 km of hair a month. • About 50–100 hairs are shed daily without a reduction in density. • The scalp contains, on average, 100 000 hair follicles. • The hair follicle is subject to melanocytic activity. • At least 25% of hair must be shed before a noticeable loss of density occurs. • Hair loss counts consistently above 100 per day indicate excessive hair loss. • Significant hair loss tends to block the shower drain or be visible all over the pillow.

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Hair disorders Key history • Onset, duration, quantity and rate of loss • Localised or generalised loss • Associated symptoms (e.g. pruritus, scaling, pustules) • Systems review including fever, acute illness, surgery, stressors • Endocrine features • Past history including skin disorders, cancer, thyroid disorders • Family history of hair loss

Associations

Key examination • General review with emphasis on endocrine system and examination of scalp • Look for exclamation mark hair, ‘white bulb’ hair, state of bald patch (clean, scaly, scarred or inflamed) and the unusual pattern of trichotillomania

• topical potent class III steroids (especially in children) bd, 12 weeks • topical irritants (e.g. dithranol 0.5% ointment initially, increasing in strength to 2% applied once daily) • intralesional steroids—triamcinolone 10 mg/mL or betamethasone acetate/phosphate 5.7 mg/mL bd (caution needed on face—risk of cutaneous atrophy). Multiple injections required. • topical minoxidil 5%—1 mL bd (for 4 or more months) only when hair growing • topical immunotherapy with DNCB antigen

Key investigations Consider: • • • • • •

FBE/ESR pituitary hormones (FSH/LH/prolactin/FSH) hair pull test trichogram scalp biopsy skin scrapings and hair sample for fungal microsurgery and culture

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• Loss of facial (beard in men) or body hair • Nail changes—dystrophy or pitting

Alopecia areata3 The course taken may be as follows. Localised patches Small patches may recover spontaneously (usually 80%), while others depend on the extent of loss and general factors. Treatment (options) includes:

Extensive area (>50% loss) • Treatment • Counselling • Alopecia areata support group • Use of cosmetic aids (e.g. wigs, hair pieces, scarves) and camouflage

Alopecia areata, alopecia totalis and alopecia universalis Alopecia areata is a disorder of the hair follicle causing a sudden onset of localised or diffuse hair loss. It is thought to be an autoimmune disorder that has a genetic susceptibility (20% have a positive family history). The hairs are affected during the growth phase, resulting in cessation of anagen. DxT patch of complete hair loss + clean scalp + exclamation-mark hairs alopecia areata

Clinical features • Complete hair loss (small patch or diffuse) • Pigmented hairs often lost first • Clean normal scalp • No or minimal inflammation • Exclamation-mark hairs, especially around the periphery (see FIG. 128.2)

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FIGURE 128.2 Exclamation-mark hair (a feature of alopecia areata)

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• Topical steroids not recommended—ineffective • Topical immunotherapy under specialist care may help • Psoralen and ultraviolet A (PUVA) phototherapy may also help • Systemic steroids only for active and progressive cases: prednisolone 0.75 mg/kg (o) daily for 3–4 weeks, then taper off over 2 months A solitary patch of hair loss will recover within 6 months in 33% of cases, while 50% of cases will recover over a year and 33% will never recover. Unfortunately, most patients (86% in one study) relapse.3

Alopecia totalis • This is where the alopecia extends over the total scalp. • There is, at best, a 50% chance of hair recovery in a fit adult but only a very small chance in childhood.

Telogen effluvium4 Telogen effluvium, which is increased shedding of hairs in the telogen phase, is one of the most common causes of diffuse hair loss and can be triggered by a variety of stressors. It is worth noting that follicular matrix cells have a high metabolic rate second only to haematological tissue and stress can result in shunting into premature telogen with cessation of anagen.1 An obligatory delay occurs between the ‘insult’ or precipitating event and the onset of hair shedding because the hair follicle cycles through catagen and telogen—approximately 2–3 months when the club hairs with white bulbs of telogen are shed. Greater than 25% of hair must be lost before there is a perceptible thinning and in this disorder up to 50% loss is common. DxT stressful event + 2–3 month gap to diffuse hair loss + ‘white bulbs’ telogen effluvium

Alopecia universalis • This is where the alopecia involves the eyebrows and eyelids as well. Recovery is rare.

Scarring alopecia1 In this condition, the hair follicles are damaged and if the follicular openings cannot be seen with a magnifying lens, regrowth of hair cannot be expected. Thus, the process is irreversible and a scalp biopsy is essential to determine the diagnosis. Apart from obvious causes such as trauma, severe burns, a carbuncle and scalp ringworm with kerion, the causes of scarring alopecia are as follows. • Lichen planopilaris—this is a variant of lichen planus that produces small follicular papules in the scalp that tend to heal with scarring and destruction of hair follicles; treatment, which is difficult, includes corticosteroids, antimalarials and etretinate1 • Discoid lupus erythematosus—this gives a similar picture to the former and tends to be treated in a similar manner • Folliculitis decalvans—a chronic folliculitis of the scalp, probably as a response to staphylococci on the scalp; treated with long-term tetracyclines • Pseudopelade—a slowly progressive, noninflammatory, scarring condition causing patchy areas of hair loss without any obvious preceding skin disease

Patients usually complain of large clumps of hairs with white bulbs coming out with gentle tugging on combing or shampooing (this can exceed 150 hairs per day compared with the normal average of 50–100 hairs).

Stress precipitants of acute telogen effluvium • • • • • • • •

Any severe stress Childbirth (common) High fever Weight loss, especially crash dieting Trauma—surgical or accidental Oral contraceptive pill (OCP) cessation Malnutrition Haemorrhage

Course of telogen effluvium If uncomplicated, spontaneous recovery can be expected in 6 months so reassurance with explanation is all that is required. If it persists longer than 6 months, consider the chronic idiopathic form or an unmasked androgenetic alopecia. However, if there is concern about non-recovery and the stress factors are corrected, topical minoxidil 5% lotion (2% if too irritant) twice daily for a minimum of 4 months is an option.3 Referral to a specialist is advised for relapsing episodes or incomplete recovery.

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Hair disorders

Chronic telogen effluvium5 This occurs usually in perimenopausal and postmenopausal women. It may be primary and idiopathic or secondary to hypothyroidism, hyperthyroidism, malnutrition or cancer. The feature is episodes of dramatic hair shedding that recover but recur weeks to months later and last up to several days. It does not result in obvious balding—it is selflimiting and does not usually need treatment.

Table 128.3

This is hair loss during the anagen phase and is typically seen in association with cancer chemotherapy and radiotherapy to the scalp, which results in immediate metabolic arrest. Hair loss is diffuse, involving the whole scalp. Anagen hair shafts are identified by their long and pigmented hair bulb. The follicle may remain in anagen, leading to a quick recovery, or move into telogen, thus delaying growth by about 3 months.3

Cytotoxic agents/thallium Amphetamines Anticoagulants: heparin, warfarin Anti-epileptics: phenytoin, sodium valproate, carbimazole Antigout agents: allopurinol, colchicine Anti-inflammatories: indomethacin, gold, penicillamine, salicylate Antiparkinson: levodopa, bromocriptine Antithyroid agents/thyroxine/iodine Cardiovascular agents: • amiodarone • statins, clofibrate • selected ACE inhibitors • selected β-blockers Cimetidine Gentamicin

Drug-induced alopecia Drugs are a very important cause of alopecia (see TABLE 128.3). They may cause telogen effluvium, anagen effluvium or accelerate androgenetic alopecia. Drugs tend to cause telogen effluvium but cancer chemotherapy, radiation to the scalp, thallium/ mercury/arsenic and colchicine in high dosage cause anagen effluvium. Acceleration of androgenetic alopecia is caused by hormone therapy, namely the OCP, danazol, testosterone and anabolic steroids.

Hormones: OCP, androgens, danazol Interferon Lithium Methysergide Vitamin A derivatives/retinoids: Roaccutane

Androgenetic alopecia (male pattern baldness) This is the most common form of alopecia, which is age related and is genetically determined in addition to being androgen dependent. The key androgen is dihydrotestosterone, which is produced from testosterone by 5α reductase. The hair loss is reasonably predictable, with some men losing hair quickly and others more slowly in a familial pattern. In others it is unpredictable. The diffuse pattern loss seen in women tends to progress slowly. About 50% of women have significant hair loss by the age of 60. The typical male pattern is shown in FIGURE 128.3. Alopecia affects 30% of men by age 30 and 50% by age 50.

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Drug-induced causes of alopecia generally from prolonged use2,3

Antihelminthic agents: albendazole/mebendazole

Anagen effluvium

9

FIGURE 128.3

Typical male pattern baldness

Androgenetic alopecia in women • In women, the pattern of hair loss is different from men. • Diffuse thinning occurs, usually on the top of the head (the crown). The front hairline usually remains but in some women this can recede with bitemporal loss (see FIG. 128.4).

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FIGURE 128.4 Typical female pattern baldness

• Although hair loss can appear in men and women as early as the 20s, it may not appear before the age of 50 in women. • Some women notice a short period of considerable hair loss but this may be followed by a long stable period of no loss. Total loss of hair rarely occurs in women. • It may be unmasked after an episode of diffuse hair loss such as after childbirth or an acute illness. Treatment (men) It is appropriate to counsel men to accept their balding as part of a natural ageing process. This includes cutting the hair short to make it look better cosmetically. If baldness is not acceptable, some options include wearing a toupee, a wig or other hair substitute or having a hair transplant operation. However, with hair transplantation, the new hair is often just as likely to disappear as the original hair. The use of medicated oils and shampoos should be discouraged. The androgen receptor antagonists such as spironolactone and cyproterone acetate are unsuitable for men because of adverse effects.3

Available medications3 • Minoxidil 2% and 5%, 1 mL applied bd to the dry scalp for a minimum of 12 months. The results vary from good to no change. One study showed that one-third of men using 2% minoxidil for 12 months experienced ‘cosmetically significant hair growth’. However, a lifetime of expensive treatment is required in these people and hair loss resumes, with loss of that being maintained by the treatment, when it is ceased. • Finasteride 1 mg tablet taken daily for a minimum of 2 years. This can halt the balding process in over 85% of men and may initiate some modest regrowth in 65% over a 12-month period, with further improvement if it is continued over a longer period. However, it is

expensive, is not a cure and balding resumes when it is discontinued. Treatment (women)

Physical treatments/hair styling This includes the use of wigs, hair transplantation and camouflage. Wigs can be worn on the whole head or on the bald spot, or fibres can be interwoven into the remaining hairs. Camouflage can be used either by having the existing hair bleached by a skilled hairdresser or by colouring the scalp the same colour as the hair. Mascara can be lightly brushed into the roots of the hair at receding hairlines or along gaps.

Medications2 minoxidil 2% and 5% topical application bd for minimum of 12 months (to assess efficacy) although one large trial has approved its effectiveness generally in women6 or spironolactone 100 mg increasing to 200 mg daily for 6 months or cyproterone acetate 100 mg (o) daily (course of 10 tablets a month) usually with OCP (coinciding with 10 active pill days) • If postmenopausal, cyproterone acetate 50 mg (o) daily in consultation with an endocrinologist As for men, these drugs tend to prevent further loss and, if effective, need long-term use.

Trichotillomania (hair pulling) This is patchy hair loss caused by deliberate plucking or twisting of hair shafts. It is reasonably common in young children, where it may be of little significance, simply being a ‘habit’. In older children and adults it may be an obsessive compulsive disorder often associated with stress.1

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Hair disorders Clinical features • Incomplete patchy alopecia • Hairs of different length • Hairs broken and twisted • Strange pattern of loss • Tends to occur on side of dominant hand • Eyelashes or eyebrows may be involved

Hair disorders in children Loose anagen (growing hair) syndrome7 This is a disorder of the hair follicle characterised by the ability to pluck anagen hairs painlessly from the scalp by gentle pulling. It presents as very thin, wispy new hair growth. It is an autosomal dominant trait.

are usually on the anterior and temporal areas of the head (see FIG. 128.6). The areas are never completely bald. A characteristic feature is an irregular-shaped area of incomplete patchy alopecia containing hairs of different length. The variable length is due to the fact that some hairs will not break with pulling while others will break at varying distances from the scalp surface. There may be associated follicular pustules. However, scrapings should be taken to exclude a particular type of tinea capitis (black dot ringworm) caused by Trichophyton tonsurans. The management is similar to thumb sucking or nail biting with a low-key approach. It does not imply a significant psychological problem.

Clinical features • Thin wispy hair with tatty ends • More common in girls; can affect boys • Onset in early childhood—usually 95% • Salbutamol 12 puffs (adult) in a spacer (4 × 4 × 4 rule) or • Continuous nebulised 0.5% salbutamol by face mask, using compressed (8 L/min) oxygen for nebulisation ↓ insert IV line • hydrocortisone 250 mg IV or IM ↓ if poor response • magnesium sulphate 25–100 mg/kg IV over 20 minutes • adrenaline 0.5 mg 1:1000 SC or IM or 1:10 000 IV If not responding, exhausted and moribund: • intubation with intermittent positive pressure ventilation (IPPV) • hydration with IV fluids

Opioid respiratory depression4 • Attend to airway (e.g. pocket mask and bag) • naloxone 0.1–0.2 mg IV boluses titrated to clinical effect Beware of recurrence of respiratory depression or neurogenic pulmonary oedema from excess naloxone.

Severe hypoglycaemia (confirm by blood glucose) glucagon 1 mL IM or SC (most practical option) then oral glucose—can repeat glucagon or 50% dextrose 20 mL IV through securely positioned canula (if IV line difficult, administer rectally by pressing the nozzle of a large syringe into the anus and injecting slowly)

Myocardial infarction/unstable angina Refer to CHAPTER 40.

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First-line management • Oxygen (face mask) 6 L/min • Insert IV line • Glyceryl trinitrate (nitroglycerin) 300 mcg (1/2 tab) SL, or spray if BP >100 mmHg • Aspirin 300 mg (1/2 or 1 tab) • Morphine 1 mg per minute IV until pain relief (up to 15 mg)—usually 2.5–10 mg (lower dose if elderly/frail) • ECG (set up by an assistant) • Arrange ambulance and hospitalisation

Hyperventilation Rebreathe slowly from a paper (not plastic) bag or into cupped hands.

Status epilepticus and serial seizures Status  epilepticus  =  repeated convulsions without regaining consciousness after initial tonic–clonic seizure. Serial  seizures  =  repeated convulsions after regaining consciousness. Management (Refer CHAPTER 84.) • Lie patient on side • Ensure adequate oxygenation: attend to airway (e.g. Guedel tube); give oxygen 8 L/min (check blood sugar) If persisting >5 minutes: (summarised) midazolam 5–10 mg IM or IV over 2–5 minutes or midazolam 5–10 mg buccally (tear top off plastic ampoule,5 slowly drip into patient’s mouth between gums and cheek—with syringe or from ampoule) or midazolam 5–10 mg intranasal—1–3 drops at a time into alternate nostrils repeat once in 15 minutes (if necessary) or diazepam 0.05 mg/kg/minute IV until the seizures cease or respiratory depression begins (beware of respiratory depression and other vital parameters): usually 10–20 mg bolus in adult When seizures cease, follow immediately with: • phenytoin 15–20 mg/kg IV over 30 minutes or • sodium valproate 10 mg/kg by slow IV infusion Other drugs to consider: • phenobarbitone, thiopentone

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BITES AND STINGS Bites and stings from animals, spiders and insects are common in Australia and the US but fatal bites are uncommon.

Snake bites

130

Snake bites are more common and severe in those handling snakes and in those trying to kill the snake. Snakes are more aggressive when mating or sloughing their skin (about four times a year). They strike for one-third of their length at 3.5 metres/second. Over 70% of bites are on the legs. Sea snakes are not a major problem in Australian waters. First aid 1 Keep the patient as still as possible. 2 Do not wash, cut, manipulate the wound, apply ice or use a tourniquet. 3 Immediately bandage the bite site very firmly (not too tight). A 15 cm crepe bandage is ideal: it should extend above the bite site for 15 cm (e.g. if bitten around the ankle the bandage should cover the leg to the knee). 4 Splint the limb to immobilise it: a firm stick or slab of wood would be ideal. 5 Transport to a medical facility for definitive treatment. Do not give alcoholic beverages or stimulants. Note: A venom detection kit is used to examine a swab of the bitten area or a fresh urine specimen but only to identify the snake species involved. The bandage can be removed when the patient is safely under medical observation. Observe for symptoms and signs of envenomation. Antivenom for most venomous Australian snakes in addition to a polyvalent vaccine is available . Envenomation Not all patients become envenomated and the antivenom should not be given unless there is evidence of this. Envenomation is more likely when the snake has a clear bite, such as in snake handlers or barefooted people or hands placed in burrows. Apart from non-specific systemic effects (as listed) there may be major organ effects according to the type of snake and its toxin. These include coagulopathy, neurotoxicity, myolysis and kidney damage.

Important early symptoms of snake bite envenomation include: • • • • • • • •

nausea and vomiting (a reliable early symptom) abdominal pain excessive perspiration severe headache dizziness, blurred vision difficulty speaking or swallowing coagulation defects (e.g. haematuria) tender lymphadenopathy

The greatest danger is respiratory obstruction and failure or unexpected catastrophic bleeding (e.g. intracerebral haemorrhage). Refer to FIGURE 130.2 for detailed effects. Investigations and observation • Careful observations (e.g. vital signs, conscious state) • Test all urine for blood and protein • FBE, serum electrolytes, LFTs, KFTs • Watch for coagulopathy (e.g. spitting and coughing blood, bleeding from wounds/IV site, haematuria) • Serial whole blood clotting time (a plain glass tube): normal 15 min significant • Coagulation screen—APTT and PT or INR • Venom detection kit: wound site (best) or urine (not always indicator) Treatment of envenomation See note 2 (below). • • • •

Reassure patient at all times Set up a slow IV infusion of N saline Keep adrenaline on standby Dilute the specific antivenom (1 in 10 in N saline) and infuse slowly over 30 minutes via the tubing of the saline solution • Have adrenaline, antihistamines, oxygen, and steroids on standby • Monitor vital signs • Provide basic life support as necessary Note 1: The use of prophylactic adrenaline is controversial and some authorities reserve it for a reaction to the antivenom. It is best avoided with brown snake envenomation and with coagulopathy. Note 2: Do not give antivenom unless clinical signs of envenomation or biochemical signs (e.g. positive urine, or abnormal clotting profile). Note 3: One ampoule may be sufficient but three or more may be needed, especially if coagulopathy.

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Emergency care

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Symptoms of envenomation vomiting/nausea haematemesis dizziness headache coughing or spitting blood sweating muscle pain

abdominal pain

Pain in groin tender lymphadenopathy haematuria

CNS stuporose loss of consciousness or neurotoxic effects (esp. cranial nerves): – ptosis – blurred, double vision – difficulty swallowing and speaking – central voluntary muscle weakness

Bite site one or paired puncture mark (may not be visible) ± pain, swelling or local reaction continued bleeding

FIGURE 130.2 How to recognise snake bite envenomation

Spider bites4 The toxin of most species of spider causes only localised pain, redness and swelling, but the toxin of some, notably the deadly Sydney funnel-web spider (Atrax robustus), can be rapidly fatal. Rule: a bite from a large black spider should be managed initially as for a funnel-web spider. First aid • Sydney funnel-web: as for snake bites • Other spiders: apply an ice pack, do not bandage

Treatment

1 Sydney funnel-web Signs of envenomation (in order): • • • • •

muscle fasciculation—limb → tongue/lip marked salivation or lacrimation piloerection dyspnoea neurological symptoms (e.g. disorientation, coma) Treatment of envenomation

• specific antivenom (usually 4–8 vials) • admit to a hospital critical care area • resuscitation and other supportive measures

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2 Other spider bites The toxins of most species of spiders cause only localised symptoms but the venom of a selected few, namely the red-back spider of Australia (Latrodectus hasseltii) and the related black widow spider of the US (Latrodectus mactans), can cause envenomation. This is rarely fatal but is more serious in the young, the frail and the elderly. The bite wounds are prone to infection. Treatment of envenomation (rarely needed): • antivenom given IM or diluted IV injection

130

Bee stings First aid 1 Scrape the sting off sideways with a fingernail or knife blade. Do not squeeze it with the fingertips. 2 Apply 20% aluminium sulphate solution (Stingose) or methylated spirits. 3 Apply ice to the site. 4 Rest and elevate the limb that has been stung. If anaphylaxis, treat as outlined earlier. Preventive measures (if hypersensitive) • Avoid bees (and wasps) if possible. • Immunotherapy to honey bee (or wasp) venom. There is no cross-allergy between the honey bee, the ‘yellow jacket wasp’ and the paper wasp. Specific hyposensitisation against the Vespula species is required. For the bee, use pure venom antigen. • Immunotherapy should be offered to those: — with a history of asthma who have had a single severe reaction to a bee sting — who have had a minimum of three stings with serial crescendo reactions — occupationally exposed who manifest severe reactions — with elevated venom-specific IgE (RAST) antibodies, or positive venom prick tests

Centipede and scorpion bites The main symptom is pain, which can be very severe and prolonged. Usually minor systemic symptoms. First aid 1 Apply local heat (e.g. hot water with ammonia— household bleach). 2 Clean site. 3 Local anaesthetic (e.g. 1–2 mL of 1% lignocaine) infiltrated around the site.

4 Consider opioids—morphine or fentanyl—for pain. 5 Consider promethazine injection. 6 Check tetanus immunisation status.

Box jellyfish or sea wasp (Chironex fleckeri)4 This is the most dangerous jellyfish in Australian waters and has been responsible for at least 80 extremely painful and sudden deaths.4 Death can occur in minutes due to cardiopulmonary failure, especially in children. There can be up to 180 metres of stinging tentacles. The sting gives a ‘frosted ladder’ appearance. The jellyfish is limited to tropical waters north of the Tropic of Capricorn (Exmouth in west to Gladstone in east) and is found in coastal waters during the summer. Prevention • Avoid swimming, paddling and wading in ‘jellyfish alert’ areas in unsafe months. • Otherwise, use a ‘stinger suit’. Treatment4 • The victim should be removed from the water to prevent drowning. • Immediately remove tentacles. • Pour vinegar liberally to sting site and surrounding area—use up to 2 L of vinegar at a time. • Use a cold pack for small stings and ice massage for large areas. • Check respiration and the pulse. • Start immediate cardiopulmonary resuscitation if necessary. • Gain IV access and give magnesium sulphate 50%; give oxygen and up to 5 mL inotropes if necessary. • Give box jellyfish antivenom by IV injection for major stings (may need at least 6 ampoules if patient remains in cardiac arrest). • Provide pain relief if required (ice, lignocaine and analgesics—fentanyl or morphine). Note: A delayed reaction can occur—the stings can cause pain after weeks (oral steroids are used). Pressure immobilisation bandaging is no longer recommended for Chironex stings.

Irukandji syndrome4 This is caused by Carukia barnesi, a tiny box jellyfish that can penetrate safety nets for Chironex, and

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Emergency care possibly other species of box jellyfish. Initially a mild sting with a delayed severe syndrome (usually after 30 minutes): • severe generalised back, abdominal and muscle pain and muscle cramps • chest pain, sweating and anxiety • anxiety, restlessness, ‘impending doom’ feeling • headache, nausea, vomiting • tachycardia, hypertension There is no specific first aid or antivenom but resuscitation measures may be needed as death can occur from pulmonary oedema or cardiac arrest. Measures include morphine or fentanyl 5 mg IV every 5 minutes as required, blood pressure control (e.g. phentolamine, CPAP and oxygen for pulmonary oedema) and possibly IV magnesium.

Common jellyfish stings4 These include bluebottle (Physalia species) and others that cause intense local pain (up to an hour or more) and linear skin redness. Systemic effects are uncommon. Treatment • Wash the sting site with sea water. • Remove any tentacles with gloved hands or water. • Immerse affected site in hot water at 45°C for 20 minutes. This is quite hot so check tolerance to temperature on other limb. • Vinegar is not helpful.

Stinging fish4 The sharp spines of the stinging fish have venom glands that can produce severe pain if they spike or even graze the skin. The best known of these is the stonefish. Others include bullrout, catfish, seaurchins and crown of thorns (may need an X-ray). The toxin is usually heat-sensitive. Stingrays cause a gash wound with possible superinfection. Envenomation • Intense pain • Localised swelling • Bluish discolouration Treatment • Clean the wound—consider exploration. • Bathe or immerse the affected part in very warm to hot (not scalding, 45°C) water—this may give instant relief.4 • Give simple analgesics.

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• If pain persists, give a local injection/infiltration of lignocaine 1% or even a regional block. If still persisting, consider morphine IV or fentanyl IV. • A specific antivenom is available for the sting of the stonefish. Best given IV by slow infusion in CCU.

Mollusc bite (blue-ringed octopus, cone shell)4 Mollusc venoms usually cause numbness or paraesthesia but can be rapidly fatal because of prolonged muscular weakness leading to respiratory paralysis. Treatment • Compression bandage to bite site (usually hand/arm) • Immobilise the limb • Arrange transport (preferably by ambulance) to a medical facility • Observe (and manage) for respiratory paralysis— ensure adequate ABC

Sandfly bites For some reason, possibly the nature of body odour, the use of oral thiamine may prevent sandfly bites. Dose: thiamine 100 mg orally, daily

Other bites and stings This includes bites from ants, wasps and mosquitoes. First aid 1 Wash the site with large quantities of cool water. 2 Apply vinegar (liberal amount) or aluminium sulphate 20% solution (Stingose) to the wound for about 30 seconds. 3 Apply ice for several minutes. 4 Use soothing anti-itch cream or 5% lignocaine cream or ointment if very painful. Medication is not usually necessary unless an acute allergic reaction develops.

The embedded tick4 Some species of ticks can be very dangerous to human beings, especially to children. In Australia, tick paralysis is confined to the eastern seaboard. Be careful in children 1–5 years—they are usually found in the scalp behind the ears. If they attach themselves to the head or neck, usually behind the ear, a serious problem

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exists. As it is impossible to distinguish between dangerous and non-dangerous ticks, early removal is mandatory. The tick should be totally removed—and the mouthparts of the tick must not be left behind. Do not attempt to grab the tick by its body and tug. This is rarely successful in dislodging the tick, and more toxin is thereby injected into the host. As an office procedure, many practitioners grasp the tick’s head as close to the skin as possible with fine forceps or tweezers, and pull the tick out sideways with a sharp rotatory action. This is acceptable, but not as effective as the methods described here.

130

First aid outdoor removal method • Loop a strong thin thread (as a half-hitch lasso) around the tick’s head as close to the skin as possible, and pull sharply with a twisting motion. Suitable materials include strong silk sutures or dental floss. • A pyrethrin-based spray is often used. Office procedure • Infiltrate a small amount of local anaesthetic into the skin around the site of embedment. • With a number 11 or 15 scalpel blade, make the necessary very small excision, including the mouthparts of the tick, to ensure total removal (see FIG. 130.3). • The small defect can usually be closed with a bandaid (or Steri-Strips). • Careful observation is needed after removal.

A POTPOURRI OF EMERGENCY CALLS

Electric shock Facts • Direct current (DC) from welding machines or lightning produces more electrolyte tissue damage and burns than AC (domestic supply). • Injuries occur at sites distant from entry or exit. • Severe muscle contractions can cause bone fracture or posterior dislocation of the shoulder. • Household shocks tend to cause cardiac arrest (ventricular fibrillation) and myocardial damage is common. • Ischaemic necrosis of a limb or digit is possible. • Apparently minor initial injuries may be very misleading (see FIG. 130.4). • Neurological deficits and psychoneurotic sequelae are common in survivors.

ventricular fibrillation

ischaemic necrosis

? fracture

exit wound

mouthparts of the tick

FIGURE 130.4 Effect of electric shock passing through the body engorged tick

skin

line of excision

FIGURE 130.3 Removing the embedded tick

Human bites and animal bites These bites can cause problems of suppurative infection and management in general. They are outlined in CHAPTER 134.

Principles of management • Make the site safe: switch off the electricity. Use dry wool to insulate rescuers. • ‘Treat the clinically dead’. • Attend to ABC. • Give a precordial thump in a witnessed arrest. • Consider a cervical collar (? cervical fracture). Bystander CPR and prolonged respiratory support for electric shocks and lightning strike can be lifesaving.

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Emergency care • Provide basic cardiopulmonary resuscitation, including defibrillation (as required). • Investigate and consider: — careful examination of all limbs — X-ray of limbs or spine as appropriate — check for myoglobinuria and kidney failure — give tetanus and clostridial prophylaxis • Get expert help—intensive care unit, burns unit.

Lightning strike Prevention (during an electrical storm) • Don’t shelter under trees or tall objects (splash phenomenon—see FIG. 130.5).6 • Stay indoors—shelter in a building or closed car. • Avoid using telephone. • Avoid holding metal objects (e.g. golf clubs). • Keep as low to ground as possible (e.g. curl up in a ditch). • Avoid being in a group.

Clinical effects • Burn injury (90%): the ‘flashover’ phenomenon—clothing disintegrates • Blast injury (e.g. ruptured spleen, subdural, ruptured eardrum)

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• Electrical injury as for household shock (uncommon)

Petrol and solvent sniffing Substances commonly sniffed include petrol, glues, spirit-based paints, paint spray cans and other aerosols. The three main acute problems are: 1 shaking and fitting: give midazolam IV or IM or diazepam IV (as for convulsions) 2 agitation/aggressive behaviour, self-harm: try to calm patient in a well-lit room; give sedation with diazepam; give haloperidol for hallucinations or delusions 3 general debilitation: this may include acute infections (e.g. chest infection) or anaemia; investigation and referral for breaking the habit is necessary

Near-drowning4

FIGURE 130.5 ‘Splash effect’ where current is reflected from tree

37

Near-drowning is survival after asphyxia from submersion in a liquid medium. Hypoxia is the final common pathway in drowning or near-drowning, whether by water aspiration (wet drowning) or by glottic closure (dry drowning). The rule to remember is that victims can respond to resuscitation after considerable immersion time (up to 30 minutes) and that mouth-to-mouth resuscitation should always be attempted even if pulseless or with fixed dilated pupils. The usual routine of basic life support and CPR apply. All symptomatic patients should receive high-flow oxygen and ideally CPAP or BiPAP. Those requiring intubation should receive positive end expiratory pressure (PEEP) in an in-patient facility. Artificial surfactant given via an endotracheal tube has been used successfully in the UK. There is no significant difference in outcome and management between salt water and fresh water drowning. Hypothermia should be attended to with warming, such as a hot-air blanket if available and warm fluids.

Epistaxis Refer to CHAPTER 59.

Opioid (heroin) overdose Refer to CHAPTER 75 and earlier in this chapter.

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Migraine

Table 130.1

Refer to CHAPTER 56.

Vital emergency skills Cardiopulmonary resuscitation

130

Cardiopulmonary arrest (CPA) It is essential that all doctors are familiar with the protocol for instituting basic life support in such an eventuality. Sick patients do visit our offices daily and the potential for sudden collapse, including a cardiac arrest, is ever present. About 75% of arrests are due to ventricular fibrillation and more than 75% of victims have severe coronary artery disease.7 After 3 minutes of CPA (unconsciousness, no pulse, no respiration) there is an increasing risk of permanent cerebral dysfunction. Important causes of sudden death are outlined in 8 TABLE 130.1. The ABC basic life support for cardiac arrest should be followed, but DRABCD is best (defibrillation first if a defibrillator is available—the outcome appears to be directly related to the speed of defibrillation). The ‘chain of survival’ principle for a victim of out-of-hospital cardiac arrest is presented in FIGURE 130.6. 9

Basic life support The following represents a logical DRSABCD plan for the adult patient who collapses or is found apparently unconscious. D= R= S = A=

assess Danger assess Response Send for help Airway open

Causes of sudden death

Cardiac arrhythmias: • ventricular fibrillation (75%) • ventricular tachycardia • torsade de pointes VT (? drugs) • sick sinus syndrome • severe bradycardia Sudden pump failure: • acute myocardial infarction • cardiomyopathy Cardiovascular rupture: • myocardial rupture • dissecting aneurysm of aorta • subarachnoid haemorrhage Acute circulatory obstruction: • pulmonary embolism Others: • aortic stenosis • pulmonary hypertension • mitral valve prolapse • electrolyte abnormalities • glue sniffing

B = Breathing C = Circulation/CPR D = Defibrillation 1 Shake and shout at the patient. 2 Check breathing. 3 Check pulse (feel carotid adjacent to thyroid cartilage). 4 Call for help (if no pulse). Ring 000 (or 112 from mobile services) or 911. 5 Finger sweep oropharynx (clear it). 6 Place victim on back on firm surface. 7 Thump precordium (if arrest witnessed). 8 Tilt head back (to maximum).

CHAIN OF SURVIVAL

Early access

Early CPR

Early defillibration

Early advanced life support

to get help

to buy time

to restart heart

to stabilise casualty

FIGURE 130.6 The chain of survival for a victim of out-of-hospital cardiac arrest

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Emergency care

Table 130.2

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Basic schedule for CPR Infant 5.0) consider giving oral vitamin K e.g. 10 mg tablet. 4 If bleeding is minor, transient action as in point 2 is still appropriate.

5 If bleeding is persistent, or severe, or involves closed body cavities (such as pericardium, intracranial, fascial compartment), urgent admission to hospital is essential. The anticoagulation may need to be reversed by administering oral or parenteral vitamin K. Infusion of fresh frozen plasma and/or prothrombin complex concentrate (best option) may also be necessary. Drug interactions There are so many potential interactions between warfarin and other drugs that the following general principles should be applied: 1 Maintain the simplest possible drug regimens. Avoid polypharmacy. 2 Aspirin is contraindicated while the patient is on warfarin because of the combined antiplatelet and anticoagulation effects. The risk of gastrointestinal bleeding is also increased. Other NSAIDs should also be avoided (see TABLE 133.3). 3 If the patient’s drug regimen must be altered during warfarin therapy, then the INR should be followed closely until stable.

Advice to the patient • Keep to a consistent diet. • Do not take aspirin or liquid paraffin. • Always mention that you take warfarin to any doctor, dentist or chemist you are consulting. • Remember to take tablets strictly as directed and have your blood tests. • Report signs of bleeding, such as black motions, blood in urine, easy bruising, unusual nose bleeds, heavy periods, ‘purple toes’. Note: Give the patient the information sheet about risks, especially if ceasing warfarin.

Bleeding on heparin • Recheck APTT • Cease or reduce heparin • Admit patient—alert laboratory and haematologist Antidotes: • protamine sulfate will reverse (use with caution) • fresh frozen plasma • clotting factors (as guided by consultant)

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Thrombosis and thromboembolism

Table 133.3

Some important drug interactions with warfarin

Effects on warfarin activity

Drug

↑  Increased

Allopurinol Amiodarone Anabolic steroids

Aspirin—salicylates (high doses) Chloral hydrate

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Practice tips for warfarin10 • • •

Antibiotics (broad spectrum) Antifungals

61

• •

Consider avoiding use if patient compliance is likely to be poor. The INR result reflects the warfarin dose administered 48–72 hours earlier. Advise and encourage patients to keep a record in an ‘anticoagulant diary’ of drug dosage and INR results. An unacceptable INR is >5.0. Discontinue therapy if skin necrosis or ‘purple toes syndrome’ occurs.

Cimetidine Clofibrate Gemfibrozil Metronidazole Miconazole NSAIDs, including COX-2 inhibitors Paracetamol (large doses) Phenytoin Proton-pump blockers Quinidine/quinine Ranitidine SSRIs Sulphonamides Tamoxifen Thyroxine Herbal medicines: • dong quai • papaya • St John’s wort ↓ Decreased

Antacids Antihistamines Barbiturates Anti-epileptics (e.g. carbamazepine) Cholestyramine (reduced absorption) Griseofulvin Haloperidol Oestrogen/oral contraceptives Rifampicin Vitamin C

Increased or decreased Alcohol Chloral hydrate Diuretics Ranitidine

References 1 Kumar P, Clark M. Clinical Medicine (7th edn). London: Elsevier-Saunders, 2009: 465. 2 Joseph J. Thrombophilia. Common sense pathology. RCPA, 2004. 3 Moulds R (Chair). Therapeutic Guidelines: Cardiovascular (Version 5). Melbourne. Therapeutic Guidelines Ltd, 2012. 4 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013: 309–16. 5 Brieger D, Curnow J. Anticoagulation: a GP primer on the new anticoagulants. Aust Fam Physician, 2014; 43 (5): 254–9. 6 Gallus AS. Anticoagulation: how to treat. Australian Doctor, 4 March 2005: 29–36. 7 Walker ID et al. Guidelines on oral anticoagulation (3rd edn). Br J Haematol, 1998; 101: 374–87. 8 Gallus AS. Consensus guidelines for warfarin therapy— recommendations from the Australasian Society of Thrombosis and Haemostasis. Med J Aust, 2000; 172: 600–5. 9 Baker R et al. Australian and NZ Consensus Guidelines for Warfarin Reversal. Med J Aust, 2004; 181 (9): 492–7. 10 Campbell P, Roberts R, Eaton V et al. Managing warfarin therapy in the community. Australian Prescriber, 2001; 24: 86–9.

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134 Common skin wounds and foreign bodies The variety of foreign bodies which have found their way into the rectum is hardly less remarkable than the ingenuity displayed in their removal. A turnip has been delivered PR by the use of obstetric forceps. A stick firmly impacted has been withdrawn by inserting a gimlet into its lower end. A tumbler, mouth downwards, has several times been extracted by filling the interior with a wet plaster of Paris bandage, leaving the end of the bandage extruding, and allowing the plaster to set. Bailey and Love, Short Practice of Surgery,  Injuries to the skin, including simple lacerations, abrasions, contusions and foreign bodies, are among the commonest problems encountered in general practice. To manage these cosmetically important injuries well is one of the really basic and enjoyable skills of our profession.

Key facts and checkpoints •

• •

•

• • • • • •

A well-prepared treatment room with good sterilisation facilities, instruments, sterile dressings and an assistant facilitates management. With lacerations, check carefully for nerve damage, tendon damage and arterial damage. Beware of slivers of glass in wounds caused by glass—explore carefully and X-ray (especially with high-resolution ultrasound) if in doubt. Beware of electrical or thermal wounds because marked tissue necrosis can be hidden by slightly injured skin. Beware also of roller injuries such as car wheels. Beware of pressure gun injuries such as oil and paint. The consequences can be disastrous. Avoid suturing the tongue, and animal and human bites, unless absolutely necessary. Keep drawings or photographs of wounds in your medical records. Have a management plan for puncture wounds, including medical needle-stick injuries. Gravel rash wounds are a special problem because retained fragments of dirt and metal can leave a ‘dirty’ tattoo-like effect in the healed wound.

Contusions and haematomas A contusion (bruise or ecchymosis) is the consequence of injury causing bleeding in subcutaneous or deeper

tissue while leaving the skin basically intact. It might take weeks to resolve, especially if extensive. A haematoma is a large collection of extravasated blood that produces an obvious and tender swelling or deformity. The blood usually clots and becomes firm, warm and red; later (about 10 days) it begins to liquefy and becomes fluctuant.

Principles of management • Explanation and reassurance • RICE (for larger bruises/haematomas) for 48 hours R = Rest I = Ice (for 20 minutes every 2 waking hours) C = Compression (firm elastic bandage) E = Elevation (if a limb) • Analgesics: paracetamol/acetaminophen • Avoid aspiration (some exceptions) • Avoid massage • Heat may be applied after 72 hours as local heat or whirlpool baths • Consider possibility of bleeding disorder if bleeding is out of proportion to the injury

PROBLEMATIC HAEMATOMAS Some haematomas in certain locations can cause deformity and other problems.

Haematoma of nasal septum1 Refer CHAPTER 59.

Haematoma of the pinna1 When trauma to the pinna causes a haematoma between the epidermis and the cartilage, a permanent deformity known as ‘cauliflower ear’ may result.

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Common skin wounds and foreign bodies The haematoma, if left, becomes organised and the normal contour of the ear is lost. The aim is to evacuate the haematoma as soon as practical and then to prevent it reforming. One can achieve a fair degree of success even on haematomas that have been present for several days. Method Under aseptic conditions insert a 25 gauge needle into the haematoma at its lowest point and aspirate the extravasated blood (see FIG. 134.1a). Apply a padded test tube clamp to the haematoma site and leave on for 30–40 minutes (see FIG.  134.1b). Generally, daily aspiration and clamping are sufficient to eradicate the haematoma completely.

Subungual haematomas These important haematomas are discussed in CHAPTER 129.

Abrasions Abrasions vary considerably in degree and potential contamination. They are common with bicycle or motorcycle accidents and skateboard accidents. Special care is needed over joints such as the knee or elbow.

Rules of management

Lacerations Lacerations vary enormously in complexity and repairability. Very complex lacerations and those involving nerves or other structures should be referred to an expert.

(b)

Principles of repair

FIGURE 134.1 Treatment of haematoma of the pinna

Pretibial haematoma A haematoma over the tibia (shin bone) can be persistently painful and slow to resolve. An efficient method is, under very strict asepsis, to inject 1 mL lignocaine 1% and 1 mL hyaluronidase and follow

1443

with immediate ultrasound. This may disperse or require drainage.

• Clean meticulously, remove all ground-in dirt, metal, clothing and other material. • Scrub out dirt with sterile normal saline under anaesthesia (local infiltration or general anaesthesia for deep wounds). • Treat the injury as a burn. • When clean, apply a protective dressing (some wounds may be left open). • Use paraffin gauze and non-adhesive absorbent pads such as Melolin. • Ensure adequate follow-up. • Immobilise a joint that may be affected by a deep wound.

(a)

63

• Good approximation of wound edges minimises scar formation and healing time. • Pay special attention to debridement. • Avoid deep layers of suture material in a contaminated wound—consider drainage. • Inspect all wounds carefully for damage to major structures such as nerves and tendons and for foreign material: — shattered glass wounds require careful inspection and perhaps plain X-ray or ultrasound — high-energy wounds (e.g. motor mowers) are prone to have metallic foreign bodies and associated fractures

134

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• Be ready to take X-rays of wounds to look for foreign objects or fractures (compound fractures). • Trim jagged or crushed wound edges, especially on the face. • All wounds should be closed in layers. • Avoid leaving dead space. • Do not suture an ‘old’ wound (greater than 8 hours) if it is contaminated with primary closure: leave 4 days before suturing if not infected. • Take care in poor healing areas, such as backs, necks, calves and knees, and in areas prone to hypertrophic scarring, such as over the sternum of the chest and the shoulder. • Use atraumatic tissue-handling techniques. • Everted edges heal better than inverted edges. • Practise minimal handling of wound edges. • A suture is too tight when it blanches the skin between the thread—it should be loosened. • Avoid tension on the wound, especially in fingers, lower leg, foot or palm. • The finest scar and best result is obtained by using a large number of fine sutures rather than fewer thicker sutures more widely spread. • Avoid haematoma. • Apply a firm pressure dressing when appropriate, especially with swollen skin flaps. • Consider appropriate immobilisation for wounds. Many wound failures are due to lack of immobilisation from a volar slab on the hand or a back slab on the leg. Practical aspects See TABLE 134.1.

Examples of good-quality instruments: • • • •

locking needle holder (e.g. Crile–Wood 12 cm) skin hooks iris scissors toothed forceps

Holding the needle The needle should be held in its middle; this will help to avoid breakage and distortion, which tend to occur if the needle is held near its end (see FIG. 134.2).

Dead space

Selection of suture material (guidelines)

Skin

Instruments

FIGURE 134.2 Correct and incorrect methods of holding the needle

Suture material

Table 134.1

• Monofilament nylon sutures are generally preferred for skin repair. • Use the smallest calibre compatible with required strains. • The synthetic, absorbable polyglycolic acid or polyglactin sutures (Dexon, Vicryl) are stronger than catgut of the same gauge, but do not use these (use catgut instead) on the face or subcuticularly.

Nylon 6/0

Face

Nylon 3/0

Back, scalp

Nylon 5/0

Elsewhere

Deeper tissue (dead space)

Catgut 4/0 Dexon/Vicryl 3/0 or 4/0

Face Elsewhere

Subcuticular

Catgut 4/0

Small vessel ties

Plain catgut 4/0

Large vessel ties

Chromic catgut (CCG) 4/0

Dead space should be eliminated to reduce tension on skin sutures. Use buried, absorbable sutures to approximate underlying tissue. This is done by starting suture insertion from the fat to pick up the fat/dermis interface so as to bury the knot (see FIG. 134.3).

buried knot Introduce needle here

FIGURE 134.3 Eliminating dead space

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Common skin wounds and foreign bodies Everted wounds Eversion is achieved by making the ‘bite’ in the dermis wider than the bite in the epidermis (skin surface) and making the suture deeper than it is wide. Shown are: • simple suture (see FIG. 134.4a) • vertical mattress suture (see FIG. 134.4b)

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Method 1 Pass the needle through the skin of the non-flap side of the wound. 2 Pass it then through the subcuticular layer of the flap tip at exactly the same level as the reception side. 3 Finally, pass the needle back through the reception side so that it emerges well back from the V flap (see FIG. 134.5).

(a)

(b)

134 FIGURE 134.4 Everted wounds: (a) correct and incorrect methods of making a simple suture, (b) making a vertical mattress suture FIGURE 134.5 The three-point suture

The mattress suture is the ideal way to evert a wound.

Number of sutures One should aim to use a minimum number of sutures to achieve closure without gaps but sufficient sutures to avoid tension. Place the sutures as close to the wound edge as possible.

SPECIAL TECHNIQUES FOR VARIOUS WOUNDS

The three-point suture In wounds with a triangular flap component, it is often difficult to place the apex of the flap accurately. The three-point suture is the best way to achieve this while minimising the chance of strangulation necrosis at the tip of the flap.

Triangular flap wounds on the lower leg Triangular flap wounds below the knee are a common injury and are often treated incorrectly. Similar wounds in the upper limb heal rapidly when sutured properly, but lower limb injury will not usually heal at first intention unless the apex of the flap is given special attention. Proximally based flap A fall through a gap in flooring boards will produce a proximally based flap; a heavy object (such as the tailboard of a trailer) striking the shin will result in a distally based flap. Often the apex of the flap is crushed and poorly vascularised; it will not survive to heal after suture.

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Treatment methods (under infiltration with LA) 1 Preferred method: to attempt to salvage the distal flap, scrape away the subcutaneous tissue on the flap and use it as a full-thickness graft. 2 An alternative is to excise the apex of the flap, loosely suture the remaining flap and place a small split-thickness graft on the raw area (see FIG. 134.6). donor site (within anaesthetised area)

excised apex of skin flap and graft site

FIGURE 134.6 Triangular flap wound repair: proximally based flap

134

For both methods apply a suitable dressing and strap firmly with a crepe bandage. The patient should rest with the leg elevated for 3 days.

Repair of cut lip While small lacerations of the buccal mucosa of the lip can be left safely, more extensive cuts require careful repair. Local anaesthetic infiltration may be adequate, although a mental nerve block is ideal for larger lacerations of the lower lip. For wounds that cross the vermilion border, meticulous alignment is essential. It may be advisable to premark the vermilion border with gentian violet or a marker pen. It is desirable to have an assistant. Method 1 Close the deeper muscular layer of the wound using 4/0 CCG. The first suture should carefully appose the mucosal area of the lip, followed by one or two sutures in the remaining layer. 2 Next, insert a 6/0 monofilament nylon suture to bring both ends of the vermilion border together. The slightest step is unacceptable (see FIG. 134.8). This is the key to the procedure. 3 Close the inner buccal mucosa with interrupted 4/0 plain catgut sutures. 4 The outer skin of the lip (above and below the vermilion border) is closed with interrupted nylon sutures.

Distally based flap See FIG.  134.7. This flap, which is quite avascular, has a poorer prognosis. The same methods as for the proximally based flap can be used. Trimming the flap and using it as a full thickness graft has a good chance of repair in a younger person but a poor chance in the elderly.

FIGURE 134.8 The lacerated lip: ensuring meticulous suture of the vermilion border

Post repair

FIGURE 134.7 Triangular flap wound repair: distally based flap

1 Apply a moisturising lotion along the lines of the wound. 2 Remove nylon sutures in 3–4 days (in a young person) and 5–6 days (in an older person).

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Common skin wounds and foreign bodies

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Repair of lacerated eyelid General points • Preserve as much tissue as possible. • Do not shave the eyebrow. • Do not invert hair-bearing skin into the wound. • Ensure precise alignment of wound margins. • Tie suture knots away from the eyeball. Method 1 Place an intermarginal suture behind the eyelashes if the margin is involved. 2 Repair conjunctiva and tarsus with 6/0 catgut. 3 Then repair skin and muscle (orbicularis oculi) with 6/0 nylon (see FIG. 134.9).

FIGURE 134.10 Repair of tongue wound

The amputated finger FIGURE 134.9 The lacerated eyelid

Repair of tongue wound Wherever possible, it is best to avoid repair to wounds of the tongue because these heal rapidly. However, large flap wounds to the tongue on the dorsum or the lateral border may require suturing. The best method is to use buried catgut sutures. Method 1 Get patient to suck ice for a few minutes, then infiltrate with 1% lignocaine and leave 5–10 minutes. 2 Use 4/0 or 3/0 catgut sutures to suture the flap to its bed, and bury the sutures (see FIG. 134.10). It should not be necessary to use surface sutures. If it is, 4/0 silk sutures will suffice. The patient should be instructed to rinse the mouth regularly with salt water until healing is satisfactory.

In this emergency situation, instruct the patient to place the severed finger directly into a fluid-tight sterile container, such as a plastic bag or sterile specimen jar. Then place this ‘unit’ in a bag containing iced water with crushed ice. Note: Never place the amputated finger directly in ice or in fluid such as saline. Fluid makes the tissue soggy, rendering microsurgical repair difficult. Care of the finger stump Apply a simple, sterile, loose, non-sticky dressing and keep the hand elevated.

Bite wounds

Human bites and clenched fist injuries Human bites and clenched fist injuries can present a serious problem of infection. β-lactamase producing anaerobic organisms in the oral cavity (e.g. Vincent’s) can penetrate the damaged tissue and form a deepseated infection. Streptococcus species, staphylococcal organisms and Eikenella corrodens are common

134

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pathogens. Complications of the infected wounds include cellulitis, wound abscess and lymphangitis. A Cochrane review of antibiotic prophylaxis concluded that it significantly reduces the risk of infection.2 Principles of treatment • Clean and debride the wound carefully (e.g. aqueous antiseptic solution or hydrogen peroxide). • Give prophylactic penicillin if a severe or deep bite. • Avoid suturing if possible. • Tetanus toxoid (although minimum risk). • Consider rare possibility of HIV and hepatitis B or C infections. • For high-risk wounds, give procaine penicillin 1.5 g IM statim and/or amoxycillin/clavulanate 875/125 mg bd for 5 days.3 • If established infection in a deep wound, take a swab and give metronidazole 400 mg (o) bd for 14 days plus either cefotaxime 1 g IV 8 hourly or ceftriaxone 1 g IV daily for 14 days.

Dog bites 134

Non-rabid Dog bites typically have poor healing and carry a risk of infection with anaerobic organisms, including tetanus, staphylococci and streptococci. Puncture and crush wounds are more prone to infection than laceration. Up to 25% of dog bite wounds become infected with the first signs appearing in about 24 hours.4 Principles of treatment (see FIG. 134.11): • Clean and debride the wound with aqueous antiseptic, allowing it to soak for 10–20 minutes. • Aim for open healing—avoid suturing if possible (except in ‘privileged’ sites with an excellent blood supply such as the face and scalp). • Apply non-adherent, absorbent dressings (paraffin gauze and Melolin) to absorb the discharge from the wound. • Tetanus prophylaxis: immunoglobulin or tetanus toxoid. • Give prophylactic penicillin for a severe or deep bite: 1.5 million units procaine penicillin IM statim, then orally for 5–10 days. An alternative is amoxycillin/clavulanate for 5–7 days. Use this antibiotic for 7–10 days for an established infection (depending on swab).4 • Inform the patient that slow healing and scarring are likely.

FIGURE 134.11 Dog bite treated by antibiotics, sterile dressing and anti-tetanus vaccination

Rabid or possibly rabid dog (or other animal) Not currently applicable in Australia (see CHAPTER 15). • Wash the site immediately with detergent or saline (preferable) or hydrogen peroxide or soap (if no other option). • Do not suture. • If rabid: — human rabies immune globulin (passive) — antirabies vaccine (active) • Uncertain: capture and observe animal, consider vaccination.

Cat bites Cat bites have the greatest potential for suppurative infection with Pasteurella multocida being the most common organism. The same principles apply as for the management of human or dog bites. Use amoxycillin + clavulanate for prophylaxis for 5 days. For infection, swab the wound but start with metronidazole + doxycycline or ciprofloxacin.3 It is important to clean a deep and penetrating wound. Another problem is cat-scratch disease, presumably caused by a Gramnegative bacterium, Bartonella henselae.

Clinical features of cat-scratch disease • An infected ulcer or papule pustule at bite site (30–50% of cases) after 3 days or so5

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Common skin wounds and foreign bodies • 1–3 weeks later: fever, headache, malaise regional lymphadenopathy (may suppurate) • Intradermal skin test positive • Benign, self-limiting course • Sometimes severe symptoms for weeks, especially in immunocompromised • Treat with erythromycin or roxithromycin for 10 days3

Water-related wound infections3 These complex infections may require expert advice.

Coral cuts Wounds from coral cuts are at risk of serious infection with Vibrio organisms (marine pathogens) or Streptococcus pyogenes. Such wounds require cleaning with antiseptics, debridement, dressing and antibiotic cover with doxycycline 100 mg bd or cephalexin 500 mg bd for 7 days.

Fish tank/swimming pool granuloma Due to Mycobacterium marinum, which causes a localised papular or nodular skin lesion in people who usually clean aquaria or swimming pools. Diagnosis is by biopsy and culture (acid-fast bacilli). Treatment: single lesion excision (may suffice). May need antibiotic therapy e.g. clarithromycin (o) bd for 3–4 months plus rifampicin for severe or unresponsive infection. Aeromonas species wound infections From fresh or brackish water or mud exposure to open wounds. Treat with ciprofloxacin.

1449

Forehead and other lacerations in children Despite the temptation, avoid using reinforced paper adhesive strips (Steri-Strips) for children with open wounds. They will merely close the dermis and cause a thin, stretched scar. They can be used only for very superficial epidermal wounds in conjunction with sutures. Adhesive glue for wound adhesion A tissue adhesive glue can be used successfully to close superficial smooth and clean skin wounds, particularly in children. Commercial preparations such as Histoacryl, Dermabond and Epiglu (active ingredient enbucrilate) are available. SuperGlue also serves the purpose although sterility and toxicity have to be considered. The glue should be used only for superficial, dry, clean and fresh wounds. No gaps are permissible with this method. Avoid glues if possible. Wound anaesthesia in children New topical preparations that provide surface anaesthesia are being used for wound repair in children. They include lignocaine and prilocaine mixture (EMLA cream) and adrenaline and cocaine (AC) liquid. Use the latter with caution. Some practitioners use an ice block to freeze the lacerated site. The child is asked to hold the ice while a suture is rapidly inserted.

Removal of skin sutures

Shewanella putrefaciens From salt or brackish water contact, infecting legs with vascular compromise. Causes severe cellulitis with necrosis, even sepsis. Treat with ciprofloxacin or meropenem/imipenem.

Suture marks are related to the time of retention of the suture, its tension and position. The objective is to remove the sutures as early as possible, as soon as their purpose is achieved. The timing of removal is based on commonsense and individual cases. Nylon sutures are less reactive and can be left for longer periods. After suture removal it is advisable to support the wound with Micropore skin tape/Steri-Strips for 1–2 weeks, especially in areas of skin tension.

Scalp lacerations in children

Method

If lacerations are small but gaping use the child’s hair for the suture, provided it is long enough.

1 Use good light and have the patient lying comfortably. 2 Use fine, sharp scissors that cut to the point or the tip of a scalpel blade, and a pair of fine, nontoothed dissecting forceps that grip firmly. 3 Cut the suture close to the skin below the knot with scissors or a scalpel tip (see FIG. 134.12a). 4 Gently pull the suture out towards the side on which it was divided—that is, always towards the wound (see FIG. 134.12b).

Method Make a twisted bunch of the child’s own hair on each side of the wound. Tie a reef knot and then an extra holding knot to minimise slipping. Ask an assistant to drop compound benzoin tincture solution (Friar’s Balsam) on the hair knot. Leave the hair suture long and get the parent to cut the knot in 5 days.

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(a)

Additional aspects In children, tend to remove 1–2 days earlier. Allow additional time for backs and legs, especially the calf. Nylon sutures can be left longer because they are less reactive. Alternate sutures may be removed earlier (e.g. face in women).

(b)

Burns5,6

FIGURE 134.12 Removal of skin sutures: (a) cutting the suture, (b) removal by pulling towards wound

When to remove non-absorbable sutures

134

For removal of sutures after non-complicated wound closure in adults, see TABLE 134.2. Note: Decisions need to be individualised according to the nature of the wound and health of the patient and healing. In general, take sutures out as soon Table 134.2

Time after insertion for removal of sutures

Area

Days later

Scalp

6

Face

3 (or alternate at 2, rest 3–4)

Ear

5

Neck

4 (or alternate at 3, rest 4)

Chest

8

Arm (including hand and fingers)

8–10

Abdomen

8–10 (tension 12–14)

Back

12

Inguinal and scrotal

7

Perineum

2

Legs

10

Knees and calf

12

Foot (including toes)

10–12

Management depends on extent and depth (burns are classified as superficial or deep—otherwise first, second or third degree). First degree burns are superficial and involve only the epidermis, causing pain, redness and swelling. A scald, which is a burn caused by moist heat, is an example. Healing proceeds quickly. Second degree or partial skin thickness burns cause the epidermis to blister and become necrotic with subsequent serous ooze. In third degree or full thickness burns, there is deep necrosis and perhaps anaesthesia from destroyed nerve endings. If extensive (>9% of body surface area) and deep there is a possibility of hypovolaemia and shock. A major burn, which is a medical emergency, is an injury of more than 20% of the total body surface for an adult and 10% for a child.

First aid The immediate treatment of burns, especially for smaller areas, is immersion in cool to cold, running water such as tap water, for a minimum of 20 minutes. Do not disturb charred adherent clothing but remove wet clothing. Chemical burns should be liberally irrigated with water. Apply 1 in 10 diluted vinegar to alkali burns and sodium bicarbonate solution for acid burns. Refer the following burns to hospital: • >9% surface area, especially in a child (see ‘rule of nines’, CHAPTER 121) • >5% in an infant • all deep burns • burns of difficult or vital areas (e.g. face, hands, perineum/genitalia, feet) • burns with potential problems (e.g. electrical, chemical, circumferential) • suspicion of inhalational injury Always give adequate pain relief. During transport, continue cooling by using a fine-mist water spray.

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Common skin wounds and foreign bodies Treatment 1 Very superficial—intact skin. Can be left with application of a mild antiseptic only (e.g. aqueous chlorhexidine). Review if blistering. 2 Superficial—blistered skin. Apply a dressing to promote epithelialisation (e.g. hydrocolloid sheets, hydrogel sheets) covered by an absorbent dressing or (best option) a retention adhesive material (e.g. Fixomull, Mefix, Hypafix) with daily or twice daily cleaning of the serous ooze and reapplication of outer stretch bandage. Fixomull can be left in place for up to 2 weeks. Guidelines to patient for retention dressings • First 24 hours: keep dry. If there is any ooze coming through the dressing, pat dry with a clean tissue. • From day 2: wash over dressing twice daily. Use gentle soap and water, rinse then pat dry. Do not soak. Rinse only. Do not remove the dressing as it may cause pain and damage to the wound. If the wound becomes red, hot or swollen, or if pain increases, return to the clinic. • From day 7: return to the clinic for removal of the dressing. Two hours prior to coming into the clinic, soak the dressing with olive oil then cover with plastic wrap (e.g. Glad Wrap). Note: Dressing must be soaked off with oil (e.g. olive, baby, citrus or peanut). Debride ‘popped blisters’. Only pop blisters that interfere with dermal circulation. 3 Deep burns. If considerable ooze, apply the following in order: • SoloSite gel, Solugel or similar • non-adherent neutral dressing (e.g. Melolin) • layer of absorbent gauze or cotton wool (larger burns) Change every 2–4 days with analgesic cover. Surgical treatment, including skin grafting, may be necessary. Exposure (open method) • Keep open without dressings (good for face, perineum or single surface burns) • Renew coating of antiseptic cream every 24 hours Dressings (closed method) • Suitable for circumferential wounds • Cover area with non-adherent tulle (e.g. paraffin gauze)

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• Dress with an absorbent, bulky layer of gauze and wool • Use a plaster splint if necessary

Burns to hands For superficial blistered burns to the hand or similar ‘complex’ shaped parts of the body apply strips of the retention stretch adhesive dressings as described above. They conform well to digits. Apply an outer bandage. At 7 days soak the dressings in oil for 2 hours prior to coming in to the clinic.

FOREIGN BODIES

Penetrating gun injuries Injuries to the body from various types of guns present decision dilemmas for the treating doctor. The following information represents guidelines, including special sources of danger to tissues from various foreign materials discharged by guns.

Gunshot wounds Airgun The rule is to remove subcutaneous slugs but to leave deeper slugs unless they lie within and around vital structures (e.g. the wrist). A special common problem is that of slugs in the orbit. These often do little damage and can be left alone, but referral to an ophthalmologist would be appropriate.

0.22 rifle (the pea rifle) The same principles of management apply but the bullet must be localised precisely by X-ray. Of particular interest are abdominal wounds, which should be observed carefully, as visceral perforations can occur with minimal initial symptoms and signs.

0.410 shotgun The pellets from this shotgun are usually only dangerous when penetrating from a close range. Again, the rule is not to remove deep-lying pellets— perhaps only those superficial pellets that can be palpated.

Pressure gun injuries Injection of grease, oil, paint and similar substances from pressure guns (see FIG.  134.13) can cause very serious injuries, requiring decompression and removal of the substances.

134

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oil injections into digital pulp

high-pressure grease or paint gun injections

splinter needle

skin

FIGURE 134.13 Dangerous accidental injections into the hand

Grease gun and paint gun

134

High-pressure injection of paint or grease into the hand requires urgent surgery if amputation is to be avoided. There is a deceptively minor wound to show for this injury, and after a while the hand feels comfortable. However, ischaemia,1 chemical irritation and infection can follow, with gangrene of the digits, resulting in, at best, a claw hand due to sclerosis. Treatment is by immediate decompression and meticulous removal of all foreign material and necrotic tissue.

FIGURE 134.14 Removal of splinters in the skin

Method 1 1 Inject 1–2 mL of LA around the fish hook. 2 Grasp the shank of the hook with strong artery forceps. 3 Slide a D11 scalpel blade in along the hook, sharp edge away from the hook, to cut the tissue and free the barb (see FIG. 134.15). 4 Withdraw the hook with the forceps.

Oil injection Accidental injection of an inoculum in an oily vehicle into the hand also creates a serious problem with local tissue necrosis. If injected into the digital pulp, this may necessitate amputation. Such injections are common on poultry farms, where many fowl-pest injections are administered.

Splinters under the skin The splinter under the skin is a common and difficult procedural problem. Instead of using forceps or making a wider excision, use a disposable hypodermic needle to ‘spear’ the splinter (see FIG.  134.14) and then use it as a lever to ease the splinter out through the skin. A ‘buried’ wooden foreign body can be detected by ultrasound.

Embedded fish hooks Two methods of removing fish hooks are presented here, both requiring removal in the reverse direction, against the barb. Method 2 is recommended as firstline management.

FIGURE 134.15 Removal of fish hook by cutting a path in the skin

Method 2 This method, used by some fishermen, relies on a loop of cord or fishing line to forcibly disengage and extract the hook intact. It requires no anaesthesia and no instruments—only nerves of steel, especially for the first attempt.

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Common skin wounds and foreign bodies 1 Take a piece of string about 10–12 cm long and make a loop. One end slips around the hook, the other hooking around one finger of the operator. 2 Depress the shank with the other hand in the direction that tends to disengage the barb. 3 At this point give a very swift, sharp tug along the cord. 4 The hook flies out painlessly in the direction of the tug (see FIG. 134.16). Note: You must be bold, decisive, confident and quick—half-hearted attempts do not work. For difficult cases, some local anaesthetic infiltration may be appropriate. Instead of a short loop of cord, a long piece of fishing line double looped around the hook and tugged by the hand, or flicked with a thin ruler in the loop, will work.

Table 134.3

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Infections transmitted by needle-stick accidents

Viruses HIV Hepatitis B, C, D Herpes simplex Herpes varicella zoster Bacteria Streptococcal infections Staphylococcal infections Syphilis Tetanus Tuberculosis Other Malaria

FIGURE 134.16 Fisherman’s method of removing a fish hook intact

Needle-stick and sharps injuries Accidental skin puncture by contaminated ‘sharps’, including needles (with blood or bloodstained body fluids), is of great concern to all health care workers. Another problem that occurs occasionally is the deliberate inoculation of people such as police by angry, sociopathic individuals. A needle-stick accident is the commonest incident with the potential to transmit infections such as HIV and hepatitis B, C or D. The part of the venipuncture that is most likely to cause the accident is the recapping or resheathing of the needle. This practice should be discouraged. Infections transmitted by needle-stick accidents are summarised in TABLE  134.3. The risk from a contaminated patient is greatest with hepatitis (10–30%), while the risk of seroconversion or clinical infection after a needle-stick injury with HIV-positive blood is very low (probably about 1 in 300).7 The risk of tetanus, especially for outdoor injuries, is significant and should be addressed.

Prevention • Avoid physically struggling with overdose victims or high-risk patients for lavage or venipuncture. • Needles should not be recapped. • Dispose of needles immediately and directly into a leak-proof, puncture-proof sharps container. • Avoid contact with blood. • Wear protective gloves (does not prevent sharps injury). Postexposure prophylaxis Postexposure prophylaxis (PEP) must be considered for high-risk exposure such as hollow bloodcontaining needles, deep injury and high viral load or late-stage HIV infection of the source.3 Although in most instances of sharps injuries PEP is not justified, do seek expert advice. Management8 • Wash affected site with soap and water without scrubbing. Also wash or irrigate any areas of skin, eye/conjectiva or other mucous membrane exposed to blood or body fluids. • Do not suck or squeeze wound. • Encourage bleeding. • Reassure the patient that the risk of viral infection is very low. • Obtain information about and blood from the sharps victim and the source person (source of body fluid). A known carrier of hepatitis B surface antigen or an HIV-positive source person will facilitate early decision making.

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Note: It takes 3 months to seroconvert with HIV so the patient may be infected but negative on initial tests. Consider the exposed person’s wishes after discussing the risks/benefits of treatment including adverse effects.

HIV status tests. Commence hepatitis B vaccination if not vaccinated. Note: Informed consent for testing and disclosure of test results for involved person should be obtained.

Known hepatitis B carrier source person

Tetanus is a very serious disease but completely preventable by active immunisation. Protection should be universal, especially if the childhood immunisation program is followed. However, all patients with wounds should be assessed for their tetanus status and managed on their merits. For severe wounds the possibility of gas gangrene should also be considered. Tetanus-prone wounds:

• If injured person immune—no further action • If non-vaccinated and non-immune: — give hyperimmune hepatitis B gammaglobulin (within 48 hours) — commence course of hepatitis B vaccination, within 24 hours

Known hepatitis C carrier source person8

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Tetanus prophylaxis

• The recipient needs to have follow-up HCV antibody tests at 1 and 6 weeks and ALT levels at 4–6 months. • There is no effective immunoprophylaxis available. Consider early therapy should seroconversion occur.

• • • • • • •

Known HIV-positive source person8

For the primary immunisation of adults, tetanus toxoid (singly or combined with diphtheria if primary childhood course not given) is given as two doses 6 weeks apart with a third dose 6 months later. Booster doses of tetanus toxoid are given every 10 years or at the time of major injury occurring 5 years after previous dose.

Refer to consultant about relative merits of drug prophylaxis (ART) and serological monitoring. A case control study by the US Centers for Disease Control and Prevention indicated that giving zidovudine following a needle-stick injury decreases the rate of HIV seroconversion by 79%.9

Options (best to start within 1–2 hours) • low risk emtricitabine + tenofovir, daily for 4 weeks or zidovudine + lamivudine 12-hourly for 4 weeks • high risk add lopinavir + ritonavir 400 + 100 mg (o) 12 hourly for 4 weeks prophylaxis within 8 hours, preferably within 1–2 hours,10 for 6 weeks or serological monitoring 0, 4, 6, 12, 24 and 52 weeks11 (check with consultant and refer to national guidelines; WHO guidelines: )

Unknown risk source person Take source person’s blood (if consent is given) and sharps victim’s blood for hepatitis B (HBsAg and anti-HBs) and hepatitis C and (if high risk for HIV)

compound fractures penetrating injuries foreign bodies extensive crushing delayed debridement severe burns pyogenic infection

Passive immunisation Passive immunisation, in the form of tetanus immunoglobulin 250 units by IM injection, is reserved for non-immunised individuals or those of uncertain immunity wherever the wound is contaminated or has devitalised tissue. Wounds at risk include those contaminated with dirt, faeces/manure, soil, saliva or other foreign material; puncture wounds; and wounds from missiles, crushes and burns. The guide is outlined in TABLE 134.4.

Practice tips • • •

Have the patient lying down for suturing and parents of children sitting down. Avoid using antibiotic sprays and powders in simple wounds—resistant organisms can develop. Consider tetanus and gas gangrene prophylaxis in contaminated and deep necrotic wounds.

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Table 134.4

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Guide to tetanus prophylaxis in wound management3

Time since vaccination

Type of wound

Tetanus toxoid

Tetanus immunoglobulin

History of 3 or more doses of tetanus toxoid 10 years

Uncertain vaccination history or less than 3 doses of tetanus toxoid

•

• •

•

•

Clean minor wounds

Yes

No

All other wounds

Yes

Yes

Give a tetanus booster if patient has not had one within 5 years for dirty wounds or within 10 years with clean wounds. Give tetanus immunoglobulin if patient is not immunised or if the wound is grossly contaminated. Never send head-wound patients home before thoroughly washing their hair and carefully examining for other lacerations. Any laceration in the cheek, mandible or lower eyelid may damage the facial nerve, parotid duct or lacrimal duct respectively. When a patient falls onto glass it takes bone to halt its cutting path. Assume all structures between skin and bone are severed.

References 1 Hansen G. Practice Tips. Aust Fam Physician, 1982; 11: 867. 2 Medeiros I, Saconato H. Antibiotic prophylaxis for mammalian bites. Cochrane Database Syst Rev. 2001; (2): CD001738.

3 Moulds R (Chair). Therapeutic Guidelines: Antibiotic (Version 14). Melbourne: Therapeutic Guidelines Ltd, 2013. 4 Broom J, Woods ML. Management of bite injuries. Australian Prescriber, 2006; 29: 6–8. 5 Papadakis MA, McPhee SJ et al. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013: 1549–53. 6 Moulds R (Chair). Therapeutic Guidelines: Toxicology and Wilderness (Version). Melbourne: Therapeutic Guidelines Ltd, 2008: 253–69. 7 Trevillyan JM, Denholm JT, Spelman D. Managing community needlestick injuries. Medicine Today, 2009; 10 (9): 80–3. 8 Buckley N (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty Ltd, 2013: 189–90. 9 Papadakis MA, McPhee, SJ et al. Current Medical Diagnosis and Treatment (52nd edn). New York: The McGraw-Hill Companies, 2013: 1321. 10 Gerberding JL. Drug therapy: management of occupational exposures to blood-borne viruses. N Engl J Med, 1995; 332: 444. 11 Hammond L. AIDS and hepatitis B protection strategies. Aust Fam Physician, 1990; 19: 657–61.

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135 Common fractures and dislocations The broken bone, once set together, is stronger than ever. John Lyly (–) Common fractures and dislocations usually apply to the limbs, the shoulder girdle and the pelvic girdle and their management requires an early diagnosis to ensure optimum treatment and to prevent complications. Early diagnosis depends on the physician being vigilant and on having knowledge of the less common conditions so that a careful search for the diagnosis can be made. The diagnosis is dependent on a good history followed by a careful examination, good-quality X-rays appropriate to the injury (e.g. stress view) and, if necessary, special investigations. The golden rule is: if in doubt—X-ray. The family doctor should develop the habit of looking at a patient’s X-rays. Such a backup to the radiologist’s report can help avoid missed diagnoses. There are many pitfalls involved in managing fractures and dislocations. Many injuries, such as fractures of the arm and hand, may seem trivial but they can lead to long-term disability. This chapter presents guidelines to help avoid these pitfalls.

Key facts and checkpoints •

•

•

•

A fracture usually causes deformity but may cause nothing more than local tenderness over the bone (e.g. scaphoid fracture, impacted fractured neck of femur). The classic signs of fracture are: — pain — tenderness — loss of function — deformity — swelling/bruising — crepitus X-ray examination of the affected area of the upper limb should include views of joints proximal or distal to the site of the injury, and X-rays in both AP and lateral planes. If an X-ray is reported as normal but a fracture is strongly suspected, an option is to splint the affected limb for about 10 days and then repeat the X-ray.

•

•

•

•

•

• • • •

•

•

As a rule, displaced fractures must be reduced whereby bone ends should be placed in proper alignment and then immobilised until union occurs. Fractures should be monitored radiologically for loss of position, particularly in the first 1–2 weeks following reduction. Bone union is assessed clinically by reduced pain at the fracture site and reduced fracture mobility. It is assessed radiologically by X-ray features such as trabecular continuity across the fracture site and bridging callus. Non-union is caused by such factors as inadequate immobilisation, excessive distraction, loss of healing callus, infection or avascular necrosis. Stiffness of joints is a common problem with immobilisation in plaster casts and slings so the joints must be moved as early as possible. Early use is possible if the fracture is stable. A dislocation is a complete disruption of one bone relative to another at a joint. A subluxation is a partial displacement such that the joint surfaces are still in partial contact. A sprain is a partial disruption of a ligament or capsule of a joint. Always consider associated soft-tissue injuries such as neuropraxia to adjacent nerves, vascular injuries and muscle compartment syndromes. A stress fracture is an incomplete fracture resulting from repeated small episodes of trauma, which individually would be insufficient to damage the bone. Stress fractures, especially in the foot, are most likely to result from sport, ballet, gymnastics and aerobics. Their incidence rises sharply at times of increased activity.1 Typical stress fractures (with their usual cause) include: — navicular (sprinting sports, football) — metatarsal neck (running, walking, basketball, jumping) — base of fifth metatarsal (dancing) — femur—neck or shaft (distance running) — ulna (weight-lifting) — distal radial and ulnar epiphyses (gymnastics) — talus (running)

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Common fractures and dislocations

— — — — — —

•

proximal tibia (running, football) lumbar spine medial tibia (running, football) distal phalanges (guitar playing) cervical spinous process (gardening) lumbar vertebrae—pars interarticularis (fast bowling) — spiral humerus (throwing sports) — rib fractures—1st (weight-lifting) — rib fractures—8th (tennis) The key strategy of most reduction manoeuvres is traction, especially for dislocations. This may be supplemented with translation or leverage.

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2 Compress along the long axis of the bones by pushing in both directions, so that the forces focus on the affected area (fracture site, see FIG. 135.1a). Alternatively, compression can be applied from the distal end with stabilising counterpressure applied proximally (see FIG. 135.1b). 3 The patient will accurately localise the pain at the fracture site. (a)

Red flag pointers for fractures • • • • • • • • •

Supracondylar fracture in children Elbow fractures in children, especially lateral humeral condyle Trampoline injuries in children Scaphoid fracture Scapholunate dislocation Skull fractures, especially temporal Talar dome fractures All intra-articular fractures Avascular heads of humerus and femur

(b)

Testing for fractures2 This method describes the simple principle of applying axial compression for the clinical diagnosis of fractures of bones of the forearm and hand, but also applies to bones of the limbs. Many fractures are obvious when applying the classic methods of diagnosis but it is sometimes more difficult if there is associated soft-tissue injury from a blow or if there is only a minor fracture such as a greenstick fracture of the distal radius. If the bone suspected of fracture is compressed gently from end to end, the patient will feel pain. A soft-tissue injury of the forearm will show pain, tenderness, swelling and possibly loss of function. It will, however, not be painful if the bone is compressed axially—that is, in its long axis. Walking is another method of applying axial compression, and this is very difficult (because of pain) in the presence of a fracture in the weightbearing axis or pelvis.

Method 1 Grasp the affected area both distally and proximally with your hands.

135

FIGURE 135.1 Testing for fractures: (a) axial compression to detect a fracture of the radius or ulna bones, (b) axial compression to detect a fracture of the metacarpal

Principles of treatment of limb fractures To reduce any fracture properly, the following steps must be taken (see FIG. 135.2a).3 1 Disimpact the fragments, usually by increasing the deformity. 2 Re-establish the correct length of the bone. 3 Re-establish the correct alignment by proper reduction of the fracture. 4 Stabilise the bone in an acceptable position for as long as it takes to heal.

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fracture (impacted)

Step 1. Disimpaction

Step 2. Establish length

may require elevation of the depressed fragment. Compound fractures of the vault require careful evaluation and referral. Special care is required over the midline as manipulation (usually by elevation) of any depressed fragment can tear the sagittal sinus, causing profuse and fatal bleeding.4 Beware of the associated extradural or subdural haematoma (see CHAPTER 75).

Base of skull fractures These fractures are difficult to diagnose on radiography but their presence is indicated by bleeding from the nose, throat or ears. CSF may be observed escaping, especially through the nose, if the dura is also torn. Treatment of basal fractures is based on prevention of intracranial infection and avoidance of excessive interference with the nose or ear, such as with packing and nasogastric tubes. An appropriate antibiotic is cotrimoxazole.4

Malar fracture A fractured zygomaticomaxillary complex (malar) is a common body contact sports injury or injury resulting from a fight. See FIGURE 135.3. Step 3. Establish alignment

(b)

135

Clinical features • Swelling of cheek • Circumocular haematoma • Subconjunctival haemorrhage • Palpable step in infraorbital margin • Flat malar eminence when viewed from above • Paraesthesia due to infraorbital nerve injury • Loss of function (i.e. difficulty opening mouth)

The above steps will only be achieved with adequate anaesthesia, analgesia and relaxation. Maintenance of the reduction depends upon the moulding, which utilises the intact periosteal bridge to hold the fracture fragments in a reduced position. FIGURE  135.2b illustrates the principle of moulding to maintain reduction.3

Management • Head injury assessment • Exclude ‘blow-out’ fracture of the orbit • Exclude ocular trauma: — remove contact lenses if worn — check visual acuity — check for diplopia — check for hyphaema — check for retinal haemorrhage • Persuade patient not to blow nose (can cause surgical emphysema) • If fracture displaced, refer for reduction under general anaesthesia

INJURIES OF THE SKULL AND FACE

Reduction methods

FIGURE 135.2 (a) Principles of reduction of fractured bones, (b) Principles of moulding to maintain reduction: the arrows indicate the three point pressure areas required to maintain reduction

Skull fractures Closed fractures without any neurological symptoms do not require active intervention. Depressed fractures

• Elevation by temporal or intraoral approach— healing can be expected in 3–4 weeks • Some require interosseous wiring or plating or pinning

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FIGURE 135.4 Immobilisation of a fractured mandible in a four-tailed bandage

Treatment Refer for possible internal fixation. A fracture of the body of the mandible will usually heal in 6–12 weeks (depending on the nature of the fracture and fitness of the patient). FIGURE 135.3 Fractured malar showing circumocular haematoma and depression of the infraorbital margin

Fracture of mandible A fracture of the mandible follows a blow to the jaw. The patient may have swelling (which can vary from virtually none to severe), pain, deformity, inability to chew, malalignment of the jaw and teeth and drooling of saliva. Intraoral examination is important as submucosal ecchymosis in the floor of the mouth is a pathognomonic sign. A simple office test for a suspected fractured mandible is to ask patients to bite on a wooden tongue depressor (or similar firm object). Ask them to maintain the bite as you twist the spatula. If they have a fracture they cannot hang onto the spatula because of pain.5 X-rays:

Dislocated jaw The patient may present with unilateral or bilateral dislocation. The jaw will be ‘locked’ and the patient unable to articulate or close the mouth. Method of reduction • Get the patient to sit upright with the head against the wall. • Wrap a handkerchief or cloth around both thumbs and place the thumbs over the lower molar teeth, with the fingers firmly grasping the mandible on the outside. • Firmly thrusting with the thumbs, push downwards towards the floor (see FIG. 135.5).

• AP views and lateral obliques • an orthopantomogram provides a global view First aid management • Check the patient’s bite and airway • Remove any free-floating tooth fragments and retain them • Replace any avulsed or subluxed teeth in their sockets Note: Never discard teeth. • First aid immobilisation with a four-tailed bandage (see FIG. 135.4)

FIGURE 135.5 Method of reduction of a dislocated jaw by downward traction on the mandible

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This action invariably reduces the dislocation, but the reduction can be reinforced by the fingers rotating the mandible upward as the thumbs thrust downwards.

INJURIES OF THE SPINE Cervical fractures, especially atlas (C1), axis (C2) and odontoid process, require early referral with the neck immobilised in a cervical collar, in a supine position. A hard collar is preferred but a soft collar with sandbags either side of the head to prevent movement will suffice.

Thoracolumbar fractures Fractures or fracture dislocations of the thoracic and lumbar vertebrae, without neurological deficit, are classified as either stable or unstable. Stable fractures • Compression fractures of vertebral body with 15 mm Talar tilt >20°

II (moderate)

III (severe)

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• there was an inability to bear weight (walk four steps) both immediately after injury and during the clinical examination

Foot injury Refer for a foot X-ray (suspected midfoot fracture) if there is pain in the midfoot and any one of: • bone tenderness at fifth metatarsal base • bone tenderness at the navicular bone • inability to weight-bear immediately after injury and when seen FIGURE 136.13 Sprained ankle with tearing of the lateral ligament complex with obvious haematoma

• a common finding is rounded swelling in front of lateral malleolus (‘signe de la coquille d’oeuf’) • test stability in AP plane (anterior draw sign) • talar tilt test (inversion stress test)

Is there an underlying fracture?9 For a severe injury the possibility of a fracture— usually of the lateral malleolus or base of fifth metatarsal—must be considered. If the patient is able to walk without much discomfort straight after the injury, a fracture is unlikely. Indications for X-ray include:9

Management The treatment of ankle ligament sprains depends on the severity of the sprain. Most grade I and II sprains respond well to standard conservative measures and regain full, pain-free movement in 1–6 weeks, but controversy surrounds the most appropriate management of grade III sprains. A 2002 Cochrane Systematic Review revealed that functional recovery for grade III strains was quicker in those treated by rehabilitation compared with surgery.11

Grade I sprain

• • • • • •

R = Rest the injured part for 48 hours, depending on disability I = Ice pack for 20 minutes every 3–4 hours when awake for the first 48 hours C = Compression bandage (e.g. crepe bandage) E = Elevate to hip level to minimise swelling A = Analgesics (e.g. paracetamol ± codeine) R = Review in 48 hours, then 7 days S = Special strapping

Ottawa rules for ankle and foot X-ray10 These rules are a quick and reliable method of selecting which patients with ankle and foot injuries need X-rays to exclude a fracture.

Use partial weight-bearing with crutches for the first 48 hours or until standing is no longer painful, then encourage early full weight-bearing and a full range of movement. This can be followed by isometric exercises.7 Use warm soaks, dispense with ice packs after 48 hours. Walking in sand (e.g. along the beach) is excellent rehabilitation. Aim towards full activity by 2 weeks.

inability to weight-bear immediately after injury marked swelling and bruising soon after injury marked tenderness over the bony landmarks marked pain on movement of the ankle crepitus on palpation or movement point tenderness over the base of the fifth metatarsal • special circumstances (e.g. litigation potential)

Ankle injury An X-ray of the ankle is necessary when the patient has pain over the medial or lateral malleolar zone and any one of the following findings: • there is bone tenderness on palpation of the distal 6 cm of the fibula (posterior tip of lateral malleolus) • there is bone tenderness on palpation of the distal 6 cm of the tibia (posterior tip of medial malleolus)

Special strapping A firm support for partial tears in the absence of gross swelling provides excellent symptomatic relief and early mobilisation. Method: • maintain the foot in a neutral position (right angles to leg) by getting patient to hold the foot in that position by a long strap or sling • apply small protective pads over pressure points

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(a)

(b)

(c)

stirrups of adhesive tape

FIGURE 136.14 Supportive strapping for a sprained ankle: (a) apply protective pads and stay tape, (b) apply stirrups to hold foot in slight eversion and (c) apply an ankle lock tape

• apply one or two stirrups of adhesive low-stretch 6–8 cm strapping from halfway up medial side, around the heel and then halfway up the lateral side to hold foot in slight eversion (see FIG. 136.14) • apply an adhesive bandage (e.g. Acrylastic, 6–8 cm) which can be rerolled and reused • reapply in 3–4 days • after 7 days, remove the bandage and use a nonadhesive tubular elasticised support until full pain-free movement is achieved

Grade II sprain

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RICE treatment (as above) for 48 hours but ice (e.g. ACE wrap) should be used every 2–3 hours and no weight-bearing (use crutches) for 48 hours. Then permit partial weight-bearing with crutches and begin the active exercise program. Follow-up and supportive strapping as for grade I. Note that the ice packs can be placed over the strapping.

Grade III sprain It would be appropriate to refer this patient with a complete tear (see FIG.  136.15). Initial management includes RICE and analgesics and an X-ray to exclude an associated fracture. The three main treatment approaches appear to be equally satisfactory. Surgical repair Some specialists prefer this treatment but it is usually reserved for the competitive athlete who demands absolute stability of the ankle.

FIGURE 136.15 Complete (grade III) tear of lateral ligaments of the ankle in a netball player; note excessive movement in inversion and anterior draw

Plaster immobilisation This is usually reserved for patients who are unable actively to dorsiflex their foot to a right angle and those who need to be mobile and protected in order to work. The plaster is maintained until the ligament repairs, usually 4–6 weeks. The patient can walk normally when comfortable with a rockered sole or open cast walking shoe.

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Common sporting injuries Strapping and physiotherapy This approach is generally recommended. After the usual treatment for a grade II repair, including the strapping as described, a heel lock (see FIG.  136.14c) should be used. The patient continues on crutches and appropriate physiotherapy is given with care so that the torn ends are not distracted. Strengthened balance is achieved by the use of elastic bands, swimming and cycling.

Non-response to treatment There are some patients who, despite an apparently straightforward ankle sprain, do not respond to therapy and do not regain a full range of movement. In such patients alternative diagnoses in addition to ligament tearing must be considered (see TABLE 136.3).

Table 136.3

Unstable ankle injuries to be considered in delayed healing (after Brukner)9

Osteochondral fracture of the talar dome Dislocation of the peroneal tendons Sinus tarsi syndrome Anteroinferior tibiofibular ligament (syndesmosis) injury Post-traumatic synovitis Anterior impingement syndrome Posterior impingement syndrome Anterior lateral impingement Rupture of posterior tibial tendon Regional pain syndrome Other fractures: • base fifth metatarsal (avulsion) • lateral process of talus • anterior process of the calcaneus • tibial plafond • stress fracture navicular

These require careful clinical assessment and further investigation such as bone scans. Rocker board ‘aeroplane’ technique for ankle dysfunction This involves proprioception exercises for injured ankle ligaments. The ligaments and leg muscles can be strengthened by the use of a rocker (wobble) board. The patient stands on the board and shifts his or her weight from side to side in neutral (first), forward (after 2–3 days) or extended (later) body positions, to improve proprioception and balance.

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Tibiofibular syndesmosis injury5 The syndesmosis of the ankle joint comprises the anterior and posterior tibiofibular ligaments and the interosseous membrane. It is injured commonly in football codes by a dorsiflexion–eversion mechanism. The injury is not commonly recognised and can present as an ankle sprain that is slow to recover. Tenderness is found anteriorly over the ligament, and pain (which can radiate proximally between the tibia and fibula) can be produced by forced external rotation in dorsiflexion. An X-ray may determine a widened ankle mortise. More severe cases leading to tibiofibular diastasis require an orthopaedic opinion.

Talar dome injury12 Talar dome lesions represent chip fractures of cartilage or bone from the articular surface of the talus. These occur in about 4–5% of ankle sprains and are usually detected by MRI and/or bone scan. It should be suspected with an inability to weightbear after an ankle sprain and persistent severe pain. Symptomatic lesions are usually treated best with arthroscopic surgery.

HEEL DISORDERS Important causes of heel pain and other disorders resulting from overuse sporting activities include: • Achilles tendon disorders (see CHAPTER 68) — tendonopathy/peritendonopathy — tear: partial or complete • bruised heel • ‘pump bumps’/bursitis • calcaneal apophysitis • plantar fasciitis (see CHAPTER 68) • talon noir • blisters

Achilles tendonopathy/ peritendonopathy13 The inflammation that occurs as a combination of degenerative and inflammatory changes due to overuse may appear either in the tendon itself or in the surrounding paratendon. The latter is called peritendonopathy rather than tenosynovitis because there is no synovial sheath. Clinical features • History of unaccustomed running or long walk • Common in runners who change routine

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Usually young to middle-aged males Aching pain on using tendon Tendon feels stiff, especially on rising Tender thickened tendon Palpable crepitus on movement of tendon

Ultrasound examination This is very useful in differentiating between tendonopathy, peritendonopathy, focal degeneration and a partial tear. Preventive measures • Warm-up and stretching exercises in athletes • Good quality shoes • 1 cm heel raise Treatment • Rest: ? crutches in acute phase, plaster cast if severe • Cool with ice in acute stage, then heat • NSAIDs • 1–2 cm heel raise under the shoe • Ultrasound and deep friction massage • Mobilisation, then graduated stretching exercises Note: Ensure adequate rest and early resolution because chronic tendonopathy is persistent and very difficult to treat. Avoid corticosteroid injection in acute stages and never give into tendon: can be injected around the tendon if localised and very tender.

Partial rupture of Achilles tendon

136

Clinical features • A sudden sharp pain at the time of injury • Sharp pain when stepping off affected leg • Usually males >30 years sporadically engaged in sport • History of running, jumping or hurrying up stairs • A tender swelling palpable about 2.5 cm above the insertion • May be a very tender defect about the size of the tip of little finger Treatment If palpable gap—early surgical exploration with repair. If no gap, use conservative treatment: • initial rest (with ice) and crutches • 1–2 cm heel raise inside shoe

• ultrasound and deep friction massage • graduated stretching exercises Convalescence is usually 10–12 weeks. A poor response to healing manifests as recurrent pain and disability, indicates surgical exploration and possible repair.

Complete rupture of Achilles tendon This common problem in athletes occurs in a possibly degenerated tendon subjected to a sudden increased load (e.g. a skier with foot anchored and ankle dorsiflexed). Clinical features • Sudden onset of intense pain • Patient usually falls over • Feels more comfortable when acute phase passes • Development of swelling and bruising • Some difficulty walking, especially on tiptoe Diagnosis • Palpation of gap (best to test in first 2–3 hours as haematoma can fill gap) • Positive Thompson test (see FIGS 136.16 and 136.17) Note: The injury may be missed because the patient is able to plantar-flex the foot actively by means of the deep long flexors to the foot. Treatment • Early surgical repair (within 3 weeks)

‘Pump bumps’ A ‘pump bump’ is a tender bursa over a bony prominence lateral to the attachment of the Achilles tendon. This is caused by inflammation related to poorly fitting footwear irritating a preexisting enlargement of the calcaneus. Treatment is symptomatic and attention to footwear.

Talon noir Talon noir or ‘black heel’, which has a black spotted appearance on the posterior end of the heel, is common in sportspeople, especially squash players. It tends to be bilateral and is caused by the shearing stresses of the sharp turns required in sport. The diagnosis is confirmed by gentle paring away of the hard skin containing old blood.

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(a)

(b)

FIGURE 136.17 Thompson calf squeeze test for ruptured Achilles tendon: (a) intact tendon, normal plantar-flexion, (b) ruptured tendon, foot remains stationary FIGURE 136.16 Rupture of the left Achilles tendon. This 31-year-old woman injured her heel snow skiing. Examination by firmly compressing the gastrocnemius soleus complex of both legs shows an absent plantar reflex on the left side (positive Thompson test). Photo courtesy Bryan Walpole

136

DISORDERS OF THE FEET AND TOES Common problems include: • • • • • • • • •

fractures of toes foot strain ingrowing toenails ‘black’ nails bony outgrowth under the nail (subungual exostosis) calluses athlete’s foot (tinea pedis) plantar warts turf toe

Black nails (‘soccer toe’) Black or ‘bruised’ nails are due to subungual haematoma caused by trauma (see FIG.  136.18). The

FIGURE 136.18 Black nails (‘soccer toe’), due to subungual haematoma caused by chronic trauma to the great toes; in this case a netball player was wearing new, ill-fitting shoes

problem can be acute or chronic and is seen in the great toes. Acute cases are usually the result of the toe being trodden on, while chronic cases are the result of wearing ill-fitting shoes (too narrow or loose) or the toenails being left too long. The problem is encountered commonly in sports that involve deceleration forces and include running (especially cross-country with downhill running), netball, basketball, tennis, football and skiing.

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• Accident and emergency medicine

Treatment An acute subungual haematoma should be decompressed with a hot needle or other procedure through the nail. A chronic non-painful problem should be left to heal. The toenails will become dystrophic and be replaced by ‘new’ nails. Attention should be paid to the footwear either by changing it or by placing protective padding in the toes of the running shoes or boots.

‘Turf toe’ This is a sprain of the first metatarsophalangeal joint caused by a forced hyperextension (occasionally hyperflexion) injury to the joint. It is common in football player and athletes e.g. jamming or stubbing the great toe.14 There is pain, swelling and limitation of movement. Plain X-rays are unhelpful but isotopic scans and MRI may help. Treatment is conservative with RICE, NSAIDs and relative rest. Surgical intervention may be required.

Injuries in adolescents If an adolescent engaged in sport presents with pain in the leg it is important to consider the following problems. • SCFE (see CHAPTER 65) • Avulsion of epiphyses (e.g. ischial tuberosity— hamstring) • Stress fracture • Osgood–Schlatter disorder • Scheuermann disorder • Idiopathic scoliosis

Patient education resources 136

Hand-out sheets from Murtagh’s Patient Education 6th edition: • Calf muscle injury • Hamstring muscle injury

• • • •

Sports injuries: first aid Sprained ankle Tennis elbow Warm-up exercises for the legs

References 1 Fitzpatrick J. Shoulder pain: a real wet blanket. Australian Doctor Weekly, 5 February 1993: 56. 2 Robinson M. Hazards of alpine sport. Aust Fam Physician, 1991; 20: 961–70. 3 Elliott B, Sherry E. Common snow skiing injuries. Aust Fam Physician, 1984; 13: 570–4. 4 Brukner P, Khan K. Clinical Sports Medicine (3rd edn). Sydney: McGraw-Hill, 2007: 334. 5 Mashford L (Chair). Therapeutic Guidelines: Rheumatology (Version I) Melbourne: Therapeutic Guidelines Ltd, 2006: 168–9. 6 Soo K. Sports injuries of the hip and groin: how to treat. Australian Family Doctor, 2 October 2009; 25–30. 7 James T. Chronic lower leg pain in sport. Aust Fam Physician, 1988; 17: 1041–5. 8 Gothelf G. Assessing ankle sprains. Medical Observer, 6 July 2012: 29–31. 9 Brukner P. The difficult ankle. Aust Fam Physician, 1991; 20: 919–30. 10 Stiell I. Ottawa ankle rules. Can Fam Physician, 1996; 42: 478–80. 11 Kerhoffs GM, Handoll HH et al. Surgical versus conservative treatment for acute injuries of the lateral ligament complex of the ankle in adults. Cochrane Database Syst Rev. 2002; (3): CD000380. 12 Brukner P. Brukner & Kahn’s Clinical Sports Medicine (4th edn). Sydney: McGraw-Hill, 2009; 776–95. 13 Paoloni J. Acute ankle injuries in sports. Medical Observer, 20 May 2005: 29–31. 14 Frimenko RE et al. Etiology and biomechanics of first metatarsophalangeal joint sprains in athletes. Crit Rev Biomed Eng, 2012; 40 (1); 43–61.

Resource Brukner P, Khan K. Brukner & Khan’s Clinical Sports Medicine (4th edn). Sydney: McGraw-Hill, 2009.

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137 The health of Indigenous peoples ‘Closing the Gap’ is a long-term ambitious framework that builds on the foundation of respect and unity provided by the 2008 National Apology to the Aboriginal and Torres Strait Islander Peoples. It acknowledges that improving opportunities for Indigenous Australians requires intensive and sustained effort from all levels of government, as well as private and not-for-profit sectors, communities and individuals.’ Council of Australian Governments (COAG)  The major health challenge in Australia (and several other developed countries) is the health status of Indigenous peoples, which continues to be significantly worse than that of other people. In some cases, it appears that the gap may be widening for women and narrowing for men.1 However, at the end of 2013 the average life expectancy for Aboriginal and Torres Strait Islanders was 69.1 years for men and 73.7 years for women (compared with others—79.9 years and 84.3  years, respectively).2 The commonest cause of death is cardiovascular disease, especially ischaemic heart disease which causes about 57% of these deaths.3 The contrast with other Australians is most marked at 25–54 years. Diseases of the circulatory system, injury and poisoning, respiratory illness and neoplasms continue to be important causes of death. Deaths from infectious diseases and genitourinary disorders continue to occur at much higher rates than among other Australians. The increasing incidence of diabetes is of great concern, especially in those changing from a traditional diet to inappropriate Westernised diets. It is four times higher than for other Australians.4 The estimated lifespan prior to white settlement was 40 years, with the commonest cause of death being injury, particularly from warfare and murder. Thirteen per cent of all children died within the first year of life and 25% by the end of the fifth year.5 Records written by early settlers indicated that the Indigenous people appeared to be in good health and free from disease. It is estimated that the total Indigenous population was 750 000 in 1788. It had fallen to about 70 000 in the 1930s after 150 years of exposure to white civilisation. Significant causes were killing by the settlers (recorded as approximately 20 000) and disease predominantly.

The main diseases that decimated the population were smallpox (two severe epidemics: 1789 and 1829–30), influenza, TB (very severe), pneumonia, measles, varicella, whooping cough, typhoid and diphtheria. The Indigenous population is now estimated to be 670 000. The level of infant and maternal mortality continues to be a concern. After great reductions in infant mortality rates in the 1970s there has been a levelling off, with rates remaining 3–5 times higher than those of other Australians. Despite some improvement, we all need to work to close the gap, and general practice is an ideal service to embrace this.6,7 It is important to understand that Indigenous people and culture must not be seen as homogeneous but rather as diverse, with each group needing a special understanding of its cultural issues. Practitioners working in primary health care in rural and remote areas in Central and Northern Australia are advised to use the CARPA Standard Treatment Manual.8

Key facts and checkpoints • •

• •

Consider the importance of cultural issues in a consultation with an Indigenous person. If assistance is required with a cultural issue, consider involving an Aboriginal health worker in the consultation. Such health workers are a vital part of the team. Always consider multiple medical conditions in the sick person. Remember the importance of opportunistic screening in Indigenous patients for relatively common conditions: — type 2 diabetes (20–50% incidence) — hypertension — kidney function

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The health of Indigenous peoples

•

• • •

•

• • • • •

— other cardiovascular risk factors (e.g. hypercholesterolaemia) — hepatitis B — STI urine screening (men and women) — Pap tests — anaemia in children — hearing in children Screening investigations to consider include: — blood sugar (finger-prick test) — serum lipids — urea and electrolytes — hepatitis B serology — BMI — urinalysis Cervical cancer is 6–8 times more common in Indigenous Australian women. Other common cancers are lung and liver. Approximately 50% of Indigenous children have chronic tympanic membrane perforations, with very significant consequences for language development and school achievement. The Indigenous Australian population has an incidence of end-stage kidney failure 10 times greater than that of other Australians. In some regions BCG vaccination is recommended for newborn Indigenous children. Influenza and pneumococcal vaccines are recommended for adults over 50 years. The prevalence of asthma is higher (16.5%) compared with other Australians (10.2%). Depressive illness, like in the general community, is a significant concern. Alcohol use is a serious health and community problem. Another drinking problem is kava, a drink made from a plant native to the Pacific Islands. Its effects are similar to alcohol and benzodiazepines with marked muscle relaxation.6,8 Excessive use causes acute and long-term problems.

National survey The first national survey of the health of Indigenous Australians, completed in 1994, highlighted considerable differences in reported health status according to place of residence.1 Interestingly, most survey participants (88%) considered themselves to be in good to excellent health. The survey highlighted the following disorders: • • • • •

asthma ear and hearing problems diabetes hypertension kidney disorders

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• • • • •

heart disease skin disorders eye problems, including trachoma nutritional status (especially obesity) substance abuse (e.g. alcohol, marijuana, petrol sniffing) • dental problems (a reversed trend of dental caries)9 • pneumococcal respiratory disease According to the BEACH data, the six most common problems managed at encounters with Indigenous Australians were (in order) diabetes, hypertension, URTI, asthma, chronic bronchitis, bronchiolitis.10 The many reasons for the lower health status of Indigenous Australians include poverty, dispossession, geographical isolation, high population mobility, unemployment, poor housing, low education attainment, temperature extremes in central Australia, increased exposure to infectious diseases, especially in subtropical areas, and lack of appropriate service deliveries. Poor living conditions including overcrowding contribute to poor health outcomes, such as substance abuse, domestic violence, other social dysfunction and child malnutrition. Other environmental health issues, such as lack of adequate shelter, lack of basic amenities such as clean running water and adequate sewage disposal facilities, and often lack of refrigeration in hot climates all impact on Aboriginal health. Associated comorbidities of children admitted to the infectious diseases ward of the Royal Darwin Hospital11 included dehydration (50%), malnutrition (60%), hypokalaemia (70%), iron deficiency (90%), anaemia (25%), pneumonia (24–32%), chronic suppurative otitis media (37%), urinary tract infection (10%) and scabies (25%). Priority health problems have been identified by the National Aboriginal Health Strategy and are summarised in TABLE 137.1.

Indigenous culture and the doctor–patient relationship An understanding of Indigenous cultural issues is fundamental to successful management outcomes. Doctors should realise that, while examining Indigenous patients, they are themselves being examined. When Indigenous Australians visit the doctor they bring their own cultural expectations with them. ‘A poster or coffee table book on Indigenous culture in the waiting room may form a

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Table 137.1

• Health of specific groups

Priority Indigenous health problems

A Clinical Diabetes Cardiovascular disease Injury (and youth suicide) Kidney disease STIs Mental health Poor nutrition Ear infections Women’s problems B Socioeconomic Education of Indigenous children (particularly in rural and remote areas) Housing Water supply Alcohol and substance misuse Domestic violence and sexual abuse Child abuse Gambling Unemployment

simple bridge to acceptance.’12 Indigenous people are often rather shy and communicate more indirectly than Europeans on important sensitive issues. They may use silence while waiting for answers and this could be a cue for the doctor to use a new line of approach.13 It is important for doctors working in Indigenous communities (see FIG. 137.1) to have an appreciation of and respect for Indigenous culture and be aware of its significance in health and behaviour. An Indigenous patient may feel more relaxed if accompanied by a relative, who can witness what the doctor said and reinforce it later.

137 Women’s business

The Indigenous concept of ‘women’s business’ can be defined as the range of experience and knowledge that is the exclusive preserve and domain of Indigenous women. It encompasses issues about menstruation, pregnancy, childbirth and contraception.14 Such matters are traditionally not discussed directly but are conveyed indirectly through stories, ceremonies and songs. For more traditional women it is taboo to talk about women’s health issues to male doctors or male health workers, or to be physically examined by them. Apart from the sense of shame and embarrassment, it represents a transgression of their natural law.15

FIGURE 137.1 Doctor on an outback home visit in Central Australia Courtesy Alice Springs Rural District Department of Health and Community Services

Men’s business Similarly, the cultural issue of men’s business needs to be understood and respected. This applies to manhood initiation rites, circumcision, sexuality and sexually transmitted infections.

Sorry business Sorry business is the process of grieving, and this needs to be clearly understood. There is a cultural obligation for mourners to grieve the death of a relative in a special way. This involves changing their appearance and a deliberate avoidance of any mention of the deceased person’s name or any portrayal of his or her likeness.12 The place where the person died is deserted for a certain time and then smoked out.

Common problems in children16 Indigenous children suffer the same spectrum of health problems as children in developing countries

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The health of Indigenous peoples and communities throughout the world, and the infant mortality rate remains high. The major problems are malnutrition, diarrhoeal disease, skin infections and respiratory tract infection. Common problems are presented in TABLE 137.2. Table 137.2

Common clinical problems in children

Perinatal Low birthweight Asphyxia Infections Preschool Failure to thrive Malnutrition Anaemia Respiratory infection Diarrhoeal disease Hepatitis B Skin infection/infestation Urinary tract infection Meningitis Joint and bone infection Chronic suppurative otitis media Later childhood and adolescence Bacterial and viral infections Parasitic infestation Streptococcal infection: • rheumatic fever • glomerulonephritis Trauma Substance abuse Chronic suppurative otitis media

Acute respiratory tract infections are a common reason for admission to hospital. Bacterial pneumonias occur more commonly than in nonIndigenous children and usually present late. Chronic upper respiratory tract disease is typical in younger children and mucopurulent nasal discharge is present in most preschool children.13 Inappropriate treatment of respiratory tract infection will predispose to a high incidence of low-grade lower respiratory tract disease in later childhood and classic bronchiectasis. Chronic suppurative otitis media, which is almost universal in preschool children, is often refractory to treatment and can lead to significant hearing impairment in many children. It can develop without apparent preceding acute otitis media and may be related to poor nutrition and anaemia. The basic treatment is ear toilet with povidone–iodine solution,

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followed by dry mopping with rolled toilet paper/ tissue ‘spears’, or initial use of the ‘spears’ followed by acetic acid drops. Skin infection and infestation are almost as prevalent as respiratory tract disease. Scabies is endemic and occasionally reaches epidemic proportions. It can be a very debilitating problem and can present in very young infants, in the first few weeks of life.16 Anaemia, usually iron deficiency, is found in at least 25% of children. Apart from reduced intake, intestinal loss from hookworm and other parasitic infection is an important factor. Treatment includes deworming in addition to iron supplements. Diarrhoeal disease is a very common reason for hospital admission. Causes of infective gastroenteritis include rotavirus, bacteria including Shigella, Salmonella and Campylobacter, and parasites such as Giardia lamblia, Strongyloides and Cryptosporidium. Other important and serious problems encountered more frequently in Indigenous children include bacterial meningitis (especially due to Haemophilus influenzae), septic arthritis and osteomyelitis, pyomyositis, Streptococcus pyogenes infections with associated glomerulonephritis and rheumatic fever, urinary tract calculi, urinary tract infection (especially at 6–18 months of age), hepatitis B and petrol sniffing (see CHAPTER 130). The ability to achieve appropriate levels of immunisation in these communities will have enormous health benefits. Poliomyelitis, diphtheria, pertussis and tuberculosis are now rare and it is hoped that hepatitis B and H. influenzae infections will be drastically reduced.

Specific disorders requiring attention The GP attending Indigenous patients has to develop special skills in the diagnosis and management of the following health concerns: • diabetes mellitus, frequently with associated hypertension and kidney disease • trauma • substance abuse, including alcohol and smoking • ear and eye infections • respiratory disorders—URTIs and LRTIs, asthma • skin disorders (e.g. fungal infections, impetigo, leg ulcers, cellulitis, boils) • parasitic infestations (e.g. scabies, lice) • gastrointestinal infections (e.g. Campylobacter enteritis, giardiasis, Shigella)

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• Health of specific groups

• • • •

sexually transmitted infections psychosocial dysfunction bites and stings severe infections (e.g. meningitis, rheumatic fever, septicaemia) • hepatitis B • tropical diseases (where applicable) • worm infestation e.g. strongyloides However, the general management of medical disorders follows the principles and treatment guidelines outlined in this book. Antibiotic guidelines for use by Indigenous health workers in rural Indigenous communities are available.8,17

• Chronic suppurative otitis media

Wash with povidone–iodine 5% solution using a 20 mL syringe with plastic tubing 1, 2 or 3 times daily, then dry mop with rolled toilet paper ‘spears’. Teach this method to family members. If available, suction kits are useful. Then instil ciprofloxacillin with hydrocortisone drops 12 hourly, especially in the presence of a perforation of the tympanic membrane

• Otitis externa

Gently clean out debris with toilet paper ‘spears’ followed by acetic acid 0.25%; insert Kenacomb or Sofradex drops or ointment 12 hourly on a gauze wick (if no perforation), otherwise ciprofloxacillin with hydrocortisone drops 12 hourly

• Acute mastoiditis

Parenteral IM or IV flucloxacillin/dicloxacillin ± gentamicin IM or IV and hospitalisation

Cardiovascular disease3,18 Cardiovascular disease, especially ischaemic heart disease, is a major cause of continuing high rates of mortality and morbidity and includes ischaemic and rheumatic heart disease and stroke. Mortality from ischaemic heart disease is almost twice that in the non-Indigenous population overall and 6–8 times higher in those aged 25–64 years. Reasons for this include high smoking rates (twice the rate for others), type 2 diabetes (two to four times higher), obesity and low rates of physical activity. Rheumatic heart disease is 11 times more common in the Indigenous population. Targets for secondary prevention of cardiovascular disease and diabetes mellitus are as presented in CHAPTER 20, FIGS 20.7 and 20.8).

Ear infections8,17

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Otitis externa and otitis media with its acute and chronic complications are major health problems in rural Indigenous children. Acute otitis media should be treated early and aggressively with antibiotics to prevent chronic suppurative otitis media, which is very difficult to cure once established. Check carefully for a perforation, which may affect management.

Treatment guidelines • Acute otitis media

Amoxycillin (o) or clotrimazole (o) or procaine penicillin (IM) for 5 days; if no response, consider amoxycillin/clavulanate or cefaclor. Review in 4–6 weeks

• Acute suppurative otitis media

Antibiotics (as above) + dry mop ear

Eye infections8,17 Treatment guidelines • Peri-orbital cellulitis and penetrating eye trauma. Arrange evacuation to hospital; if critically ill or delay in transfer give empirical treatment with ceftriaxone IM or IV once daily. Add gentamicin IM or IV as single dose for a child