A Handbook of Emergencies [9 ed.] 9789389776126, 9789352705917

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A HANDBOOK OF EMERGENCIES

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A HANDBOOK OF EMERGENCIES Ninth Edition

Aspi F Golwalla MD FACC FCPS FCCP

Emeritus Professor of Medicine GS Medical College and KEM Hospital Mumbai, Maharashtra, India

Sharukh A Golwalla MD (Med) DM (Card) FCCP (Specialised in Echocardiography)

Cardiologist Breach Candy Hospital, Jaslok Hospital Sir HN Reliance Foundation Hospital Mumbai, Maharashtra, India

JAYPEE BROTHERS MEDICAL PUBLISHERS The Health Sciences Publisher New Delhi | London | Panama

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Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: [email protected] Overseas Offices J.P. Medical Ltd 83 Victoria Street, London SW1H 0HW (UK) Phone: +44 20 3170 8910 Fax: +44 (0)20 3008 6180 Email: [email protected]

Jaypee-Highlights Medical Publishers Inc City of Knowledge, Bld. 235, 2nd Floor Clayton, Panama City, Panama Phone: +1 507-301-0496 Fax: +1 507-301-0499 Email: [email protected]

Jaypee Brothers Medical Publishers (P) Ltd Bhotahity, Kathmandu, Nepal Phone: +977-9741283608 Email: [email protected] Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2019, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/ editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. The CD/DVD-ROM (if any) provided in the sealed envelope with this book is complimentary and free of cost. Not meant for sale. Inquiries for bulk sales may be solicited at: [email protected] A Handbook of Emergencies First Edition: 1955 Ninth Edition: 2019 ISBN 978-93-5270-591-7

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Preface The revised edition of this pocketbook covers in brief the diagnosis and management of common and some not so common emergencies encountered in day-to-day practice by the clinicians. Once again, we wish to express our sincere thanks to the specialists who have taken the trouble to go through the texts of their contributions in spite of busy schedules, which has allowed the handbook to achieve its popularity. Aspi F Golwalla Sharukh A Golwalla

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Contents 1. Pediatric Emergencies •• •• •• •• ••

1

Neonatal Emergencies  1 General Pediatric Emergencies  23 Accidental Poisoning in Children  46 Neonatal Critical Care  47 Neonatal Jaundice  48

2. Dermatologic Emergencies

51

•• •• •• ••

Infections 52 Autoimmune Disorders  56 Toxic Disorders  60 Allergic Reactions Anaphylaxis and Angioedema 66 •• Drug Reactions  67

3. Emergencies in Ear, Nose and Throat

•• Foreign Bodies in the External Auditory Canal  71 •• Furunculosis of the External Auditory Canal  72 •• Malignant Otitis Externa  74 •• Traumatic Perforation of the Eardrum  75 •• Bleeding from the Ear  76 •• Acute Otitis Media  76 •• Acute Mastoiditis and Mastoid Abscess  77 •• Earache 78 •• Sudden Deafness  78 •• Meniere’s Disease  80 •• Epistaxis 81 •• Foreign Body in the Nose  83 •• Cerebrospinal Fluid Rhinorrhea  83 •• Fracture of Nasal Bone  84 •• Laryngeal Emergencies  85

71

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A Handbook of Emergencies •• •• •• •• •• •• ••

Cafe Coronary  86 Foreign Body in the Bronchus  86 Burns Due to Acid or Alkali Ingestion  87 Foreign Body in the Pharynx  88 Foreign Body in Esophagus  88 Temporomandibular Joint Dislocation  89 Trismus (Not Due to Tetanus)  90

4. Ophthalmic Emergencies •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• ••

91

Sudden Loss of Vision  91 Painful Ophthalmic Emergencies  92 Acute Conjunctivitis  92 Panophthalmitis 93 Trachoma 94 Ophthalmia Neonatorum  94 Corneal Ulcer  95 Iridocyclitis 97 Episcleritis and Scleritis  98 Acute Orbital Cellulitis  100 Cavernous Sinus Thrombosis  101 Acute Dacryocystitis  101 Vitreous Hemorrhage  102 Central Retinal Artery Occlusion  102 Retinoblastoma (Glioma)  103 Optic Neuritis  104 Malignant Exophthalmos  106 Detachment of the Retina  106 Foreign Bodies (Extraocular)  107 Intraocular Foreign Body  108 Chemical Injury and Burns of the Cornea and Conjunctiva  109 Perforating Injuries  110 Effects of Contusions  111 Hyphema (Blood in the Anterior Chamber)  112 Acute Congestive Glaucoma  113

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Contents

5. Emergencies in Gynecology

115

6. Psychiatric Emergencies

140

•• Emergencies with Profuse External Hemorrhage  115 •• Injuries of the Vulva, Vagina and Perineum  119 •• Hemorrhage from Tumors of Uterus and Ovaries  120 •• Emergencies with Obvious Severe Intraperitoneal Hemorrhage  122 •• Emergencies Associated with Obvious Infection  127 •• Rupture of a Pyosalpinx, Tubo-ovarian Abscess or an Infected Ovarian Cyst  129 •• Emergencies with Acute Abdominal Conditions of Doubtful Etiology  131 •• Dysmenorrhea 133 •• Torsion of an Ovarian Tumor, Hydrosalpinx or Subserous Fibroid  134 •• Rupture of a Chocolate Cyst of Ovary  135 •• Rupture of an Ovarian Tumor  136 •• Red Degeneration of Fibroid of the Uterus  137 •• Acute Retention of Urine  138 •• •• •• •• •• •• •• •• •• ••

ix

General Approach  140 General Principles  140 Violence 142 Suicidal Behavior  144 Victims of Disaster  145 Grief 146 Rape Survivor  147 Anxiety and Panic Disorders  148 Stupor 150 Emergencies Associated with Substance Use Disorders  151

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A Handbook of Emergencies •• Alcohol 152 •• Opioids 154 •• Sedatives and Hypnotics (Barbiturates, Benzodiazepines, Methaqualone, etc.)  156 •• Cannabinoids 158 •• Central Nervous System Stimulants  159 •• Hallucinogens 160 •• Psychiatric Manifestations of Physical Disorders  161

7. Gastrointestinal, Liver and Biliary Tract Emergencies

164

8. Respiratory Emergencies

194

•• Esophageal Disorders  164 •• Acute Gastrointestinal Bleeding (Hematemesis and Melena)  165 •• Acute Lower GI Hemorrhage  170 •• Acute Abdominal Pain  172 •• Acute Appendicitis  173 •• Acute Diverticulitis  174 •• Perforated Peptic Ulcer  175 •• Acute Severe Ulcerative Colitis  175 •• Acute Pancreatitis  176 •• Acute GI Vascular Disorders  178 •• Acute Non-specific Mesenteric Lymphadenitis 180 •• Tuberculous Lymphadenitis  180 •• Abdominal Distension  181 •• Intestinal Obstruction  182 •• Emergencies in Diseases of the Biliary Tract  183 •• Liver Disorders  185 •• Acute Liver Failure  189 •• Massive Hemoptysis  194 •• Acute Severe Asthma  196

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Contents

xi

•• Acute Respiratory Failure  199 •• Acute Lung Injury and Acute Respiratory Distress Syndrome  201 •• Acute Exacerbation of COPD  205 •• Pneumonia 209 •• Massive Pulmonary Collapse  211 •• Spontaneous Pneumothorax  212 •• Massive Pleural Effusion  213 •• Acute Laryngeal Obstruction  214

9. Cardiovascular Emergencies •• •• •• •• ••

•• •• •• •• •• •• ••

10. Neurological Emergencies •• •• •• •• •• •• •• •• ••

217

Cardiac Arrest  217 Unstable Angina/NSTEMI 222 ST Elevation Myocardial Infarction  225 Cardiac Arrhythmias  229 Acute Left Ventricular Failure with Pulmonary Edema  236 Hypertensive Crises  237 Acute Massive Pulmonary Embolism  238 Cardiac Tamponade  240 Acute Aortic Regurgitation  242 Peripheral Vascular Emergencies  242 Severe Primary Antiphospholipid Syndrome 245 Syncope 245

248

Raised Intracranial Pressure  248 Ischemic Cerebrovascular Disease  252 Intracerebral Hemorrhage  259 Acute Subarachnoid Hemorrhage  261 Status Epilepticus (SE)  264 Antiepileptic Drugs  266 Intracranial Infections  268 Acute Neuromuscular Emergencies  276 Acute Spinal Cord Disturbance (Myelopathy)  292

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11. Emergencies in Hematology •• •• •• •• ••

•• •• •• ••

295

Anemia 295 Hemoglobinuria 297 Sickle Cell Crisis  298 Bleeding Disorders  299 Disseminated Intravascular Coagulation 301 Transfusion Reactions  302 Bone Marrow Failure  304 Neutropenia (Agranulocytosis)  307 Pure Red Cell Aplasia  308

12. Endocrine Emergencies

309

13. Emergencies in Urogenital Diseases

326

•• Thyroid Crisis (Thyroid Storm)  309 •• Gastrointestinal Bleeding and Cold Exposure  310 •• Myxedema Coma  311 •• Acute Adrenal Insufficiency  313 •• Diabetic Ketoacidosis  314 •• Lactic Acidosis in a Diabetic  317 •• Hypoglycemia 317 •• Hypercalcemic Crisis  318 •• Hypocalcemic Tetany  320 •• Pituitary Apoplexy  321 •• Cranial Diabetes Insipidus  321 •• Hypertensive Crisis in Pheochromocytoma 322 •• Pituitary Crisis or Coma  323 •• Hyponatremia Secondary to SIADH  324 •• •• •• •• •• •• •• ••

Hematuria 326 Renal Colic  329 Acute Retention of Urine  331 Scrotal Pain  333 Paraphimosis 335 Acute Nephritic Syndrome  335 Rapidly Progressive Renal Failure  336 Acute Renal Failure  337

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Contents

14. Emergencies in Tropical and Infectious Diseases •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• •• ••

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341

Malaria 341 Typhoid Fever  344 Fulminant Amebic Infection  345 Acute Bacillary Dysentery  347 Cholera 348 Acute Gastroenteritis (Food Poisoning)  350 Clostridium Difficile Infection  352 Tetanus 352 Leptospirosis 355 Dengue 356 Chikungunya Fever  358 Effects of Heat  359 Rabies 360 Measles 360 Chickenpox 361 Whooping Cough  362 Mumps 363 Diphtheria 364 Infectious Mononucleosis  366 Acute Disseminated Miliary Tuberculosis  367

15. Shock •• •• •• •• ••

368

Hypovolemic Shock  368 Cardiogenic Shock  369 Obstructive Shock  371 Septic Shock  371 Systemic Inflammatory Response Syndrome 373 •• Anaphylactic Shock  374

16. Rheumatological Emergencies

•• Emergencies Involving Disease Processes  377 •• Emergencies Involving Specific Organs  379 •• Emergencies Involving Peripheral Joints and Spine  380 •• Emergencies Due to Drugs  382

377

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A Handbook of Emergencies

17. Febrile Emergencies •• •• •• •• •• •• ••

383

Sepsis Syndrome  383 Febrile Neutropenia  383 Fever in Immunocompromised Host  384 Thyroid Storm  384 Pheochromocytoma 385 Heat Stroke  385 Cerebral Hemorrhage  387

18. Emergencies in HIV Infection

388

19. Emergencies Due to Fluid and Electrolyte and Acid-base Disturbances

393

20. Acute Poisoning

403

21. Venomous Bites and Stings

453

•• Emergencies due to Opportunistic Infections  388 •• Emergencies due to Antiretroviral Therapy  391

•• Disorders of Water and Electrolyte Metabolism 393 •• Water 393 •• Sodium 394 •• Potassium 396 •• Calcium 398 •• Magnesium 399 •• Acid-base Disturbances  400

•• Approach to a Case of Poisoning  403 •• Poisonous Substances  413 •• •• •• •• ••

Snakebite 453 Scorpion Stings  457 Spider Bites  458 Bee and Wasp Stings  459 Fish Stings  459

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Contents

22. Emergencies Due to Physical Causes •• •• •• •• •• ••

461

Heat Illness  461 Cold-induced Illness  461 High Altitude-induced Illness 464 Drowning and Near-Drowning  465 Diving and Dysbaric Emergencies  468 Electrical Injuries and Lightning  470

23. Emergency Management in Burns •• •• •• •• ••

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473

Causes of Burn  473 Pathophysiology 474 Management 475 Management 478 Fluid and Electrolyte Replacement Therapy  481

24. Infections in the Immunocompromised Patient 485 •• Main Groups at Risk of Infection  485 •• Factors Associated with Increased Risk of Infection  485 •• Diagnosis 486 •• Investigations 487 •• Management of Infection  487 •• HIV Infection  488

25. Emergencies in Cancer •• •• •• •• •• •• •• •• ••

491

Spinal Cord Compression  491 Superior Vena Cava Syndrome  492 Cardiac Tamponade  492 Pulmonary Complications  493 Infections 494 Metabolic Complications  494 Hemorrhage 495 Renal Failure  495 Gastrointestinal Complications  496

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A Handbook of Emergencies

26. Postoperative Medical Emergencies •• •• •• ••

497

Fever 497 Wound Infection  499 Intra-abdominal Sepsis  500 Urinary Tract Infection  502

27. Emergencies in Industrial Medicine

504

28. Medical Emergencies in the Air

512

29. Emergency Medical Procedures

517

•• Chemical Hazards  504 •• Acute Allergic Episodes  510 •• Effects of Altitude  512 •• Medical Fitness to Fly  514

•• •• •• ••

Venous Cutdown  517 Insertion of Nasogastric Tube  518 Lumbar Puncture  519 Use of Self-retaining Foley Urinary Catheter  521 •• Tracheostomy 523

Appendix •• •• •• ••

Index

525

Normal Values of CSF  525 Normal Hematological Values  525 Coagulation Tests  525 Serum Levels of Common Emergency Drugs  526

539

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CHAPTER

1

Pediatric Emergencies

Neonatal Emergencies I. Asphyxia Definition of Birth Asphyxia National Neonatology forum of India has suggested that Birth Asphyxia should be diagnosed when “baby has gasping and in adequate breathing or no breathing at 1 minute”. Every birth is a medical emergency. If the baby does not initiate breathing/crying at birth, it is at a risk of asphyxia and its serious life-threatening consequences. Prevention of asphyxia begins in the antepartum period and continues during and after the baby is delivered. Resuscitation alert is required for the following: A. Antepartum factors: 1. Placental insufficiency – raised BP, toxemia, postmaturity, diabetes mellitus 2. Malpresentation 3. Multiple pregnancy 4. Intrauterine growth restriction (IUGR) 5. Bad obstetric history 6. Polyhydramnios or oligohydramnios 7. Maternal drug abuse/alcoholism.

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B. Intrapartum factors: 1. Fetal distress 2. Premature labor 3. Cord prolapse/tight cord around the neck 4. Antepartum hemorrhage 5. Prolonged labour (> 24 hours) 6. Prolonged 2nd stage of labour (> 2 hours). American academy of pediatric has proposed that diagnostic label of perinatal asphyxia should be reserved to describe an infant who manifests all of the following: zz Cord umbilical artery pH of 7.0 with a base deficit of > 10 mfg/L zz Neonatal neurological manifestation suggestive of hypoxic-ischemic encephalopathy (HIE) zz Evidence of multiorgans dysfunction (e.g. cardio­ vascular, renal, gastrointestinal, hematologic or pulmonary).

Management A. Antepartum 1. Identify high risk fetus and monitor. 2. If fetal distress is present, give the mother – (a) Lateral position. (b) O2 through mask. (c) Liberal IV fluids. (d) Stop oxytocin. (e) Try to cut short 2nd stage of labor. B. Neonatal resuscitation (A-Airway, B-Breathing, C-Circulation) 1. At the introitus, do mucus suction. 2. On delivery, unravel loops/knots of cord (if any). Cut the cord between clamps and handover the baby to the caretakers. Cord clamping must

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be done within 45 seconds to 2 minutes after emergence of the baby. 3. On receiving the baby, dry it (especially the head) and keep it swaddled in the warmer in head-low position. Suck out oral and nasal cavities with a low pressure suction (< –5 mm Hg). 4. Assess the APGAR score (Table 1.1). If > 7, stabilize the baby. No further resuscitation is needed. Tie the cord, clean the baby and drape it in clean sheets. Give to mother to breastfeed. 5. If the APGAR ≤ 7, and the baby is apnoeic, start physical stimulation till breaths are initiated. 6. If the mother is on narcotics or heavily sedated, give Naloxone 0.1 mL/kg/IV/ET route. 7. If respirations are inadequate, begin bag-mask ventilation with a neonatal size Ambu bag using 90–100% O 2. An extension tube will improve percentage of O2 that goes in Ambu bag (Fig. 1.1). 8. Using a small-blade (size 0 or size 00) infant laryngoscope, intubate the baby with 2.5–4 mm endotracheal tube, at this point if baby respirations are not revived and HR < 100 min continue positive pressure ventilation (pressure 20–25 cm H2O), taking care not to squeeze too hard to avoid barotrauma (e.g. subcutaneous emphysema). 9. If HR falls below 60/min, initiate chest compression with tips of first 2 fingers at 140/min. 10. Administer sequentially the following drugs: (a) Epinephrine 0.2 mL/kg IT (intratracheal) (b) Sodium bicarbonate 2 mEq/kg IV (intravenous) (c) Volume expanders—saline, Ringer lactate, salt poor albumin or blood 10 mL/kg (d) Dopamine 5–10 µg/kg/min.

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Reflex response Nil Grimace Cough or sneeze 0–2 Severe 3–5 Moderate 6–7 Mild 8–10 Normal

Muscle tone Flaccid Some flexion Active motion Score

Evaluate the score at 1, 2 and 5 minutes. By inserting catheter in nostril or tactile stimulation.

Heart rate Respiration Absent Absent Slow Slow irregular < 100 2 > 100 Good cry Response to catheter in nostril

Score 0 1

Table 1.1 : The Apgar score

Pink

Color Blue or pale Body pink, extremities blue

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Fig. 1.1: Ambu bag 11. Mechanical ventilation has to be restarted if apnea/hypopnea persists but HR > 100/min and is continued if the baby’s pulsox can be brought above 86%. 12. In case of failure to revive resuscitation may be abandoned after 30 minutes. 13. Endotracheal access: IV access may fail sometimes in infants. In such situation endotracheal (ET) route can be used for some of the drugs, e.g. epinephrine, lidocaine, atropine, naloxone, vasopressin. Epinephrine 10 times of IV dose and others 2–3 times of IV dose may be given. Ionized medications such as sodium bicarbonate or calcium chloride cannot be given by ET route.

II. Respiratory Distress Respiratory rate of > 60 breaths/min at rest with intercostal retraction and expiratory grunting.

Causes 1. Respiratory Day 0–3: Meconium aspiration, transient tachypnea, pneumonia, pneumothorax, atelectasis, hyaline membrane disease (HMD), choanal atresia, laryngeal web, goiter, diaphragmatic hernia, pulmonary hypoplasia, asphyxiating thoracic dystrophy.

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Day 3–10: Milk aspiration, H-type T-0 fistula, WilsonMilky syndrome, postnatal pneumonia, cysts and tumors. Day 15 and more: Bronchopulmonary dysplasia (BPD). 2. Cardiac: Congenital heart disease . 3. Nervous system: Asphyxia neonatorum, paralysis of muscles due to myasthenia, myopathies, etc. 4. Metabolic: Organic acidemias.

Clinical Features See Table 1.2 to assess severity. Look for degree of cyanosis. Suspect a T-O fistula if child has frothing at the lips, and a diaphragmatic hernia if abdomen is scaphoid and distress increases with face-mask bagging. There will be audible peristalsis in the chest. X-ray to confirm diagnosis.

Management 1. Stop oral feeds. Pass a stomach tube and keep aspirating 4 hourly. 2. Keep infant in preheated incubator to maintain body temperature at 30.5ºC. 3. Connect a pulsoximeter device to the baby for monitoring. Give enough O2 to keep pulse-oximeter reading above 90%. On a blood gas, one should try and achieve a PaCO2 of 42 mm Hg or less. Avoid excessive O2 as it can cause oxidative damage to the retina and lungs, causing retinopathy and bronchopulmonary dysplasia. 4. Use a oxygen hood initially, or supply moist O2 with nasal prongs. Intubation may be tried if the baby has failed to respond. In case of severe distress resort to mechanical ventilation.

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Retractions

Cyanosis

Air entry

3.

4.

5.

0

Equal and good

None

None

None

< 60

1

Reduced

None on O2, present without O2

Mild

Mild

60–80

Downe’s score of 7 or move is suggestive of impending respiratory failure

2.

Score

Respiratory rate/min Grunting

S.No.

1.

Almost absent

Needs more than 40% O2

Severe

Audible to naked ear

> 80

2

Table 1.2: Downe’s scoring for assessment of severity of respiratory distress (RD)

Pediatric Emergencies

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5. Oxygen delivery devices: Low flow system Flow rate Oxygen% 1. Nasal cannula 1–6 L/min Max 45% 2. Nasal catheter 1–6 L/min Max 45% 3. Face mask 5–10 L/min Max 35–60% High flow system 1. Oxygen hood 10–15 L/min up to 80–90% 2. Partial rebreathing 10–12 L/min 50–60% mask 3. Non rebreathing mask 10–12 L/min up to 90% 4. Anesthesia bag with 10–12 L/min up to 95% non rebreathing mask 6. Suction: An installed suction unit should be capable of generating a vacuum of 300 mm Hg when tube is clamped. A suction force of 80–120 is necessary to suction the airway of an infant or a child. 7. Mask: A mask should reach from the midportion of the bridge of the nose to the protuberance of the chin without extending over the chin. 8. Bag and mask ventilation: A correct size bag is chosen. 400–500 mL is necessary for full-term newborn, infants and young children. For older children and adults 750 mL or more is recommended. Endotracheal tubes chosen according to the size and age of the child. Popular formula for ET tube size is Age (year) + 4 4 9. If IV access fails sometimes in infants, then ET route can be used for some of the drugs, e.g. epinephrine, lidocaine, atropine, naloxone, vasopressin. Epinephrine 10 times of IV dose and others 2–3 times of IV dose. (Inner diameter in mm) =

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Ionized medications such as sodium bicarbonate or calcium chloride cannot be given by ET route. 10. In HMD, exogenous surfactant can be instilled into the lungs. Infant will have to have mechanical ventilation thereafter. 11. Baby with a diaphragmatic hernia will have to be operated as soon as it is stabilized. However, even if the operation is successful overall outcome is poor because of pulmonary hypoplasia/dysplasia. 12. Transient tachypnea of the newborn is seen after Cesarean section and the outcome is variable. 13. In severe meconium aspiration, the infant will need ventilation in 50% of cases. Outcome will depend upon timing of therapy, amount of meconium in the lungs and judicious use of ventilation. Air leaks are common in this condition and can occur even without high pressure ventilation. One should be on guard for sudden deterioration; it usually implies development of tension pneumothorax—absent air entry on one side of chest, confirmed by inserting a scalp vein in subclavicular space with the other end dipped in a cup filled with water or normal saline. Emergence of bubbles and reduction of distress over next few minutes will confirm the diagnosis. Take a chest X-ray and insert an underwater ICD drain once the baby stabilizes. 14. Tension pneumothorax: 18 size IV cannula attached to a 10 or 20 mL syringe should be inserted in 2nd intercostal space in midclavicular line to suck out air followed by ICD tube. 15. Shock: A child in hypovolemic shock may require 40–60 mL/kg of crystalloids during first 15 minutes of resuscitation, e.g. saline, Ringer lactate infused rapidly

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(20 mL/kg). In later phase of shock colloids may be useful e.g. blood, fresh frozen plasma, 5% albumin, haemaccel and starch preparations. 16. Calcium: Dose is 0.2 mL/kg of 10% solution. This delivers 5–7 mg/kg of elemental calcium. 17. Atropine: It is parasympatholytic agent that increases the heart rate and shortens the AV node conduction time. Dose is 0.02 mg/kg with minimum of 0.5 mg for child and 1.0 mg for adolescent. It can be increased 2 to 3 times when given through ET tube. 18. Naloxone: When narcotic overdose or poisoning is suspected an IV or ET dose is recommended to reverse the respiratory and circulatory depression. Dose is 0.1 mg/kg. 19. Lidocaine: It is antiarrhythmic agent. It prevents or terminates ventricular arrhythmias due to accelerated ectopic foci. Bolus of 1 mg/kg is administered followed by infusion of 20–50 mg/kg per minute. 20. Supportive measures include: (a) IV fluids – D10 on 1st day and paediatric electrolyte solution from 2nd day onwards. (b) Prevention, monitoring and correction of acidosis. Bicarbonate deficit = 0.3 × wt. of child in kg × HCO3 = 0.3 × (desired HCO3 – level observed concentration of HCO 3–). (c) Use of antibiotics. In case of pneumonia, milk aspiration and sepsis. Inj. Cefotaxime 80–100 mg/kg/d in 2 divided doses plus Inj. Amikacin 15 mg/kg/d in 2 divided doses for 3–5 days. Inj. Ampicillin must be added if Listeria monocytogenes pneumonia is suspected.

III. Apnea Apnea is defined as cessation of respiration for > 20 seconds or cessation of respiration of any duration accompanied by bradycardia (HR < 100) and/or cyanosis.

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Abrupt cessation of breathing associated with bradycardia (HR < 100/min) and/or cyanosis is called apnoea. Generally, apnea > 20 secs. causes symptoms.

Causes (a) Prematurity: Gestational age (GA) < 32 weeks, weight < 1500 g. (b) Pulmonary: Respiratory distress syndrome (RDS), pneumonia, pulmonary hemorrhage, congenital lung malformations, aspiration. (c) CVS: CHD (various types). (d) CNS: Birth trauma, asphyxia, effect of maternal sedation, intracranial hemorrhage. (e) Metabolic: Hypoglycemia, severe jaundice, hypocalcemia, acidosis, dehydration. (f) Infection: Sepsis, meningitis. (g) Hypothermia due to any cause.

Management 1. Assess severity and frequency of apnoea. Check the baby’s temperature. Examine for respiratory and cardiac abnormalities. Look out for signs of neurological illness. 2. Investigations—CBC, blood gases, tests to rule out sepsis, X-ray chest and USG skull. 3. Attach an Apnoea Monitor. Set the alarm at 20 seconds. 4. Physical stimulation: Pinching of skin, tapping of foot, gentle rocking. 5. Warmth. 6. Oxygen. 7. Correction of metabolic problems. 8. Blood transfusion if anemic. 9. Antibiotics if sepsis. 10. Drugs: (a) Theophyllin 5 mg/kg IV loading dose, followed by 2 mg/kg IV/PO 8 hourly till infant improves

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(in premature baby continue till 34 weeks GA). (b) Doxapram HCl 1–2.5 mg/kg/h as IV drip is also effective. 11. Mechanical ventilation if all else fails.

IV. Convulsions Convulsions occur in 0.5–0.8% of all newborns (6–12% of those < 1500 g). Jitteriness = convulsions.

Causes Perinatal: (a) Birth asphyxia, intracranial injuries. (b) Hypocalcemia (serum calcium < 7 mg%). (c) Infections: Intrauterine (TORCH) or sepsis. Also neonatal tetanus. (d) Hypoglycemia. (e) Inborn errors of metabolism. (f ) Developmental anomalies of the brain. (g) Miscellaneous: Pyridoxine deficiency or dependency, hypomagnesemia, electrolytemia, kernicterus.

Clinical Features (a) Focal/generalized fits. (b) Signs of underlying cause. (c) Altered state of consciousness. (d) Subtle seizures – partial seizures reflecting immaturity of the brain.

Management 1. Control of seizures and work-up of underlying cause to proceed simultaneously. 2. Establish airway, resuscitate (if need be), start O2. Attach pulsoximeter and apnea monitor. 3. Do a bedside glucose estimation. If blood glucose < 30 mg% (preterm) or < 40 mg% (full term) give IV Dextrose (10%) 2–4 mL/kg as a bolus. If convulsion is terminated, maintain IV dextrose till child settles. 4. If no relief, do other investigations – CBC, platelets, ABG, blood culture, electrolytes, serum calcium, etc. and ask for USG skull as early as possible.

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5. In the mean time, inject Phenobarbitone 20 mg/kg IV slowly over 5–10 minutes. If no effect, repeat up to 2 more doses of 10 mg/kg over next 30–60 minutes. Next one can use Dilantin sodium 20 mg/kg IV (as a diluted dose in saline at 1 mg/kg/min). Maintenance for both drugs is 5 mg/kg/d in 2 divided doses. 6. If both drugs are ineffective, Inj. Diazepam 0.25–0.5 mg/kg IV. Repeat if necessary. Alternatives are Lorazepam and Clonazepam. Other drugs are Midazolam 0.15 mg/kg/dose and Paraldehyde as 5% solution in 5% dextrose 200–400 mg/kg/IV. 7. Treatment of underlying cause. 8. Pyridoxine 100 mg IV can be tried to rule out pyridoxine deficiency/dependency (In latter case repeated doses are required).

V. Bleeding Neonate Causes (a) Hemorrhagic disease of the Newborn. Vitamin K deficiency caused by prematurity and maternal use of drugs like warfarin, anticonvulsants, etc. (b) Platelets – Thrombocytopenia, consumptive coagulopathy (DIC), antiplatelet antibody (ITP), or platelet function disorders. (Salicylate overdose in mother or inherited function disorder). (c) Inherited defects of coagulation (e.g. hemophilia). (d) Sepsis neonatorum. (e) Hepatic disease. (f ) Local causes – Bruising due to birth trauma, gastric ulceration due to indwelling NG-tube. (g) Swallowed maternal blood.

Clinical Features (a) Prolonged bleeding at circumcision. (b) Upper gastrointestinal (GI) bleed (hematemesis) or lower GI

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bleed (melena, hematochezia). (c) Cutaneous bleeding (petechiae, ecchymoses). (d) Intra-articular bleeding (hemophilia). (e) Intracranial hemorrhage. (f) Hematuria.

Management 1. Document that vitamin K has been given at birth. If not possible to document, Inj. Vitamin K1 immediately. 2. Collect blood for prothrombin time (PT), partial thromboplastin time (PTT), platelet count and fibrinogen assay. Also do a bedside bleeding time and clotting time. If PT and PTT are prolonged, send for Fibrin Split products (FSP) and D-dimer assay. 3. Order fresh frozen plasma and platelets for immediate transfusion. 4. If coagulation factor deficiency is proved, the deficient factor can be supplied, e.g. cryoprecipitate for factor VIII deficiency.

VI. Necrotizing Enterocolitis Incidence 1–2/1000 newborn, 2–5% of NICU admission. Predisposing factors: (a) Prematurity. (b) Perinatal hypoxia/neonatal asphyxia. (c) RDS/Apnea/Assisted ventilation. (d) Umbilical artery catheterization. (e) Shock, blood loss. (f) Hyperosmolar feeds, large nasogastric feeds, very early initiation of feeds in VLBW baby. (g) Sepsis/ acidosis.

Clinical Features (a) Onset usually 3–4 days after starting oral/N-G feeds, and usually within 10 days of birth. (b) Gradual or explosive onset of abdominal distension, retention of feeds and/or GI bleeding. (c) Bilious vomiting. (d) Very sick baby, often with pallor, lethargy, apnea, thermal instability.

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Radiograph: (a) Dilated intestinal loops with/without fluid levels. (b) Gas in intestinal wall (pneumatosis intestinalis), in hepatic veins and in peritoneal cavity.

Management (a) Stop feeds and keep NBM. (b) Careful monitoring of abdominal girth and signs suggestive of intestinal perforation, development of ascites, guarding/rigidity, and intestinal mass, if any are found, surgery is needed. (c) General care: IV fluids, maintain BP, urine output. (d) Antibiotics: Cefatoxime 100 mg/kg/d in 2 divided doses IV plus Amikacin 15 mg/kg/d in 2 divided doses IV plus Metronidazole 22.5 mg/kg/d in 3 divided doses IV. Role of colistin sulphate, gentamicin controversial. (e) Total parenteral nutrition (TPN) is desirable and oral/enteral feeds are begun after baby has settled. Prevention: (a) Avoidance of predisposing factors. (b) Avoiding oral feeds initially in VLBW babies and very gradual introduction of oral feeds in all babies at risk. Prophylactic antibiotics have no role to play.

VII. Hemolytic Disease of the Newborn (HDN) Types 1. Due to Rh incompatibility (Rh-HDN). 2. Due to ABO incompatibility (ABO-HDN) between the baby and its mother. Rare forms are due to minor blood group problems.

Clinical Features (a) With each subsequent pregnancy, the effect on the fetus is more and more severe. The first baby will be completely normal. Severity ranges from mild jaundice to severe jaundice within 48 hours of birth needing exchange transfusion (ET) to an oedematous stillborn

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(hydrops fetalis). (b) Due to intravascular hemolysis the surviving infant will be pale, oedematous, has asphyxia, hypothermia, acidosis and even DIC. (c) Very severe jaundice, if unchecked, will lead to encephalopathy (kernicterus). This will cause lethargy, refusal of feeds, shrill cry, sunsetting of eyes, hypertonia with opisthotonus and convulsions. The baby may die or survive with brownish staining of teeth, cerebral palsy, hearing loss, mental retardation and learning disabilities.

Management 1. Prevention of hydrops and intrauterine fetal loss is possible by amniotic fluid analysis and measurement of antibodies in mother. If need be, Rh-ve blood transfusions are given to the fetus by cardiocentesis. 2. Early clamping of cord at birth. 3. If child has CCF, Inj. Frusemide 2 mg/kg/IV, and restrict fluids. 4. Monitor baby’s serum bilirubin, Hb, Coomb’s test, RBC morphology and reticulocyte count. Mother’s Coomb’s test and ABO antibody will also be sometimes needed. 5. Start phototherapy or go ahead with ET depending on bilirubin level and result of Coomb’s test. For ET, give 180 mL/kg baby weight exchange. Blood group of the donor blood should be ‘O’ Rh-ve in Rh-HDN and same ABO-Rh as the mother in ABO-HDN. Indications for exchange transfusion in HDN Sick at birth zz Cord serum bilirubin > 4.5 mg% zz Cord Hb < 12 g% zz Infant blood’s Coomb’s test positive zz

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17

Rate of rise of bilirubin > 0.5 mg/dL/h Serum bilirubin > 10 mg/dL at 12 h, 15 mg/dL at 24 h and > 20 mg/dL at any time.

VIII. Vomiting Causes (a) At birth – Swallowed amniotic fluid, meconium or maternal blood. (b) In first 24 hours – All the above plus congenital intestinal obstruction. Overfeeding. (c) After 48 hrs. within 1st week – All above plus– (i) Neonatal pneumonia/septicemia/meningitis, raised intracranial tension. (ii) Allergy to milk. (iii) Gastroesophageal reflux. (iv) Kernicterus. (v) NEC. (d) Other causes – Common cold, gastroenteritis. Inadequate burping after feeds.

Management (a) Treatment of underlying cause. (b) X-rays to rule out obstruction. Dye studies may be needed. (c) Pass a NG tube, remove gastric contents and throw them out. (d) Give stomach wash with normal saline. (e) Medicate if no relief—metoclopramide, domperidone or cisapride. (f ) Maintain hydration.

IX. Premature and Low Birth Weight Baby Any baby < 2.5 kg at birth. In Indian circumstances, the cut off for special care as newborn < 2.0 kg at birth.

Classification 1. Premature baby (born < 37 weeks at GA). 2. Small for Gest AGE baby (may be preterm or term).

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Causes (a) Placental insufficiency. (b) Poor maternal nutrition. (c) Spontaneous preterm labour. (d) Induction of preterm labor due to risk to mother or baby or both. (e) Multiple pregnancies.

Clinical Features (i) In preterm baby – Skin thin, visible veins, downy hair. Ear pinnas cartilage unformed, pinna stays folded if bent. Breast nodule unformed. Feet—creases only on anterior 1/3 rd of the sole. Genitals – Testis descend by 34–35 weeks and scrotal rugosity and pigmentation are completed by 36 weeks in male, while labia majora and labia minor only by 36 weeks. (ii) Physiological immaturity causes RDS (HMD), hypothermia, hypoglycemia, hypocalcemia, cardiac problems like PDA, increased susceptibility to infections and poor retention of oral feeds. NEC, intracranial/intraventricular hemorrhage and sepsis are dangerous complications of prematurity. (iii) In the full term LBW baby, risk of hypothermia, hypoglycemia, hypocalcemia are the same. Baby looks physically mature but has dry, wrinkled skin, long-looking nails, hyper-alert look, excessive jitteriness and often meconium-staining of umbilical cord and/or rest of the body due to chronic fetal distress. Lung maturity is usually normal. (iv) Both preterm and SGA babies are at higher risk of jaundice which has a prolonged course.

Management (a) The best way to avoid problems is to prevent onset of preterm labour and factors that lead to intrauterine growth retardation (IUGR). (b) At birth protect the small baby

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from hypothermia by giving warmer care/incubator care. Polythene wrap keeps the baby warm. It is easily available and cost effective. (c) Resuscitate/provide O2 as needed. (d) Early beginning of NG feeding in preterm and oral feeds/BF in a FT LBW baby. (e) Institute IV fluids in a very LBW baby (weight < 100 g or GA < 30 weeks) and gradually progress to oral nutrition to avoid risk of NEC. (f ) Watch for symptoms/signs of complications mentioned above. Development of a murmur in 2nd left interspace suggests opening up of ductus arteriosus. Treatment – Restrict fluids (give 2/3 of calculated requirements), O2, frusemide 1 mg/ kg IV, repeat if required. Indomethacin 2 mg/kg IV 8 hourly × 3 doses (or oral Mefenamic acid if IV indomethacin is not available). (g) Vitamins, calcium supplements from day 3 of life. Nasogastric feeds: 1. First aspirate the stomach, then give a feed. 2. Gravitational feeding is superior to pushing. 3. Flush with 0.5–1 mL normal saline after milk is given. 4. Infant should be propped up at time of feeds. 5. First feeds to be a test feed of 5 mL 5% dextrose. 6. Start milk feeds once test feed is tolerated. Use mothers milk with human milk Fortifier (HMF) or a special formula for preterm babies in case of a preterm baby. 7. Start with normal quantity and increase over days to reach a target of 120 cals/kg/d by day 7 of life. 8. N-G tube must be aspirated before every feed. If more than 25% previous feed is returned, drop one feed and re-initiate thereafter. If 50% of previous feed is returned, revert to IV fluids and NBM till baby settles. IV fluids: Start with 10% dextrose on day 1, change to 1 –1 4 5 5% or 10% dextrose saline from day 2–3 once renal sufficiency is achieved. Initial volume is 60–80 mL/kg/d till 150 mg/kg/d is reached or baby is on NG/oral feeds.

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Danger symptoms: (a) Intracranial hemorrhage – Lethargy, refusal of feeds, subtle convulsions, tonic spasms. (b) Sepsis – Lethargy, refusal of feeds, abdominal distension, tachypnoea, acidotic breathing, sclerema, cutis marmorata, peripheral circulatory collapse, shock, development of PDA and respiratory failure, thermal instability. (c) Oxygen damage – All LBW babies who are on O2/assisted ventilation should be closely monitored to prevent oxygen-induced damage to retina and lungs. (d) Anemia – Repeated testing can reduce Hb to very low levels, leading to failure of baby to gain weight. Blood transfusions may be required. Discharge and follow up. Discharge if – (a) Mother is taught how to look after the baby at home. (b) Birth weight must have been regained and baby is putting on weight (at least 20 g/d) steadily. (c) No evidence of jaundice or any complications.

X. Surgical Emergencies Perioperative management is essential to the successful outcome of neonatal surgical problems which include: zz Diaphragmatic hernia zz T-O fistula/esophageal atresia zz Imperforate anus zz Congenital intestinal obstruction zz NEC zz Ambiguous external genitalia zz Hydrocephalus zz Meningomyelocele. Timing of surgery will decide the eventual outcome in most conditions. It should be immediate in most of the above situations, i.e. after the baby is stabilized. In case of an air-leak causing tension pneumothorax, surgery should be carried out instantaneously. In lieu of this a needle may

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be inserted in 2nd or 3rd interspace to relieve the tension, with the other end of the needle under water. Respiratory system emergencies. These will prevent successful transition from intra-uterine to extra-uterine life. The baby will turn blue within minutes to hours after birth. In case of bilateral choanal atresia, the cyanosis will deepen over minutes. On passing a tube, obstruction of the posterior nares will be detected as a resistance to the forward movement of the tube. At times there is an occluding membrane which tears readily if the tube is forcibly negotiated. This will bring instant relief to the baby. In other cases, ENT specialist help must be sought for fenestration. In diaphragmatic hernia, baby has respiratory distress at birth, a scaphoid abdomen and peristaltic sounds heard in the chest area. Bag-mask intervention will worsen the baby’s condition and must be strictly avoided. If necessary, baby should be intubated and/or ventilated till it is stable for surgery. In T-O fistula, urgent surgery is indicated by progressive worsening of baby’s condition once it is fed for the first time. Earlier there will be frothing, excessive salivation and drooling at the mouth. The milk and saliva that collects in the blind upper oesophageal pouch is regurgitated and aspirated into the lungs, resulting in pneumonia. Diagnosis is established when a proper N-G tube fails to negotiate beyond 8–10 cm from the lips (oro-gastric intubation). On an X-ray, it will be seen coiled-up in upper oesophageal pouch. As the lower end of the oesophagus communicates with the trachea (Type ‘C1’ the commonest type), a stomach bubble will also be observed. The baby should be put on continuous suctions of upper pouch with head-high nursing, NBM, IV fluids and antibiotics in preparation for urgent surgery.

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GI system emergencies: Intestinal atresia, malrotation and anorectal anomalies are the commonest GI emer­ gencies. Intestinal atresia: Duodenal atresia is the commonest. It is common in infants with Trisomy 21. The baby is normal at birth. Once it is fed, there will be progressive abdominal distention and vomiting (which will turn bilious if obstruction is distal to the opening of the common bile duct into duodenum) and failure to pass meconium within a matter of hours. Baby’s condition will worsen if it is not taken up for surgery. Intestinal perforation (of the proximal segment) may occur causing catastrophic development of peritonitis. Radiographs will help to diagnose intestinal obstruction. The presence, number and distribution of gas bubbles/air-fluid levels will help locate the site of obstruction. Management: Isotonic IV fluids, correction of fluid/ electrolyte and acid base disturbances, use of broadspectrum antibiotics and stabilization. After this, a barium/gastrograffin dye study may be needed, before planning surgery, to differentiate between small intestinal obstruction and anorectal anomalies. Baby may either be subjected to one-stage or two-stage surgery. Necrotizing colitis has been discussed earlier. Neurological emergencies: Hydrocephalus and spinal defects are often co-existent and evaluation should include search for the other if one is found. Babies with a large hydrocephalus are usually neurologically abnormal. They should be examined for lower limb paralysis and neurological bladder. If a meningo-myelocele is not covered by skin, operation

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should be carried out soon after birth to cover the defect with skin. Corrective surgery can be done electively. A ventriculo-peritoneal shunt is performed for the hydrocephalus. Ambiguous external genitalia. When a clear sex assessment is not possible at birth, it leads to parental anxiety. Presence of salt-wasting type of congenital adrenal hyperplasia forms, this form of a surgical emergency into a life-threatening medical one. The condition of ambiguity can be due to chromosomal, hormonal, or gonadal problem. A chromosomal female (XX) with ambiguity is a female hermaphrodite, while a chromosomal male (XY) is a male hermaphrodite. Infants with evidence of both testes and ovaries are labelled true hermaphrodites. Management: Careful diagnostic workup in tandem with prevention/correction of salt loss in the salt-losing varieties of CAH. Parents must be counselled that their baby cannot be assigned a sex-tag till the workup is complete. In most cases, survivors are brought up as phenotypic females as this is easier and socially more acceptable.

General Pediatric Emergencies I. Dehydration Causes A. Acute gastroenteritis. 2. Burns. 3. Sepsis. 4. Hyperpyrexia. 5. Salt-losing congenital adrenal hyperplasia. 6. Addison’s disease. 7. Massive hemorrhage due to any cause. 8. Loss through lungs – hyperventilation.

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Weight loss Thirst Conscious­ness Pulse

BP Peripherals

1. 2. 3. 4.

5. 6.

Normal Circulation time normal < 2 seconds Pink extremities Warm

Mild 4 seconds

Severe 10% Increased Drowsy to unconscious Increased rate, thready

Moderate 5–9% Increased Normal to drowsy Increased rate, normal volume Normal Prolonged > 3 seconds

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Anterior fontanelle (< 6 months age) Urine output

8.

10. Skin turgor

9.

Mucous mem­branes

7.

Contd...

Normal Passed urine < 2 hours Normal colour Volume N Normal

Normal

Mild Moist tears +

Deep yellow Volume ↓↓ Reduced Rebound > 2 seconds

Much reduced to anuric

Reduced Passed urine < 4 hours Yellow Volume ↓ Reduced Rebound < 2 seconds

Flat

Severe Dry (moist if severe vomiting). Cries without tears Sunken

Moderate Moist tears +

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B. Other features to look for in acute dehydration –– Sclerema in very small infants –– Hot dry skin especially in hypertonic dehydration (Na+ > 130 mEq/L) –– ECG changes and paralytic ileus if hypokalemia (K+ < 4 mEq/L) –– Tetany if hypocalcemia (serum calcium < 8 mg%) –– Acidotic breathing in early shock and worse cases –– Symptoms related to primary cause.

Management 1. History especially regarding travel, food intake, ORS administration, nature of stools and vomits (or other symptoms), time of last urine output and breast-feeding. 2. Weight of the child. 3. Assess degree of dehydration (see Table 1.3) 4. If more than 5% loss has occurred and especially if child is vomiting ORS, inject challenge boluses of Ringer’s lactate IV (20 mL/kg over 20 minutes each × 3 in first hour). At the end of this phase of rapid rehydration, the child will pass urine, eyeball and atrial fibrillation (AF) tension will return to normal and skin elasticity will also improve. Pulse volume will go up and pulse rate will fall. 5. Collect blood now for CBC, PCV, electrolytes and blood gases. 6. Correct any acid-base disturbances (see below). If pH is over corrected, latent hypocalcemia may become manifest as tetany (alkalotic tetany). 7. Control vomiting with (a) Promethazine 0.5 mg/ kg, or (b) Domperidone 0.5–1 mg/kg po q6-8h, or (c) Ondansetron 0.06–0.08/kg/dose po q8h. 8. Start the child on WHO ORS solution orally (a) Composition/Sachet (27.5 g)

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Sodium chloride 3.5 g  Sodium bicarbonate 2.5 g or  Add to 1 L of clean Sodium citrate 2.9  water Potassium chloride 1.5 g   Glucose 20 g Use of lower sodium formula (WHO ORS-B) is not suitable for children. (b) To make WHO-ORS-A at home: For 1 glass (200 mL) For 1 liter Salt 1–2 finger pinch 1 tsp. Sugar 1 tsp. 5 tsp. Lemon Juice Few drops 1–2 mL (c) Other fluids usable in place of WHO-ORS: (i) Rice kanji (Salt added) (ii) Diluted curd (Chaas) (iii) Weak tea with salt added Note: These are not as good as WHO-ORS in terms of enhancing reabsorption of secreted fluid from bowel mucosa. (d) Super-ORS e.g. Rice-based ORS can also be used. (e) Unacceptable fluids – Non-WHO ORS (e.g. electral), sweetened fruit juices, carbonated beverages. (f ) Technique of administering ORS – In rapid rehydration phase: ORS 50 mL/kg for each grade of dehydration in first 4 hours plus 10 mL/kg for each large stool passed, plus 5 mL/kg for each large vomit. – In maintenance (2nd phase): ORS at 100 mL/ kg for each large stool passed, plus 5 mL/kg for each large vomit. (g) Breastfeeding – Stop in 1st 2–4 hours, resume thereafter ad libitum.

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9. In severe dehydration – IV fluids: 1/5th glucose saline or Isolyte P for maintenance. Total requirement will be: i. Maintenance 100–110 mL/kg/day plus ii. Deficit 50 mL/kg/grade of dehydration plus iii. Ongoing losses 5–10 mL/kg stool or vomit up to 100 mL/kg/d In first 8 hours, give 1/3 of maintenance, 1/2 of deficit and 1/3 of ongoing losses, thereafter in next 16 hours, give the balance requirements. 10. Correct electrolyte and acid base disturbances thus: (a) Formula: mEq needed = (CD-CA) × Fd × weight (kg) Where CD = Concentration desired (mEq/L) CA = Concentration present (mEq/L) Fd = Distribution factor Wt = Baseline body weight (prior to dehydration – add 5–10% to current weight) (b) Fd: Na+ 0.6–0.7 – Cl 0.2–0.3 HCO3– 0.4–0.5 (c) Water deficit in hypertonic dehydration – For every mEq/L of Na+ >145, add 4 mL/kg H2O as deficit for replacement (d) Replacement: – Na+/HCO3–: Replace as NaHCO3 or as 1/3, ½ or full strength glucose saline. – K+: Replace as Inj. KCl to the running IV drips (> 2 mL/100 mL of fluid) only after renal output is established.

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11. Use antibiotics only for invasive diarrhoea (stools show pus and blood, child has fever and tenesmus and appears toxic). 12. After the phase of rapid rehydration is over, start breastfeeds, oral feeds and easily digestible ageappropriate foods such as curds, khichdi, rice and dal, soft bananas, potatoes, apples, etc.

II. Respiratory Emergencies A. Foreign Body Obstruction and Choking Commonest site is narrow region of the larynx just above/ below the vocal folds. Common objects: Small, round objects such as ground nuts, chana, marbles, coins and fish bone (in pyriform fossa) Clinical features: Sudden onset of gagging, cough and cyanosis within minutes. Death can result if immediate help is not available. Management: (1) Do not put fingers inside the mouth to remove foreign body (FB) initially. (2) Ensure airway and breathing if there is complete airway obstruction – (a) Deepening cyanosis and drowsiness, and (b) No rise and fall of chest on attempted mouth-to-mouth breathing (if child is not breathing), then proceed as follows – 1. Infants: Take the infant in the lap face down, buttocks raised, and administer 4 thumps with the heel of the hand on the back. Turn it over and open the mouth. If FB is seen and is moving, remove it with the index and middle fingers grasping it like a pair of forceps. If no relief, lay the child supine in your lap and give 4 epigastric thrusts with the outstretched fingers, upwards. Repeat inspection and removal of FB as above. If still no relief, repeat the above procedure (both prone

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and supine) two more times. If the child does not improve, resort to bag-mask ventilation, intubation and emergency tracheostomy. 2. Older children. Stand behind the child who is also standing and put your left fist (closed) just below the sternum in the epigastrium. Cover this fist with your other hand and give upward and backward thrusts to the child (Heimlich manoeuvre). After 4 thrusts, open the child’s mouth to see if the FB is dislodged. If it is, remove it as above. If no response, administer bag-mask ventilation, intubation under observation or tracheostomy.

B. Croup Causes: (a) Acute spasmodic laryngitis (cause is uncertain—virus, anxiety. allergy). (b) Acute laryngitis (diphtheria, pertussis, virus—parainfluenza, adeno, respiratory syncytial, influenza, measles). (c) Epiglottitis. (d) Acute laryngotracheobronchitis (viral or bacterial). (e) Tetany. (f ) Foreign body. (g) Retropharyngeal abscess. Clinical features: (a) Respiratory stridor—onset usually sudden with epiglottitis, insidious with laryngotracheobronchitis. Sudden at night with past history of similar attacks suggests spasmodic laryngitis. Stridor increases with worsening condition. With critical obstruction, air flow decreases, and stridor disappears. (b) Respiratory distress—tachypnoea, nasal flaring, subcostal retraction, decreased air entry. Unilateral decrease in air entry suggests foreign body in bronchus on that side. (c) Hoarseness of voice, brassy cough. (d) Hypoxia indicated by restlessness, anxiety, diaphoresis. Cyanosis is a late sign. (e) High fever and toxemia seen with epiglottitis and diphtheria. (f ) Thready pulse and membrane in diphtheria. Swabs confirmatory. (g) Characteristic posture

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in epiglottitis to maximise patency of airway—open mouth, jaw thrust forward, tongue protruded. Child prefers to sit up leaning back on both hands. (h) Dysphagia and drooling seen with epiglottitis, retropharyngeal abscess. (i) Serosanguinous discharge from nose with diphtheria. (j) Swollen, inflamed epiglottis seen on direct laryngoscopy in epiglottitis. Note: Never have the child to lie down to examine the throat if epiglottitis is suspected. Examine the child under anaesthesia in operation theatre. Radiographs - (a) Of soft tissues of neck – (i) Area of subglottic narrowing in AP view (Steeple sign). Dilated hypopharynx with narrowed subglottic airway seen with laryngo-tracheo-bronchitis. (b) Of chest – (inspiratory and expiratory films) – air trapping, partial or complete atelectasis, over inflation on one side in expiration suggests FB. (ii) Area of increased soft tissue density anterior to cervical vertebrae – in retropharyngeal abscess. Management: 1. Acute laryngo-tracheo-bronchitis and spasmodic laryngitis – Ensure adequate airway – Rule out epiglottitis – Humidified air/O2 with a tube held near child’s face or with a face mask – Racemic epinephrine 0.25–0.75 mL with nebulization (Dilute with saline), or Salbutamol – Inj. Dexamethasone 0.25–0.5 mg/kg/dose q6h – Intubation/mechanical ventilation in nonresponsive cases. The ET should be one size smaller than the usual size. 2. Acute epiglottitis i. Intubate immediately. If it is a dire emergency remove the child to OT and do intubation under

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general anaesthesia. After the ET is in place, attempt to start IV access as even minor irritation can precipitate complete airway obstruction. ii. Collect blood and laryngeal secretions for culture. Blood for CBC. iii. Antibiotics: IV Ampicillin 150 mg/kg/d in 4 divided doses plus Chloramphenicol 75 mg/kg/d in 3 divided doses, or IV Ceftriaxone 75–80 mg/kg/d in 2 divided doses plus Amikacin 15 mg/kg/d in 2 divided doses. iv. IV fluids. Add 10% for hyperventilation. 3. Diphtheria: If suspected, give large doses of penicillin, erythromycin for 10 days. Give diphtheria antitoxin in the following doses: Tonsils or anterior nose—10,000–20,000 units. IM Pharynx, uvula, or larynx—20,000–40,000 units. Nasopharynx—40,000–75,000 units. Half the dose IM and half IV. In cases of grave severity or where lesions have lasted for more than 2 days, give double the dose. Caution: Test sensitivity to serum by giving 1:1.000 solution intradermal. When sensitivity is present desensitise very slowly. Always give antihistaminics half an hour before giving the serum and keep syringes filled with adrenaline, dexamethasone and antihistamine ready.

C. Acute Bronchial Asthma Clinical features: Breathlessness and wheezing zz Tachypnoea, flaring of alae nasi, intercostal, subcostal, and substernal retractions. zz Cyanosis is a late sign. zz Development of pulsus paradoxus and CHF in nonresponsive cases. zz Silent chest if bronchospasm is severe. zz

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Management: 1. Therapy: O2 at the rate of 3–6 litres/min to maintain saturation above 92%. 2. Repeated inhalation of beta-2-agonist aerosol. Salbutamol nebulizer sol (5 mg/mL) in a dose of 0.1–0.15 mg/kg diluted in 3 mL of normal saline is administered over a period of 10–15 minutes. Rational behind giving repeated doses of inhaled bronchodilators every 20 minutes that follows the intitial dose, allows more distal deposition of drug particles during further dosing. This results in dilatation of smaller airways and the short dosing interval prevents any deterioration of clinical status in intervening period. Alternatively metered dose inhaler (MDI) can be used with a spacer device to give inhalation of beta-2 agonist. Duration of therapy is less than a minute as compared to 15 minutes with nebulizer. In some children with severe bronchospasm, an initial dose of epinephrine is helpful prior to inhalation therapy. 2. In very small infants or those who do not allow inhaled therapy, consider SC Adrenaline 0.01 mL/kg or Inj. Terbutaline 0.0005–0.01 mg/kg/dose q15–20 minutes × 3 doses. 3. Repeat nebulized/inj. doses every 20 minutes. 4. Monitor HR, BP and O2 saturation. 5. Start IV fluids. 6. Antibiotics usually not required. 7. Aminophylline—as an adjunct. Loading dose 5 mg/ kg IV and continue with 1mg/kg/hour IV drip, or give bolus q6h at 5 mg/kg/dose. Monitor HR and look for symptoms of toxicity such as vomiting or convulsions. 8. Ipratropium bromide has generalized action throughout the lungs. It is effective when given in combination with salbutamol a beta-2 agonist. Dose of 250 µg in 1 mL of

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respirator solution may be mixed with salbutamol and given through nebulizer. 9. Steroids: Hydrocortisone 4–8 mg/kg/dose IV initial, then maintain at 8 mg/kg/d in 4 divided dose, or replace with oral steroids e.g. Prednisolone 2–2.5 mg/ kg/day in 3 divided doses if child has settled. 10. Magnesium sulphate: In cases where initial nebulization with beta-2 agonist and corticosteriods do not show improvement MgSO4 can be tried in a dose of 30–70 mg/kg over 20–30 minutes (50% solution) 0.2 mL/kg in 20 mL normal saline in 5% dextrose over 30 minutes. 11. In non-responsive cases consider mechanical ventilation. Indications (a) Failure of maximal pharmacologic therapy. (b) Cyanosis and hypoxemia (PaO2 < 60 mm of Hg). (c) PaCO2 greater than 50 mm Hg and rising by more than 5 mm Hg/h. (d) Pneumothorax or pneumomediastinum. (e) Respiratory or cardiac failure. 12. Treatment of CHF if it is present.

III. Cardiovascular Emergencies A. Congestive Heart Failure Causes: 1. In utero: (a) Arrhythmias, complete heart block. (b) A-V malformation, A-V valve regurgitations. (c) Cardiomyopathy. (d) Rh-isoimmune disease, twinto-twin transfusion. (e) PDA. 2. In neonates : (a) Myocardial dysfunction, e.g. myocarditis, sepsis. (b) Pressure overload – AS, Coarctation. (c) Volume overload – PDA, Truncus arteriosus, VSD, TAPVR. (d) Arrhythmias and CHB.

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3. In infants: (a) Volume overload (as above). (b) Myo­ cardial dysfunction—EFE, glycogen storage disease, myocarditis, Kawasaki syndrome. (c) Secondary causes—Sepsis, renal disease, hypertension, hypo­ thyroidism. (d) Arrhythmias. (e) Pressure overload (as above). 4. In childhood/adolescence: (a) Unrepaired CHD. (b) Repaired CHD defects causing pressure/volume overload. (c) Acquired heart disease—pericarditis, rheumatic fever, endocarditis, myocarditis, rheumatic valvular disease. (d) Secondary causes—thyrotoxicosis, hypertension, sickle cell anemia, cor pulmonale. Clinical features: Fatigue and breathlessness on exertion zz Feeding difficulty in infants zz Tachycardia, gallop rhythm zz Tachypnoea with wheezing and cough, especially in infants zz Increased work of breathing – Flaring of alae nasi, intercostal retractions, grunting. zz Oedema: Increased weight in infants, oedema of eyelids, pedal oedema zz Tender hepatomegaly and splenomegaly zz Poor peripheral circulation with weak pulse and increased capillary refill time (CRT), cold extremities and dusky nails zz Raised JVP – appreciable in older children. zz Pulsus alternans/paradoxus in late stages zz

Management: (a) Investigations—CBC, chest X-ray, ECG, ECHO. (b) Monitoring—electrolytes, blood gases, blood sugar, urinalysis, BP to find out cause of CCF. (c) Prop the child upon 20–30º backrest. (d) O2 by face mask/nasal prongs.

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(e) Digitalization (see further). (f ) Diuretics—frusemide 1mg/kg/dose IV (Amp. 10 mg/mL). Oral 2–3 mg/kg/day. Chlorothiazide/hydrochlorothiazide 20–40 mg/kg/day. Supplement with KCl if diuretics likely to be used for longer time. (g) After-load reduction—captopril 0.5–5 mg/kg/ day in older children. (h) Treatment of infection, acidosis and anemia if any. (i) Dopamine or Dobutamine 5–20 µg/ kg/min to revive peripheral circulation and correction of shock. (J) Surgical intervention may at times be needed.

B. Anoxic/Cyanotic Spells Causes: Congenital cyanotic heart disease with reduced pulmonary blood flow e.g Tetralogy of Fallot. Clinical features: Excessive crying, feeding or bowel movements may precipitate an acute anoxic/cyanotic spell. It may last from few minutes to few hours. Symptoms are: zz Apnoea, gasping respirations zz Restlessness, irritability zz Deepening of cyanosis zz Feeble cry zz Scratching of anterior part of chest zz Temporary reduction in loudness of murmur, or absence of murmur on auscultation zz Occasional unconsciousness, seizures, hemiparesis. Management: 1. Loosen child’s clothes and bring it to a prone position with knees drawn up to the chest. 2. Start oxygen with face mask. 3. Inj. Morphine 0.2 mg/kg if available. 4. Correct acidosis with sodabicarb. 3–5 mEq/kg. 5. Propranolol is drug of choice. Give 1mg/kg IM or IV followed by 10 mg/kg q6h PO.

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6. IV glucose 10–15 mL/kg bolus followed by maintenance IV fluids. 7. Correct anemia. 8. Prepare for surgery—B-T shunt or Waterston surgery if child has repeated apnoeic spells. Corrective surgery can be done at older age.

C. Cardiac Arrhythmias

Supraventricular tachycardia 1. Try vagotonic manoeuvres, e.g. ice to face, carotid massage, Valsalva manoeuvre. 2. Adenosine 0.1mg/kg IV push. Increase to double the dose if needed (maximum dose 2 mg/dose). 3. Digoxin: Total digitalizing dose (DD) depends on age, varying between 20–30 µg/kg in neonates to 30–50 µg/ kg in infants and older children to > 50–1250 µg/kg in children > 10 years. Give ½ TDD at once, followed by ¼ TDD at 8 and 16 hours after the first dose. Maximum at 5–10 µg/kg/day orally/IV/IM in two divided doses. 4. Synchronous cardioversion 0.25–1.0 joules/kg as soon as possible. 5. Atrial oesophageal overdrive pacing.

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Atrial flutter 1. Atrial oesophagus overdrive pacing. 2. Synchronous cardioversion. 3. Digoxin (as above). 4. Quinidine sulphate 15–60 mg/kg/d in 4 divided doses for maintenance. (This drug raises blood digoxin levels so avoid higher doses). Premature ventricular beats 1. Observe in most cases. 2. If symptomatic – Lignocaine 1mg/kg bolus IV, and then drip at 20–50 µg/kg/min. 3. Quinidine can be used as a secondary drug. Ventricular tachycardia If hemodynamically stable – IV lignocaine. If unstable, synchronized cardioversion. Treatment of underlying illness. Ventricular fibrillation Defibrillation at 2.05/kg. Double the dose on 2nd attempt and repeat if required. Also IV lignocaine. Complete heart block 1. If asymptomatic—observe 2. If symptomatic—atropine, isoproterenol or transvenous ventricular pacing Sinus bradycardia 1. Treatment of underlying cause such as raised ICT, hypoxemia or acidosis. 2. Epinephrine 0.01mg/kg IV bolus 0.1/kg by ET. Repeat every 3–5 minutes. 3. Atropine 0.02 mg/kg IV bolus (Min: 0.1 mg, Max: 0.5–1 mg). 4. Pacemaker. Sick sinus syndrome – Pacemaker Asystole – Resuscitation

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D. Hypertensive Crisis Clinical assessment: 1. Use proper sized BP cuff. The cuff should encircle the arm 1–1¼ times and cover at least 2/3rds of the total length of the arm. 2. Investigate for underlying cause – Clinical examination followed by urinalysis, BUN, creatinine, X-ray chest, ECG. Plasma renin level as baseline. 3. If BP > 95th centile but child allright – Monitor. If BP > 95th centile and child symptomatic, hospitalize and start IV drip. Management: Goal is to reduce BP to normal. Reduce slowly, say 1/3 of the goal every 6 hours. Refer Chapter 6.

E. Hyperkalemia Causes: (a) Renal failure. (b) Hypoaldosteronism. (c) Aldosterone insensitivity. (d) Decreased insulin. (e) Potassium sparing diuretics. (f) Transfusions with old blood. (g) Addisonian crisis. (h) Metabolic acidosis (K+↑ 0.2–0.4 mEq/L per 0.1 fall in arterial pH). Management: 1. Assess – Look for weakness, paresthesiae, tetany. Do an ECG. Progressive changes (Refer). 2. Therapy (i) Calcium gluconate (10%) 0.2–0.5 mL/kg, effects last up to 1 hour. (ii) Sodium bicarbonate 1–3 mL/kg, effects last several hours. (iii) Glucose insulin drip. (iv) Kayexalate resin orally. (v) Dialysis as last resort.

F. Shock Failure of circulation of O2 to tissue resulting in lactic acid production and death due to multiple system organ failure (MSOF).

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Causes: 1. Hypovolemic: Commonest in children. Blood loss, fluid loss (gastroenteritis, polyuria). 2. Distributive: Sepsis, anaphylaxis, adrenal crisis, CNS injury. 3. Cardiogenic: Myocarditis, sepsis, congenital heart disease., coronary insufficiency, arrhythmias, hyperdynamic circulatory states (thyrotoxicosis, severe anemia). 4. Obstructive: Pericardial tamponade, tension pneumothorax, coarctation of aorta, pulmonary embolism, cor pulmonale. Symptoms and assessment: (a) Early shock: Unexplained tachycardia, low pulse pressure, increased diastolic pressure, non-pulmonary tachypnoea, cold extremities, increased capillary refill time (CRT), dry mucosae, mild oliguria and restlessness. (b) Classic shock: All above plus weak pulses, anuria, altered consciousness, cold and clammy extremities. (c) Late shock: Moribund child with severe tachycardia, bradycardia, profound hypotension, absent peripheral pulses, acidotic breathing and gasping as a prelude to respiratory arrest. Management: 1. Put child in IPCU and put him on multiparameter monitor with HR, resp. ECG, apnoea, BP and SaO2 measurements. 2. Send blood for ABG, culture, electrolytes, calcium, CBC, platelet count, BUN, creatinine, LFT, PT, PTT, fibrinogen, FSP (fibrin split products). 3. Send urine for specific gravity, osmolality, glucose, ketone bodies, microscopy and if necessary electrolytes and bicarb. 4. Chest radiograph and ECG to be done.

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5. Insert a central venous line: CVP should be maintained by giving fluids between 5–10 mL of saline. If CVP 15 µg/kg/min are not advisable. (ii) Dobutamine: Pure inotrope with little effect on heart or peripheral vasculature. Start at 10 µg/kg/min and increase up to 40 µg/kg/min. 7. Chronotopic agents are used if HR is low. Start with Isoproterenol 0.1 µg/kg/min and increase in similar amounts, or give Epinephrine 0.05–0.1 µg/kg/min. 8. In cardiogenic shock, one can supplement inotropic therapy with minimal fluids with afterload reduction. Prostaglandin E infusion is needed to keep the ductus arteriosus patent in neonates with ductus dependent conditions. 9. Steroids: Hydrocortisone hemisuccinate 5 mg/kg or Dexamethasone 0.5–1 mg/kg IV q6h for 1–2 days specially in anaphylactic shock.

IV. Endocrine Emergencies A. Diabetic Ketoacidosis 1. Assess: Review current therapy, time of last insulin dose, history of infection.

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2. Initially – IV fluids 10–20 mL/kg NS/RS over 1 hour, then continue 0.45 NS –1st 8 hours: 1/2 of deficit (assumed as 10% of previous weight) plus 40% of maintenance fluids + Urine output. Next 16–24 hours: Balance of amount calculated + Urine output. 3. Insulin drip: First bolus 0.1 U/kg, then continue at 0.1 U/kg/h in drip. Monitor glucose, reduction should not be > 100 mg%/h. More rapid correction may cause cerebral oedema. If glucose is not falling optimally, increase insulin to 0.15–0.2 U/kg/h. If it is falling optimally, continue insulin at 0.1 U/kg/h in 1/5 dextrose saline instead of NS. 4. Check K+ levels and replace as needed. 5. Look for phosphate depletion and add KPO4 to IV drip as required. 6. If pH < 7.1, add bicarb. 7. Stop insulin once ketosis is resolved, blood pH > 7.3, HCO3– > 15 mEq/L. Replace with SC insulin, gradually tapering to previous maintenance dose over 1–2 days.

B. Adrenal Crisis 1. Assess: Hypoglycemia, hyponatremia, hypokalemia, metabolic acidosis and shock. 2. Infants: Most likely cause is congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Rarer causes are adrenal aplasia, adrenal hemorrhage and pituitary-hypothalamic lesions. Symptoms: Vomiting, failure to thrive, dehydration and shock. Hyperpigmentation of nipples, axillae and genitalia. 3. Older child: Commonest cause is Addison’s disease. Onset is insidious and any acute illness can precipitate adrenal crisis. Child will present with shock preceded by a short history of nausea, vomiting, abdominal pain and symptoms of worsening dehydration.

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Management: (i) Resuscitate, put child on cardiac monitor, establish 2 large IV lines, start O2 and stabilize. (ii) Collect blood for hormonal studies. (iii) Infuse crystalloids to correct dehydration/shock. (iv) Inj. Hydrocortisone 50 mg/mL as IV bolus followed by 50–100 mg/24 hours as continuous drip till child comes out of the critical state. (v) If severe hyperkalemia, treat with IV glucose, soda bicarb, calcium gluconate, salbutamol infusion, ionexchange resins, and/or dialysis. (vi) Maintenance with oral Fludrocortisone acetate (Florinef ) 0.1–0.2 mg/day.

C. Hypoglycemia Blood glucose < 40 mg/dL (or higher if symptomatic), regardless of age (in children). Causes: (i) Infants – (a) Hyperinsulinism. (b) Hepatic enzyme deficiencies. (c) GH deficiency. (ii) Children – Usually secondary to overdose of insulin in a known diabetic. Diagnosis: Symptoms – Subtle in newborn, may be accompanied by jitteriness, cyanosis, apnoea, hypotonia, crying or seizures. In older children – Coma or convulsions preceded by history of palpitations, sweating, pallor and confused mental state. Management: (a) Collect blood for glucose, lactate levels as well as extra samples if needed. (b) Inj. bolus of dextrose—(i) Newborn: 10% 2–5 mL/kg followed by 3–5 mL/kg/h as continuous drip. (ii) Children: 25% 1 mL/kg bolus, followed by 10% 2–3 mL/kg/h as a drip. (iii) Inj. Glucagon 0.03 mL/kg/h IM (Max 1mg) if IV lines are not available and child is critical. Some will respond to this therapy.

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V. Neurological Emergencies A. Seizures Consider: 1. Is it a seizure or a syncope? 2. Is the seizure primary (epileptic) or secondary (symptomatic)? Causes: (a) Febrile seizures (6 months – 5 years). (b) CNS infections – Meningitis, encephalitis, TBM. (c) Epilepsy. (d) Metabolic – Hypoglycemia, hypomagnesemia (rare), uremia, hypernatremia. (e) Raised ICP – Subdural hematoma, tumors, abscess, acute infarction, cerebral concussion, etc. (f) Tetanus. (g) Rabies. (h) Hypertension. (i) Tuberous sclerosis. (j) Poisoning. (k) Hypoxic ischemic encephalopathy of newborn period. Clinical features: 1. Seizures, focal or generalized, single or recurrent. Accompanying symptoms like aura, autonomic disturbances, automatisms, etc. 2. Fever – High or hectic suggests infective cause. (LP to rule out acute pyogenic meningitis). 3. State of conciousness – After postictal drowsiness/coma has been accounted for, persistently altered sensorium is suggestive of CNS disease. 4. Symptoms of underlying disorder, e.g. meningeal signs in meningitis, deep acidotic breathing in uremia and continuous vomiting in raised ICP. Management: 1. Stabilise the patient first. 2. Draw blood sample for glucose, calcium, electrolytes, CBC, blood culture, renal and hepatic profile (as per history and clinical features). 3. Inj. Diazepam IV 0.2–0.3 mg/kg (diluted with saline/ blood) till seizures stops. Diazepam can also be given

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4. 5.

6. 7.

8.

9.

45

as rectal solution and can be used simultaneously while blood samples are being taken. Second line drugs to be used sequentially: (i) Inj. phenobarbitone 20 mg/kg slow IV. (ii) Inj. Diphenylhydantoin 20 mg/kg slow IV. If child is febrile, measures to control temp. (i) Paracetamol 15 mg/kg/dose. (ii) Mefenamic acid 10 mg/kg/dose. (iii) Nimesulide 1.5–2 mg/kg/dose. (iv) Tepid sponging of whole body. (v) Cold compresses to forehead, armpits and groins. If metabolic disturbances – IV fluids, glucose, calcium, sodabicarb as needed. Antibiotics: (i) Meningitis: Cefotaxime 100–200 mg/ kg/d in 2–4 divided doses plus Amikacin 15 mg/kg/d in 2 divided doses (Instead of Cefotaxime, Ceftriaxone 80–150 mg/kg/d in 2 divided doses can be used). Treatment of raised ICP with Mannitol 5–10 mg/kg of 20% solution q8h × 3 or Inj. Dexamethasone 0.5 mg/ kg in 3–4 divided doses or Inj. Frusemide 1–2 mg/kg/ dose IV slowly. If convulsions do not stop, proceed with neuromuscular blockade, midazolam or GA.

B. Increased Intracranial Pressure/Coma Causes: (a) Trauma. (b) Acute cerebrovascular accident. (c) Status epilepticus. (d) Space-occupying lesions (e) CNS infection: Abscess, meningitis, encephalitis. (f ) Hydrocephalus. (g) Poisoning. Management: 1. Assessment – with clinical examination, blood tests, LP, radioimaging for cause. (2) Treatment of primary cause. (3) Place in 20–30° head-high position. (4) Intubate if comatose and hyperventilate. (5) Medications— Refer treatment of convulsions. (6) Monitor Glasgow coma scale. (Refer).

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Accidental Poisoning in Children Causes 1. Kerosene and household hydrocarbons. 2. Household products: Insecticides, rodenticides, phenol, alkalines (caustic soda, unstalked lime), acids, turpentine, eucalyptus oil, camphor, naphthalene, neem oil, alcohol, copper sulphate. 3. Pharmaceutical products: Phenothiazine, opiates, tincture opii, barbiturates, aspirin, antiseptics, anticonvulsants. 4. Plants and plant products: Dhatura, castor seeds, Chandrajyoti seeds, yellow and white oleander. 5. Food poisoning. 6. Venomous bites and stings. If diagnosis of poisoning in doubt, administration of antidote for most likely poison may help in initiating of treatment. Common antidotes are flumazenil for benzodiazepine, deferoxamine for iron, naloxone f o r o p i a t e s, a t ro p i n e f o r o r g a n o p h o s p h a t e s, diphenhydramine for phenothiazine, pyridoxine for isoniazide toxicity.

Management 1. Dilution: Both water and milk can be used in case of caustic effects on oral oesophageal or gastric mucosa, e.g. acids and alkalies. 2. Prevention of absorption. Gastric evacuation is done if patient is seen within one hour. It can be done by emesis or lavage. 3. Binding agents. Activated charcoal is most effective. Fuller’s earth, kaolin and pectine are less effective. 4. Cathartics: Sodium or magnesium sulphate (250 mg/ kg) magnesium citrate (4 mL/kg) every 2–4 hours.

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5. Whole bowel irrigation (WBI). Electrolyte solution containing propylene glycol in dose of 30 mL/kg/h by nasogastric tube. 6. Diuresis 20% mannitol 0.5 g/kg. 7. Dialysis. 8. Specific antidotes.

Neonatal Critical Care Persistent pulmonary hypertension (PPHN) is basically a failed transition of fetal circulation to neonatal circulation. Pathophysiology: Normal cardiorespirator y adaptations at birth are aeration of lungs, fall in pulmonary vascular resistance, closure of various fetal shunts, i.e. patent foramen ovale, ductus venous arterious. Alterations in this normal process leads to PPHN.. Pathological mechanisms leading to PPHN in various disease processes. zz Maladaptation of pulmonary vessels (perinatal asphyxia, meconium aspiration syndrome) zz Maldevelopment of pulmonary vessels (PPH) zz Underdevelopment of pulmonary vasculature (congenital diaphragmatic hernia) zz Structural/functional obstruction to pulmonary blood flow.

Clinical Features zz zz zz zz zz zz zz

Cyanosis in spite of high supplemental O2 Tachypnoea 80–100/min Minimal signs on auscultation Mild tachycardia Loud P2 Pre and post-ductal O2 gradient (–20 mm Hg) Hypotension

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Hyperoxia and hyperventilation test to differentiate it from cyanotic heart disease.

Diagnosis: 2D echo—Structurally normal heart with supra-systemic PA pressure, right to left shunting at the level of PFO and PDA.

Management 1. Restore functional residual capacity of the lung using conventional or high frequency oscillatory ventilation (HTOV), and optimum PEEP. 2. Reduce peripheral vascular resistance (PVR). Maintain oxygenation >80 mm Hg. Nitric oxide is a selective pulmonary vasodilator. Other adjuvant therapies include avoiding hypercarbia, maintaining pH in range of 7.4–7.5, optimal sedation and muscle relaxation. Inhaled nitrous oxide (iNO) decreases PVR and extrapulmonary venoarterial shunting. It is contraindicated in severe IVH, platelet 5 lesions)

Drugs supervised (monthly)

Rifampicin 600 mg

Rifampicin 600 mg + Clofazimine 300 mg

Not supervised (daily)

Dapsone 100 mg

Dapsone 100 mg + Clofazimine 50 mg

Treatment duration

6 months, to be completed in 9 months

12 months to be completed in 18 months

Note: Rifampicin (600 mg) ofloxacin (400 mg) and Minocycline (100 mg) given as single dose for single lesion leprosy (without any clinical nerve thickening).

Anthrax Anthrax is caused by Bacillus anthracis and is transferred to humans by contact with infected animals and their products.

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Types 1. Cutaneous 2. Inhalational due to inhalation of spores 3. Gastrointestinal anthrax from ingestion of conta­ minated meat Anthrax meningitis usually occurs secondary to cutaneous lesion. Clinical features: Topic features may appear in some cases. The disease may progress to regional lymphadenopathy. Management: Early therapy with penicillin G as some cases may be fatal.

II. Autoimmune Disorders Pemphigus Vulgaris Chief complaint: Relapsing crops of bullae with or without fever. Symptoms and signs: Generalised vesico-bullous eruption on normal skin, some lesions may be secondarily infected, typical ‘mousy’ odour, fever (sometimes); occasionally toxaemia and electrolyte imbalance. Mucous membrane bullae, erosions and ulcerations may precede or accompany. Nikolsky’s sign (superficial detachment of skin after pressure or trauma) is present. Management: 1. General measures: Hospitalize the patient at bed rest, blood transfusions and IV feeding as indicated. 2. Corticosteroids: In large doses. To start with, prednisolone (5 mg) 24 tablets per day in divided doses. This is then tapered very gradually (by one or two tablets every 10–14 days) only after there is complete control, i.e. no new lesions. IV Rituximab infusion

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3. 4. 5. 6.

7.

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Pulse therapy–100 mg Dexamethasone in 500 ml 5% dextrose show iv drip (over 2 hours) for 3 consecutive days. On second day, 500 mg cyclophosphamide is added to the drip. This constitutes one drip. Such drips are repeated at 28 days interval. In between the pulse therapy 500 mg, cyclophosphamide PO is given. Broad-spectrum antibiotic, e.g. ampicillin, amoxycillin, ciprofloxacin. Antipyretics if required. Vitamin supplements and high protein diet as consider­ able amounts of protein are lost in the blister fluid. Drugs to counteract steroid side effects, i.e., calcium supplements, ranitidine, antacids, anabolic steroids, etc. Check the blood pressure daily and the blood sugar weekly. Anti-hypertensives and anti-diabetic drugs should be given if required. Locally: (a) Skin—Proper hygienic measures and a soothing lotion to start with calamine lotion with 2% iodochlor-hydroxyquinoline (which serves as a mild anti-bacterial and anti-fungal agent). Later, for persistent lesions, a topical antibiotic ointment like fucidin, furacin, or tetracycline or a combination of neomycin, bacitracin and polymyxin or mupirocin may be used. (b) For oral lesions: Betadine mouth paint, Condy’s gargles and anaesthetic troches. (c) For eyes: Topical antibiotic + steroid ointment or drops.

Henoch-Schonlein Purpura (Anaphylactoid Purpura) Causes: (a) Upper respiratory infection—bacterial (streptococcal) or viral. (b) Drugs—Although not proved the following have been blamed—penicillin, streptomycin, chloramphenicol, sulfonamides, etc. (c) Idiopathic— occurs more frequently in children between 3–10 years.

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Chief complaint: Prodromal symptoms of headache, anorexia and fever may precede the acute attack with abdominal pain, joint pain and rash. Clinical features: a. Abdominal: Colic, vomiting, hematemesis, melena. b. Polyarthritis: Commonly of knees, elbows, ankles and hand joints with swelling, pain and tenderness. c. Renal: Hematuria gross or only microscopic. d. Skin: The eruption begins as a crop of erythematous macules which rapidly become papular, urticarial and purpuric. In more severe cases necrotic and hemorrhagic lesions occur. It is commonly confined to extremities but occasionally involves face and entire body as well. Management: 1. Bed rest. 2. Analgesics—Paracetamol. 3. Antibiotics—If a streptococcal etiology appears well founded, long-term prophylaxis. 4. In severe cases (a) corticosteroids—only in severe cases. Prednisolone 40–50 mg per day which is then tapered gradually. (b) Immunosuppressive agents like azathioprine. 5. Urine analysis must be carried out—(a) Weekly during the attack. (b) At the end of the attack and (c) 1–3 months after the attack has subsided.

Systemic Lupus Erythematosus Clinical features: Skin involvement in acute SLE may be of various types and present alone or in different combinations. 1. Erythematous rash may be localised to the ‘butterfly’ area of face or may be generalised. It may be urticarial or like erythema multiforme.

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2. Rarely bullous eruption. 3. Generalized or patchy maculopapular eruption. 4. Telangiectases. 5. Lesions of vasculitis, i.e. erythematous papules which later breakdown giving rise to erosions and ulcerations. These may, occasionally, be hemorrhagic as well. 6. Diffuse hair loss and alopecia. 7. Peri-orbital oedema. 8. Mucosal lesions: Telangiectases, erythematous papules, painful aphthous ulcerations. 9. Systemic symptoms like fatigue, fever, weight loss, may be presenting symptoms. Management of acute systemic lupus erythematosus. a. General measures: Complete bed rest, proper nursing care, maintenance of adequate nutrition. Avoid sun exposure. b. Drugs: (i) Corticosteroids are usually required in large doses—prednisolone 60 to 100 mg/day. This should be reduced very gradually only after all clinical signs of activity of the disease have abated. Tapering by 2.5 mg every 4–5 days is usually slow enough to prevent a flare of disease activity. Precautions must be taken to counteract the side effects of steroids therapy: antacids, antihypertensive drugs and anti-diabetic drugs if required, anabolic steroids, calcium supplements, etc. (ii) Antibiotics if indicated. (iii) Antimetabolites may be used in patients not responding adequately to steroids: Azathioprine 1.2 mg/kg body weight daily is probably the best although cyclophosphamide, 6-mercaptopurine and nitrogen mustard have also been used. c. Symptomatic treatment, i.e. NSAIDs for arthritis, anticonvulsants for seizures.

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III. Toxic Disorders Acute Erythroderma (Exfoliative Dermatitis) Common causes: Although drugs are a common cause of erythroderma, several skin diseases may give rise to it. The causes of erythroderma or exfoliative dermatitis are: (a) Drugs. (b) Skin diseases – (i) Ichthyrosis. (ii) Psoriasis. (iii) Various eczemas such as contact dermatitis, atopic dermatitis, seborrhoeic dermatitis, etc. (iv) Pemphigus. (v) Reticuloses and leukemias. (vi) Pityriasis rubra pilaris. (c) Idiopathic or unknown cause. Clinical features: 1. Skin: Patchy erythema rapidly generalises and may become universal in 12–14 hours. Scaling appears which varies greatly in degree and character from case to case—it may be large or fine and bran-like. The skin is bright red, hot, dry and palpably thickened. Slight or moderate lymph node enlargement. 2. Constitutional and metabolic disturbances: Persistent generalised dilatation of peripheral vessels and loss of protein, vitamins, essential elements in scales has a profound effect on all systems. a. Cardiovascular—Generalized peripheral vasodil­ ation may lead to high output cardiac failure. b. Gastrointestinal—Protein losing enteropathy develops due to intestinal villous atrophy. Hepato­ megaly and splenomegaly in 25% of patients. c. Fluid/electrolyte/temperature—Due to hypo­ proteinemia, shift of fluid from intra to extravascular compartment results in oedema feet as well as oliguria and even anuria. Electrolyte imbalances are common. Hypothermia and concealed pyrexia are serious complications.

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d. Renal—Oliguria, hyponatremia and hyperkalemia. e. Lymphadenopathy—Generalised. Chronic generalised erythroderma is associated with profound metabolic disturbances. (i) Hyperthermia—The blood flow through the skin is markedly increased which results in excessive heat loss. When the body temperature is raised, heat loss is further increased. (ii) Hypothermia— hypothermia is a serious risk. The excessive loss of heat leads to compensatory hypermetabolism and a raised BMR. (iii) Extrarenal water loss is markedly increased. (iv) Loss of protein in the exfoliated scales is considerable and may contribute to the fall in serum albumin found in most severe cases. The low albumin is partly attributable to plasma dilution as a consequence of the hemodynamic changes. (v) Miscellaneous—Tachycardia, hypervolemia, cardiac decompensation, peripheral circulatory failure or thrombophlebitis may result. Secondary cutaneous or respiratory infections are common. Management: 1. Hospitalization with bed rest and skilled nursing care is mandatory. The protein and electrolyte balance, the circulatory status and the body temperature require continual surveillance. 2. Careful regulation of environmental temperature with avoidance of cooling and overheating. 3. Corticosteroids: 40 to 60 mg of prednisolone to start with, in gradually tapering doses. Avoid steroids if psoriasis is the causative factor. 4. Antibiotics. 5. Topically: Only bland ointment or cold cream with good hygiene. It is important to remember that the percutaneous absorption of topically applied substances is much increased in erythrodermic patients.

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Staphylococcal Scalded Skin Syndrome and Toxic Epidermal Necrolysis Two severely toxic syndromes which may look alike but with different etiologies and therefore different managements are staphylococcal scalded skin syndrome (SSSS) and toxic epidermal necrolysis (TEN). The SSSS is due to exotoxin elaborated by group 2, phage type 71 staphylococci. The TEN is generally due to drug intake, the common drugs are anticonvulsions carbamazepine, phenytoin, lamotrigine, barbiturates, NSAIDs, sulfonamides, penicillin. TEN

SSSS

History

Drug intake

Usually no drug

Age

Over 40 years

Under 5 years

Exanthemata pattern

Generalized without clear distribution

Typical distribution and succession of development (face, neck, axillae, then groins and rest of the body later)

Cutaneous tenderness

Mild to moderate

Marked

Nikolsky sign

Positive only in lesions

Positive also in uninvolved skin

Mucous membranes

Severely afflicted

Uninvolved

Exfoliative cytology

Necrotic epidermal cells, debris, polymorphs

Normal appearing acantholytic cells Contd...

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Contd... TEN

SSSS

Course

Protracted, 2–3 weeks

Brief, 2–3 days

Mortality

High

Very low

Therapy

Remove trigger Corticosteroids (may help)

Antistaphylococcal antibiotics

Treatment of toxic epidermal necrolysis (Stevens-Johnson syndrome). 1. Withdrawal of all drugs. 2. Antihistamines. 3. Soothing lotion for topical application. 4. Corticosteroids, topical and systemic. 5. Adrenaline in case of anaphylaxis. 6. Others—Fluids, correction of electrolyte imbalance, wet compresses, petroleum jelly gauze. Rule of thumb: Drugs started within one week of the onset of eruption are the most responsible.

Erythema Multiforme Major Clinical features: Usually starts as erythematous wheals or patches which may become hemorrhagic and end as the Stevens-Johnson syndrome, i.e., macular, papular, urticarial, bullous or purpuric. There may be involvement of the mucocutaneous junctions as well with ulceration of conjunctivae, lips and vulva or glans. Eye involvement may lead to keratitis, corneal ulcers, uveitis or even panophthalmitis. This may be accompanied by high fever, toxemia and shock. Target lesions—Dull red or red-blue centre with surrounding pale zone, which is surrounded by a darker ring giving a ‘bull’s-eye’ effect.

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Causes: 1. Infections a. Virus infections: (i) Primary atypical pneumonia. (ii) Adenovirus infections. (iii) Influenza type A. (iv) Infectious mononucleosis. (v) Variola. (vi) Vaccinia. (vii) Hepatitis. (viii) Psittacosis. b. Bacterial infections: (i) Hemolytic streptococci. (ii) Typhoid. (iii) Cholera. (iv) Tuberculosis. c. Fungal infections: (i) Dermatophytosis. (ii) Histoplasmosis. 2. Drug reaction. 3. Carcinomas – any type. 4. Idiopathic. Management topical/systemic steroids.

Acute Primary Irritant Dermatitis (Dermatitis Venenata) Causes: Allergy to (a) Plants (e.g. porthenian poison ivy, marking nut, chrysanthemum, etc.) (b) Nickle, rubber, hair dye. (c) Topical medications - more common when applied on stasis eczema. (d) Drugs—Nitrofurantoin, neomycin. (e) Cosmetics. Clinical features: A vesiculo-bullous eruption on an erythematous base whose distribution is bizarre depending on the areas of contact with the incriminating plant or agent. There might be an erythematous, scaly dermatitis with or without oozing. Bulbs of tulips, hyacinths and narcissi cause a painful, dry, fissured and hyperkeratotic allergic dermatitis later with erosions and ulcerations. Management: 1. Remove the incriminating contactant. 2. Antiallergic tablets—Avoid oral steroids if possible.

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3. Topically calamine lotion should be used in the early stages, later, once the lesions are dry, a local steroid cream or ointment if required.

Drug Rash with Eosinophilia and Systemic Symptoms Syndrome Clinical features: 1. Cutaneous—Facial oedema. Generalized papul­o­ pustular or exanthematous rash which may evolve to exfoliative dermatitis. 2. Systemic—Lymphadenopathy, hypereosinophilia and organ involvement, e.g. hepatitis, pneumonitis, nephritis, myocarditis, encephalitis. Treatment: Soothing agents, systemic corticosteroids, IgG IV.

Severe Pruritus Causes: The following are the commoner causes of severe generalised pruritus. a. Scabies, related mite infestation, pediculosis, dermatophytosis. b. Intestinal parasitic infestations, e.g., roundworms, hookworms, threadworms, E. histolytica, G. lamblia. c. Drugs: any drug can give rise to pruritus. d. Pruritus of internal origin : (i) Hepatic disease. (ii) Leukemia. (iii) Internal carcinoma. (iv) Lymphomas. (v) DM. (vi) AIDS. (vii) Psychonecrosis. (viii) CKF. (ix) Pregnancy pruritus. Clinical features: Excoriation marks all over the body. The patient may show exhaustion from loss of sleep. Although pruritus is a feature of most skin disorders, it becomes an emergency only when it is severe and generalised.

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Management: Determine cause of pruritus 1. Antihistamine drugs for symptomatic relief. The specific drug as well as the dose often varies from patient to patient. The dose should be adequate and it is better to err on the higher side since antihistamines are quite safe. They may also be given parenterally. Antihistamines with relatively less drowsiness are cetirizine, terfenadine, loratadine, astemizole. 2. Topically: A soothing lotion such as calamine lotion. 25% benzyl benzoate or crotamiton (Crotorax) in cases of scabies, pediculosis and other mite infestations. The contacts and fomites should also be treated. 3. Treatment of the underlying causative factor. 4. Corticosteroids only if there is inadequate relief with proper doses of antihistamines.

IV. Allergic Reactions Anaphylaxis and Angioedema Causes: (a) Administration of drugs, sera, anaesthetics and radiological contrast media. (b) Rarely, following certain insect stings or bites. Clinical features: Respiratory distress due to broncho­ spasm or oedema of the mucosa of the larynx and bronchi, intestinal spasm accompanied by vomiting or diarrhoea, cutaneous changes varying from erythema to angioneurotic oedema and urticaria and shock. Only one or a combination of these signs may be present and the results vary from transient discomfort to rapid death. Management: See management of anaphylactic shock.

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V. Drug Reactions Drugs have been termed the ‘Great Imitators’ and can give rise to any type of skin lesions which may also be accompanied by constitutional symptoms like malaise, arthralgia, headache, fever, toxemia. Amongst those that require emergency or immediate treatment are: 1. Anaphylactic reaction, urticaria, angioedema. 2. Generalised exanthematic eruptions, e.g. scarlatini­ form and morbilliform. 3. Exfoliative dermatitis, erythroderma. 4. Bullous eruptions. 5. Severe photosensitive dermatoses. 6. Epidermal necrolysis. 7. Erythema multiforme. 8. Fixed drug eruption. Clinical features: The clinical picture and lesions will vary according to the type and severity of the reaction. a. Anaphylactic reactions: Drugs commonly causing anaphylactic and/or urticarial reaction in order of frequency—Penicillin, sera, toxoids, salicylates, sulphonamides, opiates, indomethacin, paracetamol. X-ray contrast media, enzymes, codeine, blood products. It must be emphasized that any drug can give rise to any reaction. The above mentioned drugs are relatively commoner incriminating agents; the list is however not all inclusive. b. Exanthematous eruptions are the most frequent of all cutaneous reactions to drugs. The clinical features are very variable—the lesions may simulate scarlatina or measles with diffuse erythema, or may consist of a profuse eruption of small papules showing no close resemblance to any infective exanthem. Distribution

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c.

d.

e.

f.

is also variable: it may be patchy or diffuse. If the drug intake is continued an exfoliative dermatitis may develop. Drugs commonly producing exanthematic eruptions in order (bacteriostatic, antidiabetic, diuretic), ampicillin, amoxicillin, butazolidines, barbiturates, nitrofurantoin, hydantoin derivatives, is oniazid, chloramphenicol, er ythromycin, benzodiazepines, phenothiazines, carbamazepine, allopurinol, tetracyclines, streptomycin, gold salts. Exfoliative dermatitis: is one of the most dangerous patterns of cutaneous drug eruptions. It may follow exanthematic eruptions or may develop as erythema and exudation in the flexures, rapidly generalizing. Drugs in order of frequency are butazolidines, carbamazepines, cotr imoxazole, hydantoin derivatives, phenindione, cimetidine, nitrofurantoin, isoniazid, lithium, gold and streptomycin. Bullous eruptions: May vary from a few lesions to extensive involvement of the skin by vesicles and bullae with a bizarre distribution. Drugs responsible may be in order of frequency—nonsteroidal antiinflammatory agents, griseofulvin, clonidine, cystostatics, frusemide, thiazides, gold salts, minoxidil, penicillamine, psoralens and rifampicin. Photosensitive eruptions: Exanthematic type of severe dermatitis with or without oozing involving only exposed areas of the skin. Drugs in order of frequency—tetracyclines, phenothiazines, benzothiadiazines, sulphonamides, (both bacteriostatic and anti-diabetic), amitriptyline, nortriptyline and protriptyline. Epidermal necrolysis: has been described earlier. Some common drugs causing it are in order of frequency—

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nonsteroidal anti-inflammatory agents, hydantoin derivatives, sulphonamides, streptomycin. g. Erythema multiforme: (See above) Common causative drugs in order of frequency are—sulphonamides especially long-acting, hydantoins, butazolidines, barbiturates, penicillin, carbamazepine and NSAIDs. h. Drug rush with eosinophilia and systemic symptoms syndrome: Drugs implicated salphonamide, anticon­ vulsants anti-TB isoniazid, rifampicin. Clinical features: (a) Cutaneous: facial oedema generalized rash (b) Systemic: Hematological—hypereosinophilia and organ involvement like hepatitis, nephritis, pneumonitis, myocarditis, hyperthyroidism and encephalitis after 3–6 weeks of drug usage. Management: I. Systemic: 1. Stop all the drugs that the patient may be taking. 2. Corticosteroids: in high doses. If the patient is very toxic, Dexamethasone IM 8 to 16 mg 6 to 8 hourly depending on the severity. Otherwise Prednisolone 10–20 mg four times a day. 3. Antibiotics: Broad spectrum oral or IM. The suspected antibiotic should be avoided. Start with one tablet 250-500 mg on the first day, 2 tablets on the second day and if well-tolerated, i.e., there should be no exacerbation of the disease, then increase tablets 3–4 times a day. Injectable may also be given. 4. Avoid analgesics as far as possible. For fever, ice bag, sponging and fan. Only if the fever is very high, paracetamol may be tried, again starting with very small doses. Any analgesic which is suspect should be avoided.

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5. If patient is in shock, then treatment of shock. 6. General nursing care of the patient. II. Topical: Only bland, soothing applications should be used such as calamine lotion to which 2% iodochlorhydroxyquinoline has been added (as mild antibiotic and anti-fungal agent). Proper hygienic measures, i.e., sponging with mild antiseptic such as dilute Condy’s lotion or 0.5% Cetavlon. Dr IK Ramchandani

Co-ordinator Department of Dermatology Jaslok Hospital Mumbai, Maharashtra, India

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Emergencies in Ear, Nose and Throat

Foreign Bodies in the External Auditory Canal The variety of foreign bodies (FBs) encountered in the external canal is legion. Pins and match-sticks, buttons, marbles, vegetable foreign bodies like seeds, and even small insects like cockroaches, fleas, and bugs have found their way into this small canal.

Causes 1. Most commonly seen in children, especially beads, grain, etc. 2. Match-sticks, etc. in adults while cleaning the ear. 3. Live insects—crawl in during sleep.

Symptoms and Signs 1. May be symptomless. 2. Anxiety on the part of parents and relatives. 3. Pain and discomfort due to trauma of foreign body or attempted removal or swelling of a vegetable foreign body with inflammatory reaction of the skin of the external auditory canal or live insect moving and crawling against the drum. 4. Conductive deafness due to blocking or trauma to the drum.

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Management Unskilled, untimely efforts cause more damage than the foreign body itself. 1. Inspect: Confirm presence, size, nature of foreign body and inflammatory reaction from skin if any. Analgesics like diclofenac sodium, ibuprofen or valdecoxib. Chymotrypsin (e.g. Alfapsin) or Serratiopeptidase (e.g. Bidanzen) may be started prior to removal of FB. 2. Gently syringe with lukewarm water, head tilted to affected side to dislodge and drive the FB out of the canal. Syringing should be avoided in case of large vegetable foreign body as it may absorb the water and swell. It makes the future removal more difficult. It should also be avoided in case of tear of the drum. 3. Removal with forceps is difficult especially if FB is round. 4. Foreign body hook: Introduce with its side against the wall of the canal (usually superior, sometimes anterior or posterior wall) and on passing beyond the FB, rotate it to bring the hook behind the foreign body. Now gently dislodge the foreign body and extract it. 5. If the FB is impacted or initial attempts fail, or if the child is very uncooperative, removal under microscope under sedation, general anaesthesia is warranted. Discretion rather than tenacity is preferable. 6. Live FB: First kill with luke warm oil or spirit and then remove by syringing.

Furunculosis of the External Auditory Canal It is a circumscribed infection mainly confined to the cartilaginous portion of the external auditory canal involving a hair follicle and a sebaceous gland. It may be single or multiple or associated with generalized furunculosis. The most common organism is Staph. aureus.

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Symptoms and Signs 1. Pain—severe, increases in intensity (pain is due to tension in the dense and minimal subcutaneous tissue present in this area). 2. Swelling of the external canal. 3. Fever. 4. Tenderness on passive movements of the pinna or pressure on the tragus. 5. Discomfort on opening the mouth, sometimes trismus. 6. Pre- or post-auricular lymph nodular swelling, rarely abscess. 7. Deafness (conductive). 8. May be complicated by a perichondritis, chondritis. Note: Absence of mucus in the discharge helps to differentiate it from otitis media and mastoiditis. Note: Hearing may be normal or minimally affected. This helps to differentiate it from an acute otitis media with mastoiditis.

Differential Diagnosis from Acute Mastoiditis Furuncle

Acute mastoiditis

Pinna pushed outwards and downwards

Pinna pushed outwards

Tragal tenderness, pain on pulling the pinna

More tenderness over mastoid antrum and tip

Minimal or no discharge in external canal

Rapid filling of mucopurulent discharge in the canal

Hearing normal or minimal, conduction deafness

Significant conduction deafness

X-ray of mastoids normal

Clouding or necrosis of septa of air cells on X-ray

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Management Local 1. Clean the external canal. 2. Keep gauze wick soaked in glycerine ichthammol in the canal. It is both antiseptic and hygroscopic. Keep changing the wick every day. 3. Local antibiotic ear drops alone or with a steroid (hydrocortisone) may be used.

Systemic 1. Antibiotics. 2. Analgesics. 3. Short course of oral steroids in nonresponding cases. 4. Incise only if the furuncle is pointing. For recurrent furuncles: Investigate for immuno compromised status, e.g. diabetes, human immuno­ deficiency virus (HIV).

Malignant Otitis Externa It is a condition characterised by severe pain and inflammation in the external ear which occurs mainly in diabetics and immunocompromised patients. It is now not considered as a localised disease but as a form of ostitis extending to the skull base.

Diagnosis It is confirmed by computed tomography (CT) scan which shows features of osteomyelitis. Magnetic resonance imaging (MRI) is also required in case of cranial nerve deficits or suspicion of CNS involvement.

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Management Management is necessarily aggressive and involves hospitalisation, IV antibiotic therapy for a period of 4–8 weeks. In the initial stages, ciprofloxacin, cephalosporins (or ceftazidine or clindamycin) and tinidazole and anti-inflammatory drugs help together with control of diabetes. Surgery is required in case with granulation, facial nerve palsy and increasing osteomyelitis. Mastoidectomy, facial nerve decompression, facial nerve grafting is needed if the continuity of nerve is broken. Patient with prolonged facial palsy needs VII-XII cranial nerve anastomosis (facial-hypoglossal).

Traumatic Perforation of the Eardrum Etiology 1. By pins or sticks put in the ear, for cleaning the ear, removing foreign bodies. 2. Trauma due to a slap over the ear. 3. Blast injury. 4. Barotrauma.

Symptoms and Signs The patient has (a) pain, (b) deafness, (c) bleeding from the ear, and (d) tinnitus. The eardrum shows an irregular tear with blood on the edges of the tear.

Treatment 1. Prevent infection: (a) Sterile cotton swab in the external canal. (b) Ear drops to be avoided. (c) Antibiotics. 2. Analgesics.

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3. Waitful watching for small tears. Under microscope with suction, inverted margins of perforation must by everted. It helps in fast healing by avoiding the epithelium to role under the perforation margin. 4. Large tears may require myringoplasty.

Bleeding from the Ear Causes Can occur due to the following causes— 1. Injury to external canal or drum. 2. Fracture of the base of the skull, trauma to temporomandibular joint. 3. Middle ear infection with granuloma or polyp formation. 4. Hemangioma and glomus tumor of middle ear and mastoid. 5. Hemorrhagic bullous myringitis.

Treatment 1. Surgical Gelfoam pieces can be used if necessary to pack the external auditory canal. 2. Prevent infection by systemic antibiotics and keeping the ear dry and protected with a sterile cotton swab in the external canal. 3. Find the cause and treat it.

Acute Otitis Media (Inflammation of the lining of the middle ear cleft.)

Symptoms and Signs In the exudative stages— 1. Otalgia due to increased pressure in the middle ear 2. Conductive deafness

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3. Fever 4. Tinnitus or autophony 5. Commonly preceded by upper respiratory tract infection (URTI) 6. The drum appears congested and bulging and its normal luster and landmarks are lost.

Management 1. Nasal decongestants (xylometazoline, etc.). 2. Avoid local fomentation and ear drops in early stages. 3. IV systemic antibiotics may be required if response is poor and drum is bulging. 4. Analgesics. 5. Myringotomy: If drum bulging and no response to parenteral antibiotic therapy after 24–48 hours. Acute necrotic otitis media is a variant of acute otitis media and follows measles infection. There is destruction of tympanic membrane and annulus resulting in large subtotal perforations. Due to annulus destruction they go into chronic suppurative otitis media (CSOM) and secondary cholesteatosis. Glue ear, also called secretory or serous otitis media is a collection of fluid that is often glue-like, in the middle ear.

Acute Mastoiditis and Mastoid Abscess (Inflammation of the lining of the mastoid air cell.)

Symptoms and Signs 1. Of acute otitis media with mastoid tenderness. 2. Pinna is pushed downward, and outwards. 3. Post-aural abscess. The abscess may sometimes present in the neck, deep to the sternomastoid

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(Bezold’s abscess) or under the temporalis muscle, or in the external canal. Rarely, it may track medially.

Management 1. Incise and drain the abscess with subsequent/ concomitant mastoid surgery. 2. Antibiotics, ear drops. 3. Analgesics and antipyretics. 4. Treat URTI.

Earache Etiology Pain in the ear may sometimes be excruciating and therefore the treatment must be immediate. This pain can be due to (a) Local causes—external otitis, tympanic membrane injury, foreign body in the ear canal, impacted wax, otitis media. (b) Referred otalgia from—toothache, temporomandibular joint dysfunction, pharyngeal and laryngeal inflammation or neoplasm or glossopharyngeal neuralgia or stylagia.

Management Depends on the cause.

Sudden Deafness Definition Sudden deafness is defined as a sensorineural hearing loss occurring over a period of hours or a few days. It may be unilateral or bilateral, transient or permanent, and may also vary in severity.

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Causes The cause of sudden deafness may be anyone of the following: 1. Traumatic—accidental or operative. 2. Viral—mumps, influenza, measles. 3. Vascular—thrombosis, embolism, hemorrhage into the labyrinth, vasospasm, hypercoagulation. 4. Acute acoustic trauma. 5. Sudden pressure changes, leading to rupture of Reissner’s membrane. 6. More recently recognized condition of spontaneous fistulization at the oval window or round window. 7. Following toxic drugs. 8. Sudden hemorrhage in vestibular schwannoma (VIII CN tumor).

Symptoms and Signs The patient usually has deafness of varying degrees and tinnitus. Vertigo with nausea and vomiting may or may not be present. Associated symptoms like pressure in the ear, fever and headache may be experienced.

Management Various forms of treatment have been advocated by different workers. The therapy currently in vogue includes: 1. Bed rest. 2. Sedation. 3. Vasodilators—cyclandelate or xanthinol nicotinate 200 mg tds with dipyridamole (Persantin) 25 mg tds, cinnarizine 25 mg tds to improve labyrinthine circulation, betahistidine hydrochloride 16 mg tds. 4. Carbogen (5% CO2) therapy—inhalation of carbogen 5 minutes in one hour is supposed to increase blood

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flow to inner ear by vasodilatation. This reduces chance of permanent damage to the ear. 5. Corticosteroids. 6. Vitamins. 7. In cases of spontaneous perilymphatic fistula, a tympanotomy and sealing of the fistula is the best treatment. 8. Rehabilitation with hearing aids in case of moderate to severe deafness, unilateral profound deafness, bone anchored hearing aid (BAHA). For bilateral deafness— Cochlear implant if auditory nerve is functioning. In non-functioning auditory nerve, auditory brain stem implant is a hope.

Meniere’s Disease Characterised by recurrent attacks of vertigo associated with deafness and tinnitus and ear fullness.

Acute Attack Symptoms and Signs 1. Vertigo—dominating symptom. 2. Sensori-neural deafness. 3. Tinnitus. 4. Fullness in the ear. 5. Spontaneous nystagmus. 6. Nausea and vomiting, cold sweat. May be a single attack lasting for minutes to hours or cluster of attacks.

Management 1. Salt restricted diet. 2. Anticholinergics—atropine 0.8 mg subcutaneously. 3. Labyrinthine vasodilators—drugs like cinnarizine improves the circulation in the cochleo vestibular

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4.

5. 6. 7. 8.

81

region and thereby brings about improvement in the symptoms. Dose 25 mg tds to 75 mg tds. Beta-histine on the other hand improves vascularity in the central areas of the brain concerned with equilibrium thereby having a prolonged effect. Dosage 8–16 mg tds for 2–3 weeks. If the attack is prolonged, stellate ganglion block may give dramatic relief. Sedatives—phenobarb or chlorpromazine hydro­ chloride (25 mg tds orally or 25 mg IM). Diazepam, about 5–15 mg may be given IV, titrated to the patient’s response. Labyrinthine sedatives—betahistidine 25 mg tds or cinnarizine or prochlorperazine 5 mg bd for prolonged period. Transtympanic gentamicin therapy is useful in patients with serviceable hearing. Surgical treatment—labyrinthectomy is advised for nonserviceable hearing. Once acute attack is over, vestibular rehabilitation exercises to be taught to the patient.

Epistaxis Etiology The etiology of epistaxis is varied. It may occur due to trauma, infections—acute and chronic; specific and non-specific, benign or malignant tumors of the nose, paranasal sinuses, or nasopharynx. It may also occur due to generalized disorders like hypertension, atherosclerosis, coagulation disorders, chronic hepatic disease, etc. Spontaneous epistaxis often occurs from the Little’s area. It may be a minor bleed but sometimes may be profuse and exsanguinating.

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Management Arrest of bleeding—if not arrested spontaneously: 1. Press the nostrils together between thumb and index finger with patient bent forward over a kidney tray. This helps to arrest bleeding from the anterior part of the nose. 2. Cauterize the bleeding point if possible, with chemical or cautery. 3. If bleeding point cannot be located, then pack the nostrils with a ribbon gauze soaked in antibiotic or antiseptic ointment or vaseline. Remove after 48–72 hours. Doyle’s tampon can be used instead of anterior nasal pack, it is less traumatic to insert. 4. For post-nasal bleeding, do a post-nasal packing with pack prepared from folded gauze. Post-nasal packing can however be easily done with a Foley’s catheter. The catheter is introduced through the nostril and the balloon is inflated and impacted in the nasopharynx. Nowadays Merocel stents are available in different sizes to deal with epistaxis and these reduce the discomfort caused by packing. 5. If above measures fail, then the ligation of either the ant. ethmoidal, or int. maxillary or ext. carotid artery. 6. Concurrently, rule out bleeding and coagulation disorders, and hypertension. Look for a local pathology like a benign or a malignant tumor and treat if present. In short treat the cause. 7. Replace the blood loss and treat the shock. If no obvious cause is found, diagnostic nasal endoscopy and/or CT scan may be necessary to rule out a neoplasm.

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Foreign Body in the Nose It is encountered most commonly in children.

Symptoms and Signs 1. Nasal blocking. 2. Bleeding. 3. Unilateral foul nasal discharge. 4. The foreign body is usually easily visualized on anterior rhinoscopy. A foreign body of some duration covered with discharge and slough, may mimic nasal diphtheria.

Management With proper visualization the foreign body can be easily removed with a blunt probe or a Eustachian catheter. Put the probe beyond the foreign body and gently drag the foreign body out. It can also be removed with a pair of forceps, but this maneuver may accidentally push the foreign body further back. General anaesthesia (GA) should be used if the foreign body is impacted or if the patient is uncooperative. Nasal endoscope is used for deep seated or missing foreign bodies. A neglected foreign body will lead to rhinolith formation.

Cerebrospinal Fluid Rhinorrhea Etiology 1. Fracture base skull. 2. As a complication of surgery on the ethmoid and sphenoid sinuses, and transnasal hypophysectomy. 3. Spontaneous.

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Symptoms and Signs 1. Presents as clear watery discharge from the nose, increasing on bending forwards, compression of the internal jugular vein and by doing Valsalva maneuver. 2. The patient may have a history of repeated attacks of meningitis.

Diagnosis (a) Glucose test—cerebrospinal fluid (CSF) contains glucose, mucus nasal discharge does not. (b) Stains on handkerchief—mucus leaves a crusted stain, CSF does not and target halo is formed. (c) Fluorescein radiography—to locate exact site of CSF leak. (d) Nasal endoscopy may help determine site of leakage.

Management 1. Patient in bed with head end raised. 2. Avoid nose blowing. 3. Avoid nasal packing. 4. Antibiotics. 5. Repeated lumbar punctures. 6. Leak may be detected and repaired endoscopically.

Fracture of Nasal Bone Etiology is always traumatic.

Symptoms and Signs Deformity of nose is clearly visible in fresh cases. After few hours, deformity is less or not visible due to oedema or haematoma. Nose or oral bleed is also present. Diagnosis is clinical, CT scan is must to look for any associated trauma to skull base, brain or maxillofacial area.

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Management In fresh cases (< 4 hr of injury) immediate reduction of nasal bone under sedation or GA. In old cases, treat medically till the swelling subsides with non-steroidal anti-inflammatory drugs (NSAIDs) and serratiopeptidase. Once oedema is gone then do the reduction of nasal bone.

Laryngeal Emergencies Any laryngeal obstruction can result in a rapid death.

Causes The obstruction to the larynx and a stridor may be due to various factors: 1. Trauma to the larynx, internal or external. 2. Foreign bodies in the larynx and subglottic region. 3. Oedema of the larynx from laryngeal infection, abscesses of the larynx and around the larynx, angioedema. 4. Benign and malignant new growths of the larynx. 5. Congenital—laryngomalacia, laryngotracheal stenosis and malformations. 6. Neurological conditions like bilateral abductor paralysis. 7. Tetanus.

Management 1. Prompt recognition and assessment of the critical airway obstruction. 2. Non-surgical manoeuvres to relieve obstruction, i.e. removal of foreign body or positioning and supporting the airways to prevent obstruction by soft tissues. This is achieved by extending the neck, pushing the mandible upwards and forwards, heliox inhalation steroid.

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3. Establishment of airway by tracheostomy. When tracheostomy is not feasible due to absence of the required instruments or personnel, airway can be maintained by a laryngotomy (cricothyroidostomy) or by a wide bore needle pushed through the cricothyroid membrane. 4. Treatment of the cause.

Cafe Coronary Accidental aspiration of a bolus of meat into the larynx in elderly subjects with slowed reflexes under the influence of alcohol. Heimlich manoeuvre is employed to dislodge the aspirated foreign body—the doctor stands behind the patient and grasps him, making a fist with one hand and clasping it with the other hand so that the fist lies thumbside against the victim’s upper abdomen. The fist is then pressed sharply into the abdomen just below the sternum with a quick upward thrust. This manoeuvre can be repeated several times if necessary. If the victim is sitting, the doctor simply stands or kneels behind the chair and follows the same procedure.

Foreign Body in the Bronchus Etiology Foreign bodies in the bronchus are encountered usually in children. The commonly encountered ones are groundnut, gram and maize seeds, or pins, tacks, buttons, etc. They are found more commonly in the right bronchus.

Symptoms and Signs 1. The patient or relatives usually give a history of foreign body being put in the mouth followed by cough, cyanosis, retching or vomiting.

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2. Breathlessness. 3. Diminished air entry on the affected side. 4. X-ray chest may show obstructive emphysema or a collapse of the affected segment of the lung.

Management Endoscopic removal as early as possible should be done, especially if vegetable foreign bodies. When facilities and instruments are not available for a bronchoscopy and the patient is breathless, a tracheostomy should be done. In case of vegetable foreign bodies, antibiotics and steroids should be administered to minimize infection and edema.

Burns Due to Acid or Alkali Ingestion Symptoms and Signs 1. Pain in the mouth, pharynx and abdomen. 2. Dysphagia. 3. Vomiting and diarrhoea of dark precipitated blood. 4. Shock. 5. Yellowish white discoloration of oral mucosa. Note: Acid burns are less destructive than alkali burns.

Management 1. 2. 3. 4. 5.

Nil by mouth. Early flexible endoscopy. Relieve pain by giving pentazocine 30 mg IM. Treat the shock. Prevent infection by giving antibiotics prophylactically. 6. Early corticosteroid therapy to prevent stricture formation.

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Foreign Body in the Pharynx Etiology A variety of foreign bodies can get lodged in the pharynx, e.g. foods—fish and chicken bones, aniseeds. Also encountered are pins, needles, tacks, etc. held by workmen in their mouth.

Symptoms and Signs 1. Pain in the throat, especially during swallowing. 2. Pain in the ear. 3. The foreign body can sometimes be easily visualized embedded in the tonsil or base of the tongue. However, at times, a thorough examination with an indirect laryngoscopy mirror may be required to locate the foreign body at base of tongue and vallecula. 4. 70° scopy and flexible nasopharyngoscope is also used to detect foreign body. 5. Small fish and chicken bones are not visualized in X-rays but metallic foreign bodies can be easily demonstrated.

Management 1. Visualize the foreign body. 2. Remove the foreign body with a pair of forceps. If necessary, use a direct laryngoscope with topical or general anaesthesia as required.

Foreign Body in Esophagus Etiology The foreign bodies most commonly encountered in the oesophagus are coins, fish and meat bones, dentures. The common site of impaction is the upper end of the oesophagus at the level of cricopharynx. A spasm of the esophageal muscles further enhances the impaction.

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Symptoms 1. Stabbing pain. 2. Dysphagia. 3. Pooling of saliva.

Management Endoscopic removal under general anaesthesia to achieve a good muscular relaxation is the recommended treatment. In some cases FB may be removed with use of flexible fiberoptic esophago-gastroscope.

Temporomandibular Joint Dislocation Etiology Anterior dislocation of the temporomandibular joint occurs when condyle of the mandible slips anteriorly over the articular tubercle of the glenoid fossa. This can occur due to trauma, wide opening of the mouth during yawning, or due to wide opening of mouth gag during oral surgery. It may be unilateral or bilateral.

Symptoms and Signs 1. Pain. 2. If unilateral—(a) Jaw is displaced towards the opposite side. (b) Saliva dribbles out. (c) A depression is palpable anterior to the tragus, with the condyle seen in front of it. 3. If bilateral—mouth is fixed in a partly open position, both the condyles are felt in front of their normal position.

Management 1. Overcome the muscle spasm—pentazocine 30–60 mg IM, general anaesthesia may sometimes be necessary.

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2. Correct the dislocation by depressing the mandible at the lower molars with the thumb and rotating the body of the mandible upward. 3. Give the patient a four-tailed bandage for 3 weeks. 4. If recurrent dislocation occurs 25% or 50% glucose injection in temporomandibular (TM) joint. Three injections once in 3 weeks can lead to fibrosis and prevent dislocation. Interdental wiring and fixation to provide rest and fibrosis in TM joint. Nonresponding cases may be subjected to meniscectomy which allows mandibular head to sink more deeply into the articular fossa. Condylar resection is required at times.

Trismus (Not Due to Tetanus) Causes 1. Muscular spasm secondary to trauma to the mandible or around the TM joint. 2. Infection in the vicinity of the TM joint, i.e. peritonsillar, parapharyngeal, parotid, dental, etc.

Management 1. Local heat. 2. Muscular relaxants, viz. diazepam 10 mg IM, diazepam 5 mg orally. 3. Treatment of infection, if present, with systemic antibiotics. 4. Anti-inflammatory drugs like Ibuprofen 400 mg tds after meals. 5. Incision of abscesses where present. Dr Nitin Gupta

MS DNB FASB (Italy), OIM (Germany)

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4

Ophthalmic Emergencies

The symptoms that make a patient urgently seek out the eye doctor are usually the following—Sudden diminution or cessation of vision; double vision; loss of part of the visual field; trauma to the eye and its adnexa; subconjuctival haemorrhage or other causes of severe redness and drooping or closure of the eyelid. In an ophthalmic outpatient setting most or all patients will present with a combination of three main complaints: Pain/redness/decreased vision.

Sudden Loss of Vision Causes zz zz zz zz zz

zz

zz

Traumatic dislocation or rupture of the lens Vitreous haemorrhage Retinal detachment Acute congestive glaucoma attack Macular haemorrhage (trauma, severe anaemia, diabetes, hypertension), age-related macular degeneration Vascular occlusion—central retinal artery or vein occlusion Optic neuritis—papillitis (nerve head swelling) or retro-bulbar neuritis, ethambutol toxicity

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Toxic amblyopia, e.g. Methyl alcohol poisoning, tobacco.

Painful Ophthalmic Emergencies Chemosis (severe conjunctival swelling) and lid edema.

Causes A. Acute inflammatory causes 1. Severe mucopurulent conjunctivitis 2. Endophthalmitis (inflammation). B. Circulatory obstruction 1. Cavernous sinus thrombosis 2. Orbital vein occlusion (from compression of surrounding lesions) 3. Malignant exophthalmos. C. Systemic causes 1. Nephritis 2. Myxoedema 3. Angioneurotic oedema 4. Congestive heart failure. The following would be considered as ophthalmic emergencies:

Acute Conjunctivitis Causes Mainly bacterial and viral infections.

Clinical Features Conjunctival congestion more marked in the fornices, mucoid or mucopurulent discharge, matting and stickiness of eyelids especially on waking in the morning, lacrimation, foreign body sensation.

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Treatment 1. Frequent washing of eye with saline lotion to remove discharge. 2. Local antibiotics: Neosporin drops. Ciprofloxacin, Moxifloxacin or Gentamicin drops during day, ointment at bed time. For indolent cases Norfloxacin or Tobramycin drops. 3. Dark glasses if patient is photophobic. 4. If uniocular, avoid touching the sound eye with the handkerchief used to wipe affected eye. Note: Do not pad the affected eye as it favours bacterial proliferation. Keep towels, handkerchiefs, pillow cases separate from other members of the family.

Panophthalmitis It is an intense suppurative inflammation of the uveal tract with involvement of the whole eye including orbital tissues.

Causes Most commonly exogenous infection due to pneumococcus, Ps. pyocyanea, Streptococcus hemolyticus, Staphylococcus aureus, Staph. epidermidis, Propionibacterium acnes. Rarely endogenous infection, e.g. perforated corneal ulcer, penetrating wounds, lens operation, or endogenous infection (metastatic panophthalmitis) after cataract operation.

Clinical Features Usually unilateral. Severe pain in eyeball, rapid loss of vision, chemosis of conjunctiva. AC filled with pus (hypopyon), the pus usually pointing through anterior part of sclera.

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Management Vitrectomy and intravitreal Vancomycin. Ceftazidine, Vancomycin and IV steroids. Evisceration if the eye has no chance of survival.

Trachoma It is a conjunctivitis caused by the Chlamydia trachomatis virus in dry, dusty and hot surroundings. It gets complicated by secondary bacterial infection often, due to unhygienic habits.

Clinical Features Initially lacrimation, redness, itching, photophobia. The catarrhal stage gradually passes into chronicity when fibrotic changes occur both in palpebral and bulbar conjunctivae. In acute stage, palpebral conjunctiva shows presence of papillae and follicles, and the cornea pannus formation at upper limbus.

Sequelae In later stages, inversion of the lid margin (entropion), lashes get distorted or inturned (trichiasis), bulbar conjunctiva becomes dry and xerosed, and corneal opacity may develop. Adhesions from between palpebral and bulbar conjunctiva (symblepharon), fibrosis of lacrimal sac, corneal ulcer.

Treatment Local: Tetracycline 1% eye ointment. Sulphacetamide (Albucid locula) drops 20–30%. Systemic: Tetracycline.

Ophthalmia Neonatorum Purulent conjunctivitis in babies.

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Causes Gonococci, Chlamydia oculogenitalis, staphylococci and other organisms.

Signs and Symptoms 1. 2. 3. 4. 5.

Chemosis (conjunctival oedema). Purulent discharge from the eyes in the first week of life. Marked redness of the eyes. Swelling of the eyelids. Enlargement of the pre-auricular lymph node.

Complications: Corneal ulcers (Gonococci can invade the intact corneal epithelium).

Management 1. Prophylactic: (a) Antenatal treatment of vaginal discharge. (b) Obstetric asepsis at the time of birth. (c) Protection of the other eye. 2. Instillation of a drop of antibiotic. 3. Penicillin drops: Freshly prepared, in a strength of 10,000 units/mL to be instilled every minute for the first 5 minutes, every 5 minutes for the first half hour, every 1 hour thereafter. 4. Atropine drops if the cornea is affected.

Corneal Ulcer Causes Exogenous infection: Bacterial, viral or fungal. Associated factors: Chronic dacryocystitis, deficient nutrition (keratomalacia), loss of corneal sensation (V N. palsy, leprosy), lagophthalmos (VII N. palsy, proptosis, trauma or foreign body).

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Symptoms and signs: Lacrimation, photophobia, blepharo­ spasm, pain, diminished vision. Ciliary congestion, white corneal ulcer stains green with fluorescein, tenderness on pressing the eyeball.

Complications 1. Hypopyon ulcer (pus in the anterior chamber). 2. Corneal perforation and its effects: Iris prolapse, anterior synechiae (adhesions between the iris and the cornea), anterior staphyloma, corneal fistula, panophthalmitis.

Management Local: a. Control of infection: Take a conjunctival swab and scrapings from the ulcer itself for smear, culture and antibiotic sensitivity. Bacteriostatic drugs and antibiotics instilled repeatedly in the form of drops e.g. Moxifloxacin, Ciprofloxacin or Ofloxacin eye drops, ointments or subconjunctival injections. Sensitivity of the organism is determined by taking a conjunctival swab. b. Atropine: 1% or Cyclopentolate 1% eye drops three times a day. c. Pad the eye. d. Cauterization of the ulcer: First stain the ulcer with Fluorescein. Anaesthetise the cornea with xylocaine 4%. Cauterize with either pure carbolic acid or trichloroacetic acid (10–20%). Avoid touching the conjunctiva. Note: Locally steroids are contraindicated in the active stage of the disease except in marginal atopic ulcers.

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Operative treatment for indolent ulcers: Therapeutic keratoplasty if perforation is imminent or has occurred, or conjunctivoplasty.

Iridocyclitis Causes 1. Exogenous infections: After a perforating injury. 2. Secondary infection: Spread from the cornea, sclera or choroid. 3. Endogenous infections: TB, syphilis, brucellosis, viral infections such as mumps. Protozoal infections like toxoplasmosis. Septicemia due to Streptococcus. 4. Allergic inflammations: Allergy to tuberculous proteins or streptococcal proteins and sarcoid. 5. Autoimmune: Bechet’s disease, VKH syndrome, ankylosing spondylitis, rheumatic fever in children.

Symptoms and Signs Redness, pain, watering. Ciliary (circumcorneal) infection. Pupil: constricted and reacting sluggishly to light. Iris ‘muddy’ coloured with loss of normal iris pattern. Aqueous: turbid. Keratic precipitates (KPs) : Deposition of leucocytes on the posterior surface of the cornea, posterior synechiae (adhesions between the iris and the lens). Flare on slit lamp examination.

Management Local 1. Atropine: Drops 1%, 3–4 times day or eye ointment 1% bd. 2. Steroids: Drops of Betamethasone, Dexamethasone or Hydrocortisone. 3. Dark glasses if photophobic.

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Systemic 1. Steroids: Prednisolone 30 mg/day. 2. Specific antibiotics: Penicillin for syphilis. Streptomycin for tuberculosis. 3. Aspirin. 4. Elimination of any septic focus. Note: Miotics like Pilocarpine and Esserine are contraindicated.

Episcleritis and Scleritis Episcleritis: Inflammation of superficial layers of the sclera. Scleritis: Inflammation of deeper layers of the sclera with associated keratitis, iridocyclitis or choroiditis. Differential Diagnosis Conjunctival congestion 1. Indicates

Conjunctivitis

Ciliary congestion An active inflammation of the cornea, iris, ciliary body or acute congestive glaucoma

2. Site

In the fornix

Circumcorneal

3. Color

Bright red

Dark purple

4. Motility

Inflamed vessels move with the movement of the conjunctiva

Inflamed vessels are stationary

5. Depth

Superficial

Deep Contd...

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Contd...

6. Vessels

7. Blood flow

Conjunctival congestion Individual vessels can be made out From the fornix towards the cornea

Ciliary congestion Diffuse red blush Individuality of vessels absent From the cornea towards the fornix (difficult to demonstrate)

Differential Diagnosis

Conjunctivitis Iritis 1. Congestion Conjunctival Ciliary 2. Discharge Mucoid or Serous purulent

Acute angle closure glaucoma Ciliary Serous

3. Onset

Acute or gradual

Gradual

Acute

4. Vision

Normal

5. Pupil

Normal

Slight reduction Consricted and sluggishly reacting Present Normal

Markedly diminished Fixed and dilated

6. Tenderness Absent 7. Cornea Normal 8. Pain

Mild discomfort in the eyes

9. Intraocular Normal pressure

Retrobulbar pain

Lowered

Present Hazy and insensitive Severe headache unilateral, with vomiting Raised

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Causes Endogenous allergy to tuberculous or strepto­c occal proteins, collagen disease, rheumatism.

Clinical Features A small, tender, recurrent nodule on the sclera with localised redness.

Management 1. Cortisone locally, e.g. Betnesol-N, Sofracort, or Decadron eye drops, or Betnesol-N, Ocupol-D, or Kemicetine eye ointment qds. 2. Atropine if associated iritis.

Acute Orbital Cellulitis Causes Extension of inflammation from the neighbour­hood, nasal sinusitis, alveolar abscess, retained foreign body, deep injuries, metastasis in pyaemia, septic operations.

Clinical Features Swelling of the lids, chemosis, proptosis, restricted eye movements, diplopia, fever, diminished vision due to optic neuritis.

Management 1. Analgesics. 2. Broad spectrum antibiotics parenterally. 3. Hot fomentations locally with hot water. 4. Incision and evacuation of the pus.

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Cavernous Sinus Thrombosis It is a dural sinus occlusion resulting from infection in the face or mastoid region, spreading through the angular vein into cavernous sinus. Paranasal sinuses may also act as infective source. Rarely metastasis as in pyaemia.

Clinical Features Fever, rigors, headache. Proptosis and limitation of movement due to paralysis of 3rd, 4th and 6th cranial nerves, cornea insensitive due to paralysis of ophthalmic division of 5th nerve. Oedema of periorbital structures and over mastoid region. Congestion and chemosis of conjunctiva.

Management Intense systemic antibiotic therapy. Anticoagulation with heparin and warfarin.

Acute Dacryocystitis (Acute inflammation of the lacrimal sac).

Signs and Symptoms Swelling, redness and pain over the region of the sac, just below the medial canthus. Fever, pain and tenderness subside once the abscess ruptures on the skin surface, but a permanent lacrimal fistula results with discharge of pus.

Treatment 1. 2. 3. 4.

Broad spectrum antibiotics for 5 days. Hot fomentations. Incision and drainage, if the abscess points. Dacryocystorhinostomy (DCR) operation after the inflammation subsides or Laser DCR or Endonasal DCR operation.

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Vitreous Hemorrhage Causes Trauma, posterior vitreous detachment, diabetes, Eale’s disease, hypertensive retinopathy, blood dyscrasias, agerelated macular degeneration, retinal tears.

Clinical Features Sudden loss of sight, black spots in front of the eyes. Eyes are externally normal. Fundi cannot be visualised. Haemorrhage in the vitreous seen with the slit lamp.

Management 1. Treat the cause with vitamin C tablets. 2. Photocoagulation of the leaking vessels once the fundus is visible. 3. Vitrectomy operation if hemorrhage does not clear in 3 months.

Central Retinal Artery Occlusion Causes 1. Angiospasm: Hypertension, vasomotor instability, migraine; quinine, tobacco or alcohol poisoning. Raynaud’s disease, toxaemia of pregnancy. 2. Embolism: Endocarditis, atheromatous plaque in the carotid artery, cardiac emboli, e.g. rheumatic vegetations; infective emboli, e.g. endocarditis, diphtheria, pneumonia; mural thrombus; blood disease: polycythaemia, neoplasms; endocardial myxomata; fat embolism: after a crush injury with fractures. 3. Thrombosis: Because of (a) Endarteritis due to carotid insufficiency. (b) Trauma to the eyeball or optic nerve. (c) Buerger’s disease, giant cell arteritis.

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Signs and Symptoms Sudden loss of vision in one eye, without any pain or sore eyes. The eye is externally normal.

Fundus Examination 1. Disc is normal. 2. Blood vessels are markedly narrowed. Smaller arteries may disappear from view. 3. Blood column in the vessels is segmented and may show a to and fro movement (“Cattletruck appearance”). 4. Pallor of the retina, especially of the macula. 5. Cherry red spot at the centre of the macula.

Management It is difficult and the prognosis is poor. Measures to dilate the artery and let the clot pass to smaller branch are undertaken. 1. Massage the eyeball by digital pressure. 2. Paracentesis operation. 3. Retrobulbar injection of acetylcholine (0.1 g). 4. Diamox 500 mg IV. 5. Hyperventilation into a plastic bag placed over nose and mouth.

Retinoblastoma (Glioma) Definition It is a congenital, malignant, often familial and bilateral tumour, arising from the layer of rods and cones, in children.

Cause Proliferation of the neural cells.

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Clinical Features Stages: 1. Quiescent stage. 2. Glaucomatous stage. 3. Extraocular extension. 4. Distant metastasis. Initially a yellow reflex from the pupils is seen (amaurotic cat’s eye). In the second stage glaucoma, enlargement of the globe, proptosis, pain, squint, hypopyon or hyphaema. Metastasis occurs in the preauricular and cervical lymph nodes, and cranial bones. Calcified spots in the tumour seen in the X-ray, USG scan and MRI of Orbit. Fundus: Large white mass with surrounding satellite lesions. Associated detachment of the retina and retinal haemorrhages may occur.

Management 1. Chemotherapy and brachytherapy. 2. Enucleation (if within the eye). 3. Exenteration of the orbit (if it has spread to the extraocular tissues). 4. Laser photocoagulation/cryopexy. 5. Diathermy application to the sclera over the tumour. 6. Radiation: Cobalt or Ruthenium applicators to the sclera over the tumour: Dose: 4000 r in 1 week. Or external beam radiation. 7. Chemotherapy: Vincristine, etoposide + carboplatin.

Optic Neuritis 1. Demyelinating diseases: Multiple sclerosis, neuro­ myelitis optica, encephalitis periaxialis diffusa.

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2. Local causes: Uveitis, retinitis, sympathetic ophthalmitis, meningitis, sinusitis, orbital cellulitis, herpes zoster ophthalmicus. 3. Endogenous infections: Influenza, malaria, measles, mumps, septic teeth or tonsillitis, vaccination, typhoid. 4. Metabolic disorders: Diabetes, anemia, pregnancy, avitaminosis, starvation. 5. Ethambutol toxicity.

Symptoms and Signs 1. Sudden loss of vision, usually unilateral. 2. Pain on moving the eyeball especially upwards and on digital pressure. 3. Pupillary reaction to light: Sluggish and ill-sustained (relative afferent pupillary defect). 4. Central scotoma.

Fundus (a) In papillitis: (Inflammation of nerve head) Disc: Margins are blurred, hyperaemic, swelling of the disc head less than 2 Dioptres, vitreous opacities, retinal exudates, macular fan and oedema. (b) In retrobulbar neuritis (inflammation is behind the site of entry of the central retinal vessels into the optic nerve), fundus is normal.

Management 1. Inj. Methyl Prednisolone IV 1 g daily for 3 days. 2. Inj. Hydrocortisone by IV drip 200 mg daily for one week. Prednisolone 30 mg/day or Betamethasone 3 mg/day. 3. Vitamins: B Complex, Inj. Hydroxycobalamin.

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Malignant Exophthalmos It is a dysthyroid exophthalmos with marked lid oedema, lid retraction and ophthalmoplegia. It is unilateral and may occur without evidence of thyroid disease. Coronal CT scanning establishes the diagnosis by demonstrating enlargement of extraocular muscles (primarily lateral and inferior recti).

Management (a) 2% methylcellulose drops for eye grittiness. (b) Guanethidine 5% eye drops for lid retraction. (c) For failure of visual acuity Prednisolone 60 mg/day, or retrobulbar injection of methylprednisolone 10–15 mg. (d) Elevation of bed and diuresis for eyelid swelling. (e) Some patients require orbital decompression in order to prevent corneal ulcertation, papilloedema and blindness, tarsorrhaphy.

Detachment of the Retina Causes A. Primary detachment: Due to a retinal degeneration and vitreous traction, following the formation of retinal holes or tears. B. Secondary detachment: 1. Exudative choroiditis. 2. Toxaemia of pregnancy. 3. Tumours of the choroid.

Clinical Features Sudden diminution of vision, seeing black spots in front of the eyes, seeing flashes of light. Eye is externally normal. Fundus examination reveals vitreous opacities, grey detached retina with increased tortuosity of the retinal blood vessels, retinal holes or tears.

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Management 1. Complete rest in bed. 2. Pad both eyes. 3. Operation for primary detachment (closure of retinal hole by diathermy, cryosurgery or photocoagulation) or vitrectomy and silicone oil injection. 4. Treat the cause in secondary detachment.

Foreign Bodies (Extraocular) Causes Particles of dust, coal, stone, metal piece, wooden splinters, insects get impacted on the cornea or conjunctiva. Shiny multiple due to cracker injury.

Clinical Features Pain, redness and watering. Foreign body may be corneal, limbal or seen only on everting the eyelids.

Management Removal of the foreign body.

Procedure 1. Topical anaesthesia (a drop of proparacaine 0.5% or xylocaine 4%). 2. Remove with a sterile cotton swab, if conjunctival foreign body. 3. Foreign body spud or a needle is used for removal of a corneal FB. 4. Antibiotic ointment (e.g. Terramycin or Chloromycetin). 5. Bandage the eye for one day or till the epithelium heals.

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Intraocular Foreign Body Causes While hammering, machines with flying particles. Chips of iron, stone, glass, wood, bullets and other fragments may get lodged within the eye if they strike with sufficient velocity. Damage to the eye may be due to : – (a) Mechanical effect. (b) Introduction of infection. (c) Specific action (e.g. iron causes siderosis and copper chalcosis, by undergoing electrolytic dissociation within the eye).

Clinical Features Pain, redness and diminished vision following the entry of the foreign body. Wound of entry in the cornea or sclera may be visible; corneal opacity, a hole in the iris, opaque track in the lens due to the passage of the foreign body. Differential Diagnosis Optic neuritis 1. Vision Markedly lost 2. Pupil Sluggish and ill-sustained reaction to light 3. Movements Painful (especially upwards) 4. Fields Central and paracentral scotoma 5. Vitreous Present ± opacities 6. Onset Acute with self-remissions 7. Disc swelling

Usually no signs on the disc

Papilledema Almost normal Normal reaction Painless Enlarged blind spot Absent Gradual and sustained Marked, more than 2D

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Fundus. If the lens is not cataractous, the foreign body may be seen lodged in the retina. Tension of the eye is reduced due to the loss of intraocular fluids. Examine the eye on a slit lamp, with a gonioscope for detection of the foreign body in the anterior chamber. X-ray of the orbit, ultrasonography and CT scan—may help to diagnose such foreign bodies. No MRI for Metallic foreign body.

Management 1. Removal of the foreign body surgically after proper localisation with X-rays. 2. Magnetic foreign bodies are removed with an electromagnet applied over the site of impaction or vitrectomy. 3. Antibiotics locally and systemically to prevent infection. 4. Corticosteroids systemically to suppress inflammation. 5. Bandage the eye. 6. Prophylactic: Protective glasses.

Chemical Injury and Burns of the Cornea and Conjunctiva Causes Burns with hot water, oil steam, molten metal, blast injury, fire-crakers, injuries by alkalis like lime, white wash, concentrated acids and strong ammonia.

Clinical Features Severe pain, lacrimation, photophobia, blepharospasm. Eye is congested, chemosis is present, cornea may be hazy and oedematous. Later corneal ulceration, necrosis and perforation may occur.

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110 A Handbook of Emergencies Symblepharon (adhesions between the palpebral and bulbar conjuctiva) develop. Alkali burns are worse than acid burns as alkalis penetrate the ocular tissues deeper than acids.

Management 1. Local anaesthetic drop (proparacaine 0.5% or xylocaine 4%) to relieve the pain. 2. Copious irrigation to wash out the noxious substance, without any delay, with water or saline for 15 to 30 minutes. 3. Neutralisation of alkalis by weak acids (Boric lotion) or milk and acids by soda bicarb solution 3%. 4. Removal of particles of lime and metal with forceps. If solid particles are seen, do not irrigate as it would spread the bums. 5. Antibiotics locally. 6. Corticosteroids locally. 7. Sweeping a glass rod in the fornix or wearing a contact lens to prevent the development of a symblepharon. 8. Mucous, conjunctival or corneal grafting in severe cases. 9. Amniotic membrane/stem cell grafts. 10. Bandage contact lens.

Perforating Injuries Causes Injury with sharp objects like knives, projecting metal pieces. needles, flying missiles.

Clinical Features Conjunctival tears, chemosis, subconjunctival haemorrhage, corneal tears with or without iris prolapse,

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hyphaema, traumatic cataract. Vitreous haemorrhage, scleral tears, sympathetic ophthalmitis in the fellow eye.

Management 1. Prevention of infection: by local and systemic antibiotics, e.g. chloramphenicol or ofloxacin drops. 2. Place eye shield over the eye. 3. Atropine is instilled whenever the cornea or iris are injured. 4. Prolapsed iris is excised and never replaced into the anterior chamber. 5. Perforating wound is sutured in layers. 6. A badly mutilated eye with no useful vision is best excised to prevent the occurrence of sympathetic ophthalmitis in the other eye (enucleation). 7. CT scan of the orbit is taken to exclude retention of an intraocular foreign body.

Effects of Contusions (Blunt injury to the eye) 1. Corneal abrasions: Patient complains of severe pain, lacrimation, blepharospasm and foreign body sensation. It is diagnosed by the distortion of the corneal reflex over the abraded area and after the instillation of fluorescein, the abrasion stains green. Management: 1. Antibiotic eye ointment. 2. Atropine eye ointment 1%. 3. Bandage the eye till there is no staining of the cornea. 2. Subconjunctival haemorrhage: It occurs after a minor injury to the eye or after fracture of the orbit

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or base of the skull. Other causes: vomiting, lifting heavy weights, whooping cough, hypertension, blood dyscrasias, conjunctivitis, scurvy, diabetes. Management: The blood gets absorbed within one to three weeks. An eye ointment may be prescribed as a placebo.

3. Other injuries to the ocular structures: a. Iris: Traumatic miosis or mydriasis, iridodialysis (iris is torn at its ciliary attachment, resulting in a ‘D’ shaped pupil). Inversion or retroflexion of the iris. b. Lens: Concussion cataract, dislocation of the lens. c. Vitreous: Haemorrhage and opacities. d. Choroid: Haemorrhage and rupture. e. Retina: (a) Comotio retinae (Berlin’s oedema) is a traumatic retinal oedema. (b) Macular degeneration with retinal hole formation followed by a detachment of the retina. f. Traumatic glaucoma (angle recession). g. Traumatic iridocyclitis. h. Fractures of the orbital bones with retrobulbar haematoma. i. Dislocation of the trochlea. j. Avulsion of optic nerve.

Hyphema (Blood in the Anterior Chamber) Causes Contusion resulting in a rupture of the vessels of the iris or following tears in the iris. It also occurs in gonococcal and herpetic iridocyclitis.

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Clinical Features Blood is seen in the anterior chamber. It forms a horizontal line due to the gravitation of the blood clots at the bottom of the anterior chamber. In full chamber hyphaema, the iris, pupil and lens are not visible.

Complications (a) Secondary glaucoma with blood staining of the cornea. (b) Iridocyclitis.

Management Conservative paracentesis (if secondary glaucoma develops).

Acute Congestive Glaucoma Causes Blockage at the angle of the anterior chamber.

Clinical Features Headache, pain in the eyes, redness, sudden loss of vision, vomiting, halos. Ciliary injection, cornea hazy and insensitive, anterior chamber very shallow, pupil fixed and dilated and vertically oval, tension raised, eyeball tender on pressure.

Management 1. First bring down intraocular pressure to below 30 mm Hg with IV mannitol, then start miotics: (a) Betablockers (i) Timolol maleate 0.5%. (b) Pilocarpine (1% to 4%) 2 to 4 times a day. (c) Latanoprost (xalatan) one drop at bed time.

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114 A Handbook of Emergencies 2. 3. 4. 5.

Tab. Diamox (250 mg) – 2 stat., 1 every 8 hours. Mannitol IV. Glucose 50 ml of 50% IV. Oral glycerol (1.5 g/kg body weight).

Operative treatment (after the tension returns to normal): (a) Iridectomy. (b) Glaucoma surgery.

Caution Do not use mydriatics (e.g. atropine and homatropine). Dr Rumi Jehangir

MS DOMS FCPS

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Emergencies in Gynecology

Emergencies with Profuse External Hemorrhage Common Causes 1. Anovulatory bleeding: Very high levels of oestrogen which fall precipitously, bleeding results from inefficient shedding of a thickened endometrium, and menses may be prolonged and profuse. 2. Complications of pregnancy: Ectopic gestation, spontaneous abortion, hydatidiform mole, retained membrane or placental bits subinvolution in immediate puerperium, choriocarcinoma. 3. Anatomic abnormalities: (a) Benign: Cervical polyps, cervicitis, endometrial polyps, leiomyomas, pelvic inflammation or vaginal adenosis secondary to prenatal stilbestrol exposure, chronic endometritis, adenomyosis or endometriosis. (b) Malignant : Leukaemias, trophoblastic disease, carcinomas, sarcomas. 4. Abnormalities of other endocrine system: Hypo- or hyperthyroidism, adrenal disorders, or diabetes rarely. 5. Coagulation disorders. 6. Female: Hyper-androgenism: Polycystic ovarian disease.

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116 A Handbook of Emergencies 7. Miscellaneous: Obesity, drug abuse, emotional disturbances.

Symptoms 1. Small amounts of irregular bleeding for only a few moments. 2. Profuse bleeding per vagina of variable duration. 3. Symptoms due to anaemia – weakness, fatigue, attacks of giddiness, fainting, palpitations, etc. 4. Associated pain in abdomen.

Signs 1. In cases of anovulatory bleeding no palpable pathology. 2. Obvious palpable pathology in cases of leiomyomas, cervical polyps, cervicitis, adenomyosis, ovarian tumours. 3. Features of endocrine disorders—hypo- or hyper­ thyroidism. 4. Anaemia—marked pallor, oedema, tachycardia, haemic murmur. 5. Local examination—Clots in the vagina and bleeding from the os on examination.

Investigations a. Hb estimation and complete blood count. b. Coagulation testing and platelet count to ascertain adequacy of the clotting mechanism. c. Serum pregnancy test – β hCG. d. Endocrine testing if signs of endocrine disorder. e. Ultrasound—Ectopic gestation, leiomyomas, ovarian masses, adenomyosis, to detect presence of intrauterine gestation sac.

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f. Laparoscopy—Method of choice for diagnosing extrauterine gestation (ectopic pregnancies).

Management A. General: (a) Complete bed rest. (b) Sedatives. (c) Blood transfusion if warranted. (d) Styptic agents like Vitamin C, K, Ca gluconate, or Gynaec CVP. B. Specific Hormonal Therapy a. In older patients with mild to moderate bleeding, haemostasis with either IM or oral progestational agents, progesterone in oil, 100–200 mg. IM; Medroxyprogesterone acetate (Provera) 10 mg bd for 5 days. b. In cases of severe bleeding, 25 mg of conjugated estrogen (Premarin) can be administered IV every 2 to 6 hours until bleeding is controlled. Oral or IM oestrogen, can also be used. High-dose orally administered oestrogen, equivalent to 2.5 to 5 mg of conjugated oestrogens should be given 4 times a day. Alternatively 10 mg of IM oestradiol valerate can also be given when there is GI intolerance to oral oestrogens. Hig h d o s e o ra l o e s t ro g e n / p ro g e s t e ro n e combination (norethindrone or ethynodiol diacetate) 5–10 mg with mestranol 0.075 mg 4 times a day. Medroxyprogesterone acetate or norethindrone can be given in doses of 10 mg daily for the last 10 days of oestrogen administration: oestrogen is given for a total of 3 weeks. A combination of oestrogen/progesterone should be continued for 3 cycles (3 weeks on + 1 week off – 1 cycle) after bleeding has been controlled.

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118 A Handbook of Emergencies C. Surgical a. D and C is a diagnostic and not a therapeutic procedure, mainly for the diagnosis of malignancy. Curettage is usually reserved for bleeding not responding to hormonal therapy, recurrent severe bleeding or suspicion of endometrial hyperplasia. b. Diagnostic hysteroscopy to visualize the uterine cavity for the presence of intractable pathology, which would otherwise be missed by routine curettage. Verifies presence of sub-mucus fibroids, endometrial polyps, focal atypical hyperplasia, retained products of conception, placental polyps, embedded IUCD and adenocarcinoma. Operative hysteroscopy is used routinely to remove polyps and intramural fibroids which may be a cause of menorrhagia. c. Operative laparoscopy—ectopic gestations can be tackled with ease by using a cautery and scissors. The advantages being, decrease in adhesions, postoperative pain and reduced hospital stay. Laparoscopic myomectomy as well as dermoids removal can be done by this technique. d. Exploratory laparotomy may be indicated for ectopic gestation and ovarian tumours. Myomectomy is indicated in patients with leiomyo­ mas. e. Internal iliac artery ligation can also be done. f. Hysterectomy is rarely performed, and only if the patient is perimenopausal, has completed child bearing or is suffering from malignancy.

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Injuries of the Vulva, Vagina and Perineum Causes 1. Postcoital in virgins, postabortal, puerperal women or soon after vaginal operations, episiotomy suturing. 2. Direct trauma due to accidental fall. 3. Indirect trauma due to falling flat on the buttocks. 4. Trauma due to foreign bodies such a sticks, safety pins, pencils, knitting needles, etc. 5. Pessaries (retained for a long time).

Symptoms 1. Profuse bleeding PV of various degrees, sometimes leading to collapse. 2. Swelling of vulva. 3. History of fall or coitus. 4. Haematoma at the labia or vagina. 5. Retention of urine.

Signs 1. Visible vulval and perineal lacerations or tears specially in periurethral region in cases of fall on buttocks. 2. Huge increasing blackish swelling of the labia due to haematoma. 3. Retention of urine in case of periurethral avulsion of perineal haematoma. 4. Vaginal tear on careful speculum examination usually placed transversely in posterior vaginal fornix higher up. 5. Signs of shock and collapse. 6. Rarely prolapse of the bowel and omentum into vagina.

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Management 1. Resuscitation of patient. 2. Immediate thorough examination and suturing of the laceration and tears of vulva, vagina or perineum under proper anaesthesia. 3. Small vulval haematoma just requires rest in bed and cold compresses. 4. In case of large haematoma evacuation and suturing under anaesthesia. 5. If peritoneum has been opened up, then exploratory laparotomy to rule out perforation of the bowel. 6. Prophylactic antibiotic therapy. 7. Catheterization of the bladder if necessary.

Hemorrhage from Tumors of Uterus and Ovaries Common Causes 1. Carcinoma cervix. 2. Choriocarcinoma. 3. Endometrial carcinoma. 4. Endometrial hyperplasia. 5. Uterine sarcoma. 6. Ovarian carcinoma. 7. Benign ovarian neoplasms (Torsion and haemorrhage). 8. Uterine fibroids (sub-mucous).

Symptoms 1. Profuse and continuous bleeding PV. 2. Foul smelling discharge in cases of carcinoma cervix. 3. Post-coital bleeding in cases of carcinoma cervix.

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4. Lump in the lower abdomen in some cases of benign ovarian neoplasms, ovarian carcinoma, uterine fibroids and sarcoma. 5. Heaviness in the lower abdomen occasionally. 6. Pain in lower abdomen.

Signs 1. General condition may be poor and cachectic. 2. Marked pallor, tachycardia, tachypnoea due to anaemia which may be moderate to marked. 3. Hypotension in cases of profuse bleeding. 4. On local examination— a. Large friable cauliflower growth on the cervix, bleeding on touch in cases of carcinoma cervix. b. Enlarged bulky uterus in cases of uterine fibroids, uterine carcinoma, choriocarcinoma. c. Normal to slightly bulky uterus in cases of uterine hyperplasia. d. Ovarian enlargement palpable PIA and bimanually in cases of benign ovarian neoplasms or ovarian carcinoma. e. Occasionally palpable inguinal lymph nodes.

Management 1. Resuscitation in cases of severe shock. 2. Haematinics to correct moderate to severe anaemia. 3. Polypectomy and diagnostic fractional curettage and cervical biopsy. 4. Ultrasonography for differentiating origin and extent of mass in abdomen, either uterine or ovarian. 5. Wertheim’s hysterectomy with pelvic lymphadenectomy in cases of stage I and IIa carcinoma cervix and radiation in cases of stage IIb, III and IV along with palliative surgery, if needed.

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122 A Handbook of Emergencies 6. Total abdominal hysterectomy for uterine sarcoma, endometrial hyperplasia and ovarian carcinoma. Omentectomy and chemotherapy should also be added to the armamentarium for ovarian carcinoma. 7. Myomectomy or total abdominal hysterectomy for uterine fibroids, depending on age and desire for future child bearing. 8. Ovarian cystectomy or oophorectomy for benign ovarian neoplasms. 9. Methotrexate and actinomycin therapy or hysterectomy and chemotherapy for choriocarcinoma. 10. Abdominal hysterectomy with bilateral salpingooophorectomy followed by radiation if indicated for endometrial carcinoma.

Emergencies with Obvious Severe Intraperitoneal Hemorrhage Ectopic Gestation It refers to an implantation of the fertilised ovum in an abnormal site. In over 95% of the cases it is tubal, although it may occur elsewhere in the uterus—cornua, cervix, rudimentary horn, or via secondary attachment in the broad ligament or anywhere in the pelvic cavity.

Etiology 1. Chronic endosalpingitis is the most common factor. 2. Pelvic tuberculosis. 3. Tubal disease causing adhesions, old inflammatory disease or endometriosis.

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4. Intrauterine device is associated with a 1 in 23 incidence of ectopic gestation. 5. The incidence of repeat ectopic pregnancy ranges from 10–25%. 6. Previous tubal surgery, either tubal ligation or tuboplasty. 7. Congenital diverticula, or long tube.

Symptoms 1. Irregular bleeding or relative amenorrhoea. 2. Sudden onset of abdominal pain, or an acute exacerbation of a previously present sharp or dul1 pain, unilaterally in the lower abdominal area followed by shoulder pain. 3. History of orthostatic dizziness and possibly a syncopal attack. 4. History of passing some clots of blood (decidual cast).

Signs 1. Signs of shock—Cold clammy skin, thready pulse and low BP hypovolemic shock in patients with hypovolemia. 2. Temperature may be raised. 3. Increasing and marked pallor of skin, tongue and conjunctiva. 4. Per abdomen—Lower abdominal distension and tenderness. 5. Pelvic examination—Unilateral adnexal tenderness and guarding, with pain on movement of the cervix and at times an adnexal mass. The cervix may be soft and cyanotic. The cul-de-sac is usually bulging with a doughy consistency, the uterus may be somewhat enlarged occasionally.

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Differential Diagnosis 1. 2. 3. 4. 5. 6. 7.

Pelvic inflammatory disease. Intrauterine pregnancy (with or without abortion). Acute salpingitis. Acute appendicitis. Corpus luteum haemorrhage. Rupture of a vein on the fibroid surface. Uterine wall perforation due to an invasive vesicular mole. 8. Torsion of ovary or fallopian tube.

Investigations 1. Haematologoic tests—Hb and haematocrit estimation to evaluate blood loss. WBC count is elevated. 2. Pregnancy tests—invariably positive. A positive radioimmunoassay (RIA) for serum beta subunit of human chorionic gonadotropin (hCG) with a low level of hCG and for the period of gestation is highly suggestive of ectopic gestation. A negative RIA excludes the diagnosis. 3. Ultrasonography—of value in diagnosing adnexal mass if patient presents with a typical history, symptoms and signs. Transvaginal sonography helps visualise intrauterine sac from 5th week of gestation and hemoperitoneum. 4. Laparoscopy—Tool of choice and single most important asset in modern gynaecology—done under general anaesthesia—helps to diagnose and treat exact site of ectopic gestation and differentiate from corpus luteum haemorrhage and to treat the pathology. 5. Colpo puncture—Posterior paracentesis under local anaesthesia and aspiration of blood which fails to clot. It can only diagnose hemoperitoneum, not specific

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for ectopic. If hemoperitoneum is present, laparoscopy is a must.

Management 1. Resuscitation of the patient—IV fluids, head low, O2, blood, plasma expanders. 2. Blood grouping and cross matching. 3. Operative laparoscopy with removal of the pathology and suction irrigation. 4. Early exploratory laparotomy is essential in the treatment of ectopic gestation, if patient is in shock. 5. Tubal abortion warrants a conservative approach and the tube is preserved. 6. Surgery—A salpingostomy may be done if indicated in an unruptured ectopic. Salpingectomy may also be done in a ruptured ectopic.

Hemorrhage from Corpus Luteum (See p. 127) Perforation of Uterus due to an Invasive Vesicular Mole 1. Gestational trophoblastic neoplasms (GTN) range from the generally benign hydatidiform mole (1 in 200 pregnancies) through the locally infiltrating invasive mole (1 in 2,000 pregnancies) to the highly malignant choriocarcinoma (1 in 4,000 pregnancies). The invasive mole is distinguished by local invasion of the myometrium, sometimes to the extent of perforation. Occasionally metastasis will occur. Symptoms: 1. Acute onset of abdominal pain. 2. Syncopal attacks. 3. Excessive amenorrhoea.

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126 A Handbook of Emergencies 4. Periods of amenorrhoea. 5. Bleeding PV of variable duration. At times vesicles may be passed. 6. No H/O quickening or foetal movements. 7. Gradual abdominal distension. 8. Hyperthyoidism. Signs: 1. Uterus is enlarged more than period of gestation. Uterus is doughy to feel. No foetal parts are felt. Cervix bluish in colour and soft to feel. 2. Ovaries develop theca-lutein cysts due to high levels of hCG with resultant marked ovarian enlargement. 3. No foetal heart sound is heard. 4. Pre-eclampsia is encountered in 10–15% cases. 5. Signs of collapse and intraperitoneal haemorrhage. Investigations: 1. Ultrasound—Highly reliable in establishing the diagnosis by picking-up multiple echoes in a honeycomb pattern, demonstrating absence of foetal activity and outlining ovarian cysts if present. 2. Laparoscopy—to look for haemoperitoneum and uterine perforation. 3. Haematology—Hb, Haematocrit and blood grouping and cross-matching. Management: 1. Resuscitation of patient. 2. Immediate exploratory laparotomy with suturing of uterine rent if conservation is necessitated or total abdominal hysterectomy followed by: 3. Chemotherapy— a. Single agents used are actinomycin-D and methotrexate.

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b. Combination therapy is Methotrexate, Actinomycin-D and Chlorambucil (MAC). 2. Haemorrhage from a follicular cyst or corpus luteum haemorrhage. Signs and symptoms: Similar to an ectopic gestation but much less severe. Differentiated from ectopic gestation by laparoscopy only or on laparotomy. Management: Conservation, only rarely proceed to exploratory laparotomy with the removal of the cyst or corpus luteum haematoma.

Emergencies Associated with Obvious Infection Acute Salpingo-oophoritis Etiology 1. Gonococcal. 2. Non-gonococcal—Tubercular, post-abortal, puerperal, secondary to pelvic infections like appendicitis, colitis, diverticulitis. Organisms: Neisseria gonorrhoeae, E. coli, Mycoplasma hominis, T-Mycoplasma and Chlamydia trachomatis.

Symptoms 1. Bilateral lower abdominal pain beginning just after the onset of menses. 2. Fever. 3. Vomiting. 4. Increased vaginal discharge. 5. Irregular bleeding. 6. Urinary symptoms—Increased frequency or burning. 7. Chills.

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Signs 1. Elevated temperature and pulse rate. 2. P/A—Lower abdomen peritonism, with guarding and tenderness. 3. Pelvic examination—(a) Bilateral tenderness of the adnexa with exquisite tenderness on motion of the cervix. (b) Occasionally bilateral tender irregular masses palpated. (c) At times a boggy feel experienced in the posterior fornix. (d) Purulent vaginal discharge seen per speculum. 4. ESR raised considerably. 5. WBC count: leucocytosis.

Differential Diagnosis 1. Appendicitis. 2. Endometriosis. 3. Ectopic pregnancy. 4. Complications of ovarian cysts.

Management Management is usually conservative. Mild cases may be treated as outpatients with combination of quinolones and metronidazole to combat mixed aerobic as anaerobic infections. Hospital regime: Criteria for hospital admission include uncertain diagnosis, suspicion of an abscess, pregnancy, upper peritoneal signs, temperature above 38°C and failure to respond to ambulatory therapy. 1. Complete bed rest. 2. Fowlers position. 3. Analgesics and antipyretics. 4. Light diet and fluids orally. 5. Heavy antibiotic cover. 6. Blood transfusion if necessary.

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7. Short wave diathermy. 8. Surgical intervention if pelvic abscess colpotomy and drainage.

Rupture of a Pyosalpinx, Tubo-ovarian Abscess or an Infected Ovarian Cyst A pelvic abscess is a major complication as an infection in the genital tract. The abscess may be confined to the tube (Pyosalpinx) or involve tube and ovary (Tubo-ovarian abscess), or may lie between the broad ligament (Broad ligament abscess). Rupture into the general peritoneal cavity, peritonitis, is the major complication of a pelvic rupture may be spontaneous or be precipitated a fall, or an abdominal blow. If not diagnosed and treated within 24–48 hours, septicemia and sepsis follow, with resultant high mortality. Organisms responsible are—(a) Exogenous : Neisseria gonorrhoeae, beta-hemolytic streptococci, and rarely Staphylococcus aureus, or Mycobacterium tuberculi. (b) Endogenous : Bacteroides, Peptococci, Peptostreptococci and rarely clostridia.

Symptoms 1. Severe lower abdominal pain, which may be an acute exacerbation of pain, with evidence of peritonitis and with a pelvic mass no longer palpable. 2. Nausea and vomiting. 3. Fever. 4. Diarrhoea.

Signs 1. Toxic patient, dry furred tongue. 2. Tachycardia.

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130 A Handbook of Emergencies 3. Hypotension. 4. Tachypnoea. 5. Raised temperature 6. PIA distension, tenderness and rigidity in lower abdomen. PN fullness in the fornices.

Special Investigations 1. Abdominal X-rays 2. IVP. 3. Pelvic sonogram. 4. Barium enema. 5. Culdocentesis and, on occasion abdominal paracentesis yield evidence of pus and organisms involved.

Management Conservative: 1. Bed rest. 2. Analgesics and antipyretics. 3. Fluid and electrolyte balance with IV fluids and nasogastric suction. 4. If evidence of septic shock a central venous line and urinary catheter are placed. 5. Heavy doses of antibiotics (usually a penicillin, an aminoglycoside and frequently a drug specific for Bacteroides fragilis). About 70% of the cases respond to this regimen. Failure to respond is indicated by persistent fever, increase in the mass size or spreading level of peritonism. Failure is evident within 48–72 hours. Immediate surgery—If intraperitoneal rupture is suspected. Exploratory laparotomy with excision of the pyosalpinx, or tubo-ovarian mass or infected ovarian cyst in a young

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patient. Intraoperative lavage is essential to minimize the danger of postoperative reaccumulation of pelvic purulent collections. In woman who has finished child bearing, usual procedure is total abdominal hysterectomy with bilateral salpingo-oophorectomy. Drainage following the procedure is usually via the vaginal cuff.

Emergencies with Acute Abdominal Conditions of Doubtful Etiology Cryptomenorrhea Common Causes 1. Congenital: Imperforate hymen or atresia of lower part of vagina, atresia of the cervix of a normal or bicornuate uterus. 2. Acquired: (i) Adhesions leading to atresia due to inflammatory conditions, e.g. gonococcal vulvovaginitis in children and rarely diphtheritic infection of the genitalia. (ii) Douching with strong antiseptic lotions as lysol, corrosive sublimates usually for criminal abortion. (iii) Occlusion of cervical canal following cervical operations like amputation, cauterisation of the endocervix or diathermy conization. Menstrual blood collects in the vagina which gets distended to form haematocolpos and later on haematometra and rarely haematosalpinx.

Symptoms 1. Severe spasmodic pain in lower abdomen at monthly intervals. 2. Primary amenorrhoea, onset of menstruation is delayed. In some cases secondary amenorrhoea. 3. Retention of urine or difficult and painful micturition.

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132 A Handbook of Emergencies 4. Associated general disturbances such as headache, constipation and malaise and backache—menstrual molimina. 5. History of constant dull pain in lower abdomen. 6. Gradual and progressively increasing swelling of lower abdomen.

Signs 1. Usual age of the patient is 6–18 years. 2. A tense, cystic and tender tumour is palpable and visible in the lower abdomen arising from the pelvis even after catheterisation of the bladder which is dull on percussion. 3. On vulval examination a thin translucent bluish membrane is seen bulging out due to retained dark coloured blood. 4. A gentle pressure on the abdomen over the tumour causes further bulging of the hymen or makes the bulge tenser. 5. On rectal examination, a tense, cystic tender mass is felt anteriorly, filling the pelvis. 6. In case of haematocolpos, uterus is felt on the top of the cystic mass on abdominal examination.

Management 1. Catheterisation of the bladder. 2. Excision of the septum (hymen) under anaesthesia and with all aseptic precautions by cruciate incision and excision of flaps. 3. Few haemostatic catgut sutures in the cut edges. 4. No bimanual examination or dilatation of the cervix should be done under any circumstances. Forceful expulsion of the contents is not advisable. 5. Vulva is cleaned and covered by a sterile pad.

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6. A full course of prophylactic antibiotics. 7. Postoperatively raise the head end of the bed.

Dysmenorrhea Primary—is painful menstruation in the absence of pelvic disease. Secondary—related to organic pelvic disease such as endometriosis, pelvic inflammatory disease, presence of an intrauterine device, adenomyosis or fibroid.

Etiology The cause of primary dysmenorrhoea is probably multifactorial; psychological and social factors including a low pain threshold, over anxious parents, faulty sexual education and outlook have been implicated. The main cause is the excessive uterine production of prostaglandins.

Symptoms and Signs Primary dsymenorrhea starts with the first ovulatory cycles, is worse just before or at the beginning of the menses and is improved with increased age, regular intercourse and after pregnancy. Nausea, dizziness, headaches and diarrhoea are frequently associated. Physical examination is negative. Secondary dysmenorrhea—Pain often starts well before the period, lasts several days and occurs in later life. Deep dyspareunia and menorrhagia may be related symptoms. Physical examination reveals the associated organic disease.

Management 1. Counselling and reassurance of girls and mothers. 2. Simple analgesics.

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134 A Handbook of Emergencies 3. Use of prostaglandin-synthetase inhibitor drugs alleviates pain in 60–100% of cases. These include mefenamic acid, ibuprofen and naproxen. 4. Oral contraceptive drugs to inhibit ovulation are also effective. 5. In a few patients, resistant to all drug therapies, laparoscopy to exclude pelvic disease is called for. 6. At that time cervical dilatation and curettage should be done to exclude or treat the rare instances of cervical stenosis or adhesions. 7. Very occasionally a presacral neurectomy or laparoscopic uterine nerve ablation (LUNA) may be required for serious and refractory dysmenorrhoea.

Torsion of an Ovarian Tumor, Hydrosalpinx or Subserous Fibroid Most commonly torsion occurs with an adnexal mass greater than 6 cm in diameter. Usually a benign ovarian tumour such as a dermoid or a simple cyst of the ovary is responsible, but approximately 20% of the ovarian masses which undergo torsion will be malignant. Either a paraovarian cyst or a hydrosalpinx is responsible for most tubal torsions.

Symptoms 1. Acute lower abdominal pain which varies in location from groin to flank and also occasionally radiates to the thigh of the involved side. The pain is a dull ache with acute exacerbation of sharp pain. 2. Nausea and vomiting may be present with acute exacerbation. 3. Abnormal bleeding. 4. Many patients may relate a past history of similar pain.

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Signs 1. PA – Abdominal guarding on the involved side with a palpable tender adnexal mass. 2. PV – Pain on motion of the cervix, palpable tender adnexal mass. 3. Patient is usually afebrile.

Management If torsion is untreated, necrosis of the involved organ can lead to peritonitis and shock. It is treated laparoscopically with very good results.

Rupture of a Chocolate Cyst of Ovary Causes Rupture is spontaneous and usually during menstruation due to increased tension, may be provoked by coitus.

Symptoms 1. Acute abdominal pain. 2. Nausea, vomiting and syncope. 3. History of menstrual disorder—menorrhagia and congestive dysmenorrhoea which is peculiarly premenstrual, menstrual and post-menstrual.

Signs Signs of peritonism— 1. Fast pulse. 2. No distension or minimal fullness in lower abdomen. 3. Abdomen tender and rigid. 4. PV—Marked tenderness and mass in the lateral fornices usually bilateral and adherent to the uterus.

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Management 1. Conservative therapy usually produces good response. Bedrest, IV fluids, analgesics, antibiotics, Ryle’s tube. 2. Laparoscopic peritoneal lavage and ovarian cystectomy. 3. Operative laparoscopy with removal of chocolate cyst and cauterization of the base of the cyst wall. Postoperatively pseudopregnancy state may be produced by administering injection Leupride Depot SC every month for 3 months or oral Danazol therapy. The treatment of choice for a young infertile patient is to concieve. Indications for surgery: Doubtful diagnosis or failure to respond to conservative therapy.

Rupture of an Ovarian Tumor Causes 1. Trauma, accidental fall or direct violence to the abdomen. 2. During labour when the cyst is impacted in the pelvis. 3. Thin walled retention cyst may rupture during bimanual examination. 4. Spontaneous—specially papillary serous cystadenoma, pseudomucinous cystadenoma benign as well as malignant, granuloma cell tumour and dermoid.

Symptoms and Signs of Peritonism 1. Acute pain in abdomen—generalised, severe and constant. 2. Feeling of something giving way in the abdomen. 3. Nausea and vomiting.

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4. 5. 6. 7. 8.

History of abdominal swelling and menstrual disorder. Signs of shock. Abdomen distended and tender with muscle guarding. Absent peristalsis. May be associated with signs of intraperitoneal haemorrhage. 9. PV—A large irregular mass felt through one or more fornices, separate from the uterus depending upon the size of the tumour.

Management 1. Treat shock. 2. Ryle’s tube aspiration. 3. IV fluids and blood transfusion. 4. Antibiotics. 5. Laparoscopic lavage and removal, or laparotomy.

Red Degeneration of Fibroid of the Uterus Causes Usually during pregnancy in an intramural large fibroid.

Symptoms and Signs 1. Acute abdominal constant pain. 2. Nausea and vomiting. 3. Slight fever. 4. Constipation. 5. Enlarged uterus with localised tenderness. 6. Fast pulse. 7. Muscle guarding. 8. Moderate leucocytosis and raised ESR.

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Management Always conservative and symptomatic. When diagnosis is doubtful, always explore to rule out appendicitis or other surgical emergencies. 1. Rest in bed. 2. Analgesics. 3. Antipyretics, electrolytes. 4. Antiemetics. 5. Sedatives. 6. Antibiotics. 7. Fluid balance.

Acute Retention of Urine Causes 1. 2. 3. 4.

Retroverted gravid uterus at 14–16 weeks of gestation. Haematocolpos in young girl of 16–18 years. A big haematocele of extrauterine pregnancy. Cervical fibroid, uterine fibroid specially of posterior wall impacted in the pelvis. 5. Ovarian tumour impacted in pelvis, or a large malignant ovarian tumour filling the whole pelvis in old women.

Symptoms 1. Pain in lower abdomen may be severe. 2. Symptoms due to associated condition.

Signs 1. Palpable abdominal tumour—Bladder which is tense and tender. 2. Palpable pelvic tumour such as pregnant retroverted uterus, fibroid, ovarian tumour, etc.

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3. Palpable mass in the pouch of Douglas in case of pelvic haematocele. 4. History of difficulty in passing urine before.

Management 1. Put the patient to bed. 2. Slow evacuation of bladder with a self-retaining catheter inserted in bladder. 3. Urine is sent for routine examination and culture and sensitivity. 4. Advise to lie in prone position 3 times in a day for a period of minimum 10 minutes. 5. Urinary antiseptics. 6. Permanent treatment consists of removal of cause in non-pregnant patient like fibroid uterus and ovarian tumour, etc. 7. Rarely incarcerated gravid uterus may require surgical correction. Dr (Mrs) Anahita Pandole MD, DNB, FCPS

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6

Psychiatric Emergencies

Psychiatric emergencies are conditions in which there is an alteration in a person’s behaviour, emotions and thinking for which an urgent psychiatric intervention is deemed necessary in order to prevent harm or danger to the person or others. This has become a challenging speciality in the face of rise in incidence of violence, rape, abuse, addiction, terrorism and murder in society.

General Approach Psychiatric emergencies are seen mostly in emergency room (ER) of a hospital, but these can be encountered in any routine psychiatric set up. Psychiatric emergencies do not mean that patients are suffering from only psychiatric disorders. They may be present due to medical conditions or conditions unrelated to it.

General Principles Approach to a Patient The proper assessment of a psychiatric emergency depends on the correct attitude and tact displayed by a physician. The latter must approach each psychiatric

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emergency in an open-minded manner as a prejudicial attitude could interfere with proper diagnosis and management. A sympathetic, friendly and confident attitude of the physician arouses a sense of trust in the patient and gives the physician better access to a patient’s emotional turmoil. The physician should always talk to the patient first and other relevant information can be obtained later from the accompanying persons.

Assessment The scheme for the emergency assessment of a psychiatric patient is as follows: 1. Observation of the patient’s behaviour. 2. Interview with the patient. 3. Objective data and other relevant information pertaining to the patient from the persons accompanying the patient. 4. Detailed physical examination. 5. Mental status examination. 6. Relevant biochemical, hematological, radiological and psychometric investigations, when indicated. If a patient is too excited or disturbed to comply with a physical examination, then the latter should be done later as soon as possible. Psychiatric emergencies are often bizarre in their presentation. Also a hostile and uncooperative patient may make the diagnosis on initial assessment more difficult. Hence, emergency management in psychiatry is often symptom-oriented and specific treatment of the underlying psychiatric disorder can be started later after the diagnosis is established. It is not necessary to hospitalize all psychiatric patients seen in an emergency situation. However, homicidal, suicidal, markedly aggressive, severely depressed, delirious, stuporous, markedly anxious patients and patients in acute drug withdrawal states should be hospitalized.

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Violence Violence is physical or verbal aggression by one person to another person or persons are on other objects. It is important to note that most violent individuals are not psychiatrically ill. Violence can be seen in the following psychiatric disorders: 1. Psychosis: Schizophrenia, schizophreniform psychosis, brief reactive psychosis delusional disorder. 2. Mood disorders: Mania, depression (rare). 3. Personality disorders: Anti-social personality disorder, paranoid personality disorder. 4. Substance use disorders, either due to drug intoxication or in drug withdrawal. 5. Organic brain disorders: Epilepsy, trauma, encephalitis, acute organic disorders characterized by delirium and dementia. 6. Impulse control disorders: Intermittent explosive disorder. 7. Conduct disorder in children. 8. Situational problems: Child abuse, spouse abuse. 9. Dissociative disorders.

Management 1. The management of violent patients is an important skill in emergency psychiatry. The following are the list of Do’s and Don’ts that a physician should follow when dealing with these patients. Do’s i. Do protect yourself. ii. Unarm the patient. iii. Keep the door open. iv. Keep others near you. v. Do restraint, if necessary

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vi. Show concern, establish rapport and assure the patient. Don’ts i. Do not keep any potential weapon near the patient. ii. Do not sit with back to patient. iii. Do not keep any provocative family member or friend in the room. iv. Do not confront. v. Do not sit close to the patient. 2. If restraint is required, it should be used judiciously for minimum period possible. It is also important to explain to the patient the reason for restraint. At least five persons are usually required for restraint. Restraint is done one limb at a time, while the other limbs are held firmly by others. Restraints in arms are placed in such a way that IM or IV injections can be given easily. 3. Sedation : a. Butyrophenones : Haloperidol 5 mg IM can be repeated q4-6 hour until sedated. b. Benzodiazepines : Lorazepam 20–30 mcg/kg body weight, IM or IV after dilution. Can be repeated q6h. c. Thioxanthenes : Zuclopenthixol acetate 50–100 mg IM, OD till maximum of 400 mg or total 4 injections. d. Atypical : Olanzapine 10 mg IM is an antipsychotics  effective tran­quilizer. Can be repeated q12-24 hours. 4. Adjuvant medication: Antiparkinsonian drugs with Haloperidol, Chlorpromazine or Zuclopenthixol if extrapyramidal reactions occur. Benzhexol 2 mg q8hr or Procyclidine 2.5 mg q8hr PO. Alternatively Phenergan 50 mg IM can be administered.

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144 A Handbook of Emergencies 5. Once the patient is adequately sedated and the psychiatric diagnosis established, appropriate treatment for the psychiatric disorder can be started (e.g. to continue antipsychotics for schizophrenia, anti-depressants for depression). 6. Electroconvulsive therapy (ECT) may be helpful in controlling aggressive behaviour in schizophrenia and mania. 7. In cases where diagnosis is not certain relevant investigations should be carried out to ascertain the diagnosis before proper treatment can be initiated.

Suicidal Behavior Suicidal behaviour is a term which includes attempted suicides, suicidal ideations, threats or gestures. The most important implication for suicidal behaviour is that it is a ‘Cry for help’. Whereas attempted suicides require psychiatric intervention only after the emergency medical or surgical management has been completed, suicidal ideations, threats or gestures which occur in a variety of psychiatric disorders, require immediate psychiatric assessment and intervention. Contrary to popular belief that people who threaten suicide, rarely make an attempt, it has been shown that majority of people who attempted suicide had previously communicated their intent of doing so.

Assessment of Suicide Risk a. Age: There is an increased risk of suicide in adolescents, elderly people and menopausal women. b. Isolation: Incidence of suicide highest in individuals who are single, separated, divorced or widowed people. c. Presence of an environmental stress, e.g. recent bereavement or financial difficulties.

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d. Presence of a psychiatric disorder especially schizophrenia, depressive disorders, substance abuse and borderline personality disorders. e. Presence of a serious or a chronic debilitating illness, e.g. malignancy, paralysis. f. Recent major surgery, especially if it involves important organs (eyes, genitals) or which produce permanent disability (amputation). g. History of previous suicide attempt. h. Repeated statements, verbal or written expressing suicidal intentions directly or indirectly. i. Method: If suicidal attempt is made when alone and when violent or potentially lethal methods are used, e.g. hanging, drowning, using fire arms.

Management 1. Hospitalisation: In cases where suicide risk is very high. The patient must be hospitalized in a special protected ward where he or she can be constantly observed. 2. Treatment of underlying psychiatric disorder, e.g. neuroleptics for schizophrenia, mood elevators for depressive disorders, detoxification for substance abuse. 3. Electroconvulsive therapy (ECT): Particularly indicated in severely depressed individuals or schizophrenics. 4. Long-term treatment for the concurrent psychiatric disorder, with drugs and psychotherapy to help patient find solutions to his problems.

Victims of Disaster Victims of disaster are people, who have survived a sudden, unexpected, overwhelming stress, that is beyond that normally expected in life, like earthquake, flood, riots,

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146 A Handbook of Emergencies terrorism, etc. Other victims are relatives of survivors or rescue workers. Anger, frustration, guilt and confusion are common features in these individuals.

Management 1. Treatment of the life-threatening physical problems. 2. Crisis intervention. i. Sympathetic and flexible attitude toward the victims. ii. Allow the victims to express their feelings about their experience. iii. Provide accurate and responsible information to the victims 3. Group therapy. 4. Pharmacotherapy: In selected cases, benzodiazepines are prescribed to reduce anxiety and induce sleep. 5. Referral to psychiatric service, if necessary for further management.

Grief Grief is a reaction of an individual to a significant loss. Factors affecting grief reaction: i. Abruptness of loss ii. Extent of loss iii. Preparation for loss iv. Significance of the loss to the individual v. Past experience of grief vi. Cultural background vii. Personality traits.

Uncomplicated Grief It is characterized by sadness, insomnia, poor appetite, loss of interest, guilt and death wish.

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Stages 1. Hours to days—Shock and disbelief 2. Weeks to months—Anger, resentment, depression 3. Six months to a year—Acceptance of reality.

Management 1. Evaluation to rule out any psychiatric disorder. 2. Crisis intervention: Patient is encouraged to talk about the deceased in private. Reassurance is given that it is a normal experience and it will subside on its own. 3. Pharmacotherapy: Avoid drug treatment, as far as possible. Prescribe night time sedatives on as needed basis (sos). 4. Referral to psychiatric service if necessary.

Complicated Grief It is characterized by suicidality, prolonged functional impairment, morbid feeling of worthlessness or unresolved uncomplicated grief.

Management 1. Facilitate grieving process by helping the patient to remember the deceased and the nature of relationship. 2. Brief supportive psychotherapy. 3. Hospitalization, if necessary.

Rape Survivor Rape is the forceful coercion of an unwilling victim to engage in a sexual act, usually sexual intercourse. As with other acts of violence, rape is a psychiatric emergency that requires immediate appropriate intervention. Rape victims may suffer sequelae that persist for a life time.

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148 A Handbook of Emergencies Typical reactions in rape include shame, humiliation, anxiety, confusion and outrage.

Management 1. If possible a female clinician should examine the patient, after obtaining a written consent from her. 2. Attend to medical conditions, if any. 3. Prescribe morning after pill to prevent possible pregnancy. 4. Send samples for sexually transmitted disease (STD) and human immunodeficiency virus (HIV) infection. 5. Be supportive, reassuring and non-judgemental. 6. Educate about the availability of medical, legal services and rape crisis centres. 7. Avoid pharmacotherapy, if needed only short-term benzodiazepines may be given. 8. Referral to a support group for rape victims. 9. Referral to psychiatric services for further treatment. 10. Psychotherapy for post-traumatic stress disorder.

Anxiety and Panic Disorders An acute anxiety attack is characterized by a sudden onset of a feeling of intense fear or of impending doom and is accompanied by strong autonomic nervous system manifestations such as chest pain, palpitations, dyspnoea, tremulousness, paraesthesias, dizziness and restlessness. These attacks of acute anxiety or panic attacks could be primary as in panic disorder or could be secondary to a general medical condition, certain drugs or a concurrent psychiatric disorder, for example: 1. Endocrine disorders: Thyroid dysfunction, pheo­ chromocytoma, hypoglycemia, hypercortisolism 2. Intoxication: Caffeine, cocaine, amphetamine.

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3. Drug withdrawal states: Withdrawal from sedativeshypnotics. 4. Iatrogenic: Anticholinergics, neuroleptics, antihypertensives, stimulants, bronchodilators, hallucinogens, adrenergic agents. 5. Psychiatric disorders: Generalised anxiety disorder, phobic disorders, obsessive compulsive disorders, conversion disorder, depressive disorders, drugdependence states, schizophrenia. 6. Physical disorders: Ischemic heart disease (IHD), anaemias, chronic obstructive pulmonary disease (COPD), pulmonary embolism. 7. Miscellaneous: Vitamin B12 deficiency, brucellosis, heavy metal poisoning.

Diagnosis Panic disorder: It is more common in women and has its onset in early adult life. The anxiety attacks can occur spontaneously or in response to an environmental stress. A family history of panic disorder or other neurotic disturbances is often present. Patients suffering from panic disorder may also suffer from varying degrees of agoraphobia or fear of open spaces.

Management 1. All patients should undergo a physical and mental status examination and relevant investigations carried out to exclude presence of a physical or concurrent psychiatric disorder. 2. Patients who are markedly anxious or agitated should be hospitalized. 3. Patients and their relatives should be reassured about patient’s mental and physical state. 4. Drugs : (a) Emergency treatment: Benzodiazepines are the drugs of choice—Lorazepam 1–2 mg IM or

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150 A Handbook of Emergencies diazepam 5–10 mg IM or by slow IV drips brings prompt relief. Once symptoms have subsided or in milder cases oral therapy can be started. Diazepam 5–10 mg BD or Lorazepam 1–2 mg BD or chlordiazepoxide 10 mg TDS or oxazepam 15 mg TDS or clobazam 5–10 mg BD or clonazepam 0.5 mg TDS or alprazolam 0.5 mg TDS. (b) Long-term management: Once the diagnosis is established either tricyclic antidepressants (TCAs) or selective serotonin reuptake inhibitors (SSRIs) coupled with appropriate psychotherapy and the benzodiazepines should be gradually withdrawn. 5. Any concurrent physical or psychiatric disorder should be treated by appropriate means.

Stupor Stupor is a state of extreme motor inactivity usually associated with mutism or diminished verbal responses. In this state, a patient lies motionless either with his/her eyes open or closed. The patient either does not reply to questions posed to him/her or gives monosyllabic responses.

Diagnosis Stupor is a symptom which is seen in psychiatric and in certain physical conditions. 1. S c h i z o p h re n i a : Cat at o n i c s c h i zo p h re n i a i s characterized by intervening periods of excitement and stupor. The stuporous phase is characterized by a blank, expressionless face, waxy flexibility of limbs. 2. Depressive disorder: Endogenous retarded type of depression may present with a stuporous state characterized by decreased psychomotor retardation, depressed facial appearance. 3. Conversion disorder (Hysteria): Hysterical stupor is usually sudden in onset and occurs in response to

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an environmental stress. It responds dramatically following hospitalization and social isolation. 4. Physical disorders: Can be seen in various organic disorders: a. Neurological disorders: Disorders of frontal lobe, basal ganglia and corpus callosum; epilepsy and postictal states. b. Metabolic disorders: Hypercalcemia, hepatic encephalopathy, diabetic ketoacidosis, pellagra. c. Drug-induced: Neuroleptics, hallucinogens, anticholinergics corticosteroids.

Management 1. Hospitalisation for all stuporous conditions. 2. Maintenance of nutritional status. 3. Lorazepam 20–30 mcg/kg IM or by slow IV drip is effective in some functional stuporous states. 4. Narcoanalysis—Interviewing patient under the influence of sub-anaesthetic doses of sodium pentothal is a useful aid in some cases of functional stuporous states. 5. Treatment of the underlying psychiatric disorder with appropriate drugs. 6. Treatment of any underlying physical disorder. 7. ECT—Useful in depressive or catatonic stupor.

Emergencies Associated with Substance Use Disorders The clinical manifestations of drug-related problems are varied—alteration in mood, perception, cognition and behaviour can result from abuse of psychoactive substances. The commonly abused drugs or substances are: (a) Alcohol. (b) Opioids—morphine, heroin, pethidine, dextropropoxyphene, methadone. (c) Sedative or hypnotic

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152 A Handbook of Emergencies drugs—barbiturates, benzodiazepines, methaqualone, meprobamate. (d) Cannabinoids—hashish, marijuana (e) Central nervous stimulants—amphetamine, cocaine, ephedrine. (f) Hallucinogens—Lysergic acid diethylamide (LSD), methylenedioxymethamphetamine (MDMA).

Alcohol Alcohol Intoxication Clinical Features 1. Odour of alcohol in breath. 2. Slurred speech. 3. Ataxia 4. Disinhibited behaviour 5. Impaired social judgement 6. Mood disturbances varying from depression to euphoria.

Management 1. Mild to moderate intoxication: No active medical intervention especially when there is no associated disruptive behaviour. Protection from harm, reassurance and allowing the patient to sleep will usually suffice. 2. Rowdy and excited patients: Sedation and physical restraint. Diazepam 10 mg orally or IM. Chlordiazepoxide 10–20 mg PO or Haloperidol 5 mg PO or IM are safe and effective. 3. For intoxicated patients who are comatose or stuporous: Supportive treatment towards maintenance of vital functions, protection of the airway, maintenance of nutrition and monitoring of fluid and electrolyte balance till patient recovers.

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Alcohol Withdrawal Syndrome Delirium tremens: Onset is usually within 24–72 hours of abstinence and symptoms usually last 7–10 days. It is characterized by. 1. Autonomic hyperactivity: Tachycardia, hypertension, diaphoresis, tremors and hyperthermia. 2. Sleep disturbances and 3. Psychological symptoms : Anxiety, agitation, irritability, confusion, restlessness, distractibility and hallucinations which are often visual in nature but other sensory modalities can be involved.

Management 1. Patients should be hospitalized. 2. Maintenance of vital signs. 3. Correction of fluid and electrolyte imbalance and maintenance of nutritional status. 4. Thiamine 100 mg IM daily. 5. Sedation : (i) Diazepam 5–10 TDS PO or IM BD. (ii) Lorazepam 1–2 mg PO or 20–30 mcg/kg IM or by slow IV drip or (iii) Chlordiazepoxide 10–25 mg TDS PO or (iv) Oxazepam 15 mg TDS PO or (v) Haloperidol 1.5 mg TDS PO or 5 mg IM BD.

Wernicke-Korsakoff Syndrome It occurs in nutritionally deficient alcoholics and is caused by deficiency of thiamine. It consists of a triad of ocular disturbances, ataxia and peripheral neuropathy. A superimposed alcohol withdrawal syndrome may be present. The diagnosis is critical since Wernicke’s encephalopathy is treatable, if untreated the condition can progress to Korsakoff’s psychosis.

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154 A Handbook of Emergencies Korsakoff’s psychosis: Clinical manifestations: 1. Disorientation 2. Retrograde amnesia 3. Confabulation 4. Euphoria. Once this syndrome emerges, the prognosis for recovery is poor with only 20% patients making a substantial improvement.

Management of Wernicke-Korsakoff Syndrome 1. Hospitalisation 2. Maintenance of nutritional status 3. Thiamine 100 mg IM (IV) 4. Treatment of associated alcohol withdrawal syndrome.

Opioids Abusers of opioids generally seek urgent medical attention because of overdosage, withdrawal or medical complications arising out of opioid use.

Overdosage Clinical Features 1. Mental clouding. In severe cases, the patient may be comatose or stuporous 2. Pupillary constriction 3. Decreased respiratory rate 4. Hypothermia, hypotension and tachycardia may be present.

Management 1. Hospitalisation. 2. Maintenance of vital signs and respiration.

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3. Correction of fluid and electrolyte imbalance. 4. Naloxone is effective in reversing the opioid induced CNS depression in a dose of 0.4 mg IV, if patient shows no response, the dose can be repeated after 15 minutes. Once the symptoms are reversed, the dose should be kept at a minimum, otherwise an acute opioid withdrawal syndrome would occur. 5. Treatment of the ensuing opioid withdrawal syndrome. 6. Treatment of medical complications arising out of opioid abuse, e.g. pulmonary edema, cellulitis, sepsis, endocarditis, HIV.

Opioid Withdrawal Syndrome 1. Onset of withdrawal symptoms may be as early as 6 hours after abstinence from opioids. 2. Early symptoms include anxiety, craving for the drug, insomnia, yawning, sweating, rhinorrhoea and lacrimation. 3. As withdrawal progress dilated pupils, gooseflesh and tremors may become apparent along with chills, anorexia, abdominal cramps. 4. 18–24 hours after the last opioid dose, hypertension, tachycardia, tachypnoea and hyperthermia may occur. 5. Nausea, vomiting, diarrhoea and dehydration sometimes occur after 24–36 hours. 6. Peak symptoms occur 48–72 hours after the last opioid dose. 7. Most symptoms subside by 7–10 days.

Management 1. Sedation with psychotropic drugs: One of the following TDS—Haloperidol 5–10 mg orally or IM, or diazepam 5–10 mg PO or Lorazepam 1–2 mg PO or 20–30 mcg

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2.

3. 4. 5.

l kg/body weight IM. The dose of the psychotropic medication should be tapered off as the severity of the withdrawal syndrome subsides. Alternatively, Clonidine in doses of 0.1–0.2 mg po bd in divided doses can be administered orally. Hypotension and lack of sedation are common drawbacks with this drug. Monitor vital signs. Maintenance of nutritional status and fluid electrolyte balance. Treat medical complications arising out of opioid abuse.

Sedatives and Hypnotics (Barbiturates, Benzodiazepines, Methaqualone, etc.) Intoxication 1. Mild to moderate intoxication resembles alcoholic drunkenness without the odour of alcohol in the breath. Patients may exhibit ataxia, dysarthria, nystagmus, drowsiness, mild confusion. Some may become disinhibited and belligerent. 2. Severe intoxication results in stupor, coma and respiratory depression.

Management 1. Mild to moderate cases of intoxication often require no active medical intervention. Reassurance, protection from harm and monitoring of vital signs till patient recovers are usually sufficient. 2. Severe intoxication is a medical emergency— (i) Hospitalisation (ii) Monitoring vital signs. (iii) Maintenance of airway patency. Oxygenation may

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be required. (iv) Maintenance of nutritional status. (v) Forced diuresis with alkalinisation of urine will promote the excretion of Phenobarbitone but not of other drugs. (vi) Oral Phenytoin 100 mg tds to prevent epileptic convulsions.

Withdrawal Syndrome Clinical Features 1. Onset of symptoms depends on the duration of action of the abused drug. For shorter acting drugs like lorazepam symptoms may appear 12–16 hours after the last dose but may not appear until as late as 7–10 days in case of long-acting drugs like diazepam. 2. Mild cases: Anxiety, agitation, anorexia, nausea, vomiting, tachycardia, postural hypotension, hyperreflexia and tremors. Severe cases may show delirium, seizures, hypothermia and cardiovascular collapse.

Management 1. Hospitalisation is a necessity, agitated patients should be restrained 2. Monitoring of vital signs 3. Maintenance of nutritional status and fluid electrolyte balance 4. Treatment of seizures Phenytoin 100 mg TDS 5. Drug treatment—In case of barbiturate withdrawal syndrome, phenobarbitone can be given orally. The dose can be gradually tapered off till all withdrawal symptoms subside. In cases of benzodiazepine withdrawal, the dose of the abused drug has to be gradually tapered off and no other drugs may be required.

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Cannabinoids Intoxication Clinical Features 1. Euphoria 2. Sense of relaxation 3. Alteration in the perception of time 4. Conjunctival injection 5. Tachycardia.

Management These symptoms are usually self-limiting and require no active medical intervention.

Withdrawal Syndrome Some abusers may have a short and mild withdrawal syndrome after cessation of use of cannabis

Adverse Reactions to Cannabinoids: 1. Panic reaction: Characterised by anxiety, agitation and fear of going insane. Mild cases do not need active medical intervention. In severe cases, Diazepam 5–10 mg orally or IM. 2. Delirium: Characterised by confusion, agitation, hallucinations and delusions. Management consists of protecting the patient from harm, even by physical restraint if necessary, and sedation with either Diazepam 5–10 mg PO or IM or Haloperidol 5 mg PO or IM. 3. Psychosis: In this state prominent symptoms are paranoid delusions, bizarre behaviours, auditory hallucination and occasionally violence. Haloperidol 5 mg BD is effective in controlling the symptoms.

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Central Nervous System Stimulants Intoxication Clinical Features 1. Mild to moderate cases: Euphoria, restlessness, grandiosity, hypervigilance, irritability, impaired judgement. Physical symptoms include tremors, tachycardia, mydriasis, hypertension, increased sweating, nausea or vomiting. 2. Severe cases: Delirium, paranoid delusions, tactile, auditory or visual hallucinations; with overdose, seizures may occur and cardiac complications lead to death.

Management a. Hospitalisation and monitoring vital signs. b. Reduction of central nervous system irritability. i. Hyperthermia: Paracetamol 500–1000 mg orally TDS. ii. Seizures: Phenytoin 100 mg TDS or Diazepam 10 mg by slow IV injection. c. Promotion of drug excretion: In amphetamine intoxication, by acidifying the urine with 500 mg of ammonium chloride orally q4hr. d. If tachycardia and hypertension are severe and persistent—Propranolol.

Withdrawal Syndrome 1. Excess fatigue 2. Hypersomnia or insomnia 3. Hyperphagia 4. Craving for the drug 5. Depression.

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Management 1. Hospitalisation and monitoring of vital signs. 2. No active medical intervention is required. 3. Depression due to stimulant withdrawal or abstinence is usually self-limiting. If the depression persists, the possibility of a co-existing affective disorder must be considered and appropriate anti-depressant medication started.

Hallucinogens Lysergic Acid Diethylamide (LSD) Intoxication Clinical features: 1. E a r l y sy mp t o m s i n c l u d e t a c hyca rd i a, m i l d hypertension, mild hyperthermia and mydriasis. 2. Peak effects are usually seen 2–3 hours after ingestion and consist of visual hallucinations and illusions, emotional lability, distortion of time perception and synesthesia in which the boundaries between sensory perceptions become blurred, so that colours are ‘heard and noises are seen’. Management: Often no active medical intervention is required. The drug effect begins to wane by 4–6 hours after ingestion and most symptoms subside after 8–12 hours. If patient is restless, diazepam 5–10 mg IM or lorazepam 20–30 mcg/kg IM.

Withdrawal Syndrome Hallucinogens do not produce a physical dependence hence there is no withdrawal syndrome experienced after cessation of their use.

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Adverse Reactions Common are panic, delirium and toxic psychosis. Clinical features, management and adverse reactions are similar to those seen with the use of cannabinoids.

MDMA (Ecstasy) MDMA (Ecstasy) has hallucinogenic and stimulant properties, and is popular among adolescent and young adults, especially in ‘rave parties’. Intoxication or overdose results in: 1. Emotional disinhibition 2. Increased physical activity 3. Tremors 4. Hyperthermia 5. Dehydration 6. Symptoms similar to neuroleptic management syndrome—altered consciousness, fever, rigidity, increased sweating, tachycardia, labile BP and convulsions. Myoglobinuria and renal failure.

Management 1. Hospitalisation 2. Restoration of fluid and electrolyte balance 3. Antipyretics 4. If sedation is required Lorazepam 20 mcg/kg body weight IM or 1–2 mg TDS PO. 5. Treatment of any associated medical disorder.

Psychiatric Manifestations of Physical Disorders Symptoms and signs of a mental disturbance may be presenting features of a physical disorder. Hence one must be open-minded and thorough in evaluating patients with psychiatric symptoms.

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Management If psychiatric management is administered it is for symptoms that are severe or disruptive, e.g. anxiolytics for anxiety, neuroleptics for delirium, etc. The following physical conditions can often exacerbate or mimic psychiatric disorders. 1. Toxic and metabolic disorders: Electrolyte distur­ bances, disturbances in acid-base balance, vitamin deficiencies, hepatic encephalopathy, uremia, heavy metal poisoning. 2. Endocrine disorders : Hypothyroidism, hyper­ thyroidism, Cushing’s syndrome, hypoglycemia, hyperglycemia, hyperparathyroidism, hypo­ parathyroidism, pheochromocytoma. 3. Infections: Meningitis, encephalitis, AIDS, cerebral abscess. 4. Collagen disorders: SLE, PAN. 5. Cardiovascular disorders: Cardiac arrhythmias, CHF, hypotension, hypertensive encephalopathy. 6. Neurological disorders: Head injury, stroke, intracranial malignancies, epilepsy, NPH, MS, Huntington’s disease, Parkinsonism, Wilson’s disease. Psychiatric problems associated with surgery: Preoperative and post-operative periods can be complicated by the sudden appearance of psychiatric symptoms. This is specially true for surgeries involving the eyes, brain, heart, limbs (e.g. amputation) and major abdominal surgeries.

Causes 1. Improper preparation of pt prior to surgery. 2. Realisation by patient of the loss of a vital body part. 3. Infection.

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4. Electrolyte imbalance. 5. Sensory deprivation.

Management Psychiatric symptoms associated with surgery can vary from mild anxiety to severe psychotic reactions. If any organic factors responsible for the psychiatric symptoms are detected, they should be corrected promptly. Additionally if the patient requires to be sedated then 10 mg of Diazepam IM or PO Most of the psychiatric reactions to surgery can be averted by a brief preoperative mental preparation of the patient and explanation of the consequences of surgery. Dr Amit Desai

MD, DPM, FIPS

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7

Gastrointestinal, Liver and Biliary Tract Emergencies

Esophageal Disorders Esophageal Spasm Pain A severe type of pain, dull or gripping felt in the centre of the chest, often radiating to neck, epigastrium, throat and sometimes to shoulders and upper arms. It lasts from a few seconds to several minutes and if prolonged and severe, may be associated with vasovagal effects.

Causes 1. Diffuse spasm and achalasia. 2. Reflux oesophagitis. 3. Symptomatic oesophageal peristalsis (nutcracker oesophagus). 4. Nonspecific oesophageal motility disorder (NEMD).

Diagnosis It can be difficult to distinguish this from cardiac pain. Oesophageal pain may have characteristic ‘anginal’ features, and cardiac pain is at times burning in character and may be associated with eating and precipitated by recumbency.

Investigation ECG would detect a cardiac cause. If thereafter suspicion moves towards an oesophageal disorder, other investigations

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which may be undertaken are oesophageal acid perfusion test, barium swallow, endoscopy, oesophageal manometry and 24 hours esophageal pH metry.

Management (a) Diffuse spasm and achalasia. Sublingual nifedipine or isosorbide dinitrate gives temporary relief. Later balloon dilatation, endoscopic injection of Botox to the lower oesophageal sphincter or cardiomyotomy or Pantoprazole 40 mg. (b) Reflux oesophagitis. Consists of bland diet, avoidance of smoking, alcohol and use of NSAIDs; weight loss if obese. Drugs—Omeprazole 20 or Lansoprazole 30 mg with breakfast or evening meal for 8 weeks, followed by Ranitidine 300 mg bd for at least 3 months. Antireflux surgery if inadequate response to therapy or maintenance therapy irksome to the patient.

Acute Gastrointestinal Bleeding (Hematemesis and Melena) GI bleeding can manifest itself in one of the following ways: Haematemesis, melaena, rectal bleeding, occult blood in stools, anaemia or at times syncope. Haematemesis indicates a site of bleeding proximal to the duodeno-jejunal junction. The colour of the vomitus depends on how long the blood has been in the stomach; large volume of bright red blood suggests a rapid and sizeable hemorrhage, a smaller volume of dark blood (coffee grounds) is consistent with a smaller bleed, which has been altered by contact with gastric acid.

Causes Common zz zz

Peptic ulcer Erosion/gastritis

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166 A Handbook of Emergencies zz zz zz zz zz

Gastric or oesophageal varices Mallory-Weiss tear Portal hypertensive gastropathy Dieulafoy’s erosion Stress ulceration.

Uncommon or Rare Oesophagogastric tumors, vascular anomalies of upper GI tract, acute pancreatitis, blood dyscrasias or coagulation defects. Note: Coagulation or platelet defects usually do not cause haematemesis or melaena in absence of a lesion in upper GI tract. Same is true for anticoagulants.

Clinical Approach and Investigations of Upper GI Bleed 1. Assessment of blood loss: (a) Syncope suggests considerable blood loss. (b) Persistent state of shock, systolic BP < 100 and pulse rate > 100/min suggests blood loss of at least 20% of the circulating volume. 2. Identification of factors suggesting high risk and poor prognosis: (a) Age over 60. (b) Need for repeated blood transfusions because of state of shock. (c) Recurrent bleeding as indicated by persistent bright red gastric aspirate, or fresh blood per rectum. (d) Co-existing disease such as cardiac, respiratory or renal. (e) Cirrhotic patient bleeding from oesophageal varices. 3. Determining the cause of bleed a. History: (i) Use of NSAlDs. (ii) Of abdominal pain or peptic ulcer. (iii) Of heartburn and acid regurgitation as in reflux oesophagitis. (iv) Dysphagia and weight loss may suggest oesophageal malignancy.

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(v) Of retching and vomiting before onset of haematemesis suggesting oesophageal rupture. (vi) History of alcohol intake or other risk factors such as hepatitis in the past or chronic liver disease. b. Investigations ŠŠ Hb level within first few hours after haemate­ mesis or melaena is not a good indicator of volume of blood lost. ŠŠ LFTs to rule out liver disease. ŠŠ Upper GI endoscopy is a primary investigation. The timing depends on severity of bleeding and hemodynamic stability of patient. As a rule once blood volume is replenished and patient is haemodynamically stable, endoscopy should be performed as soon as possible because it helps identify the lesion in majority of cases while also offering treatment at the same time. ŠŠ Selective arteriography may identify source of bleeding. ŠŠ If lesion still cannot be diagnosed, a radioisotope labelled red cell scan may be done.

Management of Acute GI Hemorrhage 1. Collect blood: for grouping and cross-matching. 2. Resuscitation: The principles of ‘airway, breathing and circulation’ apply. IV access is essential. Initially IV colloids (low molecular weight dextran or haemaccel) or plasma, followed by blood transfusion. 3. Pass nasogastric tube: Aspirate stomach contents. Do gastric lavage with room temperature potable water to which adrenaline or noradrenaline has been added. Allow the fluid to drain by gravity and aspirate gently only if required. Keep for 24 hours after cessation of bleed.

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168 A Handbook of Emergencies 4. Blood transfusion if massive bleed, patient is in shock or Hb < 10 g/dL. Fresh frozen plasma or platelet transfusion may be required to correct coagulopathy or thrombocytopenia in patients with liver disease, one unit of fresh frozen plasma for every 5 units of packed red cells. 5. Monitoring: Measurement of pulse, BP, urine output (through an indwelling catheter) and CVP. Actively bleeding patients with evidence of shock should be managed in ICU. 6. Endoscopy: It is the primary diagnostic investigation and is undertaken after optimum resuscitation has been achieved. It has 4 purposes—(a) It provides an accurate diagnosis. (b) Certain diagnoses influence management, e.g. oesophageal varices and bleeding peptic ulcers require specific endoscopic and pharmacological interventions. (c) It provides prognostic information about risk of re-bleeding. (d) Endoscopy facilitates application of specific therapies to high-risk bleeding lesions. Indications: –– Bleeding oesophageal or gastric varices –– Peptic ulcer with major stigmata of recent hemorrhage (active spurting bleeding, a nonbleeding visible vessel) –– Vascular malformations, e.g. actively bleeding AVMs, gastric antral vascular ectasia and Dieulafoy’s lesion –– Rarely, active bleeding from Mallory-Weiss tear. 7. Injection: Direct injection of fluids into bleeding ulcer. Mechanism of benefit include tamponade by compressing the artery within the fibrous confines of the chronic ulcer, vasoconstriction induced by adrenaline, endarteritis caused by sclerosants or alcohol, and blood clot formation from fibrin gel or thrombin. Polidocanol and sodium tetradecyl sulfate

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are used for esophageal varices, cyanoacrylate glue for gastric varices. Adrenaline 1:10,000 is the most widely used. Fibrin gel (a mixture of thrombin and fibrinogen) injected through separate channels of a special needle and human thrombin are the most effective materials and have a low complication rate. 8. Heat energy: In this method, the heating probe is pushed firmly on to the bleeding lesion to apply tamponade, and defined pulses of heat energy are then given to coagulate the vessel. 9. Mechanical devices: Oesophageal variceal bands are commonly used for oesophageal varices. ‘Endoclips’ can be applied to bleeding vessels and is the best option for treatment of major bleeding ulcers. Re-bleeding after endoscopic therapy. In most patients, repeat endoscopy and retreatment of the bleeding lesion. Further bleeding is an absolute indication for surgical intervention. 10. Argon plasma coagulation: A jet of ionized argon gas is directed through a probe passed through the endoscope. 11. Drug-therapy: (a) Acid suppressing drug. It is crucial that gastric pH does not fall below 6. Omeprazole 80 mg bolus followed by 8 mg/h infusion for 24 hours significantly reduces risk of re-bleeding and need for emergency surgery. (b) Somatostatin and octreotide reduce mesenteric arterial blood flow and suppress gastric acid secretion but are not much used frequently in initial management of variceal bleed 25–50 mg/hr for 48–72 hours. (c) Tranexamic acid an antifibrinolytic agent can

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170 A Handbook of Emergencies improve stability of blood clot, it is not often used because it could lead to venous thrombosis. 12. Selective coeliac or mesenteric arterial catheterization of bleeding vessel. 13. Surgery: Indications—(a) Active bleeding that cannot be controlled by endoscopic therapy because torrential hemorrhage obscures the bleeding point, or active bleeding continues despite successful endoscopic therapy. (b) Re-bleeding follows initial successful endoscopic treatment. The type of operation depends on the site of the ulcer. Bleeding duodenal ulcers are treated by under-running the ulcer, sometimes with pyloroplasty. Gastric ulcers are treated with partial gastrectomy or simple ulcer excision.

Acute Lower GI Hemorrhage Causes Anorectal conditions: Hemorrhoids, anal fissure, ‘solitary rectal ulcer syndrome’, mucosal prolapse with ulceration. Children: Meckle’s diverticulum, juvenile polyps, inflammatory bowel disease. Adults: Inflammatory bowel disease, adenomatous polyps, carcinoma, A-V malformation, Meckel’s diverticulum. Elderly: Diver ticular disease, angiodysplasia, adenomatous polyps, carcinoma, infective or ischemic colitis, inflammatory bowel disease.

Clinical Features and Diagnosis A history of abdominal pain and change of bowel habit may suggest a neoplastic lesion, diarrhoea and urgency of defecation an inflammatory process. Elderly patients with

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cardiovascular disease may have ischemic colitis. A history of dyspepsia, alcoholism, NSAID ingestion or weight loss may give clues to the causative lesion. Melaena in large bowel hemorrhage points to caecum or ascending colon as site of bleeding. Rectum—Bright red fresh blood or deep maroon coloured stool. Note: When a continuous hemorrhage from stomach or duodenum or proximal part of small bowel is severe enough to allow fresh blood per rectum, patient is in a state of shock or is likely to go into shock.

Management Initial correction of hypovolemia with plasma expanders followed by blood transfusion to stabilize the patient before definitive investigation. CVP monitoring is a sensitive indicator of continued or recurrent bleeding. Blood should be taken for Hb estimation, clotting screening, and urea and electrolytes. However, Hb is a poor indicator of the degree of blood loss in early stage because hemodilution develops only after a few hours. Any clotting abnormalities should be corrected and anticoagulants discontinued. After resuscitation, definitive investigations may be planned.

Investigations (a) Digital anorectal examination and anorectal sigmoidoscopy to exclude local conditions. Uniformly inflamed, friable rectal mucosa indicates colitis. (b) Upper GI endoscopy if no local cause is found, to exclude causes in upper GI tract (e.g. rapidly bleeding duodenal ulcer). (c) Colonoscopy can provide clues to the segments of bowel through which the hemorrhage is arising. It also allows therapeutic procedures such as snare polypectomy,

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172 A Handbook of Emergencies diathermy, endoclipping or argon plasma coagulation of bleeding tumors, AVMs or angiodysplasia. (d) Mesenteric angiography when endoscopy fails to identify a lesion, or bleeding continues at such a rate, that surgery is inevitable. It can identify the site of bleeding in majority. (e) Radionuclide techniques should be used if rate of bleeding is slow, as angiography is unlikely to be successful. (f ) Small bowel enema may be useful in identifying Meckle’s diverticulum. (g) Emergency surgery is occasionally necessary as a diagnostic procedure when hemorrhage is massive and patient is deteriorating; this should be combined with on-table colonoscopy.

Acute Abdominal Pain Causes All age groups Appendicitis

Acute pancreatitis

Diverticular disease

Intestinal obstruction

Perforated peptic ulcer

Renal colic

Acute cholecystitis

Nonspecific abdominal pain Hernia

Elderly Cancer (colorectal) Vascular (MI, aortic aneurysm, mesenteric ischemia) Volvulus Medical causes Children

Women

Intussusception Urinary tract infection Upper respiratory tract infection

Salpingitis Urinary tract infection Ovarian cyst Ectopic pregnancy

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Acute Appendicitis Clinical Features Pain begins in central location and then moves to the right lower quadrant. Pain is aggravated by movement and coughing, and is accompanied by nausea, vomiting and anorexia. Temperature is normal or only slightly raised. There is focal tenderness in right lower quadrant with rebound tenderness and guarding. Right focal (abdominal) tenderness can be detected on rectal examination. More diffuse tenderness suggests either a perforation or a different condition.

Investigation Ultrasonography or CT scan may reveal bowel thickening or abscess.

Management Uncomplicated case: Appendicectomy, if seen within 24 hours. Acute peritonitis: IV fluids. Nasogastric aspiration. Broad spectrum antibiotics. Metronidazole I g q8h for 3 days to reduce wound infection before surgery. Appendix mass: Rest in bed, fluid diet. Record pulse, temperature, and size of mass. Drainage of abscess if mass enlarges and pyrexia continues. Note: Antibiotics are not prescribed at this stage because they can produce a chronic inflammatory honeycomb of abscesses. Non-specific abdominal pain is defined as an acute selflimiting pain of short duration and indeterminate cause which requires no surgical treatment. However in patients

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174 A Handbook of Emergencies over 50 years, a diagnosis of NSAP is justified only if it is the signal for further investigation.

Acute Diverticulitis Diverticulitis is a clinical syndrome which occurs when a diverticulum becomes inflamed or perforates leading to local pericolitis.

Clinical Features Pain and tenderness in left iliac fossa start suddenly and persist. There is fever, systemic upset and leucocytosis. Patient may become extremely ill with peritonitis or Gramnegative septicemia. Right-sided diverticulitis may mimic acute appendicitis.

Pericolic Abscess The perforation may lead to an abscess in the wall or outside it. It can cause vague symptoms like anorexia and weakness. It could be detected on pelvic examination which will reveal a tender mass. An untreated abscess can erode into a neighbouring hollow organ, producing a fistula.

Management 1. Hospitalization and rest. 2. Nothing by mouth. 3. Relief of pain. Inj Pentazocine 30 mg or Pethidine 100 mg IM. (Morphine should be avoided as it increases muscle spasm and can precipitate perforation). 4. IV fluids. 5. Antibiotics: Cefuroxime 750 mg IV 8 hourly plus metronidazole 500 mg IV 8 hourly. 6. Abscess can be treated initially by drainage controlled by CT scanning, otherwise surgery.

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Perforated Peptic Ulcer Clinical Features Pain of sudden onset, constant and severe. Pain aggravated by movement, coughing or inspiration. Diminished abdominal movement. Diffuse tenderness. Silent and rigid abdomen. Diminished liver dullness. Rectal examination may show tenderness if generalized peritonitis, but this is not an early sign. X-ray will show in majority raised and immobile right hemidiaphragm with free gas beneath it.

Management 1. Surgery: Patient who is in shock should be operated after hemodynamically stable. If patient is seen within 12 hours of perforation simple closure of a perforated duodenal ulcer is safest, but if ulcer is thought to have been present for more than a year or so, vagotomy with pyloroplasty or even partial gastrectomy. 2. Conservative treatment: If perforation is present for longer period continuous gastric aspiration and IV fluids till stable surgery after hemodynamically stable.

Acute Severe Ulcerative Colitis Clinical Features Patients with severe colitis (more than 6 bloody stools per day with pulse rate > 90/min or Hb < 10.5 g/dL or ESR > 30 mm/h).

Management (a) Admission for intensive treatment. (b) Hydrocortisone 400 mg IV and rectal. (c) IV fluids. (d) Potassium supple­ ments. (e) Thromboembolism prophylaxis. (f ) 5-ASA compounds like mesalamine. (g) Infliximab injection.

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176 A Handbook of Emergencies Toxic dilatation can be treated medically for 12–24 hours, but if there is no improvement in pulse, stool frequency and colonic diameter, urgent colectomy is indicated.

Acute Pancreatitis Causes Common: Gallstones, alcoholic abuse. Others : Trauma (blunt and penetrating), ERCP, obstruction (ampullary stenosis, duodenal diverticulum, neoplasm, parasites); hypercalcemia, hypertriglyceridemia (types I and IV), infection (coxsackievirus, mumps, mycoplasma), ischemia (vasculitis, hypotension); hypothermia, cardiopulmonary bypass, drugs (thiazides, azathioprine, valproate, corticosteroids, tetracyclines, etc.). Miscellaneous (idiopathic, scorpion bite, pregnancy). Autoimmune pancreatitis.

Clinical Features 1. Sudden onset of severe abdominal pain, often radiating to back, with nausea and vomiting. 2. Hypovolemic shock with tachycardia, hypotension, and oliguria. 3. Abdominal findings vary from mild tenderness to generalized peritonism. Abdominal wall staining in the flanks and/or of periumbilical region is pathognomonic of acute pancreatitis. Investigations 1. Routine blood tests. Electrolytes, urea, creatinine, calcium, blood glucose and CBC, arterial gas analysis and routine urinalysis.

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2. Serum amylase/lipase raised 3 times the upper normal range. Urine amylase strips can provide rapid screening. Note: Levels do not reflect disease severity. 3. Imaging. (a) CXR: A pleural effusion should suggest pancreatitis. (b) Plain radiograph of abdomen may reveal gallstones or secondary ileus. (c) Ultrasonography: Looking for gallstones is needed to plan management, and in sick patients, it may be required urgently. 4. CT abdomen: To look for necrotising pancreatitis and in cases where pancreas is not visualised on ultrasound due to excess bowel gas. 5. MRCP: Especially useful as a non-invasive test for stones in common bile duct and conditions such as pancreas divisum. 6. ERCP: Now-a-days used more as a therapeutic procedure than for diagnosis.

Management Mild pancreatitis: It is defined by absence of organ dysfunction or local complications. Treatment is largely supportive. Oral intake can be reintroduced gradually in absence of pain and ileus. Severe pancreatitis: It is defined by the development of organ failure and/or local complications. It requires multidisciplinary management, often involving further radiological investigation and treatment in ICU, and may involve endoscopic or surgical intervention. 1. Initial treatment: Nil by mouth. IV hydration with crystalloids. It is often necessary to infuse colloids when patients are oliguric or hypotensive. Nasogastric tube alleviates vomiting and is often necessary when

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178 A Handbook of Emergencies secondary ileus is present. Oxygen for hypoxia. Analgesia with parenteral opiates, antibiotic IV. Urination in 5 days (10,000 to 20,000 units twice a day) to reduce chance of necrosis. 2. Monitoring: Regular reassessment of pain and tenderness. BP, urine volume, pulse and respiratory rate to be checked hourly, and temperature and blood glucose tests every 4 hours. Further assessment may be undertaken once resuscitation has begun. LFTs in first 24 hours indicate a likely biliary cause (raised transaminases or bilirubin). Within 24 hours abdominal ultrasonography reveals any stones in GB. CT and MRCP as mentioned above. Interventions in acute pancreatitis: 1. Remove the cause: If CBD dilated or presence of CBD stones, ERCP should be performed—sphincterotomy with stone extraction and CBD stenting. 2. Surgery for necrotising pancreatitis. 3. If large pseudocysts develop and fail to resolve in 6–8 weeks intervention may be required.

Acute GI Vascular Disorders Acute mesenteric ischemia (AMI) is usually caused by superior mesenteric artery embolization or thrombosis, non-occlusive mesenteric ischemia or acute mesenteric venous thrombosis.

Clinical Features The AMI presents with acute onset of abdominal pain disproportionate to the physical findings. Central abdominal pain occurs as a result of mild-gut ischemia and spasm, together with emesis and bloody diarrhoea.

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Diagnosis Early recognition is crucial because bowel necrosis develops often by the time surgery is undertaken. CT, MRI and contrast angiography have a major role. CT angiography is sensitive for mesenteric occlusion. Endovascular interventions or catheter-directed vasodilator therapy can be started immediately after angiography.

Management Regardless of the cause, the aim is to ensure good pulsatile flow to SMA, to restore adequate blood flow to the ischemic but viable gut and to resect necrotic bowel. Acute SMA embolism: Surgical revascularization using balloon embolectomy, usually with patch angioplasty of the SMA. Resection of infarcted bowel after revascularization. Acute SMA thrombosis : It occurs in a severely atherosclerotic proximal SMA, and placement of a bypass graft to the SMA distal to the occlusive segment is required. Thrombolytic therapy is considered in those with acute thrombosis and no clinical signs of peritonitis. Non-occlusive mesenteric ischemia: Any metabolic cause is corrected. SMA is selectively catheterized and vasodilating agents such as papaverine are given. Resection of non-viable bowel may be required. Mesenteric vein thrombosis: Fluids, resuscitation and systemic anticoagulation. Thrombolysis in absence of signs of peritonitis. Bowel resection if peritoneal signs and necrotic gut at laparotomy.

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Acute Non-specific Mesenteric Lymphadenitis Common Causes Believed to be due to viral infection.

Clinical Features Common in childhood, rare after puberty. Attacks of abdominal colic worse with movement. A useful sign of differentiating it from acute appendicitis (due to a pull on the mesentery) is complete relief between spasms of pain. Slight fever. Abdominal tenderness along the mesentery. Tenderness may shift leftwards on turning patient to his left side. Other lymph nodes such as cervical, axillary and inguinal may be enlarged. Leucocytosis on first day of attack.

Management 1. 2. 3. 4.

Rest in bed. Fomentation to abdominal wall. Fluids by mouth. Laparoscopy may be required in severe cases and to obtain lymph node biopsy.

Tuberculous Lymphadenitis Usually several lymph nodes are affected and the disease may present acutely.

Clinical Features 1. S i m u l a t i n g a c u t e n o n -s p e c i f i c m e s e n t e r i c lymphadenitis with central abdominal discomfort rather than pain. There is tenderness on deep palpation to right of the umbilicus and inflamed nodes

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may be felt on deep palpation as small, tender nodes. Leucocyte count is normal. 2. Symptoms like those of acute appendicitis. Acute abdominal pain with vomiting combined with tenderness and slight rigidity in right iliac fossa. X-ray abdomen may show calcified lymph nodes.

Management Laparotomy for visualization of lymph nodes and appendicectomy may be necessary. Anti-TB therapy.

Abdominal Distension Common Causes Intestinal obstruction, severe constipation, acute dilatation of stomach, over distended bladder, severe aerophagy, post-operative.

Clinical Features 1. Central distension with visible peristalsis—ileocaecal obstruction. 2. Distension in the flanks with history of bowel symptoms—colonic obstruction. 3. Rapid distension of upper abdomen with profuse vomiting—acute dilatation of stomach. 4. Globular swelling in hypogastrium dull to percussion— distended bladder.

Investigations X-ray abdomen with patient standing upright will show multiple fluid levels in intestinal obstruction. A large gas filled sigmoid colon will be noted in sigmoid volvulus.

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Intestinal Obstruction Mechanical Obstruction Common Causes (a) Neonatal—Imperforate anus, volvulus neonatorum, congenital atresia of small intestine, meconium ileus. Hirschsprung’s disease. (b) Children—Intussusception, Hirschsprung’s disease, strangulated congenital hernia. (c) Young and middle-aged adults—Postoperative adhesions and bands, strangulated hernia, Crohn’s disease. (d) Elderly—Carcinoma or diverticular disease of colon, strangulated external hernia, impacted faeces, postoperative adhesions, and volvulus of sigmoid colon.

CIinical Features Colicky severe pain, abdominal distension, particularly marked in chronic large bowel obstruction and sigmoid volvulus, absolute constipation. Vomiting early in high intestinal obstruction, late or absent in obstruction of large intestine; at first watery eventually faeculent. On examination patient usually dehydrated, toxic and in shock. The abdomen is distended and tender with hyperactive or absent bowel sounds. It is not easy to differentiate between simple and strangulated obstruction, but the latter is suggested by severity of pain, rapid progression of symptoms, fever and pulse rate.

Management Urgent surgical intervention.

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Paralytic Ileus Common Causes (a) Peritonitis. (b) Metabolic—uremia, diabetic coma, hypokalemia. (c) Drugs—Anticholinergic, e.g. probanthine. (d) Following abdominal operation. (e) Reflex, e.g. fracture of spine or pelvis, ureteric colic, retroperitoneal haemorrhage.

Diagnosis Abdominal distension, absolute constipation, vomiting, silent tender abdomen. X-ray shows gas/air fluid levels throughout small and large intestines.

Management Entirely conservative. 1. Nasogastric tube alleviates vomiting and is often necessary when secondary ileus is present. 2. IV fluids and electrolytes, with IV potassium. 3. Inj. pentazocine or buprenorphine to relieve discomfort and nausea.

Emergencies in Diseases of the Biliary Tract Gallstones 1. Gallstone (biliary colic) is a recurrent, right-sided abdominal or central abdominal pain. Pain may last for hours and usually occurs in the early hours of the morning. It can radiate to right shoulder or inferior angle of right scapula and is associated with nausea, vomiting, pallor and sweating. 2. Acute cholecystitis presents with severe abdominal pain with tenderness in right upper quadrant, fever

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184 A Handbook of Emergencies and leucocytosis. Two classical signs are sudden pain on palpation of right upper quadrant during inspiration (Murphy’s sign) and hyperaesthesia at the site of radiation of pain at the back. 3. Gallstone ileus. If the stone is large, it can become impacted in the distal ileum, causing small bowel obstruction. 4. Other complications. Gallstones can migrate into common bile duct, sometimes without arousing pain, predisposing to cholangitis, or acute pancreatitis.

Diagnosis 1. Ultrasound scanning is the best method of detecting symptomatic stones. Thickening of GB wall to more than 3 mm indicates wall inflammation. 2. MRCP is useful in distal CBD stones which may not be visualised well on ultrasound.

Management Biliary colic: Inj. of antispasmodic, e.g. Buscopan 3 mL IV followed by antispasmodic by mouth. If pain is severe Inj. Pentazocine plus Inj. Atropine 0.6 mg IM. Acute cholecystitis: 1. Nothing by mouth for first 24 hours. 2. IV fluids. 3. TPR 2 hourly. 4. Abdominal examination q2h to follow changes in tenderness, rigidity and character of any palpable mass. 5. Gastric aspiration if persistent vomiting. 6. Surgery: Early cholecystectomy because of the high incidence of recurrence during the waiting period. Broad spectrum antibiotics parenterally. Acute acalculous cholecystitis occurs in critically ill patients. A combination of visceral ischemia, starvation and consequent bile stasis and GB distension leads

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to formation of sludge, which predisposes to acute cholecystitis. Fatal perforation is a particular risk. Management: Generally supportive care. Acute suppurative cholangitis is usually due to complete biliary obstruction, with pus under pressure within the ducts. Patient presents with jaundice, rigors and upper abdominal pain (Charcot’s triad). Mental stupor and septicemia supervene in advanced cases. Management: 1. Nothing by mouth. 2. Broad spectrum antibiotics IV. 3. Urgent decompression of biliary system by endoscopic sphincterotomy with removal of stones and stenting or nasobiliary drainage.

Liver Disorders Hepatic Encephalopathy Hepatic encephalopathy is a metabolic encephalopathy that manifests as a complex neuropsychiatric syndrome.

Causes 1. Liver diseases: (a) Fulminant hepatic failure. (b) Chronic liver disease with portosystemic shunt, postsurgical shunt or post-TIPS. (c) Reye’s syndrome. (d) Urea cycle enzyme deficiencies (occasional). 2. Portosystemic shunt without liver disease.

Precipitating Causes 1. GI bleeding 2. Infection (spontaneous bacterial peritonitis, other sites of sepsis) 3. Hypokalemia, metabolic acidosis 4. High protein diet

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186 A Handbook of Emergencies 5. Constipation 6. Sedative drugs 7. Kidney failure 8. Acute liver injury 9. Large volume paracentesis 10. Post-surgical portosystemic shunt or TIPS

Clinical Features 1. Presents with alteration of consciousness (abnormal sleep pattern, drowsiness or coma). 2. Intellectual disturbances and behaviour changes. 3. Asterixis. 4. Fetor hepaticus. 5. Jaundice and stigmata of chronic liver disease.

Grades of Encephalopathy Grade 0 Normal Grade 1 Trivial lack of awareness, euphoria, anxiety Reduced attention span Impaired performance in addition or subtraction Grade 2 Lethargy, apathy, disorientation for time and place Obvious personality disorder Grade 3 Somnolence to semi-stupor, but responsive to stimuli Confusion Gross disorientation Grade 4 Coma Mental state not testable Clinical classification: There are two common types, which differ in progression, severity, pathophysiology and management.

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1. In acute liver failure, the shorter the interval between onset of hepatitis and encephalopathy, the more likely cerebral oedema (major cause of death in fulminant hepatic failure). Encephalopathy can progress from grade 1–2 to grade 4 in hours. 2. Encephalopathy complicating cirrhosis and portosystemic shunt often develops as a result of specific precipitating cause or an acute deterioration of liver function which results in acute, subclinical or chronic encephalopathy, but is almost never complicated by cerebral oedema. Patient usually improves after correction of precipitating cause.

Investigations (a) Laboratory tests include full blood count, urea, creatinine, sodium, potassium, glucose, and liver function tests. Arterial and venous blood ammonia is often elevated but does not correlate well with the degree of encephalopathy. (b) EEG to confirm diagnosis in difficult cases; bilateral synchronus slowing of frequency from alpha to theta (4–7 Hz) or even to delta range (< 4 Hz). (c) Evoked potentials, more specific than psychometric tests but less sensitive. (d) Psychometric tests such as number connection and digital symbol substitution. Asking patient to copy a five-pointed star or clock-face. (e) Investigations to rule out other causes of altered sensorium like intracranial bleed, metabolic or toxic encephalopathy, post-seizure encephalopathy and organic brain syndrome.

Management 1. Detection and correction of precipitant cause correction of hypokalemia. 2. Protein restriction until condition improves, then protein intake gradually increased. Reduction of

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188 A Handbook of Emergencies nitrogen load–Protein 40–60 g/day, or in severe cases 20 g/day, but adequate caloric intake of 2000 kcal/day. Vegetable protein is less ammoniagenic and may allow a larger protein intake, with advantage of greater fibre content. 3. Non-digestible disaccharides lower colon pH, discouraging replication of ammonia-producing bacteria. Drug Dose Disaccharides Lactulose 15–30 mL PO 2–4 times/day, or when patient is comatose or has ileus or the drug cannot be given orally—300 mL enema plus water 700 mL, or 20% lactulose (total 1 L 2 or 3 times/day) or Lactilol 0.3–0.5 g/kg/day p.o. in divided doses 20% lactilol enema (total 1 L) 2 or 3 times/day Sodium 5 g PO bd (increases ammonia benzoate excretion) Ornithine 20 g IV in 5% fructose, 250 mL over aspartate 4 hours od. 4. High bowel washes. 5. Antibiotics: Neomycin 2–4 g/day PO in divided doses for 48 hours Metronidazole 500–800 mg/day PO in divided doses Vancomycin 1000 mg PO bd Norfloxacin 400 mg bd Rifaximin 400–550 mg PO bd Prophylactic use in patients with liver disease to prevent complication, e.g. spontaneous bacterial peritonitis.

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6.

7. 8. 9.

Combined disaccharide and antibiotic: Lactulose and Neomycin. Prevention of GI bleeding: H2-receptor antagonists or protein pump inhibitors to reduce ulcers and erosions in situations of stress (e.g. concurrent illness, surgery) by primary prophylaxis against variceal hemorrhage. IV Mannitol to reduce cerebral oedema. Reduction of portosystemic shunt’s diameter or even its closure. Before closure, eradication of varices by endoscopic methods. Liver transplantation: All patients with encephalopathy should be considered for orthotopic liver trans­ plantation.

Acute Liver Failure The term ALF describes a range of clinical syndromes with the onset of coagulopathy (INR >1.5) and clinical encephalopathy within 22 weeks of jaundice in a patient without pre-existing liver disease. Three subgroups may be recognized: 1. Hyperacute: Jaundice for < 7 days before onset of encephalopathy (e.g. paracetamol poisoning). 2. Acute: Jaundice for 8–28 days before onset. 3. Subacute: Jaundice for 4–12 weeks before onset.

Causes 1. Viral infections: Viral hepatitis. Other viral infections are CMV and herpetic virus. 2. Other infections: Pl. falciparum, leptospirosis, dengue. 3. Drugs and toxins: (a) Predictable—Paracetamol. Amanita phalloides (mushrooms), carbon tetrachloride. (b) Idiosyncratic—Antituberculous drugs (isoniazid, rifampicin), sulphonamides, NSAIDs (diclofenac),

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190 A Handbook of Emergencies ketoconazole, tricyclic anti-depressants, flutamide (used in prostate cancer), anti-epileptics (sodium valproate, carbamazepine, phenytoin). 4. Miscellaneous: Wilson’s disease, pregnancy-related syndromes, hepatic vein thrombosis (Budd-Chiari syndrome), autoimmune disease, malignancy (particularly lymphoma), sepsis and hyperthermia.

Clinical Features 1. Encephalopathy: Ranges from mild drowsiness to complete unresponsiveness. In more rapidly progressive cases, a period of confusion is typical of grade 3 encephalopathy. 2. Other signs of liver dysfunction: Fetor hepaticus is usually absent. Because of rapid onset, patients with hyperacute liver failure may not be overtly jaundiced, and ascites is uncommon except in patients with slower-onset, subacute liver failure. 3. Involvement of other systems: a. Cardiovascular system (CVS): Hypertension (in association with cerebral oedema), hypotension, tachyarrhythmias and bradycardia. There is often a progression from a high-output cardiac state with reduced systemic vascular resistance, to circulatory failure with low cardiac index and arterial pressure. b. Fever may reflect liver necrosis or infection. c. Kidney failure may be an early occurrence following paracetamol overdosage; in other etiological groups it develops at a later stage and in fewer patients. d. Respiratory failure is predominantly caused by infection, fluid overload and ARDS, but aspiration and pulmonary hemorrhage may contribute. e. Coagulopathy usually manifests as bleeding from puncture sites and urinary or GI tracts.

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Investigations A. For cause of liver failure: a. Tests of infection: Blood is screened for acute hepatitis A, E, B and C by testing for anti-HAV and anti HEV IgM, hepatitis B surface antigen and antiHBC IgM and anti-HCV. Anti-HBC IgM response respectively. Some patients with acute liver failure following HBV infection no longer have detectable HBsAg in serum, hence HBV DNA levels are also required to categorise hepatitis-B related cases. (b) Herpes simplex serology. (c) Blood film for Plasmodium falciparum infection. Serology for leptospirosis, malaria and dengue. b. Tests for Wilson’s disease: Serum ceruloplasmin, slit-lamp examination for K-F ring, 24 hours urinary copper estimation. c. Ultrasonography and CT: Ultrasonography of the liver screens for patency of hepatic veins and malignant infiltration, and provides estimate of liver volume. This can be more accurately defined by CT. B. Investigations for monitoring : a. Patients with paracetamol poisoning: Paracetamol is detectable in blood within 24 hours of drug ingestion but is usually undetectable when patients present with established kidney failure. b. Other patients: Prothrombin time, liver profile, blood urea, serum creatinine, electrolytes, complete blood count.

Management The dominant problems in patients with liver failure are neurological, infection and hemodynamic instability.

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192 A Handbook of Emergencies 1. Detection and correction of cause. 2. General measures: a. Nasogastric tube b. Self-retaining bladder catheter c. Central venous line for IV fluids d. Monitor temperature, pulse, BP, ECG, I/O chart. 3. Reduction of ammomia formation in the gut: a. Protein-free diet: Fruit juices, coconut water, vegetable soups, glucose or sucrose solution 20% through nasogastric tube. Example of formula for intragastric drip: Glucose or fructose 100 g Steamed vegetable soup 100 mL Fruit juice 100 mL Common salt 1/2 teaspoon Pot chloride 1/2 teaspoon Water to make 500 mL Give every 6 hours. b. High bowel wash or enema (to which may be added 2–4 g Neomycin) daily. c. Gut sterilization: Metronidazole 400 mg q8h + Neomycin 1 g q6h via nasogastric tube or Rifaximin 400–550 mg q12h. d. Lactulose 15–30 mL tds. Dose adjusted to allow 2–4 semisolid stools per day, or Lactulose enema 200 mL in one litre of tap water q8h or Lactilol 30 g daily as powder. (Less tendency for diarrhoea or flatulence.) 4. Treatment of complications: a. Metabolic abnormalities i. Hyponatremia: Normal saline. ii. Hypocalcemia: Calcium gluconate 10 mL 10% IV.

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iii. Hypokalemia: 80–120 mEq of potassium by infusion daily. iv. Hypoglycemia: 20% dextrose by continuous infusion. v. Metabolic acidosis: Sodabicarb. b. Cerebral oedema: Mannitol 150 mL over 1 hour. IV Can be repeated once or twice daily. In presence of renal failure mannitol should be given only when hemodialysis is in progress. c. Infection: Broad spectrum antibiotics. d. Bleeding: (a) Vitamin K 10 mg IV bd. (b) H 2receptor antagonist or proton-pump inhibitor. (c) Whole blood or packed cell transfusion. (d) Fresh frozen plasma 4–6 packs daily. e. Hypotension: Blood and/or Dopamine 5–25 µg/ min as necessary. f. Subclinical seizures: Mannitol, barbiturates, inotropes, hyperoxygenation. g. Renal failure: Continuous hemofiltration, dialysis. h. Respiratory failure: Early ventilatory support. 5. Liver transplantation: May be required. Auxiliary liver transplantation for a subgroup of patients. who need the immediate benefits of complete transplantation and have the capacity to regain normal function in the native liver. 6. Other techniques: Extracorporeal circuits incorpor­ ating viable hepatocytes are being developed to offer artificial ‘liver support’. These devices will aid recovery by acting as bridges to transplantation, with or without a preliminary hepatectomy which often temporarily stabilizes critically-ill patients. Dr FP Mistry

MD, DNB

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CHAPTER

8

Respiratory Emergencies

Massive Hemoptysis Haemoptysis is coughing out of blood, the site of bleeding being in the tracheobronchial tree or lungs. In some cases, the haemoptysis may be massive (defined as 600–800 mL blood loss in 24 hours) and requires urgent care.

Causes of Massive Hemoptysis zz zz

zz zz zz zz zz zz zz

Pulmonary TB. Trauma (Pulmonary contusion, bronchial or transbronchial biopsy, etc.). Bronchiectasis. Mitral stenosis. Lung abscess. Pulmonary vasculitis, e.g. SLE. Mycetoma, e.g. aspergilloma. Vascular anomalies, e.g. A-V malformation. Idiopathic.

Clinical Features Clinical features are due to: 1. Hypoxia from aspiration of blood into lungs. 2. Hypovolemia from loss of blood.

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Diagnosis Clinical: Patient may be unsure whether the blood has been coughed up or vomited. In haematemesis, blood is coffee ground and mixed with food particles. The pharynx and larynx must also be considered as possible sources. Note: In haemoptysis patient may swallow blood and haematemesis and melena may occur subsequently.

Investigations 1. CXR. Aspiration of blood into the lungs may result in diffuse shadows. However, if lung cavity is detected, it is diagnostic. 2. Bronchoscopy to determine site and possible cause of bleeding. 3. CT scan may detect AV aneurysm, cavitary lung lesion or bronchiectasis.

Management 1. Hospitalization in ICU. 2. Airway. Intubation with a large-sized endotracheal tube may be necessary for suctioning and oxygenation. 3. Posture. If site of bleeding is located, patient must be put in a dependent position to obviate risk of aspiration into normal lung. 4. IV fluids. Colloids or crystalloids. 5. Sedation. Inj. Buprenorphine 0.3 mg IM or slowly IV. Can be repeated q8h. 6. Bronchoscopy and therapeutic procedures to arrest bleeding. Application of adrenaline or topical thrombin solution at bleeding sites. 7. Balloon tamponade for 24–48 hours. If there is no bleeding on deflating the balloon and for 6–8 hours subsequently, balloon can be removed.

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196 A Handbook of Emergencies 8. Arteriography and embolectomy. If bleeding has not been controlled by above procedures, embolectomy is carried out. 9. Surgery. Indications: (a) Severe haemoptysis with site of bleed in lung segment or lobe. (b) If embolization is unsuccessful or cannot be performed. (c) Patient continues to be unstable haemodynamically, but has good pulmonary function.

Acute Severe Asthma Asthma is one of the most common medical emergencies. Individuals at risk of developing severe attacks of asthma. 1. Patients with psychosocial problems and economic deprivation. 2. Patients with previous history of severe attacks. 3. Patients needing oral steroids and/or nebulizer treatment, intermittently or regularly. 4. Patients with increasing symptoms (esp. at night). 5. Patients with progressively declining PEFs. 6. Individuals with increasing exposure to seasonal aero­ allergens or an environment known to trigger attacks. 7. Adolescent and young adults. 8. Patients with asthma on holiday. 9. Inability of patient to gauge severity of attacks.

Assessment of Acute Severe Asthma Features of Uncontrolled Asthma zz zz zz zz

Respiratory rate 25/min. Pulse rate >110/min. Cannot complete sentence in one breath. PEF 15 mm Hg). PaCO2 high and rising.

Life-threatening Features zz zz zz zz zz zz zz zz zz zz zz

PEF 6.7 kPa with accompanying acid-base changes.

Causes 1. Upper airway obstruction. Inhaled FB, tracheal stenosis, acute epiglottitis, trauma. 2. Lung disorders. ARDS, pneumonia, acute severe asthma, acute pulmonary oedema, acute pulmonary embolism, acute fibrosing alveolitis, SARS. 3. Respiratory pump failure. (a) CNS—Overdose of sedative drugs, antidepressives, head injury, brainstem disorders, acute idiopathic polyneuritis, poliomyelitis, encephalitis, tetanus, snake venom, repeated seizures. (b) Muscle—Myasthenia gravis, muscular dystrophy. (c) Chest wall—Trauma.

Clinical Features 1. Due to hypoxemia—Central cyanosis, mental confusion, restlessness, tachycardia, hypertension, arrhythmias, metabolic disturbances. Bradycardia and hypotension if severe hypoxia.

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200 A Handbook of Emergencies 2. Due to hypercapnia. (a) From peripheral vasodilatation – Tachycardia, large volume pulse, flushing, warm extremities. (b) Due to CNS depressant effect— Confusion, behavioural disturbances, reversal of sleep rhythm, increasing drowsiness leading to stupor and coma. (c) Due to high PaO2—Early morning headache, muscle twitchings, seizures, papilloedema. Specific physical signs may be present depending on the cause of respiratory failure.

Investigation 1. Arterial blood gas analysis (pH, PaO2, PaCO2), CBC, PCV, serum electrolytes. pH indicates whether there is a tendency towards acidity (acidosis) or alkalinity (alkalosis). PaCO2 can be easily assessed to see if the change in this could account for the pH change. If it does, respiratory disturbance is present. In the acute setting, every 0.13 kPa increase in PaCO2 is associated with a 0.01 decrease in pH. In acute metabolic disturbances, every 0.5 mmol/L change in bicarbonate is associated with a 0.01 decrease in pH. 2. Central venous pressure and pulmonary wedge pressure measurements.

Management 1. Treatment of underlying cause if possible. 2. Repeated suction for sputum retention (also removal of tenacious secretions from pharynx and nasal cavities) together with physiotherapy to promote cough and in some cases bronchoscopic aspiration. Liquefaction of secretions by adequate hydration with IV fluids. Normal saline can be introduced through tracheostomy tube each time. Endotracheal intubation

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may be required if other methods inadequate to clear airway. 3. High flow O2. There is possibility of pulmonary O2 toxicity if high concentration is required more than 24 hours. 4. Mechanical ventilation. If respiration is feeble or patient is apnoeic. Mask fitted with Ambu or anaesthetic bag fed with 100% oxygen, or if life-threatening hypoxia or hypercapnia are not controlled by above measures. (a) Mechanical ventilation through endotracheal tube or (b) Noninvasive ventilation, a technique of augmenting alveolar ventilation without an endotracheal airway. The big advantage of NIPPV is its simplicity and avoidance of complications of intubation like trauma, tube malposition and aspiration. Selection criteria—(i) Hypercapnic/hypoxaemic respiratory failure unresponsive to conventional treatment. (ii) Normal bulbar function. (iii) Ability to clear bronchial secretions. (iv) Haemodynamic stability. (v) Ability to cooperate with treatment. (vi) Absence of facial trauma or upper airway injury. (vii) Staff well versed with techniques and limitations of NIPPV. 5. Respiratory stimulants. Doxepin 1–3 µg/min IV till maximum dose of 600 mg (contraindicated in presence of high BP, or IHD), or Nikethamide 2–10 mL IV in 10 mL dextrose over 10–15 minutes q2-6h.

Acute Lung Injury and Acute Respiratory Distress Syndrome The acute respiratory distress syndrome (ARDS) is a syndrome of non-cardiogenic pulmonary oedema with acute respiratory failure, secondary to a variety of serious pulmonary and extrapulmonary insults in adults.

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202 A Handbook of Emergencies

Causes Respiratory zz zz zz zz zz zz zz

Aspiration pneumonia. Oxygen toxicity. Acute pulmonary infection. Disseminate TB. Pulmonary vasculitis. Lung contusion. Thoracic irradiation.

Non-respiratory zz zz

zz zz zz zz zz zz zz zz zz zz zz zz

Severe sepsis. Drugs and toxins including organophosphorus poisoning. Major trauma/shock. Massive burns. Hepatic or kidney failure. Amniotic fluid embolism. Cerebral malaria. Tetanus. Acute pancreatitis. Amoebic infection. Multiple transfusions. Salmonella infection. Head injury/raised ICP. Stevens-Johnson syndrome.

Clinical Features Onset: Increasing dyspnoea which may be acute or develop over several hours. Refractory hypoxia, and tachypnoea leading to hypocapnia. Fine inspiratory crackles on auscultation. Often patients are peripherally

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vasodilated in contrast to vasoconstriction in cardiac failure. Course: ARDS tends to reach its maximal initial severity 24–48 hours after presentation and may be rapidly fatal if untreated. Acute deterioration of a stabilised or improving patient may result from nosocomial pneumonia, pneumothorax, or systemic complications such as septicemia, kidney or liver cell dysfunction.

Investigations 1. CXR. Diffuse, nonspecific alveolar shadowing, often with air bronchograms. 2. Arterial blood gases. Initially varying degrees of hypoxia with hypocapnia, later hypercapnia. 3. Measurement of pulmonary artery pressure. 4. CT scan for fluid-collection or occult pneumothorax. 5. Others. Renal and hepatic function tests and haematological studies.

Management The severity of acute lung injury (ALI) depends on the nature, intensity and duration of the insult to the lungs. 1. Treatment of underlying clinical condition, e.g. antibiotics for sepsis. 2. Intubation and ventilation—Indications include severe respiratory failure [e.g. mask FiO2 >0.6 required to achieve PaO2 (10 kPa)], fatigue [(rising PaCO2 or tachypnoea (>30 breaths/minute)] or evidence of circulatory inadequacy (e.g. lactic acidosis, poor tissue perfusion, hypotension). The purpose of respiratory support is to achieve adequate arterial oxygenation without exacerbating lung injury. The usual aims are low respiratory rate (10–14/min), low tidal volume

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204 A Handbook of Emergencies (6–8 mL/kg), relatively high positive end-expiratory pressure (5–20 cm H2O) titrated to lung compliance to maintain alveolar recruitment, and when possible, limitation of FiO2, to avoid oxygen toxicity. 3. Additional therapies: (a) Prone positioning is most effective in early exudative phase of lung injury, when it allows recruitment of the oedematous but relatively better perfused dorsal lung segments, improving ventilation/ perfusion matching. Periods of 8–12 hours prone may be required. (b) Corticosteroids—may be beneficial early in ARDS caused by inflammation (e.g. acute pancreatitis) rather than sepsis, and may improve outcome in persistent ARDS. (c) Reduction of lung water—Keeping the patient ‘dry’ is reasonable in well-resuscitated patients with adequate circulation, but is inappropriate in septic patients with evidence of poor tissue perfusion, in whom inadequate volume replacement increases risk of multi-organ dysfunction. 4. Prevention of complications: (a) Multiorgan failure: The most common reasons for this are failure to treat the initiating insult and failure to re-establish adequate circulation may involve large volumes of colloid or crystalloid, and combination of inotropes, vasopressors or vasodilators. It should be noted that the oedema in ARDS is an exudate rather than a transudate, and mortality is related more to multiorgan dysfunction than to hypoxia. (b) Nosocomial infections include ventilator-associated pneumonia and those from indwelling lines and catheters. The incidence can be reduced by strict hand-washing policy, aseptic line and catheter replacement. Cultures should be taken if infection is suspected (new pyrexia,

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rising WBC, deteriorating gas exchange or new shadows on chest radiography). (c) Pneumothorax—is particularly likely when excessive pressure or tidal volume is used. Suggestive signs include subcutaneous emphysema, decreasing PaO 2, increasing central venous pressure with decreasing arterial pressure. Supine chest radiographs may show a ‘deep sulcus’ sign, pneumopericardium or relative hyperlucency of one hemithorax. If pneumothorax is loculated, CT may be required for diagnosis, localization and accurate drainage. Needle thoracostomy should be avoided unless the situation is urgent, and should be followed rapidly by chest drainage. 5. Supportive measures: Feeding: Small hourly volumes of enteral feeding supplemented by parenteral nutrition. Those who cannot tolerate feeds should – be given H2 . antagonists or sucralfate as prophylaxis against stress ulcers.

Acute Exacerbation of COPD Respiratory crisis in patients with COPD presents itself as acute respiratory failure.

Precipitating Factors zz

Infectious process

–– Viral: Influenza. –– Bacteria: (Strep. pneumoniae, H. influenzae, zz

Moraxella catarrhalis, Pseudomonas spp.). Environmental conditions –– Sudden change in temperature and humidity, tobacco smoke, noxious gases or irritating chemicals.

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Host factors

–– Patients with poor general health, poor nutritional status, immunocompromised status, noncompliance with medical therapy.

Investigation for Patient Referred to Hospital 1. Chest radiograph 2. Measurement of arterial blood gas tensions 3. ECG to exclude cardiac comorbidities. Group Group A Mild exacerbations no risk factor for poor outcome

Oral treatment Patient with only one cardinal symptom need not receive antibiotics If indication then Ampicillin/Amoxicillin Doxycycline Trimethoprim/ Sulfamethoxazole

Group II Moderate exacerbation Co-amoxiclav with risk factors for poor outcome

Alternative oral transfer to parenteral treatment Co-amoxiclav Co-amoxiclav Macrolides Ampicillin/ Cephalospor- sulbactam ins (2nd or 3rd Cephalosporgeneration) ins (2nd or Telithromycin 3rd generation) Fluoroquinolones (levofloxacin/ ciprofloxacin) (high dose) β-lactam with P. aeruginosa activity

An IV combination of Co-amoxiclav together with Clarithromycin may be preferred over Fluoroquinolones or their combinations considering the tuberculosis endemicity in India.

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Indications for Hospitalization 1. Comorbid conditions: Coronary heart disease, DM, kidney and liver failure. 2. Severe breathlessness. 3. Cyanosis. 4. Worsening peripheral oedema. 5. Impaired level of consciousness. 6. Rapid rate of onset. 7. SaO2 35 breaths/min. Impaired mental status.

Pneumonia Pneumonia is caused by accumulation of secretions and inflammatory cells in alveolar spaces of the lungs. Classification according to the probable origin of infection is: 1. Community acquired. 2. Nosocomial (hospital acquired). 3. Aspiration. 4. Pneumonia in immunocompromised patient.

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Community-acquired Pneumonia Etiology of community-acquired pneumonia (CAP) in adults is predominantly caused by Streptococcus pneumoniae. Others are H. influenzae, Mycoplasma pneumoniae, and influenza viruses.

Clinical Features Abrupt onset with fever, rigors, cough, tachypnoea, prostration and perhaps pleuritic chest pain. Signs of lung consolidation. Manifestations of cerebral dysfunction such as confusion, incontinence, falls are not uncommon in the elderly.

Features of Severe Pneumonia 1. Clinical: Mental confusion. Resp. rate >30 breaths/ min. Diastolic BP 7 mmol/L. Serum albumin < 35 g/L. PaO2 < 8 kPa on air or oxygen. WBC < 4 × 109/L or 20 × 109/L. Bacteremia by blood culture. 3. CXR. Multilobar involvement.

Investigation 1. CXR. 2. WBC count. 3. Others: LFTs, urea, electrolytes and oximetry/arterial blood gases. 4. Microbiological— Sputum, blood culture, antibodies against viruses, pleural fluid culture (when present) to identify causal organism.

Management 1. Hospitalization. 2. Antibiotics. Third generation cephalosporins, e.g. Cefuroxime 750 mg TDS. plus macrolide such as

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Clarithromycin 500 mg BD IV. If Staphylococcal infection Cloxacillin 1 g IV q4h. 3. Fluid and electrolyte balance. 4. Dopamine or Dobutamine if hypotension. 5. Ventilatory support if PaO2 50 mm Hg, respiratory rate >40/min, or evidence of circulatory failure.

Massive Pulmonary Collapse Diffuse lobar collapse or massive atelectasis constitutes an emergency. Central obstructive atelectasis: The site of obstruction is the main bronchus. Absence of breath sounds is a useful indication. Chest X-ray shows ‘loss of open bronchus in addition to atelectasis sign’, i.e. the bronchus of the affected lobe or lung is not visualised. The cause may be mucus plug, foreign body, misplaced endotracheal tube. Peripheral obstructive atelectasis: (atelectasis with a patent bronchus). Most common causes are pneumonias, postoperative particularly following thoracic or upper abdominal surgery, atelectasis in critically ill patients or patients with asthma or pulmonary eosinophilic syndromes. The breath sounds and voice sounds will be conducted to the chest wall by the airless atelectatic lung. Chest X-ray: Evidence of atelectases with ‘loss of open bronchus sign’.

Management Depends on the cause—most cases in the postoperative period and in the critically ill patient due to mucus plugging recover rapidly spontaneously or with physiotherapy

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212 A Handbook of Emergencies measures like postural drainage, chest wall percussion and a forced expiration technique (huffing). Nebulised DNase may help in some cases. Major impaction of major bronchus requires therapeutic endoscopy if above measures fail. It is also indicated if a foreign body is the cause of obstruction.

Spontaneous Pneumothorax Pneumothoraces are classified as non-traumatic (spontaneous) and traumatic. Spontaneous pneumothoraces are further divided into primary (in individuals with no known history of lung disease, e.g. rupture of subpleural bleb) or bulla and secondary in patients with history of lung disease such as pulmonary TB or COPD. Tension pneumothorax develops when disruption involves visceral pleura, parietal pleura, or tracheo­ bronchial tree. A one way valve forms allowing air inflow into pleural space and stopping air outflow. As a result pressure rises within the affected hemithorax and ipsilateral lung collapses, causing hypoxia, mediastinal shift leading to further hypoxia and compromised venous return. If untreated, the hypoxia, metabolic acidosis and decreased cardiac output can result in death. Traumatic pneumothorax occurs due to penetrating trauma (stab wound, gunshot wounds) primarily injuring peripheral lung, causing both hemothorax and pneumothorax. Blunt trauma can lead to rib fracture, resulting in raised intrathoracic pressure and bronchial rupture. Pulmonary barotrauma can occur at an altitude of 3050 m, as seen in air crew personnel, in scuba divers barotrauma can occur during ascent as gas contained in the lung expands and causes pneumothorax.

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Investigation (a) Chest X-ray: Air in pleural cavity with contralateral deviation of mediastinal structures. (b) Chest CT scan is more sensitive and is ideal or detecting occult traumatic pneumothorax. (c) Ultrasonography: Diagnostic features include absence of lung sliding (high sensitivity and specificity).

Management (a) First aid: Upright posturing may be beneficial. (b) Penetrating wounds require immediate coverage with an exclusive or pressure bandage made air tight with clean plastic sheeting. (c) O2 at high concentration. (d) Simple aspiration: A thin needle is used to relieve the pressure and allow the lung to reinflate in suspected tension pneumothorax, this is done by a plastic IV cannula. An initial antibiotic is necessary. (e) Tube thoracostomy if simple aspiration is ineffective. If the lung is re-expanded rapidly, there is risk of pulmonary oedema, hence it is better to use water seal and to avoid suction for first 24 h. A pre-packed disposable plastic tube with the long central metal trocar (18–24 Gauge) is used. Correct placement of the tube is seen as a stream of bubbles during expiration and coughing and the rise in the level of fluid level in the under water seal during inspiration. (f ) Thoracoscopy or thoracotomy should be considered if the lung remains unexpanded or there is persistent air leak 72 hours after performing tube thoracostomy.

Massive Pleural Effusion Causes 1. Tuberculosis. 2. Acute idiopathic.

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214 A Handbook of Emergencies 3. Extension of inflammation from lungs, e.g. pneumonia, abscess. 4. Neoplasms: Metastatic Ca, bronchogenic Ca, lymphoma. 5. Intra-abdominal causes. Abdominal surgery, acute pancreatitis.

Symptoms Dyspnoea depending on rate of collection of fluid. Dry cough. Symptoms of toxemia such as fever, malaise.

Signs Orthopnoea or preference to lie on sound side, fullness of hypochondrium, mediastinal shift, dull note, absent breath sounds, no foreign sounds.

Management Fluid aspiration—Position patient in sitting position with arms placed over a rest. The approach is from the posterior aspect halfway between the medial border of scapula and spine. After skin preparation, infiltrate local anaesthetic into lower part of intercostal space chosen. Insert a 3-way tap with a length of tubing to allow drainage of fluid into a receiver. Precautions. Do not aspirate more than 1500 mL of fluid at a time. Discontinue aspiration if patient complains of faintness, excessive cough or increasing dyspnoea, or no further fluid can be obtained. Pleural biopsy should be performed before aspiration.

Acute Laryngeal Obstruction Acute laryngeal obstruction is a life-threatening emergency.

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Causes 1. Traumatic injury of larynx. 2. Laryngotracheobronchitis, acute epiglottitis. 3. Angioedema. 4. New growths. 5. Diphtheria (rare).

Clinical Features With partial obstruction, there is stridor, cyanosis and a hoarse voice. With complete obstruction there is inability to speak or breathe, pallor followed by increasing cyanosis and loss of consciousness and collapse. Usually a partial obstruction is not life-threatening. Sometimes however hypoxia resulting from inadequate ventilation can be fatal, especially in older patients or in those with heart disease.

Management 1. Establish airway: Give oxygen. If intubation is difficult an emergency tracheostomy may be necessary to maintain airway. It may be usefully preceded by thrusting one or more l6 G needles through the cricothyroid membrane, as even this narrow passage will allow some gas exchange. Put patient on his back with the neck extended. Ask an assistant to hold the arms. Grasping the thyroid cartilage with thumb and middle finger, use the index finger to palpate the gap. Make a horizontal skin incision with a knife or scalpel, or with a blade over the gap at the tip of the index finger, and then with stabbing movement push the scalpel blade through the larynx. Reverse the scalpel and push the handle into the larynx. Rotate the handle through 90º to enlarge the opening. Insert immediately a tube (if not available even a hollow tube such as a ballpoint pen), and attach it to an Ambu bag. 2. If angioedema : Injection methylprednisolone 100 mg IV or Inj. adrenaline 0.5 mL of 1:1000.

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216 A Handbook of Emergencies 3. For choking: Foreign body obstruction of airway usually occurs while the victim is eating (Cafe coronary). The victim gives the choking sign by bringing his hand to his throat with the thumb and index finger spread widely to form a V, or he will clutch his throat with his hand. There may be cough, dyspnoea and wheeze.

Heimlich Maneuver for Choking Victim standing or sitting: The rescuer positions himself behind the victim and encircles his waist with his arms. With one hand he makes a fist and then places the knob against the victim’s abdomen, slightly above the navel, and well below the tip of the xiphoid process. The rescuer then grasps the fist with his free hand and presses into the abdomen with a quick upward thrust (the action consisting of a sharp flexion movement at the elbows). It may be necessary to repeat the thrust as many as 6 times to clear the airway, indicated by resumption of breathing, return of normal colour and restoration of consciousness. In case the bolus is not expelled from the mouth and remains in the oropharynx, it must be manually removed, care being taken not to drive it back into the throat. Victim supine: If victim is lying face down, he should be rolled onto his back. Facing the victim, the rescuer kneels astride the victim’s hips and positions his hands one on top of the other with the heel of the bottom hand on victim’s abdomen slightly above the navel. He presses into the abdomen with a quick upward thrust; several thrusts may be necessary. The same procedure can be used with a conscious victim if the rescuer is small or weak. While kneeling astride the supine victim, he can use his own body weight to achieve sufficient force for the thrust. Note: The position of the victim’s head should be facing up and in the midline as much as possible.

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9

Cardiovascular Emergencies

Cardiac Arrest Cardiac arrest is sudden failure of the heart such that an adequate cerebral circulation cannot be maintained.

Causes 1. Coronary artery disease with or without myocardial infarction. 2. Cardiac arrhythmias. 3. Pulmonary embolism. 4. Surgical arrest: During intratracheal intubation, manipulation of the heart, air and fat embolism, abrupt fall of BP. 5. Diagnostic procedures, e.g. bronchoscopy, cardiac catheterization, pyelography. 6. Drugs. Due to overdosage or hypersensitivity—Digitalis, quinidine, adrenaline, potassium salts, saccharated iron oxide, local anaesthetics and rarely antibiotics. 7. Drowning. 8. Electric shock. 9. Anaphylaxis.

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Diagnosis Two signs required are—(a) Loss of consciousness. (b) No palpable pulse in carotid or femoral. Other late signs are—(a) Cessation of respiration. (b) Dilatation of pupils. (c) Unrecordable BP. (d) A fit, with or without incontinence. (e) Failure to bleed if arrest during surgery.

Management of Cardiac Arrest Simple manoeuvres worth trying to start with are— 1. Elevation of the legs for 30 seconds. 2. Forceful thumping of the chest. If these are not immediately effective, no further time should be wasted before applying cardiopulmonary resuscitation. Basic CPR: Airway is cleared Breathing is made effective Circulation is restored I. Airway maintenance 1. If patient is breathing, airway patency can often be obtained by simple methods—Put patient in supine position on a firm surface such as a wooden board or on the floor. (i) Jaw lift. Placing the fingers bilaterally behind mandibular angles, displace the mandible forward and anteriorly. Clear the pharynx with a finger covered with gauze piece. (ii) Give oxygen. (iii) Do endotracheal intubation unless contraindicated (injury to cervical spine, mechanical upper airway obstruction, severe restriction of cervical mobility or inability to open the mouth). In such a case do nasotracheal intubation.

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2. Pat i e nt n ot b re at h i ng : Mou t h - to - m ou t h respiration. Use fingers of left hand to hold the chin forwards while extending the neck slightly with the right hand. By placing the edge of your hand on the forehead it is possible to maintain the extended position, at the same time pinching the nose tight. Now place your lips firmly over the mouth (a handkerchief or gauze pad can be put over patient’s mouth) and having taken a large breath, exhale. Look for the chest rising as you exhale. Now release your seal and wait for passive exhalation, again checking if the chest is moving. Repeat the procedure once exhalation is complete; this usually means 12 to 15 breaths per minute. Oronasal resuscitation: The nose can be used as airway particularly when one cannot get the airtight seal over the mouth or if the mouth contains blood or vomit. Use the left hand to hold the chin forwards and upwards and keep the mouth shut. If this is not possible, use a pad over the mouth to seal it. Place your mouth over the entire nose and exhale. Then follow the same procedure as in mouth-to-mouth resuscitation. II. Circulation 1. External cardiac massage: Having established an airway and after 2–3 breaths, check the pulse. If it is absent, start external cardiac massage. Place the heel of the hands one over the other on the lower end of sternum and compress the sternum about 3–4 cm at a rate of 60/min. Femorals and carotids should be palpable with effective cardiac massage.

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If a suitable face mask is available keep the same over the patient’s mouth and nose snugly, push the lower jaw forwards and upwards with the thumb and index finger and blow the Ambu bag which is connected with the face mask. Oxygen should be connected with the Ambu bag.

2. Determination of heart action by ECG

Note: Delivering a shock will do no harm if heart is in asystole or there is electromechanical dissociation.

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Note: Recovery from asystole is rare. It is futile to continue resuscitation for more than 15 minutes.

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Acute Coronary Syndrome ACS comprises 1. Unstable angina 2. Non-ST elevation ACS (NSTEMI) 3. ST elevation MI (STEMI).

Unstable Angina/NSTEMI Unstable angina/NSTEMI suggests a seriously compromised coronary circulation with a potential risk for acute myocardial infarction. Cardiac arrhythmias or even sudden death.

Diagnostic Criteria zz zz zz

zz

Prolonged (>20 min) anginal pain at rest. New onset (de novo) severe angina. Recent destabilization of previously stable angina (crescendo angina). Post-MI angina.

Aggravating or precipitating factors 1. Increased myocardial oxygen demand, e.g. fever, tachycardia, hypoglycemia, hyperthyroidism. 2. Exacerbation of lung conditions such as asthma, COPD. 3. Fluid loss with hypovolemia. 4. Anemia. 5. Acute tension or anxiety. Clinical presentation is retrosternal pressure or heaviness radiating to left arm, neck or jaw which may be intermittent (usually lasting several minutes) or persistent. Atypical symptoms include epigastric pain, recent onset indigestion, stabbing chest pain, chest pain with pleuritic

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symptoms or increasing dyspnoea. Atypical symptoms are often observed in younger or older patients, in women, and in patients with diabetes. Electrocardiogram may show ST segment deviation. T wave changes or may remain normal. ST depression of >2 mm carries an increased mortality risk. Inverted T waves especially of ≥ 2 mm (0.2 mv) also indicates UA/NSTEMI. Biochemical markers. Cardiac troponin (CTn) is the biomarker of choice. Troponin levels usually increase after 3–4 hours. If the first blood sample for CTn is not elevated a second sample should be obtained after 6–9 hours and sometimes after 12 to 24 hours if required. Echocardiography to assess global LV function and any regional wall motion abnormality. It also helps in excluding other causes of chest pain.

Management Patients who are awaiting hospitalization are advised to chew non-enteric coated aspirin (162–325 mg) or use sublingual nitrate for pain relief. Patients who are stable should be admitted to an inpatient unit for bed rest with continuous rhythm monitoring and observation for recurrent ischemias. High risk patients including those with continuing discomfort and/or hemodynamic instability, should be admitted in CCU and observed for at least 24 to 48 hours. Thrombolytic therapy should not be used in patients with UA and NSTEMI, they can prove harmful.

Anti-ischemic and Analgesic Therapy Nitrites—Topical, oral or IV nitrates for pain relief. IV nitroglycerin is particularly helpful in those who are

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224 A Handbook of Emergencies unresponsive to sublingual NTG, in hypertension and in those with heart failure. Nitrates should be used with caution if systolic BP 48 hours anticoagulation for 3 weeks before and 4 weeks after. 3. Bradyarrhythmias: (a) Isolated sinus bradycardia if associated with hypotension, IV atropine. (b) Heart block- (i) 1st degree - β-blockers and calcium antagonists (not nifedipine) prolong AV conduction and discontinuation of these increases ischemic injury. Atropine can be given. May progress to higher degrees of block. (ii) 2nd degree AV block- Type I - Atropine if patient becomes symptomatic, ventricular rate falls below 50 bpm, PVC and BBB or heart failure develops. Type II – Temporary external or transvenous pacemaker. (c) Complete heart block – Pacing is usually not necessary unless the ventricular rate is 4 weeks have elapsed since AMI, NSAIDs and steroids for severe symptoms. E. Embolic complications: Most often occur in first 10 days. Tr. - IV heparin for 3 or 4 days to elevate PTT to 1.5 to 2 times that of control followed by oral anticoagulants for 3 to 6 months.

Cardiac Arrhythmias Tachyarrhythmias Tachycardia is a common problem which usually presents with palpitations, though syncope, presyncope, dyspnoea and chest pain may also be presenting features.

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230 A Handbook of Emergencies Tachycardias emanate from all parts of the heart and the most common are supraventricular tachyarrhythmias such as atrial fibrillation and junctional tachycardia. Ventricular tachycardia also occurs commonly. Diagnosis of tachycardias is based on ECG. I. Narrow QRS complex (QRS < 0.12 sec) tachyarrhythmias A. Regular rhythm 1. Sinus tachycardia. Normal P waves. Pulse rate 100–200/min can reduce cardiac output in presence of myocardial dysfunction such as MI. Management: Propranolol in doses of 10 mg TDS can slow the heart rate and thus reduce myocardial O2 demand. 2. Junctional tachycardia (JT) a. Paroxysmal Supraventricular Tachycardia (PSVT due to AV nodal re-entry). A benign disorder usually and the most common form of PSVT. ECG: P waves buried within QRS or appear immediately after. Management: Vagal manoeuvres such as carotid sinus massage, first on right for 3–5 seconds at a time. Valsalva manoeuvre, induction of gagging by placing a finger in the oropharynx. Drugs – Adenosine 6 mg as initial rapid IV bolus. If ineffective within 2 mins, further 12 mg bolus which may be repeated once, or Verapamil 5 mg slowly IV. Can be repeated q5m until conversion or total dose of 20 mg, or Digoxin 0.5 mg. over 10 min IV followed by 0.25 mg q4h to maximum of 1.5 mg in 24 hours. b. PSVT in WPW syndrome (AV re-entry). ECG: P waves seen in ST segment. Management: Quinidine or Profcainamide. Digitalis,

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Verapamil or b-blockers should not be used. DC cardioversion may be necessary. c. Multifocal atrial tachycardia: Varying shape of P waves and varying PR intervals. Management: Treatment of precipitating factor, e.g. COPD, electrolyte im­balance, metabolic abnormalities, thyrotoxicosis. d. Nonparoxysmal junctional tachycardia usually due to digitalis toxicity, can occur after MI, or open heart surgery, or in severe lung disease. Management: Treatment of underlying disease. Often spontaneous conversion to sinus rhythm. 3. Atrial flutter: More often associated with heart disease than atrial fibrillation – IHD, hypertensive heart disease, cardiomyopathy, hypoxia, etc. ECG – Saw tooth P waves. Management: (a) If hemodynamically unstable (low BP, restlessness, shock) – DC shock 25–50 J or atrial pacing at frequency higher than atrial flutter rate. (b) In presence of LV dysfunction – (i) If HD stable – Pulse rate> 140/min and LV dysfunction – Digoxin IV. 0.25–0.5 mg, repeated after 2–4 hrs. Total dose in 24 hrs 1–1.75 mg. (ii) No LV dysfunction, pulse rate > 140. Verapamil IV 0.075–0.15 mg/kg over 2–3 mins. Can be repeated if required after 30 mins. Heart rate will be lowered even if sinus rhythm is not restored. If hypotension due to Verapamil give IV calcium. B. Irregular rhythm 1. Atrial fibrillation: Causes—IHD, hypertensive heart disease, hyperthyroidism, hypoxia due to lung disease. ECG – Presence of fibrillatory waves.

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232 A Handbook of Emergencies Management: (a) Paroxysmal AF – If no associated heart disease, sedatives and if necessary digitalis. If patient’s HD stable Flecainide 300 mg OR Propafenone 600 mg orally. (b) Sustained AF: Emergency termination. Conversion to sinus rhythm if most of the following criteria are met – AF has been present for less than one year, LA size (echo) is 0.12 sec) 1. Ventricular tachycardia (VT): A series of three or more consecutive ventricular premature beats at rate 100 or more beats/min.

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Cs. MI commonest cause. Others are aortic valve disease, cardiomyopathies, following coronary bypass surgery.

Management I. Non-sustained VT: Correction of potentially reversible factors such as IHD, hypoxia, electrolyte imbalance (hypokalemia, hypomagnesemia), acidosis, digitalis toxicity, hyperthyroidism. II. Sustained VT a. Patient HD unstable. Immediate DC cardioversion with 150 J, followed by 150 J and if still no reversion 250 J, followed by lidocaine infusion 2–4 mg/min for 24–48 h. b. Patient’s HD stable. Lidocaine 1 mg/kg IV. Repeat after 10 mins. if not reverted to sinus rhythm. After reversal prophylactic drip of Lidocaine 2–4 mg/ min. If this fails Amiodarone infusion. c. If failure of DC shock and drugs: QT interval normal – IV Procainamide, or IV Amiodarone. QT prolonged – Amiodarone 300 mg IV bolus followed by IV infusion. d. Repeated recurrences after DC shock and no response to drugs – Catheter and surgical ablation is possible for some patient with stable monomorphic VT and the implantable cardioverter defibrillator (ICD) is favoured in patient with poor LV function or drug refractory VT, especially when associated with previous cardiac arrest, and for those patients where there is no good method of forecasting the success of drug therapy. 1. Polymorphic VT and Torsade de pointes is a form of VT characterised by a twisting pointed appearance

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234 A Handbook of Emergencies on ECG. It is often caused by anti-arrhythmic drugs such as Quinidine or Procainamide, or tricyclic antidepressants, or other conditions which prolonged QT interval like IHD, myocarditis, organophosphorus poisoning. Management: (a) Stop all drugs. (b) Correct hypokalemia or hypomagnesemia. Magnesium sulphate 2 g IV followed by infusion of 3–20 mg/min. If arrhythmia recurs or there is bradycardia (relative) temporary atrial or ventricular pacing at about 100 beats/min. 2. Ventricular ectopics are common after MI, and may increase in frequency just before VT or VF. Frequent ectopics may often indicate hypokalemia. Treatment: should be started if PVCs are multiform or of the R on T variety. Lidocaine is drug of choice for suppressing the arrhythmia. Bolus of 50-75 mg i.v. followed by maintenance of 2 mg/ min. PVCs not due to IHD can be suppressed by treatment of causative conditions such as hypocalcemia, hypomagnesemia, hypoxia, digitalis toxicity, or metabolic disturbance, e.g. respiratory alkalosis.

Bradyarrhythmias Bradycardia is defined as a heart rate below 60 beats/min. A rate below 50/min should be regarded as abnormal. The most common pathological forms are sinoatrial (SA) dysfunction where the generation of cardiac impulse in sinus node is slow or fails to reach the atrial muscle or atrioventricular (AV) block, where conduction of the depolarising wave through the AV node and/or throughout the ventricle is faulty. Both SA dysfunction and AV block predispose to episodes of ventricular arrest leading to Adams-Stokes attacks, and are a relatively uncommon cause of blackouts.

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Sino-atrial Dysfunction 1. Sinus bradycardia needs attention when it is due to IHD (common after inferior infarction) or sick sinus syndrome since it can cause lowering of cardiac output resulting in syncope and potentiate VPCs occurring as a result of use of antiarrhythmic drugs to suppress them. 2. S-A block: Acute SA dysfunction is most commonly associated with early stages of MI and disappears within 24–48 hrs. S-A block can occur in patients with hyperkalemia and sinus node function may be disturbed temporarily after DC shock, particularly in patients on digitalis. Management: (a) Stop drugs which can slow heart rate. (b) Increase heart rate with Atropine 0.3–1 mg slowly IV or in an emergency with Isoprenaline 1 mg in 500 mL dextrose IV infusion 1–4 mg/min to start with, then gradually increased till desired heart rate. (c) Transvenous pacing if drugs fail. (d) If hyperkalemia calcium gluconate 10–20 mL 10%, followed by infusion of insulin in dextrose. 3. Sick sinus syndrome (Bradycardia-tachycardia syndrome) presents special problems because antiarrhythmic drugs which suppress tachycardia tend to worsen bradycardia. An artificial pacemaker protects the patient against dangerously slower cardiac rhythms and the increase in basic heart rate may reduce the incidence of tachycardia. Some pts however require a combination of pacemaker and anti-arrhythmic drugs. 4. Atrioventricular block. Acute heart block occurs in initial phases of MI in about 10% of patients Inferior infarction usually involves the AV node and anterior

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septal infarction is associated with a ‘low’ block (one below the bifurcation of bundle of His). Block associated with inferior infarction is transient and may be reversed by atropine 0.5–1.2 mg IV. Infections may cause transitory conduction disturbances, e.g. viral myocarditis, infective endocarditis, diphtheria and rheumatic fever. Symptoms: Effort syncope, breathlessness, occasional angina. Cardiac failure may occur if ventricular rate is very slow. Management: (a) First degree block does not require treatment and if due to any drug, the same can be stopped. (b) 2nd degree block – Mobitz type II block is often forerunner of high grade or complete heart block. Causes – MI, acute myocarditis, drugs like Digitalis, Quinidine, Procainamide. Temporary transvenous pacing must be done. (c) Complete heart block and intraventricular block are common in acute MI, rarely due to myocarditis or hyperkalemia. Urgent transvenous pacing is necessary. Pacing also in bilateral bundle branch block and trifascicular block. IV Isoprenaline 1 mg in 500 mL 5% Dextrose at 1–4 µg/ min, can be tried.

Acute Left Ventricular Failure with Pulmonary Edema Common causes: 1. Systemic hypertension. 2. Ischemic heart disease. 3. Aortic valve disease. 4. MR or MS. 5. Cardiomyopathy. Precipitating factors in LV dysfunction – (a) Severe illness. (b) Fluid overload. (c) Severe sepsis.

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Clinical features: Breathlessness, often orthopnoea. Tachycardia, diastolic gallop. Crackles at lung bases initially, then all over the chest with expectoration of pinkish froth. Investigation: 1. CXR: Bat’s wing appearance of pulmonary oedema. 2. ECG. Evidence of IHD or LV hypertrophy.

Hypertensive Crises Hypertensive crisis usually presents as an acute lifethreatening condition with extreme increases in BP, that requires prompt management strategies. 1. Hypertensive emergencies (malignant hypertension) are characterized by severe elevation in BP (>180/120 mm Hg) complicated by evidence of impending progressive target organ dysfunction. They require immediate BP reduction over a period of 6 to 8 hrs often with parenteral drugs with constant monitoring to prevent or limit target organ damage like hypertensive encephalopathy, intracerebral hemorrhage, acute MI, acute LVF with pulmonary oedema, unstable angina, aortic dissection or eclampsia. Treatment a. IV nitroglycerine though not very effective, it is useful in patients with ischemic heart disease and LVF. Dose: Initial 5 mg/min then titrate by 5 mg/min at 3–5 minute time intervals, up to 100 mg/min. b. IV Enalapril especially useful in presence of heart failure. Dose: 0.625–1.2 mg bolus q6h. c. IV Labetalol– Dose: 2–10 mg and infusion of 2.5–30 mg/kg/min. d. IV Esmolol especially useful for perioperative accelerated hypertension. Dose: 80–500 mg/kg

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238 A Handbook of Emergencies bolus over one minute followed by infusion of 50–300 mg/kg/min. e. IV Nitroprusside is required rarely in situations like aortic dissection or subarachnoid hemorrhage with very high BP. Dose: 0.3 mg/kg/min to maximum of 10 mg/kg/min. 2. Hypertensive urgencies (Accelerated hypotension) are situations associated with severe elevation in BP without progressive target organ dysfunction. Patients complain of severe headache, shortness of breath, epistaxis or severe anxiety. Majority of them are noncompliant or inadequately treated hypertensives, often with little or no evidence of target organ dysfunction. Treatment – The aim is safe, prompt and gradual lowering of BP with oral medication over a period of 3–4 days with Calcium channel blockers and ACEI/ARB. Note: Sublingual nifedipine should not be used as it can cause precipitous fall in BP, reflex tachycardia and may precipitate renal, cerebral or coronary ischemia.

Acute Massive Pulmonary Embolism Pulmonary embolism is commonly a sequel of deep vein thrombosis. Predisposing factors for DVT are either in the legs, thighs or pelvis. Predisposing factors: Immobility, hip/knee replacement, abdominal/pelvic surgery, lower limb fracture, malignancy, long distance air travel and oral contraceptives. Clinical features: PE should be considered in presence of unexplained dyspnoea, chest pain, tachypnoea, hemoptysis and syncope in patient with one or more risk factors.

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Diagnosis Procedures for a definite diagnosis are – 1. Multidetector computed tomography with CT angiography of pulmonary vasculature. 2. Pulmonary angiography. 3. Nuclear lung scan, ventilation/perfusion scan (V/Q scan). A positive D-Dimer test should be followed by above 3 tests. When CTPA and V/Q are not available, pulmonary angiography is the gold standard investigation to confirm PE. After diagnosis of PE is established, it is necessary to confirm the status of RV function. ECG, ECHO, right heart catheterization, increased levels of biomarkers (Troponin T, pro-brain natriuretic peptide).

Management 1. Analgesics to relieve hypoxia. 2. Oxygen. 3. Central venous line should be inserted for IV administration of colloid, inotropes and thrombolytic agents. 4. Thrombolysis. Streptokinase 250,000 U IV over 20–30 min (with or without Hydrocortisone 100 mg) followed by 100,000 U/hr for up to 72 hrs, followed by Warfarin and if necessary heparin, until adequate anticoagulation has been achieved or Reteplase ‘double bolus’ administration of (10 + 10 units) or Tenecteplase 0.5 mg/kg body weight. 5. Anticoagulation. (a) Heparin 5000 U IV bolus, then continuous infusion at rate of 1000 U/hr. The dose is adjusted to keep APTT to twice the normal. (b) Warfarin started from 5th day. Dose 10 mg/day for 48 hrs, subsequent dosage adjusted to keep the patient 1.5–2 times normal. After heparin is discontinued, Warfarin is continued for at least 3 months or longer.

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240 A Handbook of Emergencies 6. Cardiopulmonar y support. (a) Dopamine or Dobutamine. (b) Colloid infusion of Dextran or Haemaccel 500 mL. 7. Pulmonar y embolectomy. Indications—(a) If thrombolysis is contraindicated or deterioration despite thrombolysis. (b) More than 50% obstruction on angiography. (c) Persistent shock or marked right sided heart failure. 8. Procedures on IVC. For patients at high risk of further emboli and in whom anticoagulation is contraindicated, or in those who have recurrent emboli despite adequate anticoagulation, an IVC filter may be beneficial. However in the acute phase of massive PE, any procedure on IVC that reduces venous return is potentially detrimental. 9. Prevention of further embolization: (a) Elevation of legs. (b) Anticoagulation. (c) Use of elastic stockings. (d) Leg exercises in the form of pressing the foot of the bed, several times in a day.

Cardiac Tamponade A large pericardial effusion if it causes rise in intrapericardial pressure (cardiac tamponade) impairs venous return with consequent fall in cardiac output.

Clinical Symptoms Hemorrhagic effusion caused by cardiac trauma by chest injury, following cardiac surgery, during mechanical ventilation (barotrauma), oesophageal perforation during gastroscopy or sclerotherapy, cardiac perforation during pacing or angiography or balloon angioplasty. Anticoagulant therapy. Dissecting aneurysm.

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Clinical Features Patient presents with restlessness and malaise, leading (often rapidly) to collapse. Examination shows raised venous pressure, tachycardia, hypotension and marked pulsus paradoxus. Heart sounds are quiet.

Investigations l. CXR – Rapidly increasing cardiac shadow with clear lung fields. 2. ECG – Low voltage QRS. Electrical alternans. 3. Echo – Demonstrates even small effusions. In tamponade, it is possible to see diastolic collapse of right atrium and ventricle caused by compression of these chambers as the heart fills.

Management 1. Relief of pain if necessary with Morphine or Pentazocine. 2. Urgent pericardiocentesis. Aspiration should be carried out under ECG monitoring. Skin and chest wall are infiltrated with 2% xylocaine. A 12–16 gauge spinal needle is attached to a 20 mL syringe with a three-way tap. Site – Among the sites, the subxiphoid approach (between xiphoid and left costal margin) is safest. Patient must be put in upright or semireclining position. The needle is slowly advanced with its tip pointing towards the left shoulder under echo guidance. A gentle suction is applied whilst the needle is advanced. Another site of approach is 5th left interspace 2 cm within the outer cardiac dullness. If drainage of a large effusion is required, a soft intrapericardial catheter can be inserted with a needle stylet or guide wire, and the catheter connected to a closed sterile collection system.

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Acute Aortic Regurgitation Acute AR can result from aortic dissection, endocarditis or blunt chest trauma. Typically patient presents in a low output state with dyspnoea, marked sinus tachycardia and pulmonary congestion. Clinical diagnosis can be difficult because though the pulse upstroke is sharp, the early diastolic murmur is short and many of the physical signs of chronic AR are absent. Trans-thoracic echocardiography and Doppler assess the mechanism and severity of AR but transesophageal echo provides important additional information.

Management Acute severe AR usually requires urgent surgery and interim reduction of afterload with vasodilators.

Peripheral Vascular Emergencies Aortic Dissection Aortic dissection is a serious emergency, it is more common in males over age of 50. It can be associated with hypertension, atherosclerosis, pregnancy, coarctation of aorta or Marfan’s syndrome.

Clinical Features 1. Excruciating pain in center of chest, which may radiate to epigastrium, interscapular region, lumbar region and elsewhere. Pain is maximal at onset. 2. Dyspnoea is rare, but if present haemothorax should be suspected. 3. Shock may be severe and result in syncope. 4. Peripheral pulses (carotid, radial and femoral) may be weak, unequal on the two sides or absent. 5. Diastolic murmur of AR may develop. 6. Pericardial friction and tamponade may occur.

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Investigations 1. 2. 3. 4.

CXR may show widening of mediastinum. ECG may be normal. Echo. Oesophageal echo will demonstrate dissection. CT scan and MRI will reveal double lumen in the aorta.

Management 1. Admission to ICU and complete bed rest. 2. Relief of pain with Pentazocine or Morphine or Pethidine. 3. Lowering of systolic pressure to around 100–120 mm Hg with IV nitroprusside infusion. Propranolol 0.5–1 mg IV till adequate beta-blockade. Can be repeated q6h, or Methyldopa 250 mg p.o. q6h may be combined with above drugs to maintain stable systolic BP. 4. Surgery. Indications (a) According to Debakey’s classification of type of dissection. Type A (dissection proximal to origin of left subclavian artery and Type C (dissection extending both proximally and distally to origin of left subclavian artery). (b) Presence of AR. (c) Large hemorrhagic pleural effusion. (d) Cardiac tamponade. (e) Hypertension not responding to drug therapy. 5. Medical therapy – to be continued in type B dissection (tear distal to origin of left subclavian artery).

Acute Limb Ischemia It is caused either by an arterial embolus, originating from the heart or proximal artery, or by a thrombus superimposed on local atheromatous disease. Unless there is an obvious source of emboli, it is difficult to make the distinction between these causes on clinical grounds.

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244 A Handbook of Emergencies Risk factors include smoking, diabetes, hypertension and hyperlipidemia.

Diagnosis Clinical: Confirmatory signs such as absent femoral or popliteal pulses and pulse at the ankle. Legs should be examined for any differences of temperature of the two limbs. Investigation: Measurement of resting ankle: arm Doppler pressure index. The peak systolic pressure in the arteries at the ankle can be related to that in the arm, and the ratio of the two pressures is the simplest method of judging the severity of occlusions of arteries supplying the legs.

Management 1. Heparin. Should be given as soon as the diagnosis of acute leg ischemia is made, and patient prepared for surgery. 2. Surgery. Results of early surgical removal of the acute obstruction are good. The procedure can be carried out under local anaesthesia. After exposing the femoral artery at the groin, a special balloon catheter is passed beyond the occlusion. The balloon is inflated and the thrombus or embolus withdrawn. Oral anticoagulation should be continued. 3. Percutaneous re-opening procedures using catheter techniques can be an alternative first choice in the treatment of acute ischemia. (a) Percutaneous transluminal angioplasty (PTA) is the simplest catheter reopening procedure and carries no mortality. (b) Local fibrinolytic therapy is an alternative or additional technique to PTA, particularly if there is suggestion of recent thrombosis. Streptokinase 6000 U/hr is delivered directly on to the occlusion through

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a catheter, with repeat arteriography after 6–12 hrs of treatment. If there is no change in the occlusion, the treatment is stopped. If there is significant improvement, treatment must be continued for 24–48 hrs, with repeat arteriograms ql2h. Combination of PTA and local fibrinolysis is increasingly being used with good results.

Saddle Embolus Clinical features: Sudden severe pain in the legs, lumbosacral area and perineum, numbness in the affected areas, absent lower limb pulsations, cold and pale lower extremities and total paralysis of the legs. Management: 1. Relief of pain. Inj. Pentazocine 100 mg IM. 2. Heparin 5,000 units IV every 4 hours. 3. Low molecular dextran (Lomodex) 500 mL. slowly IV. 4. Aortography to localise the lesion. 5. Insertion of a balloon catheter to extract the clot, or 6. Direct surgical removal of the clot.

Severe Primary Antiphospholipid Syndrome APS is characterized by recurrent venous or arterial thrombosis and/or fetal losses. Deep vein thrombosis with or without pulmonary embolism is the most common manifestation followed by arterial occlusion of cerebral, coronary and other arteries, as also peripheral gangrene. Treatment: For severe cases, combination of anticoagulant and aspirin. Corticosteroids and IV immunoglobulins are beneficial in severe or catastrophic APS.

Syncope Syncope is brief loss of consciousness as a result of inadequate blood supply to the brain. Because it is a

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246 A Handbook of Emergencies symptom, not a disease, there are a wide variety of causes, both benign and life-threatening. Although syncope has to be differentiated from seizures, coma, shock and head trauma, these disorders may initially present with syncope.

Causes and Management 1. Cardiac syncope: Structural cardiac syncope occurs most commonly during or shortly after physical exertion. Occasional precipitants include sudden changes in posture or a hot bath causing vasodilatation. a. Arrhythmias: Sinus node disease, AV node disease, tachycardia (particularly VT). b. Cardiac structural disease: Aortic stenosis, HOCM, extensive myocardial ischemia, cardiac tamponade, aortic dissection. c. Reduced ventricular filling: Pulmonary embolism, cough syncope, atrial myxoma, ball valve thrombus. Obstruction of a prosthetic cardiac valve is almost always thrombotic and occurs more commonly with mechanical valves than with bioprostheses. Manifestations include peripheral embolism, unexplained cardiac failure, cardiogenic shock and syncope. Soft or absent prosthetic valve clicks strongly suggest the diagnosis. Management usually involves thrombectomy with or without valve replacement; however, thrombolytic therapy may be successful in some patients. 2. Inappropriate vasodilatation: a. Vasovagal attack (simple faint) is the most common form of syncope due to excessive vagal tone, usually triggered by pain, emotion, unpleasant sights, long periods of standing in one

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position, exhaustion or hot atmosphere. Treatment is to lay the subject at once in recumbent position and loosen any tight clothing in order to restore cerebral perfusion. b. Carotid sinus hypersensitivity: Here patients may develop dizziness or syncope when pressure is applied to the neck (e.g. when wearing a tight collar). c. Drug-induced: Anti-anginal, antihypertensive, neuroleptic medication. d. Orthostatic hypotension: Diabetes, Parkinson’s disease, elderly. e. Micturition syncope. 3. Neurogenic syncope: Vertebrobasilar ischemia (drop attacks). 4. Metabolic: Hypoglycemia – Diabetic patient on insulin/oral hypoglycemic drugs. Diagnostic pointers: Loss of consciousness may be sudden, without any premonitory symptoms. Usually however the patient has some warning sensation of faintness, dizziness, nausea, or blurring of vision. More minor attacks without complete loss of consciousness are not uncommon and are sometimes labelled as pre-syncope or near syncope. If a patient who falls describes being aware of hitting the ground or of vertigo without loss of consciousness, an alternative diagnosis should be considered. Typically, the period of consciousness is very short, unless patient remains propped up with the head raised.

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10

Neurological Emergencies

Raised Intracranial Pressure Raised intracranial pressure (ICP) is defined as an increase of ICP high enough to impair the normal flow of cerebral circulation. A sustained pressure above 15 mm Hg in an adult is abnormal and above 20 mm Hg is high.

Causes 1. Focal lesions: (a) Head injury causing intracranial h a e m a t o m a a n d c o n t u s i o n s . ( b ) Tu m o r s . (c) Inflammatory lesions (granuloma, abscess, cerebritis). (d) Vascular lesions (infarcts, hematomas). (e) Congenital malformations. 2. Diffuse causes: (a) Hydrocephalus. (b) Cerebral oedema (metabolic encephalopathy, hypertensive encephalopathy, hypoxic, pseudotumor cerebri). (c) Elevated venous pressure (CHF, SVC obstruction). (d) Venous sinus thrombosis. (e) Increased production of CSF (choroid plexus papilloma). (f ) Head injury causing diffuse axonal injury. (g) Status epilepticus. (h) Meningitis. (i) Acute subarachnoid hemorrhage.

Clinical Features of Raised ICP 1. Headache may be paroxysmal at first, but then recurs as a dull ache, present most mornings on waking up.

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There may be superadded paroxysms of agonising intensity, often provoked by straining, coughing or vomiting. 2. Vomiting is an early and prominent feature in obstructive hydrocephalus and in posterior fossa lesions especially if 4th ventricle is involved. 3. Altered mental status and somnolence. 4. Papilloedema is the only reliable clinical sign of raised ICP. 5. Diplopia due to lateral rectus palsy can occur. The abducent nerve may be torqued as it enters the petroclinoid ligament. This is a false localising sign. 6. Cushing’s reflex (hypertension, bradycardia and irregular breathing) indicates severe intracranial hypertension. Raised ICP in children. In children whose fontanelles have not closed, raised ICP is manifested by enlargement of head circumference. There may be accompanying vomiting and failure of upgaze from pressure on brainstem structures.

Herniation Syndromes Transtentorial Herniation (a) Central herniation. Expanding lesions of frontal, parietal or occipital lobes or midline extracerebral tumors may produce a downward movement of midline intracranial structures into the posterior fossa. Initial focal features relating to lobe of origin are soon replaced by diencephalic symptoms as herniation begins. Depressed consciousness occurs early followed by bilateral medium-sized non-reacting pupils. Wide fluctuations in temperature, diabetes insipidus and impairment of upgaze. Later brainstem symptoms including respiratory and hemodynamic disturbances appear.

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250 A Handbook of Emergencies (b) Uncal herniation produces deterioration of sensorium, ipsilateral dilatation of pupil, contralateral hemiparesis and decerebrate posturing. (c) Cerebellar tonsillar herniations through the foramen magnum can occur due to rapidly expanding hemorrhage, infarcts or mass lesion in the posterior fossa. Cerebellar symptoms and signs rapidly evolve to medullary dysfunction with coma, decerebrate posturing and respiratory impairment. (d) Subfalcine or cingulate herniation is usually caused by a frontal or parietal mass lesion with shift of cingulate gyrus under falx. Occlusion of anterior cerebral artery causes contralateral hemiparesis especially of the leg and coma.

Hydrocephalus Hydrocephalus is defined as an increase in the volume of CSF within the skull. Causes: 1. Subarachnoid hemorrhage. 2. Aqueduct stenosis. 3. Meningitis (esp. tuberculous). 4. Posterior fossa lesions. 5. III and IV ventricular tumors (esp. colloid cysts). 6. Arnold-Chiari malformation. 7. Head injury. Clinical features of acute hydrocephalus: In infants, there is rapid enlargement of the head with tense fontanelles. The infant is fretful, feeds poorly and may vomit. There is retraction of upper eyelids, downturning of eyes and paralysis of upgaze (‘Setting sun’ sign). In adults, papilloedema occurs with prominent headaches. There is bilateral frontal lobe disturbance with inattention, lack of spontaneity and gait abnormality. Grasping and sucking reflexes are present and sphincter incontinence may occur.

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Management of Raised ICP 1. Posture with head elevated at about 30°. 2. Mechanical hyperventilation reduces arterial PCO2 which in turn reduces blood volume and blood flow. PCO2 is reduced from baseline levels of 30–35 mm Hg to therapeutic levels of 25–30 mm Hg. Raised ICP begins to fall 10–30 seconds after hyperventilation, reaches its nadir in 30 minutes and returns to its original level in less than an hour. There is thus a limited time of effective ICP control with hyperventilation. 3. Hyperosmolar therapy. (a) Mannitol 0.25 g/kg is infused rapidly and given 3–4 times a day. (b) Hypertonic saline (HTS): It causes rapid reduction of intracranial pressure (ICP) and its benefit may last longer than mannitol. It is preferred in hypovolemic and hypotensive patients. It is infused as 3% solution at 10–40 mL/h. (c) Glycerol 1.5 g/kg body wt/day in 3–4 divided doses mixed with fruit juice to mask the unpleasant taste. Serum osmolarity and urine output should be measured frequently. (d) Frusemide (lasix) 20–40 mg bd or tds by causing diuresis. BP and electrolytes to be checked. (e) Acetazolamide (Diamox) 250–500 mg/day helps to restrict CSF formation and may be used. 4. Surgical decompression. If all other measures fail, subtemporal decompression may be tried.

Management of Hydrocephalus If high pressure hydrocephalus is caused by an obstructing mass, primary management may be either shunt placement or removal of the mass. The distal end of the shunt is usually placed in the peritoneal cavity (V-P shunt), only occasionally in the right atrium. In some

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252 A Handbook of Emergencies cases of hydrocephalus complicating TB meningitis where insertion of a shunt would result in shunt blockage caused by infection, a temporary external ventricular drainage tube (EVD) is placed to drain the CSF for a few days.

Ischemic Cerebrovascular Disease Stroke is defined as the sudden or rapid onset of a focal neurological deficit caused by a cerebrovascular disease. There are two broad categories of strokes: 1. Ischaemic strokes (80%) due to narrowing or occlusion of cerebral vessels. 2. Haemorrhagic strokes (20%) which include intracerebral and subarachnoid haemorrhage.

Types of Ischemic Strokes 1. Primary thrombotic occlusion of a vessel: This is usually caused by atherosclerosis of large cerebral arteries or lipohyalinosis of small penetrating vessels. 2. Embolic occlusion of a vessel from a distant source: The common sources of embolic material are the heart and the large neck vessels. Common cardiac causes of cerebral embolism: (a) Atrial fibrillation (especially with rheumatic heart disease). (b) Acute myocardial infarction. (c) Prosthetic valves. (d) Infective endocarditis. (e) Mitral valve prolapse. (f ) Cardiomyopathy. (g) Left atrial myxoma. The clinical profiles of ischaemic cerebrovascular disease are varied and include: 1. Transient ischemic attacks (TIAs) in which there is complete resolution of neurologic deficit within 24 hours. In the new definition of TIA, emphasis is laid

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on the fact that MRI must not show evidence of acute ischaemia, irrespective of the period of recovery. 2. Reversible ischemic neurologic deficits (RIND) in which complete recovery occurs but the time taken is more than 24 hours. 3. Stroke-in-evolution in which the deficit worsens in a step-wise fashion over hours or days with a series of sudden events. 4. Completed stroke in which the deficit is complete. 5. Lacunar stroke causing small, often cystic infarcts in the brain parenchyma due to hyaline thickening of the small penetrating arteries of the brain (lipohyalinosis).

Transient Ischemic Attacks and Minor Strokes A transient ischemic attacks (TIA) is a warning sign of cerebrovascular disease and must be taken seriously. A patient with TIA must be thoroughly investigated in an attempt to find the cause. The aim should be to prevent a major stroke in future.

Clinical Features Depend on the artery involved and the vascular territory it supplies. For example a TIA of internal carotid artery would produce ipsilateral transient monocular blindness with or without contralateral hemiplegia, and one in the posterior cerebral artery territory would cause homonymous hemianopia, memory loss and vertigo. In the examination care must be taken to examine the heart and peripheral pulsations and a bruit over the carotids.

Investigation Hemogram, ESR, sugar, urea, LFTs, CXR, ECG, lipid profile, VDRL, 2 D echo.

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254 A Handbook of Emergencies Serum homocysteine should also be estimated. A high homocysteine level increases the risk of stroke.

Neuroimaging (a) Cranial CT scan should be performed as soon as possible to rule out a haemorrhage in every case at the outset. (b) MRI scan. This is more sensitive than CT scan in recognizing early cerebral infarction. MRI brain with angiography is preferred to CT scan in TIAs as it cannot only detect tiny acute infarct but also detect stenosis of major cerebral vessels causing TIA. (c) Duplex ultrasound Doppler study of neck vessels. (d) Transcranial Doppler may be useful in assessing the blood velocities in some intracranial arteries and evaluating vasospasm due to subarachnoid haemorrhage. (e) Digital subtraction angiography (DSA): Intra-arterial to visualise arteries with a small quantity of contrast as compared to conventional angiography.

Management of Severe Carotid Stenosis If unfractionated heparin is used, activated partial thromboplastin time (aPTT) must be monitored and kept at about twice the normal. Carotid endarterectomy: Symptomatic patients (TIAs/ minor strokes) with severe (70–90%) carotid stenosis at or near the carotid bifurcation are much less likely to suffer stroke in the territory of that artery following an endarterectomy. In mild carotid stenosis ( 180 mm Hg or diastolic BP > 120 mm Hg). In an unconscious patient it is best to maintain on IV fluids only for the first few days. This also applies to conscious patients who are dysphagic. Later Ryle’s tube feeds can be started. Aspiration must be prevented while giving feeds. 5. Treatment of raised ICP and herniation. Endotracheal intubation, mechanical hyperventilation and mannitol/glycerol are indicated. Steroids have not been shown to be very effective in ischaemic brain oedema. Subcutaneous heparin 5000 units q12h may be given to prevent deep vein thrombosis. If seizures – anticonvulsants.

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258 A Handbook of Emergencies 6. Thrombolysis. Patients who present to hospital within 4–5 hours of acute ischaemic stroke whose CT does not show a bleed are considered for IV recombinant TPA (rt-PA). Dose: 0.9 mg/kg with 10% dose as bolus and remainder of the drug in infusion over 1 hour (For contraindication see under ischaemic heart disease). There is increased risk of intracranial haemorrhage (about 6%). BP prior to use and during rt-PA should be 6 hrs with occlusion of major carotid or basilar artery, intra-arterial thrombolysis can be considered, if the hospital has facility for DSA. Mechanical removal of devices like MERCI device or stent retrievers are also being implemented. 7. Piracetam (Nootropil) IV can also be used but its value and efficacy have yet to be confirmed. 8. Low molecular weight dextran (Lomodex) decreases aggregation of platelets and RBC, thus decreasing blood viscosity. However, its benefit in the treatment of acute ischaemic stroke remains unproven.

Ischemic Stroke Special considerations Lateral medullary infarct causes dysphagia, vertigo, ipsilateral palatal weakness, Horner’s syndrome, cerebellar ataxia and contralateral spinothalamic loss over the body. Patient is unable to swallow and has to be kept on Ryle’s tube. If dysphagia does not improve over a long period, a feeding gastrostomy has to be done. zz Acute cerebellar infarct is due to vertebrobasilar ischemia and presents with severe vomiting, vertigo, headache and altered sensorium. Being in the posterior fossa, patient can deteriorate fast and herniate and has to be monitored carefully. A ventricular drainage of

zz

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CSF may be necessary if hydrocephalus develops. If impending herniation, posterior fossa surgical decompression may be required.

Venous Infarct Common Causes Infections of paranasal sinuses, ears and face; pregnancy, oral contraceptives, postpartum, postoperative, dehydration, collagen vascular disease, elevated homocysteine levels, acquired and congenital abnormalities of blood and coagulation system like thrombocytosis, polycythemia vera, antiphospholipid antibody syndrome, sickle cell disease, protein C and protein S deficiency and antithrombin III deficiency.

Clinical Features Patients usually present with focal neurologic deficits, seizures and raised ICP, with papilloedema.

Investigation MRI venography is the investigation of choice to detect cerebral venous thrombosis.

Management Low MW heparin initially and then oral anticoagulants for about 6 months or till recanalization occurs.

Intracerebral Hemorrhage Intracerebral hemorrhage (ICH) accounts for 20% of all strokes.

Causes Hypertension commonest, others include bleed from A-V malformations, bleeding diathesis (especially

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260 A Handbook of Emergencies anticoagulants and thrombocytopenic purpura), bleed in tumors, drugs like cocaine and amphetamine; trauma and amyloid angiopathy.

Clinical Features Onset is usually during activity, onset during sleep is rare. Patient has headache and vomits and develops focal neurological features depending on location of the bleed. As the hematoma enlarges, ICP rises resulting in altered level of consciousness. Compression of brainstem structures by enlarging hematoma leads to coma and death. With cerebellar hematoma vomiting is early and persistent. Seizures at onset are more likely with lobar hemorrhage.

Investigation CT scan of head shows location and magnitude of the bleed. MRI is not usually indicated in acute hypertensive bleed unless some other cause is suspected (AVM, tumor). The advent of CT/MRI have made CSF examination redundant.

Management Medical 1. Admit in ICU. 2. Control hypertension. Overzealous lowering of BP can lead to underperfusion and clinical deterioration. 3. Control of ICP. (a) Mechanical hyperventilation with PCO 2 in range of 25–30 mm Hg can lower ICP in minutes. (b) IV mannitol 0.25–1 gm/kg or glycerol. (c) Dexamethasone 4 mg/6–8 h. 4. Surgical evacuation can prove lifesaving in the following situations: (a) Cerebellar hematomas.

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(b) Lobar right putaminal hematomas. Ventricular drainage of CSF by drain or shunt may be done if hydrocephalus occurs due to obstruction of CSF pathway in cerebellar and thalamic bleed.

Acute Subarachnoid Hemorrhage Acute subarachnoid hemorrhage (SAH) is one of the commonest causes of sudden death due to neurological disease.

Causes 1. Rupture of saccular aneurysm which mainly occurs at sites of arterial bifurcation or branching and are mainly located around circle of Willis. 2. Non-aneurysmal causes: Vascular malformations (AVMs), trauma, hypertension, coagulopathies and bleeding diathesis.

Clinical Features Sudden excruciating headache. Prior to rupture a few patients have minor leaks (sentinel hemorrhage). A high index of suspicion is required to diagnose the condition at this early stage so that major rupture could be prevented. Headache is usually accompanied by profuse vomiting and altered sensorium. Transient loss of consciousness at onset is common. On examination meningeal signs and neck stiffness are common and mild fever. Fundoscopy may reveal subhyaloid hemorrhage. There may be one or more cranial nerve palsies depending on the location of the aneurysmal bleed. For example 3rd nerve palsy with ptosis and dilated pupil would suggest a posterior communicating aneurysm, and a 6th nerve palsy, raised ICP. If there is extension of SAH into brain parenchyma with formation of intracerebral

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262 A Handbook of Emergencies hematoma, then focal neurologic deficit would be detected at onset of SAH.

Clinical Grading of SAH Grade Features 0 Unruptured aneurysm – asymptomatic. 1 Asymptomatic or minimal headache and slight neck stiffness. 2 Moderate or severe headache, neck stiffness, no neurologic deficit. 3 Drowsy, confused or mild focal deficit. 4 Stupor moderate to severe hemiparesis, early decerebrate rigidity. 5 Deep coma, decerebrate rigidity.

Investigation 1. CT scan to detect presence of blood in subarachnoid space. Majority of patients scanned within 5 days of the bleed will have positive scans. CT scan also gives clues to location of an aneurysm and ventricular size. 2. Lumbar puncture if CT scan not available or does not show blood. CSF may be bloody, and there is xanthochromia of supernatant fluid. Xanthochromia will be present if LP is done after 6 hours of bleed. 3. Four vessel angiography and DSA are carried out after confirming SA bleed to detect presence and location of the aneurysm.

Complications of SAH 1. Rebleed: Maximum risk of rebleed is in first 24 hours, but the risk continues to be high over 1–2 weeks. 2. Vasospasm is a significant cause of morbidity. It has peak incidence between 7th and 14th day following

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SAH, though it can occur at any time up to 14 days post bleed. Vasospasm can cause hemiplegia and worsening sensorium. 3. Hydrocephalus should be suspected if there is gradual deterioration in patient’s clinical condition. 4. Electrolyte disturbances. Hyponatremia may occur either due to SIADH or primary salt wasting.

Management 1. Hospitalization: Patient must be transferred without delay to an advanced neurosurgical unit. If an aneurysm is detected, surgery must be performed as early as possible to prevent rebleed. In case of stuporous patients surgery may be deferred till clinical improvement since surgery on grade 4 to 5 patients carries a high morbidity and mortality. 2. Medical measures a. Control of hypertension with drugs. b. Keep patient in a dark, quiet room. c. Sedatives. d. Stool softener to prevent straining at stool. e. Treat raised ICP. f. Management of vasospasm. (i) Nimodipine 30–60 mg po q4h from the onset. BP should be monitored because the drug produces hypotension. (ii) Induction of hypervolemia and systemic hypertension once vasospasm occurs. This must be done in ICU with CVP, arterial pressure and, preferably, Swan-Ganz pressure monitoring. Volume expansion with IV 5% albumin or other plasma protein fraction solutions and systemic hypertension with dopamine. Complications of this therapy include pulmonary oedema, CHF, cerebral oedema, and myocardial infarction.

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264 A Handbook of Emergencies 3. Surgery (a) Clipping—of the aneurysm as early as possible unless patient is stuporous or comatose. If hydrocephalus develops, a ventricular peritoneal shunt may have to be inserted. (b) Coiling— sometimes aneurysms are situated at locations (e.g. at basilar tip) and are difficult to tackle surgically. In such cases coiling is resorted to - Guglielmi detachable coils (GDC) are soft radiopaque platinum coils that can be delivered through a microcatheter into an aneurysm and occlude the aneurysm. Indications for GDC embolization are—medically unstable patient, poor neurologic grade of SAH, posterior fossa aneurysms with small neck, early vasospasm, and multiple aneurysms in different arterial territories.

Status Epilepticus (SE) The newer definition of status epilepticus denotes any seizure lasting more than 5 minutes or 2 or more seizures with incomplete recovery of consciousness between them.

Classification A. Generalised SE 1. Convulsive: ŠŠ Tonic-clonic ŠŠ Tonic ŠŠ Clonic ŠŠ Myoclonic 2. Non-convulsive: Absence B. Partial SE 1. Simple partial: Epilepsy partialis continua 2. Complex partial

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Tonic-clonic SE is the commonest form. The extent of brain damage is directly dependent on the time taken to control the attack.

Etiology a. In a known epileptic the commonest cause is antiepileptic drug withdrawal, or noncompliance. Precipitating factors include intercurrent illness, inadequate sleep, alcohol indulgence and drugs such as isoniazid, theophylline amitriptyline and penicillins. b. SE as initial episode may occur due to meningoencephalitis, head injury, metabolic disturbance (e.g. hypoglycemia, hyponatremia), brain tumors, cerebrovascular disease (especially cortical thrombophlebitis), lead poisoning, Reye’s syndrome (in children).

Medical Complications in Tonic-Clonic SE 1. Cerebral. Hypoxic brain damage, raised ICP and cerebral oedema, damage due to persistent electrical discharge. 2. Metabolic. Dehydration, metabolic acidosis, hyponatremia, hypoglycemia, hyperkalemia, acute renal failure (rhabdomyolysis may cause acute tubular necrosis). 3. Cardiorespiratory and autonomic. Hypotension, hypertension, arrhythmias, pulmonary oedema, aspiration pneumonia, hyperpyrexia, excessive sweating and hypersecretion.

Management of Tonic-Clonic SE For the new patient presenting as an emergency in status, it is useful to plan therapy in stages.

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266 A Handbook of Emergencies Stage I: (a) Check vital signs at once. (b) Insert soft plastic airway. (c) Oxygen. (d) If severe respiratory distress, intubate and put on ventilator. Stage II: (a) Set up IV line. (b) Collect blood for emergency investigations (blood count, arterial blood gases, sugar, liver and renal functions, calcium, magnesium, electrolytes, anticonvulsant drug levels). (c) Give antiepileptic drug therapy (see protocol). (d) If hypoglycemia is suspected, give 50 mL 50% glucose IV. (e) If alcoholism is suspected thiamine 50 mg IM and 50 mg IV before giving glucose. (f ) In infants possibility of SE due to pyridoxine deficiency should be kept in mind and a trial of 100–200 mg of the drug given IV at the onset. Stage III: (a) Establish the etiology or precipitating factors. CT scan of head and CSF examination may be necessary at this stage. (b) Manage the medical complications of SE: (i) IV sodabicarb if severe metabolic acidosis. (ii) If hypotension, pressor agent like dopamine by slow IV infusion 2–5 µg/kg/ min, can be increased to more than 20 µg/kg/min if severe hypotension. (iii) Detection and prevention of hyperthermia as it has an adverse effect on prognosis. Rectal temperature must be monitored throughout treatment. (iv) Raised ICP is treated with cerebral decongestants like mannitol and glycerol and by mechanical hyperventilation. (v) Start longterm anticonvulsant therapy in tandem with emergency treatment.

Antiepileptic Drugs Protocol for Antiepileptic Drug (AED) Initial Management IV Lorazepam 4 mg over 2–3 mins or IV Diazepam 5 mg. Repeat dose if necessary.

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If IV access not available give Midazolam 10 mg intranasally or IM, or rectal Diazepam 10 mg. Usually IV Phenytoin 15–20 mg/kg or IV Fosphenytoin 20 mg/kg infusion at rate of less than 50 mg/min (Phenytoin) is started soon after. Alternatives to phenytoin are inj. Valproate 500–1000 mg bolus or IV Levitiracetam 1 g bolus. Refractory status. If seizures continue despite the above antiepileptic drugs intubate and administer one of the following: a. IV Midazolam drip load with 0.2 mg/kg and IV infusion at rate of 0.03 to 0.2 mg/kg/h. b. IV propofol - Load with 1–2 mg/kg, repeat every 5 minutes till seizures stop, then IV infusion of 2–10 mg/h. Propofol is a short acting anaesthetic agent with a rapid metabolic clearance and less pronounced hypotensive effect compared to thiopental or IV phenobarbitone bolus 6–8 mg/kg at a rate not more than 60 mg/min. Partial (focal) motor SE consists of frequent seizures involving an extremity or facial muscles with preservation of consciousness and no tendency for generalisation. As focal SE is not a life-threatening emergency, treatment may be initiated with oral loading dose of phenytoin or phenobarbitone. In adults 100 mg of oral phenytoin during an 8–12 hour period followed by maintenance dose of 300–400 mg/day. Non-convulsive SE is essentially a behavioural manifestation without significant motor involvement. EEG helps in diagnosis. Two main types are: (a) Generalised absence status. (b) Complex partial status. Clinically, patients present with clouding of mental processes varying from simple slowing of ideation to

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268 A Handbook of Emergencies complete unconsciousness. Automatism may be present. In generalised absence SE, EEG shows bilateral discharges of spike wave complexes, while in complex partial SE, a temporal spike and slow activity is usually seen on EEG.

Management In both types the most effective drug is IV Diazepam in the same dosage as in convulsive status. In generalised absence SE, ethosuximide or valproate should be started along with diazepam, while in complex partial SE, phenytoin may be concomitantly given. Once the SE is controlled, the patient should be on maintenance antiepileptic drugs. Standard drugs used are phenytoin, carbamazepine, sodium valproate and phenobarbitone. Clonazepam can be used for myoclonic epilepsy. Some of the newer antiepileptic drugs like lamotrigine, topiramate, lacosamide, oxcarbazepine and levetiracetam can be tried as adjunctive therapy to the primary anti-epileptics if seizures are not well controlled.

Intracranial Infections Acute Bacterial Meningitis Pneumococcal meningitis is frequently associated with acute otitis media, lobar pneumonia, CSF rhinorrhoea, sickle cell disease, splenectomy, immunoglobulin deficiency and chronic alcoholism. Clinical features: Acute onset with fever, vomiting and altered sensorium. Seizures may occur during the course of illness. 25% of patients could become seriously ill within 24 hrs. Neck stiffness is as a rule present except in immuno-compromised or very old, debilitated patients. Cr. Ns. may be involved.

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Meningococcal meningitis is generally seen in epidemics and patients usually present with a morbilliform, petechial or purpuric rash with ecchymosis. Investigation: 1. Lumbar puncture. (It may be preceded by CT scan to rule out mass lesion.) CSF will show increased pressure, elevated proteins, reduced sugar and large number of WBCs, mainly polymorphs, but in partially treated meningitis, mononuclear cells may predominate. Gram’s stain usually identifies the organism which is then confirmed on culture. 2. WBC count. Neutrophilic leucocytosis. 3. CXR may show evidence of pneumonia. Complications of acute bacterial meningitis. 1. Circulatory collapse and shock, DIC. 2. SIADH. 3. Brain abscess, subdural empyema. 4. Raised ICP. 5. Vasculitis with cerebral infarction. 6. Obstructive hydrocephalus. 7. Cranial nerve palsies, hearing loss. Management: 1. General measures. (a) Isolation of patient initially if meningococcal, or unknown etiology. (b) Treatment of raised ICP. (c) Treatment of septic shock, if present, with volume replacement and pressors. (d) Corticosteroids if Waterhouse- Friedreichsen syndrome. (e) Anti-convulsants if seizures. 2. Management of predisposing factors. (a) Foci of systemic sepsis may require prolonged antibiotic therapy (e.g. infective endocarditis, osteomyelitis). (b) Parameningeal infections are treated concurrently with meningitis, with surgical drainage if necessary. (c) Minor CSF leaks need not be repaired until after CNS infection is controlled.

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270 A Handbook of Emergencies 3. Systemic antibiotic therapy. If the causative organism is isolated, the antibiotic of choice for that particular organism is given. Often, however CSF fails to reveal the organism; in such a case, the ‘best guess’ antibiotic should be started, taking into account the likely pathogen. Patients are hospitalised for the entire duration of treatment and the full course of antibiotics given parenterally. In meningitis with common organisms, the full dose should be given for at least 10 days, and at least 7 days after patient is afebrile. In complicated cases and difficult to treat organisms, LP should be repeated 24 hours after initiation of antibiotics. Organism H. influenzae

S. pneumoniae

N. meningitidis E. coli P. aeruginosa

First choice (Dose) Ampicillin (300–400 mg/ kg/day) + Chloramphenicol (100 mg/kg/day) Penicillin G (20–24 million U/ day) Vancomycin 500 mg IV bd + Ceftriaxone Penicillin G Cefotaxime (8–12 g/day) Ceftazidine 6–12 g/ day or Cefipime

Second choice (Dose) Cefotaxime (200 mg/kg/day) or Ceftriaxone (100 mg/kg/day) Cefotaxime/ Ceftriaxone or Chloramphenicol (4–6 g/day) Cefotaxime/ Ceftriaxone (4 g/day) Aztreonam or Fluoroquinolone Macropenem or piperacillin (12–18 g/day) Contd...

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First choice (Dose) Ceftazidine (6–12 g/day)

Staph. aureus

Vancomycin (2 g/day)

Listeria monocytogenes Immunocom­ promised host or Nocardia

Ampicillin (8–12 g/day) Ampicillin + third generation cephalosporin. Co-trimoxazole Vancomycin 1g 8 hourly in children 60 mg/kg/day + 3rd generation cephalosporin ceftriaxone 100 mg/ kg/day Vancomycin 1g 8 hourly + ceftriaxone 2g 12 hourly + ampicillin 3g 4–6 hourly

16–50 years

> 50 years

Post-surgical or post-head injury

Second choice (Dose) Carbenicillin (18–30 g/day) Ticarcillin (12–20 g/day) Piperacillin (12–18 g/day) Cloxacillin or Nafcillin (Bacitracin may be used intrathecal) Co-trimoxazole + Chloramphenicol Aminoglycoside

S. pneumoniae N. meningitidis H. influenza

S. pneumoniae L. monocytogenes anaerobic Gram negative bacilli

Ceftazidine 2g 8 Staph. aureus hourly + vancomycin S. pneumoniae 1g 8 hourly anaerobic Gram negative bacilli

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Tuberculous Meningitis Though tuberculous meningitis (TBM) is usually a subacute or chronic meningitis, it can present acutely, and if diagnosis is delayed, its complications may represent a neurologic emergency.

Clinical Features TBM may initially present as PUO. Usual accompaniments are headache, vomiting and altered sensorium. Neck stiffness may be foci of TB elsewhere (lungs, GI tract.).

Complications Hydrocephalus, stroke due to vasculitis, hyponatremia due to SIADH.

Investigation 1. CSF: Raised pressure, markedly elevated proteins (at times 1–2 g%), reduced sugar (30–40 mg%) and lymphocytic pleocytosis. Gram stain may show presence of AFB. 2. Polymerase chain reaction (PCR) to amplify tubercle bacillus. DNA may prove useful.

Management For initial therapy: Isoniazid 300 mg/day zz Rifampicin 450–600 mg/day zz Pyrazinamide 15–30 mg/kg/day zz Streptomycin 15 mg/kg/day IM or zz Ethambutol 15–20 mg/kg/day Pyrazinamide and ethambutol may be discontinued after 1–4 months. INH and rifampicin are given for 1–1/2 years. zz

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Pyridoxine supplement may be given to prevent neuropathy. Ciprofloxacin, ofloxacin or moxifloxacin can also be used as one of the primary anti-tuberculous drugs. TBM is treated 50% longer in patients with concurrent HIV infection. In case of resistance to primary drugs second line drugs should be used. Indications for steroids: (a) Raised ICP. (b) Vasculitis. (c) Hydrocephalus. (d) Arachnoiditis. For hydrocephalus, a shunt may need to be inserted. Fungal meningitis is seen mainly in those with compromised immune function due to cancer, lymphoma, immunosuppressive therapy or AIDS. Etiology: Commonest organism is Cr yptococcus neoformans. Coccidioides immitis and Candida albicans may also be responsible. Mucormycosis is a virulent fungal infection usually seen in uncontrolled diabetics. It produces a characteristic rhinocerebral syndrome with or without associated meningeal inflammation. Diagnosis: Clinical and CSF picture is similar to that of TBM. CSF will detect cryptococci. Management a. Amphotericin B IV initial dose 0.2 mg/kg/day, gradually increased to 1 mg/kg/day dissolved in 5% dextrose and given through a central line over 4–6 hours. Three lipid formulations of amphotericin B are lipid complex, colloidal dispersion and liposomal form. These significantly reduce the renal and systemic toxicity of amphotericin B. b. 5-Flucytosine especially useful for Cryptococcus and Candida. Good CSF penetration. Dose 150 mg/kg/day

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274 A Handbook of Emergencies in 4 divided doses. It is usually combined with amphotericin to prevent drug resistance. c. Fluconazole: Useful in cryptococcal meningitis. Well tolerated. Dose 400 mg/day po. d. Ketoconazole: Absorbed well orally but CSF penetration poor. Dose 200–400 mg/day, increased to 1200 mg/day. Indicated if amphotericin ineffective. Duration of therapy: If patient responds to initial therapy, the regimen should be continued for at least 6 weeks and till 4 consecutive CSF samples are sterile. Often the meningitis lingers for much longer and prolonged therapy is warranted.

Acute Viral Meningitis (Aseptic Meningitis) Etiology: Common viruses are mumps, coxsackie and echovirus. Lymphocytic choriomeningitis, herpes viruses and arthropod borne viruses are less common. HIV can cause acute aseptic meningitis. Clinical features: It is a benign disease and usually presents acutely with headache, fever and vomiting, preceded often by upper respiratory infection. Neck stiffness is present and patient may be slightly drowsy. Seizures and markedly depressed sensorium, and focal neurologic signs are mostly absent; if they do occur, it suggests meningo-encephalitis. Cerebrospinal fluid (CSF): Pleocytosis (mainly lymphocytic) with normal sugar and slightly elevated proteins. Management: Supportive measures. No specific therapy. Neurosyphilis is rarely encountered nowadays. In the early stages may present as acute aseptic meningitis with CSF picture similar to that in acute viral meningitis. VDRL in blood and CSF are positive as also FTA-absorption test in blood.

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Meningovascular syphilis presents with acute ischemic episodes in brain and spinal cord. Treatment: Crystalline penicillin 24 million units/day IV for 14–21 days, or Procaine penicillin 2.4 million units IM daily plus Probenecid 500 mg qds for 14 days. Later Benzathine penicillin 2.4 million units IM once a week for 3 weeks. If patient allergic to penicillin Tetracycline 500 mg po qds for 30 days or Erythromycin 500 mg po qds for 30 days or Chloramphenicol 1 g IV qds for 6 weeks or Ceftriaxone 2 g IV daily for 14 days. Acute viral encephalitis (VE): Unlike acute viral meningitis, the illness is more severe and prolonged with a significant mortality and high incidence of permanent and disabling sequelae. Etiology: The most frequent agents are mumps, herpes simplex and the arboviruses, and rabies encephalitis. Clinical features: It presents as an acute febrile illness with headache, vomiting and behavioural changes. Meningeal signs may be present. Later, focal neurological deficits, seizures (often as status epilepticus) and coma may ensue. Herpes simplex is the commonest cause of sporadic, focal encephalitis and in addition to above clinical features, patient may have dementia, loss of memory and aphasia. In Japanese B encephalitis, there may be predominantly extrapyramidal involvement. Investigation: (i) CSF: Lymphocytic pleocytosis with elevated protein but normal sugar. In HSV encephalitis fluid may be blood- stained. (ii) MRI scan: Herpes simplex encephalitis mainly involves the temporal lobes which is clearly seen. (iii) EEG is also helpful in diagnosis. Management: Except for HSV infection, there is no specific therapy and treatment is largely symptomatic. For HSV

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276 A Handbook of Emergencies Acyclovir 10–12.5 mg/kg IV q8h by IV infusion over 1 hour, for 10–15 days. For CMV infection Ganciclovir 5 mg/kg IV ql2h, infused over 1 hour may be tried. Amebic meningoencephalitis is due to Naegleria, an amoeba present in warm, fresh water. CSF is purulent and the organism can be identified as mobile large organisms on a wet preparation of fresh CSF. There is no known effective therapy. Subdural empyema is a potentially lethal infection. Causes: Spread of infection from nose and sinuses, skull osteomyelitis, complication of meningitis, following head injury, and rarely hematogenous spread from distant focus. Clinical features: Acute onset with fever, tachycardia, local tenderness over sinuses, headache, vomiting and altered sensorium. Papilloedema and focal neurological signs may occur. Seizures, often focal. A parafalcine involvement may cause paraparesis and sphincter disturbance. Investigation: CT/MRI of head demonstrates the pus. Management: Craniotomy and evacuation of pus along with appropriate antibiotics. Cerebral malaria: See under Tropical diseases.

Acute Neuromuscular Emergencies Acute Guillain-Barr Syndrome Clinical Features Onset is usually preceded by a viral illness of a few days duration. Initially patient may complain of paraesthesiae in feet and hands followed by weakness in the limbs.

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Usually weakness starts in lower limbs, increases in severity over next few days and then ascends up to involve the trunk muscles, upper limbs and, in some cases the neck, face and bulbar muscles with inability to swallow and nasal regurgitation. Respiratory muscle weakness, if not recognised early, can progress rapidly to hypoxia and death. Sensations are usually preserved and deep tendon reflexes are absent. Signs of autonomic dysfunction in the form of sudden bradycardia, tachycardia, hypotension, hyperpyrexia, sweating are seen occasionally and may be the cause of death.

Investigation (a) Urine for porphobilinogen to rule out acute porphyria. (b) Electrophysiological studies. Evidence of demyelinating neuropathy with multifocal conduction block would confirm the diagnosis. (c) CSF: Markedly elevated proteins with few or no cells. (CSF may be normal in early stages). A marked pleocytosis in CSF along with an asymmetric onset should alert the physician to possibility of poliomyelitis which often mimics GBS.

Management General All patients who are in the deteriorating phase must be admitted to ICU and closely monitored. 1. Ryle’s tube for nasogastric feeding if bulbar weakness. 2. Monitoring of respiratory rate, chest expansion, cough reflex and single breath count. If tidal volume falls to about 1000 mL (10–15 mL/kg) then elective intubation is required and artificial respiration started. Clinical signs of mild hypoxia are tachycardia, sweating, sleeplessness and confusion. After 5–7 days on

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278 A Handbook of Emergencies respirator, a tracheostomy should be done and artificial respiration given through the tracheostomy tube. While on the respirator, meticulous care must be taken to prevent bedsores, ensure adequate nutrition and prevent nosocomial infections. 3. Heparin in patients who have no movements in the legs and trunk, prophylactic anticoagulase. Heparin 5000 U bd, SC is indicated to prevent deep vein thrombosis. 4. Faecal impaction is a common problem in these patients who are bedridden and suppositories and enemas may have to be given. Specific Measures 1. Plasma exchange if worsening GBS as it has been shown to hasten recovery. 4 to 5 sessions of plasma exchange over 14 days, at each of which about 50 mL/ kg is exchanged. 2. IV immunoglobulin may be used as an alternative to plasma exchange. Dose 0.4 g/kg/day for 5 days. Note : Both plasma exchange and IV immunoglobulin are found to be equally effective in acute worsening GB syndrome and shorten the recovery time. Steroids have no role to play in acute GBS. 3. Rehabilitation. Patients with GBS may take a long time to recover functionally and may need use of braces and splints.

Myasthenia Gravis Clinical Features Weakness and fatigability with exercise are the hallmarks of generalised myasthenia. Muscles involved include ocular (diplopia and ptosis), neck, jaw, proximal muscles of upper and lower limbs, bulbar and respiratory muscles. There is diurnal variation of weakness, with patients feeling well in the

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morning and progressively deteriorating as the day advances. Course is variable with remissions and exacerbations.

Diagnostic Tests 1. Edrophonium test. Atropine 0.6 mg is given prior to the test. Edrophonium 10 mg is used in the adult. First 2 mg is infused, and patient observed for any muscarinic side-effects. If none, remaining dose is infused over 30 secs. If test is positive, an improvement in power will be noted in few secs., and last 2–20 minutes. 2. Neostigmine test. 1–1.5 mg neostigmine IM after initial atropine. The effect if present will be evident after 15–20 minutes and last 2–3 hours. 3. EMG studies will show significant decremental response on repetitive nerve stimulation. 4. Acetylcholine receptor (Ach-R) antibody assay is present in 50% patients with ocular myasthenia and in 80–90% with generalised myasthenia. 5. Muscle-specific kinase (MUSK) antibodies are detected in some AchR antibody negative myasthenia gravis patients. 6. CT/MRI of chest to rule out thymoma which occurs in 15% myasthenic patients.

Myasthenic Crisis Myasthenic patient may present with acute respiratory distress. Management 1. The patient must be admitted to ICU and intubated, if tidal volume < 1000 mL or signs of hypoxia, it is safer to put him on mechanical ventilation. Most often the crisis is due to exacerbation of muscle weakness, rarely due to the anticholinergic drugs (cholinergic crisis).

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280 A Handbook of Emergencies 2. Plasma exchange is treatment of choice in myasthenic crisis. Usually 4–5 exchanges of 50 mL/kg each. There is usually dramatic response. 3. High dose steroids are started simultaneously. 4. IV immunoglobulin if plasma exchange is not feasible. Dose 0.4 g/kg/day for 5 days. 5. Avoid drugs known to exacerbate myasthenia. Quinine, quinidine, procainamide, propranolol, aminoglycoside antibiotics, fluoroquinolones, polymyxin, morphine, barbiturates. 6. Remission inducing agents in myasthemia gravis include corticosteroids, azathioprine, mycophenolate mofetil. 7. Thymectomy is indicated in patients with thymoma and also in nonthymomatous young patients with generalized myasthenia.

Botulism It is an acute intoxication caused by the exotoxin of Cl. botulinum. The clinical syndrome is acute with rapidly progressive muscle weakness which begins in the extraocular or pharyngeal muscles and becomes generalised. There may be prominent GI symptoms. Pupils are fixed and dilated but patient remains alert.

Management (a) Trivalent antitoxin horse serum 10,000 U IV in one dose. Prior skin testing and precautions for anaphylaxis must be taken. (b) Emetics, cathartics and enemas to eliminate any toxin remaining in GI tract. (c) Guanidine hydrochloride, an acetylcholine agonist may be given 35–40 mg/kg/day orally q4h. (d) Meticulous watch must be kept on respiration. If vital capacity falls below 1000 mL, it is advisable to intubate and give mechanical ventilation.

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Scorpion, snake and insect bites may sometimes produce generalised muscle weakness similar to that in botulism.

Polymyositis It is an inflammatory autoimmune muscle disease which may be idiopathic or associated with occult malignancy or collagen vascular disease.

Clinical Features Usually subacute to chronic course but at times may present acutely with muscle pains and rapidly progressing proximal muscle weakness of limbs along with bulbar and respiratory muscle involvement. It may be associated with erythematous skin rash (dermatomyositis).

Investigation Raised ESR and significantly raised muscle enzymes (OT, PT, CK and LDH). A myopathic EMG with fibrillation in paraspinal muscles, and inflammatory exudate on muscle biopsy.

Management (a) Assess respiratory function and if significantly compromised, need for intubation and mechanical ventilation. (b) Steroids: Prednisolone 60–100 mg/day till clinical improvement. Dose reduced by 5 mg every week. Most patients are maintained on 15–20 mg/day for a long period. Repeated muscle enzyme estimations must be done to monitor activity of the disease. (c) Immunosuppressive therapy if steroids fail or adverse effects. Azathioprine 1.5–2 mg/kg/day orally. (d) Other

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282 A Handbook of Emergencies therapies like plasma exchange, immunoglobulins and methyl prednisolone may be of benefit.

Periodic Paralysis This is an important cause of episodic muscle weakness. There is acute flaccid quadriplegia with sparing of respiratory and bulbar muscles. Any conditions causing hypokalemia may give rise to this syndrome but it also occurs as an autosomal dominant trait. Attacks are usually induced by heavy carbohydrate meal and exercise.

Management of Acute Attack Potassium either orally or IV infusion 40–60 mEq in 500 mL dextrose over several hours. To prevent such attacks, oral potassium supplements, low carbohydrate diet and acetazolamide to cause mild metabolic acidosis may be prescribed. Any acquired cause of hypokalemia to be corrected.

Rhabdomyolysis Muscle cell necrosis on a large scale may release myoglobin and other muscle proteins into the plasma. Major associated conditions include trauma, strenuous exercise, polymyositis, viral myositis, licorice ingestion, hypokalemia, statins.

Clinical Features Patient presents with acute muscle pain, tenderness and swelling. There is also proximal muscle weakness which may rarely lead to respiratory compromise. Acute renal failure may result from clogging of renal tubules with myoglobin. Hyperkalemia may lead to dangerous cardiac arrhythmias.

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Investigation Muscle enzymes markedly elevated.

Management Mainly conservative with bed rest, osmotic diuresis to prevent renal failure and maintenance of electrolytes. Mechanical ventilation if respiratory failure, dialysis if renal failure.

Medical Coma Few problems are more difficult to manage than the unconscious patient because the potential causes of loss of consciousness are considerable and the time for diagnosis and effective intervention is relatively short.

Diagnostic Classification of Medical Coma Coma without focal or localising signs and without meningism 1. Hypoxic-ischemic conditions 2. Metabolic disturbances 3. Intoxications 4. Systemic infections 5. Hyperthermia/hypothermia 6. Epilepsy especially nonconvulsive status epilepticus Coma without focal or lateralising signs but with meningeal irritation 1. Subarachnoid hemorrhage 2. Meningitis 3. Encephalitis Coma with focal brainstem or lateralising signs 1. Cerebral tumor 2. Cerebrovascular disease 3. Cerebral abscess 4. Cerebral infection

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284 A Handbook of Emergencies Note: A comatose patient with no evident signs of trauma may yet be harbouring delayed effects of trauma such as subdural hematoma or meningitis from a basal skull fracture. Hence in medical coma, head injury as the cause must be excluded. Approach to a comatose patient 1. Resuscitation: (a) Establishment of a good airway and care of respiration. (b) If spontaneous respiration is inadequate, intubation and artificial respiration may be necessary. Intubation would also prevent aspiration of vomit. (c) Care of circulation. Insert a large bore IV catheter. Check BP, if hypotension IV fluids and dopamine. (d) Withdraw blood for hemogram, biochemical estimations and toxicology, then give 25–50 mL 50% dextrose; this in a hypoglycemic patient may be life saving. If likelihood of Werincke’s encephalopathy, give thiamine 100 mg IV to prevent acute deficiency from administration of glucose. 2. History: Once patient is stable, obtain as much information as possible from those who accompanied the patient or watched the onset of coma. Circumstances in which consciousness was lost is important, e.g. a history of fever, headache and vomiting of a few days duration may suggest intracranial infection, or a sudden onset of excruciating headache and vomiting followed by unconsciousness may point to a SAH. Important clues in the history are trauma, previous illness, medications, use of drugs or alcohol, and psychiatric disorders. 3. General physical examination: a. Temperature. Combination of fever and coma as a rule indicates systemic infection like pneumonia or septicemia, or a cerebral cause such as meningitis,

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b. c.

d.

e. f.

g.

encephalitis or abscess, or cerebral malaria. Heat stroke may present as a febrile comatose patient, rarely a brainstem or diencephalic lesion may cause hyperthermia. Hypothermia is most commonly seen as a complication of a stroke or an accident in an elderly individual who is dishoused leaving him for hours or days in an underheated room. It may also be seen with barbiturate intoxication, peripheral circulatory failure or profound myxoedema. Heart rate. Irregular heart rate as in atrial fibrillation raises possibility of an embolic stroke. BP. Reactive elevation of BP may occur following a cerebrovascular accident. Hypotension may indicate shock, myocardial infarction, septicemia, intoxication or Addison’s disease. Skin. Look for evidence of trauma, stigmata of liver disease, needle marks, anemia and infective or embolic phenomena. An exanthema may mean a viral infection causing meningoencephalitis or meningococcal septicemia. Hypopigmentation is suspicious of Addison’s disease. Breath. Odour of breath may suggest alcoholic intoxication, diabetes, uremia or hepatic failure. Head. (i) Neck stiffness may indicate infection, trauma or SAH. Do not manipulate the neck if suspicion of cervical spine fracture. (ii) Battle’s sign (hematoma over mastoid process), or bleed from nose or ears suggest basal skull fracture. Others. Chest, abdomen, heart and extremities must be examined routinely. Also rectal and pelvic examination and stool test for blood.

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Neurological Examination 1. Level of consciousness Glasgow coma scale Indication Response Score Eye opening Spontaneous 4 To speech stimulus 3 To pain stimulus 2 None 1 Motor response Obeys 6 (best limb) Localizes 5 Withdraws 4 Abnormal flexion 3 Extensor response 2 None 1 Verbal response Orientated 5 Confused conversations 4 Inappropriate words 3 Incomprehensible sounds 2 None 1 Glasgow coma score (total) 3–15 2. Pupillary reactions (a) Unilateral fixed dilated pupil suggests temporal lobe herniation or a posterior communicating artery aneurysm. Ptosis may also be present. Midbrain lesions typically cause loss of light reflex with midposition pupils. Pontine lesions result in pinpoint pupils which react to light. (b) Bilateral fixed pupils indicate central diencephalic herniation. 3. Corneal response. Corneal reflex is usually retained until deep coma. Loss of corneal response, when drug overdosage is excluded is a poor prognostic sign. 4. Spontaneous eye movement. (a) Conjugate deviation of the eyes implies unilateral hemispheric or contralateral brainstem lesion. (b) Roving eye movements are usually

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seen in light coma. (c) Ocular bobbing, an intermittent jerky downward movement of eyes in brainstem lesions, cerebellar hematoma or hydrocephalus. (d) Dysconjugate eye movement may occur if damage to oculomotor or abducent nerves. 5. Reflex eye movement. (a) Oculocephalic (doll’s eye response) is tested by rotating patient’s head from side to side and observing the eyes. In coma with an intact brainstem, the eyes will move conjugately and in direction opposite to the head movement. This response is lost in brainstem damage and there is no movement of the eyes when the head is turned. In a conscious individual this response is suppressed and hence doll’s eye movements cannot be tested. (c) Ice water caloric test (oculovestibular response) tests the integrity of the vestibulo-ocular reflex. The head is positioned at 30º with respect to the horizontal. 30 mL of ice water is instilled into external auditory canal of one ear, and after 3–5 minutes into opposite ear. In a conscious patient, there is nystagmus with the slow phase towards the irrigated ear (brainstem), and a fast, corrective phase in opposite direction (hemisphere). In a comatose patient with intact brainstem, there is a tonic conjugate movement of the eye towards the stimulated side. A dysconjugate or no response at all indicates brainstem damage. This test is also a way of identifying individuals in psychogenic coma who will show normal nystagmus and often be distressed by the manoeuvre. Fundus. Papilledema would suggest raised ICP, a subhyaloid hemorrhage SAH.

Investigations 1. Blood. In patient without focal or meningeal signs, metabolic or hypoxic causes are likely. Hepatic failure,

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288 A Handbook of Emergencies renal failure, hypoglycemia, hyperglycemia and disturbances of electrolytes or acidosis should be ruled out. If drug overdosage is likely, blood should be sent to toxicologic laboratory. Blood alcohol levels may also help. Possibility of CO poisoning can be excluded by measurement of carboxyhemoglobin. 2. CT scan of head in presence of focal signs to define a structural abnormality if present and in many cases to define the etiology. 3. Lumbar puncture to rule out infective cause or SAH. A prior CT scan is advisable to exclude a space occupying lesion. Also if it shows clear evidence of subarachnoid bleed, LP may not be necessary. 4. EEG has major role in identifying patients who are in subclinical status epilepticus or have complex partial status because this will significantly alter their outcome.

Management General nursing care of the comatose patient. 1. Circulation. Fluids to maintain BP at sufficient levels to ensure adequate cerebral and renal perfusion. 2. Ventilation. (a) Adequate oxygenation and prevention of infection. Remove dentures. (b) Insert and tape a short airway to prevent the tongue from obstructing airflow. (c) Prevent aspiration by suction of secretions. (d) If ventilation is unsatisfactory or secretions uncontrollable, insert a cuffed endotracheal tube. If intubation is necessary for longer than 7 days, consider tracheostomy. (e) Obtain arterial blood gases as often as necessary to ensure that ventilation is adequate. 3. Skin. The position of the patient should be changed every 1–2 hours. Bony prominences should be padded to prevent bedsores.

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4. Nutrition. Initially by IV solution. Later tube feeding with vitamin supplements. 5. Bowel care. Enema if constipation. Keep a watch for ‘pseudo-diarrhoea’ due to faecal impaction. If necessary manual evacuation of faeces. 6. Bladder care. A condom catheter for male patients. If indwelling catheter becomes necessary, it should be clamped intermittently to maintain bladder tone. 7. Eyes. Avoid corneal injury by taping the eyelids closed and put ointment or drops.

Severe Head Injury Common causes. In adults automobile and work related accidents, in children falls and accidents at play.

Classification 1. Primary brain injury (diffuse axonal injury) due to initial insult. 2. Secondary brain injury compounds primary injury and may be due to intracranial complications (e.g. haematoma, brain oedema, CNS infection), or extracranial complications (pneumonia, pulmonary embolism and haemodynamic instability).

Management of Head Injury A. Immediate medical management should begin with a well trained emergency medical team that is responsible for transporting severely injured patients. All precautions especially immobilization must be taken whenever the patient is moved. 1. Adequate airway is the first priority. Patient who is deteriorating or unresponsive will need to be intubated. When in doubt it is best to intubate the patient.

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290 A Handbook of Emergencies 2. Mechanical ventilation if spontaneous breathing is irregular or arterial blood gases show hypoxia or hypercarbia. Mechanical hyperventilation, by reducing PaCO2 would also lower raised ICP. 3. Circulation. Replacement of blood volume and maintenance of BP. If a peripheral vein is not easily placed, a subclavian or jugular vein catheter is placed or expeditious cutdown performed. Packed RBCs if significant blood loss. The haematocrit should be kept at more than 30% for neuronal oxygenation. Presence of haemorrhagic shock usually suggests an associated injury with blood loss into chest, abdomen or pelvis. Possible site of such a bleed should be identified as soon as possible. B. History. The ambulance team may provide information about the accident. Occasionally, a neurologic event like a seizure, stroke or SAH may be witnessed to precede an accident. C. Neurologic examination 1. Glasgow coma scale (see coma). 2. Detailed neurologic examination as in coma. 3. Herniation syndromes when attributable to a discrete mass lesion, they represent a true neurological emergency. Each syndrome can be associated with systemic hypertension, bradycardia and irregular respirations. 4. Spinal cord injury. In severe head injury, lateral X-rays of cervical spine are taken and if there is evidence of fracture dislocation, the neck should be immobilised. Signs of cervical compression should be looked for. 5. Skull fractures. ‘Racoon eyes’ and CSF rhinorrhoea suggest fracture through anterior cranial fossa, and bluish discoloration over mastoid and CSF

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rhinorrhoea with often loss of smell posterior cranial fossa fracture. 6. Traumatic carotid and vertebral artery dissection. With carotid artery clinical presentation may be that of an acute ‘carotid’ stroke with ipsilateral Horner’s syndrome. Vertebral artery injury causes brainstem stroke. DSA or MRI angio will be needed to diagnose the dissection. 7. Injury list. A list of definite and possible injuries should be made with the most serious injury at the top. Patient should generally be placed under the specialist treating the most threatening organ injury.

Investigations CT scan for diagnosis of: (a) Intracranial haematomas. (b) Contusions. (c) Raised ICP. (d) Intracranial air indicates sinus injury, penetrating wound or compound fracture. FBs should be noted. MRI scan is inferior to CT scan in acute setting. Surgical management: Acute subdural or extradural haematomas : Surgical evacuation. Intracerebral haematomas (haemorrhage within brain substance) can be managed conservatively, but if it is surgically accessible and patient deteriorates then surgical evacuation. Intraventricular haematoma usually get absorbed, but if acute hydrocephalus develops (due to blockage of CSF pathway), ventricular drainage of CSF. Medical management: General measures similar to that of a comatose patient once surgical lesion is excluded. Raised ICP. Most patients with severe head injury have elevated ICP. Measures to lower it are—elevation of head end of bed, mechanical hyperventilation, cerebral decongestants (mannitol, glycerol), frusemide. In very severe cases surgical decompression of the brain may

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292 A Handbook of Emergencies be attempted. Steroids are not indicated in acute head injury. In fact they have been shown to worsen outcome. Prophylactic anti-epileptic drugs as seizures in such patients could prove fatal. Leakage of CSF is a common complication of basilar skull fracture. It often stops spontaneously. If it does not, continuous lumbar drainage may decrease the pressure sufficiently to allow the tear to seal. If this fails surgical repair of the dural tear. Persistent CSF leak is a common cause of meningitis.

Acute Spinal Cord Disturbance (Myelopathy) Acute myelopathy is a neurological emergency with a sudden onset of motor, sensory and sphincter changes. Prognosis depends on severity and duration of the deficit at time of diagnosis.

Classification I. Compressive myelopathies account for majority of cases. Spinal cord trauma Rupture of intervertebral disc Extradural absecess Haematomyelia II. Non-compressive myelopathies 1. Infective myelitis: Viral, tuberculous, fungal, syphilitic. 2. Demyelination: Multiple sclerosis (MS), post viral or post vaccinal demyelination. 3. Nutritional myelopathies: Subacute combined degeneration, pellagra. 4. Toxic myelopathies: Lathyrism; subacute myelooptic neuropathy (SMON) due to long-standing ingestion of clioquinol, alcohol. 5. Spinal cord infarction. 6. Eales disease with myelopathy.

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Investigations 1. Haematological: Investigations for megaloblastic anemia including MCV, elevated LDH and presence of macrocytes in peripheral smear and megaloblasts on bone marrow examination. B12 and folate levels. 2. Plain X-ray of cervical and dorsal spine may be helpful in some cases. Atlantoaxial dislocation, Pott’s spine and metastatic bone disease are well seen. 3. MRI scan for diagnosing spinal cord compression and demyelinating lesions. 4. Myelogram if MRI not feasible, to rule out extrinsic spinal cord compression. CT myelogram is a sensitive means of detection of spinal cord pathology. 5. CSF. Xanthochromic with elevated protein in cord compression. In MS and other demyelinating myelopathies, CSF proteins elevated with increased IgG and presence of oligoclonal bands in MS. VDRL positive in neurosyphilis. 6. Evoked potentials : Visual, auditory and somatosensory evoked potentials to rule out multiple sclerosis.

Management Trauma. Fracture dislocation of cervical spine can give rise to complete paraplegia. Often there is complete transection of spinal cord with spinal shock below level of lesion. If significant cord compression by bone fragments, early surgical decompression, correction of bony displacements, removal of herniated disc tissue and fixation of spine by bone graft or wiring. If no significant demonstrable compression, traction and immobilization till skeletal immobility is obtained and then rehabilitation. Extradural abscess. After initial period of fever, backache and radicular pain, there is rapidly progressive paraparesis

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294 A Handbook of Emergencies with sensory loss in lower parts of the body and urine and stool retention. CSF contains small number of WBCs (both neutrophils and lymphocytes) unless the needle penetrates the abscess, when pure pus is obtained. Treatment is immediate laminectomy and surgical drainage to prevent irreversible cord damage. Antibiotics to be given simultaneously. Disc herniation. Rupture of disc occurs at cervical and lumbar levels, less commonly at dorsal cord level. If there is central herniation cord compression results. Surgery with removal of herniated disc tissue should be undertaken as early as possible. Myelitis. Specific treatment for syphilis, tuberculosis and parasitic infection. In demyelinating myelopathy steroids, e.g. Methyl prednisolone 0.5–1 g/day IV for 3–5 days followed by 3–4 weeks of tapering doses of oral steroid. Vitamin B12. In case of suspected vitamin B12 deficiency, injections of vitamin B12 500–1000 µg/day 3–4 times per week for few months. General measures for paraplegia. Prevention of bed sores, frequent change of position, passive physiotherapy for lower limbs, care of skin, bladder and bowels. Intermittent catheterization if upper limbs are normal. Dr. Jimmy A. Lalkaka M.D., D.M. (Neuro)

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Anemia Causes 1. Severe nutritional deficiency (Fe, B12, Folic acid) which has remained unattended for a long time. 2. Acute blood loss (accidental, surgical or spontaneous from diseases like ulcer, malignancy etc.). 3. Primary blood diseases— aplastic or haemolytic anaemia, thalassemias, sickle cell anaemia, PNH, hereditary enzyme defects (G6PD deficiency). Acquired autoimmune haemolytic anaemia; acute leukemia. 4. Acute renal or liver failure.

Clinical Features Breathlessness, palpitations, syncope, signs of congestive cardiac failure. In addition signs of chronic anaemia like pallor, paraesthesia, fatigue, weakness, oedema, glossitis, menstrual disturbances in females, signs of causative disorder.

Management Emergency treatment as necessary in cases having symptoms of cardiac or cerebral anoxia. Otherwise investigate and treat the cause of anaemia.

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296 A Handbook of Emergencies I. Transfusion therapy 1. Packed cell transfusion: For patients with CHF first treat cardiac failure and then give packed cells. Packed cell transfusion is given to bring the Hb level to such a stage that patient is out of danger of developing anoxia or CHF. Hb level is preferably brought upto 8–10 g%. It can be given as 2–4 packed cells per day till the Hb is brought to the desired level, care being taken not to overload the circulation particularly in cases of anaemia of long duration. One transfusion of packed cells will raise the Hb by 0.8 to 1.0 gm% depending upon the patient’s blood volume and Hb content of transfused blood. First transfusion should be started at a slow rate of 75 mL/h or about 15 drops/min and subsequently the rate can be doubled if there are no untoward signs of circulatory overload. If symptoms of cardiac or cerebral anoxia, e.g. anginal pains, insomnia are present, immediate packed red cells transfusion 300–450 mL. In a young patient with otherwise healthy heart, rate of transfusion can be 4–6 mL/min. In elderly patients with suspected ischaemic heart disease transfusion rate should be 1–2 mL/min. Such patients may also be given 20–40 mg frusemide IV before starting the transfusion. 300 mL of packed cells would raise the hemoglobin level by about 1 to 1.5 g%. Oxygen therapy would be helpful. 2. Fresh frozen plasma (FFP): This is indicated when anaemia is due to a congenital or acquired bleeding disorder due to deficiency of clotting factors. 3. Platelet concentrates: When platelet count is 1000/mL for 3 consecutive days or maximum for 7 days. 3. Immunosuppressive therapy is effective in producing remission. Antithymocyte globulin (ATG) or antilymphocyte globulin (ALG) IV into central vein 15 mg/kg/day over 12–16 hours for 5 days. Fever, rigor and rashes are common side-effects during first

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2 days. Addition of cyclosporin to ALG may increase likelihood of remission. Steroids are usually given with ALG/ATG. 4. Stem cell transplantation is treatment of choice for curing the disease; results are best seen in children and young adults.

Neutropenia (Agranulocytosis) Neutropenia suggest a neutrophil count of 6 mEq/L or associated with ECG changes. (a) Calcium gluconate 10%, 10 mL slow IV. (b) Sodium bicarbonate 7.5%, 50–100 mL slow IV. (c) 16U plain insulin in 100 cc 25% dextrose over 4–6 hours. (d) Polystyrene sulfonate resin 15 g qds orally or 30 g as retention enema is used for milder cases. 8. General care: (a) antacid and ranitidine prevent stress ulcers. (b) Bedsore prevention and mouth toilet

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340 A Handbook of Emergencies for immobile patients. (c) Nystatin mouthwash or swallows prevent fungal infection. (d) Antibiotics if indicated. 9. Specific treatment of the underlying etiology along with treatment of ARF is mandatory. 10. Dialysis used as a temporary supportive measure till kidneys recover if: (a) Uncontrolled hyperkalemia, (b) Severe acidosis, (c) Severe fluid retention or pulmonary edema, (d) Rapidly rising creatinine. Revised by Dr Percy Chibber

MS FCPS FRCS MNAMS (Urology)

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Malaria Morbidity and mortality from malaria are increasing owing to the increasing drug resistance and lack of effective methods to control prevalence in those areas where transmission is most intense. The infection can pose different problems depending on the species of the parasite. Falciparum malaria in an adult is a multisystem disorder. A thick blood film establishes the diagnosis.

Manifestations of Complicated, Severe Malaria 1. Encephalopathy: Altered consciousness, coma, convulsions (cerebral malaria). Coma may be moderate or profound, and may be accompanied by hypertonicity, opisthotonus, conjugate deviation of gaze, or by generalized hypotonia. Convulsions may be focal or generalized, brief or protracted. 2. Acute renal failure is caused by acute tubular necrosis, and is therefore reversible if patient can be kept alive. 3. Severe anaemia may be present at time of diagnosis, or may develop rapidly during early stages of treatment. 4. Adult respiratory distress syndrome has a poor prognosis.

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342 A Handbook of Emergencies 5. Pulmonary oedema is usually caused by excessive fluid input in a patient with renal impairment or failure. 6. Hyperlacticacidemia is caused by impaired tissue perfusion in tissues occupied by sequestered parasites, and is exacerbated by dehydration and hypoglycemia. 7. Hypoglycemia occurs especially in pregnancy. It is caused by impaired hepatic gluconeogenesis. It may also result from quinine therapy, when the stimulatory effect of the drug on pancreatic beta cells raises plasma insulin concentration. 8. Intravascular hemolysis leads to hemoglobinemia and hemoglobinuria. 9. Jaundice, which is seldom deep, is a combination of hemolysis and impaired hepatic function. 10. Disseminate intravascular coagulation is occasionally severe enough to cause overt bleeding. 11. Shock may be a feature of severe anemia. In individuals with indwelling venous or urethral catheters it may be caused or accompanied by bacteremia. 12. High fever and hyperpyrexia.

Management 1. Hospitalization in ICU. 2. Pass nasogastric tube if patient semiconscious or in coma. 3. Fluids IV according to urine output and JVP. Excess of fluids should be avoided because of danger of pulmonary oedema. 4. Antimalarial drugs (i) Artesunate monotherapy 4 mg/ kg loading dose on first day followed by 2 mg/kg od × 6 days. Severe malaria 2.4 mg/kg IM, followed by 1.2 mg/kg at 12 and 24 h daily, then 1.2 mg/kg daily for 6 day; or 2.4 mg/kg IV on first day followed by 1.2 mg/kg daily until patient can take orally or another effective

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antimalarial drug. (ii) Artemether—Severe malaria 3.2 mg/kg IM as loading dose on first day followed by 1.6 mg/kg daily for minimum of 3 days until patient can take oral therapy to complete a 7 day course. (iii) Artemether (120 mg) and lumefantrine (120 mg). Dose: Standard 3 days treatment schedule with total of 6 doses as follows 4 tablets as a single dose at time of diagnosis, again 4 tablets after 8 hours and then 4 tablets bd for 2 days (total 24 tablets). (iv) Quinine sulphate 20 mg/kg in 5% saline as IV infusion over 4 hours till parasites clear, then 8 hourly till patient can takes oral medication. (v) Arterolane maleate 150 mg and piperaquine phosphate 750 mg one tablet daily for 3 days.

Management of Complications a. ARF: Fluid restriction, reduction of maintenance dose of antimalarial drug by one-third, and daily measurements of creatinine and electrolytes. Peritoneal dialysis or hemodialysis. b. Anemia: Blood transfusion. Exchange transfusion using packed cells may be required. c. Hypotension and shock: Volume replacement and dopamine. d. Hpoglycemia: 5–10% dextrose IV. e. Convulsions: Diazepam. f. Hyperpyrexia: Tepid water or alcohol sponging, covering with wet sheet and fanning, paracetamol. g. Pulmonary oedema: Oxygen, frusemide IV and positive pressure ventilation. h. ARDS or shock: Ventilatory support. i. Associated bacterial infection: Pneumonia, gramnegative bacteremia, urinary infection. Treatment with appropriate antibiotics.

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344 A Handbook of Emergencies j. Coagulopathy: Fresh frozen plasma, or platelet infusion. DIC may be caused by gram-negative sepsis which should be covered by antibiotics. Management of malaria in pregnancy: High degrees of pyrexia can initiate premature labour, hence temperature must be lowered promptly. Chloroquine can be prescribed. Quinine is safe and in the usual dosage does not produce uterine stimulation. Arterolane 150 mg and piperaquine phosphate 750 mg tablet one od × 3 days is safe and clears parasitemia more effectively than quinine. Exchange transfusion if heavy parasitemia (>20% parasitized cells). It also allows replacement of RBCs and clotting factors without volume overload.

Typhoid Fever Salmonella infection can cause typhoid (and paratyphoid) fevers, a bacteremic illness with systemic manifestations. Fulminant states may be due to heavy infection or delayed diagnosis.

Clinical Features Clinical features are those of septicemic state. Patient is toxic with high fever and a delirious confusional state sets in. Marked abdominal distension with ‘pea soup’ stools. Hemorrhage and perforation are likely to occur. Toxic myocarditis is another serious complication. Hypotension, shock, a persistent lactic acidosis and acute kidney failure may result in death.

Diagnosis S. typhosus can be grown by blood or bone marrow culture. Blood culture is the usual diagnostic method. Widal test lacks specificity and sensitivity.

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Management (1) Hospitalization. (2) Correction of dehydration with IV fluids. (3) Inotropic support. (4) Antibiotics—Ofloxacin 500 mg bd for 10 days and/or ceftriaxone 2 g IV daily for 10 days. Chloramphenicol 500 mg IV q6h, then 500 mg q8h for 10 days may be tried. Levofloxacin 250 gm bd PO, cefotaxime 500 mg IM bd.

Fulminant Amebic Infection Amoebiasis is a common infection of the GI tract. Manifestations which present as emergencies are severe acute amoebic dysentery and liver abscess or abscesses from blood-borne dissemination of amoebae. Fulminating amoebic colitis is characterised by numerous bloody stools (20 or more/day), generalised abdominal discomfort, colicky pain preceding evacuation, and rectal tenesmus, which tends to be constant and intense. Advanced lesions may cause GI hemorrhage or perforation with peritonitis. Fulminating amoebic colitis may be encountered in pregnancy, malnourished, immunocompromised individuals and those receiving corticosteroids for erroneous diagnosis of ulcerative colitis. Amebomas usually have an acute evolution with bloody diarrhoea or dysentery of moderate severity, abdominal pain and a palpable mass in the colonic area. Acute appendicitis has clinical features similar to those of bacterial appendicitis, but in many cases, there is no involvement of the caecum, giving rise to bloodstained diarrhoea.

Diagnosis (a) Stools may reveal trophozoites with ingested RBCs. (b) Rectosigmoidoscopy and immediate microscopic

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346 A Handbook of Emergencies examination of rectal smears will reveal presence of motile, haematophagus trophozoites. (c) Serology—Anti-amoebic antibodies can be detected in more than 75% of patients with colonic invasive amoebiasis.

Management (a) Correction of dehydration. (b) Metronidazole 500 mg IV q8h for 10 days. (c) Tetracycline 250 mg qds for 10 days. Fulminating colitis and amoebic appendicitis require surgical treatment in addition to chemotherapy. In fulminating colitis, only partial or complete resection of the colon offers some hope of recovery. Amebic liver abscess is more common in adult males excessive alcohol and malnutrition are predisposing factors. The abscess is usually single, and the most common location right lobe of the liver.

CIinical Features In most patients there is an abrupt onset with pain in the region of the liver, which is intense and constant, and radiates to the scapular region and right shoulder. Local oedema of chest and abdominal wall and signs of effusion nay be detected. Fever is common. Nausea and vomiting may occur.

Complications Liver abscesses may heal following, adequate chemotherapy, increase in size, rupture or disseminate. Rupture may occur into—(a) Peritoneum presenting as acute abdomen. (b) Pericardium. A left lobe abscess may extend into the pericardium. (c) Into pleural space causing empyema, or into lung giving rise to lung abscess. (d) Retroperitoneal into posterior abdominal wall with swelling over kidney region. (e) Right paracolic gutter with tenderness in right iliac fossa. (f) Into subphrenic space giving rise to subphrenic abscess.

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Diagnosis (a) Imaging—CXR, ultrasound or CT scan of abdomen. (b) Serology—Anti-amoebic antibodies can be detected in serum of 95% of patients.

Management 1. Chemotherapy: Metronidazole or tinidazole as for amoebic dysentery. 2. Percutaneous aspiration: Preferably under CT guide. Indications—Left lobe abscess, massive abscess, a palpable mass, persistent localized tenderness, markedly raised hemidiaphragm, pleuritic pain suggesting an impending leak, failure of symptoms to remit on drug therapy. Technique: The needle is introduced into area of maximum tenderness or into 8th or 9th intercostal space in midaxillary line. All available pus should be removed. If abscess is on lower surface of left lobe, aspiration should be performed through an open abdomen. If perforation—Gastric suction, IV fluids, and electrolytes together with ceftriaxone 1g daily and metronidazole IV. Surgery should be avoided.

Acute Bacillary Dysentery The passage of blood and pus cells associated with infective diarrhoea constitutes acute dysentery. Infection with species of Shigella. Sh. dysenteriae can produce fulminating illness.

Clinical Features In more severe forms of the disease, there is acute phase response with high fever, anorexia, headache and malaise with frequent passage of small volumes of stool, progressing to passage of frank blood and pus.

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Complications (1) Bacteremia can occur in immunocompromised subject. (2) Hemolytic-uremic syndrome consisting of microangiopathic hemolytic anemia, thrombocytopenia and renal failure.

Diagnosis It is made by isolating the organism from the stool using a selective medium.

Management (a) Hospitalization. (b) IV fluids and electrolytes to correct dehydration. (c) Antibiotics—ciprofloxacin 500 mg qds and co-trimoxazole 2 tablets bd. Antimotility drugs should be avoided.

Cholera Cholera is usually the result of infection with strains of Vibrio cholerae. Infection is confined exclusively to the lumen of GI tract where a powerful enterotoxin is formed, which stimulates secretion of isotonic fluid. Morbidity and mortality of the disease is attributable to the consequences of dehydration.

Clinical Features Watery diarrhoea starts abruptly and soon the stools acquire a ‘rice water’ appearance. Vomiting is common. Within a few hours the patient becomes rapidly dehydrated. A state of shock may ensue. Fever is uncommon, but severe muscle cramps do occur.

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Diagnosis Bacterial confirmation is not necessary during epidemics. V. cholerae can be cultured from stool or rectal swab.

Management 1. Management of diarrhoea: A cholera bed can be fashioned from a canvas stretcher by cutting in the centre a hole through which liquid stool drains directly into a bucket beneath. Thus, fluid losses can be easily measured, or use of bedpan, or absorbent pads if stools numerous. 2. Oral rehydration solution: Constituents (g/L) Sodium chloride 3.5 Sodium bicarbonate 2.5 Potassium chloride 1.5 Glucose 2.0 Small volumes of ORS should be given frequently with cup or glass or if necessary through nasogastric tube. If the above salts are not available, an appropriate solution can be prepared by mixing 5 g of household salt with 40 g sucrose (or 20 g glucose) in 1 litre of water. Depending on the amount or extent of dehydration and ongoing losses, pts may require 100–300 mL/kg/day. 3. IV rehydration should be reserved for those who are much dehydrated, shocked or vomiting so severely that oral rehydration is impossible. Solution containing sodium chloride 5 g, sodium bicarbonate 4 g and potassium chloride 1 g in distilled water. Or 2 litres of isotonic saline can be alternated with 500 mL 1/6 molar sodium lactate or isotonic sodium bicarbonate.

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Access to circulation may be difficult to maintain in shocked, dehydrated patients, and central venous cannulation may be necessary. Sometimes even this is not possible, alternative approaches such as intraperitoneal or subcutaneous infusion may be required. Initial infusion should be rapid until pulse and BP have been restored. 4. Antibiotics: One of the following can be prescribed— (a) Tetracycline 50 mg/kg/day in 4 divided doses for 3 days. (b) Ampicillin 500 mg q6h can be given IV. Appropriate drug in pregnancy. (c) Doxycycline 300 mg as single dose. (d) Ciprofloxacin 500 mg bd for 5 days.

Acute Gastroenteritis (Food Poisoning) Severe food or water-borne infection may present as an urgency. 1. Acute staphylococcal food poisoning occurs after ingestion of food which has been improperly cooked or stored. Although it may be severe and prostrating, it is usually short-lived. 2. Salmonellae food poisoning comes from ingestion of food (e.g. meat, eggs) or dairy products. Host factors (extremes of age, debilitating disease, immunosuppression, gastric hypoacidity), increase susceptibility to severe illness and bacteremia. 3. Seafood poisoning results from algae-produced toxins and also from poisoning caused by eating contaminated fish or prawns. Without emergency treatment, the victim can suffer respiratory failure.

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Clinical Features Acute enterocolitis manifests itself in severe illness as passage of voluminous, watery stools every half hour or more frequently leading to rapid dehydration and renal insufficiency. The illness begins with nausea and vomiting, abdominal cramps often with vomiting, chills and fever. Later the volume may decrease and blood and mucus appear. Abdominal tenderness is common.

Management (a) IV fluids and electrolytes. (b) Antibiotics—Ciprofloxacin 500 mg bd PO or 200 mg IV for 5 days. Campylobacter enterocolitis: Infection occurs by consumption of contaminated beef, under cooked poultry, or milk.

Clinical Features Typical symptoms begin with headache, malaise, backache, myalgia and pyrexia of about to 40°C. A few hours later severe abdominal cramps and diarrhoea begin. The stools may be loose or watery or mainly bloody. Nausea is common but vomiting rare.

Diagnosis Isolation of the organism from stool. Blood culture may be positive in the immunocompromised host.

Management (1) Fluid and electrolyte replacement. (2) Antibiotics— Ofloxacin 400 mg q6h or Ciprofloxacin 500 mg BD.

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Clostridium Difficile Infection Risk factors: Gastric acid suppression with proton pump inhibitors, enteral feeding, GI surgery, cancer chemotherapy, immunosuppression with corticosteroids and haemopoietic stem cell transplantation.

Diagnosis (a) Presence of diarrhoea—Passage of 3 or more stools in 24 hours or fewer consecutive hours. (b) Stool test positive for presence of toxigenic C.difficile or its toxins or colonoscopic or histopathologic findings demonstrating pseudomembranous colitis.

Treatment (i) Oral rehydration therapy. (ii) Single dose octreotide 100 mg stat as antisecretory agent together with antibiotics.

Tetanus Tetanus is caused by a powerful neurotoxin produced by strains of Clostridium tetani when introduced into the tissues. Portals of entry are contamination of wounds by manure or rusty instruments, bums, otitis media, septic abortions, child birth, surgery, animal bites and stings.

Clinical Features 1. Rigidity: Spasm of masseters produces lock jaw (trismus) and of face muscles, risus sardonicus. Spasm of erector spinae and of abdominal muscle gives rise to exaggerated lumbar lordosis, neck retraction and abdominal rigidity. 2. Muscle spasms occur in severe tetanus. Seizures can be induced by external stimuli. Spontaneous seizures

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may result in continuous convulsive state. Spasm of pharynx causes dysphagia and of larynx can lead to asphyxia. Patient may be hypoxic and cyanosed due to spasm of respiratory ms. 3. Symptoms due to sympathetic overactivity: Tachycardia, cardiac arrhythmias, fluctuating BP, fever, excessive sweating and salivation. Features of fulminant tetanus are generalised spasticity with prolonged spasms, tachypnoea (>40 breaths/ min), apnoeic spells, marked tachycardia and severe hypertension and tachycardia alternating with bradycardia and hypotension, or severe persistent hypertension or hypotension.

Complications 1. Respiratory: (a) Bronchopneumonia can result from aspiration of stomach contents, blockage of airways by sticky secretions and lung collapse. (b) Asphyxia. (c) Respiratory fixation—Chest fixation in which general hypertonicity involves pectoral, intercostal and ms of abdominal wall reducing vital capacity markedly. 2. Due to spasms: Muscle tear and wedge fracture of thoracic vertebrae. 3. Autonomic instability: Death may occur from ventricular arrhythmia or from profound shock. 4. Miscellaneous: Hyperpyrexia, dehydration, paralytic ileus, development of catabolic state and adverse effects of drugs.

Management 1. Admission into ICU. 2. Mechanical support if neuromuscular blockade is required to control muscle spasms and impaired respiration. If hyperventilation occurs danger of

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354 A Handbook of Emergencies aspiration secondary to gastric tube feeding. Bladder catheterization if urinary retention, frequent turning and chest physiotherapy. 3. Wound care: Thorough debridement especially if deep puncture wound. 4. Antitoxin to neutralise-free toxin for adults human tetanus immunoglobulin 3000 units IM given at separate sites. If horse serum tetanus antitoxin has to be used dose’s 50,000 U IM or IV (risk of serum sickness). 5. Sedatives and muscle relaxants: Diazepam dose depends on severity. In a severe case 10–20 mg IV q3h. For less severe cases 5–10 mg PO 92 hours. Midazolam. Adults 0.1–0.3 mg/kg in IV infusion is preferred for prolonged therapy. 6. Antibiotics : Doxycycline 100 mg PO BD and metronidazole 500 mg PO q8h. 7. Tracheostomy and ventilation should be undertaken early in patients whose disease is not controlled with conservative sedative regimen, because inadequate control of muscle spasms results in asphyxia and depression of swallowing reflex. 8. Induced neuromuscular paralysis: Pancuronium 2–4 mg every 1/2-1 hr by bolus IV injection or continuous IV infusion to have a well-regulated subtotal paralysis for efficient ventilatory support. 9. Management of autonomic circulatory disturbances: (a) Hypotensive spells—Volume load or if ineffective dopamine. (b) Hypertensive spells (Refer). (c) Bradycardia—IV atropine. (d) Sustained tachycardia— Verapamil 40 mg TDS PO. 10. Nutrition: Adequate calories with 75–100 g protein through nasogastric tube.

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11. Care of the wound: Removal of foreign material and debridement of non-viable tissue of entry wound. Tetanus toxoid injection. Other clinical types which can be severe are: (a) Cephalic tetanus results from injuries to head and neck and infections of eye and orbit. One or more cranial nerves mostly Vth may be involved with spasm and paralysis of muscles they supply. Cephalic tetanus can evolve into generalised form. (b) Neonatal tetanus due to sepsis of the umbilical stump carries a high mortality. Typically the week-old infant presents with inability to suck because of spasm of facial, pharyngeal muscles, or with generalised convulsions. Crying is hoarse and the face screwed up. Cyanosis and apnoea accompany the more severe spasms.

Leptospirosis Infected rodents are typically the source of human infection which are most commonly due to contact with water or environmental surface contaminated with infected urine. Risk of leptospirosis is especially during rainy season.

Clinical Features 1. Anicteric leprospirosis: (a) Septicemic stage: Abrupt onset of fever, chills and rigors, persistent headache, photophobia, conjunctival suffusion, cough, etc. (b) Immune stage: Most of the symptoms return after 1–3 days period of minimal symptoms but are decreased. In addition, aseptic meningitis is the hallmark of the immune stage. 2. Icteric leptospirosis (Weil’s syndrome): Liver enlarged and tender with increasing severity of jaundice, the

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356 A Handbook of Emergencies patient is at greater risk of developing renal failure, hemorrhage and cardiovascular collapse.

Diagnosis Isolation of the pathogenic leptospira is the only definite proof of infection, though serological methods can be used.

Management (a) Hospitalization in ICU in patients with severe infection and Weil’s disease. (b) Antibiotics—Ampicillin 500–1000 mg IV q6h. In less severe cases, amoxycillin 500 mg PO q6h for 5–7 days or doxycycline 100 mg PO BD. (c) Doxycycline if penicillin allergy 200 mg PO qds or tetracycline 500 mg initial, then 250 mg qds × 6d or ceftriaxone 1 g od × 7d.

Dengue Diagnostic Criteria Dengue hemorrhagic fever 1. Fever for 2 or more days. 2. Thrombocytopenia (5 days. 2. Intractable pain. 3. Postural dizziness, cold extremities. 4. Decreased urine output. 5. Incessant vomiting. All patients must be assessed for dehydration and proper rehydration therapy (preferably oral) to be started quickly. Severe dehydration is characterized by two of the following: zz Abnormal sensorium, excessive sleepiness or lethargy zz Sunken eyes zz Poor fluid intake zz Dry parched tongue zz Reduced skin turgor (very slow skin pinch taking 2 sec to retract).

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Effects of Heat Clinical manifestations needing emergency attention: 1. Heat syncope: A fainting spell or ‘blackout’ from excessive heat and humidity. The individual drops to the floor if standing and there is transient loss of consciousness. Treatment: Laying down the person flat in cool surroundings is followed by quick recovery. 2. Heat stroke (Sunstroke, heat hyperpyrexia) is characterised by sudden loss of consciousness which may be preceded by prodromal signs of cerebral irritation namely headache, dizziness, nausea, convulsions and visual disturbances. There is very high fever (105–107°F) and cessation of sweating. The skin is flushed and dry, pulse rapid, irregular and weak and hypotension. Management: (a) Cooling by fanning after sprinkling water, immersion in cold water or use of ice packs to neck, axillae and groins, or ice water enemas. (b) Massage of extremities to maintain circulation. (c) Normal saline 1000 mL infusion if dehydration or cramps. (d) Do not give antipyretics like paracetamol, aspirin. 3. Exertional heat injury occurs in those who indulge in physical exertion in hot and humid environment. Patients suffer from headache, nausea, incoherent speech and muscular incoordination. Body temperature is increased with sweating. There is tachycardia and hypotension. Treatment: (1) Patient should be nursed in cool environment and covered with weight cold sheets. (2) IV Dextrose saline infusion. (3) Massage of extremities, helps in increasing peripheral blood flow.

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Rabies Since rabies is a fatal infection, it is solely of academic interest.

Measles In developing countries, measles is a major cause of childhood morbidity and mortality since a large number of children are not vaccinated. It is also a significant factor in the development of—(a) Protein-energy malnutrition which contributes to a large number of deaths, and (b) pneumonia which can be fatal in young children, and (c) Vitamin A deficiency which can increase child mortality.

Complications 1. Pneumonia is a common complication and the main cause of death. It is caused by the measles virus itself, the pneumonia usually occurs in the first 2 weeks of the illness. It is often however the result of superinfection by other viruses or bacteria, including Staph. aureus or Gram-negative organisms. During the latter part of the exanthematous stage, herpes simplex virus and adenoviruses can cause bronchiolar and interstitial necrosis. A combination of measles and adenovirus produces the most severe symptoms, the most prolonged course and the highest mortality. 2. Laryngotracheobronchitis may occasionally be severe and present with signs of upper airways obstruction (e.g. stridor). 3. Encephalitis can occur just before, during or after the rash. It may be due to direct invasion of the brain by the virus or by an allergic response to the infection. It can prove fatal.

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4. Hepatitis: Young adults generally react unfavourably to measles. A few adult pts. who have severe disease may develop hepatitis with frank jaundice. 5. Hemorrhagic measles is very rare. Encephalopathy, bleeding, confluent hemorrhagic rash and pneumonia are present, and the condition is usually fatal.

Management Antibiotics for lung infection. Treatment of secondary bronchopneumonia must include an anti-staphylococcal antibiotic. Vitamin A 200,000 IU for 2 days to children with severe measles will prevent ocular complications and reduce respiratory infections and measles-related mortality. Uncommon complications in the post-measles state: Gangrene of tips of fingers and toes, cancrum oris, septicemia, pyogenic infections, reactivation of pulmonary tuberculosis. Possible abortion or prematurity if infection occurs during pregnancy.

Chickenpox The disease generally affects children under 10 years of age. Recovery is usually uneventful but complications, some of them serious, do occur. 1. Pneumonitis has an insidious onset and is more common in adults, and very young children. Tachypnoea, cyanosis, cough and haemoptysis signify severe disease. CXR shows widespread nodular infiltrates. 2. Neurological complications: Acute meningitis or encephalitis may develop soon after onset of the rash, but more commonly, an allergic encephalopathy develops, Reye’s syndrome, especially if aspirin has been given to the child, transverse myelitis and Guillain-Barré syndrome may also occur.

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362 A Handbook of Emergencies 3. Hemorrhagic chickenpox is rare but potentially fatal form of the disease. Extensive bleeding may occur into unaffected skin as well as into the rash. 4. Immunocompromised child, patient on corticosteroids. The disease is more severe.

Management (a) Antibiotics for secondary infection. (b) Antiviral drug Acyclovir 20 mg/kg (up to 800 mg) qds in severe disease with complication like pneumonitis. (c) Secondary infection may be averted by daily antiseptic baths.

Whooping Cough Whooping cough is a highly infectious disease of the respiratory tract. With the introduction of vaccination there has been a decline in the incidence of the disease, but in children not immunised, it remains a major health hazard. The disease can be potentially fatal particularly in young infants because of various complications.

Complications 1. CNS complications: Cerebral, subarachnoid and subdural hemorrhages are rare. Convulsions, mainly a result of cerebral anoxia, may occur in young infants and prove fatal. 2. Respiratory: Prolonged apnoeic episodes may occur before or after paroxysms of cough. Bronchopneumonia is due to secondary bacterial infection, infective organisms include Strep. pneumoniae, H. influenzae type B and group A β-hemolytic streptococci. 3. Pressure effects of paroxysmal cough: Common are epistaxis, subconjunctival hemorrhage, umbilical hernia, prolapse of rectum. Rarely pneumothorax.

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Management 1. Hospitalization for all children less than 1 year of age and older children who look ill. ICU for infants with severe symptoms. 2. Erythromycin 50 mg/kg/24 hours to eliminate organisms from nasopharynx. 3. O2 for recurrent or sustained hypoxemia. 4. Periodic gentle suction to remove secretions. 5. Nutrition: Small frequent feeds especially after a paroxysm. Adequate hydration.

Mumps The mumps virus has a predilection for causing nonpurulent inflammation in salivary glands and the meninges. It usually affects children and young adults. Serious complications include encephalomyelitis, orchitis and pancreatitis.

Complications Complications of mumps can occur in absence of parotid swelling. 1. Neurological: (a) Aseptic meningitis is common and mimics that of enteroviral infections, except that the fever in mumps is higher and the CSF pleocytosis greater. (b) Encephalitis or encephalomyelitis is uncommon compared with meningitis but carries a more severe prognosis. 2. Orchitis: One or both testes become tender and inflamed a few days after onset of parotitis. Fever often recurs with severe testicular pain. 3. Abdominal pain: Nausea and vomiting with acute abdominal pain may occur early in the attack and

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364 A Handbook of Emergencies should suggest oophoritis in women or pancreatitis in either sex. As the serum amylase level is usually raised in acute mumps, the test does not help in ruling out pancreatitis.

Management In an infant with history of fits, temperature should be lowered by tepid sponging and paracetamol. For orchitis oral prednisolone 40 mg/day often reduces testicular pain and swelling. In mumps meningitis, bed rest is advised until fever and headache have subsided.

Diphtheria Diagnostic Features of Severe Diphtheria 1. 2. 3. 4. 5. 6.

No previous immunization against diphtheria. Relative lack of pharyngeal pain. Severe toxemia without high fever. Extension of membrane beyond tonsillar fossa. Diffuse cervical swelling. Palatal paralysis.

Severe Types of Diphtheria Pharyngeal diphtheria: In severe cases-foetor oris (nonspecific), hemorrhage and marked oedema of tissues, resulting in the appearance of ‘bull-neck’ diphtheria. General symptoms are severe with waxy pallor, extreme lassitude and drowsiness progressing to stupor. Laryngeal diphtheria: Pharyngeal infection can spread to the larynx, or less commonly, can start there and, with further spread, can involve the trachea and bronchi. The symptoms resemble those of croup with cough, stridor and respiratory distress.

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Management 1. DAT: The therapeutic dose is based on duration of symptoms and severity of the disease and ranges from 40,000 U for pharyngeal disease, and 150,000 U in malignant cases. Measures to combat anaphylaxis must be taken. 2. Antibiotics: Azithromycin 500 mg qds for patients allergic to the drug, given for 14 days. For children 10–15 mg/kg.

Management of Severe Complications Complications Respiratory obstruction Myocarditis Circulatory failure Cardiac failure Cardiac arrhythmias Bulbar paralysis

Respiratory paralysis

Clinical features and management Aspiration of membrane in laryngeal diphtheria. May necessitate intubation tracheostomy Faint heart sounds, tictac rhythm, ST-T changes. Complete bed rest Acute toxemia in severe case. Signs of shock Low output failure, rapid weak pulse Heart block, A-V dissociation. Cardiac pacing. High mortality Muscles of swallowing paralysed with risk of aspiration, which may require intubation or tracheostomy. Tracheostomy may be preferable to intubation if risk of pushing membrane further into trachea Diaphragm and intercostal muscles paralysed, which may require intubation and artificial ventilation

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366 A Handbook of Emergencies

Infectious Mononucleosis The infectious mononucleosis (IM) is an acute self-limiting illness caused by primary infection with EBV virus, lasting for 2–3 weeks unless complications which may need special care.

Clinical Features Fever which may be as high as 40°C, widespread maculopapular rash in some, periorbital oedema. Tonsillar enlargement with erythema and purulent exudate, which may occasionally be sufficiently severe to cause pharyngeal obstruction. Generalised lymphadenopathy, particularly cervical is common.

Diagnosis (a) WBC 10–20 × 109/1 with increase in mononuclear cells of which 20% are atypical lymphocytes. (b) Nonspecific heterophile antibodies (positive Paul-Bunnell and monospot tests). (c) Specific antibody responses. Complications though uncommon can be serious. 1. Autoimmune hemolytic anemia: Occasionally profound thrombocytopenia with purpura and hemorrhages. 2. Splenic rupture: Abdominal pain is uncommon in IM, and splenic rupture should be considered and excluded. 3. Neurological: Rarely encephalitis presenting with predominant cerebellar features, Guillain-Barré syndrome, transverse myelitis. 4. Myocarditis.

Management No specific antiviral treatment. Corticosteroids may be prescribed in management of hemolytic anemia,

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thrombocytopenia, neurological complications and myocarditis. If tonsillar enlargement causes airway obstruction prednisolone 60 mg/day for 5–6 days. Tracheostomy may be required very occasionally.

Acute Disseminated Miliary Tuberculosis Acute hematogenous TB can occur mainly in immunocompromised individuals and victims of AIDS.

CIinical Features Patient may present as pyrexia of unknown origin, or with tachypnoea, lymphadenopathy, tuberculoma of brain or multiple organ dysfunction, palpable liver and spleen, liver dysfunction with increased serum bilirubin, anemia and hypoproteinemia.

Investigations (a) Repeated blood cultures for gram-negative infections. (b) Fibreoptic bronchoscopy (if pulmonary involvement) with bronchial aspirates for acid-fast bacilli. (c) Liver biopsy for presence of caseating granulomas. (d) CT scan of head for tuberculoma. (e) CXR may show miliary lung shadows.

Management 1. Antituberculous therapy: INH, RIF, PZI and EMB with addition of one or more second-line drugs with a fluoroquinolone and an aminoglycoside. 2. Circulatory support: (a) Fluid and electrolyte balance. (b) Dopamine. (c) Packed cell transfusion. (d) IV nutrition if GI intolerance, or via nasogastric tube if patient too weak to swallow.

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Shock

Shock is a life-threatening state in which there is a serious reduction in cardiac output with inadequate perfusion of organs such as the kidneys, brain and liver. It can occur because the function of the heart is impaired, or because the heart is inadequately filled.

Hypovolemic Shock Hypovolemic shock is due to failure of venous return to the heart due to decreased circulatory blood volume.

Causes 1. Hemorrhagic: GI bleeding, penetrating wounds (liver, spleen, kidney, artery); ruptured aneurysm. 2. Hypovolemic: Burns, fluid loss from vomiting or diarrhoea, diabetes mellitus, diabetes insipidus, adrenal insufficiency. Intestinal obstruction, pancreatitis (sequestration of fluid).

Clinical Features Restlessness, cold and clammy skin, profuse sweating, rapid thready pulse, hypotension. Oliguria may progress to anuria, stupor.

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Management 1. Rapid fluid replacement—2 L of normal saline or Ringer lactate. 2. Blood transfusion for replacement of Hb. 3. Treatment of cause—Tetracycline for cholera, treatment of GI blood loss, insulin in diabetic ketoacidosis. 4. Infusion of colloids (Haemaccel or 5% albumin) if hypovolemia associated with hypotension. Crystalloids can be given via one vein and colloid solution through another. After initial infusion of 2 L of normal saline in severe hypovolemic shock, alternate N saline with Ringer lactate or 5% dextrose saline. Hypokalemia is common hence 40–60 mEq of potassium in dextrose saline infusion. Repeated if necessary depending on serum potassium levels. 5. Blood transfusion to bring up Hb once volume replacement is achieved. If type specific blood is not available in an emergency Type O Rh negative blood can be given.

Cardiogenic Shock Causes AMI (commonest cause), acute myocarditis. Cardio­ myopathy (HOCM and congestive), severe AR or MR, cardiac tamponade, severe cardiac arrhythmia. Following open heart surgery.

Clinical Features Fall of BP (20/min or a PaCO2 12000/mm3 or 10% band forms. Septic shock is defined as severe sepsis with organ dysfunction that does not respond to adequate fluid replacement.

Investigations zz zz zz

X-ray chest USG of abdomen and pelvis Identification of source of sepsis –– Blood culture –– Sputum examination (smear culture sensitivity) –– Examination discharges from wound secretions –– CSF if necessary.

Management 1. Stabilizing the airway and breathing 2. Antibiotics (a) Combination of carbapenem plus aminoglycoside or piperacillin-tazobactam to begin with. (b) If suspected penicillin resistant. Vancomycin or Linezolid should be added. (c) Severe septic shock due to community acquired pneumonia. (d) Amoxicillin-clavulanate in addition to antibiotics that cover other likely organisms. (e) In neutropenic patients with septic shock piperacillin-tazobactam plus aminoglycoside. If there is no improvement and fever persists Amphotericin B or fluconazole is added to cover fungal infections. 3. Ventilatory support 4. Blood transfusion of Hb falls to < 7g/dL.

Anaphylactic Shock Anaphylaxis is an acute and dramatic life-threatening immunological reaction to a drug or other stimulus.

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Common Stimuli for Anaphylaxis 1. 2. 3. 4. 5. 6. 7.

Antibiotics: Penicillin, streptomycin, tetracycline. Radiocontrast media. Anaesthetic agents: Lignocaine, thiopentone, scoline. Blood and blood products including sera. Hormones: Insulin, growth hormone. Venoms: Bees, wasps, spiders. Others: NSAIDs, narcotic agents, heparin thrombolytic agents, parenteral iron dextran, foods such as shellfish, eggs.

Clinical Features Onset may be instantaneous or within a few minutes after IV injection or at times after 1/2 hour after exposure. (a) Hypotension and circulatory collapse. (b) Severe laryngeal oedema/obstruction, angioedema. Bronchospasm or pulmonary oedema may occur singly or in combination. (c) Tachycardia, arrhythmia, syncope and seizures on occasions constitute predominant presentation. Diaphoresis, abdominal pain and diarrhoea may occur. Urticaria may or may not occur.

Management 1. Airway: Intubation or if it is not possible secure emergency airway by puncturing the cricothyroid membrane with a large bore needle. Perform tracheostomy if intubation is not possible. 2. Oxygen in high concentration. 3. Injection adrenaline 0.5–1 mL of 1:1000 solution IM. Repeat every 5–10 minutes if necessary. If no response or bronchospasm or cardiovascular collapse 5–10 mL of 1:10000 solution IV, or instil it through endotracheal tube.

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376 A Handbook of Emergencies 4. Fluids: ½–1 L of fluid usually restores BP but 6–9 L may be required for adequate restoration of fluid volume. 5. Hydrocortisone 300 mg IV followed by 100 mg q6h to prevent late manifestations of anaphylaxis. 6. Aminophylline 250 mg IV in 20 mL dextrose to relieve bronchospasm. 7. Diphenhydramine 50 mg (1 mg/kg) IV slowly repeated if necessary. 8. Dopamine if hypotension persists. 5 µg/kg/min increased to 10–20 µg/kg/min. If ineffective infusion of adrenaline 3–4 µg/mL initially slowly increased till rise in BP. 9. IV atropine and glucagon if patient on β-blocker failing to respond. 10. Ventilatory support may be necessary if patient is critical. In absence of airway obstruction there is little or no role of tracheal intubation in patients who do not require ventilation. Leaving an endotracheal tube in situ and allowing spontaneous breathing serves no useful purpose as excess secretions are rarely a problem in drug associated emergencies. The tracheal tube increases the work of breathing and is uncomfortable to the conscious patient.

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Rheumatological Emergencies

Rheumatic diseases involve multiple systems and may present as a wide variety of medical emergencies. Some may be due to the disease process itself, others the result of therapy.

Emergencies Involving Disease Processes Rheumatoid Vasculitis Although uncommon, it is usually seen in patients with long-standing nodular and seronegative RA.

Clinical Features Skin ulceration, gangrene of digits, neuropathy (especially mononeuritis multiplex), bowel infarction and occasionally, cerebral and coronary vasculitis. Ulcers are deep, painful and punched out and develop suddenly.

Diagnosis Can be confirmed by biopsy (e.g. sural nerve or rectum). Angiography may demonstrate microaneurysms of mesenteric vessels.

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378 A Handbook of Emergencies

Management Intermittent IV bolus Cyclophosphamide 0.5–1 g single dose with bolus Methyl Prednisolone 0.5 mg daily for 3 days. This is repeated intermittently every 3–4 weeks. Additional plasma exchange for severe cases to tide over crisis.

Ocular Emergencies a. Painful red eye due to iridocyclitis that complicates seronegative spondyloarthropathies, or scleritis associated with rheumatic diseases. It is unilateral, associated with lacrimation, photophobia and blurring of vision. Management—Mydriatics and corticosteroid drops. For scleritis, in addition to corticosteroid drops, Prednisolone 50 mg/day with Azathioprine or Cyclophosphamide if inflammation does not settle. b. Painful white eye: Ischemic optic neuropathy due to vasculitis may be seen in temporal arteritis, polyarteritis nodosa (PAN) or systemic lupus erythematosus (SLE), while retinal vasculitis is observed in Bechet’s syndrome. These conditions are more serious than painful red eye and need specialist attention.

Temporal Arteritis Occurs predominantly in the elderly and causes sudden blindness if not treated promptly.

Clinical Features Headache, scalp tenderness, weight loss, and occasionally fever, anemia and raised ESR. Also jaw claudication and carotid sinus hypersensitivity. Ocular involvement with transient visual symptoms leading to sudden blindness may occur.

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Management Prednisolone 1 mg/kg/day initially. After treatment has been commenced, diagnosis can be confirmed by temporal artery biopsy within 1 week.

Emergencies Involving Specific Organs Neurological Emergencies a. Lupus crisis can occur in SLE. Patient is severely ill with extreme weakness and severe headache often with chest and abdominal pain, and neuropsychiatric involvement. Management – High doses of Corticosteroids with Cyclophosphamide or Azathioprine. b. Vasculitis may manifest as encephalopathy, focal or multifocal CNS disturbances, hemorrhagic or ischemic stroke and myelitis. Treatment – Corticosteroids and immunosuppressives.

Pulmonary Emergencies a. Acute lupus pnueumonitis (shrinking lung syndrome) is the characteristic emergency in SLE. Clinical features: Progressive dyspnoea, fever, cough and sometimes hemoptysis. CXR: Bilateral or unilateral basal, patchy, acinar infiltrates with elevation of hemidiaphragm. Treatment: Oral Prednisolone. If deterioration, addition of Cyclophosphamide or Azathioprine. Plasmapheresis in refractory, lifethreatening situations. b. Acute pulmonar y hypertension from acute involvement of pulmonary vasculature may be seen in progressive systemic sclerosis.

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380 A Handbook of Emergencies c. Bronchiolitis obliterans is a rapidly progressive disorder in RA specially in association with Penicillamine and to a lesser extent with gold therapy. d. Respiratory muscle dysfunction if rapidly progressing, may present as an emergency. It may rarely be seen in PSS, ankylosing spondylitis, dermatomyositis/ polymyositis.

Renal Emergencies a. Malignant hypertension and irreversible kidney failure are encountered in patient with diffuse skin involvement and usually appear within 2 years of onset of the disease. Management: Control of BP. Occasionally bilateral nephrectomy is life-saving. b. Rapidly progressive glomerulonephritis may occur in SLE, Wegener’s granulomatosis, PAN. Management: Initially pulse Methyl Prednisolone 1 mg/kg/day. If pulse therapy raises BP, mini-pulses of 250 mg Methyl Prednisolone. Cyclophosphamide 0.5–1 g to be added in patients with associated systemic vasculitis. Plasmapheresis if failure of drug therapy.

Emergencies Involving Peripheral Joints and Spine a. Septic joint is a medical emergency as it has a high mortality if untreated. Individuals at risk are the elderly, those with pre-existing joint diseases especially RA. Bacteria from any source, e.g. pneumonia may lead to localised joint involvement. In RA, skin ulcers and infected rheumatoid nodules can be responsible. Diagnosis is confirmed by joint aspiration. Management: Appropriate antibiotics parenterally for first 2 weeks followed by oral antibiotics for further 6 weeks.

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In case of effusion, joint aspiration by closed needle aspiration as often as necessary. Sterile saline can be used for irrigation. Occasionally open surgical drainage, especially in case of relatively inaccessible joints, e.g. the hip or if there is inadequate response after 48–72 hours. b. Atlanto-axial and subaxial dislocation in RA can lead to quadriplegia and even death. This can be precipitated, for example, while giving anaesthesia for surgery. Pain radiating from occiput to forehead due to irritation of nerve roots is the most common feature. Subaxial dislocation at C5 level may present suddenly with quadriplegia, but usually there is sensory impairment, UMN signs and/or sphincter dysfunction. MRI can define the abnormality. Management: Urgent surgical decompression often with fusion. c. Acute synovial rupture: Patients with early knee effusions are particularly at risk and it can be precipitated by muscle exertion. Symptoms produced by leakage of inflamed synovial fluid into calf muscles may simulate those of deep vein thrombosis. An additional sign is discoloration around the ankle due to local bruising. Management: Rest and elevation of the leg with aspiration of the knee followed by intraarticular injection of long-acting corticosteroid to prevent reaccumulation of fluid. d. Acute spinal cord injury: While an elective surgery is to be performed on the spine (particularly cervical and dorsal spine), it is worthwhile to start with Methyl Prednisolone as a bolus dose and continuing as a maintenance dose throughout the duration of surgery. After completing the surgery, ice cold saline is used to irrigate the dura for a few minutes. This not only helps

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382 A Handbook of Emergencies in hemostasis but is also neuroprotective and likely to reduce any postoperative neurological deficits.

Emergencies Due to Drugs 1. GI side-effects: (a) Gastric ulceration or erosive gastritis from NSAIDs can cause GI bleeding. (b) Attack of severe diarrhoea with use of Indomethacin. 2. Kidney failure may be precipitated by NSAIDs especially in elderly, and in those with impaired renal function. (NSAIDs should not be used with ACE inhibitors). Acute interstitial nephritis may result from idiosyncratic reaction to NSAIDs. 3. Skin: Exfoliative dermatitis and Stevens-Johnson syndrome are the dreaded complications of antiepileptics (Carbamazepine, Lamotrigine), Penicillamine, Sulphasalazine and other DMARDs, Calcium channel blockers, antimalarials, Dapsone. 4. Acute adrenal insufficiency may be precipitated by corticosteroid withdrawal in patients who have received Prednisolone in doses as low as 3 mg/day for prolonged duration or within 7–28 days with doses of 20–30 mg/day. 5. Hematological complications: Profound neutropenia may lead to fatal infection and thrombocytopenia to severe bleeding. 6. Lungs: Interstitial pneumonitis is a rare but dangerous side-effect of Methotrexate. Penicillamine is occasionally associated with obliterative bronchiolitis.

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Febrile Emergencies

A fever of >41.5ºC (106.7ºF) is called hyperpyrexia. Such high fever can occur in a variety of conditions. The outcome and mortality of febrile emergencies depend on prompt intervention and treatment in first 24 hours after presentation. Major categories of febrile emergencies are:

Sepsis Syndrome Sepsis is caused by the systemic response to severe infection. When sepsis is associated with dysfunction of distant organs from the site of infection, the patient has severe sepsis. The type of organism and the site play an important part in infection. Treatment: (a) Broad spectrum antibiotics in combination initially IV. (b) Removal of cause of infection where possible (c) Cardiorespiratory support.

Febrile Neutropenia Fever in a neutropenic patient contributes to 50% of deaths associated with leukemias, lymphomas and solid tumors. Bacterial infections are common in patients with febrile neutropenia. Besides fever the absolute

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384 A Handbook of Emergencies neutrophil count (ANC) is 40.6ºC (105ºF), CNS dysfunction, metabolic derangement and coma. Two forms of heat stroke exist. (a) Exertional heat stroke (EHS) usually occurs in young, fit individuals who do strenuous physical exercise for a prolonged period in a hot environment. (b) Non-exertional heat stroke (NEHS) more commonly occurs in sedentary individuals who are chronically ill and in very young persons. Classical NEHS occurs during heat waves and is more common in areas that have not experienced heat waves in many years. Management: (a) First aid – Move the victim to a cool place, remove

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386 A Handbook of Emergencies heavy clothing. Keep victim’s head and shoulders slightly elevated. (b) External cooling – sprinkle water at 20º over the body combined with fanning. Put ice packs in neck, arm pits and groins (areas with abundant blood supply). Wet towels are also effective. Clothes should be kept wet with cool water. Internal cooling – Refrigerated IV saline solution, cold water lavage (gastric, peritoneal), extracorporeal cooling/cardiac bypass, hemodialysis). Note: Antipyretics have no role to play. To prevent hypothermia, continue cooling till temperature drops to 102ºF. Body cooling equipment (BCE) can be used if available. Use Benzodiazepines to treat agitation, shivering and seizures. Drug–induced hyperthermia be caused by Amphetamine, Cocaine, Phencyclidine, Lysergic acid, (Ecstacy), Salicylates, Lithium, anticholinergics and sympathomimetics. Malignant hyperthermia occurs in individuals with inherited abnormality of skeletal muscle and allows rapid increase in intracellular calcium levels in response to halothane and other inhalational anesthesias or to succinylcholine. Besides elevated temperature there is rapid development of increased muscle rigidity, rhabdomyolysis, acidosis and cardiovascular instability. The condition is often fatal. Neuroleptic malignant syndrome has been reported to occur with all drugs that affect the central dopanergic system—Phenothiazines, Butyrophenones, Fluoxetine, Loxapine, Tricyclics, Domperidone, as well as withdrawal dopaminergic agents. NMS is an idiosyncratic, lifethreatening syndrome characterised by fever, severe muscular rigidity and autoimmune and mental changes. Patients may have rhabdomyolysis with subsequent

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myoglobinuric kidney failure. Also metabolic acidosis, hypoxia, decreased serum iron, elevated CPK and leucocytosis. Management: Withdrawal of offending agent, aggressive volume replacement, serial monitoring and correction of electrolyte abnormalities and physical cooling methods for hyperthermia. Benzodiazepines (oral or IV) may ameliorate symptoms. Dantrolene may be useful in cases with extreme temp. elevation, rigidity and hypermetabolism. Dose 1–2.5 mg/kg body weight initial, then 1 mg/kg q6h with tapering after first few days. Cocaine toxicity can lead to hyperthermia, dysrhytmias, acute coronar y syndrome, agitation, delirium, rhabdomyolysis and acidosis. Management: Cardiac monitoring, pulse oximetry, O2, infusion of dextrose 5% in water and thiamine followed by activated charcoal to patients with oral ingestion of cocaine. Neuromuscular blockade with Vecuronium to control muscle activity and subsequent development of acidosis. Control of BP with nitroprusside and conventional cooling for hyperthermia.

Cerebral Hemorrhage Intracerebral SAH can cause fever. In pontine hemorrhage there is hyperpyrexia with pinpoint pupils, hyperpnoea and severe hypertension. Hypothalamic fever is at times used to describe elevated temp. due to abnormal hypothalamic function due to trauma, hemorrhage, tumor or intrinsic hypothalamic malfunction. However most patients with hypothalamic damage have hypothermia rather than hyperthermia. Regional and seasonal febrile emergencies include malignant malaria, dengue, leptospirosis and even typhoid and cholera.

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Emergencies in HIV Infection

Human immunodeficiency virus (HIV) infection is now a chronic managable disease. It is associated with several emergencies which could be related to opportunistic infections that are seen at presentation, or occur as the immune system gets weaker, or may be HIV-induced diseases, or result from use of anti-HIV drugs.

Emergencies due to Opportunistic Infections The site of opportunistic infection (OI) determines the clinical presentation and hence, the emergencies encountered become system specific, or they may involve more than one system.

Pulmonary Emergencies a. Pneumocystis pneumonia (Jiroveci) which is a fungus. Clinical mainfestation is subacute or chronic with a triad of shortness of breath, fever and nonproductive cough. Severity is determined by determination of PaO2. Diagnosis is confirmed by sputum examination or bronchoalveolar lavage. Treatment: Trimethoprim Sulphamethoxazole (1.5–2 mg/kg/d) is the drug of choice. It is given for 21 days followed by prophylactic therapy. In case of severe PCP (PaO2 < 60 mm Hg),

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extensive bilateral interstitial and alveolar markings. Prednisolone 40 mg od × 6–10 days, and 20 mg od from 11th to 21st day, and oxygen. b. Bacterial pneumonia: Most patients have fever, cough and sputum production with dyspnoea in majority. A lobar infiltrate on chest X-ray generally suggests bacterial pneumonia. Treatment should be initiated with second or third generation Cephalosporin or β-lactam-lactamase inhibitor or with TPS-SMX. Antibiotic selection should include to treat patients with pseudomonas infection—a regimen containing a third generation Cephalosporin plus an Aminoglycoside.

Emergencies due to CNS Involvement a. Cerebral toxoplasmosis is the most common cause of focal brain lesion in patient with AIDS. Symptoms are headache, confusion or altered mental state and fever (in about 50%). Diagnosis is based on low T cell count, positive IgG antibodies against toxoplasma and CT scan or MRI of head. Treatment : Combination of Pyrimethamine, Sulphadiazine and Folinic acid in addition to one of the following – Clindamycin, Clarithromycin, Dapsone, or Azithromycin for 4–6 weeks. Corticosteroids should be given for 2 weeks in patients with toxoplasmic encephalitis with cerebral oedema. b. Cryptococcal meningitis: Symptoms include fever, headache, altered mental state, nausea, vomiting and malaise. Diagnosis depends on level of cryptococcal antigen in CSF or CSF fungal culture. Treatment: Amphotericin B IV for 2 weeks with or without Flucytosine followed by oral Fluconazole for 8–10 weeks. Then suppressive therapy with oral Fluconazole.

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390 A Handbook of Emergencies c. Progressive multifocal leukoencephalopathy (PML): Symptoms are due to demyelination that is multifocal with a predelection for white matter of cerebral hemisphere. Cognitive disorders range from mild impairment of concentration to dementia. Also focal neurological deficits such as mono- or hemiparesis. MRI helps in diagnosis. Treatment: Nonspecific. HAART is the only therapy that can help. d. Tubercular meningitis: Basal meninges are usually involved with palsies of 3rd and 6th cranial nerves CSF is diagnostic. Treatment: Anti-TB therapy with standard drugs for one year. e. Primary CNS lymphoma is a typical endstage complication of HIV. Treatment : No cytotoxic chemotherapy. Irradiation is palliative.

Diarrheal Diseases Diarrhoea occurs in over 90% of patients with AIDS. It may be acute (7 days) or chronic. Diagnosis: Stool examination for ova and parasites. Management: Principles: (a) More than one pathogen may be involved. (b) Dissemination from the gut can occur in some bacterial infections (MAC, Salmonella, Shigella, Campylobacter, C. difficile). (c) Relapse following successful treatment is common. (d) Symptomatic treatment if diarrhoea does not subside and with progressive weight loss.

Ocular Emergencies a. Cytomegalovirus infection: Manifestations of retinitis consist of blind spots, visual field loss, flashing lights, floaters, or decreased or blurred vision. Treatment: Intravitreal inj of 0.1 mL of Ganciclovir (drug of choice) at a dose of 200–4000 mg thrice weekly for

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induction and 200–4000 mg weekly for maintenance. Foscarnet 1.2–2.4 mg twice weekly for induction and maintenance 1.2 mg/week. Maintenance therapy can be discontinued once CD4 count increase to > 200 cells/mm3 for at least 6 months following HAART. Note: None of the drugs used reverse the disease, they are only helpful in halting it. b. Varicella zoster infection – can present as (i) Acute retinal necrosis. Patients may have history of cutaneous shingles occurring either before or at the same time as retinitis. Treatment: Acyclovir for 10–14 days followed by long-term suppression with a lower dose. (ii) Progressive outer retinal necrosis syndrome occurs in patients with cell count < 50. Majority of these patients will develop retinal detachment. Treatment: IV Acyclovir 10 mg/kg for 7–10 days and continued till lesions are clearly resolving.

Emergencies due to Antiretroviral Therapy 1. Lactic acidosis is an important class side effect for the NRTI group and can occur with combinations Zidovudine (AZT) or Stavudine (d4T) with Didanosine (dd1) or rarely Lamivudine (3TC). Initial symptoms include nausea, vomiting, abdominal pain, weight loss, fatigue, shortness of breath and occasionally fever, in addition to diarrhoea, tachycardia and tachypnoea. Treatment: Stopping anti-HIV drugs, dextrose and bicarbonate IV. Riboflavin may help in some cases. 2. Abacavir hypersensitivity reaction usually starts within first 6 days of taking the drug. If symptoms such as fever, skin rash, vomiting and diarrhoea develop, the drug must be stopped immediately.

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392 A Handbook of Emergencies 3. Idinavir-induced nephrolithiasis: The drug tends to form crystals in the kidneys, these can form kidney stones made up completely of the drug. Confirmation may be difficult because these stones are not visible on plain radiography or CT scans. Treatment: IV fluids, pain control and maintaining kidney function. 4. Marrow suppression by AZT: Neutropenia and/or anemia after weeks or months of therapy Treatment: Discontinuation of the drug and G-CSF injections. Blood transfusions are often required. 5. Hepatic necrosis with Nevirapine: Elevation of liver enzymes is not uncommon and severe hepatotoxicity can occur. Side effects may continue even after stopping the drug. Role of corticosteroids is doubtful. 6. Stevens-Johnson syndrome is the most serious form caused by NNRTIs. Also known as toxic epidermal necrolysis, manifestations are a diffuse peeling of large areas of skin, blistering inside the mouth, conjunctivitis, bronchitis and fever, myalgia and arthralgia. Treatment is in burns unit with LV fluids and antibiotics. Short course of Prednisolone 80 mg daily may be given during acute phase. 7. Pancreatitis may occur with Didanosine, less commonly with Stavudine - Lamivudine and Zalcitabine. Alcohol consumption and treatment with IV Pentamidine are risk factors. Treatment is same as pancreatitis of other etiologies. 8. CNS side effects such as dizziness, insomnia, nightmares, even mood fluctuations and depression and paranoid delusions can occur with Efavirenz. Treatment: Lorazepam can diminish CNS side effects and Haloperidol can be given for panic attacks and nightmares. Both these drugs should be restricted to severe cases.

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19

Emergencies Due to Fluid and Electrolyte and Acid-base Disturbances Disorders of Water and Electrolyte Metabolism Fluid and electrolyte disturbances create complex therapeutic problems.

Water Water Excess (Overhydration) Causes 1. Acute kidney failure with oliguria or anuria. 2. Excessive infusions of saline or blood transfusion. 3. CHF, liver disease and other causes of sodium retention.

Clinical Features Oedema, raised jugular venous pressure (JVP), pulmonary congestion. Ascites and pleural effusion may develop later.

Management Restriction of fluids, salt. Frusemide. Phlebotomy for overhydration due to excess blood or fluid transfusion.

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394 A Handbook of Emergencies

Water Deficiency Causes 1. Dehydration with isotonic loss of salt and water, e.g. vomiting, diarrhoea, gastric suction, intestinal fistulae, after burns. 2. Dehydration with loss of water in excess of salt: Comatose patients, diabetes mellitus, excessive sweating as in high fever, diabetes insipidus. 3. Deficit of salt in excess of water: Diuretics, adrenal insufficiency, chronic renal insufficiency. 4. Extracellular volume depletion due to sequestration of fluid as in extensive burns, peritonitis, ileus or intestinal obstruction.

Clinical Features Anorexia, nausea, vomiting, thirst, apathy, confusion, coma. Signs are poor skin turgor, dry, shrunken tongue; sunken eyes, postural hypotension, weak thready pulse, and in severe cases state of shock.

Management 1. IV fluid infusions. 2. Correction of electrolyte and acidbase balance. Accurate I/O chart. 3. Treatment of primary cause, e.g. insulin in diabetic acidosis, hydrocortisone for adrenal insufficiency.

Sodium Hypernatremia Causes Heart failure, hypoalbuminemic conditions, renal insufficiency, Cushing’s syndrome, primary aldosteronism, venous or lymphatic obstruction, excessive IV saline infusions.

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Clinical Features 1. Oedema both peripheral and pulmonary. Pleural effusion, ascites. 2. Hypertension. 3. Postural hypotension.

Management 1. Diuretics. 2. Albumin infusion if hypovolemia is lifethreatening. 3. Spironolactone for hyperaldosteronism. 4. Hemo-or peritoneal dialysis if response to diuretics not adequate.

Hyponatremia Causes 1. Sodium depletion from diarrhoea, vomiting, exces­ sive sweating, diuretic therapy, adrenal or renal insufficiency. 2. Dilutional hyponatremia in CHF, nephrotic syndrome. cirrhosis. 3. Inappropriate ADH secretion: Benign and malignant tumors of lung, head injury, encephalitis, cerebral tumors. 4. Excessive ultrafiltration by hemo-or peritoneal dialysis. 5. Artifactual hyponatremia associated with hyper­ glycemia.

Clinical Features Altered sensorium, restlessness. Weakness. Cold hands and feet. Skin inelastic and sunken eyes and cheeks. Tachycardia, weak pulse, postural hypotension. Ultimately circulatory failure and death may occur.

Management Isotonic saline (0.9% solution) IV. In presence of severe shock. simultaneous infusion of colloids. If volume of fluid has to be restricted as in kidney failure, hypertonic saline

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396 A Handbook of Emergencies may be used. Amount of sodium required can be calculated from the formula, e.g. in an adult of 60 kg weight if serum sodium is 125 mEq/L, amount of sodium required will be: 135 − 125 ×

60 × 60 = mEq 100

(Total body water constitutes 60% of body weight) Dilutional hyponatremia should be treated with water restriction and judicious use of diuretics. Correction of acidosis with IV sodium bicarbonate and of hypokalemia.

Potassium Hyperkalemia Causes 1. Inadequate excretion. Renal failure, adrenal insuf­ ficiency, Addison’s disease, hyper-aldosteronism. Potassium-sparing diuretics, e.g. aldactone. 2. Shift of potassium from tissues. Respiratory or metabolic acidosis. Tissue injury (muscle damage, hemolysis, internal bleeding). Uncontrolled diabetes mellitus. 3. Excessive intake especially in patients with renal insufficiency or those on hemodialysis.

Clinical Features 1. Generalised muscle weakness of skeletal muscles. 2. Conduction disturbances: Bradycardia, heart block and hypotension. Cardiac arrest may be fatal.

Diagnosis 1. Serum K levels > 5.0 mEq/L. 2. ECG – Stages: (a) Shortening of QT interval and tall peaked T waves.

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(b) Widening of QRS complex, prolongation of PR interval, disappearance of P waves, nodal and ventricular arrhythmia. (c) Finally QRS complex merges with T wave with ventricular asystole or fibrillation.

Management 1. Calcium gluconate 20 mL 10% as bolus. Repeat after 10 mins if ECG remains unchanged. 2. Dextrose insulin drip. Dextrose 500 mL 20% plus soluble insulin 20 units over 1 hour. 3. Soda bicarb 50 ml 7.5% in 5–10 minutes. Should be given 1/2 hour after calcium injection. 4. Frusemide 40 mg IV. 5. Ion exchange resin. Polystyrene sulphate (Kayexlate) 30 g in 50 mL 2% sorbitol PO or 50 g in 200 mL as retention enema. 6. Hemodialysis if other methods fail especially in presence of kidney failure.

Hypokalemia Causes 1. GI loss as in vomiting, diarrhoea, nasogastric suction, intestinal or biliary fistulae. 2. Renal loss, e.g. diuretic, mannitol infusions, steroids, renal tubular disorders. 3. Transcellular shifts, e.g. metabolic alkalosis.

Clinical Features 1. Neuromuscular—apathy, weakness, paraesthesiae, hyporeflexia. Hyperventilation if muscles of respiration affected. 2. Cardiac—cardiac arrhythmias such as PVCs followed by VPT and VF. 3. Others—Paralytic ileus

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398 A Handbook of Emergencies and urinary retention may be the presenting features occasionally.

Investigation 1. Serum potassium. ECG: Flat or inverted T waves with ST depression, prominent U waves.

Management KC1 1 g TDS PO if possible. If serum K < 3 mEq/L 180–120 mEq of KC1 in dextrose infusion over 24 hours. But if serum K < 2 mEq/L or evidence of cardiac dysfunction 60–80 mEq in dextrose infusion can be given over 2 hours. Note: IV potassium should be administered very slowly in patients with renal insufficiency or metabolic acidosis. Also when giving high doses two separate veins should be used because of danger of thrombophlebitis.

Calcium Hypocalcemia Causes 1. Hypoparathyroidism. 2. Vitamin D deficiency. 3. Alkalosis. 4. Magnesium depletion. 5. Sepsis. 6. Renal failure. 7. Acute pancreatitis. 8. Hypoalbuminemia.

Clinical Features Tetany, seizures in severe cases. Prolonged QT interval.

Management Calcium gluconate 10–20 mL 10% IV slowly. Since the effect lasts a few hours. IV infusion of 20 mL of the drug in 500 mL dextrose over 2–3 hours.

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Hypercalcemia Causes 1. Excessive osteolysis – Hyperparathyroidism, meta­ static cancer, myelomatosis, Vitamin D intoxication, hyperthyroidism, immobilization. 2. Excess GI calcium absorption and/or intake—Milk-alkali syndrome, sarco­ idosis, vitamin D intoxication. 3. Elevated concentration of plasma proteins. 4. Uncertain mechanism—Addison’s disease, myxoedema, thiazide diuretics.

Clinical Features Constipation, anorexia, nausea, vomiting, abdominal pain and ileus. Also nocturia, polyuria and polydipsia. More severe elevation of serum Ca (> 12 mg/dL) is associated with irritability, confusion, delirium, stupor, and coma.

Management 1. N saline infusion 2L followed by 60–80 mg Frusemide q2-4 hours for 24 hours. 2. Calcitonin 4–8 IV/kg SC or IM q6-l2h can reduce serum Ca within 12 hours. 3. Mithramycin 25 µg/kg as infusion over 6 hours. Action slower than clacitonin. 4. Hemodialysis if above methods fail. Treatment of choice in presence of kidney failure.

Magnesium Hypomagnesemia Causes 1. Diuretics such as frusemide. 2. Chronic alcoholism. 3. Malabsorption. 4. Reduced intake. 5. Use of aminoglycosides.

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400 A Handbook of Emergencies

Clinical Features Usually associated with hypokalemia. Muscle weakness, arrhythmias, carpopedal spasm.

Management Mag. sulphate 1 mEq/kg for 2 h, and 0.5 mEq/kg for 3 days. (5 mL of 10% solution = 4 mEq of elemental Mg). If cardiac arrhythmia or seizures 4 mL of 50% solution infused over 2 minutes followed by 10 mL 50% in 500 mL N saline over 6 h, then bd for another 5 days. Half the dose at slower rate of infusion if renal insufficiency.

Hypermagnesemia Causes 1. Administration of magnesium containing antacids in CKF. 2. Diabetic ketoacidosis complicating kidney failure.

Clinical Features Hypotension and with very high levels complete heart block, respiratory failure, mental obtundation progressing to coma.

Management 1.20 mL 10% calcium gluconate IV. 2. Frusemide. 3. Hemodialysis if kidney failure.

Acid-base Disturbances A large number of metabolic events are pH sensitive and maintenance of stable acid-base balance is therefore of critical importance. For assessment of degree of acid- base disturbance estimation of blood pH is essential.

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Metabolic acidosis (Reduced pH not explained by increased PaCO2). Causes: 1. Normal anion gap: Diarrhoea, intestinal and pan­ creatic fistula, renal tubular acidosis, treatment with carbonic anhydrase inhibitors. 2. Increased anion gap: Diabetic ketoacidosis, starvation ketoacidosis, lactic acidosis, renal failure, salicylate or methyl alcohol poisoning. Clinical features: 1. Hyperventilation. 2. Drowsiness progressing to coma. 3. Odour of breath: Fruity in diabetic acidosis, ammoniacal in uremia. Management: 1. Soda bicarb 75–100 mL 7.5% as bolus. Further administration to keep pH above 7.3. Amount of carbonate to be given can be calculated from the formula: Soda bicarb = Body wt (kg) × 0.3 base deficit. 2. Hemodialysis if other methods ineffective or in pts. with renal failure when saline diuresis is not advisable. 3. Treatment of the cause. Metabolic alkalosis (Raised pH out of proportion to changes in PaCO2) Causes: 1. Vomiting or nasogastric aspiration. 2. Diuretics especially frusemide. 3. Excessive administration of alkali esp. in presence of associated renal dysfunction. 4. During corticosteroid therapy, Cushing’s syndrome. Clinical features: Mental obtundation, seizures, cardiac arrhythmias. Investigation: Raised serum bicarbonate and raised pH.

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402 A Handbook of Emergencies Management: 1. N saline infusion; volume depending on degree of fluid loss and electrolyte disturbance. Chloride deficit can be estimated from the formula: Chloride deficit = 0.27 × weight (kg) × 100 – present Cl in mEq/L. 2. KCl infusion 20–40 mEq. 3. Hemofiltration if severe metabolic alkalosis. It can be combined with careful use of N saline and KCl dextrose infusion. Respiratory acidosis (that is ventilatory failure) due to rise an PaCO2 and drop in pH and can complicate both acute and chronic respiratory failure. For causes and management refer to respiratory emergencies section. Respiratory alkalosis (that is alveolar hyperventilation): The decreased PaCO2 explains the increased pH. Causes: 1. Stress hyperventilation. 2. Hypoxic stimulus to ventilation—alveolar disease, right to left shunt, high altitude. 3. Salicylate poisoning. Clinical features: Obvious hyperventilation. Tetany. Circumoral paraesthesiae. Giddiness and syncope may occur. Diagnosis: Fall in arterial PaCO2 and in a carbonic acid content of plasma. Management: Reassurance if due to anxiety. Rebreathing from a paper bag may be useful. Correction of overventilation if on ventilator. Note: Guidelines to estimate the degrees of abnormality resulting from acute changes in PaCO2. For every increase in PaCO2 of 20 mg Hg (2.6 kPa) above normal, the pH falls by 0.1. For every decrease of PaCO2 of 10 mm Hg (1.3 kPa) below normal, the pH rises by 0.1. Any change in pH outside these parameters is therefore metabolic in origin.

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20

Acute Poisoning

Acute poisoning as a result of accidental or deliberate ingestion or inhalation of drugs or chemicals is a common medical emergency. Acute poisoning is diagnosed through history taking and examination and occasionally in unconscious patients by exclusion of other causes.

Approach to a Case of Poisoning In any case of poisoning, the priority is to assess, and if necessary offer life support to keep the patient alive.

Immediate Management 1. Respiration: Food, vomit, secretions and dentures should be removed from patient’s mouth and the pharynx and tongue prevented from falling back. If patient is comatose and the gag or cough reflex absent or weak, either an airway or preferably, an endotracheal tube should be inserted. Patient should be nursed with the head down in left lateral position to minimise risk of aspirating gastric contents into the lungs. Oxygen should be given in 100% concentration. Ventilation may be required in severe cases. If respiratory depression is due to an overdose of opioid,

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404 A Handbook of Emergencies Naloxone, or if Benzodiazepine, Flumazenil should be given at once. 2. Cardiovascular function should be assessed by measuring pulse, BP and temperature. ECG should be recorded in patients who are moderately or severely poisoned. If patient is in shock, he should be placed in head low position. A large peripheral vein should be secured and a plasma expander or 200 mL of crystalloid given to start with. If this is not effective, Dobutamine 5–40 µg/kg/min is helpful in maintaining effective cardiac output. Dopamine 2–5 µg/kg bw/ min is an alternative. Low dose Dopamine 2.5 µg/ kg/min may prevent onset of acute kidney failure in such patients. A self-retaining Foley catheter should be passed to measure urine output every hr. 3. Trial of antidotes: (a) Dextrose 25 mL of 50% for correction of possible hypoglycemia. Thiamine 100 mg can be given in addition in alcoholics with severe hypoglycemia. (b) Naloxone 2 mg IV if no response to Dextrose. Improvement in respiration will be shown in 2 minutes. (c) Flumazenil l mg IV has been used to make a clinical diagnosis of Benzodiazepine poisoning. 4. Admission to hospital is necessary if there is cardio­ respiratory depression or other complications. In patients without such depression, the toxic substance ingested and the time elapsed since ingestion, circum­ stantial evidence, clinical features and toxicological and biochemical results can determine whether hospitalization is required.

Diagnosis of Poisoning 1. History: In adults, a diagnosis of acute poisoning is usually made on the basis of patient’s history,

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though statements about the nature and quantity of what has been taken may not be taken for granted. This is because acute poisoning in this age group is usually deliberate. Vital clues may be obtained from circumstantial evidence such as empty bottles or tablets or capsules found nearby. Suicide notes are reliable indicator of drug overdose. 2. Physical signs are important in trying to elucidate the cause of unexplained coma. a. Neurological examination: (i) Localizing signs exclude diagnosis of acute poisoning unless they can be explained by some pre-existing illness. (ii) Pyramidal tract signs (hypertonia, hyperreflexia and extensor plantars) are found commonly in tricyclic antidepressant poisoning of mild-to-moderate severity, and also with other drugs with marked anticholinergic action (e.g. the older antihistamines). However, all these signs may be abolished in deep coma. (iii) Abnormal movements: Acute dystonic movements, including acute torticollis, orolingual dyskinesias and oculogyric crises are usually caused by Meto­ clopramide, less often by Haloperidol, Proclorpera­ zine and Trifluoperazine. Choreo-athetosis can be a presenting feature of poisoning with O.P. insecticides and pemoline. (iv) Pupillary changes: Widely dilated pupils that react poorly to light may be caused by toxins with anticholinergic action (e.g. tricyclic antidepressants) or sympathomimetic effects, or which cause blindness. (e.g. quinine and methanol). Miosis is usually due to opioid analgesics or toxins with anticholinesterase action (e.g. O.P. insecticides). The degree and speed of reaction of the pupils to light is of no clinical value.

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406 A Handbook of Emergencies (v) Ocular movements: Transient strabismus has been attributed to Phenytoin, Carbamazepine and Tricyclic antidepressants. Dysconjugate roving eye movements have been reported in poisoning with Tricyclic antidepressants, Phenothiazines, Benzodiazepines, Barbiturates and Ethanol. (vi) Loss of oculocephalic and oculovestibular reflexes is usually evidence of brainstem damage. In acute poisoning, however overdose with Carbamazepine, Phenytoin and Tricyclic antidepressants can be assooiated with loss of these reflexes, but patients recover completely. b. Lungs: Pulmonary oedema can be the result of a number of drugs. Cholinergic drugs can induce bronchospasm and increase in bronchial secretions. c. Skin: Sweating and moist skin are often seen with poisons having a cholinergic and sympathomi­ metic action. Skin is dry and hot in poisons with anticholinergic effect. Skin blisters while not diagnostic of specific poisons, are sufficiently common in poisoned patients, and sufficiently uncommon in patients unconscious from other cause, to be of diagnostic value. Feature cluster Coma, pyramidal tract signs, myoclonus, strabismus, mydriasis, sinus tachycardia, skin hot and dry, coma, hyporeflexia, flexor plantars, hypotension

Likely poisons Tricyclic antidepressants; less commonly orphenadrine, thioridozine antihistamines, barbiturates, benzodiazepines and alcohol combinations, severe tricyclic antidepressant poisoning Contd...

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Acute Poisoning 407 Contd... Feature cluster

Likely poisons

Coma, miosis, reduced respiratory rate Nausea, vomiting, tinnitus, deafness, sweating, hyperventilation, vasodilatation, tachycardia Coma, miosis, sweating, fasciculations, seizures, bronchospasm, severe respiratory and circulatory depression Restlessness, agitation, mydriasis, anxiety, tremor, tachycardia, arrhythmias, convulsions Metabolic acidosis, pulmonary oedema, peripheral circulatory failure, acute renal failure Blindness (usually with other features)

Opioid analgesics Salicylates

Organophosphorus poisoning

Sympathomimetics (cocaine, amphetamine, ephedrine, phencyclidine) Ethylene glycol, methanol

Quinine, methanol. Occasionally ethylene glycol

Investigations Non-toxicological Investigations a. Inspection of blood: (i) Chocolate-coloured blood indicates presence of methaemoglobinemia caused by such drugs as Dapsone, or ingestion of nitrates and nitrites. (ii) Pink plasma suggests hemolytic poisons e.g. Sodium chlorate. (iii) Brown plasma points to presence of circulating myoglobin secondary to rhabdomyolysis. b. Inspection of urine: (i) Brown discoloration may be due to presence of Hb, intravascular hemolysis, myoglobin

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408 A Handbook of Emergencies secondary to rhabdomyolysis or metabolites of paracetamol. (ii) Crystals may be prominent after overdose with Primidone or ingestion of Ethylene glycol. c. Laboratory investigations: (i) Prolongation of pro­ thrombin time could be secondary to anticoagulant ingestion or liver necrosis from excess paracetamol. (ii) Plasma K–hypokalemia can be due to Theophylline and sympathomimetic agents. (iii) Plasma bicarbonate – reduced levels may indicate respiratory alkalosis (Salicylates) or metabolic acidosis which is more serious and usually indicates severe intoxication with CO, cyanide, ethylene glycol, iron salts, isoniazid, methanol, paracetamol, or tricyclic antidepressants. (iv) Hypoglycemia is usually due to overdose with insulin or oral hypoglycemic agents and is a feature of severe liver damage (mainly by paracetamol). (v) Hyperglycemia can occur in intoxication with a large number of agents, notably sympathomimetic drugs e.g. Theophylline. (vi) Hypocalcemia may be a feature of poisoning with fluoride salts, hydrofluric acid burns and ethylene glycol ingestion. (vii) Liver function tests. Paracetamol overdose can cause rise in plasma alanine aminotransferase activity exceeding 5000 U/L. d. Radiology is of little diagnostic value. Some enteric coated or sustained release formulations may show up on plain abdominal radiographs but, with exception of iron salts, ordinary formulations seldom do. e. EGG: Presence of sinus tachycardia, with prolonged PR and QRS intervals in an unconscious patient should prompt consideration of tricyclic antidepressant as the cause. Overdosage with cardiac glycosides or potassium salts also induces characteristic ECG changes.

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Analytical Toxicology Measurement of the concentration of a specific toxin in blood or urine can also be used to establish a diagnosis of poisoning. Known toxins: Emergency measurement of plasma concentrations is indicated in case of ethanol, ethylene glycol, organophosphorus, iron, lithium, paracetamol, methanol, theophylline, salicylates. Unknown toxins: Plasma paracetamol concentration should be measured in each unconscious poisoned patient Urine is usually a more appropriate fluid for detecting unknown poisons. Once identified, their concentration in blood or plasma can be determined by specific methods, if necessary.

Further Management of Poisoning Reducing Absorption a. Gastric lavage: Efficacy of a stomach washout decreases with time, therefore lavage should be considered only if a patient has ingested life-threatening amounts of a toxic agent up to 1 hour previously. It is dangerous to perform gastric lavage on an unconscious patient without having a cuffed endotracheal tube in place. Put patient in head down position and pass a well lubricated orogastric tube into the stomach. Aspirate the stomach contents and introduce 250 mL lukewarm water. Aspirate after 2–3 minutes. Repeat the procedure until 2 litres have been used or until the lavage fluid is clear. Gastric lavage is contraindicated in case of consumption of petroleum distillates or of corrosive poisons.

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410 A Handbook of Emergencies b. Emesis: (i) Making patient drink a glass of salt water or stimulating the pharynx with the fingers are home remedies though the efficacy is low. (ii) Syrup of Ipecacuanha 30 mL in 16 oz of water for adults, 15 mL in 50 oz of water for children. However, there is no clinical evidence that it significantly reduces drug absorption as an emetic. c. Activated charcoal absorbs a wide variety of drugs, exceptions being acids and alkalis, cyanide, ethanol, ethylene glycol, iron, lithium, methanol. Single dose 50–100 g (1g/kg) of charcoal mixed with 4 parts of water, lemon barley or fruit juice or sorbitol instilled via lavage tube will prevent significant absorption of drugs such as aminophylline, aspirin, carbamazepine, digoxin, paracetamol, phenobarbitone, phenytoin, dapsone, theophylline, piroxicam. 50 g of charcoal should be repeated q4h till patient has recovered. d. Use of antidotes is discussed in the management of poisoning by specific substances after this section.

Management of Associated Conditions 1. Hypothermia: A core temperature below 35°C may be recorded in deeply unconscious patients who have been exposed in cold weather for several hours. Hypothermia is best treated by placing the patient in a room with a temperature at 27–29°C and covering him with a blanket to minimize heat loss. 2. Convulsions caused for example by tricyclic anti­ depressant drugs can usually be controlled with IV Diazepam, once hypoxemia and acidosis have been corrected. Rarely muscle relaxation and mechanical ventilation are required together with a drug such as Phenytoin.

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Acute Poisoning 411

3. Fluid, acid-base and electrolyte balance: Patients who are vomiting should be given fluids IV. Severe hypokalemia (such as that caused by theophylline and β2-agonist poisoning) should be corrected by infusing potassium to prevent onset of arrhythmias. Metabolic acidosis is a common complication of severe poisoning and, after correction of hypoxia, infusion of sodium bicarbonate may be necessary. 4. Hypoglycemia may follow overdose of insulin, sulpho­ nylureas and ethanol and may occur in paracetamolinduced liver failure. It is corrected by infusion of 10% Dextrose if necessary after bolus injection of 50 mL 50% Dextrose. 5. Hypertension: A few drugs (e.g. monoamine oxidase inhibitors) may produce severe systemic hypertension. To prevent this α-adrenergic blocking agent such as Prazosin 1–4 mg IV should be given. 6. Pain: If a corrosive substance has been ingested patient will probably have severe pain which can be relieved with an opioid. 7. Nursing care. Unconscious patients should be turned from side to side at least every 2 hours. Bullous lesions should be left until they burst to reduce the risk of infection. Deroofing should be performed when the blister bursts and a non-adhesive dressing then applied.

Increasing Elimination 1. Alkaline diuresis increases the elimination of salicylates, phenobarbitone and barbitone. Before commencing alkaline diuresis it is important to correct plasma volume depletion, and electrolyte and metabolic disturbances. Sodium bicarbonate is

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412 A Handbook of Emergencies administered as 7.5% solution IV infusion to ensure that the pH of urine is more than 7.5, preferably close to 8.5. Alkaline diuresis is a metabolically invasive procedure which requires frequent biochemical monitoring. Multidose charcoal is easier to use, though in patients severely poisoned with salicylic acid, combination of both techniques is effective. 2. Multiple-dose activated charcoal (MDAC): Use of MDAC should be considered if patient has ingested a life-threatening amount of one of the following drugs – Aspirin, Carbamazepine, Phenobarbitone, Dapsone, Quinine, Theophylline. Charcoal should be adminis­ tered in initial dose of 50–100 g and then at a rate of not less than 12.5 g/h, via nasogastric tube. Smaller doses (10–25 g) can be used in children. If patient has ingested a drug which induces protracted vomiting (e.g. Theophylline), IV Ondansetron 2–4 mg is effective as antiemetic and this allows administration of MDAC. 3. Dialysis and hemoperfusion are indicated for patients with a combination of severe clinical features and high plasma toxin concentrations. Peritoneal dialysis increases elimination of ethylene glycol and methanol, but is less effective than haemodialysis. Haemodialysis significantly enhances elimination of salicylate, lithium, methanol, isopropanol, ethy­ lene glycol and ethanol. Charcoal hemoperfusion can, within 4–6 hours, significantly reduce body burden of compounds with a low volume of distri­ bution namely barbiturates, carbamazepine, disopyramide, glutethimide, meprobamate, methaqualone, theophylline and trichlorethanol derivatives. How­ever MDAC is as effective as haemoperfusion in

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phenobarbitone, carbamazepine and theophylline poisoning and is simpler to use.

Poisonous Substances For sake of convenience the specific substances are discussed in alphabetical order.

ACE Inhibitors (Captopril, Enalapril, Amlodipine Lisinopril).

Clinical Features Anorexia, nausea, abdominal discomfort, predominate initially, and are followed by headache and paresthesiae. Hypotension, sinus tachycardia, bronchospasm and hyperkalemia can also develop.

Management (a) Gastric lavage if patient presents within 1 hour of substantial overdose. (b) Activated charcoal 50–100 g. (c) Supportive measures to correct hypotension. (d) If marked hyperkalemia 50 g glucose and soluble insulin 15 units.

Alcohol Ethanol Severe ethanol intoxication can follow consumption of 300–500 mL of a strong spirit (e.g. whisky or gin). Clinical features: Depending on blood ethanol con­ centration. (a) Inebriation—slurred speech, emotional instability, incoordination, loss of sensory perception. (b) Intoxication—blurred vision, loss of sensory perception, muscular incoordination, ataxia, coma, convulsions.

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414 A Handbook of Emergencies Very severe intoxication—coma, hyporeflexia, respiratory depression, poor airway protection. Management: (a) Supportive measures with particular care to protect the airway. In more severe cases acidbase status should be determined 2-hourly. Blood sugar should be determined hourly. If blood sugar falls in spite of infusion of 5–10% dextrose, 50 mL 50% dextrose should be given because hypoglycemia is usually unresponsive to glucagon. (b) Management of lactic acidosis requires not only correction of hypoglycemia, hypovolemia and circulatory insufficiency, if present, but also infusion of sodium bicarbonate. (c) Alcoholic ketoacidosis is usually corrected by infusion of 5% glucose alone; insulin is necessary only in diabetics. (d) Hemodialysis if blood ethanol exceeds 7500 mg/L, and/or metabolic acidosis is present which is not easily correctable by above measures.

Methanol Methanol is found in antifreeze solutions, paint removers, varnishes and shoe polishes, and is widely used as solvent to denature ethanol. Methylated spirit contains 5% methanol; it is toxic, not because of the methanol, but as a result of the 95% ethanol it contains. Clinical features: When ingested alone, methanol causes mild and transient inebriation and drowsiness. After a latent period (usually 8–36 h), nausea, vomiting, abdominal pain, headache, dizziness and coma supervene. Blurred vision and diminished visual acuity may follow, and the presence of dilated pupils nonreactive to light suggests likelihood of permanent blindness. A severe metabolic acidosis develops in all serious cases. This may be associated with hyperglycemia and raised serum amylase activity.

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Management: (1) GL. (2) Ethanol. Loading dose 50 g (e.g. 150 mL gin, whisky or vodka) p.o. followed by either further oral doses or IV infusion of 10–12 g ethanol/h to produce a blood ethanol concentration of about 1 g/L. Ethanol should be continued until methanol is undetected in blood. Sodium bicarbonate for metabolic acidosis. Hemodialysis if patient has ingested more than 30 g methanol, develops metabolic acidosis or mental, visual or fundoscopic abnormalities, or blood methanol concentration >50 mg/L. Folinic acid 30 mg IV q6h may protect against ocular toxicity.

Amiodarone Clinical Features Nausea and vomiting, headache, flushing, paraesthesiae. ataxia, tremor, vertigo. Marked bradycardia, hypotension.

Management GL, AC 25–100 g. Dobutamine for severe hypotension 5–15 µg/kg/min IV after adequate circulating blood volume is established. Dopamine 2–5 µg/kg/min IV should also be given for its effect on renal vasculature.

Ammonia Clinical Features Mild to moderate exposure leads, within minutes, to irritation of eyes and upper respiratory tract, headache, nausea, throat pain, bronchospasm, increased mucus production, coughing and mild-to-moderate respiratory distress. Severe exposure may cause pain during breathing, hemoptysis and life-threatening swelling of mucous membranes of larynx and airway leading to

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416 A Handbook of Emergencies bronchospasm, pulmonary oedema and severe respiratory distress. Exposure of skin and eyes to concentrated ammonia water may cause corrosive damage. Ingestion produces severe caustic lesions of mucous membranes of oropharynx, oesophagus and stomach. Oesophageal and gastric perforation may occur.

Management (i) Airway: Early inspection of upper airways because the mucous membranes may be very oedematous in severe cases, precluding oral endotracheal intubation; tracheostomy or cricothyrotomy may be necessary. Early intubation should be avoided because an endotracheal tube may increase risk of infection. (ii) Eyes and skin exposed to ammonia water to be irrigated with water immediately and continued for 15–30 minutes. Topical antibiotics may prevent secondary infection of the eye. Corticosteroids may retard epithelialization and cause thinning of corneal strauma. (iii) GI tract: Neutralizing agent should not be administered because the resultant exothermic reaction may worsen the injury. Following severe exposure, oesophagoscopy should be performed to introduce an NG tube to prevent complete obstruction of oesophagus.

Anticonvulsants Carbamazepine Clinical features: Anticholinergic effects: Dry mouth, convulsions. In addition drowsiness progressing to coma, nystagmus, ataxia and incoordination may occur. Pupils dilated and divergent strabismus may be present. Hallucinations may occur, particularly in recovery phase.

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Management: AC 50–100 g initially with repeated doses of 12.5 g/h.

Phenytoin Clinical features: Acute poisoning results in nystagmus, dysarthria, ataxia, drowsiness and coma. Management: Single dose of 50–100 g AC will reduce absorption.

Sodium Valproate Clinical features: Fever, muscle spasms, hypocalcemia, liver damage and thrombocytopenia. Drowsiness is common and toxic encephalopathy and optic atrophy have been described. Management: Supportive treatment. Correction of electrolyte and metabolic abnormalities. Neither MDAC nor dialysis promote elimination.

Antidepressants Trycyclic Antidepressants and Related Drugs (Amitriptyline, Imipramine, Doxepin, Nortriptyline, Clomipramine, Fluoxetine, Sertraline, Mianserin, Trazodone). Clinical features: Symptoms of overdose usually appear within 4 hours. Initially dry mouth, blurred vision, sinus tachycardia and drowsiness. In addition pyramidal signs may develop. In more severe poisoning—coma, con­vulsions, respiratory depression, hypotension and ECG disturbances (prolonged QT interval and intra­ ventricular conduction defects). Further complications include acidosis (respiratory and metabolic) and hypokalemia.

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418 A Handbook of Emergencies Management: (a) GL should be avoided because it may wash quantities of the drug into the duodenum, leading to rapid drug absorption and increased risk of acute toxicity. (b) AC 50–200 g will reduce drug absorption significantly. Repeated doses not useful. (c) Supportive management: (i) Acid-base balance should be monitored and acidosis corrected. (ii) Arrhythmias should be managed conservatively with sodium bicarbonate. Antiarrhythmic drugs are not used because they may aggravate adverse effects of tricyclics on the myocardium. (d) Convulsions should be controlled with diazepam, though this carries a risk of respiratory depression and patient may subsequently require ventilation. In recovery phase, patient becomes acutely disturbed and needs sedation with Diazepam.

Selective Serotonin Re-uptake Inhibitors Toxicity following overdose is considerably less than with tricyclic drugs. Clinical features: Nausea, vomiting, agitation and tachycardia, convulsions may develop after large doses (> 1.5 g). Patients who have taken SSRIs in combination with serotoninergic effects (e.g. Tryptophan) or an MAOI are at risk of serotoninergic syndrome (restlessness, hyperpyrexia, rhabdomyolysis and kidney failure). Management: is supportive and symptomatic. Sero­ toninergic syndrome requires more intensive therapy, particularly for hyperpyrexia. Use of dantrolene to reduce muscle spasm, or paralysis and ventilation may be required in severe cases.

Monoamine Oxidase Inhibitors (Phenelzine Iproniazid) Clinical features: Agitation, abnormal movements, hyper-reflexia, muscular rigidity, convulsions, sweating,

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hyperpyrexia, hyperventilation, tachycardia, urinary retention, coma. Management: Supportive therapy. For agitation parenteral Diazepam or Chlorpromazine. Ventilation may be required for respiratory embarrassment due to muscular spasm; Dantrolene may reduce muscular spasm. Acute interactions can occur when MAOIs are given concurrently with opiates, sympathomimetic drugs, Levodopa or anaesthetic agents leading to dramatic rises in BP. These are managed with α-blockers by slow infusion.

Antipsychotics (Phenothiazines, Thioxanthenes, Butyrophenones).

Clinical Features (a) General: Depression of consciousness, hypotension, respiratory depression, hypothermia, cardiac arrhythmias, convulsions. (b) Extrapyramidal reactions (which may occur even with therapeutic doses): Dystonia, dyskinesia, akathisia. (c) Neuroleptic malignant syndrome: Hyperthermia, fluctuating consciousness, muscular rigidity, and secondary kidney failure if rhabdomyolysis occurs.

Management Supportive therapy. For arrhythmia first correction of acidosis with sodium bicarbonate and then cardiac pacing. Symptomatic treatment for other features. Elimination techniques have no role.

β-blockers Clinical Features Earliest feature of overdose is sinus bradycardia, and if overdose is large, severe hypotension, coma and

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420 A Handbook of Emergencies convulsions may occur. Cardiorespiratory arrest may supervene. ECG may show conduction defects, ST elevation, VPCs and absent P waves.

Management (a) GL if substantial overdose 1 hour previously. (b) AC 50–100 g. (c) Atropine 0.6–1.2 mg IV may prevent vagal-induced collapse during the procedure. (d) For severe hypotension Glucagon 50–150 µg/kg as bolus over 1 min, followed by infusion of 1–5 mg/h according to response. In severe cases further doses may be necessary. Temporary transvenous pacemaker wire may have to be inserted. Convulsions are usually short-lived.

β2-agonists (Salbutamol, Terbutaline, Fenoterol, Pirbuterol, Rimiterol). Poisoning may follow ingestion or therapeutic IV infusion.

Clinical Features Excitement, tremor, palpitation, which may be followed by agitation and convulsions. Electrolyte and acid-base disturbances are common. Hypokalemia may precipitate arrhythmias. Hyperglycemia and lactic acidosis may occur, as also changes of myocardial ischemia on ECG.

Management (a) GL. (b) AC. (c) Potassium 40–60 mmol/h in 5% Dextrose. (d) Propranolol 1–5 mg slow IV will also relieve hypokalemia, but may aggravate pre-existing obstructive airway diseases. (e) Convulsions are usually transient, if necessary, Diazepam 5 mg IV.

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Benzodiazepines (Chlordiazepoxide, Diazepam, Lorazepam, Oxazepam, Alprazolam).

Clinical Features Drowsiness, dizziness, ataxia, dysarthria, nystagmus, less commonly coma and hypotension. Respiratory depression is a potential complication, particularly when ethanol and other CNS depressants have also been ingested, or patient has pre-existing COPD.

Management Flumazenil 0.5 mg IV over 1 minute. Same dose is repeated if no response or only partial response, or IV infusion 0.1–0.5 mg/h. Most patients respond to Flumazenil 1 mg.

Calcium Channel Blockers (Verapamil, Diltiazem, Amlodipine, Felodipine, Nifedipine, Isradipine, Nimodipine).

Clinical Features (a) CVS: Hypotension, flushing, bradycardia (sinus bradycardia, AV block, sinus arrest); tachycardia (sinus tachycardia, AV nodal escape rhythms), asystole; cardiac failure and cardiogenic pulmonary oedema, worsening or precipitation of angina. (b) Neurological: Headache, lethargy, fatigue, stupor, delirium, respiratory depression, coma, seizures. (c) GI: Nausea, vomiting, ileus. (d) Metabolic: Hyperglycemia, lactic acidosis. (e) Others: Non-cardiogenic pulmonary oedema. Acute overdosage of even a few tablets can produce toxicity in patients with pre-existing heart disease and those receiving interacting drugs (such as β-blockers and Digoxin).

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422 A Handbook of Emergencies

Management (a) Normal saline bolus (10–20 mL/kg). (b) 10% calcium chloride 5–10 mL, or 10% calcium gluconate 10–20 mL over 5 minutes. Repeat q3–5 minutes up to 3–5 doses. If response, institute calcium infusion (10% calcium chloride 1–10 mL/h, (monitor) serum calcium after 30 mL of calcium chloride or equivalent. (c) Glucagon 0.075–0.15 mg/kg IV (use water for injection as diluent). Repeat q5–10 minutes as needed. If response, consider infusion of 0.075–0.15 mg/kg/h. (d) Atropine, isoprenaline and/or pacing may be tried if associated symptomatic brady­ cardia. (e) Dopamine infusion, if persistent hypotension. (f ) If no response to the above, begin insulin euglycemia therapy – Insulin bolus IU/kg with 50% Dextrose 25 mL IV, followed by insulin infusion 0.5 g/h with 50% dextrose infusion 0.5 g/h, adjusted according to hourly glucose checks. (g) As a last resort, extracorporeal BP support (e.g. cardiopulmonary bypass) may be considered.

Cannabis Smoking is the usual route of abuse, but is occasionally ingested, or made into a ‘tea’ and injected IV.

Clinical Features Clinical features of acute intoxication include euphoria with drowsiness, distorted and heightened images, colours and sounds, altered tactile sensations, sinus tachycardia, conjunctival suffusion, hypotension, ataxia with visual and auditory hallucinations, depersonalization and acute psychosis {with heavier use). Cannabis infusions injected IV may cause nausea, vomiting and chills within minutes; after about 1 hr, profuse watery diarrhoea, tachycardia, hypotension and arthralgia may develop.

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Management Sedation with Diazepam 5–10 mg IV repeated as necessary. Chlorpromazine 50–100 mg IM or Haloperidol 2.55 mg IM is occasionally required.

Carbon Monoxide Most common sources of the gas in acute poisonings are motor vehicle exhaust fumes and smoke from fires. Also use of charcoal grills in confined spaces or badly installed domestic gas heating appliances.

Clinical Features Early features are headache, dizziness, nausea, vomiting and progressive impairment of consciousness, Hyperventilation, hypotension, increased muscle tone, hyperreflexia, clonus and extensor plantar responses develop as the severity of poisoning increases. Skin is more likely to be cyanosed than have the cherry-pink colour wrongly considered to be classical. Metabolic acidosis with normal oxygen tension but reduced O2 saturation is characteristic. Rhabdomyolysis, MI, pulmonary oedema and papilloedema secondary to cerebral oedema are potential complications.

Management Patient should be removed from the toxic atmosphere. A clear airway, adequate ventilation and BP should be assured. Assisted ventilation may be necessary. Dantrolene 1 mg/kg by rapid IV injection, repeated as necessary to cumulative dose of 10 mg/kg can correct metabolic acidosis. Administration of alkalis is contraindicated as it further impairs O2 release to the tissues. If cerebral oedema–Mannitol or Dexamethasone. Hyperbaric O2

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424 A Handbook of Emergencies for 2 hours or longer at pressure of 2–3 atmospheres. Indications: Patient in coma at any stage since exposure to CO, neurological or psychiatric features, COHb content >2%, or pregnancy.

Chlorine Clinical Features Mild-to moderate exposure leads within minutes to irrita­ tion of eyes and upper respiratory tract, nausea, headache, throat pain, bronchospasm, increased mucus production, cough and mild-to-moderate respiratory distress. Severe exposure may cause pain during breathing, hemoptysis, and life-threatening swelling of larynx and airways, bronchospasm, pulmonary oedema and severe respiratory distress.

Management There is no specific treatment for airway injury caused by chlorine. Tracheostomy or coniotomy may be necessary in exposed individuals who suffer severe oedema of mucosal membranes. Systemic antibiotics are not recommended because risk of infection with resistant organisms is increased.

Clonidine Clonidine poisoning may be life-threatening, particularly in children.

Clinical Features Respiratory depression, bradycardia, hypotension, coma. Also dry mouth, headache, irritability, hypotonia, loss of tendon reflexes, constricted pupils. When plasma concentrations are high, peripheral α-agonist activity predominates, causing vasoconstriction and hypertension.

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Management Gastric emptying. Atropine 1–2 mg IV for bradycardia. If severe hypertension Phentolamine 5–60 mg IV over 10–30 minutes, or Phenoxybenzamine 1 mg/kg diluted in 250–500 mL 5% dextrose infused over 60 minutes.

Copper Copper sulphate is available as a blue coloured solution.

Clinical Features Phase 1 (1–24h) GI symptoms. Phase 2 (24–72h): Hepatorenal damage. Phase 3: Hepatic failure and kidney failure. Complications more common in patients seen or brought to hospital 6 hours after ingestion and if more than 15 mL is consumed. Death may result from massive hemolysis or methemoglobinemia.

Management (a) GL preferably with potassium ferrocyanide. (b) Removal of absorbed CuSO4 by chelating agent Penicillamine 0.25–2 g/day until recovery. (c) Dimercaprol 3 mg/kg q8h for 2 days, then bd for 5 days. (d) Dialysis for kidney failure. (e) Forced alkaline diuresis may help since hypovolemia and acidic urine are predisposing factors for pigmentinduced acute renal failure.

Corrosives Strong acids and alkalis have corrosive effects on the gut.

Acids Inorganic acids in cases of poisoning include HCL, hydrofluric, nitric, phosphoric and sulphuric acids. Organic acids include acetic, formic, lactic and trichloracetic acid.

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426 A Handbook of Emergencies Clinical features: (a) Skin: Blistering, ulceration and penetrating necrosis. (b) GI: In 80% of cases oesophagus is unaffected by the acid. Immediate pain in mouth, pharynx and abdomen, intense thirst, vomiting, haematemesis and diarrhoea. Gastric and oesophageal perforation may occur, with resultant chemical peritonitis. (c) Non-GI features include hoarseness, stridor, respiratory distress, laryngeal and epiglottic oedema. Circulatory shock, metabolic acidosis, leucocytosis, acute tubular necrosis, renal failure, hypoxemia, respiratory failure, intravascular coagulation and haemolysis may also occur. Hydrofluoric acid ingestion results in chelation of calcium with resultant weakness, paraesthesiae, tetany, convulsions and disturbed coagulation. Management: Acid burns of skin should be irrigated with water or saline for 15–20 minutes. Hydrofluric acid burns require application of 2.5% calcium gluconate gel and/or SC injection of calcium gluconate 0.5 mL of 10% solution/ cm2 burnt skin, to achieve pain relief; calcium gluconate may also be given intra-arterially. Immersion in ice-cold water if gel is not available. Eyes splashed with acid should be irrigated with saline or water for 15–30 minutes. Local anaesthetic may be required to relieve pain. Specialist ophthalmic advice should be sought. Acid ingestion. Clear airway should be established. Endotracheal intubation or tracheostomy may be required for pharyngeal or laryngeal oedema. Parenteral analgesics for pain. Soluble calcium tablets 10–20 g should be given if hydrofluoric acid ingestion, if patient is able to swallow, followed by 10 mL 10% calcium gluconate IV. Dilution and/or neutralization of the acid are contraindicated. Endoscopy as soon as possible.

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Patients with circumferential ulceration or multiple deep ulcers with areas of necrosis should be admitted to ICU. Laparotomy with resection of necrotic tissue and surgical repair is necessary if there is blackened, ulcerated mucosa of stomach or oesophagus, or evidence of GI perforation.

Alkalis Alkaline substances encountered are sodium hydroxide, sodium carbonate or silicate, sodium phosphate, etc. Clinical features: Alkalis typically damage the oesophagus and spare the stomach. A burning sensation develops in mouth and pharynx with epigastric pain, vomiting and diarrhoea. Oesophageal ulceration with or without perforation may occur. Also stridor, respiratory distress, laryngeal and epiglottic oedema. Management: (a) Clear airway. If life-threatening pharyn­ geal or laryngeal oedema, endotracheal intubation or tracheostomy. (b) Analgesics for pain. (c) Induced emesis and gastric aspiration and lavage are contraindicated as also neutralization of the alkali. (d) Diagnostic endoscopy to beyond the site of first observed oesophageal/gastric lesion should be performed within 12–24 hours. If perforation of GI tract is suspected or if severe hypopharyngeal burns are present, radiographic studies using water-soluble contrast media may be performed as an alternative. Patients with severe burns should be managed in ICU. Total parenteral nutrition or a feeding jejunostomy may be required until GI lesions have healed. Laparotomy should be performed and necrotic tissue resected, if at endoscopy there are second or third degree oesophageal burns, evidence of gastric necrosis, or persistently alkaline gastric pH. (e) Corticosteroids may decrease need for surgical repair of strictures arising from second or third degree burns if they

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428 A Handbook of Emergencies are used in conjunction with oesophageal dilation. Dose: Methyl Prednisolone 40 mg IV q8h or Prednisolone 2 mg/ kg/day IV until oral intake is resumed, when equivalent dose of Prednisolone can be given orally and tapered off over 3–6 weeks. Broad spectrum antibiotics may encourage normal healing process.

Cocaine Clinical Features Acute intoxication produces euphoria, agitation, sinus tachycardia, hypertension, sweating, hallucinations, pro­ longed convulsions, hyperthermia and rhabdomyolysis. Ventricular arrhythmias, acute myocardial infarction, acute myocarditis, stroke, renal or intestinal infarction and cardiorespiratory arrest may complicate severe poisoning.

Management (a) Sedation with Diazepam 10 mg IV repeated as necessary for agitation and convulsions. (b) Active external cooling if the patient’s temperature exceeds 41ºC. (c) Hypertension and tachycardia usually respond to cooling and sedation. β-agonists are contraindicated because of risk of pre­ cipitating paradoxical hypertension. Phentolamine 2–5 mg IV can be used if necessary. (d) Early use of Lora­ zepam with nitrates can relieve chest pain.

Cyanide Clinical Features Ingestion by an adult of 50 mL of liquid hydrogen cyanide or 200–300 mg of one of its salts is likely to be fatal without treatment, though death is likely to be delayed for at least 1 hour. In contrast, when hydrogen cyanide is inhaled,

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symptoms occur within seconds and death within minutes. Acute poisoning is characterised by—Anxiety, dizziness, palpitations, headache and weakness are usually initial features. Loss of consciousness, convulsions, cerebral oedema, pulmonary oedema, cardiovascular collapse, cardiac conduction defects, dysrhythmias and metabolic acidosis are seen in severe cases. Cyanosis does not occur.

Management (1) O 2 with cardiorespiratory support. (2) Antidotes: Dicobalt edetate 300 mg IV (if diagnosis is certain otherwise cobalt toxicity may result), or sodium nitrite 2.25 mg/kg or 4-DMAP 3.25 mg/kg will achieve adequate methemoglobinemia. Sodium thiosulphate 50 mL. 25% solution IV after sodium nitrite is given for synergistic effect. (3) Inj. vitamin B12 5 g IV over 30 minutes.

Digoxin Digoxin toxicity often develops because of the small difference between therapeutic and toxic doses of the drug. Clinically significant increases in serum concentrations can be produced by the addition of Amiodarone, Erythro­ mycin, Quinidine, Quinine or Verapamil to the Digoxin regimen.

Clinical Features (a) GI tract: Anorexia, nausea, vomiting, abdominal pain, diarrhoea, dysphagia. (b) Cardiac: Atrial tachycardia, flutter or fibrillation, sinus arrest, S-A block, A-V block, A-V dissociation. (c) CNS: Malaise, fatigue, stupor, delirium, hallucinations, headache, seizures, photophobia, transient blindness or scotomata, disturbance of colour vision (green-yellow).

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430 A Handbook of Emergencies Assessment of severity: (a) ECG – Early changes include extrasystoles and minor degrees of A-V nodal block, there may be ST depression. Bradyarrhythmias include 2nd and 3rd degree heart block and slow atrial fibrillation and ventricular tachycardias. (b) Electrolytes particularly magnesium and potassium. (c) Digoxin concentration. (Samples taken after 6 hours allow a more accurate estimate of the body’s Digoxin burden).

Management (a) Activated charcoal: If acute overdose of > 0.1 mg/kg less than 2 hours previously. (b) Endotracheal intubation and gastric lavage can lead to increased vagal tone and worsen bradyarrhythmia, premedication with atropine if these are undertaken. (c) Cardiac minitoring and IV access. Normal saline IV. (Glucose may worsen hypokalemia). (d) Correction of hypokalemia and hypomagnesemia. (e) Digoxin Fab binds to digoxin in a 1:1 ratio; thus the dose of Digoxin Fab required depends on the amount of Digoxin to be neutralised. Indications for Digoxin Fab are any of the following: (i) Life-threatening dysrhythmias (VT/VF, 3° heart block). (ii) Cardiac compromise—in patients with underlying cardiac disease. (iii) Serum potassium > 6 mmol/L. (iv) Digoxin level > 7.8 µg/L. Calculation of dose: (a) From dose ingested—one 40 mg vial of Digoxin Fab binds 0.6 mg of Digoxin; thus ingestion of 3 mg of Digoxin requires 5 vials. (b) From serum Digoxin concentration: This method uses the estimated volume of distribution (adults 8 L/kg, children 2–10 years 13 L/kg, infants 2–24 months 16 L/kg) and measured Digoxin concentration. Total body burden of Digoxin = concentration in µg/L (nmol/L × 1.28) × weight (kg) × volume of distribution. Number of 40 mg

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vials of Digoxin Fab required = total body burden/0.6. (c) By titration: The Digoxin Fab dose may be titrated against the clinical response: 4–6 vials of Digoxin Fab are given and further vials are administered depending on their clinical effect. This method may be more useful in patients with ventricular arrhythmias, in whom treatment is more urgent. If Digoxin hyperkalemia or heart block than in those with ventricular arrhythmias, in whom treatment is more urgent. If Fab is not available, heart block should be treated with pacing and tachycardia may be treated with magnesium. Magnesium: Its calcium channel blocking properties make it useful in tachyarrhythmias. Other drugs: Atropine 1 mg IV repeated as necessary to patients with bradyarrhythmias. If other antiarrhythmic drugs are required, class 1B drugs should be used because they do not impair AV nodal conduction.

Ecstasy Clinical Features Mild poisoning: Agitation, tachycardia, hypertension, widely dilated pupils, trismus and sweating. More severe cases: Hyperthermia, hyponatremia, DIC, rhabdomyolysis, severe hepatic damage including fulminant hepatic failure, and acute renal failure.

Management Diazepam 10 mg IV for agitation. IV fluids and dantrolene 1 mg/kg IV for hyperthermia and dehydration. In most cases, hyponatremia responds to fluid restriction. Trans­ plantation has been undertaken in patients who develop MDMA-induced fulminant hepatic failure.

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Ethylene Glycol Ethylene glycol is most commonly used as an antifreeze. It may be drunk accidentally by children or intentionally by adults, sometimes as a substitute for ethanol.

Clinical Features Stage 1 (30 minutes–12 hours): GI and NS involvement: Apparent intoxication with alcohol (but no ethanol on breath). Nausea, vomiting, hematemesis. Coma and convulsions (often focal). Nystagmus, ophthalmoplegia, papilloedema, depressed reflexes, myotonic jerks, tetanic contractions. Stage 2 (12–24 hours): Cardiorespiratory involvement – Tachypnoea, tachycardia, mild hypertension, pulmonary oedema, congestive heart failure (CHF). Stage 3 (24–72 hours): Renal involvement: Flank pain, renal angle tenderness, acute tubular necrosis.

Management (a) Supportive measures. (b) Correction of metabolic acidosis and hypocalcemia. (c) Ethanol 50 g PO (e.g. 125 mL of gin, whisky or vodka), followed by further oral doses, or IV infusion of 10–12 g ethanol/h to achieve a blood ethanol concentration of 50–100 mg/L. The dose must be increased to 17–22 g/h if hemodialysis is undertaken, because ethanol is dialysable. (d) Fomepizole is an alternative antidote. Loading dose of 15 mg/kg over 30 minutes, followed by four to 12-hourly doses of 10 mg/kg until ethylene glycol concentration is < 200 mg/L. If hemodialysis is used, frequency of dosing should be increased to 4-hourly. (e) Dialysis removes ethylene glycol. It may also be required to treat renal failure and correct sodium overload if substantial amount of sodium

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bicarbonate has been given to correct acidosis. Dialysis should be continued until ethylene glycol is no longer detectable in blood.

Household and Industrial Products Poisoning is usually accidental, and most common among young children.

Petrolium Distillates (kerosene, white spirit) Clinical features: Nausea, vomiting, diarrhoea. If large quantities are ingested, initial excitation followed by impaired consciousness. Major problem is that of aspiration into respiratory tract resulting in hemorrhagic pneumonitis, which causes breathlessness, wheezing, cyanosis which may be fatal. Management: No attempt should be made to empty the stomach unless a large amount is ingested (>1 mL/kg). Both emesis and lavage may lead to aspiration of the distillate. For lavage, lung should be protected by insertion of cuffed endotracheal tube. Supportive measures are required in serious cases. Corticosteroids and antibiotics are of no value in treatment of lipoid pneumonia, unless presence of secondary infection is proven.

Bleaches, Disinfectants and Drain Cleaners For example, phenol, cresol. Ingestion may lead to death from corrosive effects on upper respiratory tract or upper alimentary tract and systemic toxicity (Refer corrosive poisoning). Mercury thermometers may be swallowed if the bulb of clinical thermometer is broken in a child’s mouth. Very

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434 A Handbook of Emergencies little mercury is likely to be absorbed and there may be greater risk from the broken glass.

Iodine Burning pain in mouth and oesophagus. Laryngeal oedema. Vomiting, abdominal pain, diarrhoea. Shock and circulatory collapse. Treatment: Milk or starch orally. Gastric lavage. Fluid and electrolytes. Treatment of shock, tracheostomy for laryngeal oedema. Disc (button) batteries often swallowed by small children. There are 3 hazards: (a) Batteries larger than about 20 mm in diameter may become stuck in the oesophagus. Chest X-ray is indicated. (b) Leakage due to breaking of ingested batteries, however it is rare for a potentially toxic amount of mercury to be absorbed from mercury cells. (c) Corrosive effect may occur on gut wall with subsequent perforation. Management: Batteries stuck in the oesophagus must be removed, preferably by endoscopy with or without magnets. In about 60%, batteries transit the gut within 48 hours. In the remainder, transit may take up to a week. This may be accelerated by a laxative. Batteries whose casings are seen radiologically to be disintegrating should be removed.

Hair Dye Poisoning Hair dye (paraphenylene diamine) is highly toxic. Severe oedema of face, neck and floor of the mouth, kidney failure and myocarditis are poor prognostic factors. No specific antidote.

Management 1. Gastric lavage followed by IV Methyl Prednisolone 1 mg/d for 5 days or Hydrocortisone 100 mg q8h for 7 days.

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2. Oxygen if patient is hypoxic. 3. Sodium bicarbonate (to prevent myoglobin pre­ cipitation in kidney). Dose: 1 ampoule containing 22.5 mEq in 500 mL normal saline q8h, along with Furosemide or Torsemide. 4. Chlorpheniramine maleate 1 ampoule IV q8h till cervical oedema subsides. 5. Calcium gluconate 10% 10 mL q8h for hypocalcemia. 6. IV Dopamine if persistent hypotension. 7. Dialysis in cases with renal shut down and resistant hyperkalemia. 8. IV amiodarone and defibrillation for ventricular tachyarrhythmias.

Hydrogen Sulphide Workers in petrochemical and gas industries and in tanning are at risk of exposure. The gas is also found in mines and sewers.

Clinical Features Low concentrations cause blepharospasm, pain and redness in the eyes, blurred vision and seeing of coloured haloes around lights. Headache, nausea, dizziness, drowsiness, sore throat and cough may occur. Cyanosis, confusion, pulmonary oedema, coma and convulsions are common with higher concentrations.

Management (a) Casualties must be removed into fresh air. Rescuers must wear breathing apparatus, because of risk of sudden respiratory arrest. (b) O2. (c) Sodium nitrate converts hemoglobin to methemoglobin, which may accelerate sulphide excretion. However, it is likely to increase tissue hypoxia in patients who are already hypoxic, and therefore cannot currently be recommended.

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436 A Handbook of Emergencies

Iron Serious toxicity is unlikely unless more than 60 mg of elemental iron/kg body weight has been ingested; 180–300 mg/kg is fatal.

Clinical Features Initial GI symptoms (nausea, vomiting, abdominal pain, diarrhoea and bleeding) result from direct effects of iron on gut mucosa. Shock, acidosis, impaired consciousness, convulsions and features of hepatocellular necrosis and its complications reflect systemic toxicity secondary to absorption of excessive amounts of elemental iron. In most patients, only signs of gut irritation are present.

Management (a) Hospitalization if > 20 mg elemental iron/kg body weight ingested. (b) Preventing absorption: GL if seen within 1 hour of ingestion. (c) Whole-bowel irrigation if slow-release iron formulation and tablets remain in bowel. (d) Desferrioxamine in severe poisoning (coma or shock) as IV infusion 15 mg/kg/h; total dose should not exceed 80 mg/kg in 24 hours. Administration must be stopped when clinical improvement occurs. The non-desferriox­ amine complex (Ferrioxamine) is excreted in urine, and may be eliminated by dialysis if kidney failure develops. (e) Supportive measures: Replacement of fluid and blood losses and conventional measures for liver and kidney failure.

Isoniazid Clinical Features CNS stimulation, seizures, obtundation, and coma.

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Management GL. Diazepam for sedation. Pyridoxine 200 mg slow IV for seizures, repeated if necessary. Sodium bicarbonate for acidosis.

Isopropanol Isopropanol is found in after-shave lotions, disinfectants and window cleaning solutions.

Clinical Features Effects on nervous system are similar to those of ethanol, but more severe and persistent. Acetone odour in breath. Coma and respiratory depression may occur. Also gastritis, hematemesis, hypotension, renal tubular necrosis and hemolytic anemia.

Management In severe cases hemodialysis. There is no advantage in administering ethanol.

Lithium Clinical Features Gr. 1 Drowsiness, nausea, vomiting, tremor, hyperreflexia, agitation, muscle weakness, ataxia Gr. 2 Stupor, rigidity, hypertonia, hypertension Gr. 3 Coma, convulsions, myoclonus, collapse.

Management (a) GL. (b) Hemodialysis: Patients who may benefit are those who present during first 8–12 hours, following admission with severe poisoning (grade 3), progressive clinical deterioration, renal impairment. May need to be repeated

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438 A Handbook of Emergencies over several days since lithium is extensively distributed in the body. (c) Forced diuresis is less effective than hemodialysis but can be used in less severe cases if careful monitoring of electrolytes is possible (especially danger of hypernatremia) and if dialysis facilities are not available.

LSD Clinical Features Distorted images, visual hallucinations, agitation and excitement, dilated pupils, sinus tachycardia, hyper­ tension, hyper-reflexia, tremor and hyperthermia are common. Coma, respiratory arrest and coagulation disturbances have been reported in those who have snorted large amounts of pure LSD.

Management Most patients need only reassurance and sedation. Those who are paranoid require chlorpromazine 50–100 mg IM or haloperidol 2.5–5 mg IM, repeated as necessary.

Mercury Clinical Features (a) Elemental mercury vapour is absorbed rapidly following inhalation and causes headache, conjunctivitis, cough, nausea and vomiting, metallic taste in the mouth, dyspnoea and chest pain. Chemical pneumonitis may ensue, and in severe cases kidney and/or liver failure. (b) Inorganic mercury salts are corrosive and substantial ingestion can cause hemorrhagic gastroenteritis.

Management DMPS 30 mg/kg/day po increases urinary mercury elimination and reduces blood mercury concentrations.

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Mushrooms Cytotoxic Mushrooms Clinical features: Intense GI symptoms with severe watery diarrhoea start 10–24 hrs post-ingestion and persist for 24 hrs or longer. Patients often become dehydrated, exhausted and acidotic. Signs of liver damage appear during the second day and hepatic failure may ensue. Impaired kidney function is often seen, initially because of dehydration and shock and later as a result of toxic renal damage. Management: (a) Correction of fluid, electrolyte and acidbase disturbance and support for kidney and hepatic failure. (b) AC initial dose followed by repeat doses until 3 days post-ingestion. (c) Moderately increased diuresis for first 24–48 hours. (d) Silibinin if significant ingestion. Dose 5 mg/kg IV over 1 hour followed by 20 mg/kg/24 hours continuous infusion, for 3 days. (e) Neurological symptoms, if any, are treated with pyridoxine 25 mg/kg.

Neurotoxic Mushrooms Clinical features: Diarrhoea, abdominal pain, diaphoresis, salivation, lacrimation, miosis, bronchorrhoea, broncho­ spasm, bradycardia and hypotension. Management: Atropine 1–2 mg IV (children 0.02 mg/kg) antagonizes muscarine overstimulation and related symptoms. Repeated as necessary.

Antabuse Syndrome Clinical Features Clinical features are similar to those of antabuse syndrome caused by Disulfiram and ethanol (flush, sweating, nausea, headache, anxiety, tachycardia, hypotension, dyspnoea, collapse) when mushrooms are ingested with alcohol.

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Management Symptomatic and supportive care.

Nitrogen and Nitrous Oxides NO2 is the most toxic nitrogen oxide.

Clinical Features NO2 has a low solubility in water; dissolves little in upper airway mucus, exposing lower respiratory tract to relatively high concentrations. Patients are generally symptomfree during first hours post-exposure. After several hrs (depending on concentration and duration of exposure) ARDS may manifest—dyspnoea, tachypnoea, hypoxemia, decreased lung compliance, and diffuse pulmonary infiltrates on chest radiography.

Management (a) Hospitalization. (b) In severe cases, supportive therapy and maintenance of gas exchange by mechanical ventilation if needed. Corticosteroids do not reduce pulmonary damage and prophylactic antibiotics are not recommended.

Non-steroidal Anti-inflammatory Drugs Clinical Features Severe poisoning may be complicated by disordered consciousness, convulsions, GI toxicity and renal failure. Phenylbutazone can cause liver damage. Mefenamic overdose may result in muscular twitching and convulsions but recovery is usually rapid. Ibuprofen in large amounts (plasma concentration > 600 mg/L) can cause serious

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problems, including coma, acidosis, pyrexia, respiratory distress syndrome, muscle damage and renal failure.

Management (a) GL. (b) Supportive measures: Diazepam for convul­ sions, maintenance of normal fluid, electrolyte and acid-base balance. (c) Repeated oral AC may enhance elimination of the longer-acting drugs in this group.

Opioids (Heroin, Morphine, Methadone, Dihydrocodeine, Penta­ zocine, Buprenorphine). Opioid analgesics are potent respiratory depressants and a relatively small overdose can kill with alarming rapidity particularly if injected IV.

Clinical Features Very slow respiratory rate, pin-point pupils, depression of consciousness, vomiting, delayed GI motility (particularly delayed gastric emptying), and reduced BP and pulse rate. The principal differences in the effects of the different drugs relate to their speed of action, which may be influenced by the route of administration.

Specific Opioids Diamorphine and morphine. Diamorphine is rapidly broken down to morphine. Morphine is excreted primarily by the kidneys and accumulates in patients with renal insufficiency, and in the elderly. Codeine and dihydrocodeine are weakly effective on their own. Methadone has slow onset of action, and it therefore gives less hit than morphine or diamorphine.

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442 A Handbook of Emergencies Dextropropoxyphene is usually marketed in combination with paracetamol. It has no opioid properties but as marked effects on sodium channels on myocardial membrane causing prolonged QRS, and in overdose risk of severe ventricular arrhythmia, VF and death. Tramadol is an opioid agonist and in overdose can cause convulsions. Risk of respiratory depression is increased. Management: Emergency Management – (a) Clear airway, O2, placing patient in semi-prone position to reduce risk of aspiration in event of vomiting. Injection of Naloxone initial dose of 0.8–1.2 mg IV for adult. Assisted ventilation if Naloxone is not immediately available. (b) Reversal of intoxication. Dose required for complete reversal depends on severity of poisoning and opioid involved. A single dose of 2 mg Naloxone will produce dramatic improvement in level of consciousness, increase in respiratory rate, dilatation of pupils. If response is only partial, larger doses should be given q1–2 minutes to total dose of 5 mg. Subsequent doses should be given according to return of toxic features. Much larger doses may be necessary to reverse the effects of partial antagonists such as Pentazocine. Failure to respond to Naloxone may be due to – poisoning with other drug than narcotic analgesics, severe hypoxic brain damage, intoxication with a partial antagonist such as Buprenorphine. (Effects of Buprenorphine cannot be reversed by any reasonable dose of Naloxone and assisted ventilation may be necessary). Repeated doses of Naloxone may be required to maintain reversal of intoxication with long-acting narcotics, such as Methadone. In such a case, Naloxone may be given by IV infusion.

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The complete, sudden reversal of severe narcotic poisoning with IV Naloxone is characterised by maximal dilatation of pupils, hyperventilation, muscle tremor and rigidity, pilo-erection, tachycardia and hypertension. Cardiac arrest can occur. Hence if the situation allows, it is probably safer to give Naloxone in small repeated doses than in one large dose. Methods to increase elimination are none. Supportive measures are required. Management of complications: Some complications do not respond to Naloxone. Convulsions and cardiac arrhythmias are more likely to be controlled by correction of hypoxia and hypercabia. Acute pulmonary oedema can be treated with high flow oxygen, and if necessary intermittent positive pressure ventilation. Peripheral failure may respond to Dopamine.

Paracetamol (Acetaminophen) Clinical Features Symptoms and signs of poisoning are initially nonspecific, and may be minimal, even when a fatal dose has been taken. Nausea and vomiting occur within a few hours of ingestion of hepatotoxic dose. Upper abdominal pain and hepatic tenderness are seldom seen before the 2nd day. Maximal liver damage as assessed by plasma ALT or AST activity or PT, occurs 72–96 hours after ingestion. Hepatic failure (jaundice and encephalopathy) may then develop between 3rd and 5th day. Renal failure due to acute tubular necrosis develops in about 25% with severe hepatic damage. Hypophosphatemia may contribute to morbidity and mortality by inducing mental confusion, irritability, coma and abnormalities of platelet, WBC and RBC

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444 A Handbook of Emergencies function. Increased PT, hyper-bilirubinemia. In severely poisoned patients – Fulminant hepatic failure on 3rd to 6th day, encephalopathy, cerebral oedema, hyper­ ventilation, acidosis, hemorrhage. Stages of Acetaminophen poisoning Stage Time post-ingestive Clinical features 1 0–24 h Anorexia, nausea, vomiting 2 24–72 h Right upper quadrant abdominal pain, elevated liver enzymes 3 72–96 h Symptoms of hepatic failure, AST, ALT, bilirubin and INR peak Sometimes kidney failure and pancreatitis 4 75 days Resolution of hepatotoxicity or progression to multiple organ failure

Management: Patients who present 8–10 hours after overdose of more than 150 mg/kg or 12 g (in an adult) should be given antidotes: 1. N-acetylcysteine (a) IV—150 mg/kg in 5% dextrose, 200 mL over 15 minutes, then 50 mg/kg in 5% dextrose 500 mL over next 4 hours and 100 mg/kg in 5% dextrose 1000 mL over next 20 hours (total dose 174–300 mg/kg 24 hours). (b) Oral—140 mg/kg initially, then 70 mg/kg 4 hourly doses of 60 mg/kg. Total dose 1330 mg/kg over 72 hours given diluted in fruit juice or carbonated beverage. 2. Methionine (oral)—2.5 g initially, then three 4-hourly doses of 2.5 g. Total dose 10 g over 12 hours. General measures: Use of AC is more effective than GL but is contraindicated if antidotes are to be given orally.

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Patients with fulminant hepatic failure may require transplantation.

Pesticides Organophosphate insecticides—Organophosphate.

Clinical Featrues 1. Muscarinic effects : (a) Eye – Miosis, blurred vision, eye pain. (b) Ingestion – Hypersalivation, nausea, vomiting, abdominal cramps, diarrhoea, tenesmus. (c) Inhalation – Cough, expectoration of frothy secretions, chest tightness and wheeze, pulmonary oedema. 2. Nicotinic effects – Fasciculation, progressive flaccidity, and weakness of all muscle groups including extraocular muscles and those of respiration. Respiratory failure is common. In patients with severe poisoning, initial mild excitation is followed by anxiety, restlessness, dizziness, followed by convulsions and impairment of consciousness. Hyperglycemia and glycosuria are common.

Management (a) Supportive measures including clear airway, adequate ventilation and removal of bronchial secretions. Diazepam IV reduces anxiety and is given even in absence of convulsions. (b) Antidotes – (i) Atropine IV, initially 2 mg/kg in adult, (child 0.02 mg/kg) and repeated q10–30 minutes unitl bronchorrhoea and bronchospasm are abolished or there is Atropine intoxication (dry mouth, tachycardia, dry skin, vasodilatation). In severe poisoning Atropine dose can be > 30 mg in first 24 hours. but the amount may be less if oximes are also given. Pralidoxime

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446 A Handbook of Emergencies restores muscle power, reduces fasciculations and convulsions, and improves consciousness level within 30 minutes. Dose 30 mg/kg by slow IV injection q4–6 hours in severe cases (i.e. if features of poisoning persist and if RBC and plasma cholinesterase activities are low). Alternatively an infusion of Pralidoxime 8–10 mg/kg/h may be given. Carbamate insecticides. Poisoning is generally less severe and of shorter duration. Atropine can be used, but oximes are seldom needed.

Paraquat Clinical Features Nausea, vomiting, diarrhoea. Very large doses may cause death from coma, metabolic acidosis, pulmonary oedema and myocardial depression within a few hours. Patients who survive for 3–4 days exhibit severe, painful ulceration of lips, tongue, pharynx and larynx, leading to dysphagia, cough, dysphonia and inability to clear saliva and other secretions. ARF is common by 4–5 days after ingestion.

Management (a) GL if seen within 1 hour. (b) AC 50–100 g. If plasma concentration indicates a fatal outcome it is best to keep the patient comfortable.

Aluminum Phosphate It is used as a grain preservative.

Clinical Features Garlicy taste and smell, retrosternal burning, epigastric discomfort and recurrent vomiting, tremors and drowsiness. Liberated phosgene gas causes dyspnoea,

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pulmonary oedema, bradycardia and circulatory collapse. ARDS develops if patient survives for 24 hours.

Management No specific antidote. AC 90 g to absorb PH3 from GI tract. GL with 3–5% sodium bicarbonate minimizes conversion to phosgene. Supportive measures.

Quinine and Chloroquine These are the most common antimalarial drugs encoun­ tered in acute poisoning. Their severe toxicity in overdose results from cardiotoxicity.

Clinical Features Severity of poisoning: Severity

Symptoms

Chloroquine Mild

Quinine

Visual disturbances, vomiting. ECG normal Moderate Vomiting, visual disturbances, QT prolonged, T wave decreased Severe Cardiac failure, convulsions, QRS increased Mild Cinchonism Moderate Blurred vision. QT increased. T wave decreased Severe Blindness, cardiac failure, QRS increased

Cardiovascular toxicity is more common in Chloroquine poisoning, severe oculotoxicity is a major feature in Quinine poisoning. Hypokalemia is almost always present in severe Chloroquine poisoning.

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Management a. Cardiovascular disturbances – (i) Shock : Isoprenaline or Adrenaline is for severe hypotension in Chloroquine poisoning, but the dose must be titrated carefully to avoid adverse effects. (ii) Intraventricular block: Sodium bicarbonate 250 mL IV. (iii) VT or VFs: Cardioversion. (iv) Ectopic beats, torsades de pointes: If associated with severe hypokalemia – Potassium. b. Diazepam: For protective effect for Chloroquine poisoning. Dose: 2 mg/kg within 30 mins, followed by infusion of 2–4 mg/kg/24 hours. c. Gut decontamination: Gastric lavage once patient is stabilised if a substantial doses of Quinine or Chloroquine has been ingested less than 1 hour previously. Activated charcoal 50–100 g may be given.

Salicylates Ingestion of Aspirin is the most common form of salicylate poisoning. It can also result from ingestion of Methyl Salicylate oil (oil of wintergreen).

Clinical Features Mild to moderate intoxication • Deafness • Tinnitus • Nausea • Vomiting • Hyperventilation • Sweating • Vasodilatation • Tachycardia • Respiratory alkalosis • Metabolic acidosis

Severe intoxication • All symptoms of less severe poisoning • Confusion • Delirium • Hypotension • Cardiac arrest • Acidemia

Less common complications • Non-cardiogenic pulmonary oedema • Convulsions • Coma • Encephalopathy • Kidney failure • Tetany • Hyperpyrexia • Hypoglycemia

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Management (a) AC 50–100 g. (b) Plasma salicylate concentration should be measured 2–3 hours after first measurement. (c) Correction of dehydration, electrolyte imbalance, and metabolic acidosis. (d) Urine alkalization with 225 mL 8.4% sodium bicarbonate, further doses as required. Hypokalemia should not be corrected before sodium carbonate administration because it lowers serum potassium concentration further. (e) Hemodialysis when severe acid-base abnormalities are present.

Sulphur Dioxide Risk of occupational exposure in paper mills, steel works and oil refineries.

Clinical Features Lacrimation, rhinorrhoea, cough, increased bronchial secretions, bronchoconstriction and in severe cases, pulmonary oedema and respiratory arrest. Corneal burns can follow eye exposure and liquified SO2 can cause skin burns.

Management (a) Removal of casualty from exposure. (b) Irrigation of eye and skin with plenty of water. (c) Supportive measures. (d) Mechanical ventilation with positive end-expiratory pressure.

Theophylline Clinical Features Nausea, vomiting, abdominal pain, diarrhoea, GI hemorrhage. Hypokalemia, hyperglycemia, respiratory alkalosis, metabolic acidosis. Sinus tachycardia, SVT, VT, VF.

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450 A Handbook of Emergencies Hypotension, rhabdomyolysis, acute renal failure. Restlessness, irritability, headache, hyper-reflexia, tremor, convulsions, coma.

Management (a) GL may reduce absorption if undertaken within 1 hour of overdose. This is unlikely to be very effective because most formulations of Theophylline are of slow-release type and tend to form bezoars in the stomach. (b) AC 50–l00 g will reduce absorption and in multiple doses increase elimination significantly. (c) Vomiting can be controlled by Ondansetron 8 mg IV. (d) Potassium supplements are always needed 40–60 mmol/h, appropriately diluted, may be required initially. (e) Tachyarrhythmias – Propranolol 1–5 mg slow IV. (f ) GI hemorrhage – Ranitidine. (g) Blood transfusion may be required. (h) Convulsions – Diazepam 5–10 mg IV.

Stimulants Amphetamine Clinical features: Intoxication is characterized by increased alertness and self-confidence, euphoria, extrovert behaviour, talkativeness, rapid speech, loss of desire to eat or sleep, tremor, dilated pupils, tachycardia and hypertension. In severe cases, excitability, agitation, paranoid delusions, hallucinations with violent behaviour, hypertonia and hyper-reflexia may occur. Convulsions, rhabdomyolysis, hyperthermia and cardiac arrhythmias are uncommon. Management: (a) AC 50–100 g. (b) Supportive measures. (c) Diazepam 5–10 mg IV, or Chlorpromazine 50–100 mg is an effective sedative. (d) Propranolol 40–80 mg po to antagonize peripheral sympathomimetic actions of

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Amphetamines. (e) Acidification of urine increases renal elimination.

Thyroxine and Tri-iodothyronine Clinical Features Symptoms may develop within a few hours of T3 ingestion, but are not usually maximal for 3–6 days after T4 ingestion. Palpitations, tremor, anxiety, irritability, hyperactivity, fever, tachycardia and insomnia are most common. Atrial fibrillation, sweating and loose stools are rare.

Management (a) AC in patients seen within 1 hour of substantial dose. (b) Propranolol 40 mg tds for 5 days in patients in whom serum T3, T4 concentrations are high. There are no longterm complications of acute overdose.

Volatile Substance Abuse Commonly inhaled substances include toluenecontaining glue, chlorinated hydrocarbons (cleaning fluids, paints, varnishes, lacquers, dyes), fluorocarbon (areosolpropellants, fire extinguishers, petrol, acetone (nail polish remover), butane, propane.

Acute Intoxication Clinical features are similar to those of alcohol intoxication (initial CNS stimulation followed by depression). Features include euphoria, impaired judgement, feelings of omnipotence, blurred vision, tinnitus, slurred speech, ataxia, headache, abdominal pain, anorexia, nausea, vomiting, chest pain and bronchospasm. Occasionally a delirious state with clouding of consciousness and hallucinations. Convulsions, respiratory depression and

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452 A Handbook of Emergencies coma may ensue if inhalation of the volatile substance continues. Arrhythmias are a significant cause of death. Inhalation may cause the additional problem of severe methaemoglobinemia (slategrey cyanosis). Management is essentially supportive. Patient may have to be sedated with Diazepam 10 mg IV. For methaemo­ globinemia methylene blue 1–2 mg/kg IM, if concentration > 30%.

Warfarin, Nicoumalone and other Anticoagulants Clinical Features Epistaxis, gingival bleeding, spontaneous bruising, hematomas, hematuria, bilateral flank pain, rectal bleeding and hemorrhage into any organ may occur. Severe blood loss may result in hypovolemic shock, coma and death.

Management a. Intention to continue anticoagulation: (i) When INR < 6.0 but > 0.5 above target value, reduce the dose or stop anticoagulant; restart when INR < 5.0. (ii) INR 6–8 and patient not bleeding (or only minor bleeding), stop anticoagulant and restart when < 5. (iii) INR > 8.0 and patient not bleeding, stop anticoagulant and restart when INR < 5. (iv) When there are other risk factors for bleeding, give vitamin K1 0.5 mg IV slowly. If major bleeding – Vitamin K1 by slow IV injection, with prothrombin complex concentrate, 50 U/kg, or if complex is not available, fresh frozen plasma 15 mg/kg. b. Continued anticoagulation unnecessary – (i) INR > 6.0, vitamin K1 5 mg. repeated if necessary. (ii) If active bleeding, prothrombin complex concentrate 50 U/kg in addition, or if complex not available, fresh frozen plasma 15 mL/kg.

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CHAPTER

21

Venomous Bites and Stings

Snakebite Common poisonous snakes are: (1) Elapidae (cobras, kraits, coral snakes). (2) Viperidae (vipers, adders, pit vipers, rattle-snakes). Most bites are inflicted on feet or ankles when the snake is trodden on in the dark or in undergrowth. In these circumstances, the reflex strike may be mechanically inefficient and explains why only about 50% of bites by venomous snakes result in significant envenoming.

Elapids Local effects: Bites by kraits or coral snakes, produce little pain and negligible local changes, but cobras cause immediate pain and rapid swelling with enlargement of regional lymph nodes. Local blistering may develop within a few hours, and necrosis within a few days. Systemic effects: (a) Vomiting may begin within 30 minutes and is an early sign of systemic envenoming. (b) Neurotoxicity is the most important effect. Neurologic symptoms may develop within 15–20 minutes after the bite or after many hours. Preparalytic symptoms include blurred vision, paresthesiae around mouth and gums,

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454 A Handbook of Emergencies hypersalivation, conjunctival congestion and drowsiness. Objective signs progress thus—ptosis, paralysis of upward gaze, total external ophthalmoplegia, inability to open mouth, protrude tongue or swallow, respiratory paralysis. (c) Systemic bleeding and incoagulable blood may be caused by some elapids.

Vipers Local effects: Pain, local swelling and bruising is usually within 1–2 hours. It may spread to involve the whole limb and adjacent trunk over next 2–3 days. Tender enlargement of regional lymph nodes is common. Systemic effects: (a) Hemostatic abnormalities—Spon­taneous bleeding can occur from gingivae, nose, gastrointestinal (GI) tract and skin. Intracranial, retroperitoneal and GI hemor­ rhage may prove to be fatal. (b) Shock and hypotension are commonly caused by hypovolemia from leakage of blood and plasma into the bitten limb. Some venoms cause generalised increase in capillary permeability resulting in facial and pulmonary oedema, serous effusions, hypoalbuminemia. (c) Acute renal failure is common after bites by Russell’s viper. (d) Neurological effects— Venoms of a few species produce neurotoxic symptoms with myoglobinuria and other evidence of generalised rhabdomyolysis. Sea snake bite produces progressive curare-like paralysis with respiratory failure.

Management First Aid 1. Reassurance: As mentioned earlier, a bite from a poisonous snake need not always result in enveno­ mation. Also the limb might have been protected by clothing. Severe fright and emotional upset may

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2.

3.

4. 5.

occur after snakebite and patient may faint just because of anxiety. Injury marks. Characteristic are two fang marks. There may be single mark if the bite is sideways on. Inverted U-shaped marks as a rule suggest nonpoisonous snakebite. Also if the victim is well after say 6h it is likely to be nonpoisonous. Measures to retard absorption of poison—(a) Immobi­ lization of the bitten limb with a splint. If a crepe bandage is available the whole limb should be bandaged firmly to a splint. Application of pressure bandage 5 cm proximal to the site of bite. (b) Cruciate incisions at site of bite and suction of blood and oozing fluid by breast pump, or a funnel attached to a central suction for about 15 minutes may succeed in removing as much as 50% of the venom. Admission to hospital for observation is essential unless the snake can be reliably identified as non-venomous. Antivenom is most effective if given within 1–4 hours after the bite. It is available as freeze-dried powder and is reconstituted by adding distilled water. Sensitivity tests should be done by giving intradermal test dose. 30 mL of the polyvalent serum is added to 500 mL N saline and given IV over 1–2 hours. The dose can be repeated if neurotoxicity or shock persist, or recur few hours after initial dose. If patient is sensitive, desensitization can be carried out using small dose, SC and then increasing doses IM. But this is time consuming and potentially dangerous. Antivenom reactions can be prevented by pretreatment with adrenaline, antihistamine and hydrocortisone. Dose for children is same as for adults. If a vein cannot be secured in a child, 40–60 mL is given IM with hyalase to help absorption.

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456 A Handbook of Emergencies Neutralization of procoagulant venoms can be monitored by whole blood clotting test. A few millilitres of blood are placed in a clean, dry, glass test tube and left at room temperature for 20 minutes. The tube is tipped to see if there is clotting. The test should be repeated at 6h intervals. If the blood is still incoaguable 6h after first dose, a second dose should be given. To summarise, the successful management of neurotoxic snakebite includes administration of initial bolus dose of 10 vials of ASVC and repeat 10 vials of ASVC in patients with respiratory distress along with neostigmine 0.4 mg/kg every 1–3 hours to maximum of 10 mg/24 hours IM or IV, atropine and prompt ventilatory support appears to be the most effective treatment protocol.

Supportive Treatment a. Cardiorespiratory support: In patients with severe envenomation endotracheal intubation and mechani­ cal ventilation may be necessary. An endrophonium chloride test may be tried in patient with neurotoxi­ city. If patient responds, he can be given neostigmine 2.5–5 mg IM. For patients in severe shock ventilatory and inotropic support are necessary. Also hydro­ cortisone hemisuccinate 300 mg IV, followed by slow infusion for 24 h, then 100 mg q8h for 2–3 days. b. Hypovolemia should be corrected. c. Hemofiltration or dialysis may be necessary in pre­ sence of kidney dysfunction. d. Hemolysis is treated by small packed cell transfusions. Severe bleeding due to deficiency of clotting factors requires infusions of fresh frozen plasma 5–8 units. If fibrinolysis, epsilon aminocaproic acid 0.1 g/kg slow IV infusion.

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e. Metabolic acidosis if present, IV sodium bicarbonate may be given to keep arterial pH below 7.3. f. Care of the wound: Necrotic tissue should be surgically debrided and the wound washed with antiseptic solu­ tion and an antibiotic ointment applied. Prophylactic azithromycin or a third generation cephalosporin and a tetanus-toxoid booster should be given.

Scorpion Stings Scorpions sting through the telson at the end of their tails. The Indian red scorpion is small in size with segmented tail and is very poisonous, the black scorpion less so.

Clinical Features (a) Local—Intense pain and mild local swelling, ecchymosis, numbness. (b) Systemic—Vomiting, diarrhoea, hypersalivation, profuse sweating, hypertension, toxic myocarditis and pulmonary oedema. Fasciculations, muscle spasm, respiratory paralysis, acute pancreatitis and hemostatic abnormalities.

Management 1. Local infiltration of 1% lidocaine if severe pain and systemic analgesics. Cold therapy at the site. 2. Correction of fluid balance. 3. Scorpion antivenom (SAV) must be given (without skin test) as early as possible. Dose: 30 mL of antivenom IV, however, more may be required for severe sting. High circulating catecho­ lamine induced by venom prevent a reaction to anti­ venom and act as prophylaxis against anaphylaxis.

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458 A Handbook of Emergencies 4. Prazosin—250–500 mg orally every 3 hours is useful antidote to scorpion venom. 5. Dobutamine infusion 5–20 µg/kg/min improves cardiac dysfunction and reduces pulmonary congestion. 6. Nitroglycerin drip 0.5–5 µg/kg/min reduces preload of the heart and improves intrapulmonary shunting. Noninvasive or mechanical ventilation or helmetderived noninvasive pressure support ventilation may be necessary. 7. Pulmonary oedema cases improve with dobutamine and noninvasive or mechanical ventilation.

Spider Bites Clinical Features There are two main syndromes of clinical envenoming: 1. Necrotic araneism: Local burning pain, transient fever and erythematous rash, intravascular hemolysis and development of ischemic local lesion, which forms a necrotic black eschar. Treatment: Antivenom is available for Loxosceles species. Dapsone may reduce extent of necrosis. 2. Neurotoxic araneism is commonly the result of bite by black widow or red-back spiders. Bite is very painful and causes local swelling. Systemic symptoms include headache, vomiting, muscle spasms, priapism, pulmonary oedema and coma. Treatment: Absorption of rapidly acting neurotoxin can be delayed by applying arterial tourniquet or splinting with crepe bandage. Specific antivenom. Calcium gluconate for muscle spasms.

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Bee and Wasp Stings Clinical Features People who have been sensitized to consecutive stings suffer from increasingly severe reactions to succes­ sive stings. Systemic anaphylactic reactions consist of generalized urticaria, angio-oedema of tongue, lips and throat; bronchospasm, shock, diarrhoea and vomiting. Multiple stings by bees, wasps or hornets can be lifethreatening even in patients who are not hypersensitive to the venoms. Bee venom causes generalised rhabdomyo­ lysis, intravascular hemolysis, hypertension, renal failure, airway obstruction and epidermal necrolysis.

Management (a) The sting with its attached venom gland should be removed by scraping off with the finger nail or blade or a knife. (b) If multiple bites—Admission to ICU, adrenaline 0.75–1 mL SC or IM, or IV. (c) Anaphylaxis or hypotension— Cardiorespiratory support and endotracheal intubation if increasing urticaria. Also IV hydrocortisone and antihistamines.

Fish Stings Venomous fish are found in temperate and tropical water, especially near coral reefs.

Clinical Features Most stings occur when the fish is trodden on by a wader. Pain is immediate and agonizing. It is associated with local swelling, inflammation and blistering and occasion­ ally with systemic symptoms of autonomic stimulation, vomiting, hypotension and collapse.

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460 A Handbook of Emergencies Treatment: First aid is immersion of the area stung in uncomfortably hot water about 45°C. Patients with severe envenoming may require cardiorespiratory resuscitation. Venomous jellyfish (Blue bottles, Portuguese-manof war): Clinical features depend on the species. Most cause immediate pain at site of contact and an acute local inflammatory response. The pattern of wheals may help identify the envenoming species. The box jellyfish can cause full-thickness skin damage and systemic involvement, death may occur from myocardial toxicity. Some tiny carybdied jellyfish cause pain, hypertension and cardiopulmonary decompensation can occur 30–40 minutes after the sting. Treatment: Victim must be taken out of the sea to prevent him from drowning. Vinegar (4–6% acetic acid) should be applied to box jellyfish (blue bottle) stings, as this inhibits discharge of further nematocysts. For pain ice packs. CPR on the beach may be life-saving. Echinoderms (Star fish or sea urchin): If a wader treads on it, venomous spines may penetrate the sole of the foot. The stings may cause inflammation, secondary infection and rarely systemic symptoms. Treatment: The epidermis should be pared down after it has been softened with 2% salicylic ointment. Injection of xylocaine 2% in and around the wound. Analgesics for pain. Molluscs (sea snails) can implant a venomous dart containing potent neurotoxins, which can cause fatal respiratory paralysis. Treatment: No specific remedy, but CPR can be life-saving.

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CHAPTER

22

Emergencies Due to Physical Causes

Heat Illness Clinical manifestations due to effects of heat which require urgent attention have been described in Chapter 16.

Cold-induced Illness Profound Hypothermia Hypothermia is said to be present when the core (rectal, oesophageal) temperature is below 35°C and profound hypothermia, where the body temperature decreases to less than 28°C. It is an acute medical emergency. If survived, severe hypothermia can also be associated with serious systemic illnesses. Causes of profound hypothermia: (1) Prolonged exposure to cold air with slow cooling, e.g. accident while mountain climbing, a fall into a crevasse, constant exposure to low temperatures as in the case of homeless people. (2) Immersion and submersion, e.g. ocean, lake, pond, cold rivers, in Himalayan regions. (3) Any kind of snow accident such as avalanches. (4) Myxoedema (hypothermia usually not severe). Risk factors: (a) Children because of greater body surface area, and immature thermoregulation. (b) Old people

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462 A Handbook of Emergencies because of reduced metabolism, reduced muscle mass and subcutaneous tissue. Clinical features: (1) Cardiac: Bradycardia, atrial fibrillation, ventricular arrhythmia and non-specific and specific (pathognomonic j-wave) ECG changes. At temperatures less than 30ºC, ventricular fibrillation and asystole will occur. If cardiac arrest occurs without adequate cooling of the body prognosis will be poor due to lack of cerebral protection. Resuscitation can only be successful if cardiac arrest is a consequence of hypothermia and not of anoxia and acidosis. This is the reason why victims of drowning or avalanche often suffocate before the cold can protect their central nervous system. (2) Hyperkalemia: Markedly increased serum potassium levels are an indicator of asphyxia and a grave prognostic sign. (3) Viscosity and hematocrit are increased because of loss of intravascular fluid (plasma) to the extravascular compartments. Hyperviscosity favours the development of intravascular thrombi and coagulopathy. Management of profound hypothermia A. Non-arrested patients: This group has severely depressed but still preserved cardiocirculatory function and extremely slow spontaneous breathing. Rough handling during recovery or transport should be avoided. Mechanical stimulation (attempts at intubation, insertion of central venous catheters or pacing wires) can convert a perfusion rhythm to non-perfusion VF. Active core rewarming. The most effective method is hemodialysis. Rewarming using forced hot air via a plastic or paper blanket can be used as an assisting device.

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B. Patients with cardiocirculatory arrest: Extracorporeal blo o d rewar ming is the metho d of choice. Rewarming attempts at the time of transportation are disadvantageous for the patient as they increase metabolic demand before cardiac function and oxygen delivery are improved. Patient should receive intubation, ventilation, chest compression, IV fluid therapy. Extracorporeal blood rewarming, cardio pulmonary bypass (CPB) and extra corporeal circulation warrant rapid rewarming of the core. Passive rewarming methods with slow rewarming are of limited value. Frostbite is the most common freezing injury of the tissues and occurs whenever tissue temp. falls below 0ºC. Direct exposure to cold wind quickly freeze certain areas (fingers, toes, ears, nose). Various conditions can impair peripheral circulation and predispose to frost bite, e.g. constrictive clothing and immobility. As tissue temperature drops below 10ºC, anaesthesia develops. Epithelial cells leak plasma and microvascular vasoconstriction occurs. Symptoms: Sensory deficiency affecting light touch, pain and temperature perception. Signs: Frozen tissues appear yellow, waxy, mottled, violaceous white. Early bleb formation is followed by hemorrhagic blebs. Management: Rapid thawing of the affected parts by immersion in circulating water at 40–41°C. Reestablishment of perfusion is very painful and analgesics must be given. Rubbing or friction massage may be harmful. Following thawing, tissues must be handled gently and injured part must be elevated to minimise oedema formation. Avoid compressive dressings. Daily whirlpool hydrotherapy if available. Clear blisters may be temporarily left intact or debrided and ibuprofen given PO.

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464 A Handbook of Emergencies Hemorrhagic blisters should be left intact to prevent tissue desiccation. Streptococcal and tetanus prophylaxis.

High Altitude-induced Illness The range of illness associated with altitude hypoxia is described by three syndromes—Acute mountain sickness, high altitude cerebral oedema and acute pulmonary oedema. Acute mountain sickness is short-lived and does not require emergency care.

Acute Mountain Sickness It is the mildest form and is characterised by headache plus at least one of the following fatigue, anorexia, nausea, vomiting, dizziness and sleep disturbance. Symptoms typically develop 6–10 hours after ascent and subside in 24–48 hours, but they occasionally evolve into high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE) or both.

Management Acute mountain sickness (AMS) patients should halt ascent reduce exertion until symptoms resolve. Other treatments include fluids, analgesics for headache and light dose acetazolamide 200 mg bd may relieve symptoms and improve sleep.

High Altitude Cerebral Edema Some individuals with symptoms of acute mountain sickness, may suddenly deteriorate, developing ataxia, irrational behaviour, hallucinations, clouding of consciousness and coma as high altitude cerebral oedema develops. This may respond to descent, supplementary oxygen, and dexamethasone 8 mg initially, and then 4 mg 6 hourly will facilitate descent in an emergency.

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Emergencies Due to Physical Causes 465

High Altitude Pulmonary Edema Initial symptoms of dry cough associated with breathlessness, palpitation and precordial discomfort, pronounced weakness and fatigue. As the condition progresses, pulmonary edema develops with tachycardia, tachypnoea, and pink frothy sputum, cyanosis, and rales all over the lungs.

Management (a) If anyone looks very fatigued and weak, he should be brought down the mountain immediately. An alternative to evacuation to lower altitudes would be to place the patient in a recompression chamber. A portable bag (gamow bag) is available commercially, is pressurised by means of a foot pump and is useful in remote areas. (b) Oxygen at high flow rates (6–8 L/min). (c) Morphine has a traditional use in pulmonary oedema and helps to allay anxiety and restlessness. (d) Antibiotics may be needed to control superadded respiratory infection. (e) Diuretics (furosemide are contraindicated).

Drowning and Near-Drowning Drowning is death by suffocation within 24 hours of submersion in fresh or salt water. Near-drowning (DND) is death occurring more than 24 hours after suffocation or partial suffocation due to submersion in water.

Drowning Sequence 1. Laryngospasm: Swallowing and aspiration of water triggers profound laryngospasm which, in about 15% of cases does not remit and results in asphyxia without flooding of the tracheobronchial tree (so called ‘dry drowning’).

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466 A Handbook of Emergencies 2. Water in the lungs: Much more water enters the tracheobronchial tree either initially on submersion or subsequent to the easing of the laryngospasm and leads to development of noncardiac pulmonary oedema. 3. Other problems: Hemolytic, hypervolemic and hyponatremic problems are seldom seen clinically in fresh water drowning. Sea water contains sodium chloride and therefore may be associated with pro­ found pulmonary oedema, hypovolemia and hyper­ natremia. Sea water is less likely to be contaminated than fresh water, and there may be lower incidence of secondary pneumonia. 4. Changes in blood gases: Hypoxemia, hypercarbia and mixed respiratory and metabolic acidosis are usual. 5. Cerebral and other responses: The brain swells producing increased ICP and decreased cerebral perfusion pressure. Vasospasm and hypoxemia probably account for the albuminuria and elevation of enzymes. 6. Hypothermia: Immersion in very cold water produces a rapid fall in core temperature. The rate of fall of temperature in a DND victim is dependent upon surface area to mass ratio (highest for children), volume of cold water swallowed and aspirated, body to water temperature gradient, thickness of subcutaneous fat and type of clothing worn. With progressive cooling and unconsciousness due to asphyxia, there is bradycardia progressing to asystole and diminished metabolic requirements of all organs including the brain.

Management 1. Hospitalization for at least 24 hours, even if victim seems to be fully awake and conscious, without

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2. 3.

4.

5.

6. 7.

respiratory distress; late developments of hypoxemic respiratory failure and cerebral oedema may occur. CPR should be immediately initiated and maintained until patient has been warmed and resuscitated and warmed and assessed to be unresuscitable. Warming: If core temperature is above 32°C, external rewarming with blankets, over bed radiant heaters or immersing patients in warm water. For a core temperature below 32°C, active core warming is required—gastric and rectal lavage with warmed saline, use of warmed humidified inspired gases via ventilator, peritoneal lavage, diathermy and if necessary extracorporeal blood warming. IV fluids: 5% dextrose in water in sea water drowning, and N saline, Ringer lactate or solution of two-thirds 5% dextrose in water and one-third N saline, in fresh water DND. However, it is best to keep the patient slightly on the ‘dry side’. Cardiac support: Some victims may develop VF spontaneously in the 28–32°C range. Use of anti­ arrhythmic drugs which are myocardial depressant is not advisable and, with warming, sinus rhythm returns. Antibiotics: If aspirated fluid is obviously contaminated (e.g. DND in canals or cesspools or wells), antibiotic to cover gram-negative organisms should be used. Treatment of cerebral oedema with mannitol. There is no evidence that corticosteroids favourably influence cerebral oedema associated with DND.

Prognosis Unfavourable prognostic factors are: Age less than three years, maximum submersion time >5 minutes, no attempts

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468 A Handbook of Emergencies at CPR for longer than 10 minutes after rescue, coma on admission to hospital, arterial blood pH12 >5000 ng/mL >100 >40 >20 >100

10–20 µg/mL 10–50 µg/mL 100–250 µg/mL

>250 100–700 µg/mL >300

10–20 µg/mL

>20

0.8–2.0 µg/mL >2.4 2–5 µg/mL >5 1.5–5.0 µg/mL >5 4–10 µg/mL >16 50–100 µg/mL Variable 2–5 µg/mL >10

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30 Appendix.indd 527

Drug Preparation Dose Dopamine 600 mg in 500 mL 1–10 µg/kg/min 5% dextrose Dobutamine 500 mg in 500 mL 5–15 µg/kg/min 5% dextrose Noradrenaline 4 mg in 500 mL 1–50 µg/min saline Nitroprusside 50 mg in 500 mL 2.5 mg/kg/min 5% dextrose Nitroglycerin 100 ug in 500 mL 1–50 µg/min 5% dextrose Procainamide 1 g in 250 mL in 5% dextrose 1–4 mg/min Lignocaine 2.5 5 mL 2% solution 4 mg/min in dextrose Amiodarone 50 mg/mL 0.5–1 g/24 hr Milrinone 10 mg in 10 mL 0.375–0.7 µg/min

Common IV Drugs Used as Infusions

50 mg/mL 1 mg/mL

4 mg/mL 21.5 mg/mL

100 µg/mL (1.67 µg/micro drop) 200 ug/mL (3.33 µg/micro drop)

Concentration 1200 ug/mL (12 µg/micro drop) 1000 µg/mL (16.7 µg/mL) 8 mg/mL

Appendix 527

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528 A Handbook of Emergencies

30 Appendix.indd 528

Psychopharmacological drugs Amitryptiline 120–150 ng/mL Chlorpromazine 50–300 ng/mL Desipramine 15–300 ng/mL Diazepam 100–100 ng/mL Imipramine 150–300 ng/mL Lithium 0.5–1.0 mEq/L Nortryptiline 50–150 ng/mL Opioids Pentazocine 0.1–1 mg/mL Pethidine 600–650 µg/mL

>500 >750 >500 >5000 >500 >2 >500 >2 >610

Blood Chemistry (Whole Blood, Plasma and Serum) Content Normal value Acid phosphatase 0.11–0.60 U/L Alanine aminotransferase 5–30 U/L Albumin 3.5–5.5 g/dL Alkaline phosphatase 20–90 U/L Ammonia nitrogen 15–49 µg/dL Amylase 25–125 U/L Anion gap 8–16 mEq/L Aspartate aminotransferase 10–30 U/L Bicarbonate Venous 29–39 mEq/L Arterial 18–23 mEq/L Bilirubin Conjugated 0.1–0.4 mg/dL Unconjugated 0.2–0.7 mg/dL Total 0.3–101 mg/dL Calcium 9.0–11.0 mg/dL Calcium ionized 4.25–5.25 mg/dL Carbon dioxide, total 24–30 mEq/L Carbon dioxide tension 35–45 mm Hg (PaCO2) Ceruloplasmin 23–50 mg/100 mL. Chloride 98–106 mEq/L Copper 70–140 µg/dL

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Appendix 529 Cortisol 8 AM 4 PM 10 PM Creatine Creatine kinase MB isozyme Creatinine Ferritin Fibrinogen γ-Glutamyl transferase Gastrin Glucose G6PD Haptoglobin 17-Hydroxycorticosteroids Homocysteine Insulin (fasting) Iodide (protein bound) Iron Iron binding capacity 17-ketosteroids Lactic acid Lactic dehydrogenase Lipase Magnesium Non-protein nitrogen Osmolality Oxygen Capacity (varies with Hb) Content, arterial Saturation arterial Oxygen tension PaO2 pH, arterial blood Potassium Proteins, total Albumin

30 Appendix.indd 529

6–23 ng/dL 3–15 ng/dL 50% of 8 AM value 0.2–0.8 mg/dL 0.0–4.7 ng/mL 0.6–1.3 mg/dL 20–200 ng/dL 200–400 mg/dL 5–38 U/L 0–200 pg/mL 70–115 mg/dL 5–10 IU 26–185 mg/dL Male 7–19 µg/100 m Female 50–80 µg/100 mL 5–15 µmol/L 5–25 nU/mL 4–8 µg/100 mL 50–180 µg/100 mL 300–360 µg/100 mL Male 40–150 µg/100 mL Female 38–130 µg/100 mL 6–20 mg/100 mL 40–60 ImU/mL 0.2–1.5 U/mL 1.8–3.0 mg/dL 25–40 mg/100 mL 286–295 mOsm/kg water 16–24% vol% 15–23% vol% 75–100 mm Hg 75–100 mm Hg 7.35–7.45 3.5–5.0 mEq/L 6–8 g/dL 3.4–5 g/dL

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Globulin 2.5–4 g/dL A/G ratio 0.9–2.0 Phosphatase, acid 0.1–1.0 U (Bodansky) Phosphatase, alkaline 15–20 U (Armstrong) 1.4–4.1 U (Bodansky) Phosphorus 1.45–2.76 mEq/L Pyruvate 0.3–0.9 mg/dL Sodium 136–145 mEq/L Sugar (blood) Fasting 65–110 mg/dL PP up to 125 mg/dL TSH 0–7 µU/mL Thyroxine, free 1.0–2.1 ng/dL Thyroxine (T4) 4.4–9.9 µg/dL Tri-iodothyronine (T3) 150–250 ng/dL Urate Males 2.5–8.0 mg/dL Females 1.5–7.0 mg/dL Urea 24–49 mg/dL Urea nitrogen 11–23 mg/dL Uric acid 2.6–7.2 mg/dL Viscosity 1.4–1.8 times water Serum lipids Appearance Clear Triglycerides 30–200 mg/dL Total cholesterol 125–225 mg/dL HDL cholesterol 32–54 mg/dL LDL cholesterol 6–40 mg/dL LDLC/HDLC ratio 3.0–5.0 Serum transaminases CPK 21–232 IU/L LDH 100–190 IU/L AST (SGOT) 15–37 IU/L ALT (SGPT) 30–65 IU/L γGT (GGTP) 5–85 IU/L Immunology Autoantibodies Serum negative at 1:10 dilution

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Appendix 531 Antidouble stranded (DNA) Antiglomerular basement serum membrane antibody Antinuclear antibody C-reactive protein Total complement Immunoglobulins IgG IgA IgM IgD IgE

Serum negative at 1:10 dilution < 5U/mL Negative out 1:40 dilution Serum 0.08–3.1 mg/L Serum 17–42 mg/dL 550–90 1900 mg/dL 60–33 mg/dL 45–145 mg/dL 0.5–3.0 mg/dL