John Murtagh’s General Practice [5th ed.] 0070285381, 9780070285385

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general practice

ctice

To all our medical colleagues, past and present, who have provided the vast reservoir of knowledge from which the content of this book was made possible

fifth edition

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 eforts 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 conirm 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 ifth edition published 2011 First edition published 1994, Second edition published 1998, Third edition published 2003, Fourth edition published 2007 Text © 2011 John Murtagh Illustrations and design © 2011 McGraw-Hill Australia Pty Ltd Additional owners of copyright are acknowledged in on-page credits/on the acknowledgments page Every efort 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 via www.mcgraw-hill.com.au or marked for the attention of the Permissions editor at the address below. National Library of Australia Cataloguing-in-Publication Data: Author: Murtagh, John, 1936Title: General practice / John Murtagh. Edition: 5th ed. ISBN: 9780070285385 (hbk.) Notes: Includes index. Bibliography. Subjects: Family medicine. Physicians (General practice) Dewey Number: 610 Published in Australia by McGraw-Hill Australia Pty Ltd Level 2, 82 Waterloo Road, North Ryde NSW 2113 Publisher: Elizabeth Walton Associate editor: Fiona Richardson Art director: Astred Hicks Cover design: Astred Hicks Cover and author photographs: Gerrit Fokkema Photography Internal design: David Rosemeyer Production editor: Michael McGrath Permissions editor: Haidi Bernhardt Copy editor: Rosemary Moore Illustrator: Alan Laver/Shelly Communications and John Murtagh Cartoonist: Chris Sorell Proofreader: Karen Jayne Indexer: Garry Cousins Typeset in Scala by Midland Typesetters, Australia Printed in China on 70 gsm matt art by iBook Printing Ltd 987654321

The authors

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

J

ohn 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 Emeritus Professor of General Practice in 1993 until retirement from this position in 2000. He now holds teaching positions as 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.

v

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The authors

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

J

ill 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 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 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 a 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 38 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 34 years and for the Australian Medical Council for 12 years. She was awarded a life membership of the Royal Australian College of General Practitioners in 2010.

Foreword I

n 1960 a young schoolmaster, then teaching biology and chemistry in a secondary school in rural Victoria, decided to become a country doctor. He was admitted to the first intake of students into the Medical School of the newly established Monash University and at the end of the six-year undergraduate medical course and subsequent intern and resident appointments his resolve to practise community medicine remained firm. During his years of undergraduate and early postgraduate study Dr Murtagh continued to gather and record data relating to the diagnostic and therapeutic procedures and clinical skills he would require in solo country practice. These records, subsequently greatly expanded, were to provide at least the foundation of this book. Happily, after graduation, he married Dr Jill Rosenblatt, a young graduate from Melbourne University, who shared his vocational interests. Subsequently they also shared the fulfilment of family life and the intellectual and emotional satisfaction of serving as doctors in a rural setting. In the meantime the Royal Australian College of General Practitioners had established postgraduate training programs that had a significant influence on standards of professional practice. At the same time Monash University established a Department of Community Medicine at one of its suburban teaching hospitals, under the Chairmanship of Professor Neil Carson and staffed by practitioners in the local community. While in practice Dr Murtagh gained a Fellowship of the College through examination. The College recognised his unique clinical, educational and communication skills and immediately commissioned him to prepare educational programs, especially the CHECK programs. His outstanding expertise as a primary care physician led to his appointment as a senior lecturer in the University Department of Community Medicine. The success of the initial academic development in Community Medicine at Monash University, and its influence on the clinical skills of its graduates as they relate to primary care, led to a University decision to establish a further Department of Community Medicine at another suburban teaching hospital in Melbourne. It was considered by the University to be entirely appropriate that Dr Murtagh be invited to accept appointment as Professor and Head of that Department. Four years later Professor Murtagh was appointed Head of the extended Department and the first Professor of General Practice at Monash University. John Murtagh has now become a national and international authority on the content and teaching of

primary care medicine. As Medical Editor of Australian Family Physician from 1986 to 1995 he took that journal to the stage where it was the most widely read medical journal in Australia. This textbook provides a distillate of the vast experience gained by a once-upon-a-time rural doctor whose career has embraced teaching from first to last, whose interest is ensuring that disease, whether minor or life-threatening, is recognised quickly, and whose concern is that strategies to match each contingency are well understood. General Practice is the outcome of the vision of a schoolteacher of great talent who made a firm decision to become a country doctor; through this book his dream has become a reality for all who are privileged to practise medicine in a community setting. It is most appropriate that Jill Rosenblatt, John’s partner in country practice has joined him as co-author of this fifth edition. 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 in an extraordinary way the book became 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 edition was updated and expanded, and retained the successful format of previous editions but with a more attractive and user-friendly format including clinical photographs and illustrations in colour. John Murtagh’s works 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 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 Professor of Anatomy, Monash University, 1961–77 Dean of Medicine, Monash University, 1977–88

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Contents The authors Foreword Acknowledgments Preface Making the most of your book Reviewers Normal values: worth knowing by heart Abbreviations

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v vii xii xiii xiv xviii xxi xxii

Part 1

The basis of general practice

1

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19

The nature 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 healthand illness Palliative care Pain and its management Research and evidence-based medicine Travel medicine Tropical medicine and the returned traveller Laboratory investigations Inspection as a clinical skill A safe diagnostic strategy Genetic conditions

2 7 14 21 29 39 43 48 62 72 81 90 103 112 125 136 145 150 158

Part 2

Diagnostic perspective in general practice

177

20 21 22 23 24 25 26 27 28

Depression Diabetes mellitus: diagnosis Drug problems Anaemia Thyroid and other endocrine disorders Spinal dysfunction Urinary tract infection Malignant disease HIV/AIDS—could it be HIV?

178 186 193 204 211 222 225 233 241

Contents

29 30 31 32 33 34

Baffling viral and protozoal infections Baffling bacterial infections Infections of the central nervous system Chronic kidney failure Connective tissue disease and the vasculitides Neurological dilemmas

251 258 270 275 282 291

Part 3

Problem solving in general practice

307

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 71 72 73

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 Sleep disorders Sore mouth and tongue

308 329 351 359 373 394 403 423 434 449 458 474 491 500 510 514 526 539 554 564 573 581 584 601 604 620 629 634 638 651 663 679 691 708 727 744 751 764 773

ix

x

Contents

74 75 76 77 78 79 80

Sore throat Tiredness/fatigue The unconscious patient Urinary disorders Visual failure Weight gain Weight loss

783 791 798 806 817 829 837

Part 4

Child and adolescent health

843

81 82 83 84 85 86 87 88

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

844 851 868 878 891 899 906 920

Part 5

Women’s health

925

89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104

Cervical cancer andPap smears Family planning Breast pain (mastalgia) Lumps in the breast Abnormal uterine bleeding Lower abdominal and pelvic pain in women Premenstrual syndrome The menopause Osteoporosis Vaginal discharge Vulvar disorders Domestic violence and sexual assault Basic antenatal care Infections in pregnancy High-risk pregnancy Postnatal care

926 934 943 948 959 966 979 983 990 994 1002 1009 1013 1021 1026 1040

Part 6

Men’s health

1047

105 106 107 108 109

Men’s health: an overview Scrotal pain Inguinoscrotal lumps Disorders of the penis Disorders of the prostate

1048 1051 1056 1066 1072

Part 7

Sexually related problems

1079

110

The subfertile couple

1080

Contents

111 112

Sexual health Sexually transmitted infections

1087 1099

Part 8

Problems of the skin

1111

113 114 115 116 117 118 119 120 121

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

1112 1122 1131 1152 1164 1172 1188 1197 1206

Part 9

Chronic disorders: continuing management

1215

122 123 124 125 126 127 128 129 130 131

Alcohol problems Allergic disorders including hay fever Anxiety disorders Asthma Chronic obstructive pulmonary disease Epilepsy Hypertension Dyslipidaemia Diabetes mellitus: management Chronic heart failure

1216 1223 1230 1239 1251 1258 1266 1285 1289 1302

Part 10

Accident and emergency medicine

1309

132 133 134 135 136 137 138

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

1310 1324 1330 1336 1342 1355 1377

Part 11

Health of specific groups

1393

139 140 141

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

1394 1402 1407

Appendix Index

1413 1421

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Acknowledgments The author would like to thank the Publication Division of the Royal Australian College of General Practitioners for supporting my past role as Medical Editor of Australian Family Physician, which has 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 Chris Sorrell, graphic designer, for his art illustration, and to Nicki Cooper, Jenny Green

and Caroline Menara for their skill and patience in typing the manuscript. Figure 67.5 was provided by Dr Levent Efe. 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 are also due to Dr Bruce Mugford, Dr Lucie Stanford, Dr Mohammad Shafeeq Lone, Dr Brian Bedkobar and to Lesley Rowe, for reviewing the manuscript, and to the publishing and production team at McGraw-Hill Australia for their patience and assistance in so many ways. Finally, thanks to Dr Ndidi Victor Ikealumba for his expert review of General Practice fourth edition and his subsequent contribution.

Photo credits Photographs appearing on the pages below are taken from The Color Atlas of Family Medicine by Richard P Usatine MD, McGraw-Hill US 2009, with the kind permission of the following people: Dr Richard Usatine: Fig 65.13, pg. 673; Fig 73.6, pg. 781; Fig 82.4, pg. 862; Fig 82.5, pg. 862; Fig 82.6, pg. 863; Fig 98.5, pg. 1000; Fig 112.5, pg. 1106; Fig 118.20, pg. 1182; Fig 120.5, pg. 1202; Fig 120.6, pg. 1202; Fig 99.1, pg. 1004 and Fig 115.12, pg. 1143. Dr Marc Solioz: Fig 17.1, pg. 146. Dr Brad Neville: Fig 73.1, pg. 776. Dr Edwin A Farnell: Fig 121.3a, pg. 1208. Journal of Family Practice, December 2007; 56(12):1025, Dowden Health Media: Fig 86.4, pg. 903.

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McGraw-Hill USA: Fig 51.5, pg. 529; Fig 51.9, pg. 532; Fig 58.1, pg. 603; Fig 91.2, pg. 947; Fig 92.2, pg. 950; Fig 114.5, pg. 1126; Fig 121.2a, pg. 1208; Fig 140.1, pg. 1404; Fig 15.6, pg. 134 and Fig 22.2, pg. 197. Photographs from Infectious Diseases: Atlas, Cases, Text by Robin Cooke, McGraw-Hill Australia 2008, with the kind permission of Professor Robin Cooke and Brian Stewart: Fig 15.2, pg. 129; Fig 15.3, pg. 130 and Fig 31.2, pg. 271.

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 have been added 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 fifth 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 Guideline series. To provide updated accuracy and credibility the authors have had the relevant chapters peer reviewed by independent experts in the respective discipline. These consultants are acknowledged in the reviewers section. The revised edition also has the advantage of co-authorship from an experienced general practitioner, Dr Jill Rosenblatt, who in fact provided considerable input into previous editions, especially regarding women’s health. Such a comprehensive book, 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 those 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, it is hoped that all primary-care practitioners will gain useful information from the book’s content.

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Making the most of your book

Patient presentation Patient presentation provides the overall structure of the book, mirroring clinical presentation in practice. General Practice is renowned for this unique and powerful learning feature which the book introduced from its first edition.

The staff of Asclepius The staff of Asclepius icon is a new feature highlighting diseases for when you are specifically searching for information on a particular disease.

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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 62 633 6

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 Dyspepsia (indigestion) Dysphagia Dyspnoea The painful ear The red and tender eye Pain in the face Fevers and chills Faints, fits and funny turns Haematemesis and melaena Headache Hoarseness Jaundice Nasal disorders Nausea and vomiting Neck lumps Neck pain

x x x x x x x x x x x x x x x x x x x x x x x x x x x x x

Schistosomiasis (bilharzia) The infestation is caused by parasite organisms (schistosomes) whose eggs are passed in human excreta, which contaminates watercourses (notably stagnant water) and irrigation channels in Egypt, other parts of Africa, South America, some parts of South-East Asia and China. Freshwater snails are the carriers (vectors).

Key facts and checkpoints

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

xiv

• The main diseases facing the international traveller are traveller’s diarrhoea (relatively mild) and malaria, especially the potentially lethal Plasmodium falciparum malaria. • Most cases of traveller’s diarrhoea are caused by enterotoxigenic Escherichia coli and Campylobacter specus. • Enteroinvasive E. coli (a different serotype) produces a dysentery-like illness similar to Shigella. • Traveller’s diarrhoea is contracted mainly from contaminated water and ice used for beverages, washing food or utensils or cleaning teeth. • Poliomyelitis is endemic in at least 20 countries and thus immunisation for polio is still important.

Making the mostWhat of your is new? book

Yellow flag pointers

Red and yellow flags Red and yellow flags alert you to potential dangers. The severity rates red as the most urgent with yellow requiring very careful consideration.

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: • abnormal illness behaviour • compensation issues • unsatisfactory restoration of activities Red flags for organic disease 12 • failure to return to work • unsatisfactory response to treatment • Older patient • treatment refused • atypical physical signs • Nocturnal pain or diarrhoea • Progressive symptoms • Rectal bleeding • Fever • Anaemia • Weight loss • Abdominal mass • Faecal incontinence or urgency (recent onset)

Clinical features

Clinical framework 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.

• Peak incidence 50–70 years • Risk factors: — age — obesity — nulliparity — late menopause — diabetes mellitus

Symptoms 80% present with abnormal bleeding, especially postmenopausal bleeding.

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

Management • Urgent gynaecological referral

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

Seven masquerades checklist

A.

Depression

✓

Diabetes

–

Drugs

✓

Anaemia

–

Thyroid disorder

–

Spinal dysfunction UTI

✓ ✓

DxT: febrile illness + vomiting + stupor = Japanese B encephalitis

Seven masquerades checklist Seven masquerades checklist is a unique feature of the book that reminds you of potential and hidden dangers underlying patient presentations.

xv

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Part Onethe most of your book Making

Evidence-based research

13

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.

Research and evidencebased medicine Not the possession of truth, but the effort of struggling to attain it brings joy to the researcher. G O F F H O L D L A S S I N G (1729–81)

Effective research is the trademark of the medical developed in the context of Australian general practice profession. When confronted with the great responsibility and now beyond that. The focus of EBM has been of understanding and treating human beings we need to improve health care and health economics. Its development has gone hand in hand with improved as much scientific evidence as possible to render our decision making valid, credible and justifiable. information technology. EBM is inextricably linked Research can be defined as ‘a systematic method to research. The aim of this chapter is to present a brief overview in which the truth of evidence is based on observing of research and EBM and, in particular, to encourage and testing the soundness of conclusions according to GPs, either singly or collectively, to undertake research— consistent rules’1 or, to put it more simply, ‘research is organised curiosity’,2 the end point being new and simple or sophisticated—and also to publish their work. improved knowledge. The benefits of such are well outlined in John Howie’s In the medical context the term ‘research’ tends to classic text Research in General Practice.5 conjecture bench-type laboratory research. However, the Why do research? discipline of general practice provides a fertile research The basic objective of research is to acquire new area in which to evaluate the morbidity patterns and knowledge and justification for decision making in the nature of common problems in addition to the medical practice. Research provides a basis for the processes specific to primary health care. acquisition of many skills, particularly those of critical There has been an excellent tradition of research thinking and scientific methodology. The discipline of conducted by GPs. Tim Murrell in his paper ‘Nineteenth general practice is special to us with its core content of century masters of general practice’3 describes the continuing, comprehensive, community-based primary contributions of Edward Jenner, Caleb Parry, John care, family care, domiciliary care, whole-person care Snow, Robert Koch and James MacKenzie, and notes and preventive care. To achieve credibility and parity that ‘among the characteristics they shared was their with our specialist colleagues we need to research this capacity to observe and record natural phenomena, area with appropriate methodology and to define the breaking new frontiers of discovery in medicine using discipline clearly. There is no area of medicine that an ecological paradigm’. involves such a diverse range and quantity ity of decisions This tradition was carried into the 20th century by 101 erefor Pain and its management each day as general practice, and therefore patient GPs such as William Pickles, the first president of the management needs as much evidence-based e-bas rigour Royal College of General Practitioners, Keith Hodgkin as possible. and John Fry, all of whom meticulously recorded data ural practice p Our own patch, be it an isolated rural or that helped to establish patterns for the nature of For antiplatelet effects use low doses 2–5 mg/kg/ Hydromorphone ts own ow microan industrial suburban practice, has its primary health care. In Australia the challenge was taken day. Usual dosage: epidemiological fascination. Thus, it provides ovides a unique up by such people as Clifford Jungfer, Alan Chancellor, NSAIDs opportunity to find answers to questions ons aand make Charles Bridges-Webb, Kevin•Cullen and Trevor 0.04 mg/kg (o) 4Beard hourly 4 muni observations about that particular community. in the and nowfor the research activities of the new NSAIDs have a proven safety and effi1960s, cacy in children generation GPs, academic-based or practice-based, There are also personal reasons to undertake u Methadone mild to moderate pain and can be used inofconjunction research. The process assists professional al development, deve havesuch beenastaken to a higher with themg/kg development with paracetamol and opioids codeine and level • 0.1–0.2 (o) 8–12 hourly of evidence-based encouraging clear and critical thinking,, improvement imp morphine. The advantage is their opioid-sparingmedicine effect. (EBM). usedCollaboration for opioid weaning rotationand the satisfaction of developing Based on the work of the Often Cochrane evelo of and knowledge new Contraindications include known hyper-sensitivity, skills and opening horizons. and the initiatives of Chris Silagy in particular it has severe asthma (especially if aspirin sensitive), bleeding Fentanyl diatheses, nasal polyposis and peptic ulcer disease. Fentanyl citrate can be administered orally (transThose commonly used for analgesia are: mucosal) as ‘lollipops’, transcutaneous as ‘patches’,

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

12

• ibuprofen: 5–10 mg/kg (o) 6–8 hourly (max. 40 mg/kg/day) • naproxen: 5–10 mg/kg (o) 12–24 hourly (max. 1 g/day) • indomethacin: 0.5–1 mg/kg (o) 8 hourly (max. 200 mg/day) • diclofenac: 1 mg/kg (o) 8 hourly (max. 150 mg/day) • celecoxib 1.5–3 mg/kg (o) bd

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.

The rectal dose is double the oral dose (e.g. indomethacin 2 mg/kg) but only administered twice a day.

Opioid analgesics Oral opioids These have relatively low bioavailability but can be used for moderate to severe pain when weaning from parenteral opioids, for ongoing severe pain (e.g. burns) and where the IV route is unavailable.

• 0.3 mg/kg (o) 4 hourly prn

Sustained release:

Some general rules and tips2

• 0.6–0.9 mg/kg, 12 hourly

• Give analgesics at fixed times by the clock rather than ‘prn’ for ongoing pain. • Regularly monitor your patient’s analgesic requirements and modify according to needs and adverse effects. • Start with a dose towards the lower end of the dose range and then titrate upwards depending on response. • Provide ongoing interest and support. This will magnify any placebo effect. • Avoid using compound analgesics and prescribe simple and opioid analgesics separately. • Never cut suppositories in half with the intention of halving the dose.

More effective if used combined with paracetamol or ibuprofen.

Morphine Immediate release:

• 1–2 mg/kg (o) 4 hourly (avoid with SSRIs)

numbness

Oxycodon Oxycodone Immediate release: • 0.2–0.3 mg/kg m (o) 4 hourly (max. 10 mg)

pins and needles

intolerable pain

Sustained release: Back

10

Front

• morphine: 0.2 mg/kg (max. 10–15 mg), 4 hourly prn • pethidine: 2 mg/kg (max. 25–100 mg), 3 hourly prn

Older patients have the highest incidence of painful disorders and also surgical procedures. As a general rule, most elderly patients are more sensitive to opioid analgesics and to aspirin and other NSAIDs but there may be considerable individual differences in tolerance between patients. Patients over 65 years should receive lower initial doses of opioid analgesics with subsequent doses being titrated according to the patient’s needs.2

• 0.5–1 mg/kg (o), 4–6 hourly prn (max. 3 mg/kg/day)

Tramadol Usual dosage:

pain

Parenteral opioids8 These are the most powerful parenteral analgesics for children in severe pain and can be administered in intermittent boluses (IM, IV or SC) or by continuous infusion (IV or SC). Infants under 6 months are more sensitive and need careful monitoring (e.g. pulse oximetry). This management is invariably in the hospital. Administration of parenteral opioid should not be undertaken without the availability of oxygen, resuscitation equipment and naloxone to reverse overdose. Maximum dosage of IM opioids:

Analgesics in the elderly

Codeine Usual dosage:

Mark the areas on your body where you feel the various sensations

or intranasally via a mucosal atomiser device (for painful procedures).

• 0.6 mg/ mg/kg (o) 12 hourly

9

8

Full colour illustrations

7

6 moderate pain

5

4

3 Left

Right

Right

2

1

0 no pain Mark your level of pain on this scale

Figure 12.2 Assessing pain using a visual analogue scale and body chart: ideal for lumbosacral pain

Left

Full colour illustrations with over 600 diagrams retaining the clean and simple style that has proved so popular.

Making the mostWhat of your is new? book

Clinical photos Clinical photos provide authentic and visual examples of many conditions and serve as either a valuable introduction or confirmation of diagnosis.

PRACTICE TIPS Figure 15.4 Cutaneous leishmaniasis in a serviceman after returning from the Middle East

Practice tips Practice tips consists of key points of use in the clinical setting.

Significantly enhanced index Enhanced index has more subcategories with bold page numbers indicating main treatment the topic, enabling you to quickly pinpoint the most relevant information. Page numbers in italics refer to figures and tables. Entries with ‘see also’ have cross-references to related, but more specific information on the topic.

• Morphine is the gold standard for pain. • Consider prescribing antidepressants routinely for patients in pain. • Remember the ‘sit down rule’ whereby the home visit is treated as a social visit—sitting down with the patient and family, having a ‘cuppa’ and sharing medical and social talk.3 • Early referral of terminal patients with difficult-tocontrol problems, especially pain, to a hospice or multidisciplinary team can enhance the quality of care. However, the patient’s family doctor must still be the focus of the team.

Index

dental trauma 773, 776 dentition, and weight loss 842 denture therapy 776 dependent personality disorders 489 Depo-Provera 939, 962, 975 depression 178–85 in adolescents 795, 922–4 antidepressant medication 181–3 anxiety symptoms due to 1238 assessment of 485 back pain due to 373, 375–6, 392 cause of 181 in children 180, 486 classifications of 178 cognitive behaviour therapy 32 complementary therapies 183 constipation due to 425 contrasted with dementia 55, 55 counselling for 36–7 delirium due to 476 depression scales 180–1 diagnosis of 179, 180–1 drugs that may cause 179 due to alcohol abuse 1219 dyspepsia due to 500 ear pain due to 528 in the elderly 49, 55, 58, 180, 476 faints and fits due to 574 headache due to 587 major and minor depression 178–9 management of 181 masked depression 179–80 as a masquerade 154 ‘missing chemical’ theory 37 non-pharmacological interventions 924 in patients with myocardial infarction 420 perinatal depression 180 postnatal depressive disorders 1045–6 psychogenic pain 102 recurrent depression 184 as a side effect of oral contraceptives 938 tiredness due to 791, 792, 793 treatment of bipolar depression 485 weight loss due to 838, 842 see also suicide depressive personality disorder 489 de Quervain tenosynovitis 663, 671, 673–4, 673–4, 678 de Quervain thyroiditis 215–16, 641 dermal skin lesions 1115, 1115 Derma Oil 734, 1134 Dermatec 1176 Dermatech Wart Treatment 866 dermatitis 1131–8 causes 1131 in children 864–5, 864–5 effect on nails 1116 irritant dermatitis 864–5, 1141 peri-oral dermatitis 1145, 1145–6

pruritus due to 1122, 1126 with umbilical discharge 863 vulvar dermatitis 1002–3, 1007 see also atopic dermatitis; eczema; seborrhoeic dermatitis dermatitis artefacta 1170 dermatitis herpetiformis 1114, 1122, 1125, 1125, 1129 dermato-conjunctivitis 543 dermatofibroma 1172, 1178–9, 1188, 1194 dermatomes 362, 363, 556 dermatomyositis 155, 234, 282–3, 287, 287–8, 330, 330, 343 dermatosis 1002, 1150 Dermeze 1133 dermoid cysts 636, 869 desensitisation 32 desferrioxamine 162, 207, 911 desipramine 1160 desloratadine 1227 desmoplastic melanoma 1193 desmopressin acetate 401, 860 desogestrel 935 desonide 1137 desvenlafaxine 182 detergent worker’s disorder 523 detrusor instability 813 developmental disability and delay 166–9, 850, 857–8 developmental dysplasia of the hip 679, 681, 684–5, 685, 690, 746, 874 developmental problems 846, 853–8 DEXA 991, 993 dexamethasone for altitude sickness 123 for anorexia 87 for cerebral metastases 87 for croup 914 for meningitis 271, 912 for migraine 593 for nausea and vomiting 632 for pressure pain 84, 86 dexamphetamines 197, 579, 768 dexchlorpheniramine 447 dexedrine 199 dextrin 430 dextromethorphan 202, 203, 447 dextropropoxyphene 96, 910 dextrose 74, 916 DHA 75 DHEA 202 Dhobie itch 1126 diabetes insipidus 218 diabetes ketoacidosis 310, 328, 799 diabetes ketosis 476 diabetes mellitus age of onset 48 air travel by diabetics 121 with arthropathy 329 association with facial nerve palsy 305

causes of secondary diabetes 187 in children 189–90 clinical features 187–8 complications of 190, 191, 192 deafness due to 455 delirium due to 476 diagnosis of 186–9 dietary control of 77 in the elderly 49, 190 erectile difficulties 1088 gestational diabetes 187, 189–90 hyperhidrosis due to 1149 kidney failure due to 275, 275 as a masquerade 154, 186 microvascular disease 190 neuropathy in 190, 192, 727, 729 painful diabetic neuropathy 101–2, 694 penile lesions due to 1070 peripheral neuropathy due to 302 prediabetes 189 in pregnancy 1030 preventing nephropathy 190 prevention of 192 retinopathy of 190, 817 as a risk factor for maternal disorders 1028 role of exercise and diet 67 skin signs of 187 with skin ulcers 1164 susceptibility to infections 192 types 186, 186, 282 visual failure due to 818 weight loss due to 837–8, 840 diabetic ketoacidosis 192 diabetic lumbosacral r adiculoplexopathy 190 diabetic maculopathy 828 diabetic proteinuria 813 diagnosis application of the model 156–7 basic model of 150, 150–6 communication of to patients 18–19 components of 3–4 conditions often missed 152–3 defining the problem 17 diagnostic triads 150, 155, 306 of difficult and demanding patients 39 failure to make 18 hidden agendas of patients 154–6 history-taking in 15–17 inspection as a clinical skill 145–9 masquerades in 153–4, 154–5 mnemonics for 151–2 most common disorders 5–6 ordering further tests 17–18 psychosocial reasons for malaise 154–6, 156 see also specific conditions and diseases diagnostic triads 150, 155, 306 dialysis 280

1421

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Attention Deficit Hyperactivity Disorder, page 14 • Autism, page 15 • Autism: Asperger’s Syndrome, page 16 • Bullying of Children, page 21 • Stuttering, page 57 • Tantrums, page 58

Patient education resources Where you can find relevant information from Murtagh’s Patient Education 5th edition to photocopy and hand out to patients.

xvii

Reviewers The fourth edition underwent a rigorous peer review process to ensure that General Practice remains the gold standard reference for general practitioners around the world. To that end, the author and the publishers extend their sincere gratitude to the following people who generously gave their time, knowledge and expertise.

Content consultants The author is indebted to the many consultants for their help and advice after reviewing various parts of the manuscript that covered material in their particular area of expertise.

Dr Rob Baird

laboratory investigation

Dr Roy Beran

epilepsy; neurological dilemmas

Dr Peter Berger

a diagnostic and management approach to skin problems

Professor Geoff Bishop

basic antenatal care

Dr John Boxall

palpitations

Dr Jill Cargnello

hair disorders

Dr Paul Coughlin and Professor Hatem Salem

bruising and bleeding; thrombosis and thromboembolism

Mr Rod Dalziel

shoulder pain

Dr David Dunn and Dr Hung The Nguyen

the health of Indigenous peoples

Dr Robert Dunne

common skin wounds and foreign bodies

Professor John Emery

genetic disorders, malignant disease

Genetic Health Services, Victoria

genetic disorders

Dr Lindsay Grayson and Associate Professor Joseph Torresi

travel medicine, the returned traveller and tropical medicine

Dr Michael Gribble

anaemia

Mr John Griffiths

pain in the hip and buttock

Professor Michael Grigg

pain in the leg

Dr Gary Grossbard

the painful knee

Dr Peter Hardy-Smith

the red and tender eye; visual failure

Professor David Healy

abnormal uterine bleeding

Assoc Professor Peter Holmes

cough; dyspnoea; asthma; COPD

Dr Ndidi Victor Ikealumba

refugee health

Professor Michael Kidd, Dr Ron McCoy human immunodeficiency virus infection and Dr Alex Welborn

xviii

Professor Gab Kovacs

abnormal uterine bleeding; the infertile couple

Professor Even Laerum

research in general practice

What Reviewers is new?

Dr Barry Lauritz

common skin problems; pigmented skin lesions

Mr Peter Lawson (deceased) and Dr Sanjiva Wijesinha

disorders of the penis; prostatic disorders

Dr Peter Lowthian

arthritis

Mr Frank Lyons

common fractures and dislocations

Professor Barry McGrath

hypertension

Dr Joe McKendrick

malignant disease

Professor Robyn O’Hehir

allergic disorders, including hayfever

Dr Michael Oldmeadow

tiredness

Dr Frank Panetta

chest pain

Professor Roger Pepperell

high risk pregnancy

Dr Geoff Quail

pain in the face, sore mouth and tongue

Mr Ronald Quirk

pain in the foot and ankle

Dr Ian Rogers

emergency care

Dr Jill Rosenblatt

the menopause; cervical cancer and Pap smears

Professor Avni Sali

abdominal pain; lumps in the breast; jaundice; constipation; dyspepsia; nutrition

Dr Hugo Standish

urinary tract infection; chronic kidney failure

Dr Richard Stark

neurological diagnostic triads

Dr Paul Tallman

stroke and transient ischaemic attacks

Dr Alison Walsh

breastfeeding, post-natal breast disorders

Professor Greg Whelan

alcohol problems, drug problems

Dr Sanjiva Wijesinha

men’s health, scrotal pain, inguinoscrotal lumps

Dr Alan Yung

fever and chills; sore throat

Dr Ronnie Yuen

diabetes mellitus; thyroid and other endocrine disorders

A substantial number of people were involved in reviewing this book through surveys and their invaluable contribution is acknowledged below. We also take the opportunity to thank the other participants who preferred not to be named in this collective.

Survey respondents Ashraf Aboud Mehdi Alzaini Anne Balcomb Jill Benson Ibrahim K Botros Chris Briggs Kathy Brotchie Shane Brun

Daniel Byrne Paul Carroll Louisa Case Ercelle Celis Peter Charlton Tricia Charmer Rudolph W M Chow Patrick Clancy

Jennifer Cook-Foxwell Barrie Coulson Therese Cox Roxane Craig Gordana Cuk Alice Cunningham Fred De Looze Rudi De Mulder

xix

xx

Part One Reviewers

Gabrielle Dellit Michael Desouza Yock Seck Ding Matthew Dwyer Judith Ellis Jon Emery Say Poh Eng Iain Esslemont Marian Evans Wes Fabb N Fajardo Cyril Fernandez Danika Fietz Clare Finnigan Anthony Fok Oliver Frank Brett Garrett Tarek Gergis Ben Gerhardy Elena Ghergori Naomi Ginges Jim Griffin Ranjan Gupta Hadia Haikal-Mukhtar Pedita Hall Nazih Hamzeh Erfanul Haque Abby Harwood Mark Henschke Edward C Herman D Ho David Holford Sue Hookey Elspeth Horn Seyed Ebrahim Hosseini Faline Howes Brett Hunt Rosalyn Hunt Farhana Hussein Robyn Hüttenmeister Anwar Ikladios John Inkwater

Daljit Janjua Diosdado Javellana Aravinda Jawali Les Jenshel Fiona Joske Meredith Joslin Gloria Jove Mohammed Al Kamil Inas Abdul Karim Sophia Kennelly George Kostalas Jim Kourdoulos Ivan S Lee Mohammad Shafeeq Lone Christine Lonergan Dac Luu Justin Madden Hemant Mahagaonkar Meredith Makeham Shahid Malick Muhammad Mannan Luke Manestar Linda Mann Cameron Martin Kohei Matsuda Ronald Mccoy Mark McGrath Robert Meehan Scott Milan Kirsten Miles Vahid Mohabbati Megha Mulchandani Patrick Mulhern Brad Murphy Charles Mutandwa Keshwan Nadan Ching-Luen Ng Mark Nelson Harry Nespolon Brent O’Carrigan Christopher Oh John Padgett

George Pappas Peter Parkes W J Patterson Anoula Pavli Matthew Penn Satish Prasad Tereza Rada Jason Rajakulendran Muhammad Raza Kate Roe Daniel Rouhead Fiona Runacres Safwat Saba Amin Sauddin Kelly Seach Leslie Segal Isaac Seidl Rubini Selvaratnam Theja Seneviratne Karina Severin Pravesh Shah Mitra Babazadeh Shahri Jamie Sharples G Sivasambu Russell Shute Sue Smith Jane Smith Lucie Stanford Sean Stevens S Sutharsamohan Hui Tai Tan Marlene Tham Heinz Tilenius Judy Toman Khai Tran Joseph V Turner Susan Wearne Anthony Wickins Kristen Willson Melanie Winter Jeanita Wong Belinda Woo Belinda Wozencroft

Normal values: worth knowing by heart The following is a checklist that one can use as a template to memorise normal quantitative values for basic medical conditions and management. Vital signs (average)

< 6 months

6 months – 3 years

3 – 12 years

Adult

Pulse

120–140

110

80 – 100

60 – 100

Respiratory rate

45

30

20

14

BP (mmHg)

90/60

90/60

100/70

≤ 130/85

Children’s weight

1–10 years

Rule of thumb:

Wt = (age + 4) × 2 kg

Fever—temperature (morning)(a) (a) There is considerable diurnal variation in temperature so that it is higher in the evening (0.5–1°C). I would recommend the definition given by Yung et al. in Infectious Diseases: a Clinical Approach: ‘Fever can be defined as an early morning oral temperature > 37.2°C or a temperature > 37.8°C at other times of the day’.

Oral

> 37.2°C

Rectal

> 37.7°C

Diabetes mellitus—blood sugar Random 1 reading if symptomatic 2 readings if asymptomatic

> 11.1 mmol/L

Fasting

> 7.0 mmol/L

or

the 2 values from an oral GTT

< 3.5 mmol/L

Jaundice Serum bilirubin

Serum potassium

> 19 µmol/L

> 5.0 mmol/L

Hypertension BP

> 140/90 mmHg

Alcohol excessive drinking Males

> 4 standard drinks/day

Females

> 2 standard drinks/day

Alcohol health guidelines Males and females

Hypokalaemia Serum potassium

Hyperkalaemia

≤ 2 standard drinks/day < 4 standard drinks/occasion

Anaemia—haemoglobin Males

< 130 g/L

Females

< 115 g/L

Body mass index

Wt (kg)/Ht (m2)

Normal

20–25

Overweight

> 25

Obesity

> 30

xxi

Abbreviations AAA AAFP ABC ABCD ABFP ABI ABO AC AC ACAH ACE ACL ACR ACTH AD AD ADHD ADT AFI AFP AI AICD AIDS AIIRA AKF ALE ALL ALP ALT ALTE AMI AML ANA ANCI ANF a/n/v AP APF APH APTT AR ARC ARR ASD ASIS ASOT

xxii

abdominal aortic aneurysm American Academy of Family Physicians airway, breathing, circulation airway, breathing, circulation, dextrose American Board of Family Practice ankle brachial index A, B and O blood groups air conduction acromioclavicular autoimmune chronic active hepatitis angiotensin-converting enzyme anterior cruciate ligament albumin creatine ratio adrenocorticotrophic hormone aortic dissection autosomal dominant attention deficit hyperactivity disorder adult diphtheria vaccine amniotic fluid index alpha-fetoprotein aortic incompetence automatic implantable cardiac defibrillator acquired immunodeficiency syndrome angiotension II(2) reuptake antagonist acute kidney failure average life expectancy acute lymphocytic leukaemia alkaline phosphatase alanine aminotransferase apparent life-threatening episode acute myocardial infarction acute myeloid leukaemia antinuclear antibody antineutrophil cytoplasmic antibody antinuclear factor anorexia/nausea/vomiting anterior–posterior Australian pharmaceutical formulary ante-partum haemorrhage activated partial thromboplastin time autosomal recessive AIDS-related complex absolute risk reduction atrial septal defect anterior superior iliac spine antistreptolysin 0 titre

AST ATFL AV AVM AZT

aspartate aminotransferase anterior talofibular ligament atrioventricular arteriovenous malformation azidothymidine

BC BCC BCG bDMARDs

bone conduction basal cell carcinoma bacille Calmette-Guérin biological disease modifying antirheumatic drugs bone mass density body mass index bladder outlet obstruction blood pressure benign prostatic hyperplasia benign paroxysmal positional vertigo breast self-examination

BMD BMI BOO BP BPH BPPV BSE Ca CABG CAD CAP CBE CBT CCF CCP CCT CCU CD4 CD8 CDT CEA CFL CFS cfu CHD CHF CI CIN CJD CK CK–MB CKD CKF

carcinoma coronary artery bypass grafting coronary artery disease community acquired pneumonia clinical breast examination cognitive behaviour therapy congestive cardiac failure cyclic citrinullated peptide controlled clinical trial coronary care unit T helper cell T suppressor cell combined diphtheria/tetanus vaccine carcinoembryonic antigen calcaneofibular ligament chronic fatigue syndrome colony forming unit coronary heart disease chronic heart failure confidence interval cervical intraepithelial neoplasia Creutzfeldt-Jakob disease creatinine kinase creatinine kinase–myocardial bound fraction chronic kidney disease chronic kidney failure

Abbreviations What is new?

CRF CRFM CRH CR(K)F CRP CSF CSFM CSIs CSU CT CTD CTG CTS CVA CVS CXR

carpometacarpal chronic myeloid leukaemia cytomegalovirus central nervous system compound chronic obstructive airways disease combined oral contraceptive combined oral contraceptive pill catechol-O-methyl transferase chronic obstructive pulmonary disease cyclooxygenase cardiopulmonary arrest continuous positive airways pressure creatine phosphokinase calcium pyrophosphate dihydrate cardiopulmonary resuscitation complex partial seizures controlled release computerised reference database system calcinosis cutis; Raynaud’s phenomenon; oesophageal involvement; sclerodactyly; telangiectasia chronic renal failure chloroquine-resistant falciparum malaria corticotrophin-releasing hormone chronic renal (kidney) failure C-reactive protein cerebrospinal fluid chloroquine-sensitive falciparum malaria COX-2 specific inhibitors catheter specimen of urine computerised tomography connective tissue disorder cardiotocograph carpal tunnel syndrome cerebrovascular accident cardiovascular system chest X-ray

DBP DC DDAVP DDH DDP DEXA DHA DI DIC DIDA DIMS

diastolic blood pressure direct current desmopressin acetate developmental dysplasia of the hip dipeptidyl peptidase dual energy X-ray absorptiometry docosahexaenoic acid diabetes insipidus disseminated intravascular coagulation di-imino diacetic acid disorders of initiating and maintaining sleep

CMC CML CMV CNS co COAD COC COCP COMT COPD COX CPA CPAP CPK CPPD CPR CPS CR CRD CREST

DIP dL DMARDs DNA DOM DRE DRABC drug dosage ds DS DSM DU DUB DVT DxT

distal interphalangeal decilitre disease modifying antirheumatic drugs deoxyribose-nucleic acid direction of movement digital rectal examination defibrillation, resuscitation, airway, breathing, circulation bd—twice daily tid, tds—three times dailyqid, qds—four times daily double strand double strength diagnostic and statistical manual (of mental disorders) duodenal ulcer dysfunctional uterine bleeding deep venous thrombosis diagnostic triad

esp. ESR ET ETT

expired air resuscitation Epstein-Barr mononucleosis (glandular fever) Epstein-Barr nuclear antigen Epstein-Barr virus external chest compression electrocardiogram electroconvulsive therapy emergency department expected due date electroencephalogram enzyme linked immunosorbent assay electromyogram extractable nuclear antigen ethinyloestradiol eicosapentaenoic acid extensor pollicis longus expressed prostatic secretions external rotation end-stage renal failure end stage renal (kidney) failure endoscopic retrograde cholangiopancreatography especially erythrocyte sedimentation rate embryo transfer endotracheal tube

FAD FAP

familial Alzheimer disease familial adenomatous polyposis

EAR EBM EBNA EBV ECC ECG ECT ED EDD EEG ELISA EMG ENA EO EPA EPL EPS ER ESRF ESR(K)F ERCP

xxiii

xxiv

Part One Abbreviations

FTT FUO FVC FXS

foreign body full blood count fetal death in utero flexor digitorum longus forced expiratory volume in 1 second flexor hallucis longus femto-litre (10–15) functional residual capacity follicle stimulating hormone fluorescent treponemal antibody absorption test failure to thrive fever of undetermined origin forced vital capacity fragile X syndrome

g GA GABHS GBS GCA GESA GFR GGT GI GIFT GIT GLP GnRH GO GORD GP G-6-PD GSI GU GV

gram general anaesthetic group A beta-haemolytic streptococcus Guillain-Barré syndrome giant cell arteritis Gastroenterological Society of Australia glomerular filtration rate gamma-glutamyl transferase glycaemic index gamete intrafallopian transfer gastrointestinal tract glucagon-like peptide gonadotrophin-releasing hormone gastro-oesophageal gastro-oesophageal reflux general practitioner glucose-6-phosphate genuine stress incontinence gastric ulcer growth velocity

HAV anti-HAV Hb HbA anti-HBc HBeAg anti-HBs HBsAg HBV HCG HCV anti-HCV

hepatitis A virus hepatitis A antibody haemoglobin haemoglobin A hepatitis B core antibody hepatitis Be antigen hepatits B surface antibody hepatitis B surface antigen hepatitis B virus human chorionic gonadotropin hepatitis C virus hepatitis C virus antibody

FB FBE FDIU FDL FEV1 FHL fL FRC FSH FTA–ABS

HDL HDV HEV HFA HFM HFV HGV HHC HIDA HIV HLA-B27 HMGCoA HNPCC HPV HRT HSIL HSV H

high-density lipoprotein hepatitis D (Delta) virus hepatitis E virus hydrofluoro alkane hand, foot and mouth hepatitis F virus hepatitis G virus hereditary haemochromatosis hydroxy iminodiacetic acid human immunodeficiency virus human leucocyte antigen hydroxymethylglutaryl CoA hereditary nonpolyposis colorectal cancer human papilloma virus hormone replacement therapy high grade squamous intraepithelial lesion herpes simplex viral infection hypertension

IBS ICE ICHPPC

irritable bowel syndrome ice, compression, elevation International Classification of Health Problems in Primary Care inhaled corticosteroid intercondylar separation intracytoplasmic sperm injection immunochromatographic test insulin dependent diabetes mellitus injecting drug user immunoglobulin E immunoglobulin G immunoglobulin M interferon gamma release assay ischaemic heart disease International Headache Society intramuscular injection intermalleolar separation including international normalised ratio International Olympic Committee intraocular foreign body interphalangeal intermittent positive pressure variation internal rotation idiopathic (or immune) thrombocytopenia purpura intrauterine contraceptive device intrauterine growth retardation intravenous

ICS ICS ICSI ICT IDDM IDU IgE IgG IgM IGRA IHD IHS IM, IMI IMS inc. INR IOC IOFB IP IPPV IR ITP IUCD IUGR IV

Abbreviations What is new?

IVF IVI IVP IVU

in-vitro fertilisation intravenous injection intravenous pyelogram intravenous urogram

JCA JVP

juvenile chronic arthritis jugular venous pulse

KA kg KOH

keratoacanthoma kilogram potassium hydroxide

LA LABA LBBB LBO LBP LCR LDH/LH LDL LFTs LH LHRH LIF LMN LNG LPC LRTI LSD LSIL LUQ LUTS LV LVH

local anaesthetic long acting beta agonist left branch bundle block large bowel obstruction low back pain ligase chain reaction lactic dehydrogenase low-density lipoprotein liver function tests luteinising hormone luteinising hormone releasing hormone left iliac fossa lower motor neurone levonorgestrel liquor picis carbonis lower respiratory tract infection lysergic acid low grade squamous intraepithelial lesion left upper quadrant lower urinary tract symptoms left ventricular left ventricular hypertrophy

MAIS

Mycobacterium avium intracellulare or M. sacrofulaceum in morning monoamine oxidase inhibitor medical anti-shock trousers myocardial base micrograph (also µg) medial collateral ligament metacarpal phalangeal microscopy and culture of urine mean corpuscular volume metered dose inhaler multi-drug resistant TB myaesthenia gravis

mane MAOI MAST MB mcg MCL MCP MCU MCV MDI MDR MG

MI MIC MID MND MRCP MRI MRSA MS MSM MSU MTP MVA

myocardial infarction mitral incompetence minor intervertebral derangement motor neurone disease magnetic resonance cholangiography magnetic resonance imaging methicillin-resistant staphylococcus aureus multiple sclerosis men who have sex with men midstream urine metatarsophalangeal motor vehicle accident

N N saline NAAT NAD NET NF NGU NHL NH&MRC NIDDM NNT nocte NR NRT NSAIDs NSCLC NSU

normal normal saline nucleic acid amplification technology no abnormality detected norethisterone neurofibromatosis non-gonococcal urethritis non-Hodgkin’s lymphoma National Health and Medical Research Council non-insulin dependent diabetes mellitus numbers needed to treat at night normal range nicotine replacement therapy non-steroidal anti-inflammatory drugs non-small cell lung cancer non-specific urethritis

(o) OA OCP OGTT OSA OSD OTC

taken orally osteoarthritis oral contraceptive pill oral glucose tolerance test obstructive sleep apnoea Osgood-Schlatter disorder over the counter

PA PAN Pap PBG PBS pc PCA PCB PCL

posterior–anterior polyarteritis nodosa Papanicolaou porphobilinogen Pharmaceutical Benefits Scheme after meals percutaneous continuous analgesia post coital bleeding posterior cruciate ligament

xxv

xxvi

Part One Abbreviations

PTFL PU PUO PUVA pv PVC PVD

polycystic ovarian syndrome pneumocystitis pneumonia polymerase chain reaction packed cell volume Parkinson’s disease patent ductus arteriosus pervasive development disorders peak expiratory flow peak expiratory flow rate pre-eclamptic toxaemia positron emission tomography patent foramen ovale pulmonary function test persistent generalised lymphadenopathy past history personal health record pelvic inflammatory disease proximal interphalangeal phenylketonuria permission: limited information: specific suggestion: intensive therapy periodic limb movements premenstrual dysphoric disorder premenstrual syndrome premenstrual tension plaster of Paris progestogen-only pill proton-pump inhibitor preterm premature rupture of membranes per rectum as and when needed penicillin-resistant gonococci premature rupture of membranes prostate specific antigen post streptococcal glomerulonephritis posterior superior iliac spine paroxysmal supraventricular tachycardia prothrombin time percutaneous transhepatic cholangiography posterior talofibular ligament peptic ulcer pyrexia of undetermined origin psoralen + UVA per vagina polyvinyl chloride peripheral vascular disease

qds, qid

four times daily

PCOS PCP PCR PCV PD PDA PDD PEF PEFR PET PET PFO PFT PGL PH PHR PID PIP PKU PLISSIT PLMs PMDD PMS PMT POP POP PPI PPROM PR prn PRNG PROM PSA PSGN PSIS PSVT PT PTC

RA RACGP RAP RBBB RBC RCT RF Rh RIB RICE RIF RPR RR RRR RSD RSI RSV RT rtPA RUQ s SABA SAH SARS SBE SBO SBP SC/SCI SCC SCFE SCG SCLC SIADH SIDS SIJ SL SLD SLE SLR SND SNHL SNPs SNRI SOB sp

rheumatoid arthritis Royal Australian College of General Practitioners recurrent abdominal pain right branch bundle block red blood cell randomised controlled trial rheumatic fever rhesus rest in bed rest, ice, compression, elevation right iliac fossa rapid plasma reagin relative risk relative risk reduction reflex sympathetic dystrophy repetition strain injury respiratory syncytial virus reverse transcriptase recombinant tissue plasminogen activator right upper quadrant serum short acting beta agonist subarachnoid haemorrhage severe acute respiratory distress syndrome subacute bacterial endocarditis small bowel obstruction systolic blood pressure subcutaneous/subcutaneous injection squamous cell carcinoma slipped capital femoral epiphysis sodium cromoglycate small cell lung cancer syndrome of secretion of inappropriate antidiuretic hormone sudden infant death syndrome sacroiliac joint sublingual specific learning disability systemic lupus erthematosus straight leg raising sensorineural deafness sensorineural hearing loss single nuceotide polymorphisms serotonin noradrenaline reuptake inhibitor shortness of breath species

Abbreviations What is new?

SPA SPECT SPF SR SSRI SSS statim STI STD SUFE SVC SVT

suprapubic aspirate of urine single photon emission computerised tomography sun penetration factor sustained release selective serotonin reuptake inhibitor sick sinus syndrome at once sexually transmitted infection sodium tetradecyl sulfate slipped upper femoral epiphysis superior vena cava supraventricular tachycardia

TPHA TSE TSH TT TUE TUIP TURP TV

tri-iodothyronine thyroxine temporal arteritis tuberculosis three times daily transcutaneous electrical nerve stimulation thyroid function tests triglyceride transient ischaemic attack total iron binding capacity tympanic membrane temporomandibular joint tissue necrosis factor transoesophageal echocardiography tracheo-oesophageal fistula toxoplasmosis, rubella, cytomegalovirus, herpes virus Treponema pallidum haemoglutination test testicular self-examination thyroid-stimulating hormone thrombin time therapeutic use exemption transurethral incision of prostate transurethral resection of prostate tidal volume

U UC U&E µg UMN URTI US UTI U

units ulcerative colitis urea and electrolytes microgram upper motor neurone upper respiratory tract infection ultrasound urinary tract infection ultraviolet

T3 T4 TA TB tds, tid TENS TFTs TG TIA TIBC TM TMJ TNF TOE TOF TORCH

VAS VBI VC VDRL VF VMA VPG VRE VSD VT VUR VVS VWD WBC WBR WCC WHO WPW

visual analogue scale vertebrobasilar insuffiency vital capacity Venereal Disease Reference Laboratory ventricular fibrillation vanillylmandelic acid venous plasma glucose vancomycin-resistant enterococci ventricular septal defect ventricular tachycardia vesicoureteric reflux vulvar vestibular syndrome von Willebrand’s disease white blood cells white _ blue _ red white cell count World Health Organization Wolff-Parkinson-White

XL

sex linked

xxvii

Part 1

The basis of general practice

1

The nature and content of general practice Medical practice is not knitting and weaving and the labour of the hands, but it must be inspired with soul and be filled with understanding and equipped with the gift of keen observation; these together with accurate scientific knowledge are the indispensable requisites for proficient medical practice. MOSES

General practice is a traditional method of bringing primary health care to the community. It is a medical discipline in its own right, linking the vast amount of accumulated medical knowledge with the art of communication.

Definitions General practice can be defined as that medical discipline which provides ‘community-based, continuing, comprehensive, preventive primary care’, sometimes referred to as the CCCP model. The Royal Australian College of General Practitioners (RACGP) uses the following definitions of general practice and primary care: General practice is that component of the health care system which provides initial, continuing, comprehensive and coordinated medical care for all individuals, families and communities and which integrates current biomedical, psychological and social understandings of health. General practitioner is a medical practitioner with recognised generalist training, experience and skills, who provides and co-ordinates comprehensive medical care for individuals, families and communities. Primary care involves the ability to take responsible action on any problem the patient presents, whether or not it forms part of an ongoing doctor–patient relationship. In managing the patient, the general/family practitioner may make appropriate referral to other doctors, health care professionals and community services. General/ family practice is the point of first contact for the majority of people seeking health care. In the provision of primary care, much ill-defined illness is seen; the general/family practitioner often

2

BEN

M A I M O N (113 5–1204)

deals with problem complexes rather than with established diseases. The practitioner must be able to make a total assessment of the person’s condition without subjecting the person to unnecessary investigations, procedure and treatment.

The RACGP has defined five domains of general practice: • communication skills and the doctor–patient relationship • applied professional knowledge and skills • population health and the context of general practice • professional and ethical role • organisational and legal dimensions

The American Academy of Family Physicians (AAFP)1 and the American Board of Family Practice (ABFP) have defined family practice as: … the medical specialty that provides continuing and comprehensive health care for the individual and the family. It is the specialty in breadth that integrates the biological, clinical and behavioural sciences. The scope of family practice encompasses all ages, both sexes, each organ system and disease entity.

The AAFP has expanded on the function of delivery of primary health care.1, 2 Primary care is a form of delivery of medical care that encompasses the following functions: 1 It is ‘first-contact’ care, serving as a point-ofentry for patients into the health care system. 2 It includes continuity by virtue of caring for patients over a period of time, both in sickness and in health.

The nature and content of general practice

3 It is comprehensive care, drawing from all the traditional major disciplines for its functional content. 4 It serves a coordinative function for all the health care needs of the patient. 5 It assumes continuing responsibility for individual patient follow-up and community health problems. 6 It is a highly personalised type of care.

Pereira Gray3 identifies six principles—primary care, family care, domiciliary care and continuing care all designed to achieve preventive and personal care. ‘We see the patient as a whole person and this involves breadth of knowledge about each person, not just depth of disease.’ General practice is not the summation of specialties practised at a superficial level and we must avoid the temptation to become ‘specialoids’. In the current climate, where medicine is often fragmented, there is a greater than ever need for the generalist. The patient requires a trusted focal point in the often bewildering health service jungle. Who is to do this better than the caring family doctor taking full responsibility for the welfare of the patient and intervening on his or her behalf? Specialists also need highly competent generalists to whom they can entrust ongoing care.

Apart from these processes the GP has to manage very common problems including a whole variety of problems not normally taught in medical school or in postgraduate programs. Many of these problems are unusual yet common and can be regarded as the ‘nitty gritty’ or ‘bread and butter’ problems of primary health care. In considering the level of care of symptoms, 25% of patients abandon self-care for a visit to the GP. Ninety per cent of these visits are managed entirely within primary care. Levels of care are represented in Figure 1.1.5

self-care (75%)

General practice care 25%

Unique features of general practice Anderson, Bridges-Webb and Chancellor4 emphasise that ‘the unique and important work of the general practitioner is to provide availability and continuity of care, competence in the realm of diagnosis, care of acute and chronic illness, prompt treatment of emergencies and a preventive approach to health care’. The features that make general practice different from hospital- or specialist-based medical practices include: • • • • • • • • • • • • • •

first contact diagnostic methodology early diagnosis of life-threatening and serious disease continuity and availability of care personalised care care of acute and chronic illness domiciliary care emergency care (prompt treatment at home or in the community) family care palliative care (at home) preventive care scope for health promotion holistic approach to management health care coordination

The GP has to be prepared for any problem that comes in the door (Figure 1.1).

Hospital 2.5%

Figure 1.1 Degrees of care of symptoms

Holistic approach to management The management of the whole person, or the holistic approach, is an important approach to patient care in general practice. Whole-person diagnosis is based on two components: 1 the disease-centred diagnosis 2 the patient-centred diagnosis

The disease-centred consultation is the traditional medical model based on the history, examination and special investigations, with the emphasis on making a diagnosis and treating the disease. The disease-centred diagnosis, which is typical of hospital-based medicine, is defined in terms of pathology and does not focus significantly on the feelings of the person suffering from the disease. The patient-centred consultation not only takes into account the diagnosed disease and its management but

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The basis of general practice

also adds another dimension—that of the psychosocial hallmarks of the patient, including details about: • • • • • • •

the patient as a person emotional reactions to the illness the family the effect on relationships work and leisure lifestyle the environment

Continuing care The essence of general practice is continuity of care. The doctor–patient relationship is unique in general practice in the sense that it covers a span of time that is not restricted to a specific major illness. The continuing relationship involving many separate episodes of illness provides an opportunity for the doctor to develop considerable knowledge and understanding of the patient, the family and its stresses, and the patient’s work and recreational environment.

Strategies to enhance continuing care A philosophical commitment Underlying appropriate patient care is the attitude of the provider. A caring, responsible practitioner who is competent, available and a trusted friend is ‘like gold’ to his or her patients.

Medical records An efficient medical record system is fundamental. Ideally, it should include a patient profile, a database, problem lists, special investigation lists, medication lists, adverse drug reactions and ‘at risk’ details.

Checklists The use of checklists or questionnaires to assemble information on presenting problems may enhance knowledge as well as assist earlier diagnosis.

Home visits Home visits are a goldmine of information about intrafamily dynamics. They should cement the doctor–patient relationship if used appropriately and discretely. We are the only doctors who practise domiciliary care. We must treasure it. Sitting in the office chair practising ‘conveyor belt’ medicine is contrary to the ideals of general practice.

Anticipatory guidance Unfortunately patients do not usually perceive the family doctor as a counsellor, but opportunities should be taken to offer advice about anticipated problems in

situations such as premarital visits, antenatal care and pre-adolescent contact.

Patient education Whenever possible, patients should be given insight into the nature of their illness, and reasons for the treatment and prognosis. Patient education leaflets, such as those published in journals, can be used as a starting point, although there is no substitute for careful personal explanation. This should lead to better compliance and an improved relationship between doctor and patient.

Personal health records These excellent wallets, which are handed to parents of newborn babies, have a very important place in the ongoing care of children. Their purpose is to supply an outline of preventive health care, beginning from birth. They provide an inbuilt recall list directed at a most compliant source—mothers. In fact, they provide a complete record of health care throughout a person’s lifetime.

Patient register An age-and-sex register of all patients in the practice is a very useful acquisition. The main strategy is to find out who the patients are, their basic characteristics and which patients suffer from chronic diseases, such as cancer, diabetes and emphysema.

Recall lists Use of recall lists based on the patient register should significantly improve health care delivery. Dentists have been using this technique successfully for some time. In the US, Canada and many other countries doctors use recall lists regularly to remind patients that preventive items, such as immunisation schedules and cancer smear tests, are due.

Computers Computers have simplified and streamlined the design and use of practice registers and patient-recall systems in addition to their use for accounting purposes. Their potential for patient education and doctor education is considerable.

Common presenting symptoms Common presenting symptoms in Australian practices are presented in Table 1.1,6 where they are compared with those in the US.7 The similarity is noticed but the different classification system does not permit an accurate comparison. In the third national survey of morbidity in general practice in Australia6 the most common symptoms described by patients were cough (6.2 per 100 encounters), throat complaints (3.8 per 100), back complaints (3.6 per 100) and upper

The nature and content of general practice

respiratory tract infection (URTI) (3.2 per 100). In addition, very common presentations included a check-up (13.7 per 100) and a request for prescription (8.2 per 100). McWhinney lists the 10 most common presenting symptoms from representative Canadian and British practices but they are divided between males and females.8 For males in the Canadian study these symptoms are (in order, starting from the most common) cough, sore throat, colds, abdominal/pelvic pain, rash, fever/ chills, earache, back problems, skin inflammation and chest pain. For females the five other symptoms that are included are menstrual disorders, depression, vaginal discharge, anxiety and headache. In the British study the most common symptoms are virtually identical between males and females and include cough, rash, sore throat, abdominal pain, bowel symptoms, chest pain, back pain, spots, sores and ulcers, headache, muscular aches and nasal congestion.9 Table 1.1 Most frequent presenting problems/ symptoms (excluding pregnancy, hypertension, immunisation and routine check-up) Australia

United States

Cough

1

1

Throat complaint

2

2

Back pain

3

4

URTI

4

11

Rash

5

5

Abdominal pain

6

6

Depression

7

Ear pain

8

3

Headache

9

10

Fever

10

7

Weakness/tiredness

11

Diarrhoea

12

Asthma

13

Nasal congestion/ sneeze

14

12

Chest pain

15

13

Knee complaint

16

8

Visual dysfunction

Most frequent presenting symptoms in the author’s practice The most common presenting symptoms in the author’s practice10 were identified, with the emphasis being on pain syndromes: • • • • • • • • • • • • • •

cough disturbance of bowel function pain in abdomen pain in back pain in chest pain in head pain in neck pain in ear pain in throat pain in joints/limbs rashes sleep problems tiredness/fatigue vaginal discomfort

These symptoms should accurately reflect Australian general practice since the rural practice would represent an appropriate cross-section of the community’s morbidity, and the recording and classification of data from the one practitioner would be consistent.

Symptoms and conditions related to litigation Medical defence organisations have highlighted the following areas as being those most vulnerable for management mishaps: acute abdominal pain acute chest pain breast lumps children’s problems, especially the sick febrile child 8 years only 2 mg/kg/day up to 100 mg

Photosensitivity reactions

Mefloquine (Lariam)

250 mg (1 tab) same day each week, 1 week before, during, 4 weeks after

Not recommended 45 kg as for adults

Side effects: dizziness, ‘fuzzy’ head, blurred vision, neuropsychiatric Beware of beta-blockers

Proguanil (Paludrine)

200 mg (2 tabs) same day each week 1 day before, during, 4 weeks after

< 1 year: ¼ tablet 1–4 years: ½ tablet 5–8 years: 1 tablet 9–14 years: 1 ½ tablet > 14 years: adult

Safe in lactation and pregnancy (give folic acid) Side effects: GIT disturbances, headache, dizziness, rash

Atovaquone+ proguanil (Malarone)

250 mg / 100 mg (1 tab) with food same day each week 2 days before, during, 7 days later

Junior tablets 62.5 mg/ 25 mg 11–20 kg: 1 tablet/day 21–30 kg: 2 tablets/day 31–40 kg: 3 tablets/day >40 kg: 1 adult tab/day

Avoid in pregnant women or women breastfeeding infants 10 years since last dose if >5 years for third world travel give CDT 8 years All travellers to developing countries free of malaria Tetanus toxoid booster Polio immunisation if >10 years Measles immunisation (consider MMR) Influenza Pneumococcus (for those at risk) Yellow fever (if compulsory) Preventive measures against gastrointestinal infections, sexually transmitted infections, mosquito bites Travellers to developing and other countries at high risk of infection As above plus: • malaria prophylaxis • hepatitis A • hepatitis B • typhoid • tuberculosis (BCG if Mantoux –ve) Other vaccinations—consider: • meningococcus (required in some countries) • Japanese B encephalitis • rabies • typhus • plague • anthrax • cholera

international travel. The requirements of some countries are in excess of international health regulations. However, vaccination against yellow fever is strongly recommended to all travellers who intend to visit places other than the major cities in the countries where the disease occurs in humans.

Meningococcal infection Meningitis due to this organism is a contagious lethal disease. It is common in Nepal, Mongolia, Vietnam and parts of Africa and Asia, especially in the dry season. Travellers trekking through the Kathmandu valley of Nepal and those attending the Haj pilgrimage to Saudi Arabia are at special risk and should have the vaccine. However, some countries require immunisation for entry.

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Voluntary immunisation Precautions against the following diseases are recommended for those travellers who may be at special risk.5

Hepatitis A, B Hepatitis A is a common problem in rural areas of developing countries. There is a declining level of antibodies to hepatitis A in developed countries and adults are at special risk so one or two doses of hepatitis A vaccine should be given. A blood test for hepatitis A antibodies can be carried out to determine a person’s immunity.

Prevention The rules of avoiding contaminated food and water apply (as for traveller’s diarrhoea). Hepatitis A vaccine is given as a course of two injections. Hepatitis B is endemic in South-East Asia, South America and other developing countries. Vaccination is recommended, especially for people working in such countries, particularly those in the health care area or those who may expect to have sexual or drug contact. If patients have a ‘negative’ HBV core IgG titre, then vaccination would be worthwhile (three doses: 0, 1 and 6 months). Hepatitis E has a high mortality rate in pregnant women. The usual approach for non-immunised people is to give the combined hepatitis A and B vaccine (Twinrix) as a course of three injections.

Typhoid Typhoid immunisation is not required for entry into any country but is recommended for travel to third world countries where the standards of sanitation are low. It should be considered for travellers to smaller cities, and village and rural areas in Africa, Asia, Central and South America and Southern Europe. The parenteral (subcutaneous) vaccine can be used but the single dose typhi Vi vaccine or the oral vaccine, which have fewer side effects, are generally preferred. The oral vaccine, which is given as a series of three or four capsules, appears to afford protection for about 5 years but is contraindicated in the immunocompromised.

Cholera Cholera vaccination is not officially recommended by the WHO because it has only limited effectiveness. It is advisable for health care workers or others at risk entering an endemic area. Cholera is given as an

oral vaccine (Dukoral) over 1 week prior to exposure. It is not recommended in children under 5 years or pregnant women.

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 bound 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

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 several countries, such as Vietnam, Brazil, Peru, Ecuador, Kenya and Malagasy Republic. 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 256 is suggestive of infection. • Sputum microscopy and culture is the quickest and most reliable test if Legionella sp. are identified. • Urine antigen tests for Legionella pneumophila type I

Leptospirosis • Blood for antibodies will give a diagnosis according to levels matched with clinical features. • Use PCR to identify the numerous serovariants.

Malaria • Thick and thin blood films for microscopic examination—usually require repeat examination (at least three at separate times) • Serological tests (ELISA) are not commonly used but field-based card assays using agglutination tests are useful for travellers e.g. Paracheck V test, ICT card test • PCR methods are highly specific and sensitive but not widely practical at present because specialised laboratory methods are required.

Mumps • Blood for antibody testing: diagnoses immune status and mumps infection (acute and convalescent sera) with IgM assays • CSF: the presence of IgG in CSF confirms the diagnosis of mumps meningitis although levels may be low for 2–3 days after the onset of the illness.

• Sputum (three separate samples)/bronchial brushing or washings: acid-fast staining and microscopy and culture for susceptibility testing • PCR testing on sputum

Mycoplasma pneumoniae

Q fever • Blood in acute phase and 2–3 weeks after onset of illness for antibody levels. PCR testing of tissues.

Parvovirus B19 • Blood for antibody detection. Suspected fifth disease (erythema infectiosum) and other clinical conditions, such as maternal infection with hydrops foetalis, aplastic crisis in chronic haemolysis, polyarthritis and rash in adults. PCR for confirmation.

Rubella • Blood for antibody tests—acute phase and convalescent (after 10–14 days) • A fourfold increase in IgG indicates recent infection. • IgM antibody becomes positive about 7 days after onset of the illness but will become undetectable after 8 weeks. IgM antibodies in maternal serum indicates high foetal risk, while in cord blood suggests congenital infection.

Toxoplasmosis • Blood for acute and convalescent (2+ weeks) antibody testing. A fourfold rise in IgG titre is diagnostic for toxoplasmosis. IgM antibodies at a level >16 indicate recent infection. The diagnosis of congenital toxoplasmosis is supported by the presence of IgM antibodies. Avidity antibody testing will date the infection.

Viral skin rashes4 When a patient presents with a fine maculopapular skin rash, serological tests can be performed for all of the following causative agents. Invariably, a rising antibody level between acute phase and convalescent sera (2–4 weeks) is required for diagnosis. • Measles—rising IgM titre diagnostic (raised IgM = previous infection or immunisation) • Rubella—rising IgM or IgG = recent infection • Parvovirus B19 • Echovirus • EBV • CMV

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The basis of general practice

Ross River virus Barmah Forest virus Dengue fever Other arboviruses

Sexually transmitted infections4 • Neisseria gonorrhoea — Culture (urethral, cervical, rectal, pharyngeal) — PCR is excellent on cervical or urethral swabs or first-stream urine • Chlamydia trachomatis — Antigen detection (PCR recommended) on cervical or urethral swabs or first-stream urine (preferably first 20–30 mL). The first 10 mL flushes out urethral epithelial cells. — Culture available on request Serology not recommended • Syphilis — Serology (RPR, TPHA, FTA–ABS, EIA) • Hepatitis B — Serology • HIV — Serology • Trichomonas vaginalis — Microscopy from vaginal swab — PCR • Herpes simplex — Viral culture — Antigen detection (PCR best) — Serology • Lymphogranuloma venereum — Chlamydia serology — Lymph node biopsy • Chancroid — Microscopy/culture for Haemophilus ducreyi • Granuloma inguinale — Biopsy

Urinary tract infection (UTI)4 Microscopy White blood cell count >10 per µL is abnormal and reflects response to local infection. • Higher counts have greater significance. • Epithelial cells suggests the possibility of genital contamination in females (i.e. poor sample).

Culture Counts are expressed as organisms per mL. • Counts >105 organisms per mL are more significant. • UTI can occur at lower counts, especially in pure growth and supported by the clinical picture and significant pyuria. • Significant organisms are usually in pure growth (not mixed).

• Significant UTI are usually associated with a pyuria but may occur in its absence.

Fever in returning travellers • Serology — Dengue fever (acute and convalescent) — Typhoid fever (acute and convalescent)—limited use (use stool culture) — Viral hepatitis A, B — Amoebiasis—liver abscess — Typhus • Blood culture — Typhoid fever (best to detect typhoid) — Meningococcal infection • Full blood count (FBE), thick and thin film — Malaria • Spot agglutination tests — Dengue fever — Malaria • Stool examination Culture — Campylobacter, Salmonella, Shigella, Typhoid Microscopy — Amoeba, Giardia, others • Liver function tests — Hepatitis • ESR — Screening

Lymphadenopathy • FBE, ESR, mononucleosis screen (e.g. Paul Bunnell) • Serology — EBV, CMV, HIV — Toxoplasma — Rubella, syphilis, cat-scratch disorder

Interpretation of iron studies5 A sound knowledge of the metabolism of iron and its transportation helps in the interpretation of iron studies (see Table 16.3). The serum (or plasma) level of iron falls gradually below the normal range (about 14–30 µmol/L) when the amount of iron in the body decreases after the iron reserves become exhausted. The level in the serum of transferrin, the major iron-transporting protein in the circulation, rises under these circumstances to perhaps above normal levels. A subnormal level of iron plus a high or normal level of transferrin is strong evidence of iron deficiency. Transferrin, as the carrier protein, binds most of the iron in the serum. The capacity of transferrin is represented by the total amount of iron that can be bound to serum protein, meaning that the total iron-binding capacity (TIBC) provides an alternative estimation of the concentration of transferrin.

Laboratory investigations

141

Table 16.3 The interpretation of iron studies4 Condition

Serum Fe

TIBC

% Transferrin Saturation

Ferritin

Iron deficiency

↓

N or ↑

↓

↓↓

Thalassaemia

N or ↑

N

N or ↑

↑ or N

Anaemia of chronic disease

↓

N or ↓

↓

N or ↑

Sideroblastic anaemia

N or ↑

N

N or ↑

↑

Haemochromatosis

↑

↓

↑↑

↑↑

N = normal

Transferrin saturation is the extent to which the iron-binding sites on transferrin are occupied by iron. This is calculated by dividing the iron level by the serum iron-binding capacity. The percentage saturation is normally 20–55%. It is markedly elevated in haemochromatosis—above 50%—and is the key marker for that disorder. The serum ferritin level bears a direct relationship to the amount of iron stores in the body and subnormal values can be detected when iron stores are exhausted even before the serum iron level has significantly declined. The normal range varies between sexes and age groups: 20–250 µg/L in males, 10–150 µg/L in females and lower again in children.

Liver function tests (LFTs)4

Gamma-glutamyl transferase (GGT) • Present in bile canaliculi • Raised levels with cholestasis, other liver diseases and with drug and alcohol intake

Differential diagnosis of jaundice4 Differentiating jaundice due to acute hepatocellular damage from extrahepatic obstruction on routine LFTs can only be suggested in the early stages according to the following guideline. Acute hepatitis

Obstruction

ALP

Normal to 3 times normal

ALT/AST

10–100 times normal

145 mmol/L

• Muscle twitching or cramps • Severe: seizures, delirium, hyperthermia, coma

Hyponatraemia Na+ 5 mmol/L

The first sign of hyperkalaemia (e.g. >6 ) may be a cardiac arrest.

Causes • Kidney failure • Acidosis (especially metabolic) • Mineralocorticoid deficiency: Addison disease (page 219), aldosterone antagonists • Excessive intake of K+ (e.g. ↑IV fluids with K) • Drugs (e.g. spironolactone, ACE inhibitors, NSAIDs) Consider artefact, for example, haemolysed sample

Clinical features • • • •

Hypokalaemia K+ 60 ml/min/1.72 m ) 2

(Ther. 300–700 µmol/L)

Carbamazepine*

(Ther. 10–50 µmol/L)

Gentamicin (pre)

(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

Asymptomatic hyperuricaemia: • 10 times more common than gout7 • Elevated serum uric acid (>0.42 mmol/L in men, > 0.36 mmol/L in women) • 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. 36.11), 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 drinks20 Cytotoxic agents (tumour lysis) Hypothyroidism Low-dose aspirin Others

The arthritis Monoarthritis in 90% of attacks: • MTP joint great toe—75% • other joints—usually lower limbs: other toes, ankles, knees

Gout (monosodium urate crystal disorder) Gout is an abnormality of uric acid metabolism resulting in hyperuricaemia and urate crystal deposition. Urate crystals deposit in: • joints—acute gouty arthritis • soft tissue—tophi and tenosynovitis • urinary tract—urate stones

Four typical stages of gout are recognised: • • • •

Stage 1—asymptomatic hyperuricaemia Stage 2—acute gouty arthritis Stage 3—intercritical gout (intervals between attacks) Stage 4—chronic tophaceous gout and chronic gouty arthritis

Figure 36.11 Gout showing typical red, shiny, swollen arthritis of the first MTP joint with desquamation of the skin

Arthritis

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 36.12.

$PNNPO
TJUFT

345

-FTT
DPNNPO

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)

36

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. %*1
KPJOUT

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 • 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: • • • • •

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 gcomorbid conditions (e.g. alcohol dependence, obesity, CKD, polycythaemia vera, diabetes, hypertension)

The acute attack

8

NSAIDs, in full dosage, are first-line and effective. 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)

LOFFT

NFUBUBSTPQIBMBOHFBM KPJOU¬HSFBU
UPF

BOLMFT UPFT

Figure 36.12 Gout: possible joint distribution

Note: • Must be given early • Avoid if kidney impairment • Avoid use with clarithromycin especially in CKD

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 days20 • 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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Part Three Problem solving in general practice

Long-term therapy When acute attack subsides preventive measures include:

Calcium pyrophosphate crystal disorder (pseudogout)8, 22

• 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 drinks21 • 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

The finding of calcification of articular cartilage on X-ray examination is usually termed chondrocalcinosis. This is mainly a disorder of the elderly superimposed on an osteoarthritic joint. The acute attack is similar to an acute attack of gout but it affects the following joints (in order):

Prevention (drug prophylaxis)

It can affect tendons, especially Achilles’ tendon and cause a fever resembling septic arthritis. The crystals in synovial fluid are readily identified by phase-contrast microscopy. X-rays are helpful in showing calcification of the articular cartilage. Management is based on aspiration and installation of a depot glucocorticosteroid by injection into the joint (if joint infection excluded) plus analgesia. Be cautious of using NSAIDs in the elderly—paracetamol is preferred. Colchicine can be used. Treatment includes:8

Allopurinol (a xanthine oxidase inhibitor) is the drug of choice: dose 100–300 mg daily. Indications: • • • •

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

Adverse effects: • rash (2%) • severe allergic reaction (rare)

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 4–6 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 30 minutes Awoken with pain during second half of night Improvement with exercise and not relieved by rest Limitation of lumbar spine motion in sagittal and frontal planes • Chest expansion ↓ relative to normal values • Unilateral sacroiliitis (grade 3 to 4) • Bilateral sacroiliitis (grade 2 to 4) • • • • •

NPVUI
VMDFST

BPSUJUJT QFSJDBSEJUJT LJEOFZ OFQISPQBUIZ

SBSF

TQPOEZMJUJT TBSDSPJMJJUJT VSFUISJUJT DJSDJOBUF
CBMBOJUJT

Reactive arthritis Reactive arthritis is a form of arthropathy in which non-septic arthritis and often sacroiliitis develop after an acute urogenital infection (usually Chlamydia trachomatis) or an enteric infection (e.g. Salmonella, Shigella). BSUISJUJT

DxT: NSU + conjunctivitis ± iritis + arthritis = reactive arthritis

The arthritis, which commences 1–3 weeks post infection, tends to affect the larger peripheral joints, especially the ankle (talocrural) and knees but the fingers and toes can be affected in a patchy polyarthritic fashion. Mucocutaneous lesions, including keratoderma blennorrhagica and circinate balanitis, may occur,

347

"DIJMMFT
UFOEPOJUJT QMBOUBS
GBTDJJUJT

LFSBUPEFSNB
CMFOOPSSIBHJB °TBVTBHF
UPF± EBDUZMJUJT

Figure 36.13 Possible clinical features of reactive arthritis

36

348

Part Three Problem solving in general practice

Unclassified spondyloarthritis

Cautions

Patients in this category seem to be the most frequently encountered in family practice. They clearly have a spondyloarthropathy but fail to meet the criteria for any one of the individual entities within the group. A typical patient is a young male in his third decade with a painful knee or other joint, unilateral (or bilateral) back pain with one of the entheseal problems (e.g. plantar fasciitis).

• Careful monitoring is required with NSAIDs and sulphasalazine. • Systemic corticosteroids are not indicated. • Immunosuppressants (low dose weekly methotrexate) and bDMARDs may be needed for severe intractable problems with psoriasis and reactive arthritis. • These conditions should be managed in collaboration with a consultant. • Although phenylbutazone is the most effective NSAID, its side effects (especially aplastic anaemia) are a major problem.

Investigations • X-rays: — radiological sacroiliitis is central to the diagnosis — changes include narrowing of SIJs, margin irregularity, sclerosis of peri-articular bone and eventually bony fusion. Spondylitis usually follows • ESR and CRP: most patients have an elevated ESR and CRP at some stage of their disease • HLA-B27: this test has low specificity and has limited value except that it predicts risk to offspring if positive • Microbiology: in patients with a history of reactive arthritis, cultures should be obtained from the urethra, faeces, urine and blood23

Principles of management • Identify the most active elements of the disease and treat accordingly. • Provide patient and family education with appropriate reassurance: this is vital. Stress that, although the disease is non-curable, treatment is effective and long-term prognosis generally good. • Provide regular assessment and support. • Give genetic counselling—in cases of ankylosing spondylitis with positive HLA-B27 the risk to offspring is significant. • Give advice regarding work, especially with posture. • Acute anterior uveitis requires prompt treatment and monitoring by an ophthalmologist. • Refer for physiotherapy for exercises, stretching program, postural exercises and hydrotherapy. Appropriate physiotherapy slows deterioration in spinal function.24 • Consider referral for occupational therapy. • Pharmacological agents: 8 — NSAIDs (e.g. indomethacin 75–200 mg (o) or 100 mg rectally nocte daily or ketoprofen 100 mg rectally nocte to control pain, stiffness and synovitis) — sulphasalazine (if NSAIDs ineffective) — intra-articular corticosteroids for severe monoarthritis and intralesional corticosteroids for enthesopathy

Refer for advice on above and especially for DMARD and bDMARD therapy.

When to refer • Consider referring most severe true inflammatory disorders for diagnosis and initiation of treatment (e.g. RA, spondyloarthropathy, connective tissue disorders and suspicion of a vasculitide) • Osteoarthritis: — generalised joint pain — associated systemic symptoms — deteriorating joint function — intractable pain (especially at rest) — if surgical procedure is contemplated8 • Rheumatoid arthritis: — all patients initially — persistent inflammation of a joint or joints — patient ill and corticosteroids contemplated — if a surgical procedure is contemplated • Spondyloarthropathies: — initial referral for confirmation of diagnosis and initiation of treatment — disease unresponsive to conventional treatment — sudden deterioration in symptoms, especially pain — onset of uveitis or other ocular complications — adverse drug reactions • Undiagnosed arthritis in presence of constitutional symptoms • Suspicion of a suppurative or serious infective condition (e.g. septic arthritis, endocarditis, brucellosis) • Children with evidence of juvenile idiopathic arthritis (e.g. Still syndrome)

Arthritis

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Table 36.8 Diagnostic guidelines for arthritis Disorder

Sex ratio

Typical common joints Typical age involved

Associated features

Key tests X-ray

OA (generalised— primary)

FM 6:1 >50

DIP >PIP fingers Base thumb (1st CMC) 1st MTP joint Cervical and lumbar spines Hips and knees

Pain worse in evenings, relieved by rest

RA

FM 3:1

PIP, MCP hands Wrist Base of toes (MTP joints) Symmetrical

Any joint: worse at rest, RA factor better with activity; morning Anti-CCP stiffness X-ray Constitutional symptoms Carpal tunnel syndrome Many other general effects

30–50

SLE

FM 9:1 15–35

Symmetrical and variable Small joints fingers Often slight

Constitutional symptoms Fever Adverse drug reactions Any other system affected Rash (80%) Pleuritic symptoms (67%) Raynaud phenomenon

ANA dsDNA & ENA antibodies

Scleroderma

FM 3:1

20–50

Symmetrical Polyarthritis fingers

Raynaud (90%) Other skin changes Dysphagia

ANA Scl-70 centromere

Viral arthropathies (excluding HIV)

M=F

Children

Transient Usually PIP joints fingers

Rash, fever

Specific serology

Ankylosing spondylitis

MF 3:1

18–30

Sacroiliacs Vertebral column esp. lumbar, costovertebral Also knees, hips or ankles

Iridocyclitis Chest dysfunction Enthesopathy (e.g. plantar fasciitis)

ESR X-ray HLA-B27

Psoriatic arthritis

M=F

Any age

DIP joints—fingers and toes, sacroiliacs

Psoriasis rash (pre-existing) Pitted nails, ‘sausage digits’

–

Enteropathic arthritis

M=F

Any age

Lower extremity: knees, feet, ankles Hips: sacroiliacs

Ulcerative colitis Crohn disease Whipple disease

Endoscopy

15–30

As above

Preceding dysentery or urethritis Entheseal problems Circinate balanitis Other skin lesions

ESR/CRP M and C Serology

Reactive arthritis: MF Genitourinary 20:1 (e.g. Chlamydia) Post-dysentery M=F (e.g. Salmonella) Gout

MF 20:1

M 40–50 F >60

Big toe (MTP joint): any other possible, esp. lower limb DIP—osteoarthritis

Tophi Raised serum uric acid Urate crystals in joints Diuretics in elderly

s. urate Microsynovial fluid

Pseudogout

M=F

>60 especially >70

Knee

Chondrocalcinosis Pyrophosphate crystals in joint

Microsynovial fluid X-ray

Polymyalgia rheumatica

FM 3:1

>60

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

ESR ↑↑↑

ESR

Source: After Hart26

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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.25 Table 36.8 presents the diagnostic guidelines.26

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Gout, page 177 • Osteoarthritis, page 180 • Rheumatoid Arthritis, page 185

REFERENCES 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 (5th edn). London: Saunders, 2003: 538–40. 8 Mashford L (Chair). Therapeutic Guidelines: Rheumatology (Version 1). Melbourne: Therapeutic Guidelines Ltd, 2006. 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 Cleland LG, James MJ, Proudman SM. Fish oil: what the prescriber needs to know. Arthritis Research and Therapy, 2006; 8(1): 202–11. 19 Hall S. Crystal arthritis: a clinician’s view. Aust Fam Physician, 1991; 20: 1717–24. 20 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. 21 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. 22 McPhee SJ, Papadakis MA. Current Medical Diagnosis and Treatment (4th edn). New York: The McGraw-Hill Companies, 2010: 735–6. 23 Edmonds JP. Spondyloarthropathies. Med J Aust, 1997; 166: 214–18. 24 Vilitanen JV, et al. Fifteen months follow up of intensive inpatient physiotherapy and exercise in ankylosing spondylitis. Clin Rheumatol, 1995; 14: 413–19. 25 Kincaid-Smith P, Larkins R, Whelan G eds. Problems in Clinical Medicine. Sydney: MacLennan and Petty, 1989: 391. 26 Hart FD. Early clinical diagnosis of 12 forms of arthritis. Modern Medicine Australia, 1989: March: 34–40.

Anorectal disorders

37

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. V I R G I N I A W O O L F 193 4, D I A R Y

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: • • • • •

pain lumps discharge bleeding pruritus

ENTRY

Common anorectal conditions are illustrated in Figure 37.1.

Anorectal pain The patient may complain that defecation is painful or almost impossible because of anorectal pain.

Causes Pain without swelling: • anal fissure • anal herpes • ulcerative proctitis

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MJOF

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Figure 37.1 Common anorectal conditions

351

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• proctalgia fugax • solitary rectal ulcer • tenesmus

Red flag pointers for anorectal pain • • • •

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. 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.

Examination On inspection the anal fissure is usually seen in the anal margin, situated in the midline posteriorly (6 o’clock). The fissure appears as an elliptical ulcer involving the lower third of the anus from the dentate line to the anal verge (see Fig. 37.2).1

Weight loss Change in bowel habits Fever >38ºC Recurrent (consider Crohn disease)

Treatment 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. 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 to the lower anal canal) for 6 weeks. 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 is injection of botulinum toxin into the sphincter.

Proctalgia fugax (levator ani spasm) Clinical features • • • • • • •

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

Management6 Figure 37.2 Anal fissure with prominant skin tag situated in the mid posterior position of the anal verge: the 6 o’clock position

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

• Explanation and reassurance • 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

Anorectal disorders

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 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’.

Management

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 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.

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.

Antibiotics

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 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.

• metronidazole 400 mg (o) 12 hourly for 5–7 days plus • cephalexin 500 mg (o) 6 hourly for 5–7 days7

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.

353

If a perianal or perirectal abscess is recalcitrant or spreading with cellulitis, use:

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 (e.g. cephalexin and metronidazole) are given to complement surgical drainage only if there is severe surrounding cellulitis.

37

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Part Three Problem solving in general practice

Table 37.1 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 Figure 37.3 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

Pilonidal means ‘a nest of hairs’ and the problem is particularly common in hirsute young men (see Fig. 37.3). Refer for excision of the sinus network if necessary.

Fistula-in-ano5 An anal fistula is a tract that communicates between the perianal skin 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. 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, fourth-degree piles and perianal warts (see Table 37.1).

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.

Fourth-degree haemorrhoids Perianal haematoma Perianal abscess

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 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 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. 37.4). The

Anorectal disorders

355

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Figure 37.4 Classification of haemorrhoids

Figure 37.6 Severely prolapsed haemorrhoids: requiring surgery

Other symptoms include prolapse, mucoid discharge, irritation/itching, incomplete bowel evacuation and pain (see Fig. 37.6).

Treatment

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. 37.5).

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

Clinical stages and pathology3

Anal discharge

• 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.

Anal discharge refers to the involuntary escape of fluid from or near the anus. The causes may be considered as follows.5

Figure 37.5 Three sites of primary haemorrhoids, looking into the anus from below

Symptoms Bleeding is the main and, in many people, the only symptom. The word ‘haemorrhoid’ means flow of blood.

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

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Part Three Problem solving in general practice

Anal (faecal) incontinence 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 37.7. Common JTDIBFNJD
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causes are polyps, colon cancer, ischaemic colitis, diverticular disease and haemorrhoids. 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 non-prolapsing 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 37.2). 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 thickwalled 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 technetium-labelled red cell scan or colonoscopy. 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 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 DPMJUJT

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Figure 37.7 Various causes of rectal bleeding

• • • • • • • •

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

Anorectal disorders

Table 37.2 Presentation and causes of rectal bleeding6 Bright red blood in toilet separate from faeces

Internal haemorrhoids

Bright red blood on toilet paper

Internal haemorrhoids

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.

Fissure

Signs

Anal cancer

The skin changes can vary from minimal signs to marked pathology that can show linear ulceration, maceration or lichenification (see Fig. 37.8). Superficial skin changes can be moist and macerated or dry and scaly. Full anorectal examination is necessary.

Pruritus Anal warts and condylomata Blood and mucus on underwear

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

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 mucus)

Small colorectal polyps

Melaena (black tarry stools)

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

Torrential haemorrhage (rare)

Diverticular disorder

Large volumes of mucus in faeces (little blood)

Villous papilloma of rectum

Small colorectal cancer

Angiodysplasia

Villous papilloma of colon Blood in faeces with menstruation (rare)

Rectal endometriosis

Source: Orlay, G. Office Proctology, page 11. 11 © Copyright 1987 George Orlay—reproduced with permission

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

Figure 37.8 Lichen chronicus simplex. Lichenification from scratching with longstanding pruritus (see page 1126)

Causes and aggravating factors • Psychological factors: — stress and anxiety — fear of cancer • Generalised systemic or skin disorders: — seborrhoeic dermatitis — eczema — 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)

Diagnosis • Urinalysis (?diabetes) • Anorectal examination

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• 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.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Anal Fissure, page 198 • Haemorrhoids, page 250 • Pruritus ani, page 284

REFERENCES 1 Hunt P, Marshall V. Clinical Problems in General Surgery. Sydney: Butterworths, 1991: 311. 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 Mashford L (Chair). Therapeutic Guidelines: Analgesic (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2007: 261. 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 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. 38.1). • 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. • The 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.

PHYSICIAN

R A M A Z Z I N I 1713

• 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 safety diagnostic model is presented in Table 38.1.

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

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Table 38.1 Thoracic back pain: diagnostic strategy model Q.

Probability diagnosis

A.

Musculoligamentous strains (mainly postural)

Q.

Serious disorders not to be missed

A.

Cardiovascular: • myocardial infarction • dissecting aneurysm • pulmonary infarction • epidural haematoma (blood-thinning agents)

Vertebral dysfunction

Neoplasia: • myeloma • lung (with infiltration) • metastatic disease

Pneumothorax Osteoporosis Pitfalls (often missed)

A.

Angina

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 38.2 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.

Severe infections: • epidural abscess • pleurisy • infectious endocarditis • osteomyelitis

Q.

by dysfunction of the lower cervical and thoracic spinal joints, especially those of the mid-thoracic (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.

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 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.

Gastrointestinal disorders • oesophageal dysfunction • peptic ulcer (penetrating) • hepatobiliary • pancreatic Herpes zoster Spondyloarthropathies Costochondritis: • Tietze syndrome Fibromyalgia syndrome

Osteoporosis

Polymyalgia rheumatica Chronic infection: • tuberculosis • brucellosis

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.

Q.

Seven masquerades checklist

A.

Depression

✓

Diabetes

–

Drugs

–

Acute infections

Anaemia

–

Thyroid disorder

–

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.

Spinal dysfunction UTI

✓✓ ✓

Q.

Is this patient trying to tell me something?

A.

Yes, quite possible with many cases of back pain.

Thoracic back pain

Table 38.2 Non-musculoskeletal causes of thoracic back pain Heart

Myocardial infarction Angina

Great vessels

Oesophagus

The red flag pointers are similar to that for low back pain (see Chapter 39). Fracture pointer

Dissecting aneurysm

Major trauma

Pulmonary embolism (rare)

Minor trauma:

Pulmonary infarction

• osteoporosis

Pneumothorax

• female >50 years

Pneumonia/pleurisy

• male >60 years

Oesophageal rupture

Malignancy pointer

Oesophageal spasm

Age >50

Oesophagitis

Past history malignancy

Oesophageal cancer

Unexplained weight loss

Duodenum

Miscellaneous infections

Red flag pointers for thoracic back pain1

Pericarditis

Subdiaphragmatic Gall bladder disorders of: Stomach

Pain at rest

}

Constant pain including ulcers

Night pain

Pancreas

Pain at multiple sites

Subphrenic collection

Unresponsive to treatment

Herpes zoster

Infection pointer

Bornholm disease

Fever

Infective endocarditis

Night sweats

Psychogenic

Risk factors for infection Other serious conditions Chest pain/heaviness

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 38.3. The symptoms and signs that should alert the clinician to malignant disease are: • back pain occurring in an older person

361

Shortness of breath, cough

• unrelenting back pain, unrelieved by rest (this includes night pain) • 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 pre-eruption stage and the various gastrointestinal disorders. Two commonly misdiagnosed problems are a penetrating duodenal ulcer presenting with lower thoracic pain

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Table 38.3 Significant tumours affecting the thoracic and lumbar spine

Of bone

Benign

Malignant

Osteoid osteoma

Primary:

Haemangioma

• multiple myeloma

Osteoblastoma

• lymphomas (e.g. Hodgkin)

Aneurysmal bone cyst

• sarcoma

Eosinophilic granuloma Spinal

Extradural:

Secondary:

• lipoma

• breast

• neuroma

• lung

• fibroma

• prostate

Intradural:

• adrenals/kidney

• neuroma

• thyroid

• ependymoma

• melanoma

• chordoma

Direct spread:

• meningioma

• stomach • large bowel • pancreas • uterus/cervix/ ovary

Source: After Kenna and Murtagh2

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 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 pre-existing 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

to 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 38.1. 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 25.2 (see Chapter 25), while the dermatome pattern is outlined in Figure 38.2. 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

Thoracic back pain

363

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Figure 38.2 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

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. 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 38.3 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 38.3 represent those areas where the patient experiences pain following the injection of hypertonic saline into the posterior elements of the spine.

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:

The clinical approach

• 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

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.

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5 5

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5 5

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joint. Care must be taken to rule out pneumonia and pleurisy. • 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.

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. 38.4), which becomes more prominent on forward flexion (see Fig. 38.6). Look for any asymmetry of the chest wall, inequality

Thoracic back pain

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.

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: • • • •

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: 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)

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

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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 radionucleotide bone scan if neoplastic or metabolic disease is suspected

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Thoracic back pain in children 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. 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 Kyphosis is the normal curve of the thoracic spine when viewed from the side. The normal range is 20–45º (see Fig. 38.5). An excessive angle (>45–50º) 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 • • • • • • •

Figure 38.5 Illustration of kyphosis, which is measured by the angle between the uppermost and lowermost inclined vertebrae on the lateral X-ray • 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. 38.6). The routine physical screening check of an adolescent should include this area.

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.

Thoracic back pain

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Investigation A single erect PA spinal X-ray is sufficient;7 the Cobb angle (see Fig. 38.7) is the usual measurement yardstick.

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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. • 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

Figure 38.7 Scoliosis: the Cobb angle method of curve measurement • • • • •

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. 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

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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 • • • • • • •

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

Figure 38.8 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

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.

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. 38.8) 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 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

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 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,

Thoracic back pain

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’) to neurotically click 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 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

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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

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. 38.9). 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:

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1 a history of widespread pain (neck to low back) 2 pain in 11 of 18 tender points on digital palpation

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. 38.10).

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)

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

Treatment • Explanation, reassurance and counselling • Attention to sleep disorders, stress factors and physical factors • Relaxation program • Rehabilitation exercise program (e.g. walking, swimming or cycling)

Figure 38.10 Fibromyalgia syndrome: typical tender points (the tender point map represents the 14 points recommended for use as a standard for diagnostic or therapeutic studies)

• Use paracetamol for first-line analgesia

Medication (often disappointing) antidepressants (of proven short-term value): 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. Newer agents, other antidepressants (e.g. milnacipran) and the neuromodulator pregabalin are being evaluated.

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

Metastatic disease18

Figure 38.9 Injection for myofascial trigger points

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.

Thoracic back pain

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 page 238).

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. 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 page 273).

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 5th edition: • Exercises for Your Thoracic Spine, page 175 • Fibromyalgia, page 176 • Scoliosis, page 51

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Practice tips • 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, 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.

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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. 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, 2006: 176–8. 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.

Low back pain

39

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. F R A N C I S K I LV E R T 1 8 74

Low back pain accounts for at least 5% of general practice presentations. 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.4 • The most common age groups are the 30s, 40s and 50s, the average age being 45 years.3 • 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 39.1. Table 39.1 Major causes of low back ± leg pain presenting in the author’s general practice Patients

%

Vertebral dysfunction

71.8

Lumbar spondylosis

10.1

Depression

3.0

Urinary tract infection

2.2

Spondylolisthesis

2.0

Spondyloarthropathies

1.9

Musculoligamentous strains/tears

1.2

Malignant disease

0.8

Arterial occlusive disease

0.6

Other

6.4

Total

100.0

Relevant causes are illustrated in Figure 39.1.

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Anatomical and pathophysiological concepts

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. 39.2). 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

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 Maigne 4 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

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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 should also be kept in mind (see page 273). 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 39.3.

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Figure 39.2 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

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

A diagnostic approach A summary of the safety diagnostic strategy model is presented in Table 39.2.

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.

Serious disorders not to be missed It is important to consider malignant disease, especially in an older person. It is also essential to consider

The inflammatory disorders must be kept in mind, especially the spondyloarthropathies, which include psoriatic arthropathy, ankylosing spondylitis, reactive arthritis, inflammatory bowel disorders such as ulcerative colitis and Crohn disease, and reactive arthritis. The spondyloarthropathies are more common than appreciated and must be considered in the younger person presenting with features of inflammatory back pain (i.e. pain at rest, relieved by activity). The old trap of confusing claudication in the buttocks and legs, due to a high arterial obstruction, with sciatica must be avoided.

General pitfalls • Being unaware of the characteristic symptoms of inflammation and thus misdiagnosing one of the spondyloarthropathies. • Overlooking the early development of malignant disease or osteomyelitis; if suspected, and an X-ray is normal, a radionuclide scan should detect the problem. • Failing to realise that mechanical dysfunction and osteoarthritis can develop simultaneously, producing a combined pattern. • Overlooking anticoagulants as a cause of a severe bleed around the nerve roots and corticosteroids leading to osteoporosis. • Not recognising back pain as a presenting feature of the drug addict.

Seven masquerades checklist Of these conditions, depression and urinary tract infection have to be seriously considered. For the young woman with upper lumbar pain, especially if she is pregnant, the possibility of a urinary tract infection must be considered. These patients may not have urinary symptoms, such as dysuria and frequency. Depressive illness has to be considered in any patient with a chronic pain complaint. This common psychiatric disorder can continue to aggravate or maintain the pain even though the provoking problem has disappeared.

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Table 39.2 Low back pain: diagnostic strategy model

Table 39.3 ‘Red flag’ pointers to serious low back pain conditions6

Q.

Probability diagnosis

A.

Vertebral dysfunction especially facet joint and disc

Age >50 years or 37.8°C

Spondylosis (degenerative OA)

Constant pain—day and night especially severe night pain

Q.

Serious disorders not to be missed

A.

Cardiovascular: • ruptured aortic aneurysm • retroperitoneal haemorrhage (anticoagulants)

History of cancer

Unexplained weight loss Symptoms in other systems, e.g. cough, breast mass

Neoplasia: • myeloma • metastases

Significant trauma

Severe infections: • vertebral osteomyelitis • epidural abscess • septic discitis • tuberculosis • pelvic abscess/PID

Neurological deficit

Osteoporotic compression fracture

No improvement over 1 month

Cauda equina compression

Possible cauda equina syndrome: • saddle anaesthesia • recent onset bladder dysfunction/overflow incontinence • bilateral or progressive neurological deficit

Q.

Pitfalls (often missed)

A.

Spondyloarthropathies: • ankylosing spondylitis • reactive arthritis • psoriasis • bowel inflammation

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

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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 67).

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. 39.8)

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.

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.

Figure 39.8 Spondylolisthesis: illustrating a forward shift of one vertebra on another

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. 39.9).

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

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. 39.10) (refer to Chapter 36). 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. The following profile for ankylosing spondylitis serves as a typical clinical presentation of back pain for this group.

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Typical Profile continued Relief

Activity including exercise Patient may walk around during night for relief

Associations

Back stiffness, especially in morning Pain and stiffness in thoracic or cervical spine Pain and stiffness in thoracic cage

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Figure 39.9 Lumbar spondylosis with degeneration of the disc and facet joint, leading to narrowing of the spinal canal and intervertebral foramen

Treatment Typical profile of ankylosing spondylitis8 Age and sex History of injury

Young men 15–30 years (rare onset after 40) None, unless coincidental Has a slow insidious onset

Site and radiation

Low back, may radiate to both buttocks or posterior thigh (rare below knees) Can alternate sides

Type of pain

Aching, throbbing pain of inflammation

Aggravation

Often worse at night (can wake patient), turning over in bed and rising in the morning

Commonly episodic

The earlier the treatment the better the outlook for the patient; the prognosis is usually good. 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

The basic methods of management are: • advice on good back care and posture • general education and counselling • exercise programs to improve the range of movement and maintain mobility • referral to physiotherapist • drug therapy, especially tolerated NSAIDs, preferably indomethacin in optimal dosage • sulphasalazine—a useful second-line agent if the disease progresses despite NSAIDs • DMARDs (e.g. methotrexate) or bDMARDs may be necessary in severe progressive disease

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Part Three Problem solving in general practice

B

C

Figure 39.10 (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 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. 39.11). 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 39.6. 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

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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 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.

Magnuson’s method (the ‘migratory pointing’ test)

Tests for non-organic back pain 8

Paradoxical straight leg raising test

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).

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

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.

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Part Three Problem solving in general practice

Table 39.6 Comparison of general clinical features of organic and non-organic based low back pain7,8 Symptoms

Organic disorders

Non-organic disorders

Presentation

Appropriate

Often dramatic

Pain

Localised

Bilateral/diffuse Sacrococcygeal

Pain radiation Time pattern Paraesthesia/anaesthesia Response to treatment

Appropriate

Inappropriate

Buttock, specific sites

Front of leg/whole leg

Pain-free times

Constant, acute or chronic

Dermatomal

May be whole leg

Points with finger

Shows with hands

Variable

Patient often refuses treatment

Delayed benefit

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

Signs Observation

Appropriate

Overreactive under scrutiny

Guarded

Inconsistent

Tenderness

Localised to appropriate level

Often inappropriate level

Spatial tenderness

Consistent

Withdraws from probing finger Inconsistent

(Magnuson) 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’)

Appropriate

Brisk hyperactive

Reflexes

May be depressed

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

The axial loading test

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.

1 Place your hands over the patient’s head and press firmly downward (see Fig. 39.12). 2 This will cause no discomfort to (most) patients with organic back pain.

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

389

B

39

Figure 39.12 The axial loading test

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. The caring knowledgeable therapist. Evidence supports the positive value of education and reassurance from a confident, supportive and knowing 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. 39.13). Swimming is an excellent activity for back disorders. Studies support the use of exercises for chronic back pain rather than acute pain.3

C

Figure 39.13 Examples of exercises for low back pain: (a) rotation exercise; (b) flexion exercise

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

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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

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.

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 evidence for the efficacy of these modalities is still lacking: • hydrotherapy • traction

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. 39.14). Others favour the use of steroids and the lumbar epidural approach. The evidence regarding effectiveness is conflicting.5

Physical therapy Active exercises are the best form of physical therapy (see Figs 39.13a, b). Passive spinal stretching at the end range is a safe, effective method (see Fig. 39.15). 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. 39.16).3, 6, 12, 13 However, the evidence from controlled

TBDSBM
IJBUVT

Figure 39.15 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, 1989

FOE
PG
EVSBM
TBD

Figure 39.16 Lumbar spinal stretching manipulation: illustration of the specific technique for the L4–5 level with arrows indicating the direction of applied force. Figure 39.14 Caudal epidural injection: the needle should lie free in the space and be well clear of the dural sac

Source: Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 1989

Low back pain

• • • • • • • • • • •

TENS therapeutic ultrasound facet joint injection 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. It is often defined as pain that has been present for at least 3 months • Subacute pain = pain 6–12 weeks • Chronic pain = pain greater than 12 weeks

Acute low back pain6 The common problem of low back pain caused by facet joint dysfunction and/or limited disc disruption usually responds well to the following treatment. The typical patient is aged 20–55 years, is well and has no radiation of pain below the knee.15 • Explanation and reassurance • Back education program • Encouragement of normal daily activities 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 on first visit)11, 13, 15 • Prescribe exercises (provided no aggravation) • Review in about 5 days (probably best time for physical therapy) • No investigation needed initially

391

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 67).

Acute 6 • • • • • •

• •

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, 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

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)

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General guidelines for surgical intervention for radiculopathy 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 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 • 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(0), note increasing to maximum 75–100 mg(0) • a multidisciplinary team approach is recommended/ back schools

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 • 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. • 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.

Low back pain

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Backache, page 166 • Exercises for Your Lower Back, page 172 • Sciatica, page 186 • Spondylosis, page 189

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 Waddell G, et al. Non-organic physical signs in low back pain. Spine, 1980; 5: 117–25. 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. C H A R L E S D I C K E N S (1812–70), N I C H O L A S N I C K L E B Y 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. 40.1). 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. 40.2).

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 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

Figure 40.2 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

implications for surgery, pregnancy, medication and genetic counselling.

Key facts and checkpoints QFUFDIJBF

QVSQVSB

FDDIZNPTJT

Figure 40.1 Purpuric rash (petechiae and ecchymoses)

394

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

Bruising and bleeding

• 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 40.1.1

Table 40.1 Differential diagnoses of systemic bleeding disorders Vascular disorders (a)

Inherited: • hereditary haemorrhagic telangiectasia • Marfan syndrome • Osler–Weber–Rendu syndrome

(b)

Acquired: • infection (e.g. meningococcus, measles, dengue) • purpura simplex • senile purpura • Henoch–Schönlein purpura • steroid purpura • scurvy

Coagulation factor deficiency or inhibitor (a)

Inherited: • haemophilia A • haemophilia B • vWD

(b)

Acquired: • disseminated intravascular coagulation • 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

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.

Functional platelet disorders (a)

Inherited: • Glanzmann thrombasthenia • Bernard–Soulier syndrome • storage pool deficiency

(b)

Acquired: • drug-induced (e.g. aspirin, NSAIDs) • uraemia • myeloproliferative disorders • dysproteinaemias

History Factors that suggest the presence of a systemic bleeding defect include: • • • •

spontaneous haemorrhage severe or recurrent haemorrhagic episodes bleeding from multiple sites bleeding out of proportion to the degree of trauma

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).

395

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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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 40.2.

Table 40.2 Purpura: diagnostic strategy model Q.

Probability diagnosis

A.

Simple purpura (easy bruising syndrome) Senile purpura Corticosteroid-induced purpura Immune thrombocytopenic purpura Henoch–Schönlein purpura

Q.

Serious disorders not to be missed

A.

Malignant disease: • leukaemia • myeloma

Family history A positive family history can be a positive pointer to the diagnosis:

Aplastic anaemia

• sex-linked recessive pattern: haemophilia A or B • autosomal dominant pattern: vWD, dysfibrinogenaemias • autosomal recessive pattern: deficiency of coagulation factors V, VII and X

Severe infections: • septicaemia • meningococcal infection • measles • typhoid • dengue/chikungunya

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 presented in Table 40.3. 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.

Myelofibrosis

Disseminated intravascular coagulation Thrombotic thrombocytopenic purpura Q.

Pitfalls (often missed)

A.

Haemophilia A, B vWD Post-transfusion purpura

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?

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: • chloramphenicol • corticosteroids • sulphonamides • quinine/quinidine • thiazide diuretics • NSAIDs • cytotoxics • oral anticoagulants Anaemia: • aplastic anaemia

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

Q.

Psychogenic factors

A.

Factitial purpura

Bruising and bleeding

Table 40.3 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)

— gold — heparin — phenylbutazone — sulphonamides — quinine, quinidine — thiazide diuretics — 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–Scöhnlein purpura. Senile purpura in the elderly is usually seen over the dorsum of the hands, extensor surface of the forearms and the shins. 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.

• 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 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. A summary of appropriate tests is presented in Table 40.4 and of blood changes for some coagulation factor deficiencies in Table 40.5. Table 40.4 Laboratory investigation checklist for the easy bruiser Full blood count Platelet count Prothrombin time (INR) Thrombin time (TT) Activated partial thromboplastin time Table 40.5 Blood changes for specific coagulation factor disorders

PT

Haemophilia A

vWD

Vitamin K deficiency

Normal

Normal

↑

Investigations

APTT ↑

↑

↑

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

TT

Normal

Normal

• • • •

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)

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Normal

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.

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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. 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. 40.3), 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.

Figure 40.4 Henoch–Schönlein purpura in a 5-year-old boy showing the typical distribution of the rash on the lower limbs • 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 Tip: beware of CKF

Clinical features • • • • • •

All ages, mainly in children Rash, mainly on buttocks and legs (see Fig. 40.4)4 Rash can occur on hands, arms and trunk Arthritis: mainly ankles and knees Abdominal pain—colicky (vasculitis of GIT) Haematuria (reflects nephritis)

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

Associations

Abnormal bleeding in the elderly

• Kidney involvement—deposition of IgA immune complex (a serious complication) • Melaena

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

Bruising and bleeding

399

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Figure 40.3 Henoch–Schönlein purpura: typical distribution

Vascular disorders

Platelet disorders

The features are:

The features are:

• easy bruising and bleeding into skin • ± mucous membrane bleeding • investigations normal

• petechiae ± ecchymoses • bleeding from mucous membranes • platelet counts 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

Consider: • paraffin oil (e.g. Children’s Parachoc) • poloxamer drops (e.g. Coloxyl Drops) • sennoside B granules

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 45 years

1:17

One first-degree relative and one second-degree relative

1:12

One first-degree relative 85 dB) are more than twice as likely to be deaf. • There is a related incidence of tinnitus with deafness.


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It is useful to consider the causes of deafness in terms of pathophysiology (conductive or sensorineural hearing loss) and anatomical sites (see Fig. 44.2). Conductive hearing loss is caused by an abnormality in the pathway conducting sound waves from the outer ear to the inner ear,1 as far as the footplate of the stapes. Sensorineural hearing loss (SNHL) is a defect central to the oval window involving the cochlear (sensor), cochlear nerve (neural) or, more rarely, central neural pathways.1 Congenital deafness is an important consideration in children, while presbyacusis is very common in the aged. The commonest acquired causes of deafness are impacted cerumen (wax), serous otitis media and otitis externa. Noise-induced deafness is also a common problem. It is important not to misdiagnose an acoustic neuroma, which can present as acute deafness, although slow progressive loss is more typical. A summary of the diagnostic strategy, which includes several important causes of deafness, is presented in Table 44.1 and a checklist of ototoxic drugs in Table 44.2.

Symptoms The symptoms vary so that some barely notice a problem while others are severely disabled. Common symptoms include inability to:

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• hear speech and other sounds loudly enough • hear speech and music clearly, even when loud enough • understand speech even when loud enough—a problem of language reception









People with mild hearing loss notice only subtle differences and may have trouble hearing certain highfrequency sounds, such as ‘s’, ‘f’ or ‘th’. They may also have trouble hearing in certain situations, such as at a party or in a crowd where there is a lot of background noise. Those with moderate hearing loss have trouble hearing in many situations.

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A diagnostic approach

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Figure 44.1 Prevalence of hearing problems with increasing age

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The clinical approach

Examination

History

Inspect the facial structures, skull and ears. The ears are inspected with an otoscope to visualise the external meatus and the tympanic membrane (TM) and the presence of obstructions such as wax, inflammation or osteomata. The examination requires a clean external auditory canal. Gentle suction is useful for cleaning pus debris. Syringing is reserved for wax in people with an intact TM and a known healthy middle ear. It is an advantage to have a pneumatic attachment to test drum mobility. Reduction of TM mobility is an important sign in secretory otitis media. There are several simple hearing tests. The distance at which a ticking watch can be heard can be used but the advent of the digital watch has affected this traditional method.

The history should include an account of the onset and progression of any deafness, noise exposure, drug history, a history of swimming or diving, air travel and head injury and family history. A recent or past episode of a generalised infection would be relevant and the presence of associated aural symptoms, such as ear pain, discharge, tinnitus and vertigo. Vertigo may be a symptom of Meniere syndrome, multiple sclerosis, acoustic neuroma or syphilis. Several important clues can be obtained from the history. The often sudden onset of hearing loss in an ear following swimming or showering is suggestive of wax, which swells to block the ear canal completely. Patients with conductive loss may hear better in noisy conditions (paracusis) because we raise our voices when there is background noise. Conversely, people with sensorineural deafness (SND) usually have more difficulty hearing in noise as voices become unintelligible.

Whisper test Occlude far ear. Whisper ‘68’ then ‘100’ from a distance of 60 cm.

Deafness and hearing loss

Table 44.1 Deafness and hearing loss: diagnostic strategy model Q.

Probability diagnosis

A.

Impacted cerumen

Table 44.2 Known ototoxic drugs Alcohol Aminoglycosides: • amikacin • gentamicin • kanamycin • neomycin • streptomycin • tobramycin

Serous otitis media Otitis externa Congenital (children) Presbyacusis Q.

Serious disorders not to be missed

A.

Neoplasia: • acoustic neuroma • temporal lobe tumours (bilateral) • otic tumours Severe infections: • generalised infections (e.g. mumps, measles) • meningitis • syphilis

Diuretics: • ethacrynic acid • frusemide Chemotherapeutic agents Quinine and related drugs Salicylates

Hair-rubbing method

Q.

Pitfalls (often missed)

A.

Foreign body

In children and in adults with a reasonable amount of hair grab several hairs close to the external auditory canal between the thumb and index finger. Rub the hairs lightly together to produce a relatively high-pitched ‘crackling’ sound (see Fig. 44.3). If this sound cannot be heard, a moderate hearing loss is likely (usually about 40 dB or greater). Like the whisper test, this test is a rough guide only.

Temporal bone fracture

Tuning fork tests

Otosclerosis

If deafness is present, its type (conduction or sensorineural) should be determined by tuning fork testing. The most suitable tuning fork for preliminary

Perforated tympanic membrane Cholesteatoma Perilymphatic fistula (post-stapedectomy) Meniere syndrome

Barotrauma Noise-induced deafness Rarities: • Paget disease of bone • multiple sclerosis • osteogenesis imperfecta Q.

Seven masquerades checklist

A.

Depression Diabetes

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Figure 44.3 Simple hair-rubbing method of testing possible deafness

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testing is the C2 (512 cps) fork. The fork is best activated by striking it firmly on the bent elbow.

Weber test The vibrating tuning fork is applied firmly to the midpoint of the skull or to the central forehead or to the teeth. This test is of value only if the deafness is unilateral or bilateral and unequal (see Fig. 44.4). Normally the sound is heard equally in both ears in the centre of the forehead. With sensorineural deafness the sound is transmitted to the normal ear, while with conduction deafness it is heard better in the abnormal ear.

placing the tuning fork on the mastoid process and the patient indicates when it can no longer be heard. The fork is then placed at the external auditory meatus and the patient indicates whether the sound is now audible. Normally air conduction is better than bone conduction and the sound will again be heard. A comparison of the interpretation of these tests is summarised in Table 44.3. Table 44.3 A comparison of the Rinne and Weber tests State of the hearing

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Weber test

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Negative: BC >AC

Louder in the deaf ear

Very severe conduction deafness

Negative: BC >AC

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

May hear BC only

AC = air conduction; BC = bone conduction

Rinne test The tuning fork is held:

Audiometric assessment

• outside the ear (tests air conduction) and • firmly against the mastoid bone (tests bone conduction)

Audiometric assessment includes the following:

It therefore compares air and bone conduction in the same ear (see Fig. 44.5). A variation of the test includes (a)

• • • •

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

(b)

Figure 44.5 Rinne test comparing air conduction (a) with bone conduction (b)

Deafness and hearing loss

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 44.6 and 44.7 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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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.

453

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. High-risk 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 21 g/3 days]).

Coeliac disease5 Synonyms: coeliac sprue, gluten-sensitive enteropathy Note: It can appear at any age; refer to coeliac disease in children (see page 469). It is widely underdiagnosed because most patients present with non-GIT symptoms, such as tiredness. There is a genetic factor in this autoimmune disorder with a 1 in 10 chance if a first-degree relative is affected. Consider screening under 2 years if there is such an association.

Clinical features • Classic tetrad: diarrhoea, weight loss, iron/folate deficiency, abdominal bloating • Malaise, lethargy • Flatulence • Mouth ulceration • Diarrhoea with constipation (alternating) • Pale and thin patient • No subcutaneous fat

Diagnosis • Elevated faecal fat • Characteristic duodenal biopsy: villous atrophy (key test) • IgA antigliadin antibodies (screening—limited) • IgA anti-endomysial antibodies (>90% sensitivity and specificity) • IgA transglutaminase antibodies (>90% sensitivity and specificity)

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 • • • • • • • • • • •

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)

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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 whippelii. 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 • Lymphadenopathy • ± Fever

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

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 page 318–9).

Clinical features Clinical features include:

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• 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

Differential diagnoses. These include septicaemia, urinary tract infection, intussusception, appendicitis, pelvic abscess, partial bowel obstruction, diabetes mellitus and antibiotic reaction4 (see Table 45.8). Note: Exclude acute appendicitis and intussusception in the very young. Table 45.8 Differential diagnosis of acute diarrhoea and vomiting in children Bowel infection: • viruses • bacteria • protozoal • food poisoning—staphylococcal toxin

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

Systemic infection

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

Diabetes mellitus

• • • • • • • •

Note: Exclude surgical emergencies (e.g. acute appendicitis), infections (e.g. pneumonia), septicaemia, otitis media 2 seconds

Urine output

Normal

Decreased

Nil

Treatment

Oral rehydration: • small amounts of fluids often • continue breast-feeding • solids after 24 hours • provide maintenance fluid and loss

Oral rehydration: • consider nasogastric tube for steady fluid infusion or • IV infusion

Urgent IV infusion: isotonic fluid

Avoid • Drugs: antidiarrhoeals, antiemetics and antibiotics • Lemonade: osmotic load too high, can use if diluted 1 part to 4 parts water but sugar may be poorly tolerated

To treat or not to treat at home • Treat at home—if family can cope, vomiting is not a problem and no dehydration. • Admit to hospital—if dehydration or persisting vomiting or family cannot cope; also infants 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: 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). Do not worry that your child is not eating food. Solids can be commenced after 24 hours. 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 reintroduce the 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).

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 waiting for 2 weeks). Stools may be watery, frothy, smell like vinegar and tend to excoriate the buttocks. They contain sugar. 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.

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.

Cow’s milk protein intolerance8 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 pages 1224–5).

Inflammatory bowel disorder 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.6

Chronic enteric infection 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.

Diarrhoea

Coeliac disease 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 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 page 163.

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 page 114.

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, foul-smelling diarrhoea.

Principles of treatment of diarrheoa Acute diarrhoea • Maintenance of hydration: Antiemetic injection (for severe vomiting) prochlorperazine IM, statim

469

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 It is vital that you starve but drink small amounts of clear fluids such as water, tea, lemonade and yeast extract (e.g. Marmite) until the diarrhoea settles. 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). 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).

Treatment (antimicrobial drugs)3, 5 It is advisable not to use these 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.

Shigella dysentery (moderate to severe) 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 ampicillin 1 g (o) 6 hourly for 5 days

Campylobacter jejuni (if prolonged) Norfloxacin 400 mg (o) 12 hourly for 5 days (adults) or

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Part Three Problem solving in general practice

erythromycin 500 mg (o) qid for 7 days (preferable) in adults and children

If severe: administer same drug and dosage IV for first 4–5 days.

Giardiasis

Cholera

This protozoal infestation is often misdiagnosed. It should be considered for a persistent profuse watery bubbly diarrhoea (see Chapter 15, page 132).

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

Tinidazole 2 g (o), single dose 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 for 7 days

Note: Salmonella is a notifiable disease; infants under 15 months are at risk of invasive Salmonella infection.

Amoebiasis (intestinal) See Chapter 15. Metronidazole 600–800 mg (o) tds for 6–10 days plus diloxanide furoate 500 mg (o) tds for 10 days

Blastocystitis hominis 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. 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

Alternative oral regimens (based on sensitivity): Chloramphenicol 500–750 mg (o) 6 hourly for 14 days or Cotrimoxazole (DS) 1 tablet (o) 12 hourly for 14 days or Amoxycillin 1 g (o) 6 hourly for 14 days

Doxycycline 100 mg (o) 12 hourly for 3 days or Ciprofloxacin 1 g (o) as a single dose

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

Inflammatory bowel disease Inflammatory bowel disease 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)

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 • Proctosigmoidoscopy: a granular red proctitis with contact bleeding • Barium enema: characteristic changes

Diarrhoea

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 • • • • •

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

471

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

Irritable bowel syndrome (IBS) 5, 9, 10 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 45.3 • 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 • 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 II diagnostic criteria for IBS is presented in Table 45.10. IBS is a diagnosis of exclusion. A thorough physical examination, investigations (FBE, ESR and stool microscopy or culture) and sigmoidoscopy are necessary.

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Part Three Problem solving in general practice

Table 45.10 Rome II diagnostic criteria for irritable bowel syndrome*10 In the preceding 12 months, the patient has had at least 12 weeks (not necessarily consecutively) of abdominal discomfort or pain with two of the following three features: • relieved by defecation and/or • onset associated with a change in stool frequency and/or • onset associated with a change in form (appearance) of stool 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 * in absence of structural or metabolic abnormalities to explain symptoms

Red flag pointers for non-IBS disease 9 • • • • • • • • • • •

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• Normal pleural space has 10–20 mL fluid • Can be detected on X-ray if >300 mL fluid in pleural space • Can be detected clinically if >500 mL fluid • Can be subpulmonary—simulates a raised diaphragm • May be asymptomatic • Dyspnoea common with large effusion • Chest pain in setting of pleuritis, infection or trauma • Signs: refer Table 50.6 • The fluid may be transudate or exudate (diagnosed by aspirate) • If blood stained—malignancy, pulmonary infarction, TB

Transudate Protein content 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.

Pulmonary fibrosis Pulmonary fibrosis is the end result of a collection of ill-defined disorders producing interstitial pneumonitis leading to fibrosis. In many there is a hypersensitivity reaction to various unusual antigens. The fibrosis may be

Dyspnoea

localised as following unresolved pneumonia, bilateral as with tuberculosis or widespread. Causes of widespread fibrosis include fibrosing alveolitis, rheumatoid arthritis, extrinsic allergic alveolitis including various occupational lung disorders, ornithosis, sarcoidosis and drug-induced interstitial disease (see the section on interstitial lung diseases, pages 521–3).

Key features • Consider possibility of fibrosis of lungs in chronic dyspnoea and a dry cough with normal resonance • Cyanosis and/or finger clubbing is commonly present • A ‘tricky’ feature is the presence of fine crackles at the end of inspiration upon auscultation, with faint breath sounds • Imaging is diagnostic, especially high-resolution CT scanning: it may show the ‘honeycomb lung’ appearance

Dyspnoea in children 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 page 915). 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.

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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 131).

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 126.

Interstitial lung diseases

Respiratory disease in the elderly

Interstitial lung diseases comprise a group of disorders that have the common features of inflammation and fibrosis of the interalveolar septum, representing a non-specific reaction of the lung to injury of various causes.8 Causes of pulmonary infiltration include:

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.

• sarcoidosis • cryptogenic fibrosing alveolitis (interstitial pulmonary fibrosis) • extrinsic allergic alveolitis (hypersensitivity pneumonitis) • drug-induced • lymphangitis carcinomatosis

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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). 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. • 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 finger clubbing PFTs: — restrictive ventilatory deficit — decrease in gas transfer factor • characteristic X-ray changes • • • •

High-resolution CT scanning has been a major advance in diagnosis.

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 be associated with or occur independently of hilar lymphadenopathy.

Clinical features 8,9 • • • • • • •

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 video-assisted thoracoscopy. Supporting evidence: • elevated serum ACE (non-specific) • PFTs: restrictive pattern; impaired gas transfusion 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 • hypercalcaemia, hypercalciuria • erythema nodosum with arthralgia • persistent cough

Corticosteroid treatment • 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 fibrosing interstitial pneumonia Idiopathic fibrosing interstitial pneumonia (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

Dyspnoea

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.9

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 micro-organisms 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 50.7). 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, fine-mesh 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.

Table 50.7 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. pigeons’, budgerigars’ ‘bloom’ on 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

Drug-induced interstitial lung disease 9

Malt worker’s lung

Mouldy barley

Coffee worker’s lung

Coffee dust

Drugs are an important cause of this disorder and have three main effects:

Sisal worker’s lung

Sisal dust

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 antiepileptics. Treatment is drug removal and a 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

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Sericultural workers

Silkworms

Furrier’s lung

Fur dust

Sausage workers

Dust

Prawn workers

Prawn fumes

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

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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 50.8 summarises the important causes. Table 50.8 Selected pneumoconioses Fibrotic lung disease

Agent

Typical occupations

Coal dust Coal worker’s Coal dust pneumoconiosis

Coal mining

Metal dust Siderosis

Metallic iron or iron oxide

Mining Welding Foundry work

Inorganic dusts Silicosis

Silica (silicon dioxide)

Quarrying Rock mining Stone cutting Sandblasting

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 one-third 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 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, multiple transfusions, 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).

Silicate dusts Asbestosis

Asbestos

Mining Shipbuilding Insulation Power stations Wharf labouring

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 high-resolution 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.

Severe acute respiratory syndrome (SARS) 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.

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

Dyspnoea

• 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

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 29, page 255).

Practice tips • 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.

Bronchial carcinoma Dyspnoea is associated with about 60% of cases of lung cancer3 (see page 445). 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

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carcinomatosis. A special problem arises with coexisting chronic bronchitis and emphysema.

When to refer • 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

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Asthma, page 205 • Asthma in Children, page 12 • Chronic Obstructive Airways Disease, page 211 • Dangerous Asthma, page 207 • Heart Failure, page 256

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. 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 McPhee SP, Papadakis MA. Current Medical Diagnosis and Treatment (49th edn). New York: The McGraw-Hill Companies, 2010: 269–93. 9 Moulds R (Chair). Therapeutic Guidelines: Respiratory (Version 3). Melbourne: Therapeutic Guidelines Ltd, 2005: 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 McPhee SP, Papadakis MA. Current Medical Diagnosis and Treatment (49th edn). New York: The McGraw-Hill Companies, 2010: 291–3. 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 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 51.1.1 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.

A diagnostic approach The five self-posed questions can be answered using the safe diagnostic model (see Table 51.2).

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S A L L E (1651–1719 )

Table 51.1 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

Key facts and checkpoints • 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.

DE LA

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

The painful ear

Table 51.2 The painful ear: diagnostic strategy model Q.

Probability diagnosis

A.

Otitis media (viral or bacterial) Otitis externa TMJ arthralgia Eustachian tube dysfunction

Q.

Serious disorders not to be missed

A.

Neoplasia of external ear Cancer of other sites (e.g. tongue, throat) Herpes zoster (Ramsay–Hunt syndrome)

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. 51.1) that must be distinguished from the so-called ‘safe’ ear (see Fig. 51.2). 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.

Acute mastoiditis Cholesteatoma Necrotising otitis externa Q.

Pitfalls (often missed)

A.

Foreign bodies in ear

BUUJD
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TVQFSJPS
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Hard ear wax Barotrauma Dental causes Referred pain: neck, throat Unerupted wisdom tooth and other dental causes TMJ arthralgia MBUFSBM
QSPDFTT PG
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Facial neuralgias, esp. glossopharyngeal Post tonsillectomy: • from the wound • from TMJ due to mouth gag Q.

Seven masquerades checklist

A.

Depression

✓

Diabetes

–

Drugs

–

Anaemia

–

Thyroid disorder

–

Spinal dysfunction

✓

UTI

–

Q.

Is the patient trying to tell me something?

A.

Unlikely, but always possible with pain. More likely in children. Consider factitious pain.

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Figure 51.1 Infected ear: unsafe perforation

Figure 51.2 Infected ear: safe perforation

Probability diagnosis

Pitfalls

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. 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.

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.

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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.

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.

General pitfalls

Key questions (especially children)

• 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 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 are 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

• • • • • •

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. 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 51.3 and 51.4. Inspect sites supplied by the nerves V2, IX, X, XI, C1, C2 and C3 to exclude other causes of referred pain.

Investigations Investigations are seldom necessary. Hearing tests are essential, especially for children. Simple tests such as speech discrimination, hair rubbing and tuning fork

The painful ear

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DBSDJOPNB …
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UPOTJM …
UPOHVF

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UPOTJMT …
UPOTJMMJUJT …
RVJOTZ …
UPOTJMMFDUPNZ

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 Foreign bodies (FBs) are frequently inserted into the ear canal (see Fig. 51.5). 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

Figure 51.3 Pharyngeal causes of otalgia Source: Courtesy of Bruce Black

XJTEPN
UFFUI DBSJFT

Figure 51.5 Foreign body (bead) in ear canal of a 3-yearold child, showing reactive tissue in ear canal BQJDBM
BCTDFTT DBSDJOPNB

Figure 51.4 Mandibular causes of otalgia Source: Courtesy of Bruce Black

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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 (see Fig. 51.6).

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. 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 scanning may be indicated for special conditions such as a suspected extraotic malignancy.

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 (see Fig. 51.7). 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.

Ear pain in children

Insects in the ear

Important causes of primary otalgia in children include otitis media, otitis externa, external canal furuncle or abscess, chronic eczema with fissuring of

Live insects should be immobilised by first instilling Aquaear drops or olive oil, and then syringing the ear with warm water (see Fig. 51.8).

Rubber catheter suction method

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B

B

PMJWF
PJM

UZNQBOJD
NFNCSBOF NPUI C

C

VQXBSE
EJSFDUJPO
PG
XBUFS

Figure 51.6 Probe method of removing a foreign body: (a) the tip of the probe is lifted by depressing the outer end of the probe; (b) continued gentle levering ‘rolls’ the foreign body out B

C

FBS
TZSJOHF

Figure 51.8 Insect in the ear: (a) first aid; (b) office procedure

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

Figure 51.7 Extracting the foreign body using a rubber catheter; (a) catheter cut straight across near its extremity; (b) application of suction (orally or by pump)

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.

• Two peaks of incidence: 6–12 months of age and school entry • Seasonal incidence coincides with URTIs • Bacteria cause two-thirds of cases7 • 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

The painful ear

Visualisation of the tympanic membrane 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).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.9, 10 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’.11 Possible clinical indications for antibiotics in children with painful otitis media • • • • •

Sick child with fever Vomiting Red–yellow bulging TM Loss of TM landmarks Persistent fever and pain after 3 days conservative approach

The antibiotic of choice is:8 amoxycillin 15 mg/kg 8 hourly (o) for 5–7 days or amoxycillin 30 mg/kg 12 hourly (o) for 5–7 days

Amoxycillin is also the preferred choice in the US and UK.12 If β-lactamase-producing bacteria are suspected or documented, or initial treatment fails, use: cefaclor 10 mg/kg/day (max. 750 mg/day) orally in three divided doses for 5–7 days (cefaclor is second choice irrespective of cause) or (if resistance to amoxycillin is suspected or proven) amoxycillin/potassium clavulanate

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With appropriate treatment most children with acute otitis media are significantly improved within 48 hours. Parents should be encouraged to contact their doctor if no improvement occurs within 72 hours. This problem is usually due to a resistant organism or suppuration. The patient should be re-evaluated at 10 days. It is of interest that some practitioners refer to the ‘Pollyanna’ phenomenon when treating otitis media; that is, all antibiotics seem to work!

Symptomatic treatment Rest the patient in a warm room with adequate humidity. Use analgesics such as paracetamol (acetaminophen) in high dosage. Although the use of antihistamines and decongestants has not been verified scientifically, the author has found nasal decongestants (as oxymetazoline nasal drops or sprays) effective in distressed children with an associated URTI. Otherwise, avoid antihistamines and decongestants. Follow-up: adequate follow-up with hearing assessment is mandatory.

Complications • Middle ear effusion. 70% of children will have an effusion present 2 weeks from the time of diagnosis, 40% at 4 weeks, with 10% having persistent effusions for 3 months or more. If the effusion is still present at 6–8 weeks, a second course of antibiotics should be prescribed.2 If the effusion persists beyond 3 months refer for an ENT opinion. • Acute mastoiditis. This is a major complication that presents with pain, swelling and tenderness developing behind the ear associated with a general deterioration in the condition of the child (see Fig 51.9). Such a complication requires immediate referral.7 • Chronic otitis media • Rare complications. These include labyrinthitis, petrositis, facial paresis and intracranial abscess. • Serous otitis media (glue ear). This represents incomplete resolution of suppurative otitis media. Signs include loss of drum mobility, hearing loss and abnormal impedance. Most resolve spontaneously but any necessary treatment includes medications such as bromhexine elixir and Demazin syrup, auto-inflations and ‘Otovent’ assisted nasal inflation.

Note: a proposed S. pneumoniae and H. influenzae conjugate vaccine may be an effective preventive measure for childhood otitis media.

Recurrent acute otitis media 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.

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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. 51.10). The sequence of symptoms is a blocked ear feeling, pain and fever. Discharge may follow if the TM perforates, with relief of pain and fever.

Figure 51.9 Mastoiditis in a child with recurrent otitis media showing erythema and swelling behind the ear. Surgical drainage was performed • 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,

Photo courtesy Bruce Black

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Figure 51.10 Acute otitis media causing true otalgia. The ear drum bulges laterally due to pus in the middle ear. Perforation and otorrhoea imminent.

The commonest organisms are viruses (adenovirus and enterovirus), and the bacteria H. influenzae, S. pneumoniae, Branhamella (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.

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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. 51.11). 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.

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

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Antibiotic treatment7 First choice: 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)

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Consider surgical intervention for failed therapy.

Chronic otitis media 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. 51.12a), the other unsafe (see Fig. 51.12b).

Chronic discharging otitis media (safe)8 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

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Figure 51.11 The appearances of the left tympanic membrane in the progressive development of acute otitis media

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Cholesteatoma13

(a)

Refer Chapter 44, page 455. 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. 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 51.3. Table 51.3 Comparison of types of discharge

(b)

Unsafe

Safe

Source

Cholesteatoma

Mucosa

Odour

Foul

Inoffensive

Amount

Usually scant, never profuse

Can be profuse

Nature

Purulent

Mucopurulent

Management

Photo courtesy Bruce Black

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Figure 51.12 (a) Chronic otitis media with loss of the tympanic membrane this is ‘safe ear’ (b) Unsafe ear: chronic otitis media with attic cholesteatoma.

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 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. 51.1); other perforations, not involving the drum margin (see Fig. 51.2), are regarded as ‘safe’.13

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 Otitis externa (see Fig. 51.13), 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.

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Dressings

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Figure 51.13 Otitis externa • Fungi: — Candida albicans — Aspergillus sp.

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. 51.14). 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.

Topical antimicrobials8 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 (2–3 drops bd). The tragus should be pumped for 30 seconds after instillation by pressing on it repeatedly, within the limitation of any pain.

Clinical features • • • • •

Itching at first Pain (mild to intense) 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

Figure 51.14 Insertion of a wick; it is packed gradually by short back-and-forth movements of the forceps. Source: Courtesy of Bruce Black

Other measures • Strong analgesics are essential • Antibiotics have little place in treatment unless a spreading cellulitis has developed • Prevent scratching and entry of water • Use a wick soaked in combination steroid and antibiotic ointment for more severe cases

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.

Practice tip for severe ‘tropical ear’

Syringing

Prevention

This is appropriate in some cases but the canal must be dried meticulously afterwards. For most cases it is not recommended.

• Keep the ear dry, especially those involved in water sports • Protect the ear with various water-proofing methods: — cotton wool coated with petroleum jelly

prednisolone (o) 15 mg statim then 10 mg 8 hourly for 6 doses followed by: • Merocel ear wick • Topical Kenacomb or Sofradex drops

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— 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.

Ear exostoses (‘surfer’s ear’) These bony overgrowths are caused by water retention in the ear.

Prevention • Use plugs or Blu-Tack to waterproof ear • Dry thoroughly with hair dryer after swimming

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. 51.15).

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

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.

Figure 51.15 Furuncle (boil) in hair-bearing area at opening of the ear canal

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.14 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 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

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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 Figure 51.16 Mechanism of barotrauma, with blocking of the Eustachian tube due to increased pressure at the sites indicated. Source: Courtesy of Bruce Black

Otic barotrauma Barotrauma is damage caused by undergoing rapid changes in atmospheric pressure in the presence of an occluded Eustachian tube (see Fig. 51.16). It affects scuba divers and aircraft travellers. 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 if any persistent problems for consideration of the Politzer bag inflation or myringotomy.

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

Complete healing can be expected within 8 weeks in 90–95% of such cases.15

Temporomandibular joint arthralgia 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

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 two-thirds of TM)

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Practice tips • 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. • 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 5th edition: • Earache in Children, page 29 • Ear Infection: Otitis Media, page 127 • Ear: Otitis Externa, page 240 • Ear: Wax in the Ear, page 241

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 (5th edn). Sydney: McGraw-Hill, 2008: 103–5. 7 Robinson MJ, Roberton DM. Practical Paediatrics (5th edn). Melbourne: Churchill Livingstone, 2003: 744–8. 8 Spicer J et al. Therapeutic Guidelines: Antibiotics (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2006: 234–40. 9 Antibiotics, patient education and otitis media. NPS News, 1999; 3: 3. 10 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. 11 Rosser W, Shafir M. Evidence-Based Family Medicine. Hamilton: BC Decker, 1998: 111–13. 12 Gunasekera H. Otitis media in children: how to treat. Australian Doctor, 18 July 2008: 33–40 13 Black B. Otitis media: how to treat. Australian Doctor, 29 November; 2002: I–VIII. 14 McPhee SJ, Papadakis MD. Current Medical Diagnosis and Treatment (49th edn). New York: The McGraw-Hill Companies, 2010: 182–3. 15 Kruger R, Black B. Penetrating injury eardrum. Aust Fam Physician, 1986; 15: 735.

The red and tender eye

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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. D I O C H R Y S O S T O M (40– 115 ) 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 52.1.

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 well-known 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.

Table 52.1 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, amoeba, bacterial) Herpes zoster ophthalmicus Penetrating injury Endophthalmitis Orbital cellulitis

Q.

Pitfalls (often missed)

A.

Scleritis/episcleritis Foreign body Trauma Ultraviolet light ‘keratitis’ Blepharitis Cavernous sinus arteriovenous fistula

Q.

Seven masquerades checklist

A.

Depression Diabetes Drugs Anaemia Thyroid disorder Spinal dysfunction UTI

Q.

Is the patient trying to tell me something?

A.

Unlikely.

The clinical approach The five essentials of the history are: • history of trauma, especially as indicator of intra-ocular foreign body (IOFB) • vision • the degree and type of discomfort

– – ✓ hypersensitivity – ✓ hyperthyroidism – –

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• presence of discharge • presence of photophobia

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.

• 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

Red flag pointers for red eye 'golden rules'

The key eye symptoms

• • • • • • • •

The key eye symptoms are: • • • •

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?

Loss of vision in the red eye Consider: • iritis (uveitis)

• • • •

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

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

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

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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. 52.1). 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.

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

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Figure 52.1 Physical signs to search for in a patient with a red eye (eyelids everted)

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.6 In both conditions the parents must be investigated for associated venereal infection and treated accordingly (this includes contact tracing) (see page 1398). 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. 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.6 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 trachoma caused blindness.

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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)

Blocked nasolacrimal duct Delayed development of the nasolacrimal duct occurs in about 6% of infants,6 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 82, page 853)

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.

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. 52.2). Fluorescein staining is negative.

Causative organisms These include: • • • • • •

Streptococcus pneumoniae Haemophilus influenzae Staphylococcus aureus Streptococcus pyogenes N. gonorrhoeae (a hyperacute onset) Pseudomonas aeruginosa

Diagnosis is usually clinical but a swab should be taken for smear and culture with:2 • hyperacute or severe purulent conjunctivitis

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 52.2).

Clinical features • Diffuse hyperaemia of tarsal or bulbar conjunctivae • Absence of ocular pain, good vision, clear cornea • Infectious conjunctivitis is bilateral (usually) or

Figure 52.2 Acute bacterial conjunctivitis with mucopurulent discharge, no corneal stain

The red and tender eye

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Table 52.2 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— Purulent, gritty lids stuck in the morning

Normal

No

Normal

Normal

Normal

Viral conjunctivitis

Conjunctiva, lining of lids often follicular (uni or bilateral)

Gritty

Normal

No

Normal

Normal

Normal

Watery

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Allergic (vernal) Conjunctiva, conjunctivitis papillary swellings on lid linings (bilateral)

Gritty— itching

Watery

Normal

No

Normal

Normal

Normal

Contact Conjunctiva hypersensitivity and eyelids (dermatoOedema conjunctivitis)

Itching

Watery

Normal— No may be blurred

Normal

Normal

Normal

No

Normal

No

Normal

Normal

Normal

Yes

Normal

Abnormal Normal

Subconjunctival Beefy red area No haemorrhage fading at edge (unilateral)

Herpes simplex Unilateral— Yes—gritty No, reflex Blurred, keratitis circumcorneal lacrimation but Dendritic variable, ulcer depends on site Corneal ulcer

Unilateral— Yes 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 Diffuse but Yes, severe No, reflex Haloes maximum with lacrimation around circumcorneal nausea lights and vomiting

Yes

Dilated Hazy Absent light reflex

Hard, elevated

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• prolonged infection • neonates

Management Limit the spread by avoiding close contact with others, use of separate towels and good ocular hygiene.

52.3). 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.

Mild cases Mild cases may resolve with saline irrigation of the eyelids and conjunctiva but may last up to 14 days if untreated.7 An antiseptic eye drop such as propamidine isethionate 0.1% (Brolene) 1–2 drops, 6–8 hourly for 5–7 days can be used.

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 preferably7 polymyxin B sulphate 5000 units/mL + gramicidin 25 μg/mL + neomycin 2.5 mg/mL (Neosporin), 1–2 drops hourly, decreasing to 6 hourly as the infection improves Brick red eye—think of chlamydia.

Specific organisms • Pseudomonas and other coliforms: use topical gentamicin and tobramycin. • N. gonorrhoeae: use appropriate systemic antibiotics. • 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.

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.

Figure 52.3 Viral conjunctivitis: watery eye, lid swelling, typical eyelid follicles, associated local lymphadenopathy

Diagnosis is based on clinical grounds and a history of infected contacts. Viral culture and serology can be performed to identify epidemics.

Treatment • Limit cross-infection by appropriate rules of hygiene and patient education. • 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. • 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. 52.4). 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 healing7 • Atropine 1% 1 drop, 12 hourly, for the duration of treatment will prevent reflex spasm of the pupil (specialist supervision) • Debridement by a consultant

The red and tender eye

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• Treat with naphazoline or phenylephrine. • If not responding, refer for possible corticosteroid therapy.

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

Figure 52.4 Herpes simplex keratitis—gritty, watery eye with typical dendritic ulcer, stained with fluorescein

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 pages 1227–8).

Treatment

Take swabs for culture and PCR testing Systemic antibiotic treatment:7 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.

Subconjunctival haemorrhage Subconjunctival haemorrhage, which appears spontaneously, is a beefy red localised haemorrhage with a definite posterior margin (see Fig. 52.5). 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.

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)

Artificial tear preparations may give adequate symptomatic relief.

Contact hypersensitivity 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.

Figure 52.5 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

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.

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Episcleritis and scleritis

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Episcleritis and scleritis present as a localised area of inflammation (see Figs 52.1 and 52.2). 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, herpes zoster and rarely sarcoidosis and tuberculosis.

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• • • • •

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, and more extensive than with episcleritis, being uniform across the eye. The inflamed vessels are larger than the conjunctival vessels.

Management An underlying cause such as an autoimmune condition should be identified. Refer the patient, especially for scleritis. Corticosteroids or NSAIDs may be prescribed.

Uveitis (iritis) The iris, ciliary body and the choroid form the uveal tract, which is the vascular coat of the eyeball.6 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. 52.6). The iris is sticky and sticks to the lens. The pupil may

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Clinical features Episcleritis:

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Figure 52.6 Diagrammatic representation of eye structures involved in inflammatory disorders

become small because of adhesions, and the vision is blurred. 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 Table 52.2. 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. 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.

The red and tender eye

Acute glaucoma 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 • • • • • • • •

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. 52.7). A stye may be confused with a chalazion, orbital cellulitis or dacryocystitis.

Patient >50 years Pain in one eye ± Nausea and vomiting Impaired vision Haloes around lights Hazy cornea Fixed semidilated pupil Eye feels hard

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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.

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 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.

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Figure 52.7 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. 52.8) onto the enclosed eye or by hot compresses. • Perform lash epilation to allow drainage of pus (incise with a D11 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.

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) 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. 52.9). 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.

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Part Three Problem solving in general practice

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Figure 52.10 Blepharitis: common complicating features • seborrhoeic blepharitis • staphylococcal blepharitis • blepharitis associated with rosacea Figure 52.8 Steaming the painful eye: allow steam to rise from a thermos onto the closed eye for 10–15 minutes

Clinical features8 • 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

Management

Figure 52.9 Excision of a meibomian cyst, using a chalazion clamp and curette

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. 52.10). Blepharitis is frequently associated with seborrhoeic dermatitis (especially) and atopic dermatitis, and less so with rosacea.8 There is a tendency to colonisation of the lid margin with S. aureus, which causes an ulcerative infection. The three main types are:

• 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).7 • Systemic antibiotics such as flucloxacillin may be required for lid abscess. • Avoid wearing make-up and contact lenses if inflammation is present.

Dacryocystitis Acute dacryocystitis is infection of the lacrimal sac secondary to obstruction of the nasolacrimal duct

The red and tender eye

at the junction of the lacrimal sac (see Fig. 52.11). 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. • Measures to establish drainage are required eventually. Recurrent attacks or symptomatic watering of the eye are indications for surgery such as dacryocystorhinostomy.

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. 52.12) • • • • •

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Figure 52.12 Important signs in the patient presenting with orbital cellulitis

Figure 52.11 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 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

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In peri-orbital cellulitis, which usually follows an abrasion, there is no pain or restriction of eye movement (see Fig. 52.13). Immediate referral to hospital for specialist treatment is essential for both types. Treatment is 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.7

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 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, 7 and topical aciclovir ointment 4 hourly (see pages 1158–9).

Pinguecula and pterygium 9 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

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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 52.3. Table 52.3 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 • protozoa (e.g. Acanthamoeba) Neurotrophic (e.g. trigeminal nerve defect)

Figure 52.13 Peri-orbital cellulitis following an abrasion to the eye. Treat this as an urgent condition

Immune related (e.g. rheumatoid arthritis) Spontaneous corneal erosion Chronic blepharitis

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 disorders

10

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.

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).

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.

The red and tender eye

• • • •

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), 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 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.11 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

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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 measures12 • • • • • • • •

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

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Part Three Problem solving in general practice

to head injuries or may arise spontaneously, particularly in postmenopausal women. They need radiological investigation. 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 These require urgent referral to an ophthalmologist. Consider: • • • •

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:7 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

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.

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 • 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: — 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.

Practice tips • 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.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Blepharitis, page 156 • ‘Bloodshot’ eye, page 157 • Chalazion (Meibomian Cyst), page 159 • Conjunctivitis, page 160 • Foreign Body in Eye, page 162 • Stye, page 165

The red and tender eye

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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: 113–15. 3 Elkington AR, Khaw PT. ABC of Eyes. London: British Medical Association, 1990: 6–10. 4 Colvin 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 Spicer J (Chair). Therapeutic Guidelines: Antibiotics (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2006: 69–78. 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.

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53

Pain in the face It's as though the devil suddenly thrust red hot electric needles through my right cheek towards my ear. P AT I E N T ( A N O N Y M O U S ), 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, 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 Table 53.1.1 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. • Trigeminal neuralgia is relatively uncommon with a prevalence of 155 persons per million of the population.3 • 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 50.3 and 50.4). • 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.

A diagnostic approach

DESCRIBING

'TIC

DOULOUREUX'

Table 53.1 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 Migrainous neuralgia (cluster headache) Trigeminal neuralgia (tic douloureux)

A summary of the safety diagnostic model is presented in Table 53.2.

Probability diagnosis The commonest cause of facial pain is dental disorders, especially dental caries. Another common cause is sinusitis, particularly maxillary sinusitis.

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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.

Pain in the face

Table 53.2 Pain in the face: diagnostic strategy model Q.

Probability diagnosis

A.

Dental pain: • caries • periapical abscess • fractured tooth

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: • erysipelas • periapical abscess → osteomyelitis • acute sinusitis → spreading infection Temporal arteritis

Q.

Pitfalls (often missed)

A.

TMJ dysfunction

Red flag pointers for pain in the face • • • • •

Maxillary sinusitis

Migraine variants: • facial migraine • chronic paroxysmal hemicrania Eye disorders: • glaucoma • iritis • optic neuritis Chronic dental neuralgia Parotid gland: mumps, cancer, sialectasis Salivary gland: infection, calculus, obstruction Acute glaucoma (upper face) Cranial nerve neuralgias: • trigeminal neuralgia • glossopharyngeal neuralgia Q.

Seven masquerades checklist

A.

Depression

✓

Diabetes

–

Drugs

–

Anaemia

–

Thyroid disorder

–

Spinal dysfunction

✓

UTI

–

Q.

Is the patient trying to tell me something?

A.

Quite probably. Atypical facial pain has underlying psychogenic elements.

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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.

Common pitfalls • Failing to refer unusual or undiagnosed causes of facial pain

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• 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. 53.1) 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 63). 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.

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.

PWFSMBQ BSFB

$

Figure 53.1 Dermatomes of C2 and C3, with the overlap area indicated

Perform a neurological examination on the cranial nerves with special emphasis on the trigeminal, oculomotor and glossopharyngeal nerves.

Investigations 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 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).

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.

Pain in the face

557

Dental disorders Dental caries 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.

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:4 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

Tooth abscess, inflamed wisdom tooth or root canal infection 5 Dental treatment will usually alleviate the problem; however, if severe: amoxycillin 500 mg (o) tds for 5 days

If unresponsive add: metronidazole 400 mg (o) 12 hourly for 5 days

For patients hypersensitive to penicillin: clindamycin 300–450 mg (o) 8 hourly for 5 days

Gingivitis and periodontitis Refer to Chapter 73.

Alveolar osteitis (dry socket) Refer for specialised toileting. This usually heals naturally in 14 days. Antibiotics are of no proven use (see Fig. 53.2).5

Figure 53.2 Dry tooth socket: this is a very painful condition mainly in the lower molar 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.

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 The maxillary sinus is the one most commonly infected.6 It is important to determine whether the sinusitis is caused by stasis following a URTI or acute rhinitis,

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Part Three Problem solving in general practice

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

5

5 ' '

&

'

&

;

; .

.

Suspect bacterial cause if high fever and purulent nasal discharge.

Clinical features (chronic sinusitis) • • • • • •

Vague facial pain Offensive postnasal drip Nasal obstruction Toothache Malaise Halitosis

Figure 53.3 Diagnosing sinus tenderness: T (temporal) and Z (zygoma) represent no sinus bony tenderness, for purposes of comparison

Some simple office tests Diagnosing sinus tenderness7 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. 53.3), 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. Differential tenderness both identifies and localises the main sites of infection (see Fig. 53.3).

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 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 • Analgesics • Antibiotics:5, 8 amoxycillin 500 mg (o) tds for 7 days or (if sensitive to penicillin) doxycycline 100 mg (o) bd for 7 days or

Pain in the face

559

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)6 for 5–10 days only if congestion • Inhalations (a very important adjunct) • Nasal saline irrigation

DPOF
PG
QBQFS

53

Antihistamines and mucolytics are of no proven value.

Invasive methods

WBQPVS

Surgical drainage may be necessary by atrial lavage or frontal sinus trephine.

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-the-counter 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 (see Fig. 53.4) 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 60. 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

JOIBMBOU

Figure 53.4 Method of inhalation for sinusitis

may respond to intranasal corticosteroids. Surgical intervention will benefit chronic recurrence with mechanical blockage.

TMJ dysfunction 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.

Examination • Check for pain and limitation of mandibular movements, especially on opening the mouth. • 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.

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Part Three Problem solving in general practice

Method 1: ‘Chewing’ the piece of soft wood

Injection into the TMJ

• 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.

• Indications: painful rheumatoid arthritis, osteoarthritis or TMJ dysfunction not responding to conservative measures

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.

Method 3: The TMJ ‘rest’ program This program is reserved for an acutely painful TMJ condition. • For eating, avoid opening your mouth wider than the thickness of your thumb and cut all food into small pieces. • Do not bite any food with your front teeth—use small, bite-size pieces. • Avoid eating food requiring prolonged chewing (e.g. hard crusts of bread, tough meat, raw vegetables). • Avoid chewing gum. • Always try to open your jaw in a hinge or arc motion. Do not protrude your jaw. • Avoid protruding your jaw (e.g. talking, applying lipstick). • Avoid clenching your teeth together—keep your lips together and your teeth apart. • Try to breathe through your nose at all times. • Do not sleep on your jaw: try to sleep on your back. • Practise a relaxed lifestyle so that your jaws and face muscles feel relaxed.

Method • The patient sits on a chair, facing away from the therapist. The mouth is opened to at least 4 cm. • The joint line is palpated anterior to the tragus of the ear: this is confirmed by the opening and closing of the jaw. A 25 gauge needle is inserted into the depression above the condyle of the mandible, below the zygomatic arch and one finger breadth (2 cm) anterior to the tragus. The needle is directed inwards and slightly upwards to lie free within the joint cavity. The 1 mL solution containing 0.5 mL of local anaesthetic and 0.5 mL of corticosteroid should flow quite freely.9

Other treatments • 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 (0) 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 73). 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.3 Brief paroxysms of pain, often with associated trigger points, are a feature.

Clinical features • Site: sensory branches of the trigeminal nerve (see Fig. 53.5) 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

Pain in the face

• • • • •

•

• • •

Frequency: variable and no regular pattern Duration: 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 Aggravating factors: trigger points usually in the upper and lower lip, nasolabial fold or lower eyelid (see Fig. 53.6) Relieving factors: nil Associated features: rarely occurs at night; spontaneous remissions for months or years Signs: there are no signs, normal corneal reflex

53

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)4 50 mg (elderly patient) or 100 mg (o) USJHFNJOBM HBOHMJPO

PQUIBMNJD
OFSWF

Figure 53.6 Trigeminal neuralgia: typical trigger points bd initially, gradually increase the dose to avoid drowsiness every 4 days to 200 mg bd (maintenance); testing serum levels is unnecessary; higher dosage may be necessary

Alternative drugs if carbamazepine not tolerated or ineffective (but question the diagnosis if lack of response): gabapentin 300 mg daily initially, then increase phenytoin 300–500 mg daily clonazepam baclofen

Surgery NBYJMMBSZ OFSWF 7

• 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) — thermocoagulation/radiofrequency neurolysis — surgical division of peripheral branches

Glossopharyngeal neuralgia 8, 10 7

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.

7

NBOEJCVMBS
OFSWF

Figure 53.5 Typical cutaneous sensory distribution of the trigeminal nerve and its branches

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• Sites: back of throat around tonsillar fossa and adjacent fauces deep in ear • Radiation: ear canal, neck • Triggers: swallowing, coughing, talking, yawning, laughing • Treatment: as for trigeminal neuralgia

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Migrainous neuralgia (cluster headache) As described in Chapter 57, 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.

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 page 289 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 well-defined edge (see Fig. 53.7). 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 phenoxymethyl penicillin or di/flucloxacillin for 7–10 days.

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.11

Herpes zoster and postherpetic neuralgia Refer to Chapter 115. Herpes zoster may present as hyperaesthesia or a burning sensation in any division of the fifth nerve, especially the ophthalmic division.

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 deep-seated 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.

Treatment Trial of an antidepressant4, e.g.: dothiepin 25–150 mg nocte or amitriptyline 10–150 mg nocte or carbamazepine

Figure 53.7 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 • Possible need for surgical drainage of sinusitis— indications for surgery include failure of appropriate medical treatment, anatomical deformity, polyps, uncontrolled sinus pain6 • Dental root infection causing maxillary sinusitis • Other dental disorders

Pain in the face

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.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Sinusitis, page 148 • Temporomandibular Dysfunction, page 192

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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 Selby G. Trigeminal neuralgia. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 531–3. 4 Mashford ML (Chair). Therapeutic Guidelines: Analgesic (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2002: 298–300. 5 Spicer J (Chair). Therapeutic Guidelines: Antibiotic (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2006: 167–243. 6 Stevens M. The diagnosis and management of acute and chronic sinusitis. Modern Medicine Australia, 1991; April: 16–26. 7 Bridges-Webb C. Diagnosing sinus tenderness. Practice tip. Aust Fam Physician, 1981; 10: 742. 8 Tiller J (Chair). Therapeutic Guidelines: Neurology (Version 3). Melbourne: Therapeutic Guidelines Ltd, 2009: 55–60 9 Corrigan B, Maitland G. Practical Orthopaedic Medicine. Sydney: Butterworths, 1986: 220. 10 Mendelsohn M, Lance J, Wheatley D. Facial pain: how to treat. Australian Doctor, 7 November; 2003: 31–6. 11 Burns R. Pitfalls in headache management. Aust Fam Physician, 1990; 19: 1825.

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Fever and chills Why! the fever itself is nature's instrument. T H O M A S S Y D E N H A M (1624–89), M E D I C A L O B S E R VAT I O N S Although fever is a sign of disease and usually occurs in response to infection (mainly viral), its presence is recognised to play 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

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• 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 , pages 126–8). • 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/rigors 2 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 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

Fever and chills

• 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.

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

• 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 46, page 483.

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 temperature-measuring instrument.

Basic rules of usage

This is a rare hereditary disorder characterised by rapidly developing hyperpyrexia, muscular rigidity and acidosis in patients undergoing major surgery.

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.

Sweats

Oral use

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).

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.

Malignant hyperthermia

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

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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.

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Method 1 Lubricate the stub with petroleum or KY jelly. 2 Insert for 3 cm (1 in) past anal verge. 3 Keep the thermometer between the flexed fingers with the hand resting on the buttocks (see Fig. 54.1).

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 54.1 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.

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

The initial approach is to evaluate the severity of the problem and the nature of the illness. Some infections, particularly bacterial infections, are life-threatening 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 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 54.1. The careful history is mandatory as outlined for FUO. The basic examination and investigations are along similar lines.

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 54.2.

Intermittent fever This is a fever in which the temperature rises for a few hours and then returns to normal (see Fig. 54.2a).

Table 54.1 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

Fever and chills

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In this pattern the fever recurs daily (see Fig. 54.2d). 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 87.1, in Chapter 87.

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Quotidian fever

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: • shutting a child in a car on a hot day • overwrapping a febrile child

Malaria is the classic example: in quartan fever, caused by Plasmodium malariae, 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. Other examples are cytomegalovirus, EBM and various pyogenic infections (e.g. ascending cholangitis).

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.

Remittent fever

It is important to decide whether the child looks well or seriously ill. Identification of the very ill child is presented in Chapter 87. 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 87.1, in Chapter 87.

This is a fever in which the temperature returns towards normal for a variable period but is always elevated (see Fig. 54.2d). 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. 54.2b). 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. 54.2c).

Approach to the febrile infant

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

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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

Red flag pointers for fever • • • • • •

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.

• • • • • • •

Febrile convulsions

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

Refer to page 911.

Fever in the elderly 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.

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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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 54.2).

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 should be examined regularly (as for history taking)

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Table 54.2 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 (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%) Drugs Connective tissue diseases/vasculitides: • rheumatic fever • rheumatoid arthritis • SLE • polyarteritis nodosa/Wegener granulomatosis • giant cell arteritis/polymyalgia Sarcoidosis Inflammatory bowel disease (e.g. Crohn) Factitious (1–5%) Remain unknown (5–25%) Source: After Kumar and Clark16, 17

as physical signs can develop eventually. HIV infection must be excluded. Special attention should be paid to the following (see Fig. 54.3):

• • • • • • • • • • • •

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)

Investigations Basic investigations include: • • • • • • •

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

Further possible investigations: • stool microscopy and culture • culture of sputum (if any) • specific tests for typhoid, EBM, Q fever, brucellosis, psittacosis, cytomegalovirus, toxoplasmosis, syphilis 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

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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

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• Henoch–Schönlein syndrome

Neoplastic disorders (7%) • Leukaemia • Reticulum cell sarcoma • Lymphoma

Inflammatory diseases of the bowel (4%)

Septicaemia

Collagen–vascular disorders (15%)

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:

• Rheumatic arthritis • Systemic lupus erythematosus • Rheumatic fever

• fever • rash (suggestive of meningococcus) • tachycardia

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• 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 + gentamicin 4–6 mg/kg IV (statim). 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 >38ºC or 20/min heart rate >90/min WCC >12 × 109/L or 285 µmol/L—phototherapy • >360 µmol/L—consider exchange transfusion

An example of a normogram is presented in Figure 59.3.

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 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 

exchange transfusion and phototherapy

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.

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. 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.

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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

Jaundice

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.

Clinical features

Infective causes of jaundice

Icteric phase (many patients do not develop 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 59.5. 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.

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Pre-icteric (prodromal) phase: • • • • • • •

• • • •

anorexia, nausea ± vomiting malaise headache distaste for cigarettes in smokers mild fever ± diarrhoea ± upper abdominal discomfort

dark urine pale stools hepatomegaly splenomegaly (palpable in 10%)

Recovery usually in 3–6 weeks. Fulminant hepatitis with liver coma and death may occur but is rare.

Investigations LFTs and viral markers confirm the diagnosis. The antibodies to HAV are IgM, which indicates active 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.

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. • • • • • • • • •

Provide appropriate reassurance and patient education. Rest as appropriate. Follow a fat-free diet. 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.

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

59

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Part Three Problem solving in general practice

Table 59.5 Characteristic profiles of viral hepatitis A–E Characteristic

Hepatitis A

Hepatitis B

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; often subclinical—no jaundice

Mild to severe; jaundice common; arthralgia and rash common

Mild to moderate; often subclinical

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

Mortality

0.1–0.2%

1–3%

1–2%

Variable

Variable; high (10–20%) in pregnant women

Carrier state

No

Yes

Yes

Yes

Uncertain

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) HCV-RNA (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

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 59.6. 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.

Investigations9, 10 The main viral investigation for HBV is HBsAg (surface antigen), which is searched for routinely. If detected,

Jaundice

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 a carrier state (see Fig. 59.4). Hepatitis B carriage is 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.

Table 59.6 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

Monitoring and outcome

Institutionalised intellectually disabled patients

The possible course of events is shown in Figure 59.5. 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.

Intravenous drug users

9, 10

• Negative HBeAg and HBV DNA (with anti-HBe) = resolving, with anti-HBs = full recovery. • Positive HBeAg 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 especially safe sex and sharing needles. Treatment of chronic hepatitis B infection (abnormal LFTs) is with the immunomodulatory and antiviral agents—pegylated

Kidney dialysis patients

59

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

interferon alpha and lamivudine. New approved anti-viral agents are adefovir and entecavir. 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

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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 infection anti-HBc IgG = past infection

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 needlestick 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 page 1023.

Hepatitis C 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. 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 59.6. A liver biopsy is the most reliable way to assess the severity of hepatitis C. A raised ALT level which 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.

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Diagnosis and progress This is by serology: • HCV Ab (anti-HCV) +ve = exposure (current or past) • 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

Treatment5, 12 The current standard treatment for chronic hepatitis C is ribavirin orally daily and pegylated alpha-interferon by weekly SCI. 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 alpha-interferon 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.

Those at increased risk of having hepatitis B and C • Blood transfusion recipients (prior to HBV and HCV testing) • Intravenous drug users (past or present)

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 welldocumented 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

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

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Part Three Problem solving in general practice

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:

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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. 59.7): • gall bladder (asymptomatic up to 75%)—the majority remain here • 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, Table 59.7 Significant causes of cholestasis in adults Intrahepatic Alcoholic hepatitis/cirrhosis Drugs

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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

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

Older patients can present with circulatory collapse and Gram-negative septicaemia. Urgent referral is necessary.

Carcinoma of head of the pancreas 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

Jaundice

• Obstructive jaundice • Pain (over 75%)—epigastric and back • Enlarged gall bladder (50–75%)

Possible features • • • • • •

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. 59.8).

Causes Common: • alcohol excess • chronic viral hepatitis (esp. HBV, HCV)

Others: • • • • • •

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)

Signs • Spider naevi (distribution of superior vena cava)

• • • • • • •

617

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 Portosystemic encephalopathy Hepatoma Kidney failure

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. About 80% respond while 20% develop chronic liver disease.

Primary sclerosing cholangitis 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 cholangiographic findings. There is no specific therapy.

Alcoholic liver disease The main effects of alcohol excess on the liver are: • 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. Non-alcoholic causes include obesity, diabetes mellitus, hypertriglyceridaemia and corticosteroids. A significant number with this very common condition (one in five

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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 pages 118 and 126.

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 102.

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:

Jaundice

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 • • • • • •

619

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Gallstones, page 247 • Hepatitis A, page 131 • Hepatitis B, page 132 • Hepatitis C, page 133

Neonates of HBeAg positive mothers The neonates should have the following: (see page 1023) • hepatitis B immunoglobulin IM within 24 hours of birth • hepatitis B vaccine at birth, 1 month and 6 months

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.

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 Shenfield G (Chair). Therapeutic Guidelines: Gastrointestinal (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2006: 85–108. 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. C H A R L E S D I C K E N S (1812–1870), M A R T I N C H U Z Z L E W I T

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 60.1). Nasal discharge is a common and important symptom to evaluate. The characteristics of nasal discharge are summarised in Table 60.2. 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

Table 60.1 Typical symptoms for nasal disorders3 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 smell

Nasal tumour

Blockage, unilateral discharge, epistaxis

Adenoidal hypertrophy

Bilateral blockage, snoring, halitosis

Nasal vestibulitis

Local pain, crusting, malodour

Table 60.2 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

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

620

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branch of the trigeminal nerve (cranial nerve V), detect some noxious odours. The disorders can be classified as:2

Table 60.3 Causes of reduced sense of smell Conductive defects

anosmia—no smell hyposmia—reduced smell hyperosmia—increased sensitivity to odours dysosmia—distortion of smell perception — cacosmia—normal odours seem foul or unpleasant — parosmia—a perverse sense of smell

Head trauma

Disorders of smell can be caused by conductive or sensorineural disturbances or considered as idiopathic (see Table 60.3). Conductive disorders present as anosmia or hyposmia, while sensorineural disorders can present with all of the above disorders.2 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.

Nasal tumour

• • • •

The clinical approach • History: head injury or surgery, recent URTI, drugs, occupation including chemical exposure • 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)

Treatment3, 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:

621

Nasal polyps Septal deviation Rhinitis and sinusitis Rare (not to be missed) 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 • 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 122.

Clinical features Nasal symptoms: • sneezing • nasal obstruction and congestion

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• hypersecretion—watery rhinorrhoea, postnasal drip • reduced sense of smell • itching nose (usually allergic)

Throat symptoms: • dry and sore throat • itching throat

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)

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

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 53 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.

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 (see page 570) • 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’. They occur in patients with all types of rhinitis, but especially in allergic rhinitis (see Fig. 60.1). Polyps usually arise from the middle meatus and turbinates. Symptoms include nasal obstruction, watery discharge, postnasal drip and loss of smell.

Nasal disorders

TJOVTFT

623

Table 60.4 Causes of epistaxis Local causes Idiopathic Intracranial tumours Rhinitis Trauma including nose picking

OBTBM
DBWJUZ QPMZQ
GSPN NBYJMMBSZ
TJOVT

OBTBM
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Figure 60.1 Cross-section of nose, demonstrating origin of nasal polyps 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.

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.

Epistaxis This common emergency should, in some instances, be treated as a life-threatening problem. The common situation is anterior epistaxis 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. Systemic factors include hypertension, atherosclerotic vascular disease, bleeding disorders and the rare hereditary haemorrhagic telangiectasia (see Table 60.4). The secret of good

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

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, Co-Phenylcaine forte spray ± 5% cocaine solution.

Tamponade options (for difficult bleeding) 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 between thumb and finger for 5 minutes • Apply ice packs to bridge of nose

Simple cautery of Little area (see Fig. 60.2) (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:

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BOUFSJPS
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Figure 60.2 Little area on the nasal septum where several blood vessels anastomose. Bleeding is common here, especially in young people

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 mucus 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. 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 pages 1144–5) • 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 disorders

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 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.

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.3 Tips: • X-rays are generally unhelpful unless excluding other facial skeletal injuries. • 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. 60.3). It results from haemorrhage between the two sheets of mucoperiosteum covering the septum. It may be associated with a fracture of the nasal septum. Note: This is a most serious problem as it can develop into a septal abscess. The infection can pass

Nasal fractures3, 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 sport’s field)

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Figure 60.3 Inferior view of nasal cavity showing bilateral swelling of septal haematoma

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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.

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.

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 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. 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 page 290). 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.

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).

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.

Nasal disorders

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 (pages 623–4) 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 72.

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.

Treatment Reassure the parents. • Paracetamol mixture or drops for significant discomfort.

627

• 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.9 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.

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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.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Hay Fever, page 254 • Nosebleed, page 275 • Nose: Stuffy Running Nose, page 274 • Sinusitis, page 148

REFERENCES 1 Kalish L, Da Cruz M. Nasal obstruction. Medicine Today, March 2009; 10(3): 41-52. 2 Beers MH, Porter RS. The Merck Manual of Diagnoses and Therapy (18th edn). New Jersey: Merck Research Laboratories, 2006: 814. 3 Mendelsohn M, Ruhno J. The nose—form and function. Australian Doctor, 2 October 2004: 31. 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 Bochner F (Chair). Australian Medicines Handbook. Adelaide: Australian Medicines Handbook Pty. Ltd, 2006: 366. 9 Hansen G. Practice Tips. Aust Fam Physician, 1982; 11: 867. 10 Oates K, Currow K, Hu W. Child Health: A Practical Manual for General Practice. Sydney: MacLennan & Petty, 2001: 328–30.

Nausea and vomiting

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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

Haematemesis Vomiting of blood. It is presented in Chapter 56. 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.

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

INTERNAL MEDICINE, 1994

— blood = bleeding from oesophagus, stomach or duodenum (mostly) — coffee-grounds = bleeding from stomach or duodenum

Vomiting or emesis is a rather dramatic event with a diverse number of causes. It is usually preceded by nausea. Definitions

OF

The clinical approach History A careful history is essential with an emphasis on drug intake, possible psychogenic factors, including selfinduced 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 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.

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 microscopy and culture of stools radiology of GIT endoscopy

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• oesophageal motility studies • neurological investigation for suspected intracranial pressure (e.g. CT scan, MRI) • drug toxicity studies • biochemistry • cortisol/short synacthen test

Table 61.1 Vomiting: diagnostic strategy model Q. A.

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.

Q. A.

A summary of the diagnostic strategy model is presented in Table 61.1.

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

Q. A.

• 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.

Important warning signs in neonates • • • •

Excessive drooling of frothy secretions from mouth Bile-stained vomitus—always abnormal Delayed passage of meconium (beyond 24 hours) Inguinal hernias

Specific conditions Oesophageal atresia • Vomiting occurs with the first feeding. • There is excessive drooling of frothy secretions from the mouth. • Pass a French gauge 10 catheter through the mouth to aid diagnosis.

Q. A.

Congenital hypertrophic pyloric stenosis • • • • •

Usually sudden onset 3rd–6th week Projectile vomitus Failure to thrive Male:female = 5:1 Gastric peristalsis during test feeding (L → R):

Q. A.

Probability diagnosis All ages: acute gastroenteritis, motion sickness, drugs, various infections Neonates: feeding problems Children: viral infections/fever, otitis media, UTI Adults: gastritis, alcohol intoxication, pregnancy, migraine Serious disorders not to be missed Bowel obstruction: • oesophageal atresia (neonates) • pyloric obstruction 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

REFERENCES 1 2 3

4 5 6

Fry J, Berry H. Surgical Problems in Clinical Practice. London: Edward Arnold, 1987: 38. Coman WB. Neck lumps in adults. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 340–1. Cole IE, Turner J. Neck lumps: clues to the diagnosis and management. Modern Medicine Australia, 1997; April: 37–55. Hughes C, O’Brien C. Neck lumps: how to treat. Australian Doctor, 5 August 2005: 31–8. Larkins R, Smallwood R. Clinical Skills. Melbourne: Melbourne University Press, 1993: 133–4. Stokes K. Lumps in the neck in children. Proceedings notes. Box Hill Hospital Seminar, 1995: 1–2.

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Neck pain We have all heard of the courtiers who mimicked the wry neck of Alexander the Great. W I L L I A M H E B E R D E N (1710–1801) Neck pain is a very common symptom in both sexes at all ages and although most pain is experienced in the posterior aspect of the neck, anterior neck pain can occur from causes that overlap between front and back. The main cause of neck pain is a disorder of the cervical spine, which usually manifests as neck pain but can refer pain to the head, shoulders and chest. Such pain usually originates from the facet (apophyseal) joints but can arise from other musculoskeletal structures, such as the intervertebral discs and the muscles or ligaments (see Fig. 63.1). The other major symptom is limited movement or stiffness. General causes of neck pain are presented in Table 63.1.

Key facts and checkpoints • According to an Australian study, about 18% of people wake with some degree of neck pain and 4% experience neck pain or stiffness.1

• The commonest cause of neck pain is idiopathic dysfunction of the facet joints without a history of injury. • Disorders of the intervertebral discs are common, especially in the lower cervical spine, and may cause unilateral pain, paraesthesia or anaesthesia in the arm. • In a UK study radiological cervical disc degeneration was present in 40% of males and 28% of females2 between 55 and 64 years. • Strains, sprains and fractures of the facet joints, especially after a ‘whiplash’ injury, are difficult to detect and are often overlooked as a cause of persistent neck pain. • Cervical spondylosis is a disorder of ageing: radiological signs occur in 50% of people over the age of 50 and in 75% over the age of 65 years.3 • In cervical spondylosis, osteophytic projections may produce nerve root and spinal cord compression, resulting in radiculopathy and myelopathy respectively.

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Figure 63.1 Transverse section illustrating the functional unit and nervous network of the cervical spine

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Neck pain

Table 63.1 Causes of neck pain (a pathological classification)

Table 63.1 continued Referred cranial

Musculoskeletal/structural

Haemorrhage (e.g. subarachnoid)

Joint dysfunction: • apophyseal • intervertebral disc

Tumour

Muscular/ligamentous strains or sprains Trauma: • ‘whiplash’ • fracture • other disorders Inflammation Osteoarthritis* Rheumatoid arthritis Spondyloarthropathies (e.g. ankylosing spondylitis, psoriasis, reactive arthritis) Polymyalgia rheumatica Thyroiditis Infective Spinal: • osteomyelitis • tuberculosis • herpes zoster Extraspinal: • epidural abscess • cervical adenitis • poliomyelitis • tetanus Extracervical: • meningitis • febrile states (e.g. meningism, malaria) Degenerative Spondylosis* Metabolic Paget disease Neoplasia Benign Malignant Fibromyalgia syndrome Psychogenic Referred visceral Heart: • IHD • pericarditis Oesophagus Lung cancer

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Abscess * Osteoarthritis, or spondylosis, is inflammatory and degenerative.

• Radiculopathy can be caused by a soft disc protrusion (usually unilateral), a hard, calcified lump and osteophytes (may be bilateral). • Cervical disorders are aggravated by vibration (e.g. riding in a motor vehicle). • Always determine the C2, C6 and C7 levels by finding the relevant spinous processes (easily palpable landmarks) prior to palpation. • Palpation of the neck is the cornerstone of cervical management. Palpate gently—the more one presses the less one feels. • Most episodes of neck pain, including acute torticollis, are transient, lasting from about 2 to 10 days. • In one study 70% of people with neck pain who sought medical attention had recovered or were recovering within one month.2 • Effective management of neck pain is based on the theoretical principle that stiff dysfunctional joints are painful and restoration of normal movement may be associated with resolution of pain. • The optimal treatment for dysfunctional joints (without organic disease or radiculopathy) is active and passive mobilisation, especially as exercises.

A diagnostic approach A summary of the safety diagnostic model is presented in Table 63.2.

Probability diagnosis The main causes of neck pain are vertebral dysfunction, especially of the facet joints, and traumatic strains or sprains affecting the musculoligamentous structures of the neck. The so-called myofascial syndrome is mainly a manifestation of dysfunction of the facet joints. Acute wry neck (torticollis), which is quite common, is yet another likely manifestation of apophyseal joint dysfunction. Spondylosis, known also as degenerative osteoarthrosis and osteoarthritis, is also a common cause, especially in the elderly patient. Intervertebral disc disruption is also a relatively common phenomenon in the cervical spine, especially at the lower levels C5–6 and C6–7.4

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Table 63.2 Neck pain: diagnostic strategy model Q.

Probability diagnosis

A.

Vertebral dysfunction Traumatic ‘strain’ or ‘sprain’ Cervical spondylosis

Q.

Serious disorders not to be missed

A.

Cardiovascular: • angina • subarachnoid haemorrhage • arterial dissection Neoplasia: • primary • metastasis • Pancoast tumour Severe infections: • osteomyelitis • meningitis

Angina and myocardial infarction should be considered in anterior neck pain. Other visceral disorders can refer pain to the neck. Arterial dissection of the internal carotid artery or vertebral artery should be kept in mind in patients presenting with acute neck pain, especially without musculoskeletal symptoms or signs. Tumours are relatively rare in the cervical spine but metastases do occur and should be kept in mind, especially with persistent neck pain present day and night. Metastasis to the spine occurs in 5–10% of patients with systemic cancer, making it the second most common neurological complication of cancer. The cervical spine accounts for some 15% of spinal metastases.3 The commonest primary tumours are the breast, prostate or lung. Other primaries include the kidney, thyroid and melanoma.

Vertebral fractures or dislocation Q.

Pitfalls (often missed)

A.

Disc prolapse

Red flag pointers for neck pain

Myelopathy Cervical lymphadenitis Fibromyalgia syndrome Outlet compression syndrome (e.g. cervical rib) Polymyalgia rheumatica Ankylosing spondylitis Rheumatoid arthritis Oesophageal foreign bodies and tumours Paget disease Q.

Seven masquerades checklist

A.

Depression Diabetes

✓ –

Drugs

–

Anaemia

–

Thyroid disorder

✓ Thyroiditis

Spinal dysfunction

✓✓

UTI

–

Q.

Is the patient trying to tell me something?

A.

Highly probable. Stress and adverse occupational factors relevant.

Serious disorders not to be missed Conditions causing neck pain and stiffness may be a sign of meningitis or of cerebral haemorrhage, particularly subarachnoid haemorrhage, or of a cerebral tumour or retropharyngeal abscess.

• • • • • • • • • • •

History of major trauma Age >50 years Constant pain (day and night) Fever >38ºC 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

Neck pain

pain and limited movement. This involves failure to appreciate the value of physical therapy, especially exercise programs, in alleviating the problem. • 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.

• 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?

Seven masquerades checklist

Examination

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.

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:

Psychogenic considerations 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.

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. 39.3: 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? • Do you have trouble reversing your car?

• reproduce the patient’s symptoms • identify the level of lesion or lesions • determine the cause (if possible)

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.

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.

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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. 63.2).

• 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. 63.3). This provides a ready reference for serial assessments. '

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Figure 63.2 Relative sizes of spinous processes of the cervical spine 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°

Figure 63.3 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: • 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 63.3. The dermatomes are illustrated in Figure 63.4.

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.

Neck pain

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Table 63.3 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 — MRI: the investigation of choice for cervical radiculopathy, myelopathy, suspected spinal infection and tumour

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Neck pain in children $

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Figure 63.4 Dermatomes of the upper limb, head and neck

Investigations include: • • • • •

haemoglobin, film and WCC ESR rheumatoid arthritis factor HLA-B27 antigen radiology: — 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)

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 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.

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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 25.1 in Chapter 25 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.

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. • 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.

Neck pain

• Analgesia: — first line: paracetamol 1 g (o) qid — second: paracetamol + codeine — 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 63.5.

B

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)

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 pain7 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) • • • • • C

Cervical spondylosis7

D

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 • • • • • Figure 63.5 Examples of exercises for the neck (a) resisted side bending, (b) rotation, (c) chin retraction • 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

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• • • • • • • • • •

Dull, aching suboccipital neck pain (see Fig. 63.6) 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) 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

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Clinical features

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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

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 self-limiting 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.

Muscle energy therapy

Figure 63.6 Cervical spondylosis: typical pain distribution with direction of movement diagram indicating painful and restricted movements

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. • • • • •

Complications • 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.

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.

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. 63.7a). 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. 63.7b). 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.

Neck pain

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. B

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apophyseal joints appears to be severe, with possible microfractures (not detectable on plain X-ray) and long-term dysfunction. 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 suboccipital 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 63.4. Table 63.4 Complications of whiplash Referred pain (headache, arm pain) Visual problems Vertigo

Figure 63.7 Muscle energy therapy for acute torticollis: (a) isometric contraction phase for problem on the left side, (b) relaxation phase towards the affected (left) side

Dysphagia Depression Compensation neurosis Disc rupture increasing to nerve root pain

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

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.

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• 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

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Figure 63.8 Zone of possible referred pain distribution caused by a cervical disc lesion on the right side

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. 63.8) 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 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. 63.4). 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

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

Neck pain

• Electromyography—may help delineate lesions requiring surgery

Treatment Many patients respond to conservative treatment, especially from a disc prolapse. It is basically a self-limiting disorder—about 10% remain severely disabled.10 bed rest soft cervical collar analgesics (according to severity—see page 391) 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 • 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

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Investigations • MRI scan • CT scan with myelogram (most accurate)

Central cord syndrome 12 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.

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

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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. Pain X-rays 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

Practice tips • ‘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 5th edition: • Exercises for Your Neck, page 173 • Neck: Painful Neck, page 179

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 Corrigan B, Maitland GP. Practical Orthopaedic Medicine. Sydney: Butterworths, 1986: 352. 12 Young D, Murtagh J. Pitfalls in orthopaedics. Aust Fam Physician, 1989; 18: 645–6.

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Shoulder pain 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. M I C H A E L H AY E S 1 9 9 6

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. 64.1), the acromioclavicular (AC) joint or diseased viscera, especially the heart, lungs and sub-diaphragmatic structures.

• •

•

•

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 injuryprone.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.

Note: The term tendonopathy or tendonosis is preferred to tendonitis since it has been shown that overuse tendon conditions generally have a non-inflammatory pathology.

Functional anatomy of the shoulder Figure 64.1 Typical pain zone arising from disorders of the shoulder joint and the lower cervical spine (C5 level)

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

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. 64.2). The glenohumeral joint is a ball and socket 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.2 Excessive friction

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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,3 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 so-called ‘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, bicipital tendonopathy, subacromial bursitis and lesions of the supraspinatus tendon.

Serious disorders not to be missed

A diagnostic approach

Pitfalls

A summary of the safety diagnostic model is presented in Table 64.1.

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. Specific pitfalls include:

Probability diagnosis The commonest causes of pain in the shoulder zone (see Fig. 64.1) 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 various disorders of the tendons comprising the rotator cuff and biceps tendon. Of these, supraspinatus tendon disorders, which include wearing, calcific degeneration and tearing, are the commonest. It is obvious that the supraspinatus tendon is subjected to considerable friction and wear and tear.

As usual it is important to exclude any malignancy or septic infection, be it septic arthritis or osteomyelitis. Lung cancer (Pancoast syndrome) 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. 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.

• 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

Shoulder pain

Table 64.1 Shoulder pain: diagnostic strategy model Q.

Probability diagnosis

A.

Cervical spine dysfunction (referred pain) Rotator cuff tendonopathy ± a tear Adhesive capsulitis Glenoid labral tears

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 64.2.

Bicipital tendonopathy

The clinical approach

Q.

Serious disorders not to be missed

History

A.

Cardiovascular: • angina • myocardial infarction

In analysing the pain pattern it is appropriate to keep the various causes of shoulder pain in mind (see Table 64.3). 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:

Neoplasia: • Pancoast tumour • primary or secondary in humerus Severe infections: • septic arthritis (especially children) • osteomyelitis

stiffness and restriction excessive movement/instability weakness rough versus smooth

Rheumatoid arthritis

• • • •

Q.

Pitfalls (often missed)

Key questions

A.

Polymyalgia rheumatica

• 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) • 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?

Axillary vein thrombosis

Cervical dysfunction Gout/pseudogout Osteoarthritis of acromioclavicular joint Winged scapula—muscular fatigue pain Q.

Seven masquerades checklist

A.

Depression Diabetes

✓ ✓

Drugs

✓

Anaemia

–

Thyroid disorder

rarely

Spinal dysfunction

✓

UTI

–

Q.

Is the patient trying to tell me something?

A.

Shoulder is prone to (uncommonly) psychological fixation for secondary gains, depression and conversion reaction.

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.

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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 63.

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Table 64.2 Common shoulder conditions (after murrell)5 Problem

Structure affected

Typical age group

Symptoms

Instability

Labrum/capsule

15–30

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

65+

Pain, loss of movement

Crepitus

Table 64.3 Causes of shoulder pain (excluding trauma, fractures and dislocations)

Diagnostic pointers

Table 64.3 continued Winged scapula—muscular fatigue pain

Cervical: • dysfunction • spondylosis

Malignant disease: • primary or secondary in humerus • Pancoast (referred from lung)

Cervical radiculopathy

Referred pain Cardiac: • ischaemic heart disease • pericarditis Gall bladder Lung • mediastinum, including oesophagus • diaphragmatic irritation

Polymyalgia rheumatica (bilateral) Acromioclavicular joint: • dysfunction • osteoarthritis Shoulder complex Extracapsular: • subacromial bursitis • rotator cuff disorders: — supraspinatus tendonopathy — infraspinatus tendonopathy — subscapularis tendonopathy • bicipital tendonitis Intracapsular (glenohumeral joint): • adhesive capsulitis: — idiopathic — blunt trauma — diabetes — others • rheumatoid inflammation: — rheumatoid arthritis — ankylosing spondylitis — psoriatic arthropathy • osteoarthritis • avascular necrosis • septic arthritis

Herpes zoster

Examination of the shoulder2,4 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 64.4). A knowledge of the anatomical attachments of the rotator cuff tendons to the head of the humerus (see Fig. 64.3) provides an understanding of the shoulder movements powered by these muscles. With tendon disorders (rotator cuff tendons or biceps) there is painful restriction of movement in one direction, but with capsulitis and subacromial bursitis there is usually restriction in most directions.

Shoulder pain

Table 64.4 Tendon disorders: determining resisted movements Painful resisted movement at shoulder

Affected tendon

1 Abduction

Supraspinatus

2 Internal rotation

Subscapularis Teres minor*

3 External rotation

Infraspinatus Biceps*

4 Adduction

Pectoralis major Latissimus dorsi*

* Lesser role

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

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.

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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

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Abduction 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. 64.4). The commonest cause is supraspinatus tendonopathy. Other causes include infraspinatus tendonopathy and subacromial bursitis (milder degree). • Internal rotation—90° • External rotation—90°

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 movements2 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 64.4). 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

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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 ‘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.

3 Special tests 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,6 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.

ESR (especially for polymyalgia rheumatica) rheumatoid factor serum uric acid (acute pain) ECG 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. Referred causes include: • • • • • •

peptic ulceration diaphragmatic irritation ruptured viscus (e.g. perforated ulcer) intraperitoneal bleeding (e.g. ruptured spleen) pneumothorax myocardial infarction

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

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.7 Refer to Chapter 138. 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 adducted and relieved when

Shoulder pain

abducted. 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.8

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 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.9

Rotator cuff tendonopathy4 Rotator cuff tendonopathy, also referred to as ‘impingement syndrome’, is the commonest cause of shoulder pain. It can be associated with inflammation

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(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.

Supraspinatus tendonopathy Supraspinatus tendonopathy can vary in intensity from mild to extremely severe. The severe cases usually involve calcification (calcific periarthritis) of the tendon 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.4

Treatment10 Systematic reviews to date have a lack of sufficient information to provide conclusive evidence-based recommendations for treatment.11 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

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internally rotating the humerus. This manoeuvre allows the examiner to locate the tendon readily.

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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. 64.5). 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.

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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

Typical pain profile—supraspinatus tendonopathy

Figure 64.5 Injection placement for supraspinatus tendonopathy 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. 3 Calcification of the tendon. This problem usually settles but occasionally surgical intervention is necessary.

Other rotator cuff lesions

Site:

the shoulder and outer border of arm; maximal over deltoid insertion

Radiation:

to elbow

Quality:

throbbing pain, can be severe

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.

Frequency:

constant, day and night

Management

Duration:

constant

Onset:

straining the shoulder (e.g. dog on leash, working under car, fall onto outstretched arm)

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.

Offset:

nil

Aggravation:

heat, putting on shirt, toilet activity, lying on shoulder

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

Method 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 38mm 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 45–50 years Pain on outside hip referred to as far as foot Pain on lying on hip at night Limp

Treatment Figure 66.7 The Patrick (FABERE) test for right-sided hip or sacroiliac joint lesion, illustrating directions of pressure from the examiner

A trial of NSAIDs (weigh the risks) is worthwhile and physiotherapy involving hip-strengthening exercises. Injection therapy is also worthwhile.

Hip, buttock and groin pain

Method of injection

Clinical features

• 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. 66.8). • Inject aliquots of a mixture of 1 mL of long-acting corticosteroid with 5–7 mL of local anaesthetic into the tender area, which usually occupies an area similar to that of a standard marble.

• 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

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Some patients complain of a clunking, clicking or snapping hip. This represents an annoying problem which may be painful.

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 • The gluteus maximus sliding across the greater trochanter • Joint laxity

Treatment Figure 66.8 Injection technique for gluteus medius tendonitis (into area of maximal tenderness)

The injection may be very effective. Follow-up management includes sleeping with a small pillow under the involved buttock, sleeping on a sheepskin 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 may be necessary. Local application of ice and massage therapy may provide relief.

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. 66.9), to a degree that produces a stretching sensation along the lateral aspect of the thigh.

Fascia lata syndrome 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 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.

689

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Figure 66.9 Treatment for the clicking hip

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• This iliotibial stretch should be performed for 1–2 minutes, twice daily.

When to refer • 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

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.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Bursitis and Tendonitis of Outer Hip , page 169

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: 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 (5th edn). Sydney: McGraw-Hill, 2008: 127. 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. W I L L I A M S H A K E S P E A R E (1564–1616), T I M O N 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.

OF

ATHENS

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 67.1. 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.

Infections

A summary of the safety diagnostic model is presented in Table 67.1.

Severe infections are not so common, but septic arthritis and osteomyelitis warrant consideration. Superficial infections such as erysipelas and lymphangitis occur occasionally.

Probability diagnosis

Vascular problems

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.

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.

A diagnostic approach

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Table 67.1 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: • 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 Herpes zoster (early) Greater trochanteric pain syndrome Nerve entrapment ‘Hip pocket nerve’ 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

Q.

Seven masquerades checklist

A.

Depression Diabetes Drugs Anaemia Thyroid disorder Spinal dysfunction UTI

✓ ✓ ✓ (indirect) ✓ (indirect) – ✓✓ –

Q.

Is the patient trying to tell me something?

A.

Quite possible. Common with work-related injuries.

- -

5 -

4

4

4

4

- - 4 -

- -

- -

-

-

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Figure 67.1 Dermatomes of the lower limb, representing approximate cutaneous distribution of the nerve roots

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 67.2. It is important to differentiate vascular claudication from neurogenic claudication (see Table 67.2).

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.

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Figure 67.2 Arterial occlusion and related symptoms according to the level of obstruction

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. 67.3) 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 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

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Table 67.2 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

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. 67.4). 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.

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.

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Figure 67.3 Distribution of pain in the leg from entrapment of specific nerves; the sites of entrapments are indicated by an X

• 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 weightbearing (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).

Figure 67.4 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. Reproduced with permission from C Kenna and J Murtagh. Back Pain and Spinal Manipulation. Sydney: Butterworths, 1989

— Yes: If immediate onset, consider local cause at site of pain (e.g. stress fracture). If delayed onset, consider vascular claudication or neurogenic claudication. • 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.

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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 • 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. 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 page 857).

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 developed countries) and congenital disorders such as sickle-cell anaemia, Gaucher disorder 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 67.3 and 67.4.

Pain in the leg

Nerve root pain 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. 67.1) 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 67.3. A summary of the physical examination findings for the most commonly involved nerve roots is presented in Table 67.3.

Sciatica See Chapter 39. 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 page 391). 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.

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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. 67.4). Another source of referred pain is that caused by compression of a bulging disc against the posterior 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 66). 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.

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

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Table 67.3 Comparison of neurological findings of the neurological levels L3, L4, L5 and S1. Reproduced in part with permission from S Hoppenfeld. Physical Examination of the Spine and Extremities. Norwalk, Ct: Appleton & Lange

Nerve root L3

Pain distribution (see Fig. 67.1) 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

-

L4

Anterior thigh to front of knee

Lower outer aspect of thigh and knee, inner great toe

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-

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)

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S1

Buttock to back Lateral aspect of ankle, foot of thigh and (4th and 5th toes) leg, central calf, lateral aspect of ankle and sole of foot

Plantar flexion of ankle and toes, eversion of foot

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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. 67.3). 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

(see Fig. 67.5a). 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. B

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• 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)

C

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

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Figure 67.5 (a) Anatomy of the tarsal tunnel syndrome, (b) showing injection sites

Symptoms and signs • A burning or tingling pain in the toes and sole of the foot, occasionally the heel • 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.

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Treatment

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• Relief of abnormal foot posture with orthotics • Corticosteroid injection • Decompression surgery if other measures fail

Injection for tarsal tunnel syndrome Using a 23 gauge 32-mm needle, a mixture of triamcinolone 10 mg/mL or 40 mg methylprednisolone in 1% xylocaine or procaine is injected into the tunnel from either above or below the flexor retinaculum. The sites of injection are shown in Figure 67.5b; care is required not to inject the nerve.

Vascular causes of leg pain Occlusive arterial disease Risk factors for peripheral vascular disease (for development and deterioration): • • • • • •

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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. 67.6).

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

Figure 67.6 Common sites of acute arterial occlusion

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.

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. 67.7). Note that the popliteal and posterior tibial pulses are difficult to feel, especially in obese subjects.

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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.

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Listen over abdomen and femoral area for bruits. Note: Neurological examination (motor, sensory, reflexes) is normal unless there is associated diabetic peripheral neuropathy.

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). QPTUFSJPS
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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 60º 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

• 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 • 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. 67.8). 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 67.4.

Intermittent claudication The level of obstruction determines which muscle belly is affected (see Figs 67.2 and 67.7).

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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 ( thigh > buttock

Forefoot, toes, heels

Aggravation

Walking, exercise

Recumbent, walking

Relief

Rest

Hanging foot out of bed; dependency

• Check if patient is taking beta-blockers. • General tests: blood examination, random blood sugar, urine examination, ECG. • Measure blood flow by duplex ultrasound examination or ankle brachial index. • Arteriography should be performed only if surgery is contemplated.

Associations

Beta-blockers

Night cramps

Treatment

Anaemia

Swelling of feet

• General measures (if applicable): control obesity, diabetes, hypertension, hyperlipidaemia, cardiac failure. • Achieve ideal weight. • There must be absolutely no smoking. • Exercise: daily graduated exercise to the level of pain. About 50% will improve with walking; so advise as much walking as possible. • Try to keep legs warm and dry. • Maintain optimal foot care (podiatry). • Drug therapy: aspirin 150 mg daily.

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)

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

Prevention (for those at risk)

Note: • Vasodilators and sympathectomy are of little value. • About one-third progress, while the rest regress or don’t change.5

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When to refer to a vascular surgeon • ‘Unstable’ claudication of recent onset; deteriorating • Severe claudication—unable to maintain lifestyle • Rest pain • ‘Tissue loss’ in feet (e.g. heel crack, ulcers on or between toes, dry gangrenous patches, infection)

Surgery. Reconstructive vascular surgery is indicated for progressive obstruction, intolerable claudication and obstruction above the inguinal ligament: • endarterectomy—for localised iliac stenosis • bypass graft (iliac or femoral artery to popliteal or anterior or posterior tibial arteries)

Percutaneous transluminal dilation. This angioplasty is performed with a special intra-arterial balloon catheter for localised limited occlusions. An alternative to the balloon is laser angioplasty.

Venous disorders

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Table 67.5 Risk factors for varicose veins Female sex Family history Pregnancy Multiparity Age Occupation Diet (low fibre)

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Varicose veins Varicose veins are dilated, tortuous and elongated superficial veins in the lower extremity. The veins are dilated because of incompetence of the valves in the superficial veins or in the communicating or perforating veins between the deep and superficial systems (see Fig. 67.9). The cause is a congenital weakness in the valve and the supporting vein wall but there are several predisposing factors (Table 67.5), the most important being family history, female sex (5:1), pregnancy and multiparity. Previous DVT can also damage valves, especially calf perforators, and cause varicose veins. Dilated superficial veins, which can mimic varicose veins, may be caused by extrinsic compression of the veins by a pelvic or intra-abdominal tumour (e.g. ovarian cancer, retroperitoneal fibrosis). Uncommonly, but importantly, superficial veins dilate as they become collaterals following previous DVT, especially if the ilio-femoral segment is involved.

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Figure 67.9 The common sites of varicose veins

Symptoms Varicose veins may be symptomless, the main complaint being their unsightly appearance. Symptoms include swelling, fatigue, heaviness in the limb, an aching discomfort and itching.

Varicose veins and pain They may be painless even if large and tortuous. Pain is a feature where there are incompetent perforating veins running from the posterior tibial vein to the surface through the soleus muscle. Severe cases lead to the lower leg venous hypertension syndrome6 characterised by pain that is worse after standing, cramps in the leg at night, irritation and pigmentation of the skin, swelling of the ankles and loss of skin features such as hair. A careful history will usually determine if the aching is truly due to varicose veins and not to transient or cyclical oedema, which is a common condition in women.7 The complications of varicose veins are summarised in Table 67.6.

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Table 67.6 Complications of varicose veins Superficial thrombophlebitis Skin ‘eczema’ (10%) Skin ulceration (20%) Bleeding Calcification Marjolin ulcer (squamous cell carcinoma)

Examination The following tests will help determine the site or sites of the incompetent valves. Venous groin cough impulse. This helps determine long saphenous vein incompetence. Place the fingers over the line of the vein immediately below the fossa ovalis (4 cm below and 4 cm lateral to the pubic tubercle).8 Ask the patient to cough—an impulse or thrill will be felt expanding and travelling down the long saphenous vein. A marked dilated long saphenous vein in the fossa ovalis (saphena varix) will confirm incompetence. It disappears when the patient lies down. Trendelenburg test. In this test for long saphenous vein competence the patient lies down and the leg is elevated to 45º to empty the veins (see Fig. 67.10a). Apply a tourniquet with sufficient pressure to prevent reflux over the upper thigh just below the fossa ovalis. (Alternatively, this opening can be occluded by firm finger pressure, as originally described by Trendelenburg.) The patient then stands. The long saphenous system will remain collapsed if there are no incompetent veins below the level of the fossa ovalis. When the pressure is released the vein will fill rapidly if the valve at the saphenofemoral junction is incompetent (see Fig. 67.10b). This is a positive Trendelenburg test. Note: A doubly positive Trendelenburg test is when the veins fill rapidly before the pressure is released and then with a ‘rush’ when released. This indicates coexisting incompetent perforators and long saphenous vein. Short saphenous vein incompetence test. A similar test to the Trendelenburg test is performed with the pressure (tourniquet or finger) being applied over the short saphenous vein just below the popliteal fossa (see Fig. 67.11). Incompetent perforating vein test. Accurate clinical tests to identify incompetence in the three common sites of perforating veins on the medial aspect of the leg, posterior to the medial border of the tibia, are difficult to perform. The general appearance of the leg and palpation of the sites give some indication of incompetence here.

Figure 67.10 (a) Trendelenburg test: the leg is elevated to 45º to empty the veins and a tourniquet applied

Note: Venous duplex ultrasound studies will accurately localise sites of incompetence and determine the state of the functionally important deep venous system.

Figure 67.10 (b) Trendelenburg test: test for competence of long saphenous venous system (medial aspect of knee)

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Superficial thrombophlebitis Clinical features • Usually occurs in superficial varicose veins • Presents as a tender, reddened subcutaneous cord in leg • Usually localised oedema • No generalised swelling of the limb or ankle • Requires symptomatic treatment only (see below) unless there is extension above the level of the knee when there is a risk of pulmonary embolism • Venous duplex scan is diagnostic and also determines: — extent of superficial thrombosis, and — if coexisting, unsuspected DVT is present

Treatment The objective is to prevent propagation of the thrombus by uniform pressure over the vein.

Figure 67.11 Testing for competence of the short saphenous vein

• Cover whole tender cord with a thin foam pad. • Apply a firm elastic bandage (preferable to crepe) from foot to thigh (well above cord). • Leave pad and bandage on for 7–10 days. • Bed rest with leg elevated if severe, otherwise keep active. • Prescribe a NSAID (e.g. indomethacin, for 10 days).

Note:

Prevention • Maintain ideal weight. • Eat a high-fibre diet. • Rest and wear supportive stockings if at risk (pregnancy, a standing occupation).

Treatment • Keep off legs as much as possible. • Sit with legs on a footstool. • Use supportive stockings or tights (apply in morning before standing out of bed). • Avoid scratching itching skin over veins.

Compression sclerotherapy • Use a small volume of sclerosant (e.g. sodium tetradecyl sulphate—Fibro-vein 3%). • It is ideal for smaller, isolated veins, particularly below the knee joint.

Surgical ligation and stripping • This is the best treatment when a clear association exists between symptoms and obvious varicose veins (i.e. long saphenous vein incompetence). • Remove obvious varicosities and ligate perforators.

Note: Surgery for varicose veins may not relieve heavy, aching legs.

• No anticoagulants are required. • The traditional glycerin and ichthyol dressings are still useful. • Consider association between thrombophlebitis and deep-seated carcinoma. • If the problem is above the knee, ligation of the vein at the saphenofemoral junction is indicated.

Deep venous thrombosis Refer to Chapter 135—Thrombosis and thromboembolism.

Iliofemoral thrombophlebitis (phlegmasia dolens)9 This rare but life-threatening condition is when an extensive clot obstructs the iliofemoral veins so completely that subcutaneous oedema and blanching occurs. This initially causes a painful ‘milky white leg’, previously termed phlegmasia alba dolens (used to be seen in late pregnancy or early puerperium). It may deteriorate and become cyanotic—phlegmasia cerulea dolens—representing incipient venous infarction. Massive iliofemoral occlusion is an emergency as such patients may develop ‘shock’, gangrene and pulmonary embolus.

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Other painful conditions Cellulitis and erysipelas The causative organisms are Streptococcus pyogenes (commonest) and Staphylococcus aureus. Others include Haemophilus influenzae, Aeromonas and fungal infection (especially in the immunocompromised). Predisposing factors include cuts, abrasions, ulcers, insect bites, foreign matter, IV drug use, and skin disorders such as eczema and tinea pedis of toe webs. • • • •

Rest in bed. Elevate limb (in and out of bed). Use aspirin or paracetamol for pain and fever. Wound cleansing and dressing with non-sticking saline dressings.

Streptococcus pyogenes (the common cause)11 • If S. pyogenes confirmed: Phenoxymethyl penicillin 500 mg(o) 6 hourly for 10 days • If organism doubtful: flu/dicloxacillin 500 mg (o) 6 hourly for 7–10 days • If penicillin hypersensitive/allergic: cephalexin 500 mg (o) 6 hourly or (if severe) cephalazolin 2 g IV 6 hourly

Staphylococcus aureus10 • Severe, may be life-threatening: flucloxacillin/dicloxacillin 2 g IV 6 hourly for 7–10 days • Less severe: flucloxacillin/dicloxacillin 500 mg (o) 6 hourly for 7–10 days or cephalexin 500 mg (o) 6 hourly

Furuncle (boil) of groin A painful furuncle caused by S. aureus in the hairy area of the groin is common. The aim is to treat conservatively. • Localised: — local antiseptics — hot compresses — drain when ‘ripe’ • Deep/extensive: — dicloxacillin 500 mg (o) 6 hourly for 5–7 days — drain when ‘ripe’, not before

Nocturnal muscle cramps Note: Treat cause (if known)—tetanus, drugs, sodium depletion, hypothyroidism, hypocalcaemia, pregnancy.

Physical measures • Muscle stretching and relaxation exercises: calf stretching for 3 minutes before retiring,11 then rest in chair with the feet out horizontal to the floor with cushion under tendoachilles for 10 minutes. • Massage and apply heat to affected muscles. • Try to keep bedclothes off feet and lower part of legs—a doubled-up pillow at the foot of the bed can be used.

Medication for idiopathic cramps • Tonic water before retiring may help. • Drug treatment: Consider: biperiden 2–4 mg nocte magnesium co tablets (e.g. Crampeze)

Quinine sulphate may be helpful but is not recommended because of the incidence of thrombocytopenia.12

Roller injuries to legs A patient who has been injured by a wheel passing over a limb, especially a leg, can present a difficult problem. A freely spinning wheel is not so dangerous, but serious injuries occur when a non-spinning (braked) wheel passes over a limb and these are compounded by the wheel then reversing over it. This leads to a ‘degloving’ injury due to shearing stress. The limb may look satisfactory initially, but skin necrosis may follow. • Admit to hospital for observation. • Fasciotomy with open drainage may be an option for a compartment syndrome. • Surgical decompression with removal of necrotic fat is often essential. • Rehydrate the patient and monitor renal function.

When to refer • The sudden onset of pain, pallor, pulselessness, paralysis, paraesthesia and coldness in the leg • Worsening intermittent claudication • Rest pain in foot • Presence of popliteal aneurysm • Superficial thrombophlebitis above knee • Evidence of DVT • Suspicion of gas gangrene in leg • Worsening hip pain • Evidence of disease in bone (e.g. neoplasia, infection, Paget disease) • Severe sciatica with neurological deficit (e.g. floppy foot, absent reflexes)

Pain in the leg

Practice tips • Always X-ray the legs (including hips) of a patient complains of unusual deep leg pain, especially a child. • Pain that does not fluctuate in intensity with movement, activity or posture has an inflammatory or neoplastic cause. • Hip disorders such as osteoarthritis and slipped femoral epiphysis can present as pain in the knee (usually medial aspect). • Consider retroperitoneal haemorrhage as a cause of acute severe nerve root pain, especially in people on anticoagulant therapy. • Avoidance of amputation with acute lower limb ischaemia depends on early recognition (surgery within 4 hours—too late if over 6 hours).

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Cramp, page 227 • Deep Vein Thrombosis, page 229 • Sciatica, page 186

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REFERENCES 1 House AK. The painful limb: is it intermittent claudication? Modern Medicine Australia, 1990: November; 16–26. 2 Tunnessen WW. Signs and Symptoms in Paediatrics (2nd edn). Philadelphia: Lippincott, 1988: 483. 3 Hart FD. Practical Problems in Rheumatology. London: Dunitz, 1983: 120. 4 Bates B. A Guide to Physical Examination and History Taking (5th edn). New York: Lippincott, 1991: 450. 5 Fry J, Berry H. Surgical Problems in Clinical Practice. London: Edward Arnold, 1987: 125–34. 6 Ryan P. A Very Short Textbook of Surgery (2nd edn). Canberra: Dennis & Ryan, 1990: 61. 7 Hunt P, Marshall V. Clinical Problems in General Surgery. Sydney: Butterworths, 1991: 172. 8 Davis A, Bolin T, Ham J. Symptom Analysis and Physical Diagnosis (2nd edn). Sydney: Pergamon, 1990: 179. 9 Colucciello SA. Evaluation and management of deep venous thrombosis. Primary Care Rep, 1996; 2(12): 105. 10 Spicer J (Chair). Therapeutic Guidelines: Antibiotic (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2005: 275–6. 11 Murtagh JE. Practice Tips (5th edn). Sydney: McGraw-Hill, 2008: 228–9. 12 Mashford L (Chair). Therapeutic Guidelines: Analgesic (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2007.

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The painful knee The human knee is a joint and not a source of entertainment. P E R C Y H A M M O N D , 1912, R E V I E W The knee, which is a gliding hinge joint, is the largest synovial joint in the body. Its small area of contact of the bone ends at any one time makes it dependent on ligaments for its stability. Although this allows a much increased range of movement it does increase the susceptibility to injury, particularly from sporting activities. Finding the cause of a knee problem is one of the really difficult and challenging features of practice. It is useful to remember that peripheral pain receptors respond to a variety of stimuli. These include inflammation due either to inflammatory disorders or chemical irritation such as crystal synovitis, traction pain (e.g. trapped meniscus stretching the capsule), tension on the synovium capsule (e.g. effusion or haemarthrosis), and impact loading of the subchondral bone.

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•

•

•

Key facts and checkpoints

•

• Disorders of the knee account for about one presentation per 50 patients per year.1 • The commoner presenting symptoms in order of frequency are pain, stiffness, swelling, clicking and locking.1 • The age of presentation of a painful knee has varied significance as many conditions are age-related. • Excessive strains across the knee, such as a valgusproducing force, are more likely to cause ligament injuries, while twisting injuries tend to cause meniscal tears. • A ruptured anterior cruciate ligament (ACL) is a commonly missed injury of the knee.2 It should be suspected with a history of either a valgus strain or a sudden pivoting of the knee, often associated with a cracking or popping sensation. It is often associated with the rapid onset of haemarthrosis or inability to walk or weight bear. • A rapid onset of painful knee swelling (minutes to 1–4 hours) after injury indicates blood in the joint— haemarthrosis. • Swelling over 1–2 days after injury indicates synovial fluid—traumatic synovitis. • Any collateral ligament repair should be undertaken early but, if associated with ACL injuries, early surgery may result in knee stiffness. Thus, surgery is often delayed. With isolated ACL ruptures, early

•

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reconstruction is appropriate in the high-performance athlete; otherwise, delayed reconstruction is appropriate if there is clinical instability.3 Acute spontaneous inflammation of the knee may be part of a systemic condition such as rheumatoid arthritis, rheumatic fever, gout, pseudogout (chondrocalcinosis), a spondyloarthropathy (psoriasis, ankylosing spondylitis, reactive arthritis, bowel inflammation), Lyme disease and sarcoidosis. Consider Osgood–Schlatter disorder (OSD) in the prepubertal child (especially a boy aged 10–14) presenting with knee pain. Disorders of the lumbosacral spine (especially L3 to S1 nerve root problems) and of the hip joint (L3 innervation) refer pain to the region of the knee joint. If infection or haemorrhage is suspected the joint should be aspirated. The condition known as anterior knee pain is the commonest type of knee pain and accounts for at least 11% of sports-related musculoskeletal problems. The prime cause of this is patellofemoral dysfunction pain. It is a benign condition with a good prognosis.

The knee and referred pain—key knowledge Pain from the knee joint Disorders of the knee joint give rise to pain felt accurately at the knee, often at some particular part of the joint, and invariably in the anterior aspect, very seldom in the posterior part of the knee. An impacted loose body complicating osteoarthritis and a radial tear of the lateral meniscus4 are the exceptional disorders liable to refer pain proximally and distally in the limb, but the problems obviously originate from the knee.

Pain referred to the knee Referred pain to the knee or the surrounding region is a time-honoured trap in medicine. The two classic problems are disorders of the hip joint and lumbosacral spine. • The hip joint is mainly innervated by L3, hence pain is referred from the groin down the front and

The painful knee

medial aspects of the thigh to the knee (see Fig. 68.1). Sometimes the pain can be experienced on the anteromedial aspect of the knee only. It is not uncommon for children with a slipped upper femoral epiphysis to present with a limp and knee pain. • Knee pain can be referred from the lumbosacral spine. Patients with disc lesions may notice that sitting, coughing or straining hurts the knee, whereas walking does not.

L3 nerve root pressure from an L2–3 disc prolapse (uncommon) and L4 nerve root pain will cause anteromedial knee pain; L5 reference from an L4–5 disc prolapse can cause anterolateral knee pain, while S1 reference from an L5–S1 prolapse can cause pain at the back of the knee (see Fig. 68.1).

syndromes, such as the synovial plica syndrome, patellar tendonopathy and infrapatellar fat-pad inflammation (see Fig. 68.2). Low-grade trauma of repeated overuse, such as frequent kneeling, may cause prepatellar bursitis known variously as ‘housemaid’s knee’ or ‘carpet layer’s knee’. Infrapatellar bursitis is referred to as ‘clergyman’s knee’. Osteoarthritis of the knee, especially in the elderly, is a very common problem. It may arise spontaneously or be secondary to previous trauma with associated internal derangement and instability. The most common overuse problem of the knee is the patellofemoral joint pain syndrome (often previously referred to as chondromalacia patellae).

A diagnostic approach

Serious disorders not to be missed

A summary of the safety diagnostic model is presented in Table 68.1.

Probability diagnosis A UK study1 highlighted the fact that the commonest cause of knee pain is simple ligamentous strains and bruises due to overstress of the knee or other minor trauma. Traumatic synovitis may accompany some of these injuries. Some of these so-called strains may include a variety of recently described

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Neoplasia in the bones around the knee is relatively uncommon but still needs consideration. The commonest neoplasias are secondaries from the breast, lung, kidney, thyroid and prostate. Uncommon examples include osteoid osteoma, osteosarcoma and Ewing tumour (more likely in younger people). Septic arthritis and infected bursitis are prone to occur in the knee joint, especially following contaminated lacerations and abrasions. Septic arthritis from bloodborne infection can be of the primary type in children, where the infection is either staphylococcal or due to Haemophilus influenzae, or gonococcal arthritis in adults. Rheumatic fever should be kept in mind with a fleeting polyarthritis that involves the knees and then affects other joints. Inflammatory disorders such as spondyloarthropathies, sarcoidosis, chondrocalcinosis (a crystal arthropathy due to calcium pyrophosphate dihydrate in the elderly), gout and juvenile chronic arthritis have to be considered in the differential diagnosis.

Red flag pointers for knee pain

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Acute swelling with or without trauma Acute or acute on chronic erythema Systemic features (e.g. fever) in absence of trauma Unexplained chronic, persistent pain

Pitfalls

Figure 68.1 Possible area of referred pain from disorders of the hip joint

There is a myriad of pitfalls in knee joint disorders, often arising from ignorance, because there is a myriad of problems that are difficult to diagnose. Fortunately, many of these problems can be diagnosed by X-ray. A particular trap is a foreign body, such as a broken needle acquired by kneeling on carpet. The presence of a spontaneous effusion demands careful attention because it could represent a rheumatic

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Table 68.1 The painful knee: diagnostic strategy model QBUFMMPGFNPSBM
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Q.

Probability diagnosis

A.

Ligament strains and sprains ± traumatic synovitis Osteoarthritis Patellofemoral syndrome Prepatellar bursitis

Q.

Serious disorders not to be missed

A.

Acute cruciate ligament tear Vascular disorders: • deep venous thrombosis • superficial thrombophlebitis Neoplasia: • primary in bone • metastases Severe infections: • septic arthritis • tuberculosis Rheumatoid arthritis Juvenile chronic arthritis Rheumatic fever

Q.

Pitfalls (often missed)

A.

Referred pain: back or hip Foreign bodies Intra-articular loose bodies Osteochondritis dissecans Osteonecrosis Osgood–Schlatter disorder Meniscal tears Fractures around knee Pseudogout (chondrocalcinosis) Gout → patellar bursitis Ruptured popliteal cyst Rarities: • sarcoidosis • Paget disease • spondyloarthropathy

Q.

Seven masquerades checklist

A.

Depression Diabetes Drugs Anaemia Thyroid disorder Spinal dysfunction UTI

✓ ✓ (indirect) – – ✓ –

Q.

Is the patient trying to tell me something?

A.

Psychogenic factors relevant, especially with possible injury compensation.

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Figure 68.2 Lateral view of knee showing typical sites of various causes of knee pain

disorder or conditions such as osteochondritis dissecans (more common in the young) or osteonecrosis of the femoral condyle (a necrotic problem in the elderly) and perhaps a subsequent loose body in the joint. A ruptured Baker cyst will cause severe pain behind the knee and can be confused with deep venous thrombosis. It is important to bear in mind complications of varicose veins, which can cause pain or discomfort around the knee joint.

General pitfalls • Overlooking referred pain from the hip or low back as a cause of knee pain • Failing to realise that meniscal tears can develop due to degeneration of the menisci with only minimal trauma • Failing to X-ray the knee joint and order special views to detect specific problems, such as a fractured patella or osteochondritis dissecans

Ottawa knee rules for X-ray of an injured knee • • • • •

Patient aged 55 years or more Isolated tenderness of the patella Tenderness at the head of the fibula Inability to flex to 90° Immediate inability to weight bear and in the emergency room (four steps: unable to transfer weight twice onto each lower limb regardless of limping).

The painful knee

Furthermore, a knee X-ray may be indicated following blunt trauma or a fall-type injury if the patient is: • 50 years • unable to take four weight-bearing steps in front of the clinician5

Seven masquerades checklist Of these, spinal dysfunction is the prime association. Diabetes may cause pain through a complicating neuropathy and drugs such as diuretics may cause gout in the elderly.

• How much kneeling do you do? Scrubbing floors, cleaning carpets? • Could there be needles or pins in the carpet? • Does your knee lock or catch? • Does swelling develop in the knee? • Does it ‘grate’ when it moves? • Does the pain come on at rest and is there morning stiffness? • Do you feel pain when you walk on steps or stairs?

Significance of symptoms

Psychogenic considerations

Swelling after injury

Patients, young and old, may complain of knee pain, imaginary or exaggerated, to gain attention, especially if compensation for an injury is involved. This requires discreet clinical acumen to help patients work through the problem.

The sudden onset of painful swelling (usually within 60 minutes) is typical of haemarthrosis (see Figs 68.3 and 68.4). Bleeding occurs from vascular structures such as torn ligaments, torn synovium or fractured bones, while injuries localised to avascular structures such as menisci do not usually bleed. About 75% of cases are due to ACL tears.6 If a minor injury causes acute haemarthrosis suspect a bleeding diathesis or anticoagulant usage. The causes of haemarthrosis are listed in Table 68.2. Swelling of an intermediate rate of onset, stiffness and pain in the order of hours (e.g. 6–24 hours) is typical of an effusion of synovial fluid. Causes include meniscal tears and milder ligamentous injuries. Swelling gradually developing over days and confined to the anterior knee is typical of bursitis such as ‘housemaid’s knee’.

The clinical approach History The history is the key to diagnosis. If any injury is involved careful description of the nature of the injury is necessary. This includes past history. A special problem relates to the elderly who can sustain knee injuries after a ‘drop attack’, but attention can easily be diverted away from the knee with preoccupation with the cerebral pattern. It is relevant to define whether the pain is acute or chronic, dull or sharp, and continuous or recurring. Determine its severity and position and keep in mind age-related causes.

Key questions Related to an injury • • • • • • • • • • • •

Can you explain in detail how the injury happened? Did you land awkwardly after a leap in the air? Did you get a direct blow? From what direction? Did your leg twist during the injury? Did you feel a ‘pop’ or hear a ‘snap’? Did your knee feel wobbly or unsteady? Did the knee feel as if the bones separated momentarily? How soon after the injury did the pain develop? How soon after the injury did you notice swelling? Have you had previous injury or surgery to the knee? Were you able to walk after the injury or did you have to be carried off the ground or court? Does this involve work care compensation?

No history of injury • Does the pain come on after walking, jogging or other activity?

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Figure 68.3 Haemarthrosis in a sportsman presenting with an acutely painful swollen knee

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• avulsed anterior tibial spine • dislocated patella • synovial osteochondromatosis

Pseudo-locking: • • • • •

patellofemoral disorders first or second degree medial ligament tear strain of ACL gross effusion pain and spasm of hamstrings

Catching ‘Catching’ of the knee implies that the patient feels that something is ‘getting in the way of joint movement’ but not locking. Causes include any of the conditions that cause locking, but a subluxing patella and loose bodies in particular must be considered.

Causes of loose bodies Figure 68.4 Haemarthosis: Surgical release of intraarticular blood under pressure in the knee shown in Figure 68.3 Table 68.2 Causes of haemarthrosis

• Osteochondritis dissecans (usually lateral side of medial femoral condyle) • Retropatellar fragment (e.g. from dislocation of patella) • Dislodged osteophyte • Osteochondral fracture—post injury • Synovial chondromatosis

Torn cruciate ligaments, esp. ACL

Clicking

Capsular tears with collateral ligament tears

Clicking may be due to an abnormality such as patellofemoral maltracking or subluxation, a loose intra-articular body or a torn meniscus, but can occur in normal joints when people climb stairs or squat.

Peripheral meniscal tears Dislocation or subluxation of patella Osteochondral fractures Bleeding disorders (e.g. haemophilia), anticoagulants

Recurrent or chronic swelling This indicates intra-articular pathology and includes: • patellofemoral pain syndrome • osteochondritis dissecans • degenerative joint disease including degenerative meniscus tears • arthritides

Locking Locking usually means a sudden inability to extend the knee fully (occurs at 10–45°, average 30°) but ability to flex fully.7

Causes True locking: • torn meniscus (bucket handle) • loose body (e.g. bony fragment from osteochondritis dissecans) • torn ACL (remnant) • flap of articular cartilage

Anterior knee pain 8 Common causes include: • • • •

patellofemoral syndrome osteoarthritis of the knee patellar tendonopathy osteonecrosis

Lateral knee pain Consider: • osteoarthritis of lateral compartment of knee • lesions of the lateral meniscus • patellofemoral syndrome

Medial knee pain Consider: • osteoarthritis of medial compartment of knee • lesions of the medial meniscus • patellofemoral syndrome

Examination The provisional diagnosis may be evident from a combination of the history and simple inspection of the joint but the process of testing palpation, movements

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(active and passive) and specific structures of the knee joint helps to pinpoint the disorder.

Inspection Inspect the knee with the patient walking, standing erect and lying supine. Get the patient to squat to help localise the precise point of pain. Get the patient to sit on the couch with legs hanging over the side and note any abnormality of the patella. Note any deformities, swelling or muscle wasting. The common knee deformities are genu valgum ‘knock knees’ (see Fig. 68.5a), genu recurvatum ‘back knee’ (see Fig. 68.5b) and genu varum ‘bowed legs’ (see Fig. 68.5c). A useful way of remembering the terminology is to recall that the ‘l’ in valgus stands for ‘l’ in lateral.8 In the normal knee the tibia has a slight valgus angulation in reference to the femur, the angulation being more pronounced in women. B

C

Figure 68.6 Pseudocyst of the lateral meniscus: flex the knees to 45° to force lump (if present) to appear

The test will be negative if the effusion is gross and tense, in which case the patellar tap test (see Fig. 68.8) is used by sharply tapping the lower pole of the patella

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Figure 68.5 Knee deformities; (a) genu valgum (‘knock knees’): tibia deviates laterally from knee, (b) genu recurvatum (‘back knee’), (c) genu varum (‘bowed legs’)

Palpation Palpate the knee generally, concentrating on the patella, patella tendon, joint lines, tibial tubercle, bursae and popliteal fossa. Palpate for presence of any fluid, warmth, swelling, synovial thickening, crepitus, clicking and tenderness. Feel for a popliteal (Baker) cyst in the popliteal fossa. Draw the fingers upwards over the suprapatellar pouch: synovial thickening, a hallmark of chronic arthritis, is most marked just above the patella—it feels warm, boggy, rubbery and has no fluid thrill. Flex the knees to 45° and check for a pseudocyst, especially of the lateral meniscus (see Fig. 68.6).

Figure 68.7 The bulge sign with a knee effusion: fluid bulges into the medial compartment

Fluid effusion The bulge sign: compress the medial side of the joint and evacuate any fluid. The test is positive when the lateral side of the joint is then stroked and the fluid is displaced across the joint, creating a visible bulge or filling of the medial depression (see Fig. 68.7).

Figure 68.8 The patellar tap test

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against the femur with the index finger. A positive tap is when the patella can be felt to tap against the femur and then float free.

Movements Extension: normal is 0–5°. The loss of extension is best measured by lifting the heel off the couch with the knee held down. In the normal knee the heel will lift 2.5–4 cm off the couch, that is, into hyperextension. Flexion (supine or prone): normal to 135°. The normal knee flexes heel to the buttock but in locking due to medial meniscus tears there may be a gap of 5 or more centimetres between the heel and buttock. Rotation: normal 5–10°. Test at 90° with patient sitting over the edge of the couch; rotate the feet with the hand steadying the knee. Note: Normally, no abduction, adduction or rotation of the tibia on the femur is possible with the leg fully extended.

Ligament stability tests Collateral ligaments. Adduction (varus) and abduction (valgus) stresses of the tibia on the femur are applied in full extension and then at 30° flexion with the leg over the side of the couch. With ligament strains there is localised pain when stressed. With a complete (third degree) tear the joint will open out. This end-point feel should be carefully noted: firmness indicates stability, ‘mushiness’ indicates damage (see Fig. 68.9). Cruciate ligaments. Stability of the ACL can be tested with the anterior drawer test. This is done with the patient supine and the knee flexed to 90°. The tibia is pulled forwards off the femur and in the presence of a cruciate ligament injury there will be increased gliding of the tibia on the femur. An aberrant positive sign can occur in the presence of posterior cruciate ligament (PCL) insufficiency, in which case the knee is actually B

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brought back to its normal site from a dropped-back position. This gives the appearance of a positive anterior drawer sign. In that situation, a Lachman test will be negative. In the presence of medial ligament injury, the increased external rotation of the tibia against the femur may add to the positive drawer sign.

Specific provocation tests The simplest menisci function tests are those outlined in Table 68.4 (later in this chapter). • McMurray test. The patient lies on the couch and the flexed knee is rotated in varying degrees of abduction as it is straightened into extension. A hand over the affected knee feels for ‘clunking’ or tenderness. • Apley grind/distraction test. The patient lies prone and the knee is flexed to 90° and then rotated under a compression force. Reproduction of painful symptoms may indicate meniscal tear. Then repeat the rotation under distraction—tests ligament damage. • Patella apprehension test. At 15–20° flexion, attempt to push the patella laterally and note the patient’s reaction. • Patellar tendonopathy. Palpate patellar tendon (refer to see Fig. 68.19, later in this chapter). • Patellofemoral pain test. Refer to Figure 68.18, later in this chapter.

Examine the lumbosacral spine and the hip joint of the affected side.

Measurements Quadriceps. For suspected quadriceps wasting, measure the circumference of the thighs at equal points above the tibial tuberosity. It is helpful to assess quadriceps function by feeling the tone. Static Q angle (see Fig. 68.10). If the Q angle is >15° in men and >19° in women there is a predisposition to patellofemoral pain and instability.9

Investigations Investigation for the diagnosis of knee pain can be selected from:

Figure 68.9 Medial and lateral ligament instability: (a) medial instability of knee joint; (b) lateral instability of knee joint

• 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); weight-bearing views looking for degenerative arthritis — bone scan: for suspected tumour, stress fracture, osteonecrosis, osteochondritis dissecans

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overuse injuries such as patellar tendonopathy and patellofemoral pain syndrome.

First decade 2

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Figure 68.10 The Q angle of the knee gives a measure of patellar alignment

— 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

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. 68.11). On examination, the patella is usually in a high and lateral position. Surgery may be required if symptoms persist.

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) • • • • •

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

Figure 68.11 Lateral subluxation of the patella

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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

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 page 710).

Osgood–Schlatter disorder

Age-related causes of the painful knee are presented in Table 68.3.11

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.

Table 68.3 Age-related causes of painful knee

Clinical features

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

• • • • • • • • •

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

Third decade (20–30 years)

X-ray to confirm diagnosis (widening of the apophysis and possible fragmentation of bone) and exclude tumour or fracture (see Fig. 68.12).

Bursitis

Management

Anserinus tendonopathy

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

Treatment is conservative as it is a self-limiting condition (6–18 months: average 12 months). • 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

Paget disease (femur, tibia or patella) Anserinus bursitis Chondrocalcinosis and gout

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Osteoarthritis of hip (referred pain)

The little athlete 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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Figure 68.12 Features of Osgood–Schlatter disorder

The painful knee

• 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. 68.13). It usually presents as pain and effusion and locking. If the fragment has separated, surgery to reattach it can be contemplated.

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.

Osteonecrosis 7, 16 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. 68.14). 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.

Figure 68.13 Osteochondritis dissecans: on X-ray, sclerosis of the lateral aspect of the medial condyle

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. 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 crystal-associated joint diseases, including monosodium urate (gout), CPPD (pseudogout) and hydroxyapatite (acute calcific periarthritis).

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Figure 68.14 Osteonecrosis: necrosis in the medial femoral condyle can take three months to show radiologically

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Osteochondritis dissecans: adult form 7 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 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 weight-bearing 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. 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 symptoms9: — 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 — 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 Table 68.4 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 68.4) are present.

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 which may result in chronic instability. Chronic instability can result in degenerative joint changes if not dealt with adequately. Early diagnosis is essential but there is a high misdiagnosis rate. Sites of ACL rupture are shown in Figure 68.15.

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)

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Table 68.4 Typical symptoms and signs of meniscal injuries

Mechanism

Medial meniscus tear

Lateral meniscus tear

Abduction (valgus) force

Adduction (varus) force

External rotation of lower leg on femur

Internal rotation of leg on femur

Symptoms 1

Knee pain during and after activity

Medial side of knee

Lateral side of knee

2

Locking

Yes

Yes

3

Effusion

+ or –

+ or –

Medial joint line

Lateral joint line (may be cyst)

Signs 1

Localised tenderness over joint line (with bucket handle tear)

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

• May be associated with collateral ligament tears and meniscus injuries

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 • 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

Method—Lachman test 1 The examiner should be positioned on the same side of the examination couch as the knee to be tested. 2 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. 3 The patient is asked to relax, allowing the knee to ‘fall back’ into the steadying hand and roll slightly into external rotation. 4 The anterior draw is performed with the second hand grasping the proximal tibia from the medial side (see Fig. 68.16) while the thigh is held steady by the other hand. The examiner’s knee can be used to steady the thigh. 5 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.

draw test with the knee at 15–20° of flexion. At 90° of flexion, the draw may be negative but the anterior cruciate torn. 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.

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Method—Pivot shift test • 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.

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.

Management 17

Figure 68.15 Sites of rupture of the anterior cruciate ligament

The management depends on the finding by the surgeon. Surgical repair is reserved for complete ligament tears. This usually involves reconstruction of the ligament using patellar or 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.

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Clinical features

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• 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

The painful knee

Management

Overuse syndromes

• Usually managed conservatively with immobilisation and protection for 6 weeks • Graduated weight-bearing and exercises

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:

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. 68.9a)

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

Complex regional pain syndrome I 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

• 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

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. 68.17).

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). 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

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Treatment

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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. • • • •

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Figure 68.18 Special sign of the patellofemoral pain syndrome

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Figure 68.17 Typical painful areas around the knee for overuse syndromes: (a) anterior aspect, (b) medial aspect

Patellar tendonopathy (‘jumper’s knee’) ‘Jumper’s knee’, or patellar tendonopathy (see Fig. 68.2, 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 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 68.18. • 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).

• • • •

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.

The painful knee

• 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. 68.19). • Compare with the normal side. • Very sharp pain is usually produced in the patient with patellar tendonopathy.

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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.

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 68.19 Patellar tendonopathy: method of palpation

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 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 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

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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 longacting 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 means that surgical intervention is required.

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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 patellar bursitis and can be involved with inflammatory disorders or infection. Treatment is also the same.

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. 68.2, 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. 68.2, 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.

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) • 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 36) 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. 68.20) or hemiarthroplasty, especially for the medial compartment with focal arthritis and varus deformity

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.

The painful knee

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 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).

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• 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. 68.21). • 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).

When to refer BDSZMJD
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Figure 68.20 Total joint replacement of knee

• 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

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. • 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.

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Figure 68.21 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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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. • 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.

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Baker’s Cyst, page 167 • Exercises for Your Knee, page 171 • Knee: Anterior Knee Pain, page 178 • Osgood–Schlatter Disorder, page 68

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. 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. 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 Mashford ML (Chair). Therapeutic Guidelines: Analgesic (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2002: 149–52. 19 Fricker P. Anterior knee pain. Aust Fam Physician, 1988; 17: 1055–6.

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. T H O M A S S Y D E N H A M (1624– 8 9 ) 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. The main causes of foot pain are presented in Table 69.1.1

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 safety diagnostic model is presented in Table 69.2.

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 page 718.

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 trivial) and prolonged immobilisation. Complex regional pain syndrome I usually lasts 2 years and recovery to normality usually follows.

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Table 69.1 Causes of foot pain (after Johnson)1

General Arthritis—OA, gout, RA, seronegative spondyloarthropathies

Table 69.2 The painful foot and ankle: diagnostic strategy model Q. A.

Diabetes—neuropathy [sensory (Charcot), motor, autonomic, single nerve], sepsis, vasculopathy Peripheral neuropathy—alcohol, vitamin B12 deficiency Vascular—arteriosclerosis (claudication, gangrene), hemiplegia, Raynaud phenomenon, complex regional pain syndrome I Infections—cellulitis, septic arthritis, TB, actinomyces

Q. A.

Other: Paget disease of bone, osteoid osteoma, hypermobility syndrome (including Marfan) Ankle and hindfoot Tendoachilles (bursitis, tendonopathy, tear), posterior tibial tendonopathy, rupture or subluxation, plantar fasciitis, sprain, bruised heel, phlebitis, cellulitis Midtarsal Acute or chronic foot strain, synovitis of subtaloidtarsal coalition, hypomobility of transverse tarsal joints, osteochondritis of navicular (Kohler), dorsal exostosis, peroneus brevis tendonopathy, flexor hallucis longus tendonopathy Forefoot Bunion, bunionette, Tailor bunion, intermetatarsal bursitis, traumatic synovitis of MTP joint, sesamoiditis, march fracture, Freiberg disorder

Q. A.

Toes Hallux valgus, hallux rigidus, varus little toe, mallet toe, clawed toe, corn, wet corn, ingrown toenail, onychogryphosis, subungual exostosis, deep peroneal nerve entrapment, digital nerve entrapment (Morton neuralgia) Sole Callus, plantar wart, epidermoid cyst, foreign body, tarsal tunnel syndrome, Dupuytren (Ledderhose) contracture

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.

Q. A.

Osteoid osteoma Osteoid osteomas are rare but important little ‘brain teasers’ of benign tumours that typically occur in older

Q. A.

Probability diagnosis 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 Serious disorders not to be missed 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 Pitfalls (often missed) Foreign body (especially children) Gout: • Morton neuroma • tarsal tunnel syndrome • deep peroneal nerve Chilblains Stress fracture (e.g. navicular) Erythema nodosum Rarities: • spondyloarthropathies • osteochondritis: navicular (Köhler), metatarsal head (Freiberg), calcaneum (Sever) Glomus tumour (under nail) Paget disease Seven masquerades checklist ? Depression ✓ Diabetes ✓ Drugs Anaemia ? Thyroid disorder – Spinal dysfunction ✓ UTI – Is the patient trying to tell me something? A non-organic cause warrants consideration with any painful condition.

Pain in the foot and ankle

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 67, 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.

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. • 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

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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, 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

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— 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

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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 fingerpointing sign). • What happened immediately after the injury? • Were you able to walk straight away? • What happened when you cooled off?

Figure 69.1 Dorsi-flexion and plantar-flexion of the ankle joint

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 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. 69.1) • Inversion and eversion of hindfoot (mainly subtalar joint)—hold heel and abduct and adduct (see Fig. 69.2)

Figure 69.2 Testing inversion and eversion of the hindfoot • 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. 69.3) • test other joints individually (e.g. MTP, midtarsal)

Special tests • Achilles’ tendon, including calf squeeze (Thompson or Simmond test) (see Fig. 137.17 in Chapter 137) • 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

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69 Figure 69.3 Testing (a) eversion and (b) inversion of the forefoot

— 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

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 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 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

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characteristic collapse of the metatarsal head. The treatment is restriction of activity, protective footwear and protective padding.

in Chapter 137. Note the Ottawa rules for taking an X-ray of the ankle in Chapter 138 (see pages 1386–7).

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. 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

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: • note swelling and bruising • palpate over bony landmarks and three lateral ligaments (see Fig. 138.12 at page 1385) • 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 137.

Heel pain Important causes of heel pain in adults (see Fig. 69.4)6 include: • Achilles’ tendon disorders: — tendonopathy/peritendonitis (see Chapter 137) — bursitis: postcalcaneal, retrocalcaneal — tendon tearing (see Chapter 137): 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.

Pain in the foot and ankle

Achilles’ tendonopathy 6 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 • • • • •

Achilles’ tendon bursitis Bursitis can occur at two sites: • posterior and superficial—between skin and tendon • deep (retrocalcaneal)—between calcaneus and tendon (see Fig. 69.4)

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 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) + or − 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

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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 • 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

Signs 8 • 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

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 short course of NSAIDs, are effective for short-term 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

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.

Method 1 Perform a tibial nerve block. (The area of maximal tenderness should be marked prior to nerve block.) 2 When anaesthesia of the heel is present (about 10 minutes after the tibial nerve block), insert a 23 gauge needle with 1 mL of long-acting corticosteroid (e.g. methylprednisolone acetate) perpendicular to the sole of the foot at the premarked site (see Fig. 69.5). Insert the needle until a ‘give’ is felt as the plantar fascia is pierced. 3 Inject half the steroid against the periosteum in the space between the fascia and calcaneus. 4 Reposition the needle to infiltrate into the fascial attachments over a wider area.

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‘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 69.6.

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.

Pain in the foot and ankle

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a ‘sprain’. A history of alcohol consumption or diuretic treatment is relevant.

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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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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

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: • vascular: ischaemic rest pain from small vessel disease, chilblains or other cold reaction, functional vasospasm (Raynaud) • diabetic neuropathy • tarsal tunnel syndrome (see pages 715–6) • 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. 69.7) • Worse with new shoes, especially a change to high heels

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orthotics, including arch supports, to correct any deformity.

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Flat feet (pes planus)

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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 page 875). If painful, treat with exercises and insoles. Refer if concerned. Hind foot fusion can be performed for severe pain.

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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 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 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.

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 strain is based on an exercise program and

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.

Pain in the foot and ankle

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 middle-aged females, in ballet dancers and in those with pes planus with a valgus deformity. The tendon (see Fig. 69.8.), which is an invertor of the foot, is attached to the navicular tubercule.11

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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.

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 Fig. 69.9).5 The single heel raise test is also diagnostic. The most useful investigation is an ultrasound examination. Minor

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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Figure 69.9 Tibialis posterior tendon rupture (right foot): the ‘too many toes’ posterior view

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cases can be treated conservatively with orthotics, but severe problems respond well to surgical correction.

Sesamoiditis14,15 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. 15

Metatarsalgia

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 foot deformities (especially with depression of the transverse arch), 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 fractures16

Tarsals, especially navicular Stress fracture of the navicular, which is a disorder of athletes involved with running sports, presents as poorly localised midfoot pain during weight-bearing. Examination and plain X-ray are usually normal. It is a recently recognised serious disorder due to 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.16

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. The diagnosis is made on clinical grounds. An ultrasound examination may detect a neuroma.

Clinical features • • • •

•

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

Avulsion fracture of base of fifth metatarsal Known also as a Jones fracture, it is usually a traumatic fracture but can be a stress fracture and associated with severe ankle sprains.

March fracture of metatarsal Stress or fatigue fracture of the forefoot usually involves the neck of the second metatarsal (sometimes the third).

• • • •

Usually presents in adults 5 years: flucloxacillin IV for 4–6 days then oral 1000 U/L). A result >125 U/L suggests active disease.6

Note: calcium and phosphate normal. • Plain X-ray: dense expanded bone—best seen in skull and pelvis.

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Note: Can mimic prostatic secondaries so every male Pagetic patient should have a DRE and serum PSA test. • Bone isotopic scans: useful in locating specific areas. • Watch for the uncommon complication of osteogenic sarcoma.

Note: screen siblings and children every 5 years after the age of 40.6 5,6

Treatment

The two major goals are relief of pain and prevention of long-term complication (e.g. deafness, deformities). Localised and asymptomatic disease requires no treatment. Three groups of drugs are currently available: • the calcitonins • the bisphosphonates—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)

Figure 70.2 Paget disease: possible clinical features • 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.

Walking difficulty and leg swelling

• The significance of leg swelling varies according to the age group, to whether it is bilateral or unilateral, and whether the onset is sudden or gradual (see Table 70.2). • 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 serum electrolytes, urea and creatinine blood sugar serum albumin/LFTs TSH level ultrasound (DVT screen) other radiographs (e.g. CT scan, venogram)

Table 70.2 Causes of swollen legs/peripheral oedema7 Physiological Prolonged standing or walking Prolonged sitting (e.g. elderly on long journey) Pregnancy Hot weather Mechanical factors (e.g. constricting garters/ pantyhose) Local disorders Skin (e.g. allergy) Arthritis with particular oedema Infection (e.g. cellulitis, filariasis) Trauma Thrombophlebitis Vascular obstruction: • venous (e.g. DVT, varicose veins) • lymphatic → lymphoedema Generalised disease Cardiac (e.g. CCF) Kidney (e.g. nephrotic syndrome) Hepatic (e.g. cirrhosis) Endocrine: hypothyroidism, Cushing syndrome Other low-protein states

Calf swelling of sudden onset

Drugs

Causes to consider:

NSAIDs, antihypertensives (calcium channel blockers e.g. nifedipine), corticosteroids, glitazones, oestrogens, others

• • • • • •

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 67.

Lipoedema 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 Lymphoedema: primary or secondary Idiopathic (periodic or cyclical) oedema Table 70.3 Swollen legs: diagnostic perspective Q. A.

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

Probability diagnosis Chronic venous insufficiency (varicose veins) Physiological (e.g. dependency)

Q. A.

Must not be missed Deep venous thrombosis Thrombophlebitis

Clinical features • • • • •

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Obstruction from pelvic cancer Q. A.

Pitfalls Drugs (sodium retention) Idiopathic (periodic or cyclical) oedema

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Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Deep Venous Thrombosis, page 229 • Paget’s Disease of Bone, page 181 • Parkinson’s Disease, page 110

REFERENCES 1 2 3 4 5

6

7

8

Horne M. Gait and postural disorders. Monash University Neurology Notes, 1996: 1–4. Kincaid-Smith P, Larkins R, Whelan G. Problems in Clinical Medicine. Sydney: MacLennan & Petty, 1990: 190–4. Paxton G, Munro J (eds). Paediatric Handbook (7th edn). Melbourne: Blackwell Science, 2003: 550–4. Spicer J (Chair). Therapeutic Guidelines: Antibiotic (Version 13). Melbourne: Therapeutic Guidelines Ltd, 2006: 35–6. Ralson D, Langston AL, Reid IR. Pathogenesis and management of Paget Disease of bone. Lancet, 2008; 372 (9633): 155–63. Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 121–6. Diu P, Juergens C. Clinical approach to the patient with peripheral oedema. Medicine Today, October 2009; 10(10): 37–42. Piller N, Birrell S. Lymphoedema: how to treat. Australian Doctor, 6 June 2003: I–VIII.

71

Palpitations 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. H U A N G T I (T H E Y E L L O W E M P E R O R ) (2697–2597 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 safety diagnostic model is presented in Table 71.1, 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 (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

It is also important not to miss: • hypokalaemia • hypomagnesaemia

Pitfalls There are many pitfalls in the diagnosis and management of arrhythmias, especially in the elderly, where

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Table 71.1 Palpitations: diagnostic strategy model Q.

Probability diagnosis

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.

A.

Anxiety

General pitfalls

Premature beats (ectopics) Sinus tachycardia Drugs (e.g. stimulants) Q.

Serious disorders not to be missed

A.

Myocardial infarction/angina Arrhythmias: • ventricular tachycardia • bradycardia • sick sinus syndrome • torsade de pointes

Seven masquerades checklist

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 Drugs (e.g. caffeine, cocaine) Mitral valve disease Aortic incompetence Hypoxia/hypercapnia

Q.

Seven masquerades checklist

A.

Depression

✓

Diabetes

indirect

Anaemia

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 71.2); 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

Rarities: • tick bites (T1–5) • phaeochromocytoma

Drugs

• 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)

✓✓ ✓

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.

✓ ✓

The clinical approach

Spinal dysfunction UTI

possible

Careful attention to basic detail in the history and examination can point the way clearly to the clinical diagnosis.

Thyroid disorder

Q.

Is the patient trying to tell me something?

A.

Quite likely. Consider cardiac neurosis, anxiety.

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

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.

Palpitations

Table 71.2 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

An irregular tapping ‘all over the place’ suggests atrial fibrillation, while an isolated thump or jump followed by a definite pause on a background or 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.

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?

753

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. 71.1). 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 The nature of the pulse, especially the pulse pressure and rhythm, should be carefully evaluated (see Fig. 71.2). 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 prolapse (mid-systolic click; late systolic murmur). Possible signs in the patient presenting with palpitations are shown in Figure 71.3.4

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)

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Part Three Problem solving in general practice







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Figure 71.3 Signs to consider in a patient with palpitations

Palpitations in children Children may complain of palpitations which may be associated with exercise, fever or anxiety. Various arrhythmias can occur with three requiring 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 first-line 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.

71

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Part Three Problem solving in general practice

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Palpitations

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 pages 215–7).

•

Arrhythmias

•

Facts and figures • See Figure 71.4 for tracings of important arrhythmias. • Cardiac arrhythmias account for about 25% of

•

•

757

management decisions in cardiology (see Table 71.3). 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. 71.5). Electrophysiological studies are the gold standard investigation for tachycardias but are rarely needed for diagnosing most arrhythmias.

71

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758

Part Three Problem solving in general practice

Table 71.3 Types of arrhythmias Non-pathological sinus rhythms Sinus arrhythmia

BCOPSNBM DPOEVDUJOH UJTTVF

Sinus bradycardia Sinus tachycardia

CMPDLFE

Pathological bradyarrhythmias Sinus node disease (sick sinus syndrome)

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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 complexes • ventricular tachycardia • ventricular fibrillation • torsade de pointes (twisting of points)

JNQVMTF

Figure 71.5 Diagrammatic mechanism of re-entry tachycardia

• Almost all antiarrhythmic drugs have a proarrhythmic potential (i.e. they may worsen existing arrhythmias or provoke new arrhythmias in some patients) (see Table 71.4). 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. • Advise moderation in consumption of tea, coffee, caffeine-containing soft drinks and alcohol. • Advise about cessation of smoking and other drugs. • • • •

Sinus bradycardia 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 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

Premature (ectopic) complexes Atrial premature complexes • These are usually asymptomatic. • Management is based on reassurance. • Check lifestyle factors such as excess alcohol, caffeine, stress and smoking; avoid precipitating factors.

Palpitations

759

Table 71.4 Electrophysiological classification of common antiarrhythmic drugs (after Vaughan Williams)

Class

Drug

Usual dosage

Common side effects

Ia

Disopyramide

100–200 mg qid

Blurred vision, dry mouth, urinary problems in males (avoid in men >50)

Procainamide

1 g qid IV use

Anorexia, nausea, urticaria

Quinidine

2–3 SR tabs (0.25 g) bd

Diarrhoea, headache, tinnitus

Lignocaine

IV use

Nausea, dizziness, tremor

Ib

Mexiletine

200 mg tid

Nausea, vomiting, tremor, dizziness

Ic

Flecainide

100 mg bd

Nausea, dizziness, rash

II

-blockers

various

Fatigue, insomnia, nightmares, hypotension, bronchospasm Avoid in asthmatics

III

IV

Amiodarone

SVT: 200 mg daily VT: 400 mg daily

Rash, pulmonary fibrosis, thyroid, hepatic and CNS effects

Sotalol

80–160 mg bd

As for -blockers

Verapamil

(SR) 160–480 mg daily

Constipation, dizziness, hypotension

Diltiazem

(CR) 180–360 mg daily

Hypotension, headache

Note: Sotalol is a -blocker and thus is a class II and III agent. All drugs are taken orally unless IV indicated. Adenosine and digoxin are not classified.

• 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 atenolol or metoprolol 25–100 mg (o) daily or verapamil SR 160–480 mg (o) daily

• 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.

Ventricular premature complexes

• 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.

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. • • • • •

Supraventricular tachycardia7

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Part Three Problem solving in general practice

Wolff–Parkinson–White syndrome

Method

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

• Locate the carotid pulse in front of the sternomastoid muscle just below the angle of the jaw (see Fig. 71.6). • 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.

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 • 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). Secondline 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.

In general, right carotid pressure tends to slow the sinus rate and left carotid pressure tends to impair AV nodal conduction.

Precautions In the elderly (risk of embolism or bradycardia).

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. • It tends to fall into one of the ‘three Ps’ patterns: — paroxysmal AF — persistent AF — permanent (chronic) AF

All types appear to have a similar risk for thromboembolism. • Remember to look for the underlying cause: myocardial ischaemia (15% of cases), mitral valve

Prevention To prevent recurrences 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

• • •

•

• • •

•

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 calcium-channel antagonists benefited rate control but verapamil was much less effective than amiodarone at restoring cardiac rhythm.11

Atrial flutter The ECG of atrial flutter has a regular saw-tooth baseline ventricular rate of 150 with narrow QRS complexes. This is a 2:1 AV block. It is often misdiagnosed as SVT. Rarely, conduction occurs 1:1, giving a ventricular rate of 300/min.

Treatment for atrial fibrillation/flutter 8, 9 Best in consultation with a specialist. The treatment needs to control the arrhythmia either as the rate or the rhythm and also from the viewpoint of prophylaxis against thromboembolic complications. The AFFIRM12 study confirmed that there was no statistically significant difference between the rate and rhythm of control groups. However, patients fare marginally better (in terms of mortality) with just rate control rather than trying to get them back into sinus rhythm if they are asymptomatic in atrial fibrillation.

Rate control Rapid, urgent control of ventricular rate digoxin 0.5–1.0 mg (o) immediately then 0.25–0.5 mg (o) every 4–6 hours to maximum of 1.5–2.0 mg in first 24 hours or verapamil 1 mg/min IV up to maximum 15 mg

761

(provided no evidence of heart failure and wellmonitored BP)

Routine control8 digoxin 0.0625–0.25 mg (o) daily according to age, plasma creatinine and digoxin level

Maintenance digoxin (as above) ± verapamil SR 160–480 mg (o) daily or diltiazem CR 180–360 mg (o) daily or atenolol or metoprolol 25–100 mg (o) bd

Rhythm control This should be considered if the patient is symptomatic and the arrhythmia is of recent onset—less than 6 months.

Medical cardioversion Sotalol or amiodarone or flecainide If the rate cannot be well controlled despite maximal medical therapy, consider AV node ablation and a permanent pacemaker. Atrial fibrillation with a rapid ventricular response over a long period gradually causes left ventricular dysfunction.

Electrical DC cardioversion This can be given for first-line treatment or for failed medical conversion.

The use of warfarin in atrial fibrillation8 (Chapter 135) Warfarin is effective in preventing stroke in patients with lone or non-rheumatic atrial fibrillation. The decision to use it or an antiplatelet agent (e.g. aspirin), especially in the younger patient, is difficult and should be made in consultation with a cardiologist. As a general rule, all patients should start on warfarin unless they are 10 episodes per hour—is less common (accounts for

Sleep disorders

767

Table 72.2 Causes of excessive somnolence Inadequate sleep duration Sleep apnoea syndromes Narcolepsy Endocrine (e.g. hypothyroidism) Drug induced Purposeful sleep deprivation CBDL
PG
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Nocturnal myoclonus Bereavement Idiopathic

Management of sleep apnoea 7 Referral to a comprehensive sleep disorder centre especially for sleep polysomnography is advisable if this disorder is diagnosed or suspected. The general principles are as follows:

UPOHVF



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Figure 72.3 Sleep apnoea: obstructed airway when sleeping

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 disease 4 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, 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. 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 77.2.

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?

Urinary disorders

• 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?

Table 77.2 continued Q.

Seven masquerades checklist

A.

Depression

–

Diabetes

–

Drugs

✓ cytotoxics anticoagulants

Anaemia

–

Thyroid disorder

–

Probability diagnosis

Spinal dysfunction

–

Infection: • cystitis/urethrotrigonitis (female) • urethritis (male) • prostatitis (male)

UTI

Table 77.2 Haematuria: diagnostic strategy model Q. A.

✓

Q.

Is the patient trying to tell me something?

A.

Consider artefactual haematuria.

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

Q.

Pitfalls (often missed)

A.

Urethral prolapse/caruncle Pseudohaematuria (e.g. beetroot, porphyria) Benign prostatic hyperplasia Trauma: blunt or penetrating Foreign bodies

• • • • •

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. 77.2). 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 77.3. Kidney enlargement may be due to kidney tumour, hydronephrosis, or polycystic disease. Splenomegaly suggests the possibility of a bleeding disorder. Table 77.3 Differences between spleen and left kidney on abdominal examination

Bleeding disorders Exercise Radiation cystitis Menstrual contamination Rarities: • hydronephrosis • Henoch–Schönlein purpura • bilharzia • polycystic kidneys • kidney cysts • endometriosis (bladder) • systemic vasculitides

809

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

77

810

Part Three Problem solving in general practice

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CMBEEFS … QBMQBCMF … UFOEFSOFTT VSFUISB … DBSVODMF … CMPPE QSPTUBUF … JOGMBNNBUJPO … NBTT

Figure 77.2 Features to consider in the physical examination of the patient with haematuria

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. In women a vaginal examination should be performed to search for possible pelvic masses. The urethral meatus should be inspected to exclude a urethral caruncle 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. Hemastix-affected 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 — 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.

Pseudohaematuria Pseudohaematuria is red urine caused by pigments other than red blood cells that simply stain the culture red. Causes include: • anthocyanins in food (e.g. beetroot, berries) • red-coloured confectionery • porphyrins

Urinary disorders

• 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 cancer

7

Bladder cancer is the seventh most common malignancy, with 90% being transitional cell carcinomas. Other forms include squamous cell carcinoma and adenocarcinoma.

Clinical features • Haematuria • Irritative symptoms: frequency, urgency, nocturia • Dysuria

Diagnosis • Urine cytology: three specimens • Cystoscopy and biopsy • Imaging of upper tracts: IVU, ultrasound, but CT IVU is the gold standard

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

811

resection plus intravesical agents, bladder resection (partial or total) and radio–chemotherapy.

Regular patient surveillance is essential.

Glomerulonephritis8 Glomerulonephritis means kidney inflammation involving the glomeruli. It can be simply classified into: • nephritic syndrome: oedema + hypertension + haematuria • nephrotic syndrome: oedema + hypoalbuminaemia + proteinuria • asymptomatic kidney disease

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.

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

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Diagnosis • GABHS antigens • Blood urea, creatinine, C3&4 (complement), ASOT, DNase B

Treatment • • • • • • • •

Hospital admission Bed rest 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 77.4.

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 >150–300 mg/day • Microalbuminuria 30–300 mg/day • Macroalbuminuria >300 mg/day

Table 77.4 Important causes of proteinuria Transient Contamination from vaginal secretions Urinary tract infection Pre-eclampsia These all require exclusion and follow-up. 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

Urinary disorders

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.

• 2 in 3 (approx.): — idiopathic nephrotic syndrome (based on kidney biopsy) — minimal change disease (commonest) — focal glomerular sclerosis — membranous nephropathy — membranoproliferative glomerulonephritis

Diabetic microalbuminuria

Treatment

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.

• • • • • • •

Urinary incontinence Definitions

Consequences of proteinuria

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.

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 syndrome 8,9 DxT: proteinuria + generalised oedema + waxy pallor = nephrotic syndrome

Clinical features • • • • • • • • •

Proteinuria >3 g/day (3–4+ on dipstick) Swelling of eyelids and face Generalised oedema Hypoalbuminaemia 4.5 mmol/L Waxy pallor Normal BP Dyspnoea Frothy urine

Predisposes to sepsis (e.g. peritonitis, pyelonephritis, thromboembolism).

Causes • 1 in 3 (approx.): — systemic kidney disease (e.g. diabetes)

Referral to renal physician or unit Bed rest Diet: low fluid, high protein, low salt Diuretics Prednisolone Phenoxymethylpenicillin Aspirin

A summary of the types of incontinence and their causes is presented in Table 77.5. 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

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Table 77.5 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

Table 77.6 Drugs that can cause or aggravate incontinence Antihypertensive/vasodilator drugs → stress incontinence: • ACE inhibitors • phenoxybenzamine (Dibenyline) • prazosin • labetalol Bladder relaxants → overflow incontinence: • anticholinergic agents • tricyclic antidepressants Bladder stimulants → urge incontinence: • cholinergic agents • caffeine

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 77.6. 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).

Sedatives → urge incontinence: • antidepressants • antihistamines • antipsychotics • hypnotics • tranquillisers Others → urge incontinence: • alcohol • loop diuretics (e.g. frusemide), other diuretics • lithium 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 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

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) Treatment • Weak pelvic floor—exercises • Obesity—weight reduction • Menopause—HRT/vaginal oestrogen creams • Chronic cough—physiotherapy If urodynamic studies of LUT function show genuine

Urinary disorders

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

Bladder dysfunction (in women during night)

Treatment • neurological signs → neurologist • abnormal voiding pattern → bladder retraining (e.g. void more urine less frequently) 4 Is it voiding dysfunction? • symptoms of voiding difficulty (e.g. frequency, urgency, nocturia, incomplete emptying) • large residual 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

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 drugs12 These may be worth a trial for bladder instability or voiding dysfunction: • • • •

Women with urethral syndrome constantly wake at night with urge to micturate but produce only a small dribble of urine.

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 77.3.

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)

FOUFSPDFMF

Pelvic floor exercises • 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).

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 retraining13 includes getting the patient to delay micturition for 10–15 minutes whenever she wishes to void.

815

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Figure 77.3 Uterovaginal prolapse 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) • Uterine—uterus and cervix descend toward vaginal introitus: — first degree—cervix remains in vagina • • • •

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— 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 page 815). 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 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

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 5th edition: • Incontinence of Urine, page 81

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. 14 Benness C. Uterovaginal prolapse. Medical Observer, 3 June 2005: 29–31. 15 Benness C. Female urinary incontinence. Medical Observer, 25 June 2004: 31–3.

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Visual failure 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

A E G I N A (615–6 9 0 )

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.

• Suspect a macular abnormality where objects look smaller or straight lines are bent or distorted.

Criteria for blindness and driving

• Is the loss unilateral or bilateral? • Is the onset acute, or gradual and progressive?

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. • 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 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 shortsighted (myopic) people.

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:

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 78.1). Treatment for tuberculosis with ethambutol or 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

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Table 78.1 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

Reprinted from Central Nervous System: Clinical Algorithms, published by the BMJ, with permission

• 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.

Perimetry Various defects in the visual fields are depicted in Figure 78.1.

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, cataracts

Visual failure

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Figure 78.1 Diagrammatic representation of important causes of sudden painless loss of vision (right side) and typical defects in the visual fields (left side)

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. 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 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.

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• 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 83.)

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 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.

Visual failure

Presbyopia There is a need for near correction with loss of accommodative power of the eye in the 40s.

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.

Table 78.2 Causes of cataracts Advancing age Diabetes mellitus Steroids (topical or oral) Radiation: long exposure to UV light TORCH organisms → congenital cataracts Trauma Uveitis Dystrophia myotonia Galactosaemia Table 78.3 Progressive bilateral visual loss Globe

• • • • • •

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

Chronic glaucoma Senile cataracts

Retina

Macular degeneration Retinal disease: • diabetic retinopathy • retinitis pigmentosa • choroidoretinitis

Cataracts 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 78.2 and causes of progressive visual loss in Table 78.3. Typical symptoms:

Optic nerve

Optic neuropathies Optic nerve compression (e.g. aneurysm, glioma) Toxic damage to optic nerves

Optic chiasma

Chiasmal compression: pituitary adenoma, craniopharyngioma, etc.

Occipital cortex

Tumours Degenerative conditions

Note: Unilateral causes (e.g. cataract, refractive errors, uveitis, glaucoma, progressive optic atrophy and tumours) can affect the second eye.

The type of visual distortion seen by patients is illustrated in Figure 78.2.

Examination • Reduced visual acuity (sometimes improved with pinhole) • Diminished red reflex on ophthalmoscopy • A change in the appearance of the lens

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,

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Figure 78.2 Blurred vision: appearance of a subject through the eyes of a person with cataracts. Photo courtesy Allergan Pharmaceuticals

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which may be totally obscured by a very dense cataract. The setting up of the ophthalmoscope to examine intraocular structures is illustrated in Figure 78.3.

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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.

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. 78.4). Acute glaucoma, on the other hand, has a relatively rapid onset over a few days.

Clinical features (chronic glaucoma) • Familial tendency • No early signs or symptoms

Figure 78.4 Typical visual field loss for chronic simple glaucoma; a similar pattern occurs with retinitis pigmentosa and hysteria

• Central vision usually normal • Progressive restriction of visual field

Investigations 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 • 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.

Visual failure

Typical features

from secondary glaucoma and cataract. The pupil is bound to the lens by synechiae and is distorted.

• Begins as night blindness in childhood • Visual fields become concentrically narrowed (periphery to centre) • Blind by adolescence (sometimes up to middle age)

HIV infection 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.

Examination (ophthalmoscopic) • Irregular patches of dark pigment, especially at periphery • Optic atrophy

Sudden loss of vision

Trauma Trauma to the eye may cause only a little discomfort so it is important to keep this in mind.

Intraocular foreign body 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

Chronic uveitis Pain and redness may be minimal with this chronic inflammation. If untreated, visual loss often develops

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 78.4, and the diagnostic strategy model in Table 78.5. A simplified classification is: unilateral: retinal detachment retinal artery occlusion retinal vein thrombosis temporal arteritis optic neuritis migraine bilateral: bilateral optic nerve lesion hysteria

Table 78.4 Causes of sudden loss of vision7 Unilateral Vascular causes

Bilateral

Transient

Permanent

Occipital cortex ischaemia

Amaurosis fugax

Pituitary apoplexy

Transient ocular ischaemia

Central retinal artery occlusion

Homonymous hemianopia— vascular

Retinal emboli Malignant hypertension

Central retinal vein occlusion Vitreous haemorrhage Ischaemic optic neuropathy

Other causes

Bilateral optic neuritis

Acute angle closure glaucoma

Optic neuritis

Toxic damage to optic nerve: • methanol • ethanol • tobacco • lead

Uhthoff phenomenon

Retinal detachment

Papilloedema

Optic nerve compression

Posterior vitreous detachment

Carcinomatous optic neuropathy

Leber optic atrophy Quinine poisoning of retina Cerebral oedema Occipital lobe trauma Craniopharyngioma Hysteria

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Intraocular tumour

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Table 78.5 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

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

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.

Vitreous haemorrhage

Retinal detachment 8

AIDS

Benign intracranial hypertension

Retinal detachment may be caused by trauma, thin retina (myopic people), previous surgery (e.g. cataract operation), choroidal tumours, vitreous degeneration or diabetic retinopathy.

Q.

Pitfalls (often missed)

Clinical features

A.

Acute glaucoma

• 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)

Temporal arteritis Acute glaucoma

Papilloedema Optic neuritis Intraocular foreign body Q.

Seven masquerades checklist

A.

Depression

–

Ophthalmoscopy may show detached retinal fold as large grey shadow in vitreous cavity.

Drugs

✓

Management

Anaemia

–

Diabetes

✓ diabetic retinopathy

Thyroid disorder

✓ hyperthyroidism

Spinal dysfunction

–

UTI

–

Q.

Is this patient trying to tell me something?

A.

Consider ‘hysterical’ blindness, although it is uncommon.

A flow chart for the diagnosis of painless loss of vision is presented in Figure 78.5.

Amaurosis fugax 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

• • • •

Immediate referral for sealing of retinal tears Small holes treated with laser or freezing probe Pneumatic retinopathy 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

Visual failure

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Figure 78.5 Diagnosis of painless loss of vision. Reproduced with permission from Dr J Reich and Dr J Colvin

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

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

Management

Central retinal artery occlusion

If seen early, use this procedure within 30 minutes:

The cause is usually arterial obstruction by atherosclerosis, thrombi or emboli. There may be a history of TIAs. Exclude temporal arteritis (perform immediate ESR).

• massage globe digitally through closed eyelids (use rhythmic direct digital pressure) • rebreathe carbon dioxide (paper bag) or inhale special CO2 mixture (carbogen)

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• 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.

Figure 78.6 Appearance of a subject through the eyes of a person with age-related macular degeneration. Photo courtesy Allergan Pharmaceuticals

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 to prevent thrombotic glaucoma.

Macular degeneration There are two types: exudative or ‘wet’ (acute), and pigmentary or ‘dry’ (slow onset). • ‘Wet’ MD is caused by 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 78.6) 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

be injected into the vitreous humour. The 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 beta-carotene, 15 mg; vitamin C, 500 mg; vitamin E, 400 IU; and 80 mg zinc oxide.9 Advise patient to cease smoking if applicable.

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.10

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 non-pulsatile (but often normal) • Visual acuity severely impaired • Afferent pupil defect on affected side • Usually elevated ESR >40 mm

Ophthalmoscopy

Ophthalmoscopy shows optic disc swollen at first, then atrophic. The disc may appear quite normal.

• White exudates, haemorrhage in retina • Macula may look normal or raised

Management

Management No treatment is available to stop or reverse MD. For ‘wet’ MD refer urgently for fluorescein angiography and laser photocoagulation where indicated. Ranibizumab may

• 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)

Visual failure

Retinal migraine 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 • 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

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

827

• 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 52, pages 550–1 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.

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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 78.6. • 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.

Table 78.6 Time-scale guide for rate of visual loss3, 7 Sudden: less than 1 hour Amaurosis fugax Central retinal artery occlusion Hemianopias from ischaemia (emboli) Migraine Vitreous haemorrhage Acute angle glaucoma Papilloedema Within 24 hours Central retinal vein occlusion Hysteria Less than 7 days Retinal detachment Optic neuritis Acute macular problems

Table 78.6 continued Up to several weeks (variable) Choroiditis Malignant hypertension Gradual Compression of visual pathways Chronic glaucoma Cataracts Diabetic maculopathy Retinitis pigmentosa Macular degeneration Refractive errors

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Cataracts, page 158 • Floaters and Flashes, page 161 • Glaucoma, page 163 • Macular Degeneration, page 164

REFERENCES 1 Colvin J, Reich J. Check Program 219–220. Melbourne: RACGP, 1990: 1–32. 2 Beck ER, Francis JL, Souhami RL. Tutorials in Differential Diagnosis (2nd edn). Edinburgh: Churchill Livingstone, 1988: 141–4. 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 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. 10 Warne R, Prinsley D. A Manual of Geriatric Care. Sydney: Williams & Wilkins, 1988: 191–5.

79

Weight gain Persons who are naturally very fat are apt to die earlier than those who are slender. H I P P O C R AT E S 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. 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 • The cause of exogenous obesity is multifactorial, the end result being increased body fatness (greater than 30% of total body weight in females and greater than 25% in males).2 • 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.3 • 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

actual food intake and energy expenditure, and by interviewing reliable witnesses. Genetic factors are considered to play an important role.5

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, insulin-secreting 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

A diagnostic approach

The rare congenital disorders that cause obesity, such as Prader–Willi and Laurence–Moon–Biedl syndromes, should be easy to recognise in children (see pages 167 and 831).

A summary of the safety diagnostic model is presented in Table 79.1.

Chromosomal abnormalities

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

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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Table 79.1 Weight gain: diagnostic strategy model

Genetic polymorphisms

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.

Q.

Serious disorders not to be missed

Psychogenic considerations

A.

Cardiovascular: • cardiac failure

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.

Q.

Probability diagnosis

A.

Exogenous obesity

Hypothalamic disorders: • craniopharyngiomas • optic gliomas

The clinical approach

Liver failure

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

Nephrotic syndrome Q.

Pitfalls (often missed)

A.

Pregnancy (early) Endocrine disorders: • hypothyroidism • Cushing syndrome • insulinoma • acromegaly • hypogonadism • hyperprolactinaemia • polycystic ovarian disease Idiopathic oedema syndrome Klinefelter syndrome Congenital disorders: • Prader–Willi syndrome • Laurence–Moon–Biedl syndrome

Q.

Seven masquerades checklist

A.

Depression

✓

Diabetes

–

Drugs

✓

Anaemia

–

Thyroid disorder

✓ hypothyroidism

Spinal dysfunction

–

UTI

–

Q.

Is the patient trying to tell me something?

A.

Yes: the reasons for obesity should be explored.

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. An extensive working up of the CNS is not indicated in obesity without the presence of suspicious symptoms such as visual difficulties.

Some gender pointers

Investigations

Consider polycystic ovarian disease in women and obstructive sleep apnoea in obese men.

It is essential to perform two measurements:

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, corticosteroids, pizotifen,

• weight and height (to calculate BMI) • waist circumference

Important investigations • • • •

Cholesterol/triglycerides Glucose (fasting) Liver function tests Electrolytes and urea

Weight gain

Weight gain in children

Investigations to consider • • • •

831

Thyroid function tests Cortisol (if hypertensive) Testosterone (suspected sleep apnoea) ECG and chest X-ray (older than 40)

Anthropometric measurements6 Useful measuring instruments include: • BMI: ‘healthy’ range is between 20 and 25 • Waist circumference: risk of comorbidities — in men >94 cm — in women >80 cm • 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 is defined as a W/H ratio of >0.85 in women and >0.95 in men.

Body mass index The easiest and possibly most accurate assessment of obesity is the BMI (refer to Appendix V): BMI = weight (kg) height (M2)

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 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 page 167).

Laurence–Moon–Biedl syndrome

Garrow7 has produced a simple classification of the BMI associated with the relative degree of risk increase and suggested therapy (see Table 79.2).

The characteristic features are obesity, intellectual disability, polydactyly and syndactyly, retinitis pigmentation and hypogonadism.

Table 79.2 Classification of obesity (based on WHO guidelines)7

Beckwith–Wiedemann syndrome

BMI

Grading

Suggested therapy

35

>40

Grade III: morbid obesity

Combined program plus medical therapy Consider gastric surgery

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

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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.

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 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 24 page 219).

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. 79.1). Table 79.3 Factors predisposing to primary obesity Genetic

Familial tendency

Sex

Women more susceptible

Activity

Lack of physical activity

Psychogenic

Emotional deprivation, depression

Social class

Poorer classes

Alcohol

Problem drinking

Smoking

Cessation of smoking

Prescribed drugs

Tricyclic derivatives

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 79.3). 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

Figure 79.1 Comparison of two types of obesity according to distribution of body fat

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.3 In regard to the BMI reference scale it is worth noting that the risks follow a J-shaped curve (see Fig. 79.2) 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

Weight gain

Goals



1 no further weight gain 2 loss of 5–10% initial body weight 3 improve activity

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Figure 79.2 Body mass index (BMI) reference scale — 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) — psychological problems

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.3

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. 79.3). 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). TUBSUJOH
XFJHIU

Management 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:2 reduction in energy intake change in diet composition increased physical activity behavioural therapy

Pharmacological agents are not used for first-line 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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Part Three Problem solving in general practice

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. 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 on page 75). Breakfast: • oatmeal (soaked overnight in water); after cooking, add fresh or dried fruit; serve with fat-reduced 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) • slice of wholemeal toast with a thin scraping of margarine, spread with Vegemite, Marmite or sugarfree 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 tips • Have sensible goals; do not ‘crash’ diet but have a 6–12 month plan to achieve your ideal weight.9 • Go for natural foods; avoid junk foods. • 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). • Use high-fibre foods to munch on. • Drink copious water—at least 2 L a day. • A small treat once a week may add variety. • Avoid seconds and do not eat leftovers. • Avoid non-hungry eating. • Eat slowly—spin out your meal.

Pharmacological agents A variety of these is available or imminent but they have limitations and need to be used with caution, if at all. Adverse effects can be problematic. Consider for those with a BMI >35. The agents are:4,6,10 • 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 — 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

Weight gain

low-fat eating program, does produce extra weight loss over placebo.11

other cases, investigation of kidney or liver function may be required.

Meal replacements

Treatment

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.

• Treat the cause where known • Salt (sodium) restriction • Diuretics: — a loop diuretic (e.g. frusemide) — a potassium-sparing diuretic (e.g. spironolactone)

Surgery (bariatric surgery) Surgery is the most effective treatment for obesity.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 with comorbidities. 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.6,12 Gastric stapling and gastric bypass such as Roux-en-Y bypass are 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 page 749).

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 79.4).

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:

Hypoalbuminaemia (e.g. nephrotic syndrome, chronic liver disease, malnutrition)

• 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)

Increased plasma volume

Swelling of the legs

Congestive cardiac failure

Refer to Chapter 70.

Table 79.4 Causes of generalised oedema Decreased plasma volume

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

835

‘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.

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If overweight, lose it slowly and exercise to improve the muscle tone in the buttocks and thighs.

REFERENCES

When to refer

1

• Patients with grade II or III obesity (BMI >35) who are resistant to simple weight control measures.2 • Patients with associated medical problems such as angina or severe osteoarthritis who require rapid weight reduction. • Possibility of endocrine cause of obesity. • Suspicion of congenital or inherited disorder in children.

2 3

4 5 6

Practice tips • Avoid a critical or judgmental attitude to the overweight patient.13 • 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.

7 8 9 10

11

12

13

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Obesity : How to Lose Weight Wisely, page 119

Tunnessen WW Jr. Signs and Symptoms in Paediatrics (2nd edn). Philadelphia: JB Lippincott, 1988: 33–41. Marks S, Walqvist M. Obesity. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 354–6. McPhee SJ, Papdakis MA. Current Medical Diagnosis and Treatment (49th edn). New York: McGraw-Hill Lange, 2010: 1135–8. Caterson ID. Weight management. Australian Prescriber, 2006; 29: 43–7. Davey P. Medicine at a Glance (2nd edn). Oxford: Blackwell Publishing, 2008: 56–7. Moulds R (Chair). Therapeutic Guidelines: Endocrinology (Version 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 49–58. WHO Technical Report Series Number 894. Geneva: WHO, 2000. Kaczmarczyk W. The obese patient. In: How I manage my difficult problems. Aust Fam Physician, 1991; 20: 417–21. Murtagh JE. Obesity: how to lose weight wisely. In: Patient Education (5th edn). Sydney: McGraw-Hill, 2008: 119. Padwal R, Li SK, Lau DC, et al. Long term pharmacotherapy for obesity and overweight. (Cochrane Review). Cochrane Database, September 2008; (1): CD 004094. Arterburn D, Noel P. Obesity. In: Barton S (ed.) Clinical Evidence (issue 5). London: BMJ Publishing Group, 2001: 412–19. 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. Kincaid-Smith P, Larkins R, Whelan G. Problems in Clinical Medicine. Sydney: MacLennan & Petty, 1990: 105–8.

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Weight loss 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 1988 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.

Malignant disease

Key facts and checkpoints

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 high-risk groups.

• 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 safety diagnostic model is presented in Table 80.1.

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.

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

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 under-developed countries. Addison disease (page 224) can be very difficult to diagnose. Symptoms include excessive 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.

Serious disorders not to be missed

Diabetes

Many of the problems causing weight loss are very serious, especially malignant disease.

The diabetic who presents with weight loss will be young and insulin-dependent. The initial presentation

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Table 80.1 Weight loss: diagnostic strategy model (other than deliberate dieting or malnutrition) Q.

Probability diagnosis

A.

Stress and anxiety

may be ketoacidosis. The triad of symptoms is thirst + polyuria + weight loss.

Hyperthyroidism

Non-coping elderly/dementia 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

Q.

Pitfalls (often missed)

A.

Drug dependence esp. alcohol Malabsorption states: • ?intestinal parasites/infestations • coeliac disease Other GIT problems Chronic kidney failures

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

Connective tissue disorders (e.g. SLE) Dementia

Psychogenic considerations

Rarities: • Addison disease • hypopituitarism

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. 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.

Q.

Seven masquerades checklist

A.

Depression Diabetes Drugs Anaemia

✓ ✓ ✓ ✓

Thyroid disorder

✓ hyperthyroidism

Spinal dysfunction

–

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.

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,

Weight loss

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 80.1 shows the possible causes of weight loss.

• Are your periods normal (for females)? • What drugs are you taking? • How many cigarettes do you smoke?

General questions

A careful general examination is essential with special attention to:

• 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? • Do you get short of breath? • Do you have any abdominal pain?

Examination • vital parameters • the thyroid and signs of hyperthyroidism • the abdomen (check liver, any masses and tenderness) • rectal examination (test stool for occult blood) • reflexes

Investigations Basic investigations include: • • • • • • •

haemoglobin, red cell indices and film white cell count ESR thyroid function test random blood sugar chest X-ray urine analysis

Others to consider: • upper GIT (endoscopy or barium meal) TUSFTT
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Figure 80.1 Weight loss: causes to consider

839

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80

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Part Three Problem solving in general practice

• ultrasound of abdomen (or CT if suspected abnormality not found) • colonoscopy • LFTs

Table 80.2 DSM-IV criteria for diagnosing anorexia nervosa and bulimia Anorexia nervosa

Weight loss in children

A

Refusal to maintain normal body weight at or above a minimum normal weight for age and height (loss to 35 years and smoking or other risks of CAD

There appears to be no overall increase in the incidence of cancer in women using COCs.

Absolute Pregnancy (known or suspected) First 2 weeks postpartum History of thomboembolic disease, including known thrombophilia Cerebrovascular disease Focal migraine Coronary artery disease Oestrogen-dependent tumours (e.g. breast) Active liver disease Polycythaemia

Undiagnosed abnormal vaginal bleeding Breastfeeding 4 weeks before surgery 2 weeks after surgery Gall bladder or liver disease Hypertension Diabetes mellitus Long-term immobilisation Complicated valvular heart disease Hyperlipidaemia Chloasma Severe depression

Serious side effects of COCs The most serious side effects to be considered are the effects of COCs on the circulatory system and the incidence of cancer.

Cardiovascular effects3, 6 The following circulatory disorders have been linked with pill usage. • Venous deep vein thrombosis, pulmonary embolism, rarely: mesenteric, hepatic and kidney thrombosis • Arterial myocardial infarction, thrombotic stroke, haemorrhagic stroke, rarely: retinal and mesenteric thrombosis

The risk of circulatory disease has not been related to duration of use and there is no increased risk in perpetual users. The oestrogen content of the pill is considered to be the aetiological factor and the problem is increased in

• Possible effect (not absolutely proven) and possibly very low risk: — cervix (take regular smears at yearly intervals) — breast • Protective effect: — endometrial — epithelial ovarian • No effect: — melanoma — choriocarcinoma — prolactinomas

Common side effects The relatively minor side effects listed in Table 90.4 may discourage women from persisting with oral contraception in the absence of appropriate explanation and reassurance. Management of these side effects is listed in the same table. It is useful in practice to have this list available as a ready reference for manipulating the COC if necessary. A common nuisance side effect is breakthrough bleeding in the first 2 months. If minor, continue, but if heavy, stop and start a new COC, usually with 50 mcg ethinyloestradiol.

Important advice for the patient • Periods tend to become shorter, regular and lighter. • No break from the pill is necessary. • Drugs that interact with the pill and affect their efficacy include antacids, purgatives, vitamin C, antibiotics (especially griseofulvin and rifampicin) and anticonvulsants (except sodium valproate). With warfarin and oral hypoglycaemics, requirements may change for those starting the pill.

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Women's health

Table 90.4 Management of common side effects of COC7, 10 Symptom change

Change

Examples of pill change

Acne

Increase oestrogen, reduce or change progestogen

Triphasil/Triquilar to Diane ED/ Marvelon

Amenorrhoea

Increase oestrogen or decrease progestogen

Nordette/Microgynon 30 to Nordette 50/Microgynon 50

Breakthrough bleeding: • early to mid cycle

Increase oestrogen

Triphasil/Triquilar to Biphasil/ Sequilar

• late cycle

Increase progestogen or change type

Triphasil to Nordette Nordette to Norinyl-1

Breast problems: • fullness/tenderness

Decrease oestrogen

Biphasil/Sequilar to Triphasil/ Triquilar or progesterone only pill

• mastalgia

Decrease progestogen

Nordette/Microgynon 30 to Triphasil/Triquilar

Chloasma

Stop oestrogen Try progestogen-only pill Avoid direct sun (use blockout)

Depression

Decrease or change progestogen

Nordette/Microgynon 30 to Triphasil/Triquilar or Brevinor

Dysmenorrhoea/menorrhagia

Increase progestogen

Triphasil/Triquilar to Nordette/ Microgynon

Decrease oestrogen Libido loss

Increase oestrogen Change from anti-androgenic progestogen to an alternative

Headache: • focal migraine • in pill-free week

Nausea/vomiting

Microgynon 30 etc. to Femoden/ Minulet

Discontinue pill Add 10–30 mcg ethinyloestradiol daily during pill-free week or 50–100 mcg oestradiol patch Decrease or change oestrogen or stop oestrogen

Use Microgynon 20, etc. or progestogen-only pill

Weight gain: • constant

Decrease or change progestogen

Triphasil/Triquilar to Brevinor or Marvelon

• cyclic

Decrease oestrogen

Biphasil/Sequilar to Triphasil/ Triquilar or progestogen-only pill

• Diarrhoea and vomiting may reduce the effectiveness of the pill. If a woman vomits within 2 hours of taking an active pill, she should take an additional ‘active’ pill. • Yearly return visits are recommended to update the history and examination and repeat the Pap smear.

Missed pills The essential advice is ‘just keep going’ (i.e. take a pill as soon as possible and then resume usual pill-taking schedule).

Also If the missed pills are in week three, she should omit the pill-free interval.

Also Condoms or abstinence should be used for 7 days if the following numbers of pills are missed: ‘Two for twenty’ (i.e. if two or more 20 mcg pills are missed) ‘Three for thirty’ (i.e. if three or more 30–35 mcg pills are missed)

Family planning

The seven-day rule for the missed or late pill (more than 12 hours late) • Take the forgotten pill as soon as possible, even if it means taking two pills in one day. Take the next pill at the usual time and finish the course. • If you forget to take it for more than 12 hours after the usual time there is an increased risk of pregnancy so use another contraceptive method (such as condoms) for 7 days. • If these 7 days run beyond the last hormone pill in your packet, then miss out on the inactive pills (or 7-day gap) and proceed directly to the first hormone pill in your next packet. • You may miss a period. (At least seven hormone tablets should be taken.)

Other useful rules for missed pills If 1 or 2 × 30–35 mcg EO pills or 1 × 20 mcg EO pill

and • norethisterone 350 mcg/day

Providing the mini-pill is taken regularly at the same time each day, the pregnancy rate is 3 per 100 women years.1 The failure rate decreases with age. There are no serious side effects but compliance is a problem because of cycle irregularity, especially with irregular bleeding. The mini-pill often reduces the cycle length to less than 25 days or alters the regularity of the bleeding phase. Indications for the POP include age 45 years or more, smokers aged 45 years or more, contraindications to or intolerance of oestrogens, diabetes mellitus, migraine, chloasma, lactation and well-controlled hypertension. Contraindications include pregnancy, undiagnosed genital tract bleeding, past history of or increased risk of ectopic pregnancy and concomitant use of enzymeinducing drugs (absolute).

Injectable contraceptives Depo-Provera

• take the most recent missed pill ASAP • continue taking remaining pills as usual

Medroxyprogesterone acetate (Depo-Provera) is the only injectable intramuscular contraceptive available in Australia. It is very effective for up to 14 weeks.

No additional contraception or emergency contraception needed.

Dose:

If ≥3 × 30–35 mcg EO pills or ≥2 × 20 mcg EO pills • take the most recent missed pill ASAP • continue taking remaining pills • use condoms or abstinence until pill is taken for 7 consecutive days

Practice tip Delaying a period Prescribe norethisterone 5 mg bd or tds for 3 days prior to expected period. Period resumes 2–3 days after stopping tablets. If taking COC: • continue taking the hormone tablets (skip the inactive pills) until end of next pack.

Progestogen-only contraceptive pill The POP (mini-pill) is perhaps an underutilised method of contraception, although it is not as efficacious as the COC. The two common formulations are: • levonorgestrel 30 mcg/day

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150 mg by deep IM injection in first five days of the menstrual cycle. The same dose is given every 12 weeks to maintain contraception. Failure rate: 1 per 1000 women years.1

Side effects include a disrupted menstrual cycle (amenorrhoea rate 70% or irregular or prolonged uterine bleeding), excessive weight gain, breast tenderness, depression and a delay in return of fertility (average 6 months).8 There is no effect on cardiovascular disease or the incidence of cancer but long-term use is associated with accelerated bone loss. There are no absolute contraindications. Its use is not recommended for >2 years or as a first-line contraceptive in women 5 years, personal history of breast cancer, family history in a first-degree relative (raises risk about threefold), nulliparity, late menopause (after 53), obesity, childless until after 30 years of age, early menarche,6 ionising radiation exposure.

Familial breast cancer Up to 5% of cases are familial, with most being autosomal dominant. Refer to Chapter 19.

Clinical features MVNQ

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Figure 92.8 Scheme for management of a breast lump by fine-needle aspiration

• The majority of patients with breast cancer present with a lump (see Fig. 92.9). • The lump is usually painless (16% associated with pain). • Usually the lump is hard and irregular. • Nipple changes, discharge, retraction or distortion. • Rarely cancer can present with Paget disease of breast (nipple eczema) or inflammatory breast cancer (see Chapter 91, page 947). • Rarely it can present with bony secondaries (e.g. back pain, dyspnoea, weight loss, headache).

Note: There are basically three presentations of the disease: • the vast majority present with a local breast lump2 (see Fig. 92.10) • ductal carcinoma in situ • some present with metastatic disease

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Photo courtesy Dr Victor Vanco

radiotherapy, surgery and/or endocrine therapy if applicable (level IV evidence). Most relapses8 after surgery occur in the first 3 years.

Ductal carcinoma in situ DCIS is a non-invasive abnormal proliferation of milk duct epithelial cells within the ductal–lobular system and is a precursor lesion for invasive breast cancer. Since mammography screening it is readily detected and now comprises about 20% of breast cancer. It may present clinically with a palpable mass or nipple discharge or Paget disease of the nipple with or without a mass.

Management Figure 92.9 Advanced adenocarcinoma of breast in patient showing denial for a problem of 2 years duration.

Management decisions are challenging, with options being total mastectomy or breast-conserving therapy with or without radiotherapy. Patients usually have an excellent outcome with low local recurrence rates and a survival of at least 98%.9

Adjuvant therapy for breast cancer 



 



Figure 92.10 Relative frequencies of breast cancer at various anatomical segments

Of those who present with local disease, approximately 50% will develop metastatic disease.

Management Immediate referral to an expert surgeon on suspicion or proof of breast cancer is essential. The treatment has to be individualised according to the nature of the lump, age of the patient and staging. Accurate staging requires knowledge of whether the draining lymph nodes are involved with the tumour, as this is the single most powerful predictor of subsequent metastases and death. Staging for systemic disease also requires full blood examination and liver function tests (including alkaline phosphatase). A bone scan may be used as a valuable baseline. Size and histological grading of tumour plus nodal status and receptor status are the most important prognostic factors. Optimal management of locally advanced breast cancer is a combined approach that uses chemotherapy,

The consultant will choose the most appropriate surgical and adjuvant treatments for the individual patient. The National Breast Cancer Consensus report emphasised that ‘continuing care should be coordinated through the patient’s GP as the impact of treatment may last longer than therapy and support must continue’. The report made the following recommendations:10 • Tumour excision followed by whole breast irradiation was the most preferred local therapy for most women with stage I or II cancer. • Total mastectomy and breast-conservation surgery had an equivalent effect on survival. • Total mastectomy is preferred for a large tumour, multifocal disease, previous irradiation and extensive tumour on mammography. • Current recommendations for radiotherapy after mastectomy are:11 — tumours >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.12 • Cytotoxic chemotherapy has an important place in management. Newer regimens containing anthracyclines (e.g. epirubicin) and a taxane (e.g. docetaxel) have largely replaced the traditional CMF (cyclophosphamide, methotrexate and fluorouracil) regimen.12 • Adjuvant hormonal therapy by the anti-oestrogen agent tamoxifen 20 mg (o) daily, which is a specific modulating agent, is widely used and is most suitable in postmenopausal women.

Lumps in the breast

Adjunct agents available for treatment include:13 • anti-oestrogens: tamoxifen, toremifene • aromatase inhibitors: anastrozole, letrozole, exemestane • monoclonal antibodies: trastuzumab (Herceptin) • progesterones (e.g. medroxyprogesterone acetate)

Guidelines for adjuvant treatments are presented in Table 92.4, which is a general guide only as other adjunct agents may be added or substituted.

Mammary dysplasia

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 medication to alleviate mastalgia (see treatment for cyclical mastalgia in Chapter 91). • Use analgesics as necessary. • Surgically remove undiagnosed mass lesions.

Synonyms: fibroadenosis, chronic mastitis, fibrocystic disease, 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) • • • • • • • • • •

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 • 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

Table 92.4 Adjuvant treatment favoured by trial meta-analyses11 Menopausal status

Node status

Oestrogen receptor

Premenopausal

Positive

Positive

Positive Negative

Postmenopausal

Postmenopausal

Other factors

Treatment

Negative Positive

Poor prognosis*

Negative

Negative

Poor prognosis

Chemotherapy† + tamoxifen Chemotherapy Chemotherapy and/or tamoxifen Chemotherapy

Positive

Positive Positive

>60 years 70 nmol/L with cholecalciferol 1000–2000 IU daily.

Advice on when to seek medical help • If contractions, unusual pain or bleeding occur before term • If the baby is less active than usual • If the membranes rupture (with fluid loss) • The onset of regular contractions 5–10 minutes apart

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • About Your Pregnancy, page 4 • Miscarriage, page 8 • Pregnancy Planning, page 3

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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 Carroli G, Villar J, Piaggio G et al. WHO systematic review of randomised controlled trials of routine antenatal care. Lancet, 2001; 357: 1565–70. 8 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. 9 Beischer NA, Mackay EV. Obstetrics and the Newborn. Sydney: Saunders, 1986. 10 Peat B. Antenatal care: common issues facing GPs in shared care. Med Today, 2001; June: 81–5. 11 Humphrey M. Common conditions in an otherwise normal pregnancy. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996: 116–20. 12 Hammer I et al. Calcium treatment of leg cramps in pregnancy. Acta Obstet Gynaecol Scand, 1981; 60: 345–7. 13 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. 14 Burdon J. Respiratory medicine. Check Program 395. Melbourne: RACGP, 2005: 17–8. 15 MRC Vitamin Study Research Group. Prevention of neural tube defects. Lancet, 1991; 338: 131–7. 16 Grover SR, Morley R. Vitamin D deficiency in veiled or dark-skinned pregnant women. Med J Aust, 2001: 151–2, 175.

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. I G N A Z S E M M E LW E I S (1818–65), A U T O B I O G R A P H I C A L I N T R O D U C T I O N 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.

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 beta-lactam 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. • Ideally all women should be screened for bacteriuria at their first visit. • Less than 1% will subsequently develop bacteraemia. • Approximately 5% of such women subsequently develop pyelonephritis during pregnancy with an increased risk of preterm labour, mid-trimester abortion and pregnancy-induced hypertension.

Treatment Treatment is recommended according to culture sensitivities. It is preferable to delay it until the first trimester has passed.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

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canal. Chorioamnionitis is infection of the placenta 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 problems. Routine testing for GBS is recommended at 36 weeks.

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: • • • •

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

About 1–4% of neonates per 1 000 live births develop group B strep sepsis with a high mortality rate, up to 50%.4 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.

Vaginal candidiasis 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 98, pages 997–9. Clotrimazole is a first-line treatment. Oral medication with fluconazole or itraconazole should be avoided.

Transmissible viral infections Rubella Key facts and checkpoints • Fewer than 5% of women are not immune (IgG 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 on Chapter 84, pages 882–3. • Effects on fetus:5 — 41 weeks) Multiple pregnancy Polyhydramnios Need for amniocentesis: • genetic concerns • abnormal AFP • other Age >35 years; 110 kg Pre-pregnancy weight 18 h

Alcohol or drug abuse

Malpresentation Placental insufficiency Inadequate antenatal care

Late presentation (after 20 weeks) No antenatal care Failed or poor attendance

High-risk pregnancy

• 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 must 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.

Antihypertensive drugs6 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) • 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

1029

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 90th percentile—diabetes or history of large babies • uterine abnormality (e.g. fibroids) • wrong dates

Polyhydramnios Clinical features • Liquor volume: usually >2000 mL • Multiple risks (e.g. PROM, prem labour, cord prolapse, APH, malpresentation)

Causes • Fetal abnormalities: CNS, upper GIT atresia, ectopic vesicae • Hydrops fetalis • Diabetes • Multiple pregnancy • Chorioangioma of placenta • Fetal infection—cytomegalovirus, toxoplasmosis • Unknown causes

Refer for tests—diabetes, ultrasound. Refer for specialist advice.

Fundus less than dates Consider: • • • •

oligohydramnios—liquor volume usually 20% — velocity >30 microns/s

Female—ovulation status • 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 110.2).

Table 110.2 WHO classification of ovulatory dysfunction6 Group 1

Hypothalamic– pituitary failure

Low FSH, LH (e.g. anorexia nervosa)

Group 2

Hypothalamic– pituitary dysfunction

Normal FSH (e.g. PCOS)

Group 3

Ovarian failure

High FSH (e.g. ovarian failure)

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 If azoospermia or severe oligospermia:

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• 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 and inhibin (a low inhibin also indicates irreversible failure) • antisperm antibodies (in semen or serum) • sperm function tests • chromosome analysis: 46 XXY or 46 XXY/46 XY or microdeletion • testosterone • testicular ultrasound

Female (Other investigations may be necessary.) • • • • • • • •

Thyroid function tests: ?hypothyroidism Serum prolactin, FSH, LH, androgen levels Sonohysterogram Endometrial biopsy Transvaginal ultrasound Hysteroscopy/laparoscopy CT of the pituitary fossa Chlamydia (cervical culture)

Note: Ovulation or its absence is best demonstrated by luteal progesterone. Essential investigations are outlined in Table 110.3. Table 110.3 Essential investigations of the subfertile couple2 First-line Basal body temperature chart and cervical mucus diary Semen analysis Serum progesterone (mid-luteal—day 21) in female Transvaginal ultrasound Rubella immune status (female)

Management principles5 • 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.

Fertility awareness This education is helpful for couples: • women always ovulate 2 weeks 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

Polycystic ovary syndrome PCOS is a common chronic anovulatory disorder affecting 5–10% of women of reproductive age. It should not be confused with the common ultrasonographic diagnosis of cystic ovaries with no clinical features. The classic clinical features are infertility, oligomenorrhoea, hirsutism (70%) and obesity (50%). 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, which cause more egg-containing cysts to form in the ovaries without ova reaching maturation. 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 • Transvaginal ultrasound (usually at least 12 follicles 2–9 mm in size in an enlarged ovary) • Possible endometrial biopsy

Suggested screening for all women with PCOS8 • • • • • •

Smoking history Blood pressure Blood glucose levels Oral glucose tolerance test Fasting plasma insulin Fasting serum HDL and LDL levels

The subfertile couple

Management strategies8 First-line • 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 • Assisted conception • Laparoscopic ovarian diathermy (failed medical treatment)

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 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. 110.3) 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 If the problem has been identified, specific treatment needs to be prescribed by the consultant.

110

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Part Seven Sexually related problems

• 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 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 gamete intrafallopian transfer (GIFT), a modification of IVF. This method, in which eggs and sperm are placed into the fallopian tubes, is best used in the treatment of infertility of unknown aetiology and carries a pregnancy rate of about 30% per couple.3

Evidence-based RCTs The conclusion as published in Clinical Evidence10 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 • male infertility—intra-uterine insemination, donor insemination, fallopian tube sperm infusion • unexplained infertility—intra-uterine insemination

When to refer A family doctor should perform the initial investigations of a couple with infertility, including 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. How to treat: Infertility. 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 4). Melbourne: Therapeutic Guidelines Ltd, 2009: 267–73. 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 Duckitt K. Infertility and subfertility. In: Barton S (ed). Clinical Evidence. London: BMJ Publishing Group, 2001, issue 5: 1279–94.

111

Sexual health The functional form of impotence fills the coffers of the quacks, and swells the list of suicides. R U T H E R F O R D M O R R I S O N (1853 –19 39 ) Drink, sir, provokes the desire, but it takes away the performance. W I L L I A M S H A K E S P E A R E (1564–1616), M A C B E T H , A C T 2, S C E N E 1 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 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 111.1. 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 content-related, much of which is based on commonsense, but the ubiquitous problem of communication. 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

Table 111.1 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

how relatively simple it is to help so many confused people who often have unrealistic expectations of their partners and themselves.

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

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• 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 111.2). 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 111.2 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 partners and tend to be unaware of the sexual needs of elderly people (see Table 111.3). It is most appropriate to enquire about these issues in our patients—e.g. the postmyocardial infarction patient, the postprostatectomy patient, the patient taking antihypertensives or other drugs (see Table 111.4), and the post-mastectomy or posthysterectomy patient. Diabetes deserves special attention as 27–55% of diabetic men reported some erectile difficulties.2

Table 111.3 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

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,

Sexual health

Male

Female

Alcohol

Alcohol

• How often do you reach a climax during lovemaking? • How often do you have intercourse, or sexual activity without intercourse? • Do you ‘come’ together?

Anticholinergics

Anti-epileptics

Female

Anti-epileptics Antihistamines

Antihypertensives (selected)

• Do you have enough lubrication? Are you wet enough? • Do you find intercourse uncomfortable or painful?

Antihypertensives

CNS depressants

Male

Benzodiazepines

Combined oral contraceptive

Table 111.4 Drugs affecting sexual arousal and function

Cytotoxic drugs Disulfiram Marijuana

Marijuana Narcotics

Narcotics Oestrogens Psychotherapeutic drugs

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)? • 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, marijuana, nicotine)?

Specific questions about sexuality • • • • • • • •

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?

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• 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? • 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?

Examination 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.

Investigations No particular routine tests are recommended. Tests for male erectile dysfunction (impotence) are outlined on page 1093. 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.

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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

Sexual myths in the male 4 • • • • • • • • •

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.

Basic sexual counselling 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: • 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 111.5. Table 111.5 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

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. 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 exercises, fantasy conditioning with VHS/DVDs, and behaviour modification. Complex problems, especially those involving erectile dysfunction, infertility and sexual deviations or perversions, demand referral to an expert.

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: Permission giving • LI: Limited Information

Sexual health

• SS: Specific Suggestion • IT: 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. 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). reading VHS/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 (updated 2008). • Zilbergeld B. Men and Sex. A Guide to Sexual Fulfilment. Medindie SA: Souvenir Press, 1979. • Crooks R, Baur K. Our Sexuality. Menlo Park, CA: Benjamin/Cummings Publishing Co., 1984. • Williams W. It’s Up to You—a Self-Help Book for the Treatment of Erectile Problems. Sydney: Williams & Wilkins, 1989. • Rickard-Bell R. Loving Sex: Happiness in Mateship. Sydney: Wypikaninkie Publications, 1992. • Kitzinger S. Women’s Experience of Sex. Penguin, 1993. • Phelps K. Confronting Sexuality. Sydney: Harper Collins, 1993. • Heiman J, Lo Piccolo J. Becoming Orgasmic: a Sexual Growth Program for Women. Sydney: Simon & Schuster, 1988. Recommended VHS/DVDs • The Lovers’ Guide I and II. Andrew Stanway. • The Language of Love.

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

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simple model (see Fig. 111.1) 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 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. 111.1) 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 page 1031). Important causes are listed in Table 111.6. 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.

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Figure 111.1 Analogous structures in male and female genitalia Source: Reproduced with permission from G and M Cohen, Canadian Family Physician, 852, 31: 767–712

Table 111.6 Important causes of dyspareunia Pain worse on insertion Physiological—inadequate lubrication Vaginitis in chronic candidiasis Vulvar dermatoses Postnatal perineal scarring Incompletely ruptured hymen Vulvar vestibular syndrome (vestibulitis) Vulvovaginal atrophy (e.g. postmenopausal) Vaginismus Pain worse on deep penetration Endometriosis PID Pelvic adhesions Ovarian and uterine tumours Postnatal

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

vaginismus tampons will probably never have been inserted. It is often related to the vulval vestibular syndrome. 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.

Sexual health

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. 9

Causes

• 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).

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 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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Address modifiable risk factors, including medications (if feasible), psychosocial issues and lifestyle (see NEAT, Chapter 7, page 45). Management should comprise appropriate patient education including a VHS/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.

Psychogenic disorders These will involve psychotherapy and sex behavioural modification as outlined under sexual counselling. Referral to a consultant may be appropriate.

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Hormonal disorders

Intrapenile injection

• Testosterone for androgen deficiency: primary testicular disease (e.g. Klinefelter syndrome) or gonadotrophin deficiency

• Alprostadil intracavernosal injections: — self-administered after supervised teaching (use a penile model if available) — start with a lower dose, 2.5–5 mcgm — 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)

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 (PDE-5) inhibitors are the first-line oral medication (see Table 111.7). 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

The cooperation of the partner is essential and urological back-up must be arranged.

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. 111.2) • 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. For the latter the intravaginal ejaculatory time is 80 mmHg in late pregnancy is

considered unacceptable. Preferred drugs to use are methyldopa, labetalol, and β-blockers. Diuretics and ACE inhibitors should not be used. Hypertensive pregnant women should be supervised in association with a specialist unit.

Surgical patients Patients whose BP is under control before surgery should continue the same treatment. If oral medication is affected by the surgery, parenteral treatment may be needed to avoid rebound hypertension. This is a particular problem with clonidine and possibly methyldopa. Withdrawal of other drugs, such as β-blockers, may have adverse consequences.

Kidney disease Kidney function is not adversely affected by the treatment of severe or malignant hypertension. Use a loop diuretic (e.g. frusemide) initially. β-blockers, calcium-channel blockers, prazosin and methyldopa can be used, while caution is needed with ACE inhibitors, particularly if there is underlying renovascular disease. Kidney protection in diabetes requires strict BP control.

Hypertension

Heart failure First-line treatment for associated hypertension includes ACE inhibitors and diuretics. Other suitable drugs are a hydralazine–nitrate combination and methyldopa. Calcium-channel blockers should be used with care and verapamil and β-blockers should be avoided.

has been well controlled for several months to years it is often worth reducing the dosage or the number of drugs. A ‘drug holiday’ (cessation of treatment) can be hazardous, however, because satisfactory control may be temporary and hypertension will re-emerge. Careful monitoring under such circumstances is mandatory.

When to refer 4

Ischaemic heart disease Recommended drugs are β-blockers and calcium antagonists.14 The non-dihydropyridine agents should be used with care with a β-blocker but the dihydropyridine agents are quite safe.

Obstructive pulmonary disease Apart from β-blockers, all other routine antihypertensives can be used.

Erectile dysfuntion It is prudent to avoid antihypertensives that are possibly associated with erectile dysfunction (e.g. thiazide diuretics, methyldopa, reserpine and β-blockers). Suitable agents to use are ACE inhibitors and calciumchannel blockers.

Can hypertension be overtreated?

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19

Yes. Excessive BP reduction, particularly if acute, can seriously compromise perfusion in vital organs, especially if blood flow is already impaired by vascular disease. Careful monitoring of the patient, including standing BP measurement, is important. One should avoid excessive BP reduction in the setting of acute stroke, where there is a tight carotid artery stenosis (particularly if symptomatic) and in the elderly subject (especially if there is postural hypotension). The same rule applies to head injury. It has been suggested that lowering the 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. • 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 5th edition: • Hypertension, page 260

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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 Fraser A. Measurement of blood pressure. Aust Fam Physician, 1989; 18: 355–9. 6 British Medical Association. ABC of Hypertension. London: British Medical Association, 1989: 1–50. 7 Bates B. A Guide to Physical Examination and History Taking (5th edn). Philadelphia: Lippincott, 1991: 284. 8 National Heart Foundation of Australia. Guide to Management of Hypertension. Canberra: National Heart Foundation of Australia, 2008. 9 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. 10 Blair SN, Goodyear NN, Gibbons LW, Cooper KH. Physical fitness and incidence of hypertension in healthy normotensive men and women. JAMA, 1984; 252(4): 487–90. 11 Rouse IL, Beilin LJ. Vegetarian diet and blood pressure. Editorial review. J Hypertens, 1984; 2: 231–40. 12 Kestlefoot H. Urinary cations and blood pressure—

13 14

15

16

17

18

19 20

21

population studies. Annals of Clinical Research, 1984; 16 Supp. (43): 72–80. Jennings G, Sudhir K. Initial therapy of primary hypertension. Med J Aust, 1990; 152: 198–202. Smith A (Chair). Therapeutic Guidelines: Cardiovascular (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2008: 27–84. Hypertension Guideline Committee, 1991 report. Hypertension: Diagnosis, Treatment and Maintenance. Adelaide: Research Unit RACGP (South Australian Faculty), 1991. 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. Guidelines for the treatment of mild hypertension. Memorandum from a WHO–ISH meeting. Endorsed by Participants at the Fourth Mild Hypertension Conference. Bulletin of the World Health Organization, 1986; 64(1): 31–5. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. JAMA, 1991; 265: 3255–64. Vandongen R. Drug treatment of hypertension. Aust Fam Physician, 1989; 18: 345–8. Cruickshank JM, Thorp JM, Zacharias FJ. Benefits and potential harm of lowering high blood pressure. Lancet, 1987; 1: 581–4. The HOT study group. The Hypertension Optimal Treatment Study. Blood Pressure, 1993; 2: 6.

Dyslipidaemia

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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

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 KAPS,6 REGRESS7 and WOSCOPS8—all reinforce the benefits of lipid-lowering therapy for dyslipidaemia and the primary prevention of coronary heart disease. A recent 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.9 The main focus of treatment will be on primary dyslipidaemia but secondary causes (see Table 129.1) also need to be addressed. There is now a greater emphasis on high density lipoprotein (HDLP), in particular, rather than total cholesterol. LDLC is the lipid with the highest correlation with CHD.

Established facts 10,11,12 • Major risk factors for CAD include: — increased LDL cholesterol + reduced HDL cholesterol — ratio LDLC/HDLC >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

AND

M E R E D I T H 19 9 6 1

Table 129.1 Common causes of secondary dyslipidaemia Hypothyroidism Nephrotic syndrome Type 2 diabetes Cholestasis Anorexia nervosa Obesity Kidney impairment Alcohol abuse Smoking • LDLC reduction with statin therapy reduces heart attacks, stroke, the need for revascularisation and death

Investigations 10 The following fasting tests are recommended in all adult patients 18 years and over: • serum triglyceride level • serum cholesterol level and HDLC and LDLC 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 129.2. Testing should occur at least every 5 years. Recommended treatment goals12 • • • •

Total cholesterol 5.5 mmol/L 4 mmol/L

Patients not eligible under the above: • men 35–75 years • postmenopausal women up to 75 years Other patients not included in the above

Target levels Cholesterol 9 mmol/L or Triglyceride >8 mmol/L

Non-pharmacological measures

Hypercholesterolaemia

• Dietary measures: — keep to ideal weight — reduce fat intake, especially dairy products and meat — avoid ‘fast’ foods and deep-fried foods — replace saturated fats with mono or polyunsaturated fats — limit high-cholesterol foods (e.g. egg yolk, offal, fish roe) — use approved cooking methods (e.g. steaming, grilling) — always trim fat off meat, remove skin from chicken — avoid biscuits and cakes between meals — eat fish at least twice a week — high-fibre diet, especially fruit and vegetables — increase complex carbohydrates — alcohol intake 0–2 standard drinks/day — drink more water • Regular exercise • Cessation of smoking • Cooperation of family is essential • Exclude secondary causes (e.g. kidney disease, type 2 diabetes, hypothyroidism, obesity, alcohol excess— especially ↑ TG), specific diuretics

Choose one of the following.

First-line agents

• Diet therapy effective (TG ↓, LDLC ↓) within 6–8 weeks • Continue at least 6 months before considering drug therapy in all but the highest-risk category

1 HMG-CoA reductase inhibitors (statins): atorvastatin 10 mg (o) nocte, increase to max. 80 mg/day or fluvastatin 20 mg (o) nocte, increase to max. 80 mg/day or simvastatin 10 mg (o) nocte, increase to max. 80 mg/day or pravastatin 10 mg (o) nocte, increase to max. 80 mg/day or rosuvastatin 5 mg (o) nocte, increase to 40 mg/day • adverse effects: GIT side effects, myalgia, abnormal liver function (uncommon) • monitor: measure LFTs (ALT and CPK) and CK as baseline • repeat LFTs after 4–8 weeks, then every 6 weeks for 6 months 2 Ezetimibe 10 mg daily (especially if statin-intolerant) 3 Combination: ezetimibe + statin (e.g. simvastatin) (especially if statins below target) 4 Bile acid sequestrating resins: • e.g. cholestyramine 4 g daily in fruit juice increasing to maximum tolerated dose • adverse effects: GIT side effects (e.g. constipation, offensive wind) 5 Fibrates: consider if above drugs not tolerated

Pharmacological measures

Second-line agents

The choice of the lipid-lowering agent depends on the pattern of the lipid disorder.11,12 See Table 129.3. Use the following agents in addition to diet.

6 Nicotinic acid • nicotinic acid 250 mg (o) with food daily, increase to max. 500 mg tds

Checkpoints

Dyslipidaemia

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Table 129.3 Lipid-lowering drugs Drug The statins Atorvastatin Pravastatin Simvastatin Fluvastatin Rosuvastatin Bile acid binding resins Cholestyramine Colestipol Fibrates Gemfibrozil

Dose (average) Night dose 10–80 mg 10–80 mg 10–80 mg 20–80 mg 5–40 mg

Usage

Adverse effects

Safety monitoring

↑ cholesterol

Muscle pains, raised liver enzymes

Liver enzymes: creatine kinase and ALT

8 g bd 10 g bd

↑ cholesterol

GIT dysfunction, drug interactions

600 mg bd

↑ triglycerides mixed hyperlipidaemia

GIT dysfunction, myositis, interaction with statins and warfarin

Liver enzymes coagulation

Arthralgia, myalgia, myositis, liver dysfunction Flushing, raised glucose, urate and liver enzymes GIT dysfunction, arrhythmias Minimal

Liver enzymes

Fenofibrate Other agents Ezetimibe

160 mg daily 10 mg daily

↑ cholesterol

Nicotinic acid

100 mg tds to 500 mg tds

↑ cholesterol and triglycerides

Probucol

500 mg bd

↑ cholesterol

Fish oils n-3 fatty acids

2 g daily

↑ triglycerides

• adverse effects: flushing, gastric irritation, gout • minimise side effects with gradual introduction; take with food and aspirin cover 7 Probucol • probucol 500 mg (o) bd • problems: slow response, care with hepatic disease 8 Oestrogen12 • oestradiol valerate 2 mg (o) mane ± medroxyprogesterone acetate This hormone replacement therapy can reduce LDLC and is a physiological intervention in postmenopausal females, especially after hysterectomy. It has limited efficacy.

Resistant LDLC elevation 1 Combination statin + ezetimibe 2 Combined statin and resin cholestyramine 4–8 g (o) mane plus a statin (see page 1317)

Glucose urate Liver enzymes Liver enzymes ECG Bleeding time

Moderate to severe (isolated) TG elevation gemfibrozil 600 mg (o) bd or fenofibrate 145 mg (o) daily

Note: Slow response; monitor LFTs; predisposes to gallstones and myopathy. Alternatives: nicotinic acid or n-3 fish oil concentrate 6 g (o) daily in divided doses to max. 15 g/day

Note: Reduction in alcohol intake is essential.

Massive hypertriglyceridaemia (TG) 10 nmol/L: • Fibrate plus fish oil

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Mixed hyperlipidaemia (↑ TG + ↑ LDLC) • If TG 4: a fibrate

Consider combination therapy, e.g.: • fish oil + ‘statin’ • fibrate + resin

Note: Statin + gemfibrozil increases risk of myopathy and requires specialised supervision.

sterols but there is insufficient evidence to recommend vitamin E, garlic and lecithin.13

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Cardiovascular (Including Coronary) Risk Factors, page 116 • Cholesterol: How to Lower Cholesterol, page 117

Special considerations The decision to commence drug therapy should be based on at least two separate measurements at an accredited laboratory. Be careful with β-blockers and diuretics affecting lipid levels.

Length of treatment • Possibly lifelong (up to 75 years)

Follow-up investigations • Serum lipids • LFTs (ALT and CPK) • Possibly CK

Special groups Children In general there is little justification for using lipidregulating drugs in children, especially as the drugs have been shown to reduce heart disease within 2–5 years in adults.11 Initial dietary advice and avoidance of smoking is recommended. Bile acid sequestrating resins are safe to use.

The elderly11 The role of lipid therapy remains unclear. Generally, elderly patients with established CHD should receive standard lipid management unless their general medical status is poor.

Pregnancy12 As a general rule the increase in cholesterol level associated with pregnancy subsides after delivery. Systemically absorbed lipid-lowering agents may be unsafe during pregnancy and should be avoided.

Complementary therapy Claims have been made for the cholesterol-lowering properties of policosanol (derived from sugar cane), fish oils, plant sterols, vitamin E, garlic and lecithin. The evidence from RCTs to date indicates a modest benefit from policosanol, fish oils (consuming a fish-based meal at least twice a week is recommended) and plant

REFERENCES 1 Duffy SJ, Meredith IJ. Treating mildly elevated lipids. Current Therapeutics, 1996; 37(4): 49–58. 2 Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet, 1994; 344: 1383–9. 3 Pitt B, Mancini BJ, Ellis SG, et al. Pravastatin limitation of atherosclerosis in the coronary arteries (PLACI): reduction in atherosclerosis progression and clinical events. J Am Coll Cardiol, 1995; 26: 1133–9. 4 Byington RP, Furberg CD, Crouse JR, et al. Pravastatin, lipids and atherosclerosis in the carotid arteries (PLACII). Am J Cardiol, 1995; 76: 54C–59C. 5 Furberg CD, Adams HP, Applegate WB, et al. for the Asymptomatic Carotid Plaque Study (ACAPS) Research Group. Effect of lovastatin and warfarin on early carotid atherosclerosis and cardiovascular events. Circulation, 1994; 90: 1679–87. 6 Salonen R, Nyyssonen K, Porkkala-Sarataho E, Salonen JT. The Kuopio Atherosclerosis Prevention Study (KAPS): effect of pravastatin treatment on lipids, oxidation resistance of lipoproteins, and atherosclerosis progression. Am J Cardiol, 1995; 76: 34C–39C. 7 Jukema JW, Bruschke AVG, van Boven A, et al. Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation, 1995; 91: 2528–40. 8 Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolaemia. N Engl J Med, 1995; 333: 1301–7. 9 Studer M, Briel M, et al. Effect of different antilipidemic agents and diets on mortality. Arch Intern Med, 2005; 165: 725–30. 10 Department Human Services and Health. Schedule Benefits. Canberra: Commonwealth of Australia, November 1996: 25–8. 11 Colquhoun D. How to treat hypercholesterolaemia. Australian Prescriber, 2008; 31(5): 119–21. 12 Smith A (Chair). Therapeutic Guidelines: Cardiovascular (Version 5). Melbourne: Therapeutic Guidelines Ltd, 2008: 57–66. 13 Managing dyslipidaemia. NPS News, 2002; 20: 5–6.

Diabetes mellitus: management

9 130

Man may be the captain of his fate, but he is also the victim of his blood sugar. W I L F R E D G O A K L E Y (1905– 6 8 ) 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:1 1 to achieve strict glycaemic control as measured by (most importantly) glycosylated 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. 130.5 and 130.6) at the end of this chapter.

Management principles • Provide detailed and comprehensive patient education, support and reassurance. • Achieve control of presenting symptoms. • Achieve blood pressure control (≤130/80 mmHg supine). • 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.

Metabolic syndrome 2 Beware of the deadly metabolic syndrome (syndrome X or insulin resistance syndrome).

• fasting glucose ≥ 5.6 mmol • BP ≥130/85

This syndrome is associated with increased risk for the development of type 2 diabetes and atherosclerolic vascular disease.

Monitoring techniques • • • • • • • • •

Blood glucose estimation (fasting and post-prandial) Urine glucose (of limited usefulness) Urine ketones (for type 1 diabetes) Glycosylated haemoglobin (HbA1c) (essential to know glycaemic control) Microalbuminuria (regarded as an early and reversible sign of nephropathy) Blood pressure Serum lipid levels Kidney function (serum urea/creatinine eGFR) ECG

Control guidelines are summarised in Figure 130.1 and Table 130.1. Table 130.1 Suggested guidelines for glycaemic control (plasma glucose mmol/L)1, 3 Ideal

Suboptimal or unacceptable

Before meals (fasting)

7.7

After meals (2 hours postprandial)

11

HbA1c %*

11

*HbA1c is an index of the mean plasma glucose levels over the preceding 2–3 months (assume a reference range of 4.5–8%). The reference ranges vary in different laboratories.

• Upper truncal obesity ( waist circumference) plus any 2 or more of the following • ↑ triglycerides >1.7 mmol/L • ↓ HDL cholesterol 15 mm Talar tilt >20°

Clinical features (sprained lateral ligaments) Common features: ankle ‘gives way’ difficulty in weight-bearing discomfort varies from mild to severe bruising (may take 12–24 hours) indicates more severe injury (see Fig. 138.13) • may have functional instability: ankle gives way on uneven ground • • • •

Examination Perform as soon as possible: • note swelling and bruising • palpate over bony landmarks and three lateral ligaments • test general joint laxity and range of motion • a common finding is rounded swelling in front of lateral malleolus (the ‘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.

Figure 138.13 Sprained ankle with tearing of the lateral ligament complex with obvious haematoma

Indications for X-ray include:9 • • • • • • •

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)

Ottawa rules for ankle and foot X-ray 10 These rules are a quick and reliable method of selecting which patients with ankle and foot injuries need X-rays to exclude a fracture.

Common sporting injuries

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) • 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

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.

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 B

C

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A = Analgesics (e.g. paracetamol ± codeine) R = Review in 48 hours, then 7 days S = Special strapping

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 with 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. 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 • 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. 138.14) • 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 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 D

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138 Figure 138.14 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

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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. 138.15). 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.

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 138.3). Table 138.3 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

Figure 138.15 Complete (grade III) tear of lateral ligaments of the ankle in a netball player; note excessive movement in inversion and anterior draw

Surgical repair Some specialists prefer this treatment but it is usually reserved for the competitive athlete who demands absolute stability of the ankle. 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. 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. 138.14c) 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.

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.

Wobble 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 wobble board. An improvised wobble board can be constructed by attaching a small piece of wood (10 cm × 5 cm) to the centre of a 30 cm piece of plywood or simply placing a slab of wood on a dome-shaped mound of earth. 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 (see Fig. 138.16), to improve proprioception and balance.

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

Common sporting injuries

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• talon noir • blisters

Achilles tendonopathy/ peritendonopathy 11 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 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 Figure 138.16 Wobble board technique for ankle dysfunction

This is very useful in differentiating between tendonopathy, peritendonopathy, focal degeneration and a partial tear.

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.

Preventive measures

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 pages 732–3) — tendonopathy/peritendonopathy — tear: partial or complete • bruised heel • ‘pump bumps’/bursitis • calcaneal apophysitis • plantar fasciitis (see pages 733–4)

• 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 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

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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. 138.17 and 138.18)

Note: The injury may be missed because the patient is able to plantarflex the foot actively by means of the deep long flexors to the foot.

Figure 138.17 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

Treatment

Disorders of the feet and toes

• Early surgical repair (within 3 weeks)

Common problems include:

‘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 pre-existing 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.

• • • • • • • •

fractures of toes foot strain ingrowing toenails ‘black’ nails bony outgrowth under the nail (subungual exostosis) calluses athlete’s foot (tinea pedis) plantar warts

Black nails (‘soccer toe’) Black or ‘bruised’ nails are due to subungual haematoma caused by trauma (see Fig. 138.19). The 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.

Common sporting injuries

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B

Figure 138.19 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 C

Patient education resources Hand-out sheets from Murtagh’s Patient Education 5th edition: • Sports Injuries : First Aid, page 190 • Sprained Ankle, page 191 • Warm-up Exercises for the Legs, page 194

Figure 138.18 Thompson calf squeeze test for ruptured Achilles tendon: (a) intact tendon, normal plantarflexion, (b) ruptured tendon, foot remains stationary

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.

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.

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 page 702) • Avulsion of epiphyses (e.g. ischial tuberosity— hamstring) • Stress fracture • Osgood–Schlatter disorder • Scheuermann disorder • Idiopathic scoliosis

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 Litt J. The sprained ankle. Aust Fam Physician, 1992; 21: 447–56. 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 Brukner P, Khan K. Clinical Sports Medicine (3rd edn). Sydney: McGraw-Hill, 2007: 59–607. 12 Paoloni J. Acute ankle injuries in sports. Medical Observer, 20 May 2005: 29–31.

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Health of specific groups

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The health of Indigenous peoples Health does not just mean the physical well being of the individual but refers to the social, emotional and cultural well being of the whole community. This is a whole of life view and includes the cyclical concept of life-death-life. Health services should strive to achieve the state where every individual can achieve their full potential as human beings (Aborigines) and thus bring about the total well being of their communities. This is an evolving definition (process). N AT I O N A L A B O R I G I N A L C O M M U N I T Y C O N T R O L L E D H E A LT H O R G A N I S AT I O N , S E P T E M B E R 199 3

The major health challenge in Australia (and several other developed countries) is the health status of Indigenous peoples, which continues to be dramatically worse than that of other people. In some cases, it appears that the gap may be widening, especially for women.1 Life expectancies in 2001 for Aboriginal and Torres Straits Islander men and women were 17 years below those of other Australians.1 At the end of 2001 their average life expectancy was 59.4 years for men and 64.8 years for women (compared with others—77 years and 82 years, respectively).1,2 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

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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 approximately 480 000. 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. 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.6

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:

The health of Indigenous peoples

•

• • •

•

• • • • •

— type 2 diabetes (20–50% incidence) — hypertension — kidney function — other cardiovascular risk factors (e.g. hypercholesterolaemia) — hepatitis B — STI urine screening (men and women) — Pap smears — anaemia in children — hearing in children Screening investigations to consider include: — blood sugar — 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 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

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kidney disorders 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)7 • pneumococcal respiratory disease • • • • • •

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 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 Hospital8 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 139.1.

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 simple bridge to acceptance.’9 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.10 It is important for doctors working in Indigenous communities (see Fig. 139.1) to have an appreciation of and respect for Indigenous culture and be aware of its significance in health and behaviour.

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Table 139.1 Priority Aboriginal 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 Aboriginal children (particularly in rural and remote areas) Housing Water supply Alcohol and substance misuse Domestic violence and sexual abuse Child abuse Gambling Unemployment

An Indigenous patient may feel more relaxed if accompanied by a relative, who can witness what the doctor said and reinforce it later.

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.11 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.12

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.9 The place where the person died is deserted for a certain time and then smoked out.

Figure 139.1 Doctor on an outback home visit in Central Australia. Courtesy Alice Springs Rural District Department of Health and Community Services

Common problems in children 12 Indigenous children suffer the same spectrum of health problems as children in developing countries 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 139.2. Acute respiratory tract infections are a common reason for admission to hospital. Bacterial pneumonias occur more commonly than in non-Indigenous 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

The health of Indigenous peoples

Table 139.2 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

preceding acute otitis media and may be related to poor nutrition and anaemia. The basic treatment is ear toilet with povidone–iodine solution, 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.13 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

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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 page 1350). 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) • sexually transmitted infections • psychosocial dysfunction • bites and stings • severe infections (e.g. meningitis, rheumatic fever, septicaemia) • hepatitis B • tropical diseases (where applicable) • worm infestation

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.6,14

Cardiovascular disease 3,15 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.

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Targets for secondary prevention of cardiovascular disease and diabetes mellitus are as presented on page 1290 (‘Management of diabetes’).

Ear infections 6,14 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

and one for Chlamydia). Apply topical chloramphenicol eyedrops plus ointment. • Neonatal gonococcal ophthalmia and Chlamydia infection. Refer to pages 552–1. • Gonococcal conjunctivitis. Procaine penicillin (IM) statim or single dose oral therapy with amoxycillin plus probenecid (e.g. 3 g + 1 g in adult). Use ceftriaxone IM if penicillin-resistant. • Trachoma. These patients have ‘scratchy’ eyes and watery discharge ± red eye (see Fig. 139.2): — if over 6 kg and not pregnant: azithromycin (o) as single dose — if under 6 kg or pregnant: erythromycin or roxithromycin (o) for 21 days or oily tetracycline eyedrops 1 bd for 3–6 weeks — check and treat household contacts — check routinely for ‘follicles’ of trachoma

• Acute suppurative Antibiotics (as above) + dry mop otitis media ear • Chronic Wash with povidone–iodine 5% suppurative otitis solution using a 20 mL syringe media 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

Eye infections 6,14 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