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EMERGENCY MEDICINE This page intentionally left blank EMERGENCY MEDICINE Sixth edition Anthony F. T. Brown MB ChB, FRCP, FRCS(Ed), FACEM, FCEM Professor Discipline of Anaesthesiology and Critical Care School of Medicine University of Queensland, Brisbane Senior Staff Specialist Department of Emergency Medicine Royal Brisbane and Women’s Hospital Brisbane Editor-in-Chief Emergency Medicine Australasia Senior Court of Examiners Australasian College for Emergency Medicine (ACEM) Inaugural ACEM Teaching Excellence Award 2001 Mike D. Cadogan MA(Oxon), MB ChB (Ed), FACEM Staff Specialist in Emergency Medicine Department of Emergency Medicine Sir Charles Gairdner Hospital Perth Medical Editor and Founder Lifeinthefastlane.com Winner, Gold Medal/Buchanan Prize ACEM Fellowship Exam 2003 DIAGNOSIS AND MANAGEMENT First published in Great Britain by Hodder Arnold Fifth edition 2006 This sixth edition published in 2011 by Hodder Arnold, an imprint of Hodder Education, a division of Hachette UK 338 Euston Road, London NW1 3BH http://www.hodderarnold.com © 2011 Anthony Brown and Michael Cadogan All rights reserved. Apart from any use permitted under UK copyright law, this publication may only be reproduced, stored or transmitted, in any form, or by any means with prior permission in writing of the publishers or in the case of reprographic production in accordance with the terms of licences issued by the Copyright Licensing Agency. In the United Kingdom such licences are issued by the Copyright licensing Agency: Saffron House, 6-10 Kirby Street, London EC1N 8TS Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. In particular (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed. Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress ISBN-13 978 1 444 120 134 1 2 3 4 5 6 7 8 9 10 Commissioning Editor: Caroline Makepeace Project Editor: Sarah Penny Production Controller: Kate Harris Cover Design: Helen Townson Cover image © beerkoff-Fotolia Typeset in Minion Pro 9pt by Dorchester Typesetting, Dorchester, Dorset Printed and bound in India by Replika Press Ltd What do you think about this book? Or any other Hodder Arnold title? Please visit our website: www.hodderarnold.com To Regina, my beautiful and understanding wife, for her encouragement and patience. And to Edward and Lucy, who continue to impress and amaze, and bring such joy and happiness whilst reminding me what really matters. A.F.T.B. To my wonderful wife Fiona for her tolerance and support. To my enigmatic children William, Hamish and Olivia for their enduring patience and inspiration. M.D.C. DEDICATION This page intentionally left blank Contents vii Dedication v Preface xxi Acknowledgements xxiii Section I CRITICAL CARE EMERGENCIES Cardiopulmonary Resuscitation 2 Initial approach 2 Definitive care 6 Acute Upper Airway Obstruction 13 Shocked Patient 15 General approach 15 Hypovolaemic shock 19 Septic shock 21 Unconscious Patient 24 Anaphylaxis 27 Severe Head Injury 29 Critical-Care Areas Drug Infusion Guideline 34 Further Reading 41 Section II GENERAL MEDICAL EMERGENCIES Chest Pain 44 Acute coronary syndrome 44 ST elevation myocardial infarction 44 Non-ST elevation myocardial infarction and unstable angina 48 Non-cardiac chest pain 51 Pulmonary embolus 51 Venous thromboembolism with deep vein thrombosis 55 Aortic dissection 57 Pericarditis 58 Pleurisy 59 Abdominal causes of chest pain 59 Musculoskeletal and chest wall pain 60 CONTENTS viii Contents Cardiac Arrhythmias 60 Breathless Patient 64 Acute asthma 65 Community-acquired pneumonia 67 Chronic obstructive pulmonary disease 71 Pneumothorax 72 Pulmonary embolus 75 Pulmonary oedema 75 Acute upper airway obstruction 76 Upper Gastrointestinal Haemorrhage 76 Diabetic Coma and Pre-coma 78 Diabetic ketoacidosis 78 Hyperglycaemic, hyperosmolar non-ketotic syndrome 80 Altered Conscious Level 80 Confused patient 81 Alcohol-related medical problems 85 Patient with an altered conscious level and smelling of alcohol 85 Alcohol withdrawal 86 Acute Neurological Conditions 87 Syncope 87 Seizure (Fit) 89 Generalized convulsive status epilepticus 91 Transient ischaemic attack 93 Stroke 95 Headache 97 Meningitis 97 Subarachnoid haemorrhage 99 Space-occupying lesion 100 Temporal arteritis 101 Hypertensive encephalopathy 101 Migraine 102 Tension (muscle contraction) headache 104 Post-traumatic headache 104 Disease in other cranial structures 105 Acute Arthropathy 105 Acute monoarthropathy 105 Septic arthritis 105 Gouty arthritis 106 Pseudogout 107 Traumatic arthritis 107 Acute polyarthropathy 108 Rheumatoid arthritis 109 Contents ix Osteoarthritis 109 Allergic or Immunological Conditions 110 Urticaria (hives) 110 Angioedema 111 Skin Disorders 112 Blistering (vesicobullous) conditions 112 Pruritus (itching conditions) 113 Purpuric conditions 114 Exanthematous diseases 116 Malignant melanoma 117 Elderly Patient 118 Disordered behaviour in the elderly 119 Falls in the elderly 120 Further Reading 121 Section III ACID–BASE, ELECTROLYTE AND RENAL EMERGENCIES Acid–Base Disturbances 124 Arterial blood gas interpretation 124 Metabolic acidosis 126 Metabolic alkalosis 128 Respiratory acidosis 129 Respiratory alkalosis 130 Electrolyte Disorders 131 Potassium disorders 132 Hyperkalaemia 132 Hypokalaemia 134 Sodium disorders 135 Hypernatraemia 135 Hyponatraemia 136 Calcium disorders 138 Hypercalcaemia 138 Hypocalcaemia 139 Magnesium disorders 139 Hypermagnesaemia 139 Hypomagnesaemia 140 Acute Renal Failure 141 Acute kidney injury 141 Further Reading 144 x Contents Section IV INFECTIOUS DISEASE AND FOREIGN TRAVEL EMERGENCIES Febrile Neutropenic Patient 146 Hepatitis 147 Gastrointestinal Tract Infection 148 Sexually Transmitted Diseases 150 Needlestick and Sharps Incidents 151 Inoculation Incident with HIV Risk 151 Inoculation Incident with Hepatitis Risk 151 Human Immunodeficiency Virus Infection 153 Tuberculosis 155 Bites with Rabies or other Lyssavirus Risk 157 Rabies and Lyssavirus risk 157 Common Imported Diseases of Travellers 158 Malaria 159 Typhoid 160 Dengue 161 Typhus and spotted fevers 161 Helminth infections 162 Pandemic Influenza 163 Further Reading 164 Section V TOXICOLOGY Acute Poisoning: General Principles 166 Specific Poisons 169 Paracetamol 170 Salicylates 172 Tricyclic antidepressants 174 Benzodiazepines 175 Opioids 176 Iron 177 Digoxin 178 Lithium 179 Theophylline 181 Beta-blockers 182 Calcium-channel blocking drugs 183 Carbon monoxide 184 Cyanide 185 Chloroquine 185 Cocaine 186 Contents xi Organophosphates 187 Paraquat 188 Chemical Burns 189 Further Reading 190 Section VI TOXINOLOGY EMERGENCIES Snake Bites 192 Elapid snake bites 192 Viper (adder) snake bites 195 Spider Bites 196 Marine Envenomation 197 Bee and Wasp Stings 199 Further Reading 200 Section VII ENVIRONMENTAL EMERGENCIES Heat, Cold and Drowning 202 Heat illness 202 Other hyperthermia-related illness 204 Hypothermia 205 Drowning 207 Sports-Diving Accidents 208 Decompression illness 209 Decompression illness with barotrauma 210 Electrical Burns, Electrocution and Lightning Strike 212 Electrical flash burns 212 Low-voltage electrocution 212 High-voltage electrocution 213 Lightning strike 215 Further Reading 216 Section VIII SURGICAL EMERGENCIES Multiple Injuries 218 Further Diagnosis and Management of Multiple Injuries: Definitive Care 223 Head and Facial Injuries 223 Neck Injuries 224 Cervical spine injury 224 Airway injury 229 Vascular injury in the neck 229 Nerve injury in the neck 229 xii Contents Oesophageal injury 230 Neck sprain 230 Chest Injuries 231 Pneumothorax 231 Haemothorax 231 Rib and sternum fractures 232 Myocardial contusion 233 Aortic rupture 234 Diaphragm rupture 235 Oesophageal rupture 236 Penetrating chest injury 237 Abdominal and Pelvic Trauma 238 Blunt abdominal trauma 238 Penetrating abdominal trauma 240 Pelvic injury 241 Blunt renal injury 242 Penetrating renal injury 243 Bladder and urethral injuries 244 Additional Orthopaedic Injuries in Multiple Trauma 244 Thoracic and lumbosacral spine injury 245 Limb injury 246 Head Injury 247 Conscious head injury 247 Burns 250 Major burns 250 Minor burns and scalds 252 Minor burns of the hand 253 Minor burns of the face 254 Bitumen burns 254 Acute Abdomen 254 Seriously ill patient 254 Stable patient with an acute abdomen 255 Causes of acute abdominal pain 259 Acute appendicitis 260 Intestinal obstruction 260 Intussusception 261 Perforation of a viscus 262 Diverticulitis 262 Inflammatory bowel disease 263 Biliary colic 264 Acute cholecystitis 264 Ruptured abdominal aortic aneurysm 265 Ischaemic colitis 266 Contents xiii Mesenteric infarction 266 Ruptured spleen 267 Acute pancreatitis 267 Renal and ureteric colic 268 Pyelonephritis 269 Acute urinary retention 270 Acute epididymo-orchitis 271 Acute testicular torsion 271 Primary peritonitis 272 Retroperitoneal haemorrhage 272 Gynaecological causes 273 Medical disorders presenting with acute abdominal pain 273 Further Reading 274 Section IX ORTHOPAEDIC EMERGENCIES Injuries to the Shoulder and Upper Arm 276 Fractures of the clavicle 276 Acromioclavicular dislocation 276 Sternoclavicular dislocation 277 Fractures of the scapula 278 Anterior dislocation of the shoulder 278 Posterior dislocation of the shoulder 280 Fractures of the upper humerus 281 Fractures of the shaft of the humerus 282 Injuries to the Elbow and Forearm 283 Supracondylar fracture of the humerus 283 Condylar and epicondylar fractures of the humerus 284 Dislocation of the elbow 285 Pulled elbow 286 Fractures of the olecranon 286 Fractures of the radial head 287 Fractures of the radial and ulnar shafts 287 Injuries to the Wrist and Hand 288 Colles’ fracture 288 Smith’s fracture 290 Barton’s fracture-dislocation 291 Radial styloid fracture 291 Distal radial fractures in children 292 Fractures of the scaphoid 292 Dislocations of the carpus 294 Fractures of the other carpal bones 294 Fractures of the thumb metacarpal 295 Dislocation of the thumb metacarpal 296 xiv Contents Rupture of the ulnar collateral ligament 296 Fractures of the other metacarpals 297 Fractures of the proximal and middle phalanges 298 Fractures of the distal phalanges 298 Dislocation of the phalanges 299 Flexor tendon injuries in the hand 300 Extensor tendon injuries in the hand 300 Digital nerve injuries 301 Fingertip injuries 301 Cervical Spine Injuries 301 Thoracic and Lumbar Spine Injuries 302 Pelvic Injuries 302 Injuries to the Hip and Upper Femur 302 Dislocation of the hip 302 Fractures of the neck of the femur 303 Fractures of the shaft of the femur 304 Injuries to the Lower Femur, Knee and Upper Tibia 305 Supracondylar and condylar fractures of the femur 305 Fractures of the patella and injury to the quadriceps apparatus 305 Dislocation of the patella 306 Soft-tissue injuries of the knee 306 Dislocation of the knee 308 Fractures of the tibial condyles 308 Injuries to the Lower Tibia, Ankle and Foot 309 Fractures of the shaft of the tibia 309 Isolated fracture of the fibula 310 Inversion ankle injuries 310 Other ankle injuries 312 Dislocation of the ankle 312 Fractures and dislocation of the talus 312 Fractures of the calcaneus 313 Rupture of the tendo Achilles 314 Mid-tarsal dislocations 314 Metatarsal injuries and tarsometatarsal dislocations 314 Fractures of the phalanges of the foot 315 Dislocations of the phalanges of the foot 315 Further Reading 316 Contents xv Section X MUSCULOSKELETAL AND SOFT-TISSUE EMERGENCIES Soft-Tissue Injuries 318 Tetanus prophylaxis 321 Crush injury and compartment syndrome 323 Puncture injuries 324 Hand infections 325 Pre-tibial laceration 326 Non-articular Rheumatism 326 Torticollis (wry neck) 327 Frozen shoulder 327 Rotator cuff tear: supraspinatus rupture 328 Supraspinatus tendinitis 328 Subacromial bursitis 329 Tennis and golfer’s elbow 329 Olecranon bursitis 329 De Quervain’s stenosing tenosynovitis 329 Carpal tunnel syndrome 330 Housemaid’s knee 330 Back Pain 330 Direct back trauma 331 Indirect mechanical back trauma 331 Severe or atypical, non-traumatic back pain 332 Mild to moderate, non-traumatic back pain 333 Further Reading 333 Section XI PAEDIATRIC EMERGENCIES General Assessment 336 Cardiopulmonary Resuscitation 339 Breathless Child 347 Asthma 347 Bronchiolitis 349 Pneumonia 350 Anaphylaxis 351 Stridor 352 Croup (acute laryngotracheobronchitis) 352 Epiglottitis (supraglottitis) 352 Inhaled foreign body 354 Abdominal Pain, Diarrhoea and Vomiting 355 Acute abdominal pain 355 Diarrhoea, vomiting and dehydration 357 xvi Contents Febrile Child 361 Seizures and Febrile Convulsions 364 Seizures 364 Febrile convulsions 365 Acute Poisoning 367 Limping Child 369 Sudden Unexpected Death in Infancy 370 Child Abuse (Non-accidental Injury) 372 Further Reading 374 Section XII OBSTETRIC AND GYNAECOLOGICAL EMERGENCIES Gynaecological Assessment and Management 376 General principles 376 Prescribing in pregnancy 376 Gynaecological Causes of Acute Abdominal Pain 376 Ruptured ectopic pregnancy 377 Pelvic inflammatory disease (acute salpingitis) 379 Ruptured ovarian cyst 380 Torsion of an ovarian tumour 380 Endometriosis 381 Bleeding in Early Pregnancy 381 Spontaneous miscarriage 381 Induced septic abortion 383 Conditions in Late Pregnancy 383 Terminology 384 Antepartum haemorrhage 384 Pre-eclampsia and eclampsia 385 Emergency delivery 386 Trauma in late pregnancy 387 Cardiopulmonary resuscitation in late pregnancy 388 Women’s Medicine Crises 389 Post-coital contraception 389 Missed oral contraceptive pill 390 Domestic violence to females 391 Female rape 391 Further Reading 393 Contents xvii Section XIII ENT EMERGENCIES Traumatic Conditions of the Ear 396 Subperichondrial haematoma 396 Wounds of the auricle 396 Foreign body in the external ear 396 Perforated eardrum 397 Basal skull fracture 397 Non-traumatic Conditions of the Ear 398 Otitis externa 398 Furunculosis of the external ear 398 Acute otitis media 399 Mastoiditis 399 Vertigo 400 Facial nerve palsy 400 Traumatic Conditions of the Nose 401 Fractured nose 401 Foreign body in the nose 402 Non-traumatic Conditions of the Nose 402 Epistaxis 402 Traumatic Conditions of the Throat 404 Non-traumatic Conditions of the Throat 404 Tonsillitis 404 Quinsy (peritonsillar abscess) 405 Foreign body in the pharynx 405 Swallowed foreign body 406 Stridor 407 Further Reading 407 Section XIV OPHTHALMIC EMERGENCIES Visual Acuity 410 Topical Ophthalmic Preparations 410 Traumatic Conditions of the Eye 411 Periorbital haematoma (‘black eye’) 411 Subconjunctival haematoma 411 Eyelid laceration 412 Eyelid burn 412 Chemical burns to the eye 412 Conjunctival foreign body 413 Corneal foreign body 414 Corneal abrasion 414 Flash burn (arc eye) 414 xviii Contents Blunt trauma to the eye 415 Penetrating trauma to the eye 416 Conditions Affecting the Eyelids 417 Blepharitis 417 Stye (external hordeolum) 417 Meibomian abscess (internal hordeolum) 417 Meibomian cyst (chalazion) 417 Dacryocystitis 417 Orbital and periorbital cellulitis 418 Basal cell carcinoma (rodent ulcer) 418 Ophthalmic shingles (herpes zoster ophthalmicus) 418 Painful, Red Eye 419 Acute conjunctivitis 419 Acute keratitis 420 Acute iritis 421 Acute episcleritis and scleritis 421 Acute glaucoma 422 Sudden Loss of Vision in the Uninflamed Eye 422 Central retinal artery occlusion 422 Central retinal vein occlusion 423 Vitreous haemorrhage 424 Retinal detachment 424 Optic neuritis 425 Further Reading 425 Section XV MAXILLOFACIAL AND DENTAL EMERGENCIES Traumatic Conditions of the Face and Mouth 428 Lacerations 428 Tooth injuries 428 Fractured mandible 430 Dislocated mandible 430 Fracture of the zygoma or zygomaticomaxillary (malar) complex 431 ‘Blow-out’ fracture of the orbital floor 432 Le Fort middle-third of face fractures 433 Non-traumatic Conditions of the Mouth 434 Toothache 434 Dental abscess 434 Ludwig’s angina 434 Submandibular swellings 435 Further Reading 435 Contents xix Section XVI PSYCHIATRIC EMERGENCIES Deliberate Self-harm 438 Violent Patient 439 Alcohol and Drug Dependency and Abuse 441 Alcohol and drug withdrawal 441 Problem drinking 441 Opiate and intravenous drug addiction 442 Benzodiazepine and solvent addiction 443 Involuntary Detention 443 Further Reading 444 Section XVII ADMINISTRATIVE AND LEGAL ISSUES Desirable Habits of the Good Emergency Department Doctor 446 Excellence in emergency department care 446 Emergency department medical records 446 Communicating with the general practitioner 447 Breaking bad news 448 Risk management and incident reporting 449 Triage 450 Consent, Competence and Refusal of Treatment 451 Consent and competence 451 Refusal of treatment and discharge against medical advice 452 Police, Coroner and Attending Court 453 Police request for patient information 453 Police request to interview a patient 453 Police request for an alcohol breath test or blood sample 453 Request for a police medical statement 454 Coroner 454 Attending an inquest or court 455 Retrieval and Inter-hospital Transfer 456 Major Incident 456 External disaster 456 Specialized responses 459 Chemical incident 460 Biological incident 462 Radiological incident 463 Further Reading 464 xx Contents Section XVIII PRACTICAL PROCEDURES Endotracheal Intubation 466 Rapid Sequence Induction (RSI) Intubation 466 Cricothyrotomy 469 Needle Thoracentesis 471 Intercostal Catheter Insertion 473 DC Cardioversion 474 Pericardial Aspiration 475 Central Line Insertion 476 Intraosseous Line Insertion 480 Lumbar Puncture 482 Indwelling Urethral Catheter Insertion 484 Nasogastric Tube Insertion 486 Bier’s Intravenous Regional Block 488 Femoral Nerve Block 489 Digital Nerve Ring Block 491 Knee Aspiration 492 Further Reading 492 Glossary 495 Appendix: Normal Laboratory Values 503 Index 507 xxi Many changes have been made to this new edition, which incorporates the latest ideas and evidence base underpinning the best emergency medicine care. The whole text has been revised and updated from the latest 2010 international guidelines on cardiopulmonary resuscitation, right through to favourite handy hints and practical tips. Also included are brand new sections on Critical Care Emergencies and Practical Procedures, plus expanded sections on Paediatric Emergencies, Infectious Disease and Foreign Travel Emergencies, and Environmental Emergencies, and the addition of normal laboratory values and precise drug doses. A standardized approach to every condition has been retained throughout, with the text consistently formatted to maximize ease of use and the practical delivery of patient care. This book is as much designed for the bedside as it is for studying. The text is now supported by a wealth of additional online material at http:// lifeinthefastlane.com/. This includes high-resolution clinical images, procedural videos, case-based clinical questions, additional reading material and links to online references, all available for free. The emergency department is rightly regarded as the ‘front door’ to the hospital. No matter how busy it may be, or how much inpatient beds are at a premium, each new patient deserves high-quality care from the moment he or she arrives. We hope this book will help you deliver on this challenge. Anthony F T Brown Mike Cadogan December 2010 PREFACE TO THE 6TH EDITION OF EMERGENCY MEDICINE This page intentionally left blank xxiii Many thanks to Dr Peter Logan for his expert contribution on the Major Incident and to Dr Tor Ercleve for his fine illustrations. Also to Dr Chris Nickson (Critical Care), Dr Tim Inglis (Infectious Diseases) and Kane Guthrie (Practical Procedures) for reviewing and commenting on the drafts of these sections. In addition, particular thanks to the outstanding and professional help and advice from Caroline Makepeace, Head of Postgraduate and Professional Publishing, Health Sciences at Hodder Education, and from Sarah Penny, Project Editor. We could not have asked to work in a more efficient, effective or encouraging partnership. Tony Brown and Mike Cadogan December 2010 ACKNOWLEDGEMENTS This page intentionally left blank Critical Care Emergencies 1 CRITICAL CARE EMERGENCIES Section I 2 Critical Care Emergencies INITIAL APPROACH DIAGNOSIS 1 Cardiopulmonary resuscitation (CPR) is required if a collapsed person is unconscious or unresponsive, not breathing, and has no pulse in a large artery such as the carotid or femoral. (i) The following may also be seen: (a) occasional, ineffectual (agonal) gasps (b) pallor or cyanosis (c) dilated pupils (d) brief tonic grand mal seizure. 2 Sudden cardiac arrest still causes over 60% of deaths from coronary heart disease in adults. MANAGEMENT 1 This is based on the International Liaison Committee on Resuscitation (ILCOR) 2010 International Consensus on CPR Science with Treatment Recommendations (CoSTR). (i) The first person on the scene stays with the patient, checks for danger and commences resuscitation, making a note of the time. (ii) The second person summons help to organize the arrival of equipment, then assists with the resuscitation. 2 Immediate actions The aim is to maintain oxygenation of the brain and myocardium until a stable cardiac output is achieved. (i) Lay the patient flat on a hard surface such as a trolley. If the patient is on the floor and enough people are available, lift the patient onto a trolley to facilitate the resuscitation procedure. (ii) Rapidly give a single, sharp precordial thump within the first few seconds of the onset of a witnessed or monitored arrest, where the rhythm is pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF), and a defibrillator is not immediately to hand. (iii) Check the victim for a response, and then open the airway by tilting the head and lifting the chin if there is no response (‘head tilt, chin lift’): (a) this prevents the tongue from occluding the larynx (b) look, listen and feel for breathing for no more than 10 s, while keeping the airway open. (iv) If breathing is not normal or absent, check for signs of a circulation: (a) assess a large pulse such as the carotid or femoral, or look for signs of life for no more than 10 s. CARDIOPULMONARY RESUSCITATION Critical Care Emergencies 3 CARDIOPULMONARY RESUSCITATION (v) Start CPR immediately if there are no signs of life: (a) commence external cardiac massage (b) commence assisted ventilation. 3 External cardiac massage (i) Place the heel of one hand in the centre of the patient’s chest. Place the heel of the other hand on top, interlocking the fingers. (ii) Keeping the arms straight and applying a vertical compression force, depress the sternum 5–6 cm at a rate of at least 100 compressions/min (but not exceeding 120/min): (a) release all the pressure on the chest without losing contact with the sternum after each compression (b) do not apply pressure over the upper abdomen, lower end of sternum or the ribs, and take equal time for compression and for release. (iii) Perform 30 compressions, which should create a palpable femoral pulse. (iv) Use a one- or two-hand technique to compress the lower half of the sternum in small children by approximately one-third of its depth, at a rate of at least 100 compressions/min but not greater than 120/min: (a) use the tips of two fingers in infants, also at a rate of at least 100/min (see p. 343). 4 Assisted ventilation (i) Open the airway again using head tilt and chin lift. (ii) Start mouth-to-mouth/nose or mouth-to-mask respiration without delay if breathing is absent, using a pocket mask such as the Laerdal. (iii) Deliver two effective rescue breaths that should be completed within 5 s total time, and immediately resume compressions. (iv) Use a bag-valve mask setup such as an Ambu or Laerdal bag with oxygen reservoir attached and face mask instead, if trained in the technique (a) quickly look in the mouth and remove any obstruction with forceps or suction. Leave well-fitting dentures in place (b) or try inserting an oropharyngeal (Guedel) airway if necessary (c) check for leaks around the mask or convert to a two-person technique if the chest fails to inflate (d) consider possible obstruction of the upper airway, if ventilation is still ineffective (see p. 13). Warning: avoid using excessive or malpositioned force causing rib fractures, flail chest, liver lacerations, etc. ! 4 Critical Care Emergencies CARDIOPULMONARY RESUSCITATION 5 Basic life support: external cardiac massage with assisted ventilation (i) Continue with chest compressions and rescue breaths in a ratio of 30:2. (ii) Change the person providing chest compressions every 2 min, but ensure minimum interruption to compressions during the changeover. 6 Defibrillation (i) As soon as the defibrillator arrives, apply self-adhesive pads or paddles to the patient whilst continuing chest compressions (a) rapidly shave excessive male chest hair, without delay (b) place one self-adhesive defibrillation pad or conventional paddle to the right of the sternum below the clavicle, and the other adhesive pad or paddle in the mid-axillary line level with the V6 electrocardiogram (ECG) electrode or female breast (c) avoid positioning self-adhesive pads or paddles over an ECG electrode, medication patch, or implanted device, e.g. pacemaker or automatic cardioverter defibrillator. (ii) Analyse the rhythm with a brief pause, and charge the defibrillator if the rhythm is VF or pulseless VT. Continue chest compressions until fully charged. (iii) Quickly ensure that all rescuers are clear, then give the patient an immediate 150–200 J direct current (DC) shock using a biphasic waveform defibrillator (all modern defibrillators are now biphasic) (a) minimize the delay in delivering the shock, which should take less than 5 s (b) ensure good electrical contact is made when applying manual paddles by using gel pads or electrode jelly, and apply firm pressure of 8 kg force in adults (c) give a 360 J shock if an older monophasic defibrillator is used. (iv) Immediately resume chest compressions without reassessing the rhythm or feeling for a pulse. (v) The only exception is when VF is witnessed in a patient already connected to a manual defibrillator, or during cardiac catheterization, and/or early post-cardiac surgery (a) use a stacked, three-shock strategy rapidly delivering three shocks in a row before starting chest compressions. (vi) Continue external chest compressions and assisted ventilation for 2 min, then pause briefly to assess the rhythm again. Warning: adequate oxygenation is achieved by the above measures. Endotracheal intubation should only be attempted by those who are trained, competent and experienced. ! Critical Care Emergencies 5 CARDIOPULMONARY RESUSCITATION 7 Observe one of four possible traces (see Fig. 1.1 for a rapid overview of treatment): (i) Shockable rhythms such as VF (see p. 7) or pulseless VT (see p. 7). Figure 1.1 Adult advanced life support algorithm. ABCDE, airway/breathing/ circulation/disability/exposure; CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; PEA, pulseless electrical activity; VF, ventricular fibrillation; VT, ventricular tachycardia. Reproduced with kind permission from European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010. Section 1. Executive summary. Resuscitation 81: 1219–76. Call Resuscitation Team During CPR: ● Ensure high-quality CPR: rate, depth, recoil ● Plan actions before interrupting CPR ● Give oxygen ● Consider advanced airway and capnography ● Continuous chest compressions when advanced airway in place ● Vascular access (intravenous, intraosseous) ● Give adrenaline (epinephrine) every 3–5 min ● Correct reversible causes Reversible causes ● Hypoxia ● Hypovolaemia ● Hypo-/hyperkalaemia/metabolic ● Hypothermia ● Thrombosis ● Tamponade – cardiac ● Toxins ● Tension pneumothorax Unresponsive? Not breathing or only occasional gasps CPR 30 : 2 Attach defibrillator/monitor Minimize interruptions Assess rhythm Non-shockable (PEA/asystole) Shockable (VF/pulseless VT) 1 shock Immediately resume: CPR for 2 min Minimize interruptions Immediately resume: CPR for 2 min Minimize interruptions Immediate post cardiac arrest treatment ● Use ABCDE approach ● Controlled oxygenation and ventilation ● 12-lead ECG ● Treat precipitating cause ● Temperature control/therapeutic hypothermia Return of spontaneous circulation 6 Critical Care Emergencies CARDIOPULMONARY RESUSCITATION (ii) Non-shockable rhythms such as asystole (see p. 8) and pulseless electrical activity (PEA) (see p. 8). 8 Establish an initial i.v. line in the antecubital fossa. (i) Give at least 20 mL of normal saline to flush any drugs administered, that are given after the third DC shock. (ii) Elevate the limb for 10–20 s to facilitate drug delivery to the central circulation. (iii) Establish a second i.v. line unless the cardiac resuscitation is rapidly successful (a) ideally this line should be inserted into a central vein, either the external or internal jugular or the subclavian (b) a central line should only be inserted by a skilled doctor, as inadvertent arterial puncture, haemothorax or pneumothorax may invalidate further resuscitation attempts (c) also, the central venous route poses additional serious hazards should thrombolytic therapy be indicated (d) all drugs are then given via this central line. 9 Endotracheal intubation A skilled doctor with airway training may insert a cuffed endotracheal tube (see p. 466). This maintains airway patency, prevents regurgitation with inhalation of vomit or blood from the mouth or stomach, and allows lung ventilation without interrupting chest compressions. (i) Confirm correct endotracheal tube placement by seeing the tube pass between the vocal cords, and by observing bilateral chest expansion, and auscultating the lung fields and over the epigastrium. (ii) Immediately connect an exhaled carbon dioxide detection device such as a waveform capnograph, and look for a tracing, as the signs above are not completely reliable (a) never delay CPR to intubate the airway except for a brief pause in chest compressions of not more than 10 s, as the tube is passed between the vocal cords. (iii) Once the airway has been secured, continue cardiac compressions uninterrupted at a rate of at least 100/min, and ventilate the lungs at 10 breaths/min (without any need now to pause for the chest compressions) (a) take care not to hyperventilate the patient at too fast a rate. 10 Subsequent management depends on the cardiac rhythm and the patient’s condition. Keep the ECG monitor attached to the patient at all times. DEFINITIVE CARE DIAGNOSIS The ECG trace will show shockable rhythms such as VF or pulseless VT, or non-shockable rhythms such as asystole or PEA (see Fig. 1.1). Critical Care Emergencies 7 CARDIOPULMONARY RESUSCITATION MANAGEMENT 1 Ventricular fibrillation or pulseless ventricular tachycardia VF is asynchronous, chaotic ventricular depolarization and repolarization producing no cardiac output. Pulseless VT is a wide-complex, regular tachycardia associated with no clinically detectable cardiac output. (i) Give a DC shock once VF/VT is confirmed on the monitor: (a) deliver 150–200 J using a biphasic defibrillator (b) deliver 360 J if using an older monophasic defibrillator (c) deliver this shock with less than 5 s delay to cardiac compressions. (ii) Immediately resume CPR, continuing with chest compressions to ventilations at a ratio of 30:2, if the airway has not yet been secured (a) do not delay CPR by reassessing the rhythm or feeling for a pulse (b) perform compressions at 100/min and ventilations at 10/min without interruption if the airway has been secured by now. (iii) Continue CPR for 2 min, then briefly pause to reassess the rhythm on the monitor (a) if there is still VF/VT, give a second DC shock of 150–360 J biphasic or 360 J monophasic (b) immediately resume CPR after this shock. (iv) Briefly pause after another 2 min of CPR to check the monitor: (a) give by a third shock of 150–360 J biphasic or 360 J monophasic and resume CPR. (v) Continue compressions and give: (a) 10 mL of 1 in 10 000 adrenaline (epinephrine) (1 mg) i.v. (b) a bolus of amiodarone 300 mg i.v. diluted in 5% dextrose to a volume of 20 mL if VF/VT persist. 2 Irrespective of the arrest rhythm, give additional 1 in 10 000 adrenaline (epinephrine) 1 mg (10 mL) every 3–5 min until return of spontaneous circulation (ROSC). (i) This will be once every two cycles of the algorithm (see Fig. 1.1). (ii) Meanwhile continue providing CPR and make sure to change the person performing cardiac compressions every 2 min, to preserve optimum efficacy. 3 Continue the drug–shock–CPR–rhythm check sequence. (i) Analyse the rhythm again after another 2 min of CPR: (a) immediately deliver a fourth shock if still in VF/VT. 4 Look for signs of life suggesting ROSC, or palpate for a pulse once a non-shockable rhythm is present with regular or narrow complexes. (i) Resume CPR if the pulse is absent or difficult to feel. (ii) Begin post-resuscitation care when a strong pulse is felt, or the patient shows signs of life suggesting ROSC. See page 11. 8 Critical Care Emergencies CARDIOPULMONARY RESUSCITATION 5 During this period of CPR: (i) If not already done: (a) check the defibrillator pad or paddle position and contact (b) attempt/verify the endotracheal tube position, and successful i.v. access (c) review all potentially reversible causes. See the ‘4 Hs’ and the ‘4 Ts’ below (Section 7). (ii) Consider the following drugs even though there are no data in support of their increasing survival to hospital discharge: (a) amiodarone – give initial bolus of 300 mg i.v. after the third shock, repeated once at a dose of 150 mg for recurrent or refractory VF/VT. Follow with an infusion of 900 mg over 24 h (b) lignocaine (lidocaine) – give initial bolus of 1 mg/kg i.v. if amiodarone is unavailable, followed by 0.5 mg/kg if necessary. Omit if amiodarone has been given (c) magnesium – give 2 g (8 mmol or 4 mL) of 49.3% magnesium sulphate i.v., particularly in torsades de pointes, or for suspected hypomagnesaemia such as a patient on a potassium-losing diuretic, and for digoxin toxicity. Repeat the dose after 10–15 min if ineffective. (iii) Consider buffering agent: (a) 8.4% sodium bicarbonate – particular indications are for life-threatening hyperkalaemia or tricyclic antidepressant overdose (see p. 132 and p. 174) (b) give 50 mmol (50 mL) i.v., then as guided by arterial blood gases (ABGs). 6 Asystole or pulseless electrical activity These are non-shockable rhythms. See Figure 1.1 for a rapid overview of treatment. (i) Asystole is absence of any cardiac electrical activity (a) make sure the ECG leads are not disconnected or broken by observing the cardiac compressions artefact on the ECG screen during CPR (b) check appropriate ECG lead selection and gain setting, without stopping chest compressions or ventilation (c) do not rely on a gel pad-manual paddle combination to diagnose asystole, but use independent ECG electrodes (d) continue chest compressions and ventilation if there is difficulty in differentiating from fine VF, in an attempt to ‘coarsen’ unsuspected VF. Tip: if venous access is impossible, insert an intraosseous cannula, particularly in children (see p. 480). ✓ Critical Care Emergencies 9 CARDIOPULMONARY RESUSCITATION (ii) Pulseless electrical activity (PEA) was formerly known as electromechanical dissociation. It is the presence of a coordinated electrical rhythm without detectable cardiac output (a) survival is unlikely unless a reversible cause can be found and treated. See the ‘4 Hs’ and the ‘4 Ts’ below. (iii) Asystole and PEA have a poor prognosis because defibrillation is of no use (a) continue CPR at a compression/ventilation (C/V) ratio of 30:2, unless the airway has been secured, in which case give compressions at a rate of 100/min and ventilations at a rate of 10/min (b) give 1 in 10 000 adrenaline (epinephrine) 1 mg (10 mL) i.v. (c) recheck the rhythm after 2 min of CPR. If organized with a palpable pulse, begin post-resuscitation care (d) resume CPR immediately if asystole or PEA persist (e) give repeated 1 in 10 000 adrenaline (epinephrine) 1 mg (10 mL) every 3–5 min, i.e. every second cycle of the algorithm (see Fig. 1.1) (f) continue CPR unless the rhythm changes to VF/VT. If VF is identified midway through a 2-min cycle, complete that cycle of CPR before shock delivery (see above p. 7). 7 Potentially reversible causes: the 4 Hs and the 4 Ts. Always look out for the following conditions, which may precipitate cardiorespiratory arrest and/or decrease the chances of a successful resuscitation (see Fig. 1.1). (i) Hypoxaemia (a) make sure maximal up to 100% oxygen is being delivered at 15 L/min (b) confirm ventilation at 500–600 mL tidal volume (6–7 mL/kg) is creating a visible rise and fall of both sides of the chest. (ii) Hypovolaemia (a) severe blood loss following trauma, gastrointestinal haemorrhage, ruptured aortic aneurysm or ruptured ectopic pregnancy may cause cardiac arrest (b) always consider this in any case of unexplained cardiovascular collapse (c) get senior emergency department (ED) help, and search for the source of bleeding (d) give warmed fluid replacement and call the surgical, vascular, or obstetrics and gynaecology team as appropriate. (iii) Hyper/hypokalaemia, hypocalcaemia, acidaemia and other metabolic disorders (a) rapidly check the potassium and calcium initially as suggested by the medical history, e.g. in renal failure (see p. 141) 10 Critical Care Emergencies CARDIOPULMONARY RESUSCITATION (b) give 10% calcium chloride 10 mL i.v. for hyperkalaemia, hypocalcaemia or calcium-channel blocking drug overdose (c) give a bolus of potassium 5 mmol i.v. for hypokalaemia. (iv) Hypothermia (a) check the core temperature with a low-reading thermometer particularly in any drowning or exposure incident (see p. 207) (b) moderate (30–32°C) or severe (under 30°C) hypothermia will require heroic measures such as active core re-warming with warmed pleural, peritoneal or gastric lavage, or even extracorporeal re-warming, when a patient is in cardiac arrest (see p. 205) (c) get a senior ED doctor’s help. Do not cease CPR until the temperature is at least 33°C, or the team leader determines futility. (v) Tension pneumothorax (a) tension usually follows a traumatic rather than a spontaneous pneumothorax, particularly if positive-pressure ventilation is used (b) it results in extreme respiratory distress and circulatory collapse. It may follow attempts at central venous cannulation (c) the patient becomes increasingly breathless and cyanosed, and develops a tachycardia with hypotension – there is decreased chest expansion on the affected side, a hyper-resonant percussion note, and absent or diminished breath sounds – the trachea is displaced towards the other side, and the neck veins are usually distended (d) this is a life-threatening situation requiring immediate relief, without waiting for a chest radiograph (CXR) (e) insert a wide-bore needle or cannula through the second intercostal space in the mid-clavicular line. This will be followed by a rush of air outwards (see p. 471) (f) insert an intercostal drain (see p. 473). (vi) Tamponade (a) cardiac tamponade may follow trauma, usually penetrating, myocardial infarction, dissecting aneurysm or pericarditis (b) there is hypotension, tachycardia, pulsus paradoxus and engorged neck veins that rise on inspiration (Kussmaul’s sign). The heart sounds are quiet, the apex beat is impalpable and PEA may ensue (c) perform pericardiocentesis if the patient is in extremis. Insert a cardiac needle between the angle of the xiphisternum and the left costal margin at 45° to the horizontal, aiming for the left shoulder (see p. 475) Critical Care Emergencies 11 CARDIOPULMONARY RESUSCITATION (d) sometimes aspirating as little as 50 mL restores the cardiac output, although immediate resuscitative thoracotomy is usually indicated in cases resulting from trauma (see p. 237). (vii) Toxins/poisons/drugs (a) many substances cause cardiorespiratory arrest following accidental or deliberate ingestion, such as poisoning with tricyclic antidepressants (see p. 174), calcium-channel blocking drugs (see p. 183) or -blockers (see p. 182), and hydrofluoric acid burns (see p. 190) (b) consider these based on the history, recognize early, and treat supportively or with antidotes where available. (viii) Thromboembolism with mechanical circulatory obstruction (a) perform external cardiac massage, which may break up a massive pulmonary embolus (PE), and give a fluid load of 20 mL/kg (b) give thrombolysis such as alteplase (recombinant tissue plasminogen activator [rt-PA]) 100 mg i.v. if clinical suspicion is high and there are no absolute contraindications (c) consider performing CPR for at least another 60–90 min before termination of the resuscitation. 8 The prognosis is usually hopeless if a patient is still in asystole. However, consider pacing if P waves or any other electrical activity, such as a severe bradycardia, are present with poor perfusion: (i) Use an external (transcutaneous) pacemaker to maintain the cardiac output until a transvenous wire is inserted. (ii) A temporary transvenous pacemaker wire should ideally be passed under X-ray guidance, but may be inserted blind via a central vein. 9 Post-resuscitation care It is important to continue effective CPR until the heartbeat is strong enough to produce a peripheral pulse, and/or there are signs of life. (i) Titrate oxygen delivery to maintain oxygen saturation 94–98%. Avoid hyperoxaemia. (ii) Check the ABG to exclude hypocarbia from over-ventilation, which causes cerebral vasoconstriction with decreased cerebral blood flow (a) adjust ventilation to aim for normocarbia with a PaCO2 from 35 to 45 mmHg (4.5 to 6 kPa). (iii) Insert a gastric tube to decompress the stomach. (iv) Contact the cardiology service urgently after cardiac arrest in a suspected acute coronary syndrome, such as a cardiac arrest following chest pain (a) immediate percutaneous coronary intervention (PCI) may be possible 12 Critical Care Emergencies CARDIOPULMONARY RESUSCITATION (b) do not rely on any particular early ECG abnormality, or expect to see ST elevation. (v) Give 1 in 10 000 adrenaline (epinephrine) 50 μg (0.5 mL) i.v. if there is persistent hypotension, and other treatable causes such as hypoxia, hypovolaemia, tension pneumothorax, hyperkalaemia or hypokalaemia have been excluded. (a) repeat the adrenaline (epinephrine) to maintain a blood pressure similar to the patient’s usual blood pressure, or a systolic blood pressure greater than 100 mmHg, aiming for an adequate urine output of 1 mL/kg/h (b) give the adrenaline (epinephrine) and other vasoactive drugs as soon as possible via a dedicated central venous line, which should be inserted under ultrasound control if not already sited. (vi) Control seizures with midazolam 0.05–0.1 mg/kg up to 10 mg i.v., diazepam 0.1–0.2 mg/kg up to 20 mg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. (a) follow this with phenytoin 15–18 mg/kg i.v. no faster than 50 mg/min by slow bolus, or preferably as an infusion in 250 mL normal saline (never in dextrose) over 30 min under ECG monitoring. (vii) Maintain blood glucose at ≤10 mmol/L, but avoid hypoglycaemia. (viii) Commence therapeutic hypothermia measures to a temperature range of 32–34°C, according to local policy: (a) initiate cooling following out-of-hospital VF arrest, as well as in post asystole/PEA patients (b) infuse 30 mL/kg cold 4°C normal saline or Hartmann’s (c) place ice packs to the groin and axillae (d) use a cooling blanket if available. (ix) Transfer the patient to the ICU, catheter laboratory or coronary care unit (CCU). Perform the following investigations but do not delay the transfer: (a) serum sodium, potassium, glucose and ABG, if not already done (b) 12-lead ECG (c) CXR to look for correct positioning of the endotracheal tube, nasogastric tube and central line – exclude a pneumothorax, pulmonary collapse and pulmonary oedema. (x) Transfer the patient with a trained nurse and doctor in attendance. A minimum of a portable cardiac monitor, defibrillator, oxygen and suction should be available on the trolley. Critical Care Emergencies 13 ACUTE UPPER AIRWAY OBSTRUCTION 10 When to stop The decision to cease further attempts at resuscitation is difficult. Only the senior ED doctor should take this. Survival from out-of-hospital cardiac arrest is greatest when: (i) The event is witnessed. (ii) A bystander starts resuscitation, even if only chest compressions (doubles or triples survival rate). (iii) The heart arrests in VF or VT (22% survival). (iv) Defibrillation is carried out at an early stage, with successful cardioversion achieved within 3–5 min (49–75% survival), and not more than 8 min: (a) each minute of delay before defibrillation reduces survival to discharge by 10–12% (b) survival after more than 12 min of VF in adults is less than 5%. DIAGNOSIS 1 Acute upper airway obstruction may be due to choking on an inhaled foreign body, epiglottitis, croup, facial burns and/or steam inhalation, angioedema, trauma, carcinoma or retropharyngeal abscess. 2 There may be sudden wheeze, coughing, hoarseness or complete aphonia, with severe distress, ineffective respiratory efforts, stridor and cyanosis, followed by unconsciousness. 3 Attach a cardiac monitor and pulse oximeter to the patient. MANAGEMENT This depends on the suspected cause. 1 Sit the patient up and give 100% oxygen via a face mask. Aim for an oxygen saturation above 94%. 2 Inhalation of a foreign body (i) Perform up to five back blows between the shoulder blades, using the heel of your hand with the victim leaning well forwards or lying on the side. Tip: make special considerations in near-drowning, hypothermia and acute poisoning (especially with tricyclic antidepressants). Full recovery has followed in apparently hopeless cases (fixed dilated pupils, nonshockable rhythm) with resuscitation prolonged for several hours. ✓ ACUTE UPPER AIRWAY OBSTRUCTION 14 Critical Care Emergencies ACUTE UPPER AIRWAY OBSTRUCTION (ii) Perform up to five abdominal thrusts if back blows fail (Heimlich’s manoeuvre) in adults and children over 1 year: (a) stand behind the patient, place your arms around the upper abdomen with your hands clasped between the umbilicus and xiphisternum (b) give thrusts sharply inwards and upwards to expel the obstruction. (iii) Continue alternating five back blows with five abdominal thrusts if the obstruction is still not relieved. (iv) Hold babies and infants up to 1 year head-down, and deliver up to five back blows with the heel of the free hand. (v) Perform up to five chest thrusts if this fails, using the same landmark as for cardiac compression, to dislodge foreign material in the airway. (vi) Attempt removal under direct vision if the foreign body is still present, using a laryngoscope and a pair of long-handled Magill forceps. (vii) Cricothyrotomy Perform a cricothyrotomy if the patient is in extremis, and all else has failed (see p. 469): (a) achieve rapid access by inserting a large-bore 14-gauge i.v. cannula through the cricothyroid membrane (b) alternatively, make an incision through the cricothyroid membrane with a scalpel blade, and insert a 4–6 mm endotracheal tube (or small tracheostomy tube) and connect this to an Ambu or Laerdal bag and the oxygen supply (see p. 469). 3 Epiglottitis (see p. 353) Inflammation of the epiglottis presents with sudden onset of fever, difficulty in breathing, soft inspiratory stridor, dysphagia and drooling. The child looks pale, toxic and unwell. (i) Do not examine further, i.e. no temperature, blood pressure, or X-ray. Do not attempt to visualize the throat. (ii) Leave the parent holding the child upright with an oxygen mask held near the child’s face. (iii) Call for senior ED, paediatric, anaesthetic and ENT assistance immediately. 4 Croup (see p. 352) A child with croup will have a barking cough, harsh stridor and hoarseness, and will be frightened and miserable but not systemically ill. (i) Give dexamethasone 0.15–0.3 mg/kg orally or i.m., nebulized budesonide 2 mg or prednisolone 1 mg/kg orally. (ii) Refer to the paediatric team. Critical Care Emergencies 15 SHOCKED PATIENT 5 Facial burns and or steam inhalation (see p. 250) (i) Send blood for ABGs and a carboxyhaemoglobin level. (ii) Give 100% oxygen and nebulized salbutamol 5 mg, and refer to intensive care or specialist burns unit if there is an associated respiratory burn. (iii) Be prepared to intubate if gross laryngeal oedema occurs. 6 Angioedema with laryngeal oedema (see p. 111) (i) Give high-dose oxygen and 1 in 1000 adrenaline (epinephrine) 0.3–0.5 mg (0.3–0.5 mL) i.m. into the upper outer thigh, repeated every 5–10 min as necessary. (ii) Change to adrenaline (epinephrine) 0.75–1.5 μg/kg i.v. if circulatory collapse occurs, i.e. 50–100 μg or 0.5–1.0 mL of 1 in 10 000 adrenaline (epinephrine), or 5–10 mL of 1 in 100 000 adrenaline (epinephrine) for a 70 kg patient, given slowly. (iii) Endotracheal intubation may still be required, performed by a skilled doctor with airway training, or even a cricothyrotomy. GENERAL APPROACH DIAGNOSIS 1 ‘Shock’ is defined as acute circulatory failure leading to inadequate end-organ tissue perfusion with oxygen and nutrients. It is a clinical diagnosis with a high mortality that depends on the underlying cause, its duration and response to treatment. (i) Shock progresses from an initial insult to compensated (reversible), decompensated (progressive) then finally refractory (irreversible) shock. (ii) Compensated shock Physiological mechanisms initially compensate to combat the circulatory failure. These include hyperventilation as a result of acidosis, sympathetic mediated tachycardia and vasoconstriction, and the diversion of blood from the gastrointestinal and renal tracts to the brain, heart and lungs. (iii) Decompensated shock Inadequate tissue perfusion results in increasing anaerobic glycolysis and metabolic acidosis, cellular injury with fluid and protein leakage, and deteriorating cardiac output from vascular dilatation and myocardial depression. (iv) Irreversible shock This ensues when vital organs fail and cell death occurs. Severe and progressive shock states cause multi-organ failure (MOF) or SHOCKED PATIENT 16 Critical Care Emergencies SHOCKED PATIENT end in cardiac arrest with pulseless electrical activity. Once shock deteriorates to this degree, it is difficult or impossible to reverse. 2 Aim to identify abnormal tissue perfusion early, ideally before the systolic blood pressure (SBP) drops, treat aggressively and avoid the irreversible phase. Investigation and treatment are concurrent – get senior help early. (i) A normal blood pressure does not exclude the diagnosis of shock. (ii) The absolute value of the SBP associated with poor perfusion varies greatly, but an SBP <90 mmHg is usually insufficient to maintain adequate vital organ perfusion. 3 Consider causes in four broad categories (see Fig. 1.2). Often more than one mechanism is present: Cardiogenic shock Depressed contractility Acute coronary syndrome Myocarditis Cardiomyopathy Drug toxicity Acute valvular dysfunction Arrhythmia Bradyarrhythmia Tachyarrhythmia Obstructive shock Pulmonary embolism Tension pneumothorax Traumatic Non-traumatic Cardiac tamponade Traumatic Non-traumatic Dynamic hyperinflation Hypovolaemic shock (most common) Haemorrhage Traumatic 􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀦􀁙􀁕􀁆􀁓􀁏􀁂􀁍􀀁􀀉􀁓􀁆􀁗􀁆􀁂􀁍􀁆􀁅􀀊􀀁􀀁 􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀪􀁏􀁕􀁆􀁓􀁏􀁂􀁍􀀁􀀉􀁄􀁐􀁏􀁄􀁆􀁂􀁍􀁆􀁅􀀊 􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁􀀁Non-traumatic 􀀁􀀁􀀁􀀁􀀁􀀁External (revealed) 􀀁􀀁􀀁􀀁􀀁􀀁Internal (concealed) Non-haemorrhagic External fluid loss Distributive shock Anaphylaxis Sepsis Neurogenic Drug related Acute adrenal insufficiency Figure 1.2 Different types of shock. Critical Care Emergencies 17 SHOCKED PATIENT (i) Hypovolaemic shock (‘insufficient circulatory volume’) (see p. 19): (a) haemorrhagic – traumatic or non-traumatic; external (revealed) or internal (concealed) (b) non-haemorrhagic fluid losses – external (revealed), internal (concealed). (ii) Cardiogenic shock (‘pump failure’): (a) decreased contractility – acute coronary syndrome, myocarditis, myocardial contusion, end-stage cardiomyopathy, drug toxicity, severe acidaemia (b) acute valvular dysfunction – acute valve leak (papillary muscle/chordae tendinae rupture, infective endocarditis), severe aortic stenosis (c) arrhythmia – tachycardia such as SVT, AF or VT, bradycardia including heart block. (iii) Distributive shock (‘infinite circulation, unable to be filled’): (a) sepsis (see p. 21) (b) anaphylaxis (c) neurogenic – spinal cord trauma, epidural (d) drug-related – nitrates, vasodilators (e) adrenal insufficiency – inadequate steroid replacement, Addison’s. (iv) Obstructive shock (‘obstructed circulation’): (a) pulmonary embolism – thrombotic, air, fat, amniotic fluid (b) tension pneumothorax – traumatic, non-traumatic (c) cardiac tamponade – traumatic, non-traumatic such as uraemia, pericarditis, malignancy (d) dynamic hyperinflation – over-ventilated asthma, or COPD. 4 Ask about the onset whether sudden or gradual, associated symptoms such as chest pain, abdominal or back pain, and the past medical history, drugs taken including illicit drugs, allergies, recent travel abroad, alcohol use or immunosuppression and prior cardiorespiratory status. 5 Assess for features of circulatory shock including abnormal vital signs. (i) Tachycardia occasionally bradycardia, tachypnoea, hypotension, hypothermia (or hyperthermia in sepsis), reduced oxygen saturation and a reduced conscious level (Glasgow Coma Scale [GCS] score) occur (a) check for a postural change in blood pressure, if the SBP is normal – increase in heart rate of >20 beats/min, a fall in SBP of >20 mmHg, or a fall in DBP of >10 mmHg indicates postural hypotension and suggests hypovolaemia – make certain the orthostatic readings are taken after at least 2 min sitting or standing up. 18 Critical Care Emergencies SHOCKED PATIENT (ii) Look at the skin for sweating, pallor or mottling and feel if it is cold or clammy (a) check the capillary refill time (CRT) by pressing on a nailbed (held at the level of the heart) for 5 s. Observe the time taken to refill the blanched area with blood. Over 2 s is prolonged and suggests hypoperfused or cool peripheries. 6 Estimate preload volume status to help determine the cause, and to monitor treatment effect. (i) Low preload with non-visible jugular venous pressure (JVP) occurs in hypovolaemic and distributive shock states. (ii) High preload with raised JVP occurs in cardiogenic and obstructive shock. 7 Establish venous access with two large-bore (14- or 16-gauge) cannulae into the antecubital veins and attach a cardiac monitor and pulse oximeter to the patient. 8 Send blood for full blood count (FBC), coagulation profile, electrolyte and liver function tests (ELFTs), lipase, cardiac troponin I (cTnI) or troponin T (cTnT), lactate, blood cultures from two sites and a group and save (G&S) or cross-match blood according to the suspected cause. (i) Check a venous or arterial blood gas. 9 Perform an ECG, and arrange immediate review by a senior ED doctor. (i) Look for acute changes suggesting an acute coronary syndrome, or for an arrhythmia (a) acute changes may be the cause or the effect of the shock state. (ii) A normal ECG effectively rules out cardiogenic shock. 10 Request a CXR to look for cardiomegaly, pneumothorax, consolidation, pulmonary oedema and atelectasis. 11 Insert a urethral catheter to measure the urine output, and check a urinalysis for blood, protein, nitrites and sugar. Send for microscopy and culture if positive. (i) Oliguria suggests ongoing renal hypoperfusion. (ii) Check a urinary -human chorionic gonadotrophin (hCG) pregnancy test in pre-menopausal females. 12 Organize a rapid bedside ultrasound to look for a ruptured abdominal aortic aneurysm (AAA), ectopic pregnancy, cardiac tamponade or free fluid in the peritoneal cavity. MANAGEMENT 1 Commence high-dose oxygen via a face mask. Maintain the oxygen saturation above 94%. 2 Begin immediate fluid replacement: (i) Give 20 mL/kg normal saline i.v. rapidly and repeat until JVP is 3–5 cm above sternal angle Critical Care Emergencies 19 SHOCKED PATIENT (a) omit fluids if JVP is already raised, and or the patient has pulmonary oedema (b) aim for a urine output of 0.5–1 mL/kg per h. (ii) Give cross-matched blood when it is available, if the patient is shocked due to blood loss: (a) use O-negative blood if the situation is desperate. Aim for haemoglobin 70–100 g/L, or haematocrit >30%. 3 Optimize afterload: (i) Give a vasopressor such as adrenaline if vasodilated from anaphylaxis (see p. 27) or sepsis (see p. 21). 4 Treat sepsis: (i) Give broad-spectrum antibiotics early if septic shock is suspected, after taking a minimum of two sets of blood cultures from different sites (see p. 21). 5 Admit the patient to ICU, HDU, theatre or coronary care depending on the underlying cause, and response to treatment. HYPOVOLAEMIC SHOCK DIAGNOSIS 1 This follows haemorrhage or non-haemorrhagic fluid loss that results in a reduced circulatory volume with inadequate end-organ tissue perfusion. 2 Causes of haemorrhagic shock include (see also p. 17): (i) Trauma with external bleeding: (a) arterial laceration, compound fracture, limb avulsion, massive scalping injury. (ii) Trauma with internal bleeding: (a) haemothorax, haemoperitoneum from liver, spleen or mesenteric injury, retroperitoneal from aortic, pelvic or renal injury, closed long-bone or pelvic fracture. (iii) Non-traumatic, external bleeding: (a) epistaxis, massive haemoptysis, haematemesis either fresh or coffee-grounds, rectal bleeding either melaena or fresh red, vaginal bleeding either pregnancy-related or non-pregnant, or gross haematuria. (iv) Non-traumatic, internal bleeding: (a) haemothorax, haemoperitoneum including ruptured AAA or ectopic pregnancy, retroperitoneal bleeding including ruptured AAA or spontaneous from warfarin or bleeding diathesis. 3 Causes of non-haemorrhagic shock from fluid loss include: (i) External: (a) vomiting, diarrhoea, polyuria from renal disease, diabetes insipidus or diabetes mellitus, burns, extensive skin disease including erythroderma, hyperthermia, fistulae. 20 Critical Care Emergencies SHOCKED PATIENT (ii) Internal: (a) pancreatitis ‘third spacing’, bowel obstruction. 4 Ask about external bleeding, previous episodes of bleeding, chest, abdominal or back pain, drugs taken including non-steroidal anti-inflammatory drugs (NSAIDs) or warfarin, allergies, alcohol use and travel abroad. (i) Enquire about non-specific symptoms of lethargy, breathlessness, light-headedness, syncope and altered mental status such as confusion, particularly in the elderly. 5 Check the vital signs and include a postural blood pressure if SBP is normal. 6 Look for signs of anaemia with pale skin creases and conjunctivae, and for signs of dehydration such as dry mucous membranes, reduced tissue turgor or sunken eyes. (i) Assess the JVP which should be low. 7 Examine for specific causes according to the history. Include a per rectal exam for unrecognized gastrointestinal bleeding. 8 Establish venous access with two large-bore (14- or 16-gauge) cannulae into the antecubital veins and attach a cardiac monitor and pulse oximeter to the patient. 9 Send blood for FBC, coagulation profile, ELFTs, lipase, lactate and crossmatch blood according to the suspected cause. (i) Check a venous or arterial blood gas. 10 Perform an ECG and request a CXR. 11 Insert a urethral catheter to measure the urine output. (i) Oliguria suggests ongoing renal hypoperfusion. (ii) Check a urinary -hCG pregnancy test in pre-menopausal females. 12 Organize a rapid bedside ultrasound to look for a ruptured AAA, ectopic pregnancy or free fluid in the peritoneal cavity. MANAGEMENT 1 Commence high-dose oxygen via a face mask. Maintain the oxygen saturation above 94%. 2 Compress or pack any external haemorrhage such as epistaxis (see p. 402) or wound bleeding (see p. 220). 3 Begin immediate fluid replacement: (i) Give 20 mL/kg normal saline i.v. rapidly and repeat, aiming for a urine output of 0.5–1 mL/kg per h (a) then gradually correct any dehydration (rehydration), and include daily maintenance amounts. (ii) Give cross-matched blood when it is available, if the patient is shocked due to blood loss Critical Care Emergencies 21 SHOCKED PATIENT (a) remember that in healthy adults the only signs associated with loss of up to 30% of the circulatory blood volume (i.e. 1500 mL) may be a tachycardia and a narrowed pulse pressure (b) thus, a consistent fall in SBP indicates that at least 30% of the blood volume has already been lost (c) full cross-match takes 45 min, a type-specific cross-match takes 10 min, and O rhesus-negative blood is available immediately (d) use a blood warmer and macropore blood filter for multiple transfusions – give fresh frozen plasma 8–10 units and platelets after transfusing 8–10 units of blood or more, i.e. in a 1:1 ratio for a ‘massive blood transfusion’ (e) aim for haemoglobin 70–100 g/L, or haematocrit >30%. 4 Consult the surgical, vascular or gynaecological team immediately if there is suspected blood loss causing shock (e.g. ruptured spleen, AAA or ectopic pregnancy). 5 Admit the patient to theatre, intensive care unit (ICU) or a high-dependency unit (HDU) depending on the underlying cause, and response to treatment. SEPTIC SHOCK DIAGNOSIS 1 Sepsis is a heterogeneous clinical entity defined by physiological changes known as the systemic inflammatory response syndrome (SIRS) in response to a presumed infectious aetiology, which is most usually bacterial, or fungal, viral or parasitic. (i) More than 85% of the causes originate from the chest, abdominal or genitourinary systems, skin and vascular access. (ii) Worldwide sepsis is one of the most common reasons for admission to an ICU, and up to 20–50% of patients with sepsis die. 2 Definitions used in sepsis include: (i) SIRS Two or more of: (a) temperature >38°C or < 36°C (b) tachycardia with heart rate >90/min (c) respiratory rate >20/min or PaCO2 <32 mmHg (<4.3 kPa) (d) WBC >12  109/L, <4  109/L or >10% immature neutrophils (band forms). (ii) Sepsis When SIRS is the result of a confirmed infectious process. 22 Critical Care Emergencies SHOCKED PATIENT (iii) Severe sepsis Sepsis plus either organ dysfunction, or with evidence of hypotension or hypoperfusion (e.g. confusion, oliguria, raised lactate). (iv) Septic shock Subset of severe sepsis with sepsis-induced hypotension (SBP <90 mmHg), or hypoperfusion abnormality such as lactate ≥4 mmol/L persisting despite adequate fluid resuscitation (20–30 mL/kg). 3 Initial symptoms are non-specific and include malaise, fever or rigors, myalgia, nausea or vomiting and lethargy. (i) Ask specifically about focal features such as headache, neck pain, sore throat, ear ache, cough, breathlessness, abdominal pain, frequency, dysuria, joint or skin changes. (ii) Enquire about previous illnesses, use of antibiotics, allergies, immunosuppression including diabetes, chemotherapy, steroids or HIV, alcohol use or travel abroad. 4 Assess for features of circulatory shock including abnormal vital signs. (i) Early signs are non-specific such as tachypnoea, tachycardia, temperature change (high or low), and altered mental status. (ii) Some patients will be hot and flushed with a bounding pulse, but many others are normo- or hypothermic with a tachypnoea and metabolic acidosis. 5 Examine for potential source areas such as the ears, throat, chest, heart, abdomen, limbs and skin including between the toes (tinea), skin folds (intertrigo), perineum and axillae (abscess). (i) Look for a rash, particularly petechial. 6 Establish venous access with two large-bore (14- or 16-gauge) cannulae into the antecubital veins and attach a cardiac monitor and pulse oximeter to the patient. 7 Send blood for FBC, coagulation profile, ELFTs, CRP, lactate and two sets of blood cultures from different sites. (i) Check a venous or arterial blood gas. (ii) Swab any infected areas. 8 Perform an ECG and request a CXR. 9 Insert a urethral catheter to measure the urine output, and check a urinalysis for blood, protein, nitrites and sugar. Send for microscopy and culture if positive. (i) Oliguria suggests ongoing renal hypoperfusion. (ii) Check a urinary -hCG pregnancy test in pre-menopausal females. 10 Arrange an ultrasound, CT scan and/or lumbar puncture (LP) according to the suspected source of infection, but these should never delay antibiotic therapy. Critical Care Emergencies 23 SHOCKED PATIENT MANAGEMENT 1 Commence high-dose oxygen via a face mask. Maintain the oxygen saturation above 94%. 2 Begin aggressive fluid replacement: (i) Give 20 mL/kg normal saline i.v. rapidly over the first 30 min and then reassess. Multiple boluses may be required (a) intravascular fluid resuscitation often requires large volumes up to 50–100 mL/kg before volume replacement is adequate (b) ensure haemoglobin is maintained above 100 g/L. 3 Administer appropriate antibiotics early. Mortality is reduced if antibiotics are given within 1 h of onset of hypotension. Each additional hour of delay adds 7% to the mortality in septic shock. Get senior advice early and consult local antibiotic guidelines: (i) Give flucloxacillin 2 g i.v. q.d.s. plus gentamicin 5 mg/kg once daily if no source is apparent in the immunocompetent patient. (ii) Add vancomycin 1.5 g i.v. 12-hourly for possible MRSA including community-associated (CA-MRSA), suspected line sepsis and instead of flucloxacillin for immediate hypersensitivity. (iii) Give neutropenic patients piperacillin 4 g with tazobactam 0.5 g i.v. 8-hourly, plus gentamicin 5 mg/kg stat when no source is apparent, and add vancomycin 1.5 g i.v. 12-hourly for possible line sepsis. (iv) Otherwise give antibiotics to cover likely pathogens depending on a known focus, and/or once culture and sensitivities are known. 4 Start vasopressor support for continuing hypotension despite fluid resuscitation. (i) Give noradrenaline or adrenaline i.v. by infusion to maintain mean arterial pressure (MAP) >65 mmHg (see p. 35 for dose and dilution). (ii) Inotropic support with dobutamine i.v. by infusion may also be required, as myocardial depression is common in severe sepsis (see p. 35 for dose and dilution). (iii) Give hydrocortisone 50 mg i.v. q.d.s. if poorly responsive to fluid and vasopressor therapy. 5 Refer the patient urgently to the surgical team if a local cause requires source control or drainage such as wound debridement, laparotomy for perforation, percutaneous drainage for urinary obstruction, etc. Contact theatre and the anaesthetist. 6 Meanwhile arrange admission to ICU for all patients. 24 Critical Care Emergencies UNCONSCIOUS PATIENT The aim is to resuscitate the patient and treat urgent precipitating conditions while a picture of the situation is built up. The definitive diagnosis may not be made in the ED. MANAGEMENT 1 Manage the patient in a monitored resuscitation area, and call the senior ED doctor immediately. (i) Clear obstructing material using a tongue depressor or laryngoscope blade if the patient is unconscious with a noisy airway, and remove broken dentures, vomit or blood with a Yankauer sucker. (ii) Improve airway opening using a head tilt, chin lift and or jaw thrust (a) open the airway with the jaw thrust alone in trauma cases, avoiding any movement of the neck. (iii) Insert an oropharyngeal airway and give high-dose oxygen via a face mask. Attach a cardiac monitor and pulse oximeter to the patient and aim for an oxygen saturation above 94%. 2 Commence cardiopulmonary resuscitation if no pulse is felt (see p. 2). 3 An airway-skilled doctor should now insert an endotracheal tube if there is a reduced or absent gag reflex and an unprotected airway, using a rapid sequence induction technique (see p. 467). 4 Otherwise: (i) Apply a semi-rigid collar if there is any suggestion of face, head or neck trauma, before moving the patient. Tip: beware patients who are neutropenic from chemotherapy, malnourished, elderly, diabetic, have HIV or are otherwise immunosuppressed, as they have few signs of sepsis. Fever may be minimal, focal features few, and only a non-specific inflammatory response is found in the laboratory tests. Immediate blood cultures and empirical antibiotics are essential. ✓ UNCONSCIOUS PATIENT Warning: never attempt rapid sequence induction (RSI) unless you have been trained. Use a bag-valve mask technique instead, while waiting for help. ! Critical Care Emergencies 25 UNCONSCIOUS PATIENT (ii) Remove all the clothing, but keep the patient covered and avoid heat loss. 5 Insert an i.v. cannula and take blood for FBC, coagulation profile, blood sugar, ELFTs, blood culture and drug screen for salicylate and paracetamol if not already done. (i) Perform ABGs, recording the amount of oxygen being delivered (FiO2). (ii) Give 50% dextrose 50 mL i.v. if the blood glucose test strip is low (a) remember dextrose i.v. can precipitate Wernicke’s encephalopathy in alcoholic or malnourished patients, who require thiamine 100 mg i.v. immediately. 6 Record the temperature (if 35°C, repeat with a low-reading thermometer to exclude hypothermia), pulse, blood pressure, and the pupil size and reaction. (i) Consider naloxone 0.4–2 mg i.v. slowly if there are pinpoint pupils with hypoventilation to reverse narcotic poisoning, but beware of precipitating an acute withdrawal reaction. 7 Consider other critical conditions requiring immediate action: (i) Tension pneumothorax (a) this usually follows trauma, especially if positive-pressure ventilation is being given (b) insert a large-bore cannula or intercostal drain without waiting for an X-ray (see p. 471). (ii) Cardiac arrhythmia (a) treat as necessary after recording a formal 12-lead ECG (see p. 60). (iii) Exsanguination (a) bleeding may be external and obvious, or internal and concealed from the gastrointestinal tract, a ruptured AAA or ectopic pregnancy (b) cross-match blood, give i.v. fluids, arrange an ultrasound and refer the patient for an urgent surgical opinion. (iv) Anaphylaxis (a) this may follow drug therapy, food ingestion, or an insect sting (b) give 1 in 1000 adrenaline (epinephrine) 0.3–0.5 mg (0.3–0.5 mL) i.m. repeated as necessary every 5–10 min (c) give 1 in 10 000 or 1 in 100 000 adrenaline (epinephrine) 0.75–1.5 μg/kg i.v. if there is circulatory collapse, i.e. 50–100 μg or 0.5–1.0 mL of 1 in 10 000, 5–10 mL of 1 in 100 000 adrenaline (epinephrine), slowly i.v. for a 70 kg patient (see p. 27). (v) Extradural haemorrhage (a) this may follow even trivial trauma; look for a local bruise on the scalp, for instance in the temporoparietal area over the middle meningeal artery territory 26 Critical Care Emergencies UNCONSCIOUS PATIENT (b) watch out for deterioration in the level of consciousness, ultimately with the development of Cheyne–Stokes breathing and a unilateral fixed, dilated pupil (c) call an airway-skilled doctor to pass a cuffed endotracheal tube if one is not already in place (d) arrange an urgent head CT scan, and refer the patient immediately to the neurosurgical team, before critical mass lesion signs develop. DIAGNOSIS 1 The patient’s cardiorespiratory status should have been stabilized by this stage, bloods sent, a blood sugar level checked, an in-dwelling catheter and a nasogastric tube placed, and an ECG and CXR performed. 2 Now focus on the underlying cause. The most common causes of an unconscious patient are: (i) Poisoning (accidental or deliberate, including alcohol, carbon monoxide). (ii) Hypoglycaemia. (iii) Post-ictal state. (iv) Stroke. (v) Head injury. (vi) Subarachnoid haemorrhage. (vii) Respiratory failure. (viii) Hypotension (shock – see p. 15). 3 Less common causes of an unconscious patient are: (i) Meningitis or encephalitis. (ii) Hepatic or renal failure. (iii) Septicaemia. (iv) Subdural haematoma. (v) Hyperglycaemia (diabetic ketoacidosis [DKA] or hyperglycaemic, hyperosmolar non-ketotic syndrome [HHNS]). (vi) Hypothermia or hyperthermia. 4 Rare causes of an unconscious patient are: (i) Cerebral space-occupying lesion. (ii) Hyponatraemia or hypercalcaemia. (iii) Myxoedema. (iv) Addison’s disease. (v) Hypertensive encephalopathy. 5 Finally, in those who have recently been abroad, consider: (i) Cerebral malaria. (ii) Typhus, yellow fever, trypanosomiasis and typhoid. (iii) Rabies, viral haemorrhagic fever. (iv) Severe acute respiratory syndrome (SARS) or avian influenza (bird flu). Critical Care Emergencies 27 ANAPHYLAXIS 6 These four lists may seem daunting, but aim to build up a picture of the events as follows. History: (i) Any clues from relatives, passers-by or ambulance crew? (ii) Witnessed fit, trauma, alcohol or drug ingestion? (iii) Prior medical or surgical conditions? (iv) Known drug therapy or abuse? (v) Recent travel abroad? 7 Further examination: (i) Search the clothing for a diabetic card, steroid card or outpatient card. (ii) Look particularly for signs of trauma, needle puncture marks, or petechiae on the skin. (iii) Repeat the vital signs, including the temperature. (iv) Reassess the neurological state, including the level of consciousness using the GCS score (see Table 1.1, p. 30), the pupil responses, eye movements and fundi. Assess the muscle power, tone and reflexes including the plantar responses. Exclude any neck stiffness. (v) Examine the front of the chest, feel the abdomen and examine the back, inspect the perineum and perform a rectal examination. 8 Arrange: (i) CXR and pelvic X-ray in trauma (see p. 221). (ii) Head computed tomography (CT) scan with cervical spine if intracranial pathology is suspected or cannot be excluded, which is frequently the case. 9 Refer the patient to the medical (or surgical) team, or ICU if they are not already involved, having stabilized the cardiorespiratory status, treated any urgent conditions and built up a list of the likely causes of unconsciousness. DIAGNOSIS 1 IgE-mediated allergic anaphylaxis is an immunological, multi-system reaction that may rapidly follow drug ingestion, particularly parenteral penicillin, a bee or wasp sting, or food such as nuts and seafood. (i) Non-IgE-mediated, non-allergic anaphylaxis (previously termed an anaphylactoid reaction) is a clinically identical reaction most commonly seen following radio-contrast media or aspirin or NSAID exposure, but which is not triggered by IgE antibodies. ANAPHYLAXIS 28 Critical Care Emergencies ANAPHYLAXIS 2 Respiratory manifestations: (i) Dyspnoea, laryngeal oedema, hoarseness and stridor. (ii) Cough, wheeze (bronchospasm), cyanosis. (iii) Rhinitis and conjunctivitis. 3 Cardiovascular manifestations: (i) Tachycardia, occasionally bradycardia. (ii) Hypotension, with massive vasodilation. (iii) Light-headedness, confusion, collapse with loss of consciousness. 4 Other manifestations: (i) Gastrointestinal: (a) odynophagia (difficult or painful swallowing) (b) abdominal cramps or pain (c) vomiting and diarrhoea. (ii) Cutaneous: (a) erythema (b) local or widespread urticaria (c) pruritus (d) angioedema. (iii) Miscellaneous: (a) premonitory aura, anxiety, feeling of impending doom (b) back pain, pelvic cramps. 5 Attach a cardiac monitor and pulse oximeter to the patient. MANAGEMENT 1 Give high-dose oxygen via a face mask aiming for an oxygen saturation above 94%, and place the patient supine or elevate the legs. Stop the delivery of potential causative agent and call for help. 2 Laryngeal oedema and wheeze (i) Give 1 in 1000 adrenaline (epinephrine) 0.3–0.5 mg (0.3–0.5 mL) i.m. immediately into the upper outer thigh. (ii) If rapid deterioration occurs, change to 1 in 10 000 or 1 in 100 000 adrenaline (epinephrine) 0.75–1.5 μg/kg i.v.; i.e. 50–100 μg or 0.5–1.0 mL of 1 in 10 000, or 5–10 mL of 1 in 100 000 adrenaline (epinephrine) over 5 min i.v. The ECG must be monitored. (iii) Give 1 in 1000 adrenaline (epinephrine) 2–4 mg (2–4 mL) nebulized in oxygen while preparing the i.v. adrenaline (epinephrine). (iv) Give hydrocortisone 200 mg i.v. particularly for bronchospasm. 3 Shock and circulatory collapse (i) Give 1 in 1000 adrenaline (epinephrine) 0.3–0.5 mg (0.3–0.5 mL) i.m. immediately into the upper outer thigh, repeated every 5–10 min until improvement occurs. Critical Care Emergencies 29 SEVERE HEAD INJURY (ii) Lie the patient flat and or elevate the legs. (iii) Give a bolus of normal saline 20–40 mL/kg i.v. (iv) If rapid deterioration occurs, change to 1 in 10 000 or 1 in 100 000 adrenaline (epinephrine) 0.75–1.5 μg/kg i.v.; i.e. 50–100 μg or 0.5–1.0 mL of 1 in 10 000, or 5–10 mL of 1 in 100 000 adrenaline (epinephrine) over 5 min i.v. The ECG must be monitored. 4 Second-line measures only used after achieving cardiorespiratory stability include: (i) Promethazine 12.5–25 mg i.v. or chlorphenamine 10–20 mg slowly i.v. plus ranitidine 50 mg i.v. (ii) Hydrocortisone 200 mg i.v. (if not given already). (iii) Glucagon 1–2 mg i.v. repeated as necessary, for patients on -blockers resistant to the above treatment. 5 Admit any patient receiving adrenaline (epinephrine) for 6–8 h observation as late deterioration may occur in up to 5%, known as biphasic anaphylaxis. 6 Then discharge home on prednisolone 50 mg once daily, loratadine 10 mg once daily plus ranitidine 150 mg b.d., all orally for 3 days. (i) Inform the GP by fax or letter. (ii) Refer all significant or recurrent attacks to the allergy clinic, especially if the cause is unavoidable or unknown. DIAGNOSIS 1 The head injury may be obvious from the history or on immediate examination. 2 The possibility of a head injury must also be considered in every instance of coma or abnormal behaviour, in at-risk groups such as alcohol intoxication and epileptics, non-accidental injury in children, and in falls in the elderly. 3 Confirm a history from the ambulance crew, police or any witnesses as to the circumstances and nature of the injury, period of loss of consciousness or subsequent seizures. 4 Obtain other medical details, if a relative or friend is available, of current medical or surgical conditions, drug therapy, allergies and any previous head injury or epilepsy. 5 Check the temperature, pulse, blood pressure, respiratory rate, and attach an ECG monitor and pulse oximeter to the patient. Record the level of consciousness using the GCS score (Table 1.1). SEVERE HEAD INJURY 30 Critical Care Emergencies SEVERE HEAD INJURY Table 1.1 The Glasgow Coma Scale (GCS) score Score Eye opening Spontaneously 4 To speech 3 To pain 2 None 1 Verbal response Oriented 5 Confused 4 Inappropriate 3 Incomprehensible 2 None 1 Motor response Obeys commands 6 Localizes pain 5 Withdraws (pain) 4 Flexion (pain) 3 Extension (pain) 2 None 1 (i) A patient in coma has a score of 8 or less. (ii) A decrease in score of 2 or more points indicates a significant deterioration. (iii) Repeat neurological examinations, including the GCS, are essential for detecting and managing secondary brain damage. 6 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, coagulation profile, blood sugar, and G&S, and save serum for a drug screen in case alcohol or drug intoxication is subsequently suspected. 7 Send ABGs, recording the percentage of inspired oxygen administered at the time the sample was drawn. 8 Perform a neurological examination, including: (i) Conscious level: regularly record the GCS and look for any deterioration (decrease in score). (ii) Pupil size and reactions: look in particular for an unequal or dilating pupil, indicating a focal mass lesion and or rising intracranial pressure. The maximum score is 15. Any reduction in score indicates deterioration in the level of consciousness. Critical Care Emergencies 31 SEVERE HEAD INJURY (iii) Eye movements and fundoscopy: (a) intact eye movements are one indicator of brainstem function (b) fundoscopy may reveal papilloedema, subhyaloid haemorrhage or retinal detachment. (iv) Other cranial nerves: include examination of the corneal reflex, facial movements and the cough and gag reflexes. (v) Limb movements: (a) assess for abnormal tone, weakness or loss of movement, or an asymmetrical response to pain if the patient is unconscious (b) check the limb reflexes, including the plantar responses. 9 Examine the scalp for bruising, lacerations and haematomas, and palpate for a deformity indicating a depressed skull fracture. 10 Examine the face and mouth for signs of facial fracture or basal skull fracture. A basal skull fracture is indicated by: (i) Periorbital and subconjunctival haemorrhage. (ii) Haemotympanum, external bleeding, or cerebrospinal fluid (CSF) leak from the ear. (iii) Haemorrhage or CSF leakage from the nose. (iv) Nasopharyngeal haemorrhage, which may be profuse. (v) Mastoid bruising (Battle’s sign), which may not appear for many hours. 11 Perform a head-to-toe assessment for other injuries to the neck, chest, abdomen and perineum including a rectal examination (loss of anal tone may indicate spinal cord damage), back and limbs. 12 Request radiological examinations: (i) CXR and pelvic X-ray in all multiply injured patients. (ii) CT head scan with cervical spine scan. The airway must be protected first, before a head CT is performed. Indications for CT head scan include: (a) GCS <13 at any point since injury (b) GCS 14 or less 2 h post injury (c) focal neurological signs including hemiparesis, diplopia (d) neurological deterioration, i.e. 2 points or more on the GCS (e) post-traumatic seizure (f) coagulopathy (history of bleeding, clotting disorder, or patient on warfarin) (g) fracture known or suspected, including base of skull (h) penetrating injury, known or suspected. (iii) Skull X-rays are of no additional value in the early management of a major head injury, when there is ready access to CT scanning (a) only consider if CT scanning is not available. They may demonstrate a radio-opaque foreign body or depressed skull fracture, but cannot exclude serious injury if normal. 32 Critical Care Emergencies SEVERE HEAD INJURY MANAGEMENT 1 Clear the airway by sucking out any secretions, remove loose or broken dentures, and insert an oropharyngeal airway. Give 100% oxygen by tightfitting mask with reservoir bag. Aim for an oxygen saturation above 94%. 2 Immobilize the cervical spine by applying a semi-rigid collar, as up to 10% of patients with blunt head trauma have a concomitant neck injury. Use sandbags in addition on either side of the head taped to the forehead, unless the patient is excessively restless. 3 The patient must be intubated to protect and maintain the airway, prevent aspiration and guarantee oxygenation and ventilation, if the gag reflex is reduced or absent. Take great care to minimize neck movements by an assistant providing in-line manual immobilization of the neck throughout. (i) Call the senior ED doctor immediately. (ii) Prepare for an RSI intubation (see p. 467). 4 Regularly repeat the temperature, pulse, blood pressure and respiratory rate. 5 Consider whether a tension pneumothorax (see p. 231), open pneumothorax (see p. 220), massive haemothorax (see p. 231) or flail chest (see p. 232) is responsible if the respiratory rate is rapid or ineffective. 6 Commence i.v. fluid to maintain normotension. Use a crystalloid such as normal saline or Hartmann’s. (i) Aim for a MAP of >90 mmHg, to ensure adequate cerebral perfusion pressure. (ii) Avoid excessive fluid administration if the patient is normotensive, as this may contribute to cerebral oedema. 7 Search for associated injuries including chest, abdominal or pelvic bleeding, long-bone fracture and cardiac tamponade if the patient is hypotensive. Note shock is rarely due to an isolated head injury: (i) Occasionally, brisk scalp bleeding alone is found to be responsible, usually in children. (ii) Alternatively, a cervical or high thoracic spinal cord injury with loss of sympathetic vascular tone may be the cause. 8 Treat the following complications immediately, as they worsen the existing primary cerebral injury and may lead to secondary brain damage. (i) Hypoglycaemia (a) perform a bedside glucose test; if it is low, send a formal blood glucose to the laboratory and give 50% dextrose 50 mL i.v. (b) remember this especially if the patient has been drinking alcohol. Critical Care Emergencies 33 SEVERE HEAD INJURY (ii) Hypoxia (a) PaO2 <70 mmHg (9 kPa) breathing air or 100 mmHg (13 kPa) on supplemental oxygen and hypercarbia with PaCO2 over 45 mmHg (6 kPa) in the spontaneously breathing patient requires active intervention (b) call for urgent senior ED doctor help and prepare for endotracheal intubation using an RSI technique (see p. 467) to protect the airway, if not already performed. (iii) Seizures (a) give midazolam 0.05–0.1 mg/kg up to 10 mg i.v., diazepam 0.1–0.2 mg/kg up to 20 mg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. (b) follow with phenytoin 15–18 mg/kg i.v. (see p. 92). (iv) Pinpoint pupils (a) give naloxone 0.8–2 mg i.v. (b) no response may indicate pontine or cerebellar damage. (v) Restless or aggressive behaviour Check if any of the following are present: (a) hypoxia: make sure the airway is still patent and high-flow oxygen is being delivered (b) hypotension: repeat the blood pressure (c) pain: catheterize the bladder, splint fractures and exclude a constricting bandage or tight cast. (vi) Gastric distension (a) pass a large-bore nasogastric tube (b) use an orogastric tube if a basal skull or mid-face fracture is present. 9 Look out for signs of increasing intracranial pressure and uncal transtentorial herniation (‘coning’), e.g. a deteriorating level of consciousness, bradycardia, hypertension and focal neurological signs, e.g. a dilated pupil: (i) Call for a skilled doctor to perform an RSI intubation, if an endotracheal tube is not already positioned. (ii) Mildly hyperventilate the patient to maintain PaCO2 at 30–35 mmHg (4.0–4.7 kPa). (iii) Give 20% mannitol 0.5–1 g/kg (2.5–5 mL/kg) as an osmotic diuretic, provided adequate circulatory volume resuscitation has occurred. (iv) Arrange immediate neurosurgical intervention. 10 Give flucloxacillin 1 g i.v. or cefuroxime 1.5 g i.v. if a penetrating or compound skull fracture or intracranial air is found, and tetanus prophylaxis. 34 Critical Care Emergencies CRITICAL-CARE AREAS DRUG INFUSION GUIDELINES 11 Criteria for neurosurgical consultation: Refer all the following patients to the neurosurgery team: (i) Coma continues after resuscitation (GCS <9). (ii) Deterioration in neurological status, e.g. worsening in conscious state (2 points or more decrease in GCS), seizures, increasing headache, focal neurological signs. (iii) Skull fracture: (a) compound depressed fracture (b) basal skull fracture (see p. 397) (c) any skull fracture with confusion, decreased level of consciousness or focal neurological signs. (iv) Penetrating head injury. (v) Confusion or other neurological disturbance (GCS 9–13) for more than 2 h with no defined skull fracture. (vi) Radiological abnormality on CT head scan. 12 Stabilize the patient’s condition first and make sure any associated injuries have been dealt with before transferring the patient, if transfer is necessary. (i) The transport team must be trained and suitably experienced and carry appropriate monitoring equipment (see p. 456). 13 Refer all other patients for admission under the care of the surgical team. These infusion guidelines were developed for use in critical care areas only. Most require close monitoring with titration to response, and are thus inappropriate for general ward areas. All calculations assume an adult weight of 70–80 kg. Paediatric resuscitation drug doses are available in Figure 11.1 (p. 338) and Table 11.4 (p. 345) in Section XI, Paediatric Emergencies. Other paediatric doses are available in any paediatric formulary. Readers are strongly advised to re-check all doses with another medical person before commencing therapy. CRITICAL-CARE AREAS DRUG INFUSION GUIDELINES Critical Care Emergencies 35 Drug Loading dose Paediatric infusion Dilution Adult dose (70–80 kg) range (< 30 kg) Infusion pump (IP) Syringe driver Concentration Dose per hour Volume per hour Adrenaline According to condition 0.05–1.0 μg/kg/min 6 mg in 3 mg in 60 μg/mL 2–20 μg/min 2–20 mL/h (epinephrine) 1–100 μg/kg 100 mL DS 50 mL DS Aminophylline 5.0 mg/kg in 100 mL 0.5–0.9 mg/kg/h 1000 mg in — 2 mg/mL 0.5–0.9 mg/kg/h 17.5–30 mL/h bStandard DS over 20 min by IP 500 mL DS aTransport 5.0 mg/kg in 100 mL 0.5–0.9 mg/kg/h 500 mg in 250 mg in 5 mg/mL 0.5–0.9 mg/kg/h 7–13 mL/h DS over 20 min by IP 100 mL DS 50 mL DS Amiodarone 2–5 mg/kg in 100 mL 5–15 μg/kg/min 600 mg in 500 mL — 1.2 mg/mL 20–60 mg/h 17–52 mL/h bStandard DW over 30 min by IP DW glass bottle. (max. 15 mg/kg/24h) Discard at 12 h aTransport 2–5 mg/kg in 100 mL 5–15 μg/kg/min 300 mg in 100 mL 150 mg in 3 mg/mL 20–60 mg/h 7.5–22 mL/h DW over 30 min by IP DW 50 mL DW (max. 15 mg/kg/24h) Clonazepam 1.0–2.0 mg 5–10 μg/kg/h 10 mg in 5 mg in 0.1 mg/mL 0.35–0.7 mg/h 3.5–7.0 mL/h 100 mL DS 50 mL DS Dobutamine — 2–30 μg/kg/min 250 mg in 125 mg in 2.5 mg/mL 2–30 μg/kg/min 2–30 mL/h 100 mL DS 50 mL DS Dopamine — Renal: 200 mg in 100 mg in 2 mg/mL Renal: Renal: 0.5–2.5 μg/kg/min 100 mL DS 50 mL DS 0.5–2.5 μg/kg/min 1–5 mL/h Inotrope: Inotrope: Inotrope: 5–20 μg/kg/min 5–20 μg/kg/min 10–40 mL/h Fentanyl 1–5 μg/kg 1–10 μg/kg/h 1000 μg in 500 μg in 10 μg/mL 50–200 μg/h 5–20 mL/h 100 mL DS 50 mL DS a, b See key, page 40. Abbreviations see key, page 40. 36 Critical Care Emergencies Drug Loading dose Paediatric infusion Dilution Adult dose (70–80 kg) range (< 30 kg) Infusion pump (IP) Syringe driver Concentration Dose per hour Volume per hour Glyceryl — 1–10 μg/kg/min 200 mg in — 400 μg/mL 0.4–8 mg/h 1–20 mL/h trinitrate (GTN) 500 mL DW. bStandard Use glass bottle/ low-absorption set aTransport — 1–10 μg/kg/min 50 mg in 25 mg in 500 μg/mL 0.5–10 mg/h 1–20 mL/h 100 mL DW 50 mL DW Insulin 2–20 units 0.03–0.3 units/kg/h 100 units in 50 units in 1 unit/mL 2–20 units/h 2–20 mL/h (short-acting) 100 mL NS 50 mL NS Isoprenaline Low dose 50–100 μg increments 0.5–7.5 μg/min 1 mg in 0.5 mg in 10 μg/mL 0.5–7.5 μg/min 2–30 mL/h 100 mL DS 50 mL DS High dose — 0.05–1.0 μg/kg/min 6 mg in 3 mg in 60 μg/mL 2–20 μg/min 2–20 mL/h 100 mL DS 50 mL DS Ketamine IV: 1–2 mg/kg 5–20 μg/kg/min 1000 mg in 500 mg in 10 mg/mL 0.3–1.2 mg/kg/h 2–10 mL/h IM: 5–10 mg/kg 100 mL DS 50 mL DS Lignocaine (lidocaine) bStandard 1–2 mg/kg 15–50 μg/kg/min Pre-mixed: Pre-mixed: 4 mg/mL ***8 mg/min ***120 mL/h 2 g in 500 mL DW 2 g in ***4 mg/min ***for 20 min 500 mL DW ***2 mg/min ***60 mL/h for ***60 min ***30 mL/h for ***24 h aTransport 1–2 mg/kg 15–50 μg/kg/min 2 g in 100 mL DW 1 g in 20 mg/mL ***8 mg/min ***24 mL/h Critical Care Emergencies 37 50 mL DW ***4 mg/min ***for 20 min ***2 mg/min ***12 mL/h ***for 60 min ***6 mL/h for ***24 h Magnesium 0.15–0.3 mmol/kg = 0.05–0.1 mmol/kg/h 40 mmol in 20 mmol in 0.4 mmol/mL 2–8 mmol/h 5–20 mL/h sulphate 10–20 mmol (adult) 100 mL DS 50 mL DS or 0.1 g/mL 0.5–2.0 g/h 49.3% solution in Dilute in 50 mL DS 5 mL = 10 mmol Infuse: 2 min (VT) to = 2.47 g 20 min (pre-eclampsia) Methyl 30 mg/kg over 5.4 mg/kg/h 4 g in 100 mL. 2 g in 50 mL. 40 mg/mL 5.4 mg/kg/h for 23 h 10 mL/h (70 kg) prednisolone 30 min by IP Reconstitute in Reconstitute in Spinal injury water BP water BP Dilute in DS Dilute in DS Midazolam 0.05–0.1 mg/kg in 10–100 μg/kg/h 50 mg in 25 mg in 0.5 mg/mL 2.5–10 mg/h 5–20 mL/h 1–2.5 mg increments 100 mL DS 50 mL DS Morphine 2.5–15 mg in 10–50 μg/kg/h 100 mg in 50 mg in 1 mg/mL 2–10 mg/h 2–10 mL/h 2.5 mg increments 100 mL DS 50 mL DS Naloxone 0.4–2.0 mg 10 μg/kg/h 4 mg in 2 mg in 40 μg/mL 0.5–1.0 mg/h 12.5–25 mL/h (max. 10 mg) 100 mL DS 50 mL DS Nimodipine — 6–30 μg/kg/h 10 mg in 10 mg in 0.2 mg/mL 0.4–2.0 mg/h. Start 2 mL/h 50 mL 50 mL Titrate to maintain Increase 2 mL/h dispensed dispensed MAP every hour to max. of 10 mL/h Noradrenaline — 0.05–1.0 μg/kg/min 6 mg in 3 mg in 60 μg/mL 2–20 μg/min 2–20 mL/h (norepinephrine) 100 mL DS 50 mL DS a, b See key, page 40. Abbreviations see key, page 40. 38 Critical Care Emergencies Drug Loading dose Paediatric infusion Dilution Adult dose (70–80 kg) range (< 30 kg) Infusion pump (IP) Syringe driver Concentration Dose per hour Volume per hour Octreotide 50–200 μg 3–5 μg/kg/h 1000 μg in 500 μg in 10 μg/mL 25–100 μg/h 2.5–10 mL/h 100 mL DS 50 mL DS Phenobarbitone 15–25 mg/kg in — — — — — — (phenobarbital) 100 mL DS over 20–30 min (max. 50 mg/min) by IP Phenytoin 15–18 mg/kg in — — — — — — 100 mL NS over 20–30 min (max. 50 mg/min) by IP Procainamide 10 mg/kg (max. 20–80 μg/kg/min 1000 mg in 500 mg in 10 mg/mL 2–6 mg/min 12–36 mL/h 1000 mg) in 100 mL DW 50 mg DW 100 mL DW over 30 min by IP Propofol Sedation: 1–10 mg/kg/h — 500 mg in 50 mL 10 mg/mL Sedation Sedation 0.5–1.0 mg/kg (dispensed as 1–2 mg/kg/h 7–15 mL/h Induction: 20-mL and Anaesthesia Anaesthesia 2–3 mg/kg 50-mL amps, 5–10 mg/kg/h 35–70 mL/h both with 10 mg/mL) Critical Care Emergencies 39 rt-PA (alteplase) 15-mg bolus (15 ml) — 100 mg in — 1 mg/ml (a) 15-mg bolus 100 ml water BP (b) 0.75 mg/kg (max 50 mg) over 30 min (c) 0.5 mg/kg (max 35 mg) over 60 min r-PA (reteplase) 10-U bolus in — — 2 vials/prefilled 2 min. After 30 min, syringes/ second 10-U reconstitution bolus in 2 min devices and needles Salbutamol 5–10 μg/kg in 100 ml 1.0–5.0 μg/kg/min 6 mg in 3 mg in 60 μg/ml 5–50 μg/min 5–50 ml/h (asthma) DS over 10 min 100 ml DS 50 ml DS Salbutamol 5–10 μg/kg in 100 ml 0.2–1.0 μg/kg/min 6 mg in 3 mg in 60 μg/ml 10–50 μg/min 10–50 ml/h (obstetric) DS over 10 min 100 ml DS 50 ml DS Sodium — 0.05–10 μg/kg/min 100 mg in 500 mL — Min 200 0.05–10 μg/kg/min 1–210 mL/h nitroprusside DW in glass bottle μg/mL (max. 1.5 mg/kg/24h) 500 mL/24h Protect from light Max 800 Discard at 24 h μg/min Streptokinase 1.5 million units in — — — 15 000 2.5 mL/min 150 mL/h AMI 100 mL NS over units/mL 45 min by IP PE, DVT, etc. 250 000 units in 1500–2000 500 000 units in — 5000 units/mL 100 000 units/h 20 mL/h 100 mL NS over units/kg/h 100 mL NS 30 min by IP a, b See key, page 40. Abbreviations see key, page 40. 40 Critical Care Emergencies Drug Loading dose Paediatric infusion Dilution Adult dose (70–80 kg) range (< 30 kg) Infusion pump (IP) Syringe driver Concentration Dose per hour Volume per hour Thiopentone 3–6 mg/kg 1–5 mg/kg/h 2500 mg in 1250 mg in 25 mg/mL 75–350 mg/h 3–15 mL/h (thiopental) (0.5 mg/kg in shock) 100 mL water BP 50 mL water Protect from light BP Protect from light Vecuronium 0.1 mg/kg 0.05–0.1 mg/kg/h 100 mg in 100 mL. 50 mg in 50 mL. 1.0 mg/mL 4–8 mg/h 4–8 mL/h Reconstitute in Reconstitute in water BP water BP Dilute in DS Dilute in DS AMI, acute myocardial infarct; DS, dextrose saline, or any isotonic crystalloid; DVT, deep vein thrombosis; DW, 5% dextrose in water; IM, intramuscular; IP, infusion pump; IV, intravenous; MAP, mean arterial pressure; NS, normal saline; PE, pulmonary embolus; VT, ventricular tachycardia; water BP, water for injection. bStandard: use in Emergency department. aTransport: use for retrievals/interhospital transfers. Reproduced by kind permission of Associate Professor CT Myers, Director and Head, Department of Emergency Medicine, The Prince Charles Hospital, Brisbane. Critical Care Emergencies 41 Allergy UK. http://www.allergyuk.org/ (anaphylaxis). American Heart Association. http://circ.ahajournals.org/content/vol122/18_ suppl_3/ (2010 CPR and ECC guidelines). American Heart Association (2010) Part 1: Executive Summary: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S640–56. American Heart Association (2010) Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S729–67. Australian Resuscitation Council. http://www.resus.org.au/ (resuscitation guidelines 2010). Australasian Society of Clinical Immunology and Allergy. http://www.allergy.org. au/ (anaphylaxis). European Resuscitation Council. http://www.cprguidelines.eu/2010/ (2010 CPR and ECC guidelines). European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010 Section 1. Executive summary. Resuscitation 81: 1219–76. European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support. Resuscitation 81: 1305–52. Lieberman P, Nicklas R, Oppenheimer J et al. (2010) The diagnosis and management of anaphylaxis practice parameter: 2010 Update. Journal of Allergy and Clinical Immunology 126: 480.e1–41. National Institute for Health and Clinical Excellence, NHS UK. http://www.nice. org.uk/Guidance/CG/Published National Institute of Clinical Studies (Australia). http://www.nhmrc.gov.au/nics/ index.htm Scottish Intercollegiate Guidelines Network. http://www.sign.ac.uk/ Trauma.org http://trauma.org/ (severe head injury). FURTHER READING This page intentionally left blank GENERAL MEDICAL EMERGENCIES Section II 44 General Medical Emergencies DIFFERENTIAL DIAGNOSIS Always consider the life-threatening diagnoses first: ● Acute coronary syndrome (ACS), such as myocardial infarction or unstable angina. ● Pulmonary embolus. ● Aortic dissection. Other causes to consider include: ● Pericarditis. ● Pleurisy. ● Pneumonia. ● Pneumothorax. ● Abdominal – oesophagitis, oesophageal rupture, gall bladder disease, etc. ● Musculoskeletal and chest wall pain. ACUTE CORONARY SYNDROME The term acute coronary syndrome encompasses the spectrum of patients presenting with chest pain or other symptoms due to myocardial ischaemia that ranges from ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI) to unstable angina pectoris (UA). The common pathophysiology of ACS is rupture or erosion of an atherosclerotic plaque. ST ELEVATION MYOCARDIAL INFARCTION (STEMI) DIAGNOSIS 1 Predisposing factors include cigarette smoking, hypertension, diabetes, hypercholesterolaemia, male sex, increasing age and a positive family history. 2 There may be a prior history of angina, myocardial infarction or heart failure, or alternatively the condition may arise de novo. 3 ‘Typical’ pain is central, heavy, burning, crushing or tight retrosternal, usually lasting for several minutes or longer, unrelieved by sublingual nitrates, and is associated with anxiety, dyspnoea, nausea and vomiting. CHEST PAIN Warning: patients with these can present initially with few physical signs and or a non-diagnostic chest radiograph (CXR) and electrocardiogram (ECG), so may have to be managed on clinical suspicion alone. Attach a cardiac monitor and pulse oximeter to the patient, establish venous access and give 35% oxygen. ! CHEST PAIN General Medical Emergencies 45 4 The pain may radiate to the neck, jaw, one or both arms, the back and occasionally the epigastrium, or may present at these sites alone. (i) Atypical symptoms occur more frequently in people with diabetes, the elderly and in females. 5 The patient may be clammy, sweaty, breathless and pale or the patient may appear deceptively well. 6 Alternatively, the patient may present with a complication such as a cardiac arrhythmia (fast or slow), heart failure, severe hypotension with cardiogenic shock, ventricular septal rupture or papillary muscle rupture, systemic embolism or pericarditis. 7 Establish venous access with an i.v. cannula and attach a cardiac monitor and pulse oximeter to the patient. 8 Send blood for full blood count (FBC), coagulation profile, electrolyte and liver function tests (ELFTs), cardiac biomarker assay such as cardiac troponin I (cTnI) or troponin T (cTnT) and lipid profile. (i) Do not delay definitive management while awaiting a result. (ii) Cardiac biomarkers do not rise for 4–6 h after symptom onset, so can be normal early on. (iii) Higher elevated troponin levels identify an increase in adverse outcome risk. 9 Electrocardiogram (ECG). Perform this within 10 min of patient arrival, and arrange for immediate review by a senior emergency department (ED) doctor. (i) Look for ST elevation in two or more contiguous leads. (ii) The greater the number of leads affected and the higher the ST segments, the higher the mortality. (iii) Inferior myocardial infarction causes changes in leads II, III and aVF. (iv) Anterior myocardial infarction causes changes in I, aVL and V1–V3 (anteroseptal) or V4–V6 (anterolateral). (v) True posterior myocardial infarction causes mirror-image changes of tall R waves and ST depression in leads V1–V4. (vi) Repeat the ECG after 5–10 min in symptomatic patients with an initial non-diagnostic ECG. 10 Perform a CXR to look for pulmonary oedema, cardiomegaly and atelectasis. Request a portable X-ray in the ED, provided this does not delay definitive management. MANAGEMENT 1 Give high-dose 40–60% oxygen unless there is a prior history of obstructive airways disease, in which case give 28% oxygen. Aim for an oxygen saturation (SaO2) over 94%. CHEST PAIN 46 General Medical Emergencies 2 Give aspirin 150–300 mg orally unless contraindicated by known hyper - sensitivity. (i) Give clopidogrel 300 mg oral loading dose, then 75 mg orally once daily, if aspirin intolerant or in addition to aspirin if this is local policy. 3 Maximize pain relief: (i) Give glyceryl trinitrate (GTN) 150–300 g sublingually, maintaining systolic blood pressure (BP) above 100 mmHg and avoiding excessive hypotension. (ii) Add morphine 2.5–5 mg i.v. with an antiemetic, e.g. metoclopramide 10 mg i.v., if pain persists. 4 Reperfusion therapy Consider reperfusion therapy in consultation with the senior ED doctor. Aim to either commence thrombolysis within a maximum of 30 min of the patient’s arrival in hospital, without delay by transferring to the CCU, or arrange for percutaneous coronary intervention (PCI) if this is available in under 60–90 min. 5 Thrombolysis This is indicated within 12 h (ideally 6 h) of the onset of myocardial ischaemic pain in patients with a STEMI, e.g. ECG evidence of ST elevation MI, with ST elevation of at least 1 mm in two contiguous limb leads or 2 mm in two contiguous precordial chest leads, and for new bundle branch block, particularly left bundle branch block (LBBB). (i) Absolute contraindications to thrombolysis: (a) intracerebral or subarachnoid haemorrhage ever, intracranial malignancy (b) thrombotic stroke in previous 3 months (c) known bleeding diathesis or active bleeding (excluding menses) (d) significant head or facial trauma in previous 3 months (e) aortic dissection (see p. 57). (ii) Relative contraindications (thrombolysis may still be considered in those at highest risk of death, or with greatest net clinical benefit, such as a large anterior infarction presenting within 3 h of symptom onset): (a) oral anticoagulant therapy (b) pregnancy or within 1 week post partum (c) major surgery in last 3 weeks (d) non-compressible arterial puncture or central line (e) refractory hypertension (systolic BP over 180 mmHg, diastolic BP over 110 mmHg) (f) history of severe or poorly controlled hypertension (g) prolonged CPR over 10 min (h) severe hepatic or renal disease. CHEST PAIN General Medical Emergencies 47 (iii) Administer tenecteplase (TNK) as the lytic agent of first choice: (a) give tenecteplase 30 mg (weight <60 kg), 35 mg (weight ≥60 to <70 kg), 40 mg (≥70 to <80 kg), 45 mg (≥80 to <90 kg) and 50 mg (weight ≥90 kg) as a single bolus over 10 s (b) tenecteplase is easiest to administer, safe given weight-based, has greater fibrin specificity and with efficacy up to 12 h (c) continue ECG monitoring for reperfusion arrhythmias. (iv) Start unfractionated heparin by i.v. bolus 60 units/kg (maximum 4000 units), then i.v. infusion at 12 units/kg/h (maximum 1000 units/h) for 48 h in addition (a) alternatively, give low-molecular-weight (LMW) heparin such as enoxaparin 30 mg i.v. immediately, then 1 mg/kg subcutaneously (s.c.) 12-hourly, but check your local policy. (v) Other fibrin-specific lytic agents to consider if tenecteplase is unavailable include: (a) reteplase 10 units as a bolus over no more than 2 min, followed after 30 min by a further 10 units bolus i.v. (b) alteplase (rt-PA) 15 mg (15 mL) bolus, followed by an infusion of 0.75 mg/kg over 30 min (to maximum 50 mg), then 0.5 mg/kg over 60 min (to maximum 35 mg). (vi) Give streptokinase (SK) 1.5 million units over 45–60 min in 100 mL normal saline if none of the above fibrin-specific agents are available. The early infarct-related artery vessel patency rate is less than with those agents (a) avoid SK if it has been given between 5 days and 12 months previously, or immediately after a severe streptococcal infection (b) slow or stop the infusion if hypotension or rash occurs. Restart the infusion as soon as they have resolved (c) occasionally, severe hypotension and anaphylaxis may occur, requiring oxygen, adrenaline (epinephrine) and fluids, etc. (see p. 27). 6 Percutaneous coronary intervention (PCI) Organize primary percutaneous coronary intervention in preference to thrombolysis, when it is available locally in less than 90 min of patient arrival, or in less than 60 min if the chest pain onset was within previous 3 h. (i) It is superior to thrombolysis, particularly in a high-volume centre preferably with cardiac surgery capability. (ii) It is preferred in cardiogenic shock, and if thrombolysis is contraindicated. (iii) Give thrombolysis with tenecteplase if the PCI will take longer than the 60–90 min to organize. 7 Transfer the patient to the CCU following thrombolysis, or to the catheter lab for PCI, with a doctor and nurse escort, and resuscitation equipment and drugs available. CHEST PAIN 48 General Medical Emergencies NON-ST ELEVATION MYOCARDIAL INFARCTION (NSTEMI) AND UNSTABLE ANGINA DIAGNOSIS 1 The predisposing factors and pathophysiology are the same as for STEMI (see p. 44). 2 It is not possible from the character of the chest pain alone to accurately exclude ACS, unless a clear alternative cause for the pain is apparent (see Table 2.1). Table 2.1 Differential diagnosis of chest pain in patients presenting with possible acute coronary syndrome (ACS) Diagnosis Classic history Physical examination Diagnostic testing Acute coronary syndrome (see p. 44) Band-like, tight, or pressure pain with radiation to neck and arms, sweating, dyspnoea, cardiac risk factors May be normal, or may have evidence of heart failure, hypotension Cardiac biomarkers, ECG, possibly stress testing Pulmonary embolus (see p. 51) Sudden onset, pleuritic pain, dyspnoea, risks for venous thrombo-embolism Tachycardia, tachypnoea, pleural rub, low-grade fever CXR, V/Q scan, CTPA Aortic dissection (see p. 57) Sudden, sharp, tearing pain radiating to back, neurologic symptoms Unequal pulses or BP, new murmur, bruits CXR, echocardiogram, CT angiogram Pericarditis (see p. 58) Pleuritic, positional ache, worse lying down Fever, pericardial rub, tachycardia ECG, CXR, echocardiogram Pneumonia (see p. 67) Cough, fever, dyspnoea, pleuritic pain, malaise Fever, hypoxia, tachypnoea, tachycardia, abnormal breath sounds CXR, WCC Pneumothorax (see p. 72) Pleuritic pain, dyspnoea Reduced breath sounds over hemithorax CXR Oesophageal rupture (Boerhaave’s syndrome) (see p. 236) Constant, severe retrosternal pain, dysphagia Subcutaneous emphysema CXR, CT chest CHEST PAIN General Medical Emergencies 49 Gastrointestinal causes (see p. 59) Burning, nocturnal pain, gastrointestinal symptoms Abdominal tenderness, rebound or guarding Lipase, AXR, ultrasound Musculoskeletal causes (see p. 60) Pain increased with movement or muscular activity Chest-wall tenderness to palpation (may occur in ACS!) Normal ACS, acute coronary syndrome; AXR, abdominal X-ray; BP, blood pressure; CT, computerized tomography; CTPA, computerized tomography pulmonary angiogram; CXR, chest X-ray; ECG, electrocardiograph; V/Q, ventilation perfusion; WCC, white cell count. (i) Unstable angina (UA) includes increasing severity or frequency of angina, angina at rest and new-onset angina that markedly limits physical activity or following a recent myocardial infarction. (ii) Older patients, females, diabetics and chronic renal failure patients may present with atypical ACS pain. 3 Establish venous access with an i.v. cannula, and attach a cardiac monitor and pulse oximeter to the patient. 4 Send blood for FBC, coagulation profile, ELFTs, cardiac biomarker assay such as cardiac troponin I (cTnI) or troponin T (cTnT) and lipid profile, exactly as for STEMI. 5 Perform an ECG within 10 min of patient arrival, with immediate review by a senior ED doctor. (i) This may show ST depression, T wave inversion or flattening, non-specific or transient changes, or (ii) The ECG may be normal. MANAGEMENT 1 Give aspirin 150–300 mg orally unless contraindicated by known hypersensitivity. (i) Give clopidogrel 300 mg oral loading dose, then 75 mg once daily if aspirin-intolerant, or in addition if this is local policy. 2 Give GTN 150–300 g sublingually, and add morphine 2.5–5 mg i.v. with an antiemetic, e.g. metoclopramide 10 mg i.v., if pain persists. 3 Commence heparin for all patients with a suspected NSTEMI or UA, without necessarily awaiting the first cardiac biomarker results particularly with new ECG changes. (i) Give LMW heparin such as enoxaparin 1 mg/kg s.c. or dalteparin 120 units/kg s.c. both 12-hourly, or CHEST PAIN 50 General Medical Emergencies (ii) Give unfractionated (UF) heparin i.v. bolus 60–70 units/kg (maximum 5000 units), followed by an infusion at 12–15 units/ kg/h (maximum 1000 units/h) (a) UF heparin may be preferred in hospitals likely to offer coronary angioplasty (PCI) within 24–36 h of symptom onset, so check your local policy (b) titrate the UF heparin infusion to an activated partial thromboplastin time (aPTT) of 50–70 s by 6 h post infusion. 4 Admit all patients. The final diagnosis of NSTEMI (rise in cardiac troponin biomarker), UA (no rise in troponin or cardiac biomarker) or non-cardiac chest pain (normal cardiac biomarkers, normal ECGs, normal stress test) takes time to establish. (i) Admit patients with ‘high-risk’ features directly to the coronary care unit (CCU). This includes any one or more of: (a) elevated troponin on arrival blood test, repetitive or prolonged chest pain over 10 min, diabetic patient or chronic kidney disease patient with estimated glomerular filtration rate of <60 mL/min and typical symptoms of ACS, associated syncope, symptoms or signs of heart failure (see p. 75), signs of new mitral incompetence (pansystolic murmur), PCI in the last 6 months or prior revascularization (coronary artery bypass graft [CABG]), haemodynamic instability or ECG changes. (ii) Admit patients with ‘intermediate-risk’ features under the medical team, possibly to a shared chest pain assessment unit (CPAU). These include any one or more of: (a) chest pain or discomfort within the past 48 h occurring at rest, or that was repetitive or prolonged (but currently resolved), age over 65 years, two or more risk factors of hypertension, family history, active smoking or hyperlipidaemia, and diabetic patient or chronic kidney disease patient with estimated glomerular filtration rate of <60 mL/min and atypical symptoms of ACS (b) lack of CCU beds may necessitate that all diabetic or chronic renal impairment patients are treated as intermediate-risk and are admitted to a general ward (rather than to CCU as high-risk if they have typical symptoms of ACS) (c) repeat the ECG and troponin at 6–8 h post arrival in the ED (d) admit the patient to CCU if chest pain recurs, the ECG changes, or a repeat cardiac troponin is elevated, as they have now become a high-risk patient. (iii) Meanwhile, arrange an immediate stress test such as an ECG exercise stress test (EST) if the repeat ECG and cardiac biomarkers remain normal and the pain does not recur: CHEST PAIN General Medical Emergencies 51 (a) ideally this stress test is performed as an inpatient (b) only if this stress test is normal has ACS finally now been excluded and the patient may go home (c) local policy may be to arrange an outpatient stress test within 72 h of discharge instead. Make sure the general practitioner (GP) is kept informed. NON-CARDIAC CHEST PAIN DIAGNOSIS 1 A stabbing, pleuritic, positional or palpation-induced pain is less characteristic of ACS, but can not absolutely exclude it. 2 Thus non-cardiac chest pain is a diagnosis of exclusion, unless there are clear features that indicate its origin such as immediate rib pain following a fall or blow, or a sudden onset related to a sneeze or deep cough, or 3 Non-cardiac chest pain is diagnosed by finding definite features of an alternative diagnosis such as a PE, aortic dissection, pericarditis, pleurisy, pneumothorax, etc. (see Table 2.1). (i) Otherwise perform serial ECGs and troponins, and arrange a stress test. MANAGEMENT 1 Give every patient in whom the diagnosis is not immediately clear aspirin 150–300 mg orally unless contraindicated by known hypersensitivity. 2 Management will depend on which cause is suspected or found (see above or following pages). PULMONARY EMBOLUS DIAGNOSIS 1 Venous thromboembolism (VTE) includes PE and deep venous thrombosis (DVT). 2 Predisposing risk factors for VTE are best divided into acute provoking and chronic predisposing, and apply to both PE and DVT (see Table 2.2). Warning: never discharge any chest pain patient after a single normal troponin test as a second paired test plus repeat ECG at 6–8 h post-arrival are mandatory, followed by some form of stress test to definitely rule out ACS. ! CHEST PAIN 52 General Medical Emergencies Table 2.2 Predisposing risk factors for venous thromboembolism (VTE) Acute provoking factors Hospitalization, i.e. reduced mobility Surgery, particularly abdominal, pelvic, leg Trauma or fracture of lower limbs or pelvis Immobilization (includes plaster cast) Long haul travel – over 3000 miles or 5000 km Recently commenced oestrogen therapy (e.g. within previous 2 weeks) Intravascular device (e.g. venous catheter) Chronic predisposing factors Inherited Acquired Inherited or acquired Natural anticoagulant deficiency such as protein C, protein S, antithrombin III deficiency Increasing age High plasma homocysteine Factor V Leiden Obesity High plasma coagulation factors VIII, IX, XI Prothrombin G20210A mutation Cancer (chemotherapy) Antiphospholipid syndrome (anticardiolipin antibodies and lupus anticoagulant) Leg paralysis Oestrogen therapy Pregnancy or puerperium Major medical illnessa Previous venous thromboembolism (DVT/PE) aChronic cardiorespiratory disease, inflammatory bowel disease, nephritic syndrome, myeloproliferative disorders. DVT, deep vein thrombosis; PE, pulmonary embolus. Modified from Ho WK, Hankey GJ (2005) Venous thromboembolism: diagnosis and management of deep venous thrombosis. Med J Aust 182:476–81. 3 A small PE causes sudden dyspnoea, cough, pleuritic pain and possibly haemoptysis, with few physical signs. Look for a low-grade pyrexia (37.5°C), tachypnoea over 20/min, tachycardia, crepitations and a pleural rub. 4 A major PE causes dyspnoea, chest pain and light-headedness or syncope. Look for cyanosis, tachycardia, hypotension, a parasternal heave, raised jugular venous pressure (JVP) and a loud delayed pulmonary second sound. CHEST PAIN General Medical Emergencies 53 5 Establish venous access with an i.v. cannula, send blood for FBC, coagulation profile and ELFTs, and attach a cardiac monitor and pulse oximeter to the patient. (i) Only request a D-dimer test after assessing the clinical pre-test probability as low and one or more PE rule-out criteria (PERC) are positive. See points 9 to 11 below. 6 Consider a blood gas that may reflect hypocapnia from hyperventilation, and less commonly hypoxia, but that will be normal in over 20% patients with PE. (i) Do not perform an arterial blood gas (ABG) routinely, unless there is an unexplained low pulse oximeter reading on room air. ABGs rarely help. 7 Perform an ECG, mainly to exclude other diagnoses such as ACS or pericarditis. (i) It may show a tachycardia alone or possibly right axis deviation, right heart strain, right bundle branch block (RBBB) or atrial fibrillation (AF) in PE. (ii) The well-known ‘S1Q3T3’ pattern is neither sensitive nor specific for PE. 8 Request a CXR, again mainly to exclude other diagnoses such as pneumonia or a pneumothorax. (i) It may be normal in PE, or show a blunted costophrenic angle, raised hemidiaphragm, an area of linear atelectasis or infarction, or an area of oligaemia. 9 Determine the clinical pre-test probability now before requesting any further diagnostic imaging (see Table 2.3). Table 2.3 Estimation of the clinical pre-test probability for suspected pulmonary embolus (PE) Feature Score Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins. See p. 55) 3 Alternative diagnosis less likely than PE 3 Heart rate >100 beats/min 1.5 Immobilization or surgery in previous 4 weeks 1.5 Previous DVT or PE 1.5 Haemoptysis 1 Cancer 1 Low pre-test probability = score < 2 Moderate pre-test probability = score 2–6 High pre-test probability = score > 6 DVT, deep venous thrombosis; PE, pulmonary embolus. Modified from Wells PS, Anderson DR, Rodger M et al. (2001) Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer. Ann Intern Med 135:98–107. CHEST PAIN 54 General Medical Emergencies (i) A low pre-test probability on Wells’ criteria with a score of <2 has up to 3.6% probability of PE. (ii) A moderate pre-test probability with a Wells’ criteria score of 2–6 has a 20.5% probability of PE. (iii) A high pre-test probability with a Wells’ criteria score of >6 has a 66.7% probability of PE. 10 Patients under 50 years old and with a low pre-test probability: (i) Check if the PERC rule score is negative (see Table 2.4) and if all criteria are fulfilled, no further testing is required and a PE is ruled out. Table 2.4 Pulmonary embolism rule-out criteria (PERC) rule in the low pre-test probability patient Age <50 years Pulse <100 beats/min Pulse oximetry >94% No unilateral leg swelling No haemoptysis No recent trauma or surgery No prior pulmonary embolism or deep vein thrombosis No oral hormone use If all eight factors are fulfilled (negative), no further testing is required. Modified from Kline JA, Mitchell AM, Kabrhel C et al. (2004) Clinical criteria to prevent unnecessary diagnostic testing in ED patients with suspected pulmonary embolism. Journal of Thrombosis and Haemostasis 2: 1247–55. 11 Send a D-dimer test only in patients ≥50 years with a low pre-test probability, or in any patient under 50 with a low pre-test probability but with one or more PERC criteria positive (see Table 2.4). (i) Check with the laboratory which D-dimer test they use and their test’s reference ranges, in particular their normal cut-off range. (ii) Discharge the patient if this D-dimer test is negative, i.e. there is no PE. (iii) Arrange imaging if the D-dimer test is positive (see below). 12 Perform a multislice, helical computed tomography pulmonary angiogram (CTPA) if available, in all patients with a moderate or high pre-test probability, and in those low pre-test probability patients with a positive D-dimer. 13 Alternatively, start with a ventilation–perfusion isotope lung scan, the V/Q scan. (i) A V/Q scan is preferred when the patient is allergic to contrast dye, has renal failure or is younger than 40 years, particularly in females. CHEST PAIN General Medical Emergencies 55 (ii) In addition the CXR should be normal with no history of chronic lung disease. (iii) Unfortunately, over half the V/Q results will not help, i.e. are low or intermediate probability results, and must still be followed by further testing, such as CTPA or lower leg venous Doppler ultrasound. MANAGEMENT 1 Give high-dose oxygen through a face mask. Aim for an oxygen saturation above 94%. 2 Relieve pain if it is severe with morphine 5 mg i.v. and give an antiemetic such as metoclopramide 10 mg i.v. 3 Commence heparin in intermediate or high pre-test probability patients, unless a diagnostic imaging test is imminently available, and contraindications such as active bleeding, thrombocytopenia, recent trauma or cerebral haemorrhage are absent: (i) Give LMW heparin such as enoxaparin 1 mg/kg s.c. or dalteparin s.c. according to body weight, both 12-hourly. (ii) Alternatively, give UF heparin 5000 units i.v. bolus, followed by 1000–1300 units/h infusion (a) this is preferred with a major PE, as a first dose bolus or according to local policy. 4 Admit all patients with a confirmed PE under the medical team, or if the test results remain indeterminate. (i) Arrange sequential testing with a V/Q scan then a CTPA or vice versa, plus or minus a lower-limb venous Doppler ultrasound to finally rule in or out the diagnosis. (ii) Commence heparin once a positive result is confirmed, if not already started. 5 Get help from a senior ED doctor for any apparent major, life-threatening PE patient: (i) Reserve thrombolysis with recombinant tissue plasminogen activator (rt-PA) 10 mg i.v. over 1–2 min, then 90 mg over 2 h (or 1.5 mg/kg maximum if under 65 kg) for patients with a massive PE in shock, with acute right heart failure and systolic hypotension. (ii) Involve the intensive care team early. VENOUS THROMBOEMBOLISM WITH DEEP VEIN THROMBOSIS DIAGNOSIS 1 Predisposing risk factors are as for venous thromboembolism. Up to two-thirds of patients have acute provoking factors (see Table 2.2). CHEST PAIN 56 General Medical Emergencies 2 Typical symptoms include leg pain, swelling, tenderness and redness or discoloration. 3 Examination may reveal unilateral oedema, warmth, superficial venous dilatation, increased limb girth or tenderness along the deep venous system. (i) Unfortunately, a similar picture is seen in cellulitis, lymphoedema, musculoskeletal injury and varicose vein insufficiency. (ii) Homan’s sign of pain on forced ankle dorsiflexion is unreliable, unhelpful and not recommended. 4 Ask about any associated features of a concomitant PE (see p. 51), particularly in suspected proximal DVT above the knee. 5 Exactly as with PE, determine the clinical pre-test probability of a DVT now before requesting diagnostic testing (see Table 2.5). (i) A low pre-test probability on Wells’ criteria with a score ≤0 has up to a 5% probability of DVT. (ii) A moderate pre-test probability with a Wells’ score 1–2 has a 17% probability of DVT, and a high pre-test probability with a Wells’ score ≥3 has up to a 53% probability of DVT. Table 2.5 Estimation of the clinical pre-test probability for suspected deep venous thrombosis (DVT) Clinical feature Score Active cancer (treatment ongoing or within 6 months or palliative) 1 Paralysis, paresis or recent plaster immobilization of the lower extremities 1 Recently bedridden for ≥3 days, or major surgery within the previous 12 weeks 1 Localized tenderness along the distribution of the deep venous system 1 Entire leg swollen 1 Calf swelling >3 cm when compared with the asymptomatic leg (at 10 cm below the tibial tuberosity) 1 Pitting oedema: confined to the symptomatic leg 1 Collateral superficial veins (non-varicose) 1 Previously documented deep venous thrombosis 1 Alternative diagnosis as likely or greater than that of deep venous thrombosis –2 In patients with symptoms in both legs, the more symptomatic leg is scored. Low pre-test probability = score ≤0 Moderate pre-test probability = score 1–2 High pre-test probability = score ≥3 From Wells PS, Owen C, Doucette S et al. (2006) Does this patient have deep vein thrombosis? J Amer Med Assoc 295:199–207. CHEST PAIN General Medical Emergencies 57 6 Send blood for D-dimer only when the pre-test probability is low. (i) Discharge the patient if this D-dimer is negative, that is no DVT, provided alternative diagnoses do not require further care. 7 Perform Doppler ultrasound on all moderate and high pre-test probability patients, and when the D-dimer test is positive. MANAGEMENT 1 Give the patient analgesia such as paracetamol 500 mg with codeine 8 mg two tablets orally q.d.s. or an anti-inflammatory such as ibuprofen 200–400 mg orally t.d.s. or naproxen 250 mg orally t.d.s. 2 Commence heparin if the diagnosis is confirmed. (i) Give LMW heparin such as enoxaparin 1 mg/kg s.c. 12-hourly or dalteparin according to body weight s.c. 12-hourly. (ii) Alternatively, give UF heparin 5000 units i.v. bolus followed by 1000–1300 units/h infusion particularly for a large or extensive DVT, according to local policy. 3 Refer all patients to the medical team if the diagnosis is confirmed. (i) Some patients may be discharged for outpatient LMW heparin. Check your local policy. (ii) Other patients may even be sent home without any treatment at all if the DVT is confined below the knee (a) organize a repeat US scan within 5–7 days in those not treated to exclude more proximal extension of the thrombosis. 4 Get senior ED doctor advice if the diagnosis is still indeterminate. AORTIC DISSECTION DIAGNOSIS 1 Predisposed to by hypertension typically in males 60–80 years old. Other risk factors include Marfan’s syndrome, bicuspid aortic valve, coarctation, cocaine use, iatrogenic trauma or prior cardiovascular surgery. 2 The onset is abrupt with sudden pain that is sharp or tearing, retrosternal, interscapular or lower in the back or migratory, and may be severe and resistant to opiates. 3 Look for unequal or absent pulses, a difference of blood pressure in the arms, or the following complications of the dissection: (i) Aortic incompetence, myocardial ischaemia and haemopericardium with pericardial rub or cardiac tamponade (see p. 10). (ii) Dyspnoea, pleural rub or effusion. (iii) Altered consciousness, syncope, hemiplegia or paraplegia. (iv) Intestinal ischaemia or bowel infarction with abdominal pain and bloody diarrhoea. (v) Oliguria and haematuria. CHEST PAIN 58 General Medical Emergencies 4 Establish venous access with a large-bore (14- or 16-gauge) i.v. cannula, and send blood for FBC, ELFTs, cardiac enzymes and group and cross-match. Attach a cardiac monitor and pulse oximeter to the patient. 5 Perform an ECG, which may look remarkably normal despite the severity of the pain, with left ventricular hypertrophy and non-specific changes. 6 Request a CXR that may show a widened mediastinum, blurred aortic knob and a left pleural effusion, but can be normal. MANAGEMENT 1 Give high-dose oxygen via a face mask. Aim for an oxygen saturation above 94%. 2 Relieve the pain with morphine 5–10 mg i.v. and give an antiemetic. 3 Reduce the systolic BP to below 110 mmHg using a labetalol infusion or sodium nitroprusside plus propranolol i.v. in consultation with the senior ED doctor or intensive care team, when dissection is diagnosed or highly likely. 4 Organize an urgent helical CT angiogram, transoesophageal echocardiogram or aortogram to confirm the diagnosis. 5 Contact the cardiothoracic surgeons and arrange transfer without delay. Involve the intensive care team early. PERICARDITIS DIAGNOSIS 1 This may be post-viral such as Coxsackie or follow a myocardial infarction either early within 24 h or later at 2–3 weeks (Dressler’s syndrome), pericardiotomy, connective tissue disorder, uraemia, trauma, tuberculosis or a neoplasm. 2 The pain is sharp, pleuritic, retrosternal and positional, relieved by sitting forward. 3 Listen for a pericardial friction rub, best heard along the left sternal edge with the patient sitting forward, which may be transient or intermittent. 4 Send blood for FBC, ELFTs, cardiac biomarkers and viral serology. Attach a cardiac monitor and pulse oximeter to the patient. 5 Perform an ECG that may show sinus tachycardia alone or AF, widespread concave ST elevation, followed by T wave flattening then inversion. 6 Request a CXR, which is usually normal, even if a pericardial effusion is present. MANAGEMENT 1 Give high-dose oxygen via a face mask. Aim for an oxygen saturation above 94%. 2 Give the patient a non-steroidal anti-inflammatory analgesic such as ibuprofen 200–400 mg orally t.d.s. or naproxen 250 mg orally t.d.s. CHEST PAIN General Medical Emergencies 59 3 Refer the patient to the medical team for bed rest and cardiac monitoring if there are widespread ECG changes or raised cardiac enzymes. 4 Arrange urgent echocardiography and pericardiocentesis for signs of cardiac tamponade such as tachycardia, hypotension, pulsus paradoxus and a raised JVP that rises on inspiration, known as Kussmaul’s sign (see p. 10). PLEURISY DIAGNOSIS 1 Pleurisy or pleuritic pain occurs in association with pneumonia, pulmonary infarction from a PE, neoplasia, tuberculosis, connective tissue disorders, uraemia, or following trauma. 2 It may also be due to viruses, especially enteroviruses, and may be mimicked by a pneumothorax or epidemic myalgia (Bornholm’s disease). 3 The pain is sharp, knife-like, localized and exacerbated by moving, coughing or breathing, which tends to be shallow. Radiation to the shoulder or abdomen occurs with diaphragmatic involvement. 4 Listen for a pleural rub, although this may be inaudible if pain limits deep breathing, and disappears as an effusion develops. 5 Send ABGs if there are significant signs of pulmonary parenchymal disease. Perform an ECG, which should be normal. 6 Request a CXR that may reveal the underlying cause or may be quite normal. MANAGEMENT 1 Give the patient oxygen and a non-steroidal anti-inflammatory analgesic such as ibuprofen 200–400 mg orally t.d.s. or naproxen 250 mg orally t.d.s. 2 Rule out a PE if there was sudden dyspnoea, tachypnoea and risk factors for thromboembolism. A PE is possible even with a normal CXR and ECG (see p. 51). 3 Refer the patient to the medical team for treatment of the underlying cause, or discuss with the senior ED doctor before discharging. ABDOMINAL CAUSES OF CHEST PAIN DIAGNOSIS AND MANAGEMENT 1 Oesophagitis (i) This is suggested by burning retrosternal or epigastric pain, worse on stooping or recumbency, exacerbated by hot drinks or food, and relieved by antacids. (ii) It may mimic cardiac pain and may even be relieved by sublingual GTN, so consult the senior ED doctor CARDIAC ARRHYTHMIAS 60 General Medical Emergencies (a) admit the patient to rule out ACS with serial ECGs and troponins, if there is any doubt at all about the diagnosis. (iii) Otherwise give an antacid or proton-pump inhibitor orally. 2 Oesophageal rupture. See page 236. 3 Acute cholecystitis, pancreatitis and peptic ulceration may cause chest pain, but other diagnostic features should be present. MUSCULOSKELETAL AND CHEST WALL PAIN DIAGNOSIS AND MANAGEMENT 1 Musculoskeletal disorders cause pain that is worse with movement and breathing. There may have been preceding strenuous exercise, a bout of coughing, or a history of minor trauma. 2 Pain is localized on palpation and the ECG is normal. A CXR may show a fractured rib but is otherwise normal. 3 Give the patient a non-steroidal anti-inflammatory analgesic such as ibuprofen 200–400 mg orally t.d.s., or naproxen 250 mg orally t.d.s. Refer back to the GP. 4 Two specific causes are: (i) Shingles This causes pain localized to a dermatome, unaffected by breathing, associated with an area of hyperaesthesia preceding the characteristic blistering rash (a) give the patient (usually elderly) with severe pain a narcotic analgesic and aciclovir 800 mg orally five times a day for 7 days, or famciclovir 250 mg orally t.d.s. for 7 days, if seen within 72 h of vesicle eruption (b) admit to a suitable isolation area if unable to be nursed at home. (ii) Costochondritis (Tietze’s syndrome) This causes localized pain, swelling and tenderness typically around the second costochondral junction, related to physical strain or minor injury. (a) prescribe ibuprofen 200–400 mg orally t.d.s., or naproxen 250 mg orally t.d.s. Refer the patient back to the GP. CARDIAC ARRHYTHMIAS DIAGNOSIS 1 Cardiac rhythm disturbances include atrial, nodal and ventricular tachycardias, atrial flutter and fibrillation, the bradycardias and the various degrees of heart block. CARDIAC ARRHYTHMIAS General Medical Emergencies 61 2 Exclude myocardial ischaemia from ACS as a priority (see p. 44). 3 Consider other underlying precipitating factors for the arrhythmia such as hypoxia from any cause, hypovolaemia from blood or fluid loss, electrolyte disturbances particularly hyperkalaemia, thyroid disease, drug, alcohol or noxious gas toxicity whether inadvertent or deliberate, septicaemia, hypothermia, electrocution, or simple pain and fear. 4 Ask the patient about palpitations, ‘missed beats’, breathlessness, chest pain, light-headedness and fatigue. 5 Measure the temperature and vital signs and attach a cardiac monitor and pulse oximeter to the patient. (i) Abnormal vital signs including hypotension, confusion or associated features such as chest pain and breathlessness necessitate urgent management. 6 Send blood for FBC, ELFTs, cardiac biomarkers, coagulation profile, thyroid function and toxicology screen as indicated. Measure the ABGs if in respiratory distress. 7 Perform an ECG. Look systematically at the following: (i) Rate: fast or slow; paroxysmal or continuous? (ii) Rhythm: regular, regularly irregular or irregularly irregular? (iii) P waves: present, absent and relationship to QRS complexes? (iv) PR interval: shortened <120 ms or prolonged over 200 ms? (v) QRS complexes: narrow or widened >120 ms? (vi) QTc interval (corrected for rate): normal or longer than 450 ms (470 ms in females)? (vii) ST segment and T waves: elevated, depressed or inverted? 8 Request a CXR and look for cardiomegaly or evidence of acute pulmonary oedema. See page 75. MANAGEMENT This depends on the arrhythmia, cardiovascular stability and the presence of associated chest pain, breathlessness or confusion. 1 Give high-dose 40–60% oxygen unless there is a prior history of obstructive airways disease, in which case give 28% oxygen. Aim for an oxygen saturation over 94%. 2 Give aspirin 150–300 mg orally if there is possible or probable ACS, unless contraindicated by known hypersensitivity. Tip: call the senior ED doctor immediately if the patient is hypotensive with a systolic BP <90 mmHg, is breathless, is confused or has chest pain. ✓ CARDIAC ARRHYTHMIAS 62 General Medical Emergencies 3 Provide pain relief if needed with GTN 150–300 g sublingually for coronary ischaemic pain, or morphine 2.5–5 mg i.v. with an antiemetic, e.g. metoclopramide 10 mg i.v., for more severe pain, including non-ischaemic. 4 Correct any electrolyte abnormality. See page 131. 5 Tachycardia This may be sinus with normal preceding P waves, narrow-complex or broadcomplex. (i) Look urgently for and treat underlying causes such as hypoxia, hypovolaemia, fever, anaemia, pain, etc. if it is definitely a sinus tachycardia. (ii) Give a synchronized DC shock, if the patient is unstable with hypotension and a systolic BP <90 mmHg, is confused, has chest pain or heart failure (see p.75) (a) start with 120–150 J biphasic or 200 J monophasic and repeat up to three times, with stepwise increases in joules (b) a senior doctor with airway experience must first give a shortacting general anaesthetic or i.v. midazolam in the conscious patient (c) give amiodarone 300 mg i.v. over 10–20 min if three attempts at synchronized DC cardioversion failed, then repeat the DC shock and follow by an infusion of amiodarone 900 mg over 24 h. (iii) Broad-complex tachycardia When regular this may be due to ventricular tachycardia (VT) or supraventricular tachycardia with aberrant conduction (block): (a) give amiodarone 5 mg/kg i.v. over 20–60 min if the patient is stable, followed by an infusion of amiodarone 900 mg over 24 h (b) consider AF with bundle branch block if the rhythm is irregular, or AF with ventricular pre-excitation as in Wolff– Parkinson–White syndrome: – seek expert help if not already involved – give flecainide 2 mg/kg over 10 min, or amiodarone 5 mg/ kg i.v. followed by an infusion – avoid adenosine, verapamil, digoxin and diltiazem, as they block the atrioventricular (AV) node and may worsen preexcited AF leading to VT or even ventricular fibrillation (VF). Tip: frequent ventricular ectopic beats (VEBs) do not require treatment, unless they are multi-focal, in runs or arrive on the T wave of the preceding complex. ✓ CARDIAC ARRHYTHMIAS General Medical Emergencies 63 (iv) Narrow-complex supraventricular tachycardia (SVT) When regular this may be one of the re-entry tachycardias or atrial flutter with regular AV conduction (usually 2 to 1 block if the rate is about 150/min) (a) proceed directly to synchronized DC cardioversion if the patient is shocked, unstable or deteriorating, starting at 70–120 J biphasic or 100 J monophasic, after a senior doctor with airway experience has given a short-acting anaesthetic (b) use a vagal stimulus such as carotid sinus massage (CSM) if patient is stable and young with no carotid bruit, or prior transient ischaemic attack (TIA) or cerebrovascular accident (CVA) – press firmly at the upper border of the thyroid cartilage against the vertebral process with a circular motion – or get the patient to perform Valsalva’s manoeuvre (c) give adenosine 6 mg rapidly over 2–5 s i.v. if CSM fails, followed by 12 mg i.v. rapidly after 1–2 min, then a further 12 mg i.v. rapidly once more if still no response – make sure to warn the patient to expect transient facial flushing, headache, dyspnoea, chest discomfort and nausea from the adenosine (d) alternatively, give verapamil 5 mg i.v. as a bolus over 30 s to 2 min. Verapamil may cause hypotension and bradycardia, particularly in elderly patients, who may be pre-treated with calcium gluconate 10 mL given slowly i.v. to prevent these (e) never use verapamil after a -blocker, when digitalis toxicity is suspected, or if the patient has a wide complex tachycardia. (v) Irregular narrow-complex tachycardia or AF Irregularly irregular narrow-complex tachycardia is usually AF or less frequently atrial flutter with variable AV block (a) proceed directly to synchronized DC cardioversion starting at 120–150 J biphasic or 200 J monophasic, if the patient is shocked, unstable or deteriorating. In patients on digoxin therapy, temporary transcutaneous pacing may be required as asystole may follow DC reversion (b) otherwise try rhythm control, if the patient has been in the AF for less than 48 h, with amiodarone 5 mg/kg i.v. over 20–60 min, followed by an infusion of amiodarone 900 mg over 24 h (c) however, when the patient has been in AF for over 48 h, or the time duration is unclear, rhythm control with drugs or elective DC reversion is contraindicated prior to full anticoagulation, due to the risk of clot embolization: – attempt rate control only using an oral or i.v. -blocker, digoxin, diltiazem or magnesium. Seek senior ED doctor advice BREATHLESS PATIENT 64 General Medical Emergencies – commence heparinization with LMW heparin such as enoxaparin 1 mg/kg s.c. or unfractionated UF heparin 5000 units i.v. as a bolus, followed by an infusion. (vi) Admit all patients who required active treatment to a monitored CCU bed. 6 Bradycardia This may be sinus, junctional (nodal) or due to atrioventricular block. (i) Give a bolus of atropine 0.5–0.6 mg i.v. (ii) Repeat the atropine for sinus or junctional bradycardia if it persists, to a maximum of 3 mg i.v. total. (iii) Consider the insertion of a temporary transvenous pacemaker wire by an expert, if the bradycardia persists with symptomatic second- or third-degree (complete) AV block, or the patient is unstable, or (a) use an external (transcutaneous) pacemaker until X-ray guidance and expert help are available (b) small doses of a sedative such as midazolam 0.05 mg/kg and or morphine 0.05 mg/kg are needed as external pacing is uncomfortable. (iv) Avoid excessive atropine or using an isoprenaline infusion immediately following an acute myocardial infarction, as these may provoke VF. BREATHLESS PATIENT DIFFERENTIAL DIAGNOSIS Consider the following, some of which were covered in the preceding section on chest pain: ● Acute asthma ● Community-acquired pneumonia (CAP) ● Chronic obstructive pulmonary disease (COPD) ● Pneumothorax ● Pulmonary embolus (see p. 51) ● Pulmonary oedema ● Acute upper airway obstruction – see page 13 ● Metabolic causes, such as acidosis in diabetic ketosis or salicylate poisoning ● Respiratory muscle weakness from myasthenia gravis or Guillain–Barré syndrome BREATHLESS PATIENT General Medical Emergencies 65 ACUTE ASTHMA DIAGNOSIS 1 Ascertain the precipitating factors in the present attack, its duration, additional treatment given particularly steroids and the response to treatment. 2 Ask about regular medication such as inhalers, previous attacks, hospital admissions and ventilation in an ICU. 3 Risk factors for a severe or fatal attack are: (i) Previous ICU admission. (ii) A recent acute attack within the last month, especially if the patient required steroids. (iii) ≥3 ED visits, or ≥2 hospitalizations in the previous 1 year. (iv) Difficulty perceiving asthma severity, and or lack of a written asthma management plan. (v) Drug or alcohol abuse, mental illness, low socioeconomic status and non-compliance ‘denial’. (vi) Comorbidities such chronic lung disease, cardiovascular disease. 4 Assess the severity of the present attack rapidly before any nebulizer therapy is given. (i) Severe attack is indicated by any one of the following: (a) inability to complete sentences in one breath (b) respiratory rate of ≥25 breaths/min (c) tachycardia of ≥120 beats/min (d) peak expiratory flow (PEF) rate or forced expiratory volume in 1 s (FEV1) 33–50% or less of predicted or known best (see Fig. 2.1). (ii) Life-threatening attack is indicated by any one of the following: (a) PEF under 33% of predicted or best (b) silent chest, cyanosis or feeble respiratory effort (c) bradycardia, dysrhythmia or hypotension (d) exhaustion, confusion or coma (e) oxygen saturation (SaO2) <92%, PaO2 <60 mmHg (below 8 kPa), normal PaCO2 34–45 mmHg (4.6–6.0 kPa), or worse a raised PaCO2 (imminently fatal). MANAGEMENT 1 Commence high-dose 40–60% oxygen via a face mask. Maintain the oxygen saturation above 94%. 2 Give salbutamol 5 mg via an oxygen-driven nebulizer, diluted with 3 mL normal saline. BREATHLESS PATIENT 66 General Medical Emergencies 3 Add ipratropium (Atrovent™) 500 g to a second dose of salbutamol 5 mg via the nebulizer if there is no response, or there is a severe attack. 4 Involve the senior ED doctor if the patient is still wheezy, and perform the following: (i) Give prednisolone 50 mg orally or hydrocortisone 200 mg i.v. if unable to swallow. (ii) Repeat the salbutamol 5 mg via the nebulizer up to every 15–30 min, or even via continuous nebulization. (iii) Send blood for white cell count (WCC), urea and electrolytes (U&Es) and blood sugar. Commence an i.v. infusion of normal saline for dehydration, with added potassium if low. 5 Perform a CXR only when a pneumothorax, pneumomediastinum or an infection with consolidation is suspected, or the patient is not improving. Women Height (cm) 190 183 175 167 160 Height (cm) 175 167 160 152 145 Peak expiratory flow rate (L/min) 650 600 550 500 450 400 15 20 25 30 35 40 45 50 55 60 65 70 Age (Years) Men Figure 2.1 Predicted normal peak expiratory flow rates in adult men and women. Reproduced by kind permission of Clement Clark International Ltd. BREATHLESS PATIENT General Medical Emergencies 67 6 Take an ABG only if the patient is deteriorating. ABG markers of a lifethreatening attack are: (i) Normal 34–45 mmHg (4.6–6 kPa), or high PaCO2 (imminently fatal). (ii) Severe hypoxia with PaO2 under 60 mmHg (8 kPa). (iii) Low pH (or high hydrogen ion concentration). (iv) Also check potassium, which may be low. 7 Call the ICU and/or the anaesthetist if the patient remains severe or has any life-threatening features. (i) Commence an i.v. bronchodilator under ECG control (a) give salbutamol 3–6 g/kg i.v. over 10 min, followed by an infusion of 5 mg salbutamol in 500 mL of 5% dextrose, i.e. 10 g/mL at 5 g/min (30 mL/h or 0.5 mL/min) initially. Titrate to response up to 20–40 g/min (120–240 mL/h). (ii) Give magnesium 2 g (8 mmol) i.v. over 20 min. (iii) Arrange immediate ICU or high-dependency unit (HDU) admission. 8 Meanwhile, admit under the medical team the initially severe patient who stabilizes with a PEF maintained over 50%. 9 Alternatively, in the patient with a mild (PEF over 75% predicted) or a moderate (PEF 50–75% predicted) initial attack who improves with prednisolone and nebulizers to a PEF over 75% for at least 1–2 h off treatment: (i) Discharge if the GP can provide follow-up within 2 days and the patient has salbutamol and steroid inhalers (and knows how to use them), plus prednisolone 50 mg orally once daily reduced over 5 days. (ii) Admit for overnight observation if there is any doubt about discharging the patient. COMMUNITY-ACQUIRED PNEUMONIA (CAP) DIAGNOSIS 1 Common organisms include Streptococcus pneumoniae (over 50%), ‘atypical’ organisms such as Legionella spp., Mycoplasma and Chlamydia, Haemophilus influenzae (especially in COPD), and viruses including influenza and chickenpox. (i) Less common are Staphylococcus aureus (may follow the ’flu), Gram-negatives (alcoholism) and Coxiella (Q fever). (ii) Consider melioidosis in tropical areas due to Burkholderia pseudomallei, or in diabetics, alcoholism and chronic renal failure (CRF). BREATHLESS PATIENT 68 General Medical Emergencies (iii) Finally remember tuberculosis, especially in alcoholism or social deprivation and also in human immunodeficiency virus (HIV) patients, who may also get Pneumocystis jiroveci (carinii) pneumonia. See page 153. 2 Risk factors for CAP include: age over 50 years; smoking; coexisting chronic respiratory, cardiac, renal, cerebrovascular or hepatic disease; diabetes; alcoholism; neoplasia; nursing home residency; and immunosuppression. 3 Fever, dyspnoea, productive cough, haemoptysis and pleuritic chest pain may occur. 4 Less obvious presentations include septicaemia with shock, acute confusional state particularly in the elderly, referred upper abdominal pain, or diarrhoea. 5 Examine for signs of lobar infection, with a dull percussion note and bronchial breathing. Usually there are only localized moist crepitations with diminished breath sounds. 6 Send blood for FBC, ELFTs, blood sugar and two sets of blood cultures, particularly if there is an intercurrent illness. (i) Only do an ABG when there are features of severe CAP (see below). 7 Perform a CXR, which may show diffuse shadowing unless there is lobar consolidation. (i) Look at the lateral, particularly for consolidation. 8 Features of severe CAP requiring hospital admission include one or more of the following: (i) Respiratory rate ≥30/min. (ii) Systolic BP <90 mmHg or diastolic BP <60 mmHg. (iii) Acute onset of confusion. (iv) Arterial or venous pH <7.35. (v) Oxygen saturation <92%, or PaO2 <60 mmHg (below 8 kPa). (vi) Multilobar CXR changes. (vii) Urea of >7 mmol/L, or WCC <4  109/L or >30  109/L. 9 Predictors of the need for intensive respiratory or vasopressor support (IRVS) are indicated by the SMART-COP score (see Table 2.6). (i) A score of 3–4 gives a 1:8 risk of needing IRVS. (ii) A score of ≥5 indicates severe CAP with a 1:3 risk of needing IRVS. BREATHLESS PATIENT General Medical Emergencies 69 Table 2.6 SMART-COP score for assessing severity, once community-acquired pneumonia is confirmed on CXR Score S Systolic BP <90 mmHg M Multi-lobar CXR involvement A Albumen <35 g/L R Respiratory rate – age-adjusted cut-offs: Age ≤50 yr >50 yr RR ≥25/min ≥30/min T Tachycardia ≥125/min C Confusion (new onset) O Oxygen low – age-adjusted cut-offs: Age ≤50 yr >50 yr PaO2 <70 mmHg <60 mmHg or SaO2 ≤93% ≤90% or (if on O2) PaO2/FiO2 <333 <250 P Arterial pH <7.35 2 points 1 point 1 point 1 point 1 point 1 point 2 points 2 points TOTAL SCORE = (Max 11) 0–2 points: Low risk of needing IRVS 3–4 points: Moderate (1 in 8) risk of needing IRVS 5–6 points: High (1 in 3) risk of needing IRVS ≥7 points: Very high (2 in 3) risk of needing IRVS A score of ≥5 indicates severe CAP. BP, blood pressure; CAP, community-acquired pneumonia; CXR, chest x-ray; FiO2, fractional inspired oxygen concentration; IRVS, intensive respiratory or vasopressor support; PaO2, partial pressure of oxygen (arterial); RR, respiratory rate; SaO2, arterial oxygen saturation. Adapted with permission from Charles PG, Wolfe R, Whitby M et al. (2008) SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clinical Infectious Diseases 47: 375–84. MANAGEMENT 1 Give the patient high-dose oxygen, unless there is a known history of obstructive airways disease (use 28%). Aim for an oxygen saturation above 92%. 2 Start antibiotics according to the severity of the pneumonia, and or based on local guidelines. BREATHLESS PATIENT 70 General Medical Emergencies 3 Mild CAP (i) Young, fit adults with single lobe involvement may well be able to return home on oral antibiotics: (a) give amoxicillin 1 g orally 8-hourly for 5–7 days, or if Mycoplasma pneumoniae, Chlamydophila pneumoniae or Legionella is suspected, give doxycycline 200 mg orally first dose then 100 mg orally daily for 5 days instead, or clarithromycin 250 mg orally 12-hourly for 5–7 days (b) add doxycycline or clarithromycin to the amoxicillin, if the patient fails to improve by 48 h, or if review is not going to be possible (c) give doxycycline or moxifloxacin 400 mg orally daily, if the patient has a history of immediate hypersensitivity to penicillin, depending on local practice. (ii) Inform the patient’s GP by fax or a letter if the patient is discharged, and arrange review within 1–2 days. 4 Moderate severity CAP (i) Most patients need admission to hospital and parenteral antibiotics: (a) give benzyl penicillin 1.2 g i.v. 6-hourly until significant improvement then change to amoxicillin 1 g orally 8-hourly for 7 days, plus either doxycycline 100 mg orally 12-hourly for 7 days, or clarithromycin 500 mg orally 12-hourly for 7 days (b) add gentamicin 5 mg/kg i.v. daily (assuming normal renal function) if Gram-negative bacilli are identified in blood or sputum. Alternatively, change the benzyl penicillin to ceftriaxone 1 g i.v. daily (c) substitute ceftriaxone 1 g i.v. daily for the penicillin, or use moxifloxacin 400 mg orally daily as monotherapy, if the patient has a history of immediate hypersensitivity to penicillin, depending on local practice (d) in tropical areas, if the patient has risk factors for melioidosis (diabetes/alcohol/CRF) give ceftriaxone 2 g i.v. daily i.v. plus gentamicin 5 mg/kg i.v. as a single dose. (e) consider adding oseltamivir 75 mg orally b.d. for 5 days during any ’flu outbreak. (ii) Refer the patient to the medical team. 5 Severe CAP, usually with a SMART-COP score ≥5 (i) Admit these patients with severe CAP to the HDU or ICU: (a) give ceftriaxone 1 g daily i.v.; or benzyl penicillin 1.2 g 4-hourly i.v. with gentamicin 5 mg/kg daily i.v., plus with either azithromycin 500 mg daily i.v. BREATHLESS PATIENT General Medical Emergencies 71 (b) use moxifloxacin 400 mg daily i.v. with azithromycin, if the patient has penicillin allergy or significant renal impairment (c) give meropenem 1 g 8-hourly i.v. plus azithromycin 500 mg daily i.v. for severe tropical pneumonia where B. pseudomallei (melioidosis) or Acinetobacter baumannii are prevalent. CHRONIC OBSTRUCTIVE PULMONARY DISEASE DIAGNOSIS 1 Causes of chronic bronchitis with emphysema (COPD) include smoking, environmental pollution, occupational exposure such as silica, repeated or chronic lung infection, and -1 antitrypsin deficiency. 2 Productive cough, dyspnoea, wheeze and reduced exercise tolerance worsen with exacerbations, until end-stage disease when there is minimal variation. 3 Ask about normal daily exercise capacity and level of dependence. (i) Enquire about current medication, home oxygen use, previous hospital admissions and associated cardiac disease. 4 Exacerbation of COPD. This is usually multi-factorial, so consider the many underlying causes possible: (i) Infection; bronchospasm; pneumothorax; pneumonia; right, left or biventricular heart failure; cardiac arrhythmia including AF; myocardial infarction. (ii) Non-compliance with medication including steroid underdosing; iatrogenic response to excess sedatives, opiates or inadvertent -blockade; environmental allergens or weather change; malignancy and a PE. 5 Examine for fever, lip pursing, tachypnoea, tachycardia and wheeze. Also look for: (i) Cyanosis, ruddy complexion and signs of right heart failure due to cor pulmonale with a raised JVP and peripheral oedema. (ii) Carbon dioxide retention causing headache, drowsiness, tremor and a bounding pulse. 6 Establish venous access and send blood for FBC, ELFTs, glucose and two sets of blood cultures if pyrexial. Attach a cardiac monitor and pulse oximeter to the patient. 7 Take an ABG if patient is clearly unwell, to look for hypoxia PaO2 <60 mmHg (8 kPa), hypercarbia PaCO2 >45 mmHg (6 kPa) and a raised bicarbonate indicating compensated respiratory acidosis. 8 Perform an ECG and look for large P waves (P pulmonale), right ventricular hypertrophy or strain (cor pulmonale), and signs of ischaemia with ST and T wave changes. BREATHLESS PATIENT 72 General Medical Emergencies 9 Perform bedside lung function testing for PEF, FEV1 and FVC to compare with previous respiratory function tests, and to follow the response to treatment. 10 Request a CXR which may show hyperinflation, bullae, atelectasis, consolidation, pneumothorax, heart failure or a lung mass. MANAGEMENT 1 Commence controlled oxygen therapy initially at 28% via a Venturi mask if there is evidence of chronic carbon dioxide retention, with a raised PaCO2 and bicarbonate. Aim for an oxygen saturation over 90%. (i) Otherwise give higher dose 40–60% oxygen via face mask to treat hypoxaemia. Watch out for deterioration and a rising PaCO2. 2 Give salbutamol 5 mg via a nebulizer for bronchospasm repeated as needed, and add ipratropium (Atrovent™) 500 g to the initial nebulizer then 6-hourly. 3 Give prednisolone 50 mg orally or hydrocortisone 200 mg i.v. if unable to swallow, for bronchospasm and or if on long-term inhaled or oral steroids. 4 Treat infection with amoxicillin 500 mg orally t.d.s., or doxycycline 100 mg orally b.d. both for 5 days. 5 Give frusemide (furosemide) 40 mg i.v. if heart failure is suspected. 6 Admit under the medical team. 7 Call urgent senior ED doctor help if there is exhaustion, agitation or confusion; or a rising PaCO2 and a falling pH. Involve the intensive care team. (i) Commence non-invasive ventilation (NIV) if there are trained and experienced staff to supervise. PNEUMOTHORAX DIAGNOSIS 1 Spontaneous pneumothorax that occurs in an otherwise healthy patient with no lung disease, particularly in taller people, is designated a ‘primary’ pneumothorax. 2 Spontaneous pneumothorax that occurs in a patient with chronic lung disease (CLD) is termed a ‘secondary’ pneumothorax, and is associated with asthma, emphysema, fibrotic or bullous lung disease including cystic fibrosis and Marfan’s syndrome. (i) In addition, this includes patients aged over 50 years who may have unrecognized underlying lung disease. 3 Spontaneous pneumothoraces are also much more common in smokers. 4 Pneumothorax may be due to both penetrating or blunt trauma. (i) See p.231 for discussion on the management of traumatic pneumothorax. BREATHLESS PATIENT General Medical Emergencies 73 5 A spontaneous primary pneumothorax may cause only slight dyspnoea and pleuritic chest pain in a fit patient, even when the whole lung is collapsed. (i) ‘Significant’ dyspnoea is considered any deterioration in usual exercise tolerance. (ii) Significant dyspnoea or breathlessness is more common in a secondary pneumothorax with underlying chronic lung disease, even if small. 6 Look for reduced chest expansion on the affected side, increased resonance on percussion, and diminished breath sounds. Beware that lateralizing signs may be subtle and difficult to confirm. 7 Request a standard inspiratory CXR in all cases. (i) Do not wait for this if there are signs of tension, but proceed immediately to insert a wide-bore cannula or intercostal drain (see p. 471). (ii) Assess the size of the pneumothorax on the CXR: (a) small is a visible rim of <2 cm (b) large is a visible air rim ≥2 cm around all the lung edge, that represents over 50% of lung volume lost (c) expiratory CXRs are no longer routine. MANAGEMENT This is determined by the presence or absence of chronic lung disease (i.e. a secondary or a primary pneumothorax), the degree of dyspnoea (significant or not), and by the size of the pneumothorax (large or small). 1 Discharge a patient with a small ‘primary’ pneumothorax <2 cm, with no CLD and no significant dyspnoea. No active interventional management is indicated. (i) Arrange follow-up by the GP for repeat CXR within 7–14 days, and refer to a respiratory physician. (ii) Advise the patient to stop smoking, and to return immediately if they develop significant dyspnoea. (iii) Advise them not to fly for at least 1 week after the CXR has returned to normal, and never to go SCUBA diving (unless they have had bilateral surgical pleurectomies). 2 Also take no active intervention in a patient with underlying lung disease, i.e. a ‘secondary’ pneumothorax, who has a small pneumothorax <2 cm with no significant dyspnoea. (i) However, admit for observation for 24 h, and start high-flow oxygen via a face mask, unless they have COPD in which case use 28%. (ii) Repeat the CXR after 6–12 h and discharge after 24 h only if they remain asymptomatic and the pneumothorax is not progressing. Arrange early respiratory or medical follow-up within 7 days. BREATHLESS PATIENT 74 General Medical Emergencies (iii) Perform needle aspiration if the air leak has enlarged, or the patient develops significant breathlessness. Alternatively, insert a small-bore (<14 F) chest drain intercostal catheter (ICC) using a Seldinger technique, and admit the patient under the medical team (see p.471). 3 Needle aspiration (thoracentesis) Perform this for a symptomatic primary pneumothorax (no CLD) with dyspnoea, whether large or small; and in a small secondary (with CLD) pneumothorax less than 2 cm with minimal breathlessness if aged under 50 years. (i) Infiltrate local anaesthetic down to the pleura in the second intercostal space in the mid-clavicular line. (ii) Insert a 16-gauge cannula into the pleural cavity, withdraw the needle, and connect to a 50 mL syringe with three-way tap (see p.471) (a) alternatively use a proprietary chest aspiration kit, with special fenestrated cannula and one-way valve. (iii) Aspirate air until resistance is felt, the patient coughs excessively, or more than 2500 mL is aspirated. (iv) Repeat the CXR; if the lung has re-expanded, observe and repeat the CXR again after 6 h: (a) discharge patients with a primary pneumothorax if the lung remains expanded, and arrange follow-up with the GP and give discharge advice as above (b) admit patients with CLD and a secondary pneumothorax overnight even if aspiration was successful, for continued observation (c) proceed directly to insertion of an ICC if aspiration fails, suggesting a persistent air leak, particularly with a secondary pneumothorax. 4 Intercostal catheter This is therefore indicated for: (i) Failed needle aspiration, e.g. with more than just a small residual rim of air around the lung. (ii) Any secondary pneumothorax in a patient with CLD causing significant dyspnoea, or if aged >50 years. (iii) Tension pneumothorax following initial needle thoracocentesis. (iv) Traumatic pneumothorax or haemothorax (see p. 231). (v) Any pneumothorax prior to anaesthesia or positive-pressure ventilation. 5 ICC insertion (see p. 473) (i) Use a small-bore 8–14 French ICC inserted under a Seldinger technique. BREATHLESS PATIENT General Medical Emergencies 75 (ii) Alternatively use a small standard size 16–22 French gauge drain directed apically for a simple pneumothorax, or a larger 28–32 French gauge directed posterior basally for a haemothorax. (iii) Admit under the care of the medical team. PULMONARY EMBOLUS See page 51. PULMONARY OEDEMA DIAGNOSIS 1 Pulmonary oedema is usually caused by left ventricular failure due to myocardial infarction, hypertension, an arrhythmia, valvular disease, myocarditis or fluid overload. 2 Occasional non-cardiogenic causes include septicaemia, uraemia, head injury, intracranial haemorrhage, near drowning, and inhalation of smoke or noxious gases. 3 The onset may be precipitate with breathlessness, cough, orthopnoea, paroxysmal nocturnal dyspnoea (PND) and dyspnoea at rest. 4 The patient is clammy, distressed and prefers to sit upright. Look for wheeze, tachypnoea sometimes with pink froth, tachycardia, basal crepitations and a triple rhythm or gallop. 5 Establish venous access and send blood for FBC, ELFTs and cardiac biomarkers, although they do not influence the initial management. Attach a cardiac monitor and pulse oximeter to the patient. 6 Perform an ECG to look for acute ischaemia, arrhythmias and evidence of underlying cardiac disease. 7 Request a CXR that shows engorged upper-lobe veins, a perihilar ‘bat’s wing’ haze, cardiomegaly, septal Kerley B lines, and small bilateral pleural effusions. MANAGEMENT 1 Sit the patient upright and give 40–60% oxygen, unless the patient is known to have chronic bronchitis, in which case 28% oxygen should be used. Aim for an oxygen saturation above 94%. 2 Give GTN 150–300 g sublingually, which may be repeated. Remove the tablet if excessive hypotension (systolic BP <100 mmHg) occurs. 3 Give frusemide (furosemide) 40 mg i.v., or twice their usual oral daily dose i.v. if already on frusemide (furosemide). 4 Get senior ED doctor help in refractory cases, repeat the frusemide (furosemide), and commence a GTN infusion, provided the patient is not hypotensive. UPPER GASTROINTESTINAL HAEMORRHAGE 76 General Medical Emergencies (i) Add GTN 200 mg to 500 mL of 5% dextrose, i.e. 400 g/mL, using a glass bottle and low-absorption polyethylene infusion set. (ii) Infuse initially at 1 mL/h, maintaining the systolic BP above 100 mmHg. Progressively increase to ≥20 mL/h, avoiding hypotension. 5 Commence mask continuous positive airways pressure (CPAP) respiratory support: (i) Use a dedicated, high-flow fresh gas circuit, tight-fitting mask and variable resistor valve, starting at 5–10 cmH2O. (ii) A trained nurse must remain in attendance at all times, as some patients will not tolerate the mask. (iii) Never simply use wall oxygen with a black anaesthetic mask and head harness, as this will asphyxiate the patient due to inadequate fresh gas flow. 6 Morphine 0.5–2.5 mg i.v. with an antiemetic such as metoclopramide 10 mg i.v. is rarely helpful, and it may further obtund the patient particularly if the patient is tired or has COPD. 7 Admit the patient under the medical team. ACUTE UPPER AIRWAY OBSTRUCTION See page 13. UPPER GASTROINTESTINAL HAEMORRHAGE DIAGNOSIS 1 Causes of upper gastrointestinal haemorrhage include: (i) Peptic ulceration (over 40% of cases): (a) duodenal ulcer (DU) (b) gastric ulcer (GU) less common. (ii) Gastric erosions or gastritis: (a) post-alcohol (b) drug-induced (salicylates, non-steroidal anti-inflammatory drugs [NSAIDs], steroids). (iii) Reflux oesophagitis. (iv) Bleeding oesophageal or gastric varices associated with portal hypertension (due to cirrhosis, often alcoholic). (v) Mallory–Weiss tear (oesophageal tear following vomiting or retching). UPPER GASTROINTESTINAL HAEMORRHAGE General Medical Emergencies 77 (vi) Miscellaneous, including gastric neoplasm, blood coagulation disorders, angiodysplasia and aorto-enteric fistula in a patient with a past history of an abdominal aortic aneurysm (AAA) repair. 2 Mortality is 10–14%, highest with age over 60 years, variceal origin, comorbid disease, shock and coagulopathy. 3 Patients can present in a variety of ways: (i) Haematemesis: (a) fresh red blood (b) altered blood ‘coffee grounds’. (ii) Melaena (sticky black, tarry stool). (iii) Haematochezia (maroon-coloured or red rectal bleeding). (iv) Collapse and shock. (v) Syncope and postural hypotension. (vi) Fatigue, dyspnoea, angina, etc. 4 Ask about previous gastrointestinal bleeding, recent endoscopy, use of drugs and alcohol, and known chronic liver disease. 5 Look for signs of volume depletion such as pallor and sweating, tachycardia, hypotension and postural hypotension. (i) Palpate for abdominal tenderness, organomegaly, masses, and perform a rectal examination. (ii) Note in particular any signs of chronic liver disease including jaundice, bruising, spider naevi, palmar erythema, clubbing, gynaecomastia, hepatomegaly and encephalopathy. (iii) Examine for splenomegaly and ascites as signs of portal hypertension. 5 Establish venous access with a large-bore 14-gauge i.v. cannula, and attach a pulse oximeter and cardiac monitor to the patient. (i) Take blood for FBC, U&Es, blood sugar, LFTs, clotting studies including a prothrombin index (PTI) and cross-match from 2–4 units of blood, according to the presumed aetiology and degree of shock. MANAGEMENT 1 Commence high-dose oxygen via a face mask. Maintain the oxygen saturation above 94%. 2 Begin fluid replacement: (i) Start with normal saline 10–20 mL/kg, aiming for a urine output of 0.5–1 mL/kg per hour. (ii) Give cross-matched blood when it is available if the patient is shocked, or if the bleeding is continuing. (iii) Use O-negative blood if the situation is desperate. DIABETIC COMA AND PRE-COMA 78 General Medical Emergencies 3 Start a proton-pump inhibitor if peptic ulcer disease is likely. Give omeprazole or pantoprazole 80 mg i.v. followed by an infusion at 8 mg/h. (i) There is no supporting evidence for an H2-antagonist. 4 Give octreotide 50 g i.v. then 50 g/h if varices are known, or are likely from the presence of chronic liver disease and portal hypertension. Also give ceftriaxone 1 g i.v. in chronic liver disease. 5 Arrange for an urgent endoscopy, particularly in patients who have sus - pected varices, continue to bleed, remain unstable or are aged >60 years. Contact the intensive care team. (i) Endoscopy will differentiate the cause of the bleeding and allow immediate thermal or injection therapy where appropriate, or banding for varices. 6 Otherwise admit patients who have stopped bleeding and are haemodynamically stable under the medical team, for endoscopy ideally within 24 h. DIABETIC COMA AND PRE-COMA Hypoglycaemia rapidly produces coma in people with diabetes, compared with the slower onset of altered consciousness in diabetic ketoacidosis and hyperglycaemic, hyperosmolar non-ketotic syndrome (HHNS). DIABETIC KETOACIDOSIS DIAGNOSIS 1 Diabetic ketoacidosis (DKA) may occur in a known diabetic person precipitated by infection, surgery, trauma, pancreatitis, myocardial infarction, cerebral infarction or inadequate insulin therapy, e.g. insulin stopped in an unwell diabetic patient ‘because he was not eating’! 2 Alternatively, it may arise de novo in an undiagnosed diabetic, heralded by polyuria, polydipsia, weight loss, lethargy, abdominal pain or coma. 3 The predominant features arise from salt and water depletion and acidosis, hence there is dry skin, tachycardia, hypotension (especially postural) and deep sighing respirations (Kussmaul breathing). (i) The ketones may be detected on the breath as a sickly sweet, fruity smell. Warning: inserting a central venous pressure (CVP) line in a hypotensive, shocked patient is difficult and dangerous. Leave it until initial transfusion is under way for a skilled doctor to perform under ultrasound guidance (see p. 476). ! DIABETIC COMA AND PRE-COMA General Medical Emergencies 79 4 Establish venous access and send blood urgently for FBC, ELFTs, blood glucose and blood cultures if infection is suspected. Attach a cardiac monitor and pulse oximeter to the patient. 5 Take blood for a bedside venous blood gas (VBG) or an ABG, and organize an ECG, CXR and a midstream urine (MSU). (i) Look at the ECG for an early indication of critical hyperkalaemia with peaked T waves, QRS widening, then absent P waves and finally a ‘sine wave’ trace (see p. 132). MANAGEMENT 1 Give high-dose oxygen via a face mask and aim for an oxygen saturation above 94%. 2 Start an i.v. infusion and run in normal saline 1 L in the first hour, followed by a further 500 mL/h for the next 4 h if the diagnosis is confirmed. (i) Continue the i.v. normal saline resuscitation until the blood sugar is ≤15 mmol/L, then change to 5% dextrose but continue the insulin infusion until the ketones are cleared. (ii) Aim to replace the fluid deficit steadily over the first 24 h. 3 Commence short-acting soluble insulin therapy by infusion. (i) Add 50 units soluble insulin to 50 mL normal saline, i.e. 1 unit/mL. (ii) Run at 0.1 units/kg/h, i.e. 5–7 units/h or 5–7 mL/h via an infusion pump. 4 Add potassium to the i.v. fluid when the plasma K level is known. This should be within 30 min: (i) Potassium is <3.0 mmol/L – add potassium chloride (KCl) 40 mmol/L (3 g KCl). Must give via an infusion pump. Repeat the serum level within the hour and adjust rate. (ii) Potassium is 3.0–4.0 mmol/L – add 26.8 mmol KCl/L (2 g KCl). (iii) Potassium is 4.0–5.0 mmol/L – add 20 mmol KCl/L (1.5 g KCl). (iv) Potassium is 5.0–6.0 mmol/L – add 13.4 mmol KCl/L (1 g KCl). (v) Omit the potassium if: (a) no urine output is established (unusual) (b) the serum level is >6.0 mmol/L (c) the ECG shows peaked T waves or QRS complex widening. 5 Refer the patient to the medical team or ICU. Remember to have looked for any underlying precipitating factor(s) for the DKA. 6 Do not give i.v. sodium bicarbonate except on the advice of the senior ED doctor. Tip: every patient who presents with abdominal pain, vomiting or thirst must have urine tested for sugar and ketones. ✓ ALTERED CONSCIOUS LEVEL 80 General Medical Emergencies (i) It may be considered if the pH remains <7.0, particularly with circulatory failure. HYPERGLYCAEMIC, HYPEROSMOLAR NON-KETOTIC SYNDROME DIAGNOSIS 1 HHNS is more common in the elderly, non-insulin-dependent patient, with a more gradual onset than DKA. 2 It may be precipitated by infection, myocardial infarction, a stroke or by thiazide diuretic use and steroids, and like DKA, may occur in a previously undiagnosed patient. 3 The patient presents with an altered level of consciousness, profound dehydration and may develop seizures or focal neurological signs. Mortality is 20–40%, compared to DKA where it is <5% in younger patients. 4 Blood glucose and serum osmolarity tend to be higher than in DKA. The osmolarity usually exceeds 350 mOsmol/L. (i) Estimate the osmolarity by 2(Na + K) + urea + glucose (all units in mmol/L). 5 Make certain to do an ECG, CXR and an MSU early. MANAGEMENT 1 This is comparable to DKA (see above). 2 Give i.v. normal saline or half-normal saline if the serum sodium exceeds 150 mmol/L, at a similar or slower rate to DKA. Beware of over-rapid rehydration causing pulmonary oedema. 3 Use a slower insulin infusion rate of 0.05 units/kg per hour, i.e. 2–3 units/h, as there is increased insulin sensitivity compared to DKA. Lower potassium replacement rates are also usual. 4 Commence prophylactic heparin, either unfractionated (UF) heparin 5000 units i.v. bolus then an infusion at 1000 units/h, or LMW heparin such as enoxaparin 1.5 mg/kg per day, assuming there is no active bleeding, particularly intracerebral. 5 Admit under the care of the medical team. ALTERED CONSCIOUS LEVEL Patients with an altered conscious level frequently present to the ED. Although history taking is compromised, a methodical, careful approach is essential using information from the family, friends, passers-by, the police, ambulance and previous medical records. ALTERED CONSCIOUS LEVEL General Medical Emergencies 81 The following categories are covered, although they may overlap: ● Confused patient ● Alcohol-related medical problems ● Patient with an altered conscious level and smelling of alcohol ● Alcohol withdrawal. The collapsed or unconscious patient in coma is covered separately in Section I on p. 24. CONFUSED PATIENT ‘Confusion’ or delirium is a transient global disorder of cognition. It is a syndrome (not a diagnosis) with multiple causes that describes a state of clouding of consciousness or disturbed awareness, which may fluctuate. DIAGNOSIS 1 An acute confusional state may go unrecognized or be mistaken for dementia or depression particularly in the elderly (see p. 119), or for mania and even acute schizophrenia. 2 There is usually abrupt onset of: (i) Clouding of consciousness that may fluctuate, disorientation in time and place, impaired memory, visual, olfactory or tactile hallucinations and illusions. (ii) Difficulty maintaining attention, restlessness, irritability, emotional lability and poor comprehension. (iii) Hyperactive state with increased arousal and reversed sleep-wake cycle, or hypoactive and withdrawn. 3 Causes of confusion. (i) Hypoxia (a) chest infection, COPD, pulmonary embolus, cardiac failure (b) respiratory depression from drugs, or weakness, e.g. Guillain–Barré syndrome, myasthenia gravis or muscular dystrophy (c) chest injury or head injury (d) drowning, smoke inhalation. (ii) Drugs (a) intoxication or withdrawal from alcohol, sedatives, cocaine, amphetamines, phencyclidine (b) side effects (especially in the elderly and with polypharmacy) of analgesics, anticonvulsants, psychotropics, digoxin, anticholinergics and antiparkinsonian drugs such as benzhexol (trihexyphenidyl) and levodopa (c) inappropriate use, such as steroids particularly anabolic. (iii) Cerebral (a) meningitis, encephalitis (b) head injury ALTERED CONSCIOUS LEVEL 82 General Medical Emergencies (c) post-ictal state, complex partial (temporal lobe) seizures (d) cerebrovascular accident, subarachnoid haemorrhage (e) space-occupying lesion, e.g. tumour, abscess or haematoma (f) hypertensive encephalopathy (g) vasculitis such as systemic lupus erythematosus (SLE). (iv) Metabolic (a) respiratory, cardiac, renal or liver failure (b) electrolyte disorder, such as hyponatraemia, hypercalcaemia or hypernatraemia (c) vitamin deficiency, e.g. thiamine (Wernicke’s encephalopathy), nicotinic acid (pellagra) or B12 (d) acute intermittent porphyria. (v) Endocrine (a) hypoglycaemia or hyperglycaemia (b) thyrotoxicosis, myxoedema, Cushing’s syndrome, hyperparathyroidism, Addison’s disease. (vi) Septicaemia (a) urinary tract, biliary, meningococcaemia or malaria. (vii) Situational (a) post-operative (multi-factorial including drugs, hypoxia, infection, pain, etc.) (b) faecal impaction, urinary retention or change in environment in the elderly (rarely the sole cause). 4 Build up a picture of which condition or conditions are responsible from a detailed history and examination. 5 Record the vital signs including temperature, respiratory rate, pulse, blood pressure and Glasgow Coma Scale (GCS) score. (i) Any abnormality of the vital signs should be assumed to have an organic cause until proven otherwise. 6 Document a formal Mini-Mental State Examination (see Table 2.7). (i) This records cognitive impairment by assessing orientation, attention and calculation, immediate and short- term recall, language, and ability to follow simple verbal and written commands. (ii) A score of ≤20 suggests cognitive impairment, and the possibility of an organic cause. 7 Perform some or all of the following investigations based on the suspected aetiology. Always exclude hypoglycaemia: (i) FBC, coagulation profile. (ii) U&Es, blood sugar, liver function tests, calcium, thyroid function tests. (iii) Drug screen including ethanol. (iv) ABGs. ALTERED CONSCIOUS LEVEL General Medical Emergencies 83 (v) Blood cultures, MSU. (vi) ECG, CXR. (vii) CT brain scan. (viii) Lumbar puncture. See page 482. Table 2.7 Mini-Mental State Examination (MMSE) Cognition tested Score Orientation (10 points) 1. What is the date? 1 What is the day? 1 What is the month? 1 What is the year? 1 What is the season? 1 2. What is the name of this building? 1 What floor of the building are we on? 1 What city are we in? 1 What state are we in? 1 What country are we in? 1 Registration (3 points) 3. I am going to name three objects. After I have said them I want you to repeat them. Remember what they are because I am going to ask you to name them in a few minutes. Apple. Table. Penny. (Code the first attempt and then repeat the answers until the patient learns all three) Apple 1 Table 1 Penny 1 Attention and calculation (5 points max) 4. Either: Can you subtract 7 from 100, and then subtract 7 from the answer you get and keep subtracting until I tell you to stop? 93 1 86 1 79 1 72 1 65 1 5. Or: I’m going to spell a word forwards and I want you to spell it backwards. The word is W-O-R-L-D. Now you spell it backwards (Repeat if necessary) D 1 L 1 R 1 O 1 W 1 ALTERED CONSCIOUS LEVEL 84 General Medical Emergencies MANAGEMENT 1 Avoid the temptation to simply sedate the confused patient, without looking carefully for the underlying cause(s). 2 Admit all patients under the appropriate specialist team. Recall (3 points) 6. Now what were the three objects I asked you to remember? Apple 1 Table 1 Penny 1 Language (9 points) 7. What is this called? (Show wristwatch) 1 What is this called? (Show pencil) 1 8. I’d like you to repeat a phrase after me: No ifs ands or buts 1 9. Read the words on the bottom of this page and do what it says Closes eyes 1 10. (Read the full statement below before handing the respondent a piece of paper. Do not repeat or coach) I’m going to give you a piece of paper. What I want you to do is take the paper in you right hand, fold it in half and put the paper on your lap Takes with right hand 1 Folds in half 1 Puts on lap 1 11. Write a complete sentence on this piece of paper. The sentence should have a subject, verb and make sense. Spelling and grammatical errors are OK 1 12. Here is a drawing. Please copy the drawing on the same piece of paper (Hand the respondent a drawing of two intersecting pentagons) Correct if two five-sided pentagons intersect to make a foursided figure 1 Total score (out of 30) CLOSE YOUR EYES A score of 20 or less indicates cognitive impairment. Higher scores are expected in the well-educated, and lower scores in the elderly, the uneducated, and the mentally impaired. From Folstein MF, Folstein SE, McHugh PR (1975) Mini-Mental State. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 12:189–98. Table 2.7 contd ALTERED CONSCIOUS LEVEL General Medical Emergencies 85 ALCOHOL-RELATED MEDICAL PROBLEMS Acute alcohol intoxication is causally related to all types of trauma, including motor vehicle crashes, incidents in the home, deliberate self-harm, assaults, drownings, child abuse and falls in the elderly. Chronic use also predisposes to a variety of medical conditions, and sudden reduction in intake causes withdrawal problems. MEASUREMENT OF ALCOHOL LEVEL ● Various methods are available, including a breath test, a urine test, and a blood level test. None is admissible in a court of law, unless special forensic kits are used under police direction (see p. 453). ● The Australian legal limit to drive is 0.05 g/100 mL in every state or territory. ● The British legal limit for driving is a blood alcohol level below 80 mg% (0.08 g/100mL). Intoxication is marked above a level of 150 mg% (0.15 g/100mL), and coma usually occurs above a level of 300 mg% (0.30 g/100mL). PATIENT WITH AN ALTERED CONSCIOUS LEVEL AND SMELLING OF ALCOHOL DIAGNOSIS AND MANAGEMENT Never assume that a confused, obtunded or unconscious patient smelling of alcohol is simply ‘drunk’ until you have considered and excluded all of the following: 1 Hypoglycaemia (i) Check a blood sugar, and give 50% dextrose 50 mL i.v. if it is low. (ii) This may precipitate worsening of the confusion due to a Wernicke’s encephalopathy. (iii) Wernicke’s is associated with alcohol abuse and malnutrition, and causes confusion, ataxia, nystagmus, and bilateral lateral rectus palsy (a) give thiamine 100 mg i.v. immediately (b) this should be routine in suspected alcoholism and in the malnourished patient receiving dextrose. 2 Head injury (i) Always remember the possibility of an extradural or subdural haematoma from a head injury. (ii) Commence neurological observations and perform a CT head scan if confusion persists or there is a deteriorating conscious level (see p. 31). (a) a skull X-ray is reasonable only in the absence of a CT scan and may show a fracture, but if normal it does not exclude intracranial injury. ALTERED CONSCIOUS LEVEL 86 General Medical Emergencies 3 Other general medical problems in patients who drink (i) Epileptic seizure. (ii) Acute poisoning. (iii) Meningitis, chest infection, etc. (iv) Cerebral haemorrhage. (v) Unrecognized trauma such as a rib fracture, wrist fracture, abdominal injury. (vi) Hypothermia. 4 An acute condition more prevalent in chronic alcoholics (i) Pneumococcal pneumonia, aspiration pneumonia or tuberculosis. (ii) Cardiac arrhythmia, cardiomyopathy. (iii) Gastrointestinal haemorrhage, including variceal. (iv) Pancreatitis. (v) Liver failure. (vi) Hypokalaemia, hypomagnesaemia, hypocalcaemia. (vii) Withdrawal seizures or delirium tremens. (viii) Ketoacidosis. (ix) Acidic acidosis. (x) Renal failure. (xi) Wernicke’s encephalopathy. 5 Thus, many patients smelling of alcohol will require admission to exclude the above conditions. 6 Always admit if in doubt, and do not discharge until medically well, sober and safe. ALCOHOL WITHDRAWAL This is caused by an absolute or relative decrease in the usual intake of alcohol, that may be intentional through lack of funds or unintentional following detention in hospital or by the police. DIAGNOSIS AND MANAGEMENT Two conditions are recognized: the alcohol withdrawal syndrome, and the progression to delirium tremens. 1 Alcohol withdrawal syndrome (i) This is common, occurring within 12 h of abstinence and lasting a few days. It is characterized by agitation, irritability, fine tremor, sweats and tachycardia. (ii) Commence diazepam 10–20 mg orally 2–6-hourly until the patient is comfortable, plus thiamine 100 mg i.v. or i.m. once daily. ACUTE NEUROLOGICAL CONDITIONS General Medical Emergencies 87 (iii) Control seizures with midazolam 0.05–0.1 mg/kg up to 10 mg i.v., or diazepam 0.1–0.2 mg/kg up to 20 mg i.v., or lorazepam 0.07 mg/kg up to 4 mg i.v., after excluding hypoglycaemia. (iv) Refer the patient to the medical team. 2 Delirium tremens (i) This is uncommon, occurring 72 h after abstinence. There is clouding of consciousness, terrifying visual hallucinations, gross tremor, autonomic hyperactivity with tachycardia and cardiac arrhythmias, dilated pupils, fever, sweating, dehydration, and grand mal seizures that may be prolonged (status epilepticus). (ii) Delirium tremens is a medical emergency (a) control seizures with midazolam, diazepam or lorazepam i.v. (see doses above) (b) exclude other causes of status epilepticus such as head injury and meningitis (see p. 91). (iii) Replace fluid and electrolyte losses, avoiding excessive normal saline in liver failure. Give thiamine 100 mg i.v. once daily. (iv) Refer all patients immediately to the ICU. ACUTE NEUROLOGICAL CONDITIONS The following neurological conditions frequently present to the ED: ● Syncope (faint) ● Seizure (fit) ● Generalized convulsive status epilepticus ● TIA ● Stroke. Headache is covered separately on page 97. SYNCOPE DIAGNOSIS 1 Syncope or ‘faint’ is a sudden, transient loss of consciousness and postural tone due to reduced cerebral perfusion, with subsequent spontaneous recovery. (i) A brief tonic-clonic seizure may follow if cerebral perfusion remains impaired. Warning: never dispense a benzodiazepine supply or chlormethiazole (clomethiazole) capsules in the ED to take home. They are reserved for inpatient detoxification programmes only. ! ACUTE NEUROLOGICAL CONDITIONS 88 General Medical Emergencies 2 A faint may be difficult to distinguish from a seizure or acute vertigo, so an eye-witness account is vital. Always interview ambulance crew or accompanying adults. 3 Causes vary from benign to imminently life threatening. The aim is to always exclude the most serious conditions such as cardiac-related, hypovolaemia or subarachnoid haemorrhage: (i) Cardiac (a) arrhythmia, either a tachycardia or a bradycardia ‘Stokes– Adams attack’ (b) myocardial infarction (c) stenotic valve lesion (especially aortic stenosis) (d) hypertrophic cardiomyopathy (e) drug toxicity or side effect – prolonged QT from sotalol, tricyclics, erythromycin, etc. – calcium-channel or -blocker. (ii) Postural (orthostatic) hypotension (a) haemorrhage or fluid loss: – vomiting and or diarrhoea, with dehydration – haematemesis and melaena – concealed haemorrhage (such as an abdominal aortic aneurysm or ectopic pregnancy) – hypoadrenalism (Addison’s), hypopituitarism, pancreatitis ‘third spacing’ (b) autonomic dysfunction – Parkinson’s disease (multiple systems atrophy), diabetes (c) drugs: – antihypertensives, e.g. angiotensin-converting enzyme (ACE) inhibitors, prazosin – diuretics – nitrates – levodopa – phenothiazines – tricyclic antidepressants. (iii) Vascular (a) pulmonary embolism (b) carotid sinus hypersensitivity. (iv) Neurological (a) subarachnoid haemorrhage (b) vertebrobasilar insufficiency, as part of a transient ischaemic attack (TIA). (v) Cough, micturition or defecation syncope. ACUTE NEUROLOGICAL CONDITIONS General Medical Emergencies 89 (vi) Vasovagal (neurocardiogenic) – ‘simple’ faint, triggered by heat, pain or emotion. Do not diagnose if over 45 years old, but look first for the more sinister causes above. (vii) Hypoglycaemia (relative). 4 Examine all patients carefully, looking for hypotension (including postural), a cardiac lesion, an abdominal mass or tenderness, and focal neurological signs. 5 Check the blood glucose test strip for hypoglycaemia, and perform an ECG. 6 Request other investigations only as indicated clinically such as FBC, U&Es, cardiac biomarkers, pregnancy test, CXR and CT scan. MANAGEMENT 1 Refer the patient to the medical (or surgical) team for admission if a serious cause is possible, particularly a patient aged over 75 years. Be sure to admit patients with any one or more of: (i) History of congestive heart failure. (ii) Shortness of breath. (iii) Triage systolic BP <90 mmHg. (iv) Abnormal ECG. (v) Haematocrit <30%. 2 Refer other patients with no clear inciting history, a normal examination and a normal ECG for outpatient follow-up if no immediately life-threatening cause for syncope is found. (i) A 24-hour ambulatory ECG (Holter monitor) may help, particularly in unexplained recurrent syncope. 3 Inform the GP by fax or letter if the patient is discharged and arrange early follow-up. SEIZURE (FIT) DIAGNOSIS 1 An eye-witness account is essential to establish the correct diagnosis. Helpful indicators of an epileptic seizure having occurred, rather than a faint, a fall or an episode of vertigo are: (i) Preceding aura, or proceeding drowsiness. (ii) Bitten tongue, urinary incontinence. (iii) Known seizure disorder. 2 The most common causes of a seizure in a known epileptic are: (i) Not taking their medication, or rarely medication toxicity. (ii) Alcohol abuse, either excess or withdrawal. (iii) Intercurrent infection (remember meningitis). (iv) Head injury. (v) Hypoglycaemia. ACUTE NEUROLOGICAL CONDITIONS 90 General Medical Emergencies 3 Exclude all the following ‘acute symptomatic’ secondary causes of a seizure in any patient presenting with a first seizure or a sporadic seizure: (i) Hypoglycaemia. (ii) Head injury. (iii) Hypoxia. (iv) Infection – especially meningitis, encephalitis, cerebral abscess, HIV or a febrile seizure in a child. (v) Acute poisoning, e.g. alcohol, tricyclic antidepressants, anticholinergics, theophylline, cocaine, amphetamine and isoniazid. (vi) Drug withdrawal, e.g. alcohol, benzodiazepine, narcotics, cocaine. (vii) Intracranial pathology: (a) space-occupying lesion (b) cerebral ischaemia (c) subarachnoid or intracerebral haemorrhage. (viii) Hyponatraemia, hypocalcaemia, uraemia and eclampsia. 4 Check a blood glucose test strip. (i) Give 50% dextrose 50 mL i.v. if it is low, after taking blood for a laboratory glucose estimation, or give glucagon 1 mg i.m. when venous access is impossible. 5 Insert an i.v. cannula and take blood for FBC, U&Es, LFTs, and a drug and alcohol screen. (i) Proceed to ABGs, blood cultures, ECG, CXR and CT head scan as indicated clinically, and attach a cardiac monitor and pulse oximeter to the patient. (ii) Send urgent anticonvulsant levels if the patient is on treatment. MANAGEMENT 1 Give high-dose oxygen via a face mask. Aim for an oxygen saturation above 94%. 2 Make sure the head is protected from harm and turn the patient semi-prone. Do not attempt to wedge the mouth open. 3 Give midazolam 0.05–0.1 mg/kg up to 10 mg i.v., diazepam 0.1–0.2 mg/kg up to 20 mg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. if the patient is having a seizure, or if the seizure recurs. 4 Refer the following patients for admission to the medical team: (i) Suspected underlying cause such as meningitis, tumour, etc. (ii) A seizure exceeding 5 min, or recurrent seizures, especially if there is no full recovery between them. (iii) Residual focal central nervous system (CNS) signs. (iv) Seizure following a head injury (refer to the surgeons). ACUTE NEUROLOGICAL CONDITIONS General Medical Emergencies 91 5 Discharge home a known previous epileptic if: (i) A rapid, full recovery is made. (ii) The seizure lasted less than 5 min and was not associated with trauma either before or during the seizure. (iii) There are no residual focal CNS signs and the level of consciousness is normal. (iv) Their usual medication is adequate and being taken. (v) There is an adult to accompany the patient. 6 In addition, discharge home a patient under 40 years with a non-focal first seizure, with no serious underlying cause found (having considered the causes listed under point 3 on p. 90), and who makes a full recovery without focal neurology. (i) Perform a CT head scan first, or organize one within the next day or two. (ii) Confirm safe discharge with the senior ED doctor. (iii) Organize an outpatient EEG and medical clinic review. (iv) Advise the patient not to drive, operate machinery, supervise children swimming, or bath a baby alone etc. until seen by the specialist. Record this advice in writing in the notes. 7 Always inform the GP by fax or letter on discharging the patient, and if the patient was referred to the medical or neurology clinic for follow-up. GENERALIZED CONVULSIVE STATUS EPILEPTICUS DIAGNOSIS 1 Generalized convulsive, grand mal, major motor or tonic–clonic status epilepticus is defined as two or more grand mal seizures without full recovery of consciousness in between, or recurrent grand mal seizures for more than 5–10 min. 2 Over 50% patients have no prior history of seizures. (i) Thus it is essential to look for any of the underlying ‘acute symptomatic’ causes listed under point 3 on page 90. (ii) Therefore, perform all the tests mentioned under point 5 on p. 90, once the seizures have been terminated. 3 Attach a cardiac monitor and pulse oximeter to the patient on arrival. Warning: never diagnose new-onset ‘epilepsy’ in a non-epileptic patient until, as a minimum, secondary causes have been excluded by a CT brain scan, and an electroencephalogram has been performed and a specialist outpatient assessment has occurred. ! ACUTE NEUROLOGICAL CONDITIONS 92 General Medical Emergencies MANAGEMENT 1 Give the patient oxygen via a face mask, and aim for an oxygen saturation above 94%. 2 Check the blood sugar: (i) Give 50% dextrose 50 mL i.v. if it is low. (ii) Give thiamine 100 mg i.v. in addition if chronic alcoholism or malnutrition is likely, to avoid precipitating Wernicke’s encephalopathy. 3 Give midazolam 0.05–0.1 mg/kg up to 10 mg i.v., diazepam 0.1–0.2 mg/kg up to 20 mg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. (i) Beware of causing respiratory depression, bradycardia and hypotension, especially in the elderly. 4 Get senior ED doctor help if the patient is still having a seizure: (i) Repeat the midazolam, diazepam or lorazepam i.v. until seizures cease. (ii) Then give phenytoin 15–18 mg/kg i.v. no faster than 50 mg/min by slow bolus, or preferably as an infusion in 250 mL normal saline (never in dextrose) over 30 min under ECG monitoring, or (iii) Give the pro-drug fosphenytoin at an equivalent dose but faster rate. 5 Other drugs that may be used include phenobarbitone (phenobarbital) 10–20 mg/kg i.v. no faster than 100 mg/min, or clonazepam 0.5–2 mg i.v. (i) By now, make sure the ICU team is involved if seizures continue. (ii) All patients will require admission, possibly to a highdependency area. 6 Occasionally, if i.v. access is impossible, give: (i) Rectal diazepam, especially in children, using parenteral diazepam solution 0.5 mg/kg given through a small syringe (see p. 365) or midazolam 0.5 mg/kg p.r. or via the buccal route. 7 Consider the following underlying reasons when a patient fails to regain consciousness, despite the seizures stopping: (i) Medical consequences of the seizures: (a) hypoxia (b) hypo- or hyperglycaemia (c) hypotension (d) hyperpyrexia (e) cerebral oedema (f) lactic acidosis (g) iatrogenic over-sedation. (ii) Progression of the underlying disease process: (a) head injury, e.g. extradural or subdural (b) meningitis or encephalitis ACUTE NEUROLOGICAL CONDITIONS General Medical Emergencies 93 (c) cerebral hypoxia (d) drug toxicity, e.g. theophylline. (iii) Subtle generalized convulsive status epilepticus. (iv) Non-convulsive status epilepticus: (a) complex–partial (temporal lobe) seizures (b) petit mal status. TRANSIENT ISCHAEMIC ATTACK DIAGNOSIS 1 TIAs are episodes of sudden transient focal neurological deficit, maximal at the outset and lasting for <24 h, usually <10 min. (i) They may recur and are important in that they are part of a spectrum that can progress to a full-blown stroke. (ii) Thus they may be followed by a major ischaemic stroke or other serious vascular event: (a) 2.5–5% at 2 days (b) 5–10% at 30 days (c) 10–20% at 90 days. 2 The causes may be considered in three groups. (i) Embolic (a) extracranial vessels – carotid stenosis, narrowed vertebral artery (b) cardiac – post-myocardial infarction, AF, mitral stenosis, valve prosthesis. (ii) Reduced cerebral perfusion (a) hypotension from hypovolaemia, drugs or a cardiac arrhythmia (b) hypertension (especially in hypertensive encephalopathy) (c) polycythaemia, paraproteinaemia, or a hypercoagulable state such as protein C, protein S or antithrombin III deficiency, and with antiphospholipid antibodies (d) vasculitis, e.g. temporal arteritis, SLE, polyarteritis nodosa, or syphilis. (iii) Lack of nutrients (a) anaemia (b) hypoglycaemia. 3 TIAs present clinically as: (i) Carotid territory dysfunction causing hemiparesis, hemianaesthesia, homonymous hemianopia, dysphasia, dysarthria and amaurosis fugax (transitory monocular blindness). (ii) Vertebrobasilar territory dysfunction (posterior circulation) causing combinations of bilateral limb paresis, crossed sensory symptoms, diplopia, nystagmus, ataxia, vertigo and cortical blindness. ACUTE NEUROLOGICAL CONDITIONS 94 General Medical Emergencies 4 Examine the pulse rhythm, heart sounds, blood pressure (in both arms and postural), listen for carotid bruits and perform a full neurological assessment. 5 Risk stratify the patient using the ABCD2 scoring system (see Table 2.8). Table 2.8 ABCD2 score for early risk stratification in transient ischaemic attack Score Age ≥60 years Blood pressure ≥140 mmHg (SBP) and/or ≥90 mmHg (DBP) Clinical signs Unilateral weakness Speech disturbance without weakness Other Duration ≥60 min 10–59 min <10 min Diabetes 1 point 1 point 2 points 1 point 0 points 2 points 1 point 0 points 1 point Total = (Max 7) High risk ≥4 points: with a 7-day risk of completed stroke of 5.9–11.7%. Low risk 0–3 points: with a 7-day risk of completed stroke of 1.2%. DBP, diastolic blood pressure; SBP, systolic blood pressure. Adapted with permission from Johnston C, Rothwell P, Nguyen-Huynh M et al. (2007) Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 369: 283–92. (i) ABCD2 score of ≥4 points is considered ‘high-risk’, with a 7-day risk of completed stroke of 5.9–11.7%. (ii) ABCD2 score of 0–3 points is considered ‘low-risk’, with a 7-day risk of completed stroke of 1.2%. 5 Check a bedside blood glucose test strip. Send blood for FBC, ESR, coagulation profile, blood sugar, ELFTs and a lipid profile in all patients. 6 Perform an ECG and request a CXR. 7 Arrange an urgent CT brain scan to differentiate haemorrhage from infarction, and to look for a structural, non- vascular lesion. 8 Organize a duplex carotid ultrasound for a suspected carotid territory ischaemic event as soon as possible, certainly for the high-risk patient with an ABCD2 score of ≥4 points. MANAGEMENT 1 Give aspirin 300 mg orally, then 75–150 mg once daily as soon as the CT scan has excluded haemorrhage. ACUTE NEUROLOGICAL CONDITIONS General Medical Emergencies 95 2 Deciding who to admit can be difficult. Refer the patient for immediate medical admission if: (i) High-risk patient with an ABCD2 score of ≥4 points. (ii) The ECG is abnormal, and a cardiac embolic source is suspected particularly new or untreated atrial fibrillation. (iii) TIAs are recurring over a period of hours or are progressing in severity and intensity (known as crescendo TIAs). (iv) There are residual neurological findings. (v) The patient has new or poorly controlled diabetes. (vi) The patient has poorly controlled hypertension with systolic BP ≥180 mmHg, or diastolic BP ≥100 mmHg. (vii) Carotid territory disease, particularly in an otherwise healthy patient with an audible carotid bruit and possible high-grade stenosis, or a history of known carotid stenosis. 3 Refer the remaining patients to medical or neurology outpatients within 7 days, if complete recovery has occurred, and the patient is low-risk with an ABCD2 score of 0–3 points. (i) Arrange an echocardiogram (if cardiac cause suspected) as an outpatient. (ii) Inform the GP by fax and by letter. STROKE These are due to a vascular disturbance producing a focal neurological deficit for over 24 h. DIAGNOSIS 1 The causes include: (i) Cerebral ischaemia or infarction (80%) (a) cerebral thrombosis from atherosclerosis, hypertension or rarely arteritis, etc. (b) cerebral embolism from atheromatous plaques in a neck vessel, AF, post-myocardial infarction or mitral stenosis (c) hypotension causing cerebral hypoperfusion. (ii) Cerebral haemorrhage (20%) (a) intracerebral haemorrhage associated with hypertension or rarely intracranial tumour and bleeding disorders including anticoagulation Warning: remember that patients can present with the consequences of their TIA, e.g. a head injury, Colles’ fracture, or fracture of the neck of femur. Do not fail to investigate for these, or to look for the true precipitating event (i.e. the TIA). ! ACUTE NEUROLOGICAL CONDITIONS 96 General Medical Emergencies (b) subarachnoid haemorrhage from ruptured berry aneurysm or arteriovenous malformation. 2 Presentation may give a clue to aetiology: (i) Cerebral thrombosis is often preceded by a TIA and the neurological deficit usually progresses gradually. Headache and loss of consciousness are uncommon. (ii) Cerebral embolism causes a sudden, complete neurological deficit. (iii) Intracerebral haemorrhage causes sudden onset of headache, vomiting, stupor or coma with a rapidly progressive neurological deficit. (iv) Subarachnoid haemorrhage is heralded by: (a) sudden, severe ‘worst headache ever’, sometimes following exertion, associated with meningism, i.e. stiff neck, photophobia, vomiting and Kernig’s sign (see p. 99) (b) confusion or lethargy, which are common, or focal neurological deficit and coma, which are rare and serious. 3 Record the vital signs, including the temperature, pulse, blood pressure, respiratory rate and GCS score (see p. 30). 4 Perform a full neurological examination, recording any progression of symptoms and signs. 5 Gain i.v. access and send blood for FBC, ESR, coagulation profile, ELFTs and blood sugar. Attach a cardiac monitor and pulse oximeter to the patient, and catheterize the bladder. 6 Obtain an ECG and CXR, and arrange an urgent CT head scan. (i) This CT scan may initially be normal with a cerebral infarct. MANAGEMENT 1 This is essentially supportive. Make certain a bedside blood glucose test strip has been done and give 50% dextrose 50 mL i.v. if it is low. 2 If the patient is unconscious: (i) Open the airway by tilting the head and lifting the chin, insert an oropharyngeal airway, give high-dose oxygen via a face mask and pass a nasogastric tube (NGT). (ii) Place the patient in the left lateral position. Get a senior ED doctor help. (iii) Consider endotracheal intubation if there is respiratory depression, deteriorating neurological status and/or signs of raised intracranial pressure. Discuss this with the intensive care team. 3 Otherwise, commence oxygen, and aim for an oxygen saturation above 94%. 4 Keep nil by mouth (NBM) until a swallowing assessment is completed within the first 24 h. HEADACHE General Medical Emergencies 97 5 Refer the patient to the medical team or stroke unit for admission and definitive management. (i) Give aspirin 300 mg orally daily or via NGT within 48 h, once CT scan has excluded haemorrhage. (ii) Avoid the temptation to treat acutely raised blood pressure unless aortic dissection (see p. 000) or subarachnoid haemorrhage (see p. 99) are found, or (iii) In an ischaemic stroke if the BP is acutely raised >220/120 mmHg, when reduction by 10–20% may be performed (i.e. no lower than 180/100 mmHg initially). Get senior ED doctor help. 6 Seek an urgent neurosurgical opinion for acute hydrocephalus, or a cerebellar hemisphere haematoma >3 cm presenting with headache, dizziness, vertigo, truncal or limb ataxia, gaze palsy and a diagnostic CT brain scan. HEADACHE DIFFERENTIAL DIAGNOSIS Consider the serious or life-threatening diagnoses first: ● Meningitis ● Subarachnoid haemorrhage ● Space-occupying lesion ● Temporal arteritis (age >50 years; erythrocyte sedimentation rate [ESR] >50 mm/h) ● Acute narrow-angle glaucoma ● Hypertensive encephalopathy. The majority, however, will be due to: ● Migraine ● Tension or muscle contraction headache ● Post-traumatic headache ● Disease in other cranial structures. The history is vital as physical signs may be minimal or lacking, even in the serious group. A new headache or a change in quality of a usual one must be evaluated carefully, especially in the elderly. MENINGITIS DIAGNOSIS 1 Causes include meningococcus, Streptococcus pneumoniae, Listeria mono - cytogenes (adults over 50 years, in alcoholism, pregnancy, immunosuppression or cancer, and in infants <3 months along with group B streptococcus and HEADACHE 98 General Medical Emergencies Escherichia coli), viruses, and Cryptococcus neoformans and tuberculosis (immunosuppression including HIV). (i) Haemophilus influenzae is now becoming rare following vaccination programmes. 2 Prodromal malaise is followed by generalized headache, fever and vomiting, with altered mental status and irritability and drowsiness progressing to confusion or coma. 3 Pyrexia, photophobia and neck stiffness are found. Localized cranial nerve palsies or seizures may occur. 4 Eliciting signs of meningeal irritation are rarely positive (<10%): (i) Kernig’s sign: pain and spasm in the hamstrings on attempted knee extension, with a flexed hip. (ii) Brudzinski’s sign: involuntary flexion of both hips and knees on passive neck flexion. 5 Always consider meningitis in the confused elderly, sick neonate, in generalized convulsive status epilepticus, and in coma of unknown cause. 6 A petechial rash, impaired consciousness and meningism are features of meningococcal septicaemia (meningococcaemia), but are relatively late signs. Therefore look out for the earlier signs of possible meningococcaemia such as: (i) Muscle pain including leg pains, abnormal skin colour with pallor or mottling, and cold hands and feet. (ii) Rigors, vomiting, headache or abdominal pain and a rapid evolution of illness within 24 h. (iii) Progression to shock and obtundation indicate fulminant meningococcal disease. 7 Gain i.v. access and send blood for FBC, coagulation profile, ELFTs, blood sugar, viral studies and two sets of blood cultures (from different venepuncture sites). 8 Attach a cardiac monitor and pulse oximeter to the patient, and perform a CXR. MANAGEMENT 1 Give the patient oxygen and commence a normal saline infusion. 2 Seek immediate senior ED doctor help, and give antibiotics as soon as the diagnosis is suspected. (i) Give ceftriaxone 4 g i.v. daily, or 2 g i.v. 12-hourly; or cefotaxime 2 g i.v. then 6-hourly. (ii) Add benzylpenicillin 2.4 g i.v. 4-hourly if Listeria is possible, such as in immunosuppression, adults >50 years, chronic alcohol abuse, pregnancy or debilitation, or HEADACHE General Medical Emergencies 99 (iii) Add vancomycin 1.5 g i.v. 12-hourly, if patient has known or suspected otitis media or sinusitis, or Gram-positive diplococci are seen in the cerebrospinal fluid (CSF), or a pneumococcal antigen assay on CSF is positive. 4 Give dexamethasone 0.15 mg/kg up to 10 mg i.v. then 6-hourly at the same time as the antibiotics, if bacterial meningitis is strongly suspected, particularly when ill or obtunded, although its efficacy is unclear. 5 Then perform a CT scan, especially if there are focal neurological signs, papilloedema or mental obtundation. (i) Even if this CT scan is normal, omit the lumbar puncture until these signs improve or disappear. 6 Consider lumbar puncture (LP) without CT if there are no focal neurological signs and the patient has a normal mental state, particularly if a CT scan is unavailable. 7 Admit the patient under the medical team, or to the ICU if altered mental status or haemodynamically unstable. SUBARACHNOID HAEMORRHAGE DIAGNOSIS 1 The majority of cases are associated with a ruptured berry aneurysm, in patients who may have a family history, hypertension, polycystic kidneys or coarctation of the aorta. (i) The remainder are due to an arteriovenous malformation, or rarely coagulopathy and vasculitis. 2 Ask about any prodromal episodes of headache or diplopia due to a ‘warning leak’. These may precede a sudden, severe ‘worst headache ever’, sometimes following exertion. 3 Lethargy, nausea, vomiting and meningism with photophobia and neck stiffness occur, although fever is usually absent or is low grade. (i) A IIIrd nerve oculomotor palsy suggests bleeding from a posterior communicating artery aneurysm. 4 Less typical presentations include acute confusion, transient loss of consciousness with recovery, or coma when a stiff neck and sub-hyaloid (pre-retinal) haemorrhage are useful diagnostic pointers on examination. 5 Gain i.v. access and send blood for FBC, coagulation profile, U&Es, blood sugar and a group and hold. Attach a cardiac monitor and pulse oximeter to the patient. 6 Perform an ECG and request a CXR. HEADACHE 100 General Medical Emergencies MANAGEMENT 1 Give the patient oxygen and nurse head upwards. Aim for an oxygen saturation above 94%. 2 Give midazolam 0.05–0.1 mg/kg up to 10 mg i.v., or diazepam 0.1–0.2 mg/kg up to 20 mg i.v., or lorazepam 0.07 mg/kg up to 4 mg i.v. for seizures or severe agitation. 3 Give paracetamol 500 mg and codeine phosphate 8 mg two tablets orally or rarely morphine 2.5–5 mg i.v. for pain relief, with an antiemetic such as metoclopramide 10 mg i.v. 4 Arrange a CT head scan urgently to confirm the diagnosis. (i) CT scan is up to 98% sensitive in the first 12 h, but drops to 50% by day 7. 5 Proceed to perform a lumbar puncture if the CT brain scan is negative or unavailable, provided that 8–10 h have passed since headache onset and there are no focal neurological signs or papilloedema. (i) Always request xanthochromia studies by spectrophotometry of the CSF to differentiate a traumatic tap (absent) from a true subarachnoid haemorrhage (positive). 6 Refer the patient to ICU for admission, or to a neurosurgical unit. (i) Seek specialist consultation and commence nimodipine 60 mg orally 4-hourly or an infusion at 1 mg/h if comatose, increased to 2 mg/h after 2 h if the blood pressure is stable, when the diagnosis is confirmed. SPACE-OCCUPYING LESION DIAGNOSIS 1 Causes include an intracranial haematoma, cerebral tumour, or cerebral abscess. 2 The headaches become progressively more frequent and severe, worse in the mornings and exacerbated by coughing, bending or straining. 3 Vomiting without nausea occurs, and focal neurological signs develop, ranging from subtle personality changes, ataxia, and visual problems to cranial nerve palsies, hemiparesis and seizures. 4 Papilloedema may be seen, with loss of venous pulsation and blurring of the disc margin with filling in of the optic cup as the earliest signs on funduscopy. 5 Perform a CXR to look for a primary tumour and arrange an immediate CT head scan. HEADACHE General Medical Emergencies 101 MANAGEMENT 1 Give oxygen, and treat seizures with midazolam 0.05–0.1 mg/kg up to 10 mg i.v., or diazepam 0.1–0.2 mg/kg up to 20 mg i.v., or lorazepam 0.07 mg/kg up to 4 mg i.v. 2 Refer a patient with an extradural or subdural haematoma to the neurosurgical team. 3 Otherwise refer the patient to the medical team for full investigation. TEMPORAL ARTERITIS DIAGNOSIS 1 This occurs in patients over 50 years, with relentless, diffuse or bitemporal headache often associated with a history of malaise, weight loss and myalgia. (i) Occasionally there is pain on chewing (jaw claudication). (ii) Polymyalgia rheumatica (PMR) with shoulder girdle weakness and discomfort coexist in 30% of patients. 2 Look for localized scalp tenderness, hyperaesthesia and decreased temporal arterial pulsation. 3 Send blood for an urgent ESR (one of the few times this is really necessary in the ED!). 4 The immediate danger is sudden visual loss due to ophthalmic artery involvement, which may affect both eyes if steroid treatment is delayed. MANAGEMENT 1 Commence prednisolone 60 mg orally if the ESR is raised >50 mm/h, or if the result is not available immediately. 2 Refer the patient to the medical or ophthalmology team for admission for urgent temporal artery biopsy and continued high-dose steroid therapy. ACUTE NARROW-ANGLE GLAUCOMA See page 422. HYPERTENSIVE ENCEPHALOPATHY DIAGNOSIS 1 This is due to an acute accelerated or malignant hypertensive crisis, related to rapid onset hypertension with headache, nausea and vomiting, confusion, and blurred vision. 2 Ask about drug non-compliance if known hypertension, renal disease, autoimmune disease such as SLE or scleroderma, and recreational drug use such as cocaine or amphetamines. HEADACHE 102 General Medical Emergencies 3 Examine for focal neurological signs. Seizures and coma may develop later. (i) Look for papilloedema, retinal haemorrhages, exudates and cotton-wool spots on funduscopy (grade IV retinal changes). 4 Gain i.v. access and send blood for FBC, ELFTs, blood sugar and cardiac biomarker such as troponin if there are chest pains or ECG changes. Attach a cardiac monitor and pulse oximeter to the patient. 5 Perform an ECG and request a CXR. 6 Check an MSU for proteinuria and send it for microscopy to look for evidence of renal disease, with casts or abnormal urinary red blood cells (>70% dysmorphic). (i) Perform a urinary -human chorionic gonadotrophin (hCG) pregnancy test (qualitative and immediate) or send blood (quantitative but takes time). 7 Arrange an urgent CT brain scan. MANAGEMENT 1 Give the patient oxygen, and aim for an oxygen saturation above 94%. 2 Get senior ED doctor help and take expert advice. (i) Aim to reduce mean arterial pressure (MAP) initially by no more than 25%, or aim for a diastolic BP of 100–110 mmHg within the first 24 h. (ii) Use oral treatment with labetalol 100 mg, atenolol 100 mg or long-acting nifedipine 20–30 mg. (iii) Avoid an i.v. agent such as sodium nitroprusside 0.25–10 g/ kg per min i.v., unless admitted to ICU with intra-arterial blood pressure monitoring in place. 3 Refer the patient to the medical team for blood pressure control and to observe for the complications of heart failure, aortic dissection, intracranial haemorrhage and renal impairment (cause or effect). MIGRAINE DIAGNOSIS 1 ‘Common’ migraine or migraine without aura (66–75% migraineurs). This is diagnosed by a history of at least five previous attacks that: (i) Last 4–72 h if untreated. (ii) Have at least two of the following headache characteristics: (a) unilateral (b) pulsating or throbbing (c) moderate to severe (d) aggravated by movement. HEADACHE General Medical Emergencies 103 (iii) Have at least one associated symptom of: (a) nausea and/or vomiting (b) photophobia (c) phonophobia. 2 ‘Classic’ migraine, or migraine with aura, is less common (25–30% migraineurs). It has similar features to those above, plus a history of at least two previous attacks that: (i) Have a typical aura: (a) fully reversible visual, sensory or speech symptoms (or mixed), but not motor weakness (b) visual symptoms can be uni- or bilateral flashing lights, zig-zag lines (teichopsia), fortification spectra and a central scotoma, or transient hemianopia (c) sensory symptoms are unilateral positive or negative (c) these symptoms develop over 5 min, or each symptom lasts ≥5 min but <60 min. (ii) Headache precedes, accompanies, or follows the aura within 60 min, although up to 40% can have an aura with no headache, or (iii) Have a less typical aura (these are all rare): (a) hemiplegic (sporadic or familial) (b) basilar (ataxia, vertigo, tinnitus, nystagmus, diplopia, confusion) (c) ophthalmoplegic. 3 Therefore it is not possible to diagnose a first episode of migraine, without first excluding a more serious cause such as a subarachnoid haemorrhage, space-occupying lesion or other intracranial haemorrhage. (i) Also do not diagnose a ‘migraine’ if the headache is different from a typical attack, was sudden or precipitate in onset, is more longer lasting, if the aura is prolonged and or if there is residual neurology. (ii) Get senior ED doctor help and arrange investigations including a CT brain scan. MANAGEMENT 1 Nurse the patient in a darkened room, give oxygen by face mask and an oral analgesic such as aspirin 300 mg three tablets, ibuprofen 200 mg two or three tablets, or paracetamol 500 mg and codeine phosphate 8 mg two tablets. 2 Give an antiemetic with antidopaminergic effects, such as metoclopramide 10–20 mg i.v. 3 Give chlorpromazine 0.1–0.2 mg/kg i.v. if the above fail, with a fluid bolus of normal saline 10 mL/kg, or 4 Consider a triptan such as sumatriptan 6 mg s.c. for resistant headache: (i) Side effects of tingling, heat and flushing may occur, or rarely chest pain and tightness. HEADACHE 104 General Medical Emergencies (ii) Sumatriptan is contraindicated in known coronary artery disease (CAD), previous myocardial infarction, and in patients with possible unrecognized coronary artery disease, such as men over 40 years or post-menopausal women, with CAD risk factors. (iii) Sumatriptan is also contraindicated within 24 h of ergotaminecontaining therapy. 5 Discharge the patient back to the GP, after a discussion of precipitating factors such as fatigue, alcohol, caffeine, hunger, etc. that might then be avoided. TENSION (MUSCLE CONTRACTION) HEADACHE DIAGNOSIS 1 This is a ‘featureless headache’ with none of the above associated symptoms as for migraine, and that lacks a family history or trigger factors other than stress, or some craniocervical musculoskeletal problems. 2 Women are more commonly affected and the pain comes on gradually, is bilateral, mild to moderate, dull, constant and band-like. 3 Mild nausea, phonophobia and photophobia can occur, but are usually absent and vomiting is rare. Headaches often become chronic. MANAGEMENT 1 Give the patient an analgesic such as paracetamol 500 mg and codeine phosphate 8 mg two tablets orally 6-hourly. 2 Reassure the patient and discharge back to the care of the GP. POST-TRAUMATIC HEADACHE DIAGNOSIS 1 Headache following head injury may begin immediately or after a few days, and is present in up to 30% of patients at 6 weeks after mild concussion. 2 Inability to concentrate, irritability, dizziness, insomnia and even depression may develop, known as the ‘post-concussion syndrome’. 3 Request an urgent CT head scan if there is persistent worsening of headache, recurrent vomiting, clouding of consciousness, or focal neurological signs, to exclude a subdural haematoma. MANAGEMENT 1 Treatment is supportive including analgesics, rest, and reassurance that complete recovery is the rule. 2 Refer the patient back to the GP, as symptoms may persist for up to 1 year. 3 Discuss patients with an abnormal CT scan with the neurosurgeons. ACUTE ARTHROPATHY General Medical Emergencies 105 DISEASE IN OTHER CRANIAL STRUCTURES DIAGNOSIS AND MANAGEMENT 1 Iritis (see p. 421), otitis media (see p. 399), sinusitis or dental caries may all present with headache. 2 Treatment is aimed at the underlying condition. ACUTE ARTHROPATHY Acute joint pain in the ED may be divided into three main types: ● Acute monoarthropathy ● Acute polyarthropathy ● Periarticular swellings. ACUTE MONOARTHROPATHY DIFFERENTIAL DIAGNOSIS It is important to distinguish between: ● Septic arthritis ● Gout or pseudogout ● Trauma and haemarthrosis and occasionally: ● Rheumatoid arthritis ● Osteoarthritis. though these last two are more commonly polyarticular. SEPTIC ARTHRITIS DIAGNOSIS 1 This may occur with any penetrating trauma, even trivial such as a rose thorn, or following arthrocentesis. 2 Most cases, however, develop from haematogenous spread. This is predisposed to by: (i) Rheumatoid arthritis. (ii) Osteoarthritis, particularly in the elderly. (iii) Intravenous drug abuse. (iv) Diabetes mellitus. (v) Immunosuppression. (vi) Disseminated gonococcal or meningococcal infection. (vii) Sickle cell disease, often from Salmonella. ACUTE ARTHROPATHY 106 General Medical Emergencies 3 Check temperature, pulse and blood pressure. There is localized joint pain, warmth, erythema and severely restricted range of active and passive movement, but with a less precipitate onset than with gout. 4 Send blood for two sets of blood cultures, FBC, ESR and C-reactive protein (CRP). 5 Request an X-ray which will initially be normal, but subsequently may show destruction of bone with loss of the joint space. 6 Or arrange an ultrasound scan, which is most helpful in demonstrating an effusion in joints such as the hip (see p. 370), or even a CT scan for the sternoclavicular joint. MANAGEMENT 1 Give an analgesic such as paracetamol 500 mg and codeine phosphate 8 mg two tablets orally. 2 Refer the patient immediately to the orthopaedic team for joint aspiration under sterile conditions, i.v. antibiotics, rest and repeated operative drainage. (i) Joint aspiration should yield turbid, yellow fluid with a polymorph WCC >50 000/ mL. A fluid culture is positive in >50%. GOUTY ARTHRITIS DIAGNOSIS 1 Gout is much more common in men, and is associated with diabetes, hypertension, hypercholesterolaemia and myeloproliferative disease (especially following treatment), renal failure (cause or effect), thiazide diuretic therapy, or dietary excess, alcohol and trauma. 2 It is commonest in the metatarsophalangeal joint of the great toe or in the ankle, wrist and knee, sometimes with a precipitate onset waking the patient from sleep. 3 Chronic cases may be associated with gouty tophi on the ear and around the joints, polyarthropathy and recurrent acute attacks. 4 The patient may be mildly pyrexial with a red, shiny ‘angry’ joint. 5 Send blood for FBC, ELFTs, and ESR plus CRP if septic arthritis is as likely. (i) Laboratory blood results may show a mild leucocytosis, with a raised uric acid level (>0.4 mmol/L), but the serum uric acid may be normal in up to 40% of acute attacks. 6 Definitive diagnosis is by joint aspiration and polarizing light microscopy showing strongly negative birefringent crystals. (i) Joint aspiration yields cloudy yellow fluid, with a WCC of 2000–50 000/mL. Polarizing microscopy is diagnostic. ACUTE ARTHROPATHY General Medical Emergencies 107 MANAGEMENT 1 Give the patient an NSAID in a known relapsing case, or if there is strong clinical suspicion of gout, such as ibuprofen 600 mg orally once, then 200–400 mg orally t.d.s. or naproxen 500 g orally, followed by 250 mg orally t.d.s. 2 Give prednisone 50 mg orally daily for 3 days instead, then tapered over 10–14 days in patients with renal or gastrointestinal disease unable to take NSAIDs. 3 Reserve colchicine 1 mg orally then 0.5 mg orally up to 1 h later, if the patient cannot tolerate either steroids (heart failure or diabetes) or NSAIDs (renal or gastrointestinal disease). (i) Do not repeat the colchicine dose for at least 3 days. 4 Refer the patient back to the GP or to medical outpatients. 5 Refer the patient immediately to the orthopaedic team for joint aspiration if septic arthritis cannot be excluded (see p. 105). PSEUDOGOUT 1 This is much less common than gout, typically affecting the knee, wrist or shoulder, and is associated with diabetes, osteoarthritis, hyperparathyroidism, haemochromatosis and many other rare conditions. 2 X-ray may show chondrocalcinosis, and joint aspiration shows weakly positive birefringent crystals under polarizing light microscopy. 3 Treatment is as for acute gout, with referral back to the GP or to medical outpatients for follow-up. TRAUMATIC ARTHRITIS DIAGNOSIS 1 Severe joint pain is usually associated with obvious trauma, although occasionally the trauma is mild or even forgotten. 2 Haemarthroses may also occur spontaneously in haemophilia A (factor VIII deficiency), haemophilia B (Christmas disease with factor IX deficiency) or severe von Willebrand’s disease (with deficiency of both von Willebrand’s factor and factor VIII). 3 Request an X-ray, although it may not always demonstrate an obvious fracture. (i) Suspect a fracture when there is supporting evidence of a haemarthrosis with a joint effusion or periosteal elevation (e.g. scaphoid or radial head). 4 Arrange joint aspiration performed by a senior ED doctor to look for a haemorrhagic joint effusion, with fat globules floating on the surface in cases of intra-articular fracture, if there is doubt about the diagnosis. ACUTE ARTHROPATHY 108 General Medical Emergencies (i) Also perform joint aspiration when septic arthritis cannot be excluded, or refer the patient directly to the orthopaedic team. MANAGEMENT 1 Give analgesia and refer the patient to the orthopaedic team as necessary. Management varies according to the joint involved (see Section IX, Orthopaedic Emergencies). 2 Give factor VIII to a patient with known haemophilia A, factor IX to a known haemophilia B patient and von Willebrand’s factor plus factor VIII to a patient with von Willebrand’s. (i) Organize this as rapidly as possible in consultation with the haematology team. ACUTE POLYARTHROPATHY DIAGNOSIS 1 There are many causes, including: (i) Rheumatoid arthritis. (ii) SLE. (iii) Psoriatic arthritis. (iv) Ankylosing spondylitis. (v) Reiter syndrome. (vi) Viral illness, e.g. hepatitis B, rubella, parvovirus B19, and HIV. (vii) Sarcoid. (viii) Ulcerative colitis, Crohn’s disease, gonococcus (early bacteraemic phase), Behçet’s disease, and Lyme disease. (ix) Rheumatic fever, or bacterial endocarditis. (x) Osteoarthritis, haemochromatosis, acromegaly (all noninflammatory). 2 Send blood for FBC, ESR, CRP, ELFTs, uric acid, rheumatoid factor, antinuclear antibody (ANA) and DNA antibodies, viral titres and blood cultures according to the suspected cause. 3 Request X-rays of the affected joints. MANAGEMENT 1 Refer to the medical team for admission, bed rest, drug treatment and definitive diagnosis if the patient is systemically unwell. 2 Otherwise, commence an NSAID analgesic such as ibuprofen 200–400 mg orally t.d.s. or naproxen 250 mg orally t.d.s. and refer the patient to medical or rheumatology outpatients. ACUTE ARTHROPATHY General Medical Emergencies 109 RHEUMATOID ARTHRITIS DIAGNOSIS 1 This occasionally presents as a monoarthritis, although usually it causes a symmetrical polyarthritis affecting the metacarpophalangeal and proximal interphalangeal joints in particular, initially with morning stiffness. (i) Other joints affected include the elbows, wrists, hips and knees. 2 Systemic involvement may occur with malaise, weight loss, fever, myalgia, nodules, pleurisy, pericarditis, splenomegaly, episcleritis and pancytopenia. 3 Check FBC, ESR, rheumatoid factor, ANA and DNA antibodies. 4 X-rays initially show soft-tissue swelling only and juxta-articular osteoporosis, followed by joint deformity. MANAGEMENT 1 Refer the patient to the medical team for admission if systemically unwell. 2 Refer the patient to the orthopaedic team if septic arthritis cannot be excluded, remembering that rheumatoid arthritis predisposes to septic arthritis. 3 Otherwise commence an NSAID analgesic such as ibuprofen 200–400 mg orally t.d.s. or naproxen 250 mg orally t.d.s. and refer the patient to medical outpatients or the GP. OSTEOARTHRITIS DIAGNOSIS 1 This usually presents as a polyarthritis of insidious onset, typically affecting the distal interphalangeal joints, hips and knees with pain on movement, but no systemic features. 2 However, occasionally an acute monoarthritis exacerbation may be seen associated with marked joint crepitus. 3 Request an X-ray that may show loss of joint space, osteophyte formation and bony cysts. MANAGEMENT 1 Refer the patient to the orthopaedic team if septic arthritis cannot be excluded. 2 Otherwise, give the patient an NSAID analgesic and return to the care of the GP. ALLERGIC OR IMMUNOLOGICAL CONDITIONS 110 General Medical Emergencies PERIARTICULAR SWELLINGS See pp. 326–330 in Section X, Musculoskeletal and Soft-Tissue Emergencies. ALLERGIC OR IMMUNOLOGICAL CONDITIONS The following immunological conditions may present, ranging from those that are socially inconvenient to imminently life-threatening: ● Urticaria (hives) ● Angioedema ● Anaphylaxis – see page 27 (Section I, Critical Care). URTICARIA (HIVES) DIAGNOSIS 1 There are many immunological and non-immune causes, including: (i) Foods – nuts, shellfish, eggs, strawberries, chocolate, food dyes or preservatives. (ii) Drugs – penicillin, sulphonamide, aspirin, NSAIDs, codeine, morphine. (iii) Insect stings, animals, parasitic infections including nematodes (in children). (iv) Physical – cold, heat, sun, pressure, exercise. (v) Systemic illness – malignancy including Hodgkin’s lymphoma, vasculitis, viruses such as hepatitis A or Epstein–Barr virus (EBV) and serum sickness. (vi) Idiopathic (in >90% of chronic cases). 2 Itchy, oedematous, transient skin swellings are seen, which may occur in crops lasting several hours. MANAGEMENT 1 Give the patient a less sedating H1 histamine antagonist such as loratadine 10 mg orally daily. This is minimally sedating, unlike promethazine. (i) Refractory cases may respond to the addition of an H2 histamine antagonist such as ranitidine 150 mg orally b.d. 2 Attempt to identify the likely cause from the recent history. Most reactions occur within minutes but may be delayed for up to 24 h. 3 Observe for any multi-system involvement suggesting progression to anaphylaxis (see p. 27). ALLERGIC OR IMMUNOLOGICAL CONDITIONS General Medical Emergencies 111 ANGIOEDEMA DIAGNOSIS 1 This is an urticarial reaction involving the deep tissues of the face, eyelids, lips, tongue and occasionally the larynx, often without pruritus. 2 The causes are as for urticaria, especially ACE inhibitors, aspirin or a bee sting. 3 It may cause facial, lip and tongue swelling, progressing to laryngeal oedema with hoarseness, dysphagia, dysphonia and stridor. 4 Attach a cardiac monitor and pulse oximeter to the patient. 5 A rare autosomal dominant hereditary form is due to C1 esterase inhibitor deficiency. A family history of attacks without urticaria, often following minor trauma, and recurrent abdominal pain are suggestive. MANAGEMENT 1 Commence high-dose oxygen aiming for an oxygen saturation above 94%. 2 Give 1 in 1000 adrenaline (epinephrine) 0.3–0.5 mg (0.3–0.5 mL) i.m. into the upper outer thigh, repeated as necessary. 3 Call the senior ED doctor urgently and prepare for intubation, if airway obstruction persists. (i) Give 1 in 1000 adrenaline (epinephrine) 2–4 mg (2–4 mL) nebulized, repeated as necessary. (ii) Change to 1 in 10 000 or 1 in 100 000 adrenaline (epinephrine) 0.75–1.5 g/kg i.v., i.e. 50–100 g or 0.5–1.0 mL of 1 in 10 000 or 5–10 mL of 1 in 100 000 adrenaline (epinephrine) slowly over 5 min i.v., if rapid deterioration occurs with imminent airway obstruction. The ECG must be monitored. 4 Give H1 and H2 blockers and steroids, only after cardiorespiratory stability has been achieved. (i) Promethazine 12.5–25 mg i.v. slowly plus ranitidine 50 mg i.v. (ii) Hydrocortisone 200 mg i.v. 5 Hereditary angioedema responds poorly to adrenaline (epinephrine). Give urgent C1 esterase inhibitor i.v. or fresh frozen plasma. 6 Admit the patient when stable for 6–8 h observation, as late deterioration may occur in up to 5% (known as biphasic anaphylaxis). 7 Then discharge home on prednisolone 50 mg once daily, loratadine 10 mg once daily plus ranitidine 150 mg b.d., all orally for 3 days. (i) Inform the GP by fax or letter. (ii) Refer all significant or recurrent attacks to the allergy clinic, especially if the cause is unavoidable or unknown. 112 General Medical Emergencies SKIN DISORDERS The vast majority of skin disorders are managed by GPs and the dermatology department. However, some patients may present as emergencies with blistering, itching or purpuric conditions. Exanthematous diseases are common in children and young adults, and malignant melanoma particularly in areas of high sunshine. BLISTERING (VESICOBULLOUS) CONDITIONS DIAGNOSIS 1 Common causes: (i) Viral: (a) herpes zoster (b) herpes simplex. (ii) Impetigo. (iii) Scabies. (iv) Insect bites and papular urticaria. (v) Bullous eczema and pompholyx. (vi) Drugs – sulphonamides, penicillin, barbiturates. 2 Less common causes: (i) Erythema multiforme minor (1–2 cm ‘target lesions’ only) or erythema multiforme major (‘target lesions’ rash, plus one mucous membrane involved) due to: (a) Mycoplasma pneumonia (b) herpes simplex (c) drugs – sulphonamides and penicillins (d) idiopathic (50%). (ii) Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) causing epidermal detachment with mucosal erosions due to: (a) drugs such as anticonvulsants, sulphonamides, NSAIDs and penicillins. (iii) Staphylococcal scalded-skin syndrome (SSSS) usually in children. (iv) Dermatitis herpetiformis (gluten sensitivity). (v) Pemphigus and pemphigoid. 3 Rare causes: (i) Porphyria cutanea tarda. (ii) Epidermolysis bullosa (congenital). MANAGEMENT 1 Refer patients with widespread or potentially life-threatening blistering immediately to the dermatology team or medical team. SKIN DISORDERS General Medical Emergencies 113 (i) This should include any patient with SJS, TEN, SSSS, pemphigus and pemphigoid, who may die from intercurrent infection and multi-organ failure. 2 Otherwise give symptomatic treatment including: (i) Antihistamine orally such as promethazine 10 mg t.d.s. if there is associated pruritus, with a warning about drowsiness. (ii) Antibiotics orally such as flucloxacillin 500 mg q.d.s. or cephalexin 500 mg q.d.s. for secondary staphylococcal infection in herpes zoster, impetigo, insect bites and eczema. Give clindamycin 450 mg t.d.s. for patients with severe penicillin allergy. (iii) Parasiticidal preparation for scabies (see p. 114). (iv) Antiviral agent orally such as aciclovir 200 mg five times a day for 5 days for severe herpes simplex, or 800 mg five times a day or famciclovir 250 mg t.d.s. for 7 days for severe herpes zoster. (v) Topical steroid antiseptic such as 1% hydrocortisone with 1% clioquinol cream t.d.s. for papular urticaria and bullous eczema. 3 Return the patient to the care of their GP. PRURITUS (ITCHING CONDITIONS) DIAGNOSIS 1 Causes of pruritus with skin disease: (i) Scabies, pediculosis, insect bites, parasites (roundworm). (ii) Eczema. (iii) Contact dermatitis. (iv) Urticaria. (v) Lichen planus (pruritic, planar, purple, polygonal papules with chronic oral mucous membrane involvement). (vi) Pityriasis rosea (upper respiratory infection preceding ‘herald’ patch, followed after 7–14 days by a pink or red, flaky, ovalshaped rash). (vii) Drugs, which may cause any of the conditions (ii)–(vi) above. (viii) Dermatitis herpetiformis (chronic itchy, papulovesicular eruptions, usually distributed symmetrically on extensor surfaces, associated with gluten sensitivity). 2 Causes of pruritus without skin disease: (i) Hepatobiliary – jaundice, including primary biliary cirrhosis. (ii) Chronic renal failure. (iii) Haematological: (a) lymphoma (b) polycythaemia rubra vera. SKIN DISORDERS 114 General Medical Emergencies (iv) Endocrine: (a) myxoedema (b) thyrotoxicosis. (v) Carcinoma: (a) lung (b) stomach. (vi) Drugs. 3 Take a general medical history, and ask in particular about medications. MANAGEMENT 1 Refer patients unable to sleep with intractable pruritus to the dermatology team or medical team. 2 Otherwise give symptomatic treatment including: (i) Antipruritic drug orally: (a) promethazine 10 mg t.d.s. with a warning about drowsiness. (ii) Scabies: (a) scabies is suggested by itch worse at night that does not involve the head, a close partner affected, and finding burrows (often excoriated) in interdigital webs, around the genitalia, or on the nipples (b) treat the patient and close contacts with 5% permethrin aqueous lotion over the whole body including the face and hair, washed off after 8–24 h; all clothes should also be washed (c) explain to the patient that although itching may persist, it is no longer contagious (d) advise the patient to attend a genitourinary medicine clinic to exclude an associated sexually transmitted disease if the scabies followed casual sex. (iii) Urticaria, see page 110. (iv) Cease any recent drug therapy considered causal, including nonprescription drugs. 4 Return the patient to the care of their GP. PURPURIC CONDITIONS DIAGNOSIS 1 Petechiae and purpura are non-blanching, cutaneous areas of bleeding that may be non-palpable or palpable. 2 Causes of non-palpable purpura include: (i) Thrombocytopenia, with splenomegaly: (a) normal marrow: – liver disease with portal hypertension – myeloproliferative disorders SKIN DISORDERS General Medical Emergencies 115 – lymphoproliferative disorders – hypersplenism. (b) abnormal marrow: – leukaemia – lymphoma – myeloid metaplasia. (ii) Thrombocytopenia, without splenomegaly: (a) normal marrow: – immune: idiopathic thrombocytopenic purpura (ITP), drugs, infections including HIV – non-immune: vasculitis, sepsis, disseminated intravascular coagulation (DIC), haemolytic–uraemic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP). (b) abnormal marrow: – aplasia, fibrosis or infiltration – cytotoxics – alcohol, thiazides. (iii) Non-thrombocytopenic: (a) cutaneous disorders: – trauma, sun – steroids, old age. (b) systemic disorders: – uraemia – von Willebrand’s disease – scurvy, amyloid. 3 Causes of palpable purpura include: (i) Vasculitis: (a) polyarteritis nodosa (b) leucocytoclastic (allergic), Henoch–Schönlein purpura. (ii) Emboli: (a) meningococcaemia (b) gonococcaemia (c) other infections: Staphylococcus, Rickettsia (Rocky Mountain spotted fever), enteroviruses. 4 Ask about any drugs taken, systemic symptoms, bleeding tendency, travel history, alcohol use and HIV disease or risk behaviour. 5 Check the temperature, pulse, blood pressure, SaO2 and examine for lymphadenopathy and hepatosplenomegaly. Perform a urinalysis for casts. 6 Send blood for FBC and film, coagulation profile, ELFTs and blood cultures according to the likely aetiology. SKIN DISORDERS 116 General Medical Emergencies MANAGEMENT 1 Management is of the underlying cause. 2 This is urgent for suspected meningococcaemia with ceftriaxone 2 g i.v. and for Rocky Mountain spotted fever with doxycycline 100 mg orally b.d. EXANTHEMATOUS DISEASES DIAGNOSIS 1 Exanthems are generalized erythematous, often blanching, maculopapular eruptions secondary to viral or bacterial infection. (i) Some have ‘classic’ clinical presentations such as chickenpox, fifth disease, glandular fever, measles, rubella and scarlet fever (see Table 2.9). (ii) Others are non-specific rashes, secondary to enteroviruses or respiratory viruses. 2 Ask about recent known contacts, particularly at childcare or in school, as well as any constitutional symptoms such as fever and malaise. 3 Most are diagnosed on clinical features, but serology for antibody titres may aid confirmation, particularly when there is concern following contact in a pregnant person. MANAGEMENT 1 Give symptomatic treatment, or phenoxymethylpenicillin 250–500 mg orally q.d.s. for 10 days in the case of streptococcal scarlet fever. 2 Isolate the patient at home until non-infectious. (i) Rarely admission is indicated in the immunosuppressed, or patients with severe systemic features. 3 Discuss pregnant contacts of a rubella or fifth disease patient with an infectious disease specialist or obstetrician. MALIGNANT MELANOMA The incidence of malignant melanoma has doubled in many countries over the past decade. DIAGNOSIS AND MANAGEMENT 1 Look for the following suspicious signs when a malignant melanoma is possible: (i) Major signs: (a) change in size, e.g. an increase in size of a new or pre-existing cutaneous lesion (b) change in shape, especially an irregular outline (c) change in colour, including multiple (variegated). SKIN DISORDERS General Medical Emergencies 117 (ii) Minor signs: (a) inflammation or elevation (b) bleeding or crusting (c) sensory changes, including itching (d) diameter ≥7 mm. Table 2.9 Common exanthematous diseases Disease Incubation period (days) Prodrome Rash Other features and infectivity Chickenpox 10–20 None Macules, papules, vesicles and pustules of differing ages Infective until all vesicles are crusted over (usually 6 days after last crop) Fifth disease (erythema infectiosum) 7–10 Fever, malaise Raised red ‘slapped cheeks’, diffuse maculopapular Transient arthralgia, then relapsing rash; infective before onset of rash. Fetal abnormality Glandular fever 5–14 Fever, sore throat, malaise Transient maculopapular (rare); itchy drug rash with ampicillin (common) Tonsillar exudate, cervical lymphadenopathy; hepatosplenomegaly; infective for many months by close physical contact Measles 9–14 3 days of cough, cold, conjunctivitis Red, confluent, maculopapular; lasts 7–11 days Koplik’s spots; cough predominates; may be quite ill; infective for 5 days after rash appears Rubella 14–21 None Pink, maculopapular, discrete; lasts 3–5 days Occipital and preauricular lymphadenopathy; infective until rash disappears. Fetal abnormality Scarlet fever 2–5 1–2 days of sore throat, fever, vomiting Minute, red punctuate papules; last 7 days Unwell; circumoral pallor; ‘strawberry tongue’; infective until negative throat swabs following penicillin ELDERLY PATIENT 118 General Medical Emergencies 2 Refer a patient with a pigmented lesion with any major sign urgently to the dermatology team. 3 Also refer a patient with a pigmented lesion and a minor sign, although <50% will have a melanoma. 4 Remember that the most common sites for melanoma are on the back and on the legs. ELDERLY PATIENT 1 An increasing number of patients over the age of 75 years attend the ED and pose unique problems of their own. 2 These problems begin in the waiting area, where old people may become frightened or confused due to their inability to see, hear or move easily, and understand instructions. 3 Always consider all of the following factors before discharging an elderly patient: (i) Can the patient walk safely with or without a stick? (ii) Can the patient understand new or existing medication? (iii) Can the patient get home safely and easily? (iv) Once home, can the patient cope with dressing, washing, using the toilet, shopping, cooking, cleaning or relaxing? (v) Can relatives or friends cope any more? 4 Do not discharge the patient without seeking help from the following people, if any factor above is present. Keep the patient in overnight to facilitate arrangements, when there is any doubt: (i) General practitioner: (a) the key person to coordinate the care of the patient at home (b) always contact by fax as well as by letter. (ii) ‘Hospital in the Home’, or ‘Hospital in the Nursing Home’ service. (iii) District or community nursing service. (iv) Social worker (hospital- or community-based), who can offer: (a) home help (b) ‘meals on wheels’ (c) lunch and recreational clubs (d) voluntary visiting services (e) laundry service (f) chiropody service (g) home adaptation service (h) emergency accommodation. (v) Domiciliary physiotherapist or occupational therapist. ELDERLY PATIENT General Medical Emergencies 119 DISORDERED BEHAVIOUR IN THE ELDERLY A breakdown in a patient’s normal, socially acceptable behaviour is best con sidered in three broad categories, that can overlap and or be mistaken for each other: ● Delirium – acute transient organic brain syndrome with global disorder of cognition ● Dementia – progressive intellectual decline ● Depression – pathological, unrelenting and disabling low mood. DIAGNOSIS 1 Delirium (see p. 81) (i) This includes clouding of consciousness, inattention and failure of recent memory. (ii) It results in an acute or fluctuating confusional state associated with restless sometimes aggressive behaviour and non-auditory hallucinations. It is often worse at night. (iii) Causes are many, including: (a) infection – pneumonia, urinary tract infection (UTI), cholecystitis, septicaemia (b) hypoxia – respiratory disease, heart failure, anaemia (c) cerebral lesion – haematoma, tumour, infection, stroke (d) iatrogenic – many drugs (remember poisoning, both accidental and deliberate), alcohol (e) metabolic – including dehydration, electrolyte imbalance, hypoglycaemia or hyperglycaemia and thyroid disease (f) urinary retention, faecal impaction, pain, cold or change in environment (these are rarely the sole cause). 2 Dementia (i) This includes disorientation in place, time and person, abnormal or antisocial behaviour, short-term memory loss, loss of intellect, and loss of insight. There is no clouding of consciousness. (ii) The causes are many, although a definitive new diagnosis is seldom made in the ED. (iii) However, look for and exclude the causes listed in 1 (iii) above if a known demented patient is brought into the ED with a recent deterioration. 3 Depression (i) This includes difficulty in sleeping, demanding, anxious or withdrawn behaviour, hypochondriasis, a loss of self-interest and a sense of futility. (ii) Suicide is a particular risk, especially if the patient lives alone and is physically incapacitated, or has made previous attempts at suicide. ELDERLY PATIENT 120 General Medical Emergencies MANAGEMENT 1 Delirium and acutely decompensated dementia require hospital admission (do not simply sedate). 2 Depression and a high suicide risk require urgent referral to a psychiatrist and possible hospital admission. FALLS IN THE ELDERLY DIAGNOSIS Always consider the underlying cause as well as the potential result following any fall in the elderly: 1 Cause of the fall: (i) Accidental: (a) obstacles in the home, such as a trailing flex, the edge of a carpet, poor lighting, or no handrails (b) inappropriate footwear. (ii) Musculoskeletal: (a) arthritis (b) obesity (c) weakness (d) physical inactivity. (iii) Visual failure: (a) cataracts (b) senile macular degeneration (c) glaucoma. (iv) Sedating drugs: (a) benzodiazepines (b) antihistamines (c) psychotropics (d) alcohol. (v) Postural hypotension: (a) occult bleeding (b) autonomic failure (c) drug-induced. (vi) Syncopal episode: (a) cardiac arrhythmia, myocardial infarction, heart block (b) vertebrobasilar insufficiency. (vii) Cerebral disorder: (a) Parkinson’s disease (b) ataxia (c) seizure (d) stroke. FURTHER READING General Medical Emergencies 121 (viii) Balance disorder: (a) inner ear disease (b) impaired proprioception. 2 Result of the fall: (i) Fracture: (a) Colles’ (b) neck of femur or pelvis (c) neck of humerus (d) ribs (e) skull. (ii) Hypothermia. (iii) Hypostatic pneumonia. (iv) Pressure sore, rhabdomyolysis. (v) Fear, loss of confidence and independence, loss of mobility. 3 All falls in the elderly, particularly if recurrent, must be diagnosed and managed correctly, otherwise ultimately a fatal outcome will occur. MANAGEMENT 1 Refer the patient to the medical or geriatric team for admission if acute care is needed, or if there is any doubt about their ability to cope at home. 2 Otherwise, refer to outpatients, physiotherapy, occupational therapy or social services and liaise closely with the GP. FURTHER READING American Heart Association (2010) Part 10: Acute coronary syndromes: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S787–817. American Heart Association (2010) Part 11: Adult stroke: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S818–28. British Infection Association. http://www.britishinfection.org/drupal/ (meningitis and meninogococcaemia). British Society of Gastroenterology. http://www.bsg.org.uk/ (gastrointestinal bleeding). British Thoracic Society. http://www.brit-thoracic.org.uk/ (pulmonary embolus, pneumonia, chronic obstructive pulmonary disease, pneumothorax). Diabetes UK. http://www.diabetes.org.uk/ (diabetic ketoacidosis). FURTHER READING 122 General Medical Emergencies European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010 Section 5. Initial management of acute coronary syndromes. Resuscitation 81: 1353–63. Heart Foundation (Australia). http://www.heartfoundation.org.au/ Meningitis Research Foundation. http://www.meningitis.org/ (meningitis and septicaemia). National Institute for Health and Clinical Excellence, NHS UK. http://www.nice. org.uk/Guidance/CG/Published National Institute of Clinical Studies (Australia). http://www.nhmrc.gov.au/nics/ index.htm Scottish Intercollegiate Guidelines Network. http://www.sign.ac.uk/ Stroke Foundation (Australia). http://www.strokefoundation.com.au/ (stroke and TIA). ACID–BASE, ELECTROLYTE AND RENAL EMERGENCIES Section III 124 Acid–Base, Electrolyte and Renal Emergencies ARTERIAL BLOOD GAS INTERPRETATION Blood gas analysis provides information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH, and results in acidaemia. Alkalosis is an abnormal process with decrease in the hydrogen ion concentration, resulting in alkalaemia. 1 Blood gas analysis is used to: (i) Determine the adequacy of oxygenation and ventilation. (ii) Assess the respiratory function. (iii) Determine the acid–base balance. 2 Interpret the arterial blood gas result in a stepwise manner as follows (see Table 3.1): (i) Determine the adequacy of oxygenation (PaO2): (a) normal range 80–100 mmHg (10.6–13.3 kPa) (b) provides direct evidence of hypoxaemia (c) determine if there is a raised A-a gradient due to VQ mismatch/shunting, if there is a lower than expected PaO2 ACID–BASE DISTURBANCES Table 3.1 Determining the likely acid–base disorder from the pH, PaCO2 and HCO3 pH PaCO2 HCO3 Acid–base disorder ‚ N ‚ Primary metabolic acidosis ‚ ‚ ‚ Metabolic acidosis with respiratory compensation ‚ · N Primary respiratory acidosis ‚ · · Respiratory acidosis with renal compensation ‚ · ‚ Mixed metabolic and respiratory acidosis · ‚ N Primary respiratory alkalosis · ‚ ‚ Respiratory alkalosis with renal compensation · N · Primary metabolic alkalosis · · · Metabolic alkalosis with respiratory compensation · ‚ · Mixed metabolic and respiratory alkalosis Note: respiratory compensation occurs rapidly by changes in PaCO2. Renal compensation occurs more slowly by changes in HCO3. N, normal. Acid–Base, Electrolyte and Renal Emergencies 125 ACID–BASE DISTURBANCES (d) assuming 100% humidity at sea level, the A-a gradient can be calculated by: A-a gradient = PAO2–PaO2 where PAO2 = (FiO2  (760–47))–(PaCO2/0.8) (e) normal A-a gradient is <10 torr (mmHg), or approximately < (age/4) + 4. (ii) Review the pH or hydrogen ion status: (a) normal range pH 7.35–7.45 (H+ 35–45 nmol/L) (b) acidaemia is a pH <7.35 (H+ >45 nmol/L) (c) alkalaemia is a pH >7.45 (H+ <35 nmol/L). (iii) Determine the respiratory component (PaCO2): (a) normal range 35–45 mmHg (4.7–6.0 kPa) (b) PaCO2 >45 mmHg (6.0 kPa): – acidaemia indicates a primary respiratory acidosis – alkalaemia indicates respiratory compensation for a metabolic alkalosis (c) PaCO2 <35 mmHg (4.7 kPa): – alkalaemia indicates a primary respiratory alkalosis – acidaemia indicates respiratory compensation for a metabolic acidosis (iv) Determine the metabolic component (bicarbonate, HCO3): (a) HCO3 normal range 22–26 mmol/L (b) HCO3 <22 mmol/L: – acidaemia indicates a primary metabolic acidosis – alkalaemia indicates renal compensation for a respiratory alkalosis (c) HCO3 >26 mmol/L: – alkalaemia indicates a primary metabolic alkalosis – acidaemia indicates renal compensation for a respiratory acidosis. 3 This approach will determine most primary acid–base disturbances and their associated renal or respiratory compensatory changes. 4 Remember: (i) Renal or respiratory compensation is always a secondary process and should really not then be described in terms of an ‘acidosis’ or ‘alkalosis’: (a) rather, in the presence of metabolic acidaemia, think of the respiratory compensation as ‘compensatory hyperventilation’ rather than a ‘secondary respiratory alkalosis’. (ii) Chronic compensation returns the pH value towards normal, but overcompensation never occurs. 126 Acid–Base, Electrolyte and Renal Emergencies ACID–BASE DISTURBANCES (iii) The presence of a normal pH with abnormal HCO3 and PaCO2 suggests both a primary respiratory and a primary metabolic process are present: (a) pH normal: PaCO2 >45 mmHg (6.0 kPa), HCO3 >26 mmol/L – dual primary process involving a primary respiratory acidosis and a primary metabolic alkalosis (b) pH normal: PaCO2 <35 mmHg (4.7 kPa), HCO3 <22 mmol/L – dual primary process involving a primary respiratory alkalosis and a primary metabolic acidosis. 5 Alternatively, for simplicity, use an acid–base nomogram to plot and read off the interpretation of the arterial blood gas abnormality (see Fig. 3.1)! METABOLIC ACIDOSIS METABOLIC ACIDOSIS DIAGNOSIS 1 An abnormal process or condition leading to the increase of fixed acids in the blood, best determined by a fall in plasma bicarbonate to less than 22 mmol/L. 2 Metabolic acidosis may be associated with a high, normal, or low anion gap. (i) The anion gap is calculated from the equation [Na+] – ([Cl–] + [HCO3–]) with all units in mmol/L. (ii) A normal anion gap is 8–16. metabolic acidosis acute respiratory acidosis chronic respiratory acidosis metabolic alkalosis 0 2 4 6 8 10 12 14 kPa 0 20 40 60 80 100 PaCO2 HCO3 – (mmol/L) 5 10 15 20 25 30 40 100 80 60 40 20 7.00 7.10 7.20 7.30 7.40 7.50 7.60 (mmHg) NR NR NR pH H+ (nmol/L) NR acute respiratory alkalosis Figure 3.1 Acid–base nomogram for plotting interpretation of the arterial blood gas (NR is normal range) Acid–Base, Electrolyte and Renal Emergencies 127 ACID–BASE DISTURBANCES 3 Causes of a high anion gap metabolic acidosis (anion gap >16) include: (i) Increased acid production: (a) ketoacidosis, e.g. diabetic, alcoholic, starvation (b) lactic acidosis (serum lactate >2.5 mmol/L): – type A: impaired tissue perfusion in cardiac arrest, shock, hypoxia, sepsis – type B: impaired carbohydrate metabolism in hepatic or renal failure, lymphoma, pancreatitis and drugs such as metformin. (ii) Decreased acid excretion, as in renal failure. (iii) Exogenous acid ingestion: (a) methanol, ethylene glycol, iron, cyanide and salicylates. 4 Causes of a normal anion gap metabolic acidosis (anion gap 8–16) include: (i) Renal: (a) renal tubular acidosis (b) carbonic anhydrase inhibitors. (ii) Gastrointestinal: (a) severe diarrhoea (b) small bowel fistula (c) drainage of pancreatic or biliary secretions. (iii) Other: (a) administration of synthetic amino acid solutions, ammonium chloride (b) recovery from ketoacidosis. 5 The body compensates to reduce the acid load by hyperventilation. The expected compensatory reduction in PaCO2 may be calculated (see Table 3.2): Table 3.2 Predicting the expected compensatory changes in PaCO2 and HCO3 Metabolic acidosis Metabolic alkalosis Predicted PaCO2 (kPa) 0.2  [HCO3] + 1 kPa (+/– 0.25) [HCO3] + 2.5 kPa (+/– 0.7) 10 Predicted PaCO2 (mmHg) 1.5  [HCO3] + 8 mmHg (+/– 2) 0.7  [HCO3] + 20 mmHg (+/– 5) Respiratory acidosis Respiratory alkalosis Predicted HCO3 (kPa) Acute 24 + (PaCO2 – 5.33)  0.75 Chronic 24 + (PaCO2 – 5.33)  3 Acute 24 – (5.33 – PaCO2)  1.5 Chronic 24 – (5.33 – PaCO2)  3.75 Predicted HCO3 (mmHg) 24 + PaCO2 – 40 10 24 +(PaCO2 – 40)  4 10 24 – (40 – PaCO2)  2 10 24 – (40 – PaCO2)  5 10 ACID–BASE DISTURBANCES 128 Acid–Base, Electrolyte and Renal Emergencies (i) The acidosis is partially compensated if the PaCO2 value is higher than predicted. (ii) A primary respiratory alkalosis coexists if the PaCO2 value is lower than predicted. 6 There are few specific clinical features due to an acute metabolic acidosis itself, other than hyperventilation known as Kussmaul breathing. 7 Urea and electrolytes (U&Es) confirm a primary fall in plasma bicarbonate below 22 mmol/L and usually show an associated rise in plasma potassium from an extracellular shift. MANAGEMENT 1 Provide supportive treatment with oxygen, i.v. fluids and treat symptomatic hyperkalaemia (see p. 132). 2 Correct any reversible underlying disorder: (i) Administer fluid and insulin, and replace potassium in diabetic ketoacidosis. (ii) Ensure adequate oxygenation and restore the intravascular volume to improve peripheral perfusion in lactic acidosis. 3 Refer the patient to the medical team. Dialysis will be necessary for renal failure and severe methanol or salicylate poisoning. METABOLIC ALKALOSIS DIAGNOSIS 1 An abnormal process or condition leading to a serum bicarbonate level of >28 mmol/L. 2 Causes include: (i) Addition of base to extracellular fluid: (a) recovery from organic acidosis secondary to metabolism of lactate and acetate (b) milk-alkali syndrome (c) massive blood transfusion (metabolism of citrate). (ii) Chloride depletion: (a) loss of gastric acid from vomiting or gastric aspiration (b) diuretics. (iii) Potassium depletion: (a) primary (Conn’s) and secondary hyperaldosteronism (b) Cushing’s or Bartter’s syndromes (c) severe hypokalaemia. (iv) Other: (a) laxative abuse (b) severe hypoalbuminaemia. ACID–BASE DISTURBANCES Acid–Base, Electrolyte and Renal Emergencies 129 3 The body compensates to reduce the bicarbonate load by hypoventilation. The expected compensatory rise in PaCO2 may be calculated (see Table 3.2). (i) This effect can be pronounced. Compensatory arterial PaCO2 levels as high as 86 mmHg (11.5 kPa) have been recorded. (ii) However, this compensatory PaCO2 elevation is variable: (a) pain or hypoxia cause the respiratory rate to rise and the PaCO2 to fall, thereby worsening the alkalosis. 4 There are few specific clinical features other than hypoventilation. Symptoms relating to associated hypocalcaemia and hypokalaemia may be present. MANAGEMENT 1 Give high-flow oxygen to reduce complications associated with hypoventilation. Try to avoid hyperventilation, as this worsens the alkalaemia. 2 Correct any reversible underlying disorder. 3 Administer normal saline at 500 mL/h i.v to replace lost chloride, restore intravascular volume, and enhance renal bicarbonate excretion. 4 Replace potassium with potassium chloride 10–20 mmol/h i.v. if the potassium is low. 5 Consider the use of acetazolamide 250 mg orally to increase the rate of bicarbonate elimination. RESPIRATORY ACIDOSIS DIAGNOSIS 1 A primary acid–base disorder associated with respiratory failure, inadequate alveolar ventilation and an arterial PaCO2 >45 mmHg (6.0 kPa). 2 Causes include: (i) Loss of central respiratory drive: (a) drugs, e.g. opiates, sedatives, anaesthetic agents (b) cerebral trauma, tumour, haemorrhage or stroke. (ii) Neuromuscular disorders: (a) Guillain–Barré syndrome, myasthenia gravis (b) toxins, e.g. organophosphate poisoning and snake venom. (iii) Respiratory compromise: (a) chronic obstructive pulmonary disease (COPD), critical asthma, restrictive lung disease (b) pulmonary oedema, aspiration, pneumonia (c) upper airway obstruction and laryngospasm (d) thoracic trauma, pneumothorax, diaphragm splinting (e) high thoracic or cervical spinal cord trauma (f) morbid obesity. 130 Acid–Base, Electrolyte and Renal Emergencies ACID–BASE DISTURBANCES 3 Clinical manifestations of respiratory acidosis are secondary to the hypercapnia. Look for the following: (i) The patient is usually warm, flushed, sweaty and tachycardic with ‘bounding’ peripheral pulses, from cardiovascular stimulation. (ii) Acute confusion, mental obtundation, somnolence and occasionally focal neurological signs from increased cerebral blood flow, cerebral vasodilation and raised intracranial pressure. 4 The body compensates to reduce acidaemia by minimizing the excretion of bicarbonate by the kidneys. However, this renal compensatory response is slow. (i) There is no time for any significant renal compensatory response in an acute respiratory acidosis. (ii) The kidneys are able to retain bicarbonate in chronic respiratory acidosis lasting over a few days, so the plasma bicarbonate level rises and the pH returns towards normal. (iii) The expected compensatory rise in plasma bicarbonate in acute and chronic respiratory acidosis may be calculated (see Table 3.2, p. 127). MANAGEMENT 1 Give oxygen and commence assisted ventilation by bag-mask ventilation. Call for senior emergency department (ED) doctor help and prepare for emergency endotracheal intubation, or non-invasive ventilation such as continuous positive airway pressure (CPAP), for instance in acute pul monary oedema. 2 Correct any reversible underlying disorder, e.g. naloxone for opiate poisoning. RESPIRATORY ALKALOSIS DIAGNOSIS 1 A primary acid–base disturbance, associated with increased alveolar ventilation and an arterial PaCO2 of <35 mmHg (4.7 kPa). 2 Causes include: (i) Asthma, pneumonia, pulmonary embolus, pulmonary oedema and pulmonary fibrosis (mediated by intrapulmonary receptors). (ii) Hypoxia (mediated by peripheral chemoreceptors). (iii) Centrally induced hyperventilation secondary to respiratory centre stimulation: (a) head injury, stroke Warning: the pulse oximeter may record a normal oxygen saturation in a patient receiving supplemental oxygen, despite the presence of dangerous hypercapnoea from hypoventilation. ! ELECTROLYTE DISORDERS Acid–Base, Electrolyte and Renal Emergencies 131 (b) pain, fear, stress, psychogenic, voluntary (c) fever (cytokines), pregnancy (progesterone), thyrotoxicosis, liver disease (d) drugs, e.g. salicylate poisoning. (iv) Iatrogenic from excessive artificial ventilation. 3 Clinical manifestations are secondary to hypocapnoea, hypokalaemia and hypocalcaemia. Look for the specific effects of hypocapnoea: (i) Circumoral paraesthesia, carpopedal spasm and tetany from neuromuscular irritability. (ii) Light-headedness and confusion from cerebral vasoconstriction (usually adapts in 6–8 h). (iii) Cardiac arrhythmias and decreased myocardial contractility. 4 The body compensates to reduce alkalaemia by excreting or buffering bicarbonate ions. (i) A moderate compensatory response via a non-renal-mediated buffering process can reduce plasma bicarbonate levels to 18–20 mmol/L in an acute respiratory alkalosis within hours. (ii) The kidneys increase the rate of bicarbonate excretion in chronic respiratory alkalosis, and reduce serum bicarbonate levels to as low as 12–15 mmol/L returning the pH towards normal (a) this renal compensatory response is slow. The maximal effect takes 2–3 days to occur. (iii) The expected compensatory fall in plasma bicarbonate in acute and chronic respiratory alkalosis may be calculated (see Table 3.2, p. 127). MANAGEMENT 1 Give oxygen to treat any coexistent hypoxia. 2 Look for and correct any reversible underlying disorder. 3 Never diagnose ‘hysterical’ hyperventilation until subtle presentations of pneumonia, pulmonary embolism, pneumothorax, fever, etc., have been actively excluded. 4 Otherwise if no significant underlying cause for hyperventilation is likely, reassure the patient and/or ask them to rebreathe into a paper bag. ELECTROLYTE DISORDERS Electrolyte disturbances are commonly associated with cardiovascular emergencies and may cause cardiac arrhythmias and cardiopulmonary arrest. Prompt recognition and immediate treatment of electrolyte disorders can prevent cardiac arrest. ELECTROLYTE DISORDERS 132 Acid–Base, Electrolyte and Renal Emergencies POTASSIUM DISORDERS The potassium gradient across the cellular membrane is essential to maintain excitability of nerve and muscle cells, including the myocardium. Extracellular potassium levels are strictly regulated between 3.5 and 5.0 mmol/L and may be affected by many processes including serum pH. As the pH rises, serum potassium falls as potassium is shifted intracellularly; when serum pH decreases, serum potassium increases as intracellular potassium shifts into the vascular space. HYPERKALAEMIA DIAGNOSIS 1 This is the most common electrolyte disturbance associated with cardiac arrest. 2 Causes include: (i) Increased potassium intake: (a) oral or i.v. potassium supplements, transfusion of stored blood. (ii) Increased production: (a) burns, ischaemia, haemolysis (b) rhabdomyolysis, tumour lysis syndrome (c) intense physical activity. (iii) Decreased renal excretion: (a) acute or chronic renal failure (b) drugs, e.g. potassium-sparing diuretics, angiotensinconverting enzyme (ACE) inhibitors, non-steroidal antiinflammatory drugs (NSAIDs) (c) Addison’s disease, hypoaldosteronism. (iv) Transcellular compartmental shift: (a) acidosis (metabolic or respiratory) (b) hyperglycaemia (c) digoxin poisoning, suxamethonium. (v) Factitious: (a) haemolysed specimen, thrombocytosis, massive leucocytosis. 3 The risk of adverse events associated with hyperkalaemia increases with the serum concentration level. The severity of hyperkalaemia may be defined by the serum potassium level: (i) Mild hyperkalaemia: potassium >5.5 mmol/L. (ii) Moderate hyperkalaemia: potassium 6.0–6.5 mmol/L. (iii) Severe hyperkalaemia: potassium >6.5 mmol/L. 4 Patients may present with weakness, ascending paralysis, loss of deep tendon reflexes, and respiratory failure. 5 Gain i.v. access and attach an electrocardiography (ECG) monitor and pulse oximeter to the patient. Acid–Base, Electrolyte and Renal Emergencies 133 ELECTROLYTE DISORDERS 6 Look for the characteristic ECG changes that are usually progressive and determined by the absolute serum potassium, as well as its rate of increase: (i) Tall, peaked (tented) T waves. (ii) Prolonged PR interval with flattened P waves. (iii) ST segment depression. (iv) QRS widening, absent P waves and sinusoidal wave pattern. (v) Ventricular tachycardia and cardiac arrest from ventricular fibrillation, pulseless electrical activity (PEA) or asystole. MANAGEMENT 1 Give high-flow oxygen via face mask. Cease any exogenous sources of potassium supplementation. 2 Severe hyperkalaemia (>6.5 mmol/L) or hyperkalaemia with life-threatening ECG changes. Provide immediate cardioprotection to prevent cardiac arrest: (i) Give 10% calcium chloride 10 mL i.v. over 2–5 min, repeated until the ECG and cardiac output normalize (a) this does not lower the potassium level, but antagonizes the deleterious effects of hyperkalaemia on the myocardium, reducing the risk of ventricular fibrillation (onset of protection in 1–3 min). (ii) Use the other therapies outlined below to shift potassium into the cells, and eliminate potassium from the body. 3 Moderate hyperkalaemia (6.0–6.5 mmol/L). Shift potassium intracellularly with: (i) 50% dextrose 50 mL i.v. with 10 units of soluble insulin over 20 min (onset of action 15 min, with maximal effect within 1 h). (a) beware more rapid delivery of the 50% dextrose with the insulin as it may paradoxically release intracellular potassium due to its hypertonicity (b) give the soluble insulin alone in hyperglycaemic patients with a blood sugar of >12 mmol/L (i.e. without the dextrose). (ii) Salbutamol 5–10 mg nebulized. Several doses may be required (onset of action 15 min). (iii) 8.4% sodium bicarbonate 50 mL i.v. over 5 min, provided there is no danger of fluid overload, as it contains 50 mmol sodium (a) less effective as a sole agent, but works well in combination with salbutamol and dextrose/insulin (onset of action 15–30 min), and if a metabolic acidosis is present. Tip: consider hyperkalaemia in any patient with an arrhythmia or in cardiac arrest. ✓ 134 Acid–Base, Electrolyte and Renal Emergencies ELECTROLYTE DISORDERS 4 Mild hyperkalaemia (5.5–6.0 mmol/L). Remove potassium from the body with: (i) Frusemide (furosemide) 40–80 mg i.v. (onset of action with diuresis, provided not anuric). (ii) Potassium-exchange resin: calcium resonium 30 g orally or by enema (onset of action 1–3 h after administration). 5 Refer the patient to the medical team, and according to the potassium level and underlying cause, organize urgent haemodialysis or peritoneal dialysis as needed, particularly in known renal failure. HYPOKALAEMIA DIAGNOSIS 1 Hypokalaemia is associated with an increased incidence of cardiac arrhythmias especially in those patients with pre-existing heart disease, and in those treated with digoxin. 2 Causes include: (i) Inadequate intake of potassium, e.g. alcoholism, starvation. (ii) Abnormal gastrointestinal losses from vomiting, diarrhoea and laxative abuse. (iii) Abnormal renal losses: (a) Cushing’s, Conn’s and Bartter’s syndromes (b) ectopic adrenocorticotrophic hormone (ACTH) production (c) drugs, e.g. diuretics and steroids (d) hypomagnesaemia. (iv) Compartmental shift: (a) metabolic alkalosis (b) insulin (c) drugs, e.g. salbutamol, terbutaline, aminophylline (d) hypomagnesaemia. 3 Hypokalaemia occurs when serum potassium level is <3.5 mmol/L and is defined as severe if the serum potassium is <2.5 mmol/L. 4 Look for weakness, fatigue, leg cramps and constipation. (i) Polydipsia, polyuria, rhabdomyolysis, ascending paralysis and respiratory compromise may develop as the potassium level falls. 5 Gain i.v. access and attach an ECG monitor. Non-specific ECG changes include: (i) Flat or inverted T waves, prominent U waves. (ii) Prolonged PR interval. (iii) ST segment depression. (iv) Ventricular arrhythmias, including torsades de pointes. ELECTROLYTE DISORDERS Acid–Base, Electrolyte and Renal Emergencies 135 MANAGEMENT 1 Replace potassium immediately in the following situations: (i) Serum potassium <3.0 mmol/L. (ii) Serum potassium 3.0–3.5 mmol/L in patients with chronic heart failure or cardiac arrhythmias, particularly if on digoxin or following myocardial infarction. 2 Give potassium 10–20 mmol/h i.v. under ECG control using a fluid infusion device, but do not exceed 40 mmol/h. 3 Give magnesium sulphate 10 mmol (2.5 g) diluted in 100 mL normal saline over 30–45 min in severe or intractable hypokalaemia, as magnesium enhances potassium uptake and helps maintain intracellular potassium levels. 4 Change to oral supplements or maintenance i.v. replacement when the serum potassium is >3.5 mmol/L. 5 Refer the patient to the medical team as necessary for treatment of the underlying condition. SODIUM DISORDERS Sodium is the most common intravascular cation. It has a major influence on serum osmolality and determines the volume of the extracellular fluid. HYPERNATRAEMIA DIAGNOSIS 1 Hypernatraemia is defined as a serum sodium level of >145–150 mmol/L. 2 Causes include: (i) Decreased fluid intake with normal fluid loss: (a) disordered thirst perception, e.g. hypothalamic lesion (b) inability to communicate water needs, e.g. cerebrovascular accident, infants, intubated patients. (ii) Hypotonic fluid loss, with water loss in excess of salt loss: (a) skin loss from excessive sweating in hot climates, dermal burns (b) gastrointestinal loss from diarrhoea or vomiting (c) renal loss from impaired salt-concentrating ability, e.g. diabetes insipidus, osmotic diuretic agents, hyperglycaemia, hypercalcaemia, chronic renal disease. Tip: consider hypokalaemia in any patient with an arrhythmia or in cardiac arrest. ✓ 136 Acid–Base, Electrolyte and Renal Emergencies ELECTROLYTE DISORDERS (iii) Increased salt load: (a) hyperaldosteronism or Cushing’s syndrome (b) ingestion of seawater, salt tablets, and administration of sodium bicarbonate or hypertonic saline. 3 Symptoms and signs of hypernatraemia are progressive and directly related to the serum osmolality level. Look for: (i) Increased thirst, weakness, lethargy and irritability (>375 mOsm/kg). (ii) Altered mental status, ataxia, tremor and focal neurological signs (>400 mOsm/kg). (iii) Seizures and coma (>430 mOsm/kg). 4 Assess the underlying volume status. Look at the skin turgor, jugular venous pressure (JVP), measure lying and sitting blood pressures, listen for basal crackles. 5 Send blood for full blood count (FBC), U&Es, liver function tests (LFTs), and serum osmolality. 6 Perform an ECG and request a chest radiograph (CXR). MANAGEMENT 1 Give high-flow oxygen via a face mask. 2 Replace fluid orally, or via a nasogastric tube in stable asymptomatic patients. 3 Give hypovolaemic patients volume replacement with i.v. normal saline without causing too rapid a reduction in the serum sodium. (i) Aim to reduce serum sodium by 0.5–1.0 mmol/L per h. HYPONATRAEMIA DIAGNOSIS 1 Hyponatraemia is defined by a serum sodium level <130 mmol/L. 2 Causes include: (i) Factitious ‘pseudohyponatraemia’ (a) associated with hyperglycaemia, hyperlipidaemia, hyperproteinaemia (b) correct the sodium for hyperglycaemia by adjusting the serum sodium up by 1 mmol/L for every 3 mmol/L elevation in blood sugar. (ii) Hypovolaemic hyponatraemia (a) urinary sodium >20 mmol/L: renal causes including diuretics, Addison’s disease, salt-losing nephropathy, glycosuria, ketonuria (b) urinary sodium <20 mmol/L: extrarenal losses such as vomiting, diarrhoea, burns, pancreatitis. Acid–Base, Electrolyte and Renal Emergencies 137 ELECTROLYTE DISORDERS (iii) Normovolaemic hyponatraemia (a) urine osmolality > serum osmolality: – syndrome of inappropriate antidiuretic hormone secretion (SIADH) due to head injury, meningoencephalitis, CVA, pneumonia, COPD, neoplasia, human immunodeficiency virus (HIV) infection, drugs such as carbamazepine, NSAIDs and antidepressants – positive-pressure ventilation, porphyria (b) urine osmolality < serum osmolality: – hypotonic post-operative fluids such as 5% dextrose or 4% dextrose 1/5 normal saline, transurethral resection of the prostate (TURP) irrigation fluid, psychogenic polydipsia, ‘tea and toast’ diet, beer potomania. (iv) Hypervolaemic hyponatraemia (a) urinary sodium <20 mmol/L: congestive cardiac failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia, hepatorenal syndrome (b) urinary sodium >20 mmol/L: steroids, cerebral salt wasting, chronic renal failure, hypothyroidism. 3 Clinical features progress as the serum sodium level drops, but depend also on the rate of fall, i.e. the more rapid the fall the greater the symptoms: (i) Na >125 mmol/L: usually asymptomatic. (ii) Na 115–125 mmol/L: lethargy, weakness, ataxia, and vomiting. (iii) Na <115 mmol/L: confusion, headache, convulsions, and coma. 4 Assess the underlying volume status: (i) Look at the skin turgor, jugular venous pressure (JVP), measure lying and sitting blood pressure (BP), listen for basal crackles. 5 Send blood for FBC, U&Es, LFTs, thyroid function and serum osmolality. Send urine for sodium and osmolality. 6 Perform an ECG and request a CXR. MANAGEMENT 1 Commence high-flow oxygen by face mask. 2 Asymptomatic patients: (i) Discontinue implicated drug therapy and treat the underlying medical condition, e.g. antibiotics for sepsis. (ii) Restrict fluid intake to 50% of estimated maintenance fluid requirements in SIADH, i.e. around 750 mL/day. (iii) Aim to increase the serum sodium gradually by 0.5 mmol/L per h, to a maximum rate of 12 mmol/L per 24 h. 3 Get senior ED doctor help if the patient has neurological symptoms. (i) Administer 3% hypertonic saline to raise serum sodium levels by 1 mmol/h. 138 Acid–Base, Electrolyte and Renal Emergencies ELECTROLYTE DISORDERS (ii) Consult with the intensive care team if the patient develops seizures or coma, and give 20% hypertonic saline 10–20 mL by rapid i.v. infusion. CALCIUM DISORDERS Calcium is the most abundant mineral in the body and essential for bone strength, neuromuscular function and a myriad of intracellular processes. Minor degrees of hypercalcaemia may be the first clue to an underlying diagnosis of malignancy or hyperparathyroidism. HYPERCALCAEMIA DIAGNOSIS 1 Hypercalcaemia is defined by a serum calcium level of >2.6 mmol/L after correction for albumin. 2 Causes include: (i) Malignancy, sarcoidosis, thyrotoxicosis and tuberculosis. (ii) Primary or tertiary hyperparathyroidism. (iii) Drugs, e.g. thiazides. (iv) Addison’s disease. 3 Patients present with anorexia, thirst, weakness, abdominal pain, constipation, lethargy and confusion or psychosis. Coma may occur at serum calcium levels of >3.5 mmol/L. 4 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, LFTs, calcium, lipase and thyroid function. 5 Perform an ECG. Typical changes include: (i) Bradycardia. (ii) Short QT interval with a widened QRS. (iii) Flattened T waves, atrioventricular block and cardiac arrest. 6 Request a CXR that may show an underlying cause. MANAGEMENT 1 Commence rehydration with 0.9% normal saline i.v. at 500 mL/h. 2 Give frusemide (furosemide) 20–40 mg i.v. after urine output is established to maintain a diuresis. 3 Refer the patient to the medical team for longer-term therapy with steroids, bisphosphonates or dialysis. Warning: too rapid correction of hyponatraemia may cause coma associated with osmotic demyelination syndrome or central pontine demyelinosis, or the underlying disease process itself. ! ELECTROLYTE DISORDERS Acid–Base, Electrolyte and Renal Emergencies 139 HYPOCALCAEMIA DIAGNOSIS 1 Hypocalcaemia is defined by a serum calcium level of <2.1 mmol/L after correction for albumin. 2 Causes include: (i) Chronic renal failure, acute pancreatitis. (ii) Rhabdomyolysis, tumour lysis syndrome, whole blood transfusion and toxic shock syndrome. (iii) Primary respiratory alkalosis (hyperventilation). (iv) Calcium-channel blocker overdose. 3 Patients present with paraesthesiae of the extremities and face, muscle cramps, carpopedal spasm, stridor, tetany, seizures and cardiac failure. 4 Look for hyper-reflexia and a positive Chvostek’s or Trousseau’s sign: (i) Chvostek’s sign: facial twitching from percussing the facial nerve in front of the ear. (ii) Trousseau’s sign: carpal spasm after 3 min of inflation of a BP cuff above systolic pressure. 5 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, LFTs, creatine kinase (CK), magnesium and lipase. 6 Perform an ECG and look for: (i) QT interval prolongation, T wave inversion. (ii) AV block, torsades de pointes (cardiac arrest may ensue). MANAGEMENT 1 Commence rehydration with 0.9% normal saline i.v. at 250 mL/h. 2 Look for and treat the underlying cause. 3 Give calcium i.v. in symptomatic patients: (i) 10% calcium chloride 10–40 mL i.v. (ii) discuss further elemental calcium infusion with the medical team or intensive care unit (ICU) admitting team. 4 Give calcium by oral calcium supplements, or vitamin D-rich milk in asymptomatic patients. MAGNESIUM DISORDERS Magnesium is the second most abundant intracellular cation and essential for stabilizing excitable cellular membranes and facilitating the movement of calcium, potassium and sodium into and out of cells. HYPERMAGNESAEMIA DIAGNOSIS 1 Hypermagnesaemia occurs at a serum level of >1.1 mmol/L. 140 Acid–Base, Electrolyte and Renal Emergencies ELECTROLYTE DISORDERS 2 Causes include: (i) Renal failure. (ii) Iatrogenic magnesium administration i.v. (iii) Rhabdomyolysis and tumour lysis syndrome. 3 Patients present with muscular weakness, respiratory depression, confusion, ataxia and hypotension. (i) Extreme magnesium toxicity >5.0 mmol/L may be associated with bradycardia, respiratory depression, altered conscious level and cardiac arrest. 4 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, LFTs, magnesium and thyroid function. 5 ECG changes are similar to hyperkalaemia. MANAGEMENT 1 Commence i.v. rehydration with normal saline at 500 mL/h. 2 Give 10% calcium chloride 10 mL i.v. for life-threatening arrhythmias and severe magnesium toxicity. 3 Otherwise give a combination of normal saline i.v. and frusemide (furosemide) 1 mg/kg i.v. to increase the renal excretion of magnesium, provided the urine output is normal. (i) Check calcium levels regularly to prevent hypocalcaemia, which will worsen the symptoms of magnesium toxicity. 4 Refer the patient to the medical team or ICU for consideration of dialysis in severe toxicity with levels >5.0 mmol/L. HYPOMAGNESAEMIA DIAGNOSIS 1 Hypomagnesaemia occurs at a serum level of <0.6 mmol/L. 2 Causes include: (i) Increased magnesium losses: (a) gastrointestinal loss from vomiting, diarrhoea, pancreatitis (b) acute tubular necrosis (ATN) or chronic renal failure (c) drugs, e.g. alcohol, diuretics, gentamicin, digoxin. (ii) Reduced magnesium intake in starvation, malnutrition, chronic alcoholism. (iii) Metabolic with low levels of calcium, phosphate and potassium. (iv) Endocrine such as diabetic ketoacidosis (DKA), thyrotoxicosis, hyperparathyroidism, hypothermia. 3 Clinical manifestations are non-specific and may mimic hypocalcaemia and hypokalaemia. Look for tremor, paraesthesiae, tetany, altered mental state, ataxia, nystagmus and seizures. Acid–Base, Electrolyte and Renal Emergencies 141 ACUTE RENAL FAILURE 4 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, LFTs, CK, magnesium, lipase and thyroid function. 5 Perform an ECG and look for: (i) Prolongation of PR and QT intervals. (ii) ST segment depression. (iii) Widened QRS and torsades de pointes. MANAGEMENT 1 Commence rehydration with 0.9% normal saline i.v. at 250 mL/h. 2 Look for and treat the underlying cause. 3 Administer oral magnesium supplements to asymptomatic patients. 4 Start parenteral magnesium in more severe cases: (i) Give patients with seizures, torsades de pointes, or cardiac arrest 50% magnesium sulphate 8 mmol or 2 g i.v. over 5–10 min. (ii) Give other symptomatic patients 50% magnesium sulphate 8 mmol (2 g) i.v. at a slower rate over 30–60 min. 5 Refer the patient to the medical team and discuss further elemental magnesium treatment. ACUTE RENAL FAILURE ACUTE KIDNEY INJURY Acute renal failure is now encompassed in the term ‘acute kidney injury’ (AKI) that denotes the spectrum of rapid loss of kidney function from minor changes to the requirement for renal replacement therapy. The RIFLE classification is used for diagnostic staging of acute kidney injury and allows differentiation between mild and severe, as well as early and late cases. The RIFLE criteria refer to: Risk: serum creatinine ·  1.5; or urine production <0.5 mL/kg per hour for 6 h Injury: serum creat ·  2; or urine production <0.5 mL/kg per hour for 12 h Failure: serum creat ·  3 or >355 μmol/L (with acute rise >44); or urine output <0.3 mL/kg per hour for 24 h ‘oliguria’, or anuria for 12 h Loss: persistent AKI with complete loss of kidney function for >4 weeks End-stage kidney disease: complete loss of kidney function for >3 months. DIAGNOSIS 1 Acute renal failure leads to an abrupt, sustained increase in serum urea and creatinine secondary to decreased glomerular filtration rate (GFR), usually associated with oliguria or anuria. 142 Acid–Base, Electrolyte and Renal Emergencies ACUTE RENAL FAILURE 2 Causes include: (i) Pre-renal failure (decreased renal perfusion): (a) shock, burns, sepsis, dehydration, low-output cardiac failure (b) renovascular disease: renal artery stenosis, renal artery emboli. (ii) Intrinsic renal failure: (a) acute tubular necrosis (ATN): ischaemia, sepsis, toxins, e.g. gentamicin, radiographic contrast, myoglobin, ethylene glycol (b) acute interstitial nephritis: drugs (including antibiotics and NSAIDs), infection, sarcoidosis, autoimmune disease, e.g. systemic lupus erythematosus (c) acute glomerulonephritis: post-infectious, vasculitis, autoimmune disease, complement-related (d) acute cortical necrosis: profound hypoperfusion, e.g. obstetric complication with haemorrhage (e) miscellaneous: malignant hypertension, renal vein thrombosis. (iii) Post-renal failure Obstruction may be extramural, intramural or intraluminal at any point from the renal tubule to the distal urethra. Causes include: (a) ureteric obstruction to a single kidney, or bilateral ureteric obstruction to both kidneys (b) retroperitoneal fibrosis; ureteric strictures, calculi or crystal deposition; tumours such as uterine cancer; prostatic disease such as benign prostatic hypertrophy or malignancy. 3 Take a thorough history, including a drug history for potential nephrotoxic agents, and obtain an accurate weight on arrival as this will help monitor treatment progress. 4 As acute kidney injury is associated with multiple pathologies it may present in a variety of ways. (i) Pre-renal failure with symptoms and signs of hypovolaemia such as confusion, dehydration, orthostatic hypotension, oliguria and anuria. (ii) Nephritic syndrome with acute hypertension, haematuria with red cell casts and dysmorphic red cells, and generalized oedema from acute glomerular disease. (iii) Flank pain, loin pain and microscopic or macroscopic haematuria. 5 Examine patients systematically. Look for: (i) Volume status (a) signs of volume depletion: hypotension, tachycardia, decreased skin turgor, dry mucous membranes in a patient with decreased renal perfusion associated with a pre-renal condition Acid–Base, Electrolyte and Renal Emergencies 143 ACUTE RENAL FAILURE (b) signs of volume overload: raised JVP, peripheral oedema and respiratory crepitations in intrinsic renal disease. (ii) Clinical manifestations of acute uraemia: sallow complexion, asterixis (flap), pericardial or pleural rub, pulmonary oedema or pleural effusion, altered mental status, confusion, seizures. (iii) Signs of post-renal obstruction: enlarged prostate on per rectal (p.r.) examination, cervical or uterine mass lesion on vaginal examination. 6 Insert an i.v. cannula and send bloods for FBC, U&Es, LFTs, blood sugar, CK, calcium and uric acid. Take an arterial blood gas analysis. Attach a cardiac monitor to the patient. 7 Organize a bedside bladder scan to determine the presence of urinary retention, which may signal a post-renal obstruction cause. 8 Insert an indwelling catheter and send a midstream urine sample for urinary osmolality and electrolyte screen to help distinguish a pre-renal from an intrinsic renal cause of renal failure. (i) Request microscopy for signs of glomerulonephritis such as red cell casts or >70% dysmorphic red cells, and for myoglobinuria, haemoglobinuria (absent red cells) or evidence of infection. 9 Take an ECG to look for signs of hyperkalaemia, or an arrhythmia such as atrial fibrillation which may, for instance, be associated with renal embolic disease. 10 Request a CXR to look for volume overload, metastatic disease and pulmonary– renal syndromes such as Wegener’s granulomatosis. 11 Arrange an urgent renal tract ultrasound to look at the size of the kidneys, particularly looking for evidence of obstruction anywhere from the renal pelvis to the bladder outlet. (i) Shrunken kidneys suggest an acute on chronic process. (ii) Exceptions are polycystic kidneys, amyloid or HIV nephropathy, and diabetic nephropathy, which are associated with enlarged or preserved renal size even with chronic renal failure. MANAGEMENT 1 Determine the need for urgent treatment. (i) Treat severe hyperkalaemia with 10% calcium chloride 10 mL i.v. over 2–5 min, repeated until the ECG and cardiac output normalize (see p. 132). (ii) Treat accelerated hypertension and any suspected sepsis including urinary tract. (iii) Avoid nephrotoxic drugs such as NSAIDs and iodinated contrast. (iv) Arrange early haemodialysis for patients with volume overload 144 Acid–Base, Electrolyte and Renal Emergencies FURTHER READING and refractory pulmonary oedema, pericarditis, uraemic encephalopathy or if a dialysable drug is responsible such as lithium or salicylate. 2 Commence fluid resuscitation with caution. (i) Aim to optimize renal perfusion by treating hypovolaemia, but take care not to precipitate acute volume overload. (ii) Closely monitor urine output. 3 Refer the patient to the medical, renal or urology team depending on the suspected underlying pathology, response to resuscitation, and any urgent requirement for dialysis. FURTHER READING American Heart Association (2010) Part 12: Cardiac arrest in special situations: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S829–61. European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances. Resuscitation 81: 1400–33. Kellum JA, Bellomo R, Ronco C (2008) Definition and classification of acute kidney injury. Nephron Clinical Practice 109: c182–7. INFECTIOUS DISEASE AND FOREIGN TRAVEL EMERGENCIES Section IV 146 Infectious Disease and Foreign Travel Emergencies Neutropenia has a significant generalized infection risk with a temperature >100°F (38°C) in patients with an absolute neutrophil count <0.5 109/L, or <1.0 109/L if the count is rapidly falling. DIAGNOSIS 1 Neutropenic patients may already know their diagnosis and/or be receiving treatment, or can present as a new case. 2 Causes of neutropenia include: (i) Reduced neutrophil production: (a) aplastic anaemia (b) leukaemia, lymphoma (c) myeloproliferative syndrome (d) metastatic bone marrow disease (e) drug-induced agranulocytosis, including chemotherapy (f) megaloblastic anaemia crisis. (ii) Reduced neutrophil survival: (a) systemic lupus erythematosus (SLE) (b) immune-mediated (c) drug-related (d) Felty syndrome. (iii) Reduced neutrophil circulation: (a) septicaemia (b) hypersplenism. 3 Ask about constitutional symptoms including fever and malaise, plus organspecific features such as cough, frequency and dysuria, diarrhoea or headache and confusion. (i) Take a detailed drug history, contact and travel history. 4 Record the vital signs and note any focal sources of sepsis including the skin, ears, throat and perineum, indwelling catheters, and for evidence of anaemia or bruising suggesting a pancytopenia. 5 Establish venous access with strict asepsis, and send blood for full blood count (FBC), coagulation profile, electrolyte and liver function tests (ELFTs) and two sets of blood cultures from different venepuncture sites. 6 Request a chest radiograph (CXR) and send a midstream urine (MSU) sample. MANAGEMENT 1 Start empirical antibiotic therapy initially, unless there is a clear focus of infection, and discuss with an infectious disease physician or microbiologist. FEBRILE NEUTROPENIC PATIENT Infectious Disease and Foreign Travel Emergencies 147 HEPATITIS (i) Urgent empirical i.v. therapy with broad-spectrum antimicrobials is universal, although the optimal regimen will depend on local bacteriological susceptibilities and preference. Give: (a) piperacillin 4 g with tazobactam 0.5 g i.v. 8-hourly, plus gentamicin 5 mg/kg i.v. once daily when no source is apparent (b) ceftazidime 2 g i.v., t.d.s. if penicillin-sensitive, plus gentamicin 5 mg/kg i.v. once daily (c) add vancomycin 1.5 g i.v. 12-hourly for possible line sepsis, MRSA or if the patient is shocked. 2 Admit the patient under the medical team, even if the patient looks well with only a fever, as rapid deterioration may occur. (i) Refer haemodynamically unstable patients to the intensive care unit (ICU). HEPATITIS DIAGNOSIS 1 Causes of hepatitis include: (i) Viruses such as enterically transmitted hepatitis A or E, or parenterally spread hepatitis B, C, D or G, and infectious mononucleosis, cytomegalovirus (CMV) or herpes simplex virus (HSV). (ii) Bacteria such as leptospirosis, or amoebae. (iii) Toxins and drugs such as alcohol, Amanita mushrooms, methyldopa, statins, chlorpromazine, isoniazid and paracetamol (remember the possibility of acute poisoning). 2 Hepatitis presents with anorexia, malaise, nausea, vomiting, abdominal pain and joint pain. 3 Look for a raised temperature, jaundice, tender hepatomegaly and splenomegaly. Assess for confusion or an altered conscious level. 4 Send blood for serology for hepatitis A, B or C, plus FBC, coagulation profile, ELFTs and lipase. 5 Test the urine for bilirubin and urobilinogen. MANAGEMENT 1 Refer unwell patients to the medical team. (i) This should include those with persistent vomiting, dehydration, encephalopathy or a bleeding tendency with a prolonged prothrombin time. 148 Infectious Disease and Foreign Travel Emergencies GASTROINTESTINAL TRACT INFECTION 2 Otherwise, discharge the patient with advice to avoid preparing food for others and to use their own knife, fork, spoon, cup and plate (assuming the patient could have hepatitis A or E). 3 Advise the patient to avoid alcohol and cigarettes. 4 Give the patient a referral letter to medical outpatients or to their general practitioner (GP) for definitive diagnosis and follow-up. GASTROINTESTINAL TRACT INFECTION DIAGNOSIS 1 The commonest manifestation is sudden acute diarrhoea, often with vomiting. 2 Causes of infectious diarrhoea include: (i) Toxin-related diarrhoea from staphylococcal food poisoning which has a precipitate onset in hours, as does Bacillus cereus enterotoxin from rice, in which vomiting and abdominal cramps predominate. (ii) Viral diarrhoea from the rotavirus in very young children and Norwalk-like viruses in older children and adults, with an incubation period of 1–2 days, sometimes occurring in outbreaks of non-bloody diarrhoea. (iii) Salmonella with an incubation period of 6–72 h and Shigella infections with an incubation period of 1–3 days result in fever, malaise, diarrhoea (which may be blood-stained), vomiting and abdominal pain. (iv) Campylobacter infection has an incubation period of 2–5 days and presents with colicky abdominal pain, which may precede the onset of diarrhoea, that is watery and offensive, and sometimes blood-stained. (v) Giardiasis has an incubation period of 3–25 days and causes explosive watery diarrhoea, which often persists for weeks. Chronic infection may eventually cause malabsorption with steatorrhoea. Ask about travel to Russia or North America, and contact with children in day care who have had recent diarrhoea. (vi) Amoebiasis may also cause a chronic, recurring diarrhoea, with stools containing blood and mucus. Ask about travel to Africa, Asia or Latin America. Infectious Disease and Foreign Travel Emergencies 149 GASTROINTESTINAL TRACT INFECTION (vii) ‘Traveller’s diarrhoea’ is most often due to enterotoxigenic Escherichia coli, and is usually self-limiting over 2–5 days, causing watery stools and occasionally vomiting. Fever is unusual, and may indicate a more serious infection that needs active investigation, including malaria or even epidemic influenza. 3 The most important feature in all cases, after establishing a contact or travel history, is clinical evidence of dehydration. (i) Dehydration causes thirst, lassitude, dry lax skin, tachycardia and postural hypotension, leading to oliguria, confusion and coma when critical. 4 Also consider other causes of acute diarrhoea including drug-related, Clostridium difficile antibiotic-related diarrhoea (CDAD), Crohn’s disease, ulcerative colitis, ischaemic colitis, irritable bowel syndrome, and ‘spurious’ from faecal impaction. 5 Send blood for FBC and ELFTs, and commence an i.v. infusion of normal saline in all dehydrated, febrile or toxic patients. (i) Send a stool specimen for C. difficile toxin assay, if antibioticassociated diarrhoea is suspected following any antibiotic use in the previous 8 weeks. MANAGEMENT 1 Admit dehydrated, toxic, very young or elderly, and immunosuppressed patients for rehydration. 2 Allow other patients home and encourage them to drink plenty of fluid. (i) Alternatively, give the patient an oral glucose and electrolyte rehydration solution, which may also be purchased over the counter. (ii) Give an antimotility agent such as loperamide 4 mg initially, followed by 2 mg after each loose stool to a maximum of 16 mg/ day (not in children). 3 Ask the patient to return within 24–48 h if symptoms persist: (i) Send stools for microscopy and culture then. (ii) Consider empirical treatment for moderate to severe systemic illness with bloody diarrhoea or for associated rigors (a) give ciprofloxacin 500 mg orally b.d. for 5–7 days (not in children). (iii) Give tinidazole 2 g orally once if Giardia is suspected. 4 Arrange follow-up in medical outpatients or by the local GP. (i) Stop any antibiotics if CDAD is confirmed and give metronidazole 400 mg orally t.d.s. for 7 days. 150 Infectious Disease and Foreign Travel Emergencies SEXUALLY TRANSMITTED DISEASES DIAGNOSIS 1 A sexually transmitted disease (STD) may be caused by non-specific infection, Chlamydia, gonococcus, HSV, human papilloma virus, Trichomonas, scabies or lice, syphilis, and of course human immunodeficiency virus (HIV). 2 Males may present with dysuria, urethral discharge, penile ulceration, warts, epididymo-orchitis and balanitis. 3 Females may present with vaginal discharge, vaginal pruritus, ulceration, warts, menstrual irregularities and abdominal pain. (i) Pelvic inflammatory disease is commonly sexually acquired (see p. 379). 4 Take swabs for bacterial, viral and chlamydial studies for microscopy, culture and nucleic acid amplification, if you intend to commence treatment. (i) Discuss the swabs and transport medium with your microbiology lab if you are unsure (ii) Arrange a first-voided urine specimen for nucleic acid testing for Chlamydia trachomatis or Neisseria gonorrhoeae. MANAGEMENT 1 All STDs deserve expert diagnosis, treatment, follow-up and partner-contact tracing most readily available in the genitourinary medicine clinic (Special Clinic). 2 As many patients are reluctant to attend these clinics, explain carefully the local appointment system, what to expect, and how to locate the clinic, and refer the patient on. (i) Advise males not to empty the bladder for at least 4 h before attendance. 3 Commence empirical antibiotic treatment in the homeless or itinerant patient considered unlikely to attend any clinic. (i) Give azithromycin 1 g orally as a single dose plus ceftriaxone 500 mg i.m. for urethritis. 4 In addition, consider treating the patient with an immediately painful condition such as genital herpes simplex: (i) Give aciclovir 400 mg orally t.d.s. or famciclovir 250 mg orally t.d.s. for 5 days. 5 Admit a patient under the medical or gynaecology team for treatment of the acute manifestations of HIV infection, secondary syphilis, acute Reiter’s syndrome, disseminated gonococcal infection, severe primary genital herpes, or acute severe salpingitis. Infectious Disease and Foreign Travel Emergencies 151 NEEDLESTICK AND SHARPS INCIDENTS INOCULATION INCIDENT WITH HIV RISK DIAGNOSIS 1 The risk of seroconversion is 0.1–0.5% following accidental inoculation of blood or infectious material from a suspected HIV-positive person. 2 This risk depends on the nature and extent of the inoculation, and the viral disease activity of the HIV-positive source. 3 Take 10 mL clotted blood from the injured person, and if possible 10 mL with consent from the source. Send for HIV, hepatitis B and C testing, clearly marking the specimen as ‘needlestick/sharps injury’. MANAGEMENT 1 Wash wounds, and clean and flush mucous membranes immediately after exposure. Use a skin antiseptic such as 0.5% chlorhexidine in 70% alcohol and encourage bleeding by local venous occlusion. 2 When the source is known to be HIV-positive with a high viral load or latestage disease, and higher-risk exposure has occurred, e.g. a deep needlestick or laceration with blood inoculated, proceed as follows: (i) Discuss the situation immediately with an infectious diseases specialist. (ii) On their advice, commence (within hours) antiretroviral therapy such as lamivudine 150 mg with zidovudine 300 mg orally b.d., and lopinavir 400 mg with ritonavir 100 mg orally b.d. usually for 4 weeks. Check your local policy for regional variations. (iii) The side effects of these drugs are complex and significant, including rash, malaise, fatigue, headache, nausea, vomiting, diarrhoea, hepatitis, pancreatitis and blood dyscrasias. 3 When the source is HIV-positive with a low viral load and lower-risk exposure has occurred, e.g. superficial scratch or mucous membrane contamination, commence zidovudine and lamivudine alone, or according to local policy. 4 Refer the injured person to Occupational Health for follow-up with repeat serology and monitoring blood tests, advice and ongoing counselling with psychological support. (i) Report the incident to the senior ED doctor and infection control officer. (ii) The exposed person requires follow-up for up to 6 months, should practise safe sex, should not donate blood, and should avoid pregnancy. (iii) Assure confidentiality and sensitivity for all concerned. 152 Infectious Disease and Foreign Travel Emergencies NEEDLESTICK AND SHARPS INCIDENTS 5 Consider the additional possibility of transmission of hepatitis B and the need for tetanus prophylaxis (see p. 321). INOCULATION INCIDENT WITH HEPATITIS RISK DIAGNOSIS 1 The risk of seroconversion in a non-immunized person following a needlestick injury with HBV-positive blood is 5–40%, and following injury with hepatitis C virus-positive blood is 3–10%. 2 Take 10 mL clotted blood from the injured person, and if possible 10 mL with consent from the source. Send for hepatitis B and C and HIV testing, clearly marking the specimen as ‘needlestick/sharps injury’. MANAGEMENT 1 Wash the area with soap and water, dress the wound, and give tetanus prophylaxis. 2 Use Table 4.1 to determine the need for hepatitis B prophylaxis following significant percutaneous, ocular or mucous membrane exposure in persons without adequate immunity, i.e. anti-HBs levels unrecordable or <10 IU/mL. Check your local policy for regional variations. 3 Refer the injured person to Occupational Health for follow-up, with repeat serology and monitoring blood tests for up to 6 months. (i) Inform the senior ED doctor and infection control officer. Table 4.1 Hepatitis B prophylaxis following significant percutaneous, ocular or mucous membrane exposure for persons without adequate immunity Exposure source Exposed person Test for HBsAg Test for anti-HBs (unless recent satisfactory level of ≥10 IU/mL is known) HBsAg +ve, or cannot be identified and tested rapidly anti-HBs –ve or <10 IU/mL, give: HBIGa HB vaccineb HBsAg –ve anti-HBs –ve offer HB vaccinec anti-HBs, antibody to HBsAg; HB vaccine, hepatitis B vaccine; HBIG, hepatitis B immunoglobulin; HBsAg, hepatitis B surface antigen. aHBIG: 400 IU i.m. for adults, or 100 IU i.m. for children <30 kg, within 72 hours. bHB vaccine: 1 mL i.m. within 7 days, then at 1–2 months, and a third dose at 6 months. cInjury indicates evidence that the work area represents a significant exposure risk, so full vaccination is encouraged for the injured (exposed) person. Infectious Disease and Foreign Travel Emergencies 153 HUMAN IMMUNODEFICIENCY VIRUS INFECTION (ii) The exposed person requires follow-up for 6 months, should practise safe sex, should not donate blood and should avoid pregnancy. (iii) Assure confidentiality and sensitivity for all concerned. HUMAN IMMUNODEFICIENCY VIRUS INFECTION DIAGNOSIS 1 HIV is a cytopathic RNA retrovirus. It is transmitted by sexual contact, by syringe sharing in i.v. drug abusers, transplacentally and rarely now by blood transfusion. (i) Remember acute HIV infection may present after international travel. 2 HIV risk groups include: (i) Men who have sex with men. (ii) Intravenous drug users. (iii) Partners of HIV/AIDS patients. (iv) Children of HIV/AIDS affected mothers. (v) Blood product recipients in the early 1980s. 3 The revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS Among Adolescents and Adults was published by the US Centers for Disease Control and Infection in 1992 and emphasized the clinical importance of the absolute CD4+ T lymphocyte count or its percentage of the total lymphocyte count. (i) Three categories of CD4+ count were recognized for medical management purposes: (a) CD4 count ≥500/mm3 (b) CD4 count 200–499/mm3 (c) CD4 count <200/mm3 (ii) A CD4+ count <200/mm3 or 14% may be used to define acquired immune deficiency syndrome (AIDS). 4 Presentation varies according to the disease group. (i) Group 1 – Acute infection: (a) 50–70% of patients infected with HIV develop an acute illness with lethargy, fever, pharyngitis, myalgia, rash and lymphadenopathy about 2 weeks after exposure. Acute meningitis or encephalitis are occasionally seen (b) although the patient is infectious, serology for HIV antibodies at this early stage will be negative. 154 Infectious Disease and Foreign Travel Emergencies HUMAN IMMUNODEFICIENCY VIRUS INFECTION (ii) Group 2 – Asymptomatic infection: (a) the acute infection symptoms usually resolve by 3 weeks (b) infected patients seroconvert to HIV-positive over the next 4 months, most within 2–12 weeks of exposure (c) 50% of these patients will have fully developed AIDS by 10 years, with a near 100% mortality, although disease progression is slowing almost to a preserved life expectancy with modern highly active anti-retroviral therapy (HAART). (iii) Group 3 – Persistent generalized lymphadenopathy: (a) enlarged nodes in two or more non-contiguous extra-inguinal sites for at least 3 months and not due to a disease other than HIV (b) the patient is otherwise relatively well and enters a latency period of 2–10 years or more. (iv) Group 4 – Symptomatic infection: (a) subgroup A: constitutional disease with persistent fever, unexplained weight loss of 10% body mass or diarrhoea for over 1 month (b) subgroup B: neurological disease, including encephalopathy, myelopathy and peripheral neuropathy (c) subgroup C: secondary infectious diseases due to opportunistic infections occur as the CD4+ count drops usually below 200/mm3. These include Pneumocystis jiroveci pneumonia, recurrent pneumonia, Mycobacterium tuberculosis, atypical mycobacteria, toxoplasmosis, cryptosporidiosis, isosporiasis, strongyloidosis, cytomegalovirus, systemic candidiasis, cryptococcosis and many others (d) subgroup D: secondary cancers including Kaposi’s sarcoma, high-grade non-Hodgkin’s lymphoma, primary lymphoma of the brain and invasive cervical cancer (e) subgroup E: other conditions such as the HIV-wasting syndrome and chronic lymphoid interstitial pneumonitis. 5 AIDS-defining illnesses in an HIV-positive patient are in subgroups B to E, most commonly P. jiroveci pneumonia and Cryptococcus neoformans meningitis. 6 Thus, patients encountered in the ED infected with HIV range from the asymptomatic carrier state in the majority to non-specific illness or to acute problems as varied as collapse, respiratory failure, gastrointestinal bleeding, skin disorders, depression, dementia, stroke and coma. 7 Always maintain a high index of suspicion to identify an HIV-risk patient, if necessary by direct questioning. 8 Send blood preferably for HIV antigen if the patient is acutely unwell with a possible new HIV illness, requesting nucleic acid amplification (NAA) Infectious Disease and Foreign Travel Emergencies 155 TUBERCULOSIS testing such as a polymerase chain reaction (PCR) assay for HIV, viral RNA load test and the p24 antigen, rather than simple antibody testing. 9 Otherwise, routine HIV antibody testing in the ED is inappropriate if skilled counselling and follow-up are not available. (i) Also relying on a single serum test for HIV antibody to establish or exclude HIV infection is unwise as: (a) occasional false positives occur (b) false negatives occur in those infected due to: – early infection – lack of seroconversion in the first 4 months. MANAGEMENT 1 Consider every patient to be potentially infectious and adopt standard infection control precautions including designated hospital hand hygiene practice, and the use of personal protective equipment to minimize body substance exposure. (i) Precautions must be consistently observed with every patient in order to prevent any HIV dissemination and consequent exposure to disease risk. (ii) Always wash hands before and after contact with a patient. (iii) Wear gloves when handling blood specimens and body fluids. (iv) Wear a disposable apron if there is likely to be contamination of clothing (e.g. from bleeding), and a face mask and goggles if splashing is even a small possibility. (v) Take great care handling needles or scalpel blades, particularly on disposal. (vi) Clean blood spills immediately with a suitable chlorine-based disinfectant. 2 Refer the patient to the medical team in the usual way if he or she is acutely ill. (i) Otherwise refer the patient to infectious disease, genitourinary medicine (special clinic), or to the medical outpatient service for complete and ongoing care. TUBERCULOSIS DIAGNOSIS 1 Tuberculosis is an unusual diagnosis in the ED, particularly in developed countries such as Australia and the UK. However, as tuberculosis is a treatable and potentially curable disease its diagnosis should be remembered. 156 Infectious Disease and Foreign Travel Emergencies TUBERCULOSIS 2 Pulmonary tuberculosis has a significant risk of secondary transmission, although the risk to staff and other patients in the ED is small. 3 Request an acid-fast stain for Mycobacteria in the following clinical settings, even though their differential diagnosis is wide-ranging and includes malignancy: (i) Family history of tuberculosis. (ii) Previous migration from overseas, particularly Africa, Asia and southern Europe. (iii) Fever and cough in a patient with HIV/AIDS, or risk behaviour. (iv) Fever, productive cough and haemoptysis of unknown cause, particularly if homeless or indigenous. (v) Fever, chronic cough, weight loss and night sweats. 4 Perform a chest X-ray, although the appearances are not diagnostic. (i) Radiographic presentations include apical shadowing, hilar lymphadenopathy and apparent bronchial consolidation. 5 Send blood and sputum for microscopy with Ziehl–Neelsen staining, culture and polymerase chain reaction (PCR) assay for M. tuberculosis. (i) An acid-fast smear is rapid but less sensitive than culture, although culture may take several weeks to produce a definitive result. (ii) A negative sputum smear does not rule out pulmonary tuberculosis, and a positive smear does not confirm M. tuberculosis, as atypical mycobacteria have the same appearance. MANAGEMENT 1 Assess any patient with suspected pulmonary tuberculosis in a separate room (isolation room), and not in a standard ED resuscitation or observation cubicle. 2 Pulmonary tuberculosis is rarely severe enough to warrant commencing immediate antimycobacterial therapy. Rather ensure that you: (i) Send a series of sputum samples for microscopy and culture. (ii) Liaise with the on-call infectious disease team or respiratory medicine team to determine the best treatment course and area for admission: (a) standard short-course therapy consists of 2 months treatment with isoniazid, rifampicin, pyrazinamide and ethambutol followed by 4 months of isoniazid and rifampicin (b) starting therapy in the ED is rarely ever indicated. (iii) Contact the infection control service for a patient with suspected pulmonary tuberculosis to determine an infection control risk assessment and to initiate contact tracing. 3 Tuberculosis is a notifiable disease to the relevant public health authority. Infectious Disease and Foreign Travel Emergencies 157 BITES WITH RABIES OR OTHER LYSSAVIRUS RISK RABIES AND LYSSAVIRUS RISK DIAGNOSIS 1 Transmission of rabies or other lyssaviruses usually occurs from the bite of a dog, other canids such as foxes and wolves, cats, monkeys, bats, raccoons and skunks. 2 Rabies is endemic in most continents apart from Australia, but several cases of a similar disease caused by the Australian bat lyssavirus (ABLV), a zoonotic virus closely related to rabies virus, have occurred following a bat bite or scratch. 3 The incubation period is 3–8 weeks, but may be 3 months or more, by which time a travel history and animal or bat bite history may have been forgotten. 4 Clinical signs of infection include anorexia, fever, pain at the bite site and headache, progressing to confusion and agitation from encephalitis with pre-fatal hypersalivation, hyperthermia and hydrophobia. 5 Discuss any laboratory test with the infectious diseases team or pathology laboratory prior to sample collection. (i) Laboratory confirmation includes immunofluorescent stain of a skin biopsy from the nape of the neck, antibody detection in blood or CSF, or PCR assay of saliva, blood or CSF. MANAGEMENT 1 Established rabies is inevitably fatal. All cases of rabies exposure that have survived have been vaccinated before the onset of clinical disease. 2 Immediately wash and flush all bite wounds and scratches for at least 5 min. Check the patient’s tetanus immunization status, and give adsorbed diph - theria and tetanus toxoid (ADT) as required. 3 Try to evaluate the exposure risk: (i) Category I – touching or feeding animals, licks on the skin. (ii) Category II – nibbling of uncovered skin, minor scratches or abrasions without bleeding, licks on broken skin. (iii) Category III – single or multiple transdermal bites or scratches, contamination of mucous membrane with saliva from licks; exposure to bat bites or scratches. 4 Discuss post-exposure rabies and ABLV prophylaxis (post-exposure prophylaxis [PEP]) immediately with an infectious diseases specialist or the on-call population health unit specialist. 158 Infectious Disease and Foreign Travel Emergencies COMMON IMPORTED DISEASES OF TRAVELLERS (i) PEP is a combination of human rabies immunoglobulin (HRIG) and rabies vaccine, and should be given within 48 h of the bite: (a) category I exposure – no further treatment required (b) category II exposure – administer rabies vaccine i.m. (c) category III – administer rabies vaccine and HRIG i.m. (ii) Depending on the vaccine type, PEP in the non-immune includes rabies vaccine 1 mL i.m. in the deltoid muscle to a total of five doses over four weeks on day 0, 3, 7, 14 and 28–30. In addition, HRIG 20 IU/kg is infiltrated around the wound site on the first day. 5 Determine and manage the local wound infection risk. (i) A low risk wound seen within 8 h not involving a tendon or joint that can be adequately debrided and irrigated requires no further treatment. (ii) A high risk wound includes delayed presentation (8 h or more), a puncture wound unable to be debrided adequately, a wound on the hand, feet or face and a wound with underlying structures involved (e.g. bone, joint or tendons) (a) give amoxicillin 875 mg and clavulanic acid 125 mg one tablet orally b.d. for 5 days. COMMON IMPORTED DISEASES OF TRAVELLERS ● Ask any patient who has been travelling abroad specifically about the time, place and type of travel. Ask how long they spent in each foreign country and when they arrived back. ● Enquire specifically about malaria prophylaxis and whether it was taken for 4 weeks after leaving a malarial zone, and about immunizations before going abroad. ● The CDC Travellers’ Health website (see http://wwwnc.cdc.gov/travel/) has information to assist travellers and their healthcare providers in deciding on the vaccines, medications, and other measures necessary to prevent illness and injury during international travel. It covers all aspects of foreign travel, including lists of recent disease outbreaks, and information on illnesses in alphabetical order from African sleeping sickness to yellow fever. ● Remember that the returned traveller may well have a condition that is not considered ‘tropical’, such as an STD including HIV infection, meningococcal infection, pneumonia, pyelonephritis, and enteric infection other than traveller’s diarrhoea. ● Some of the tropical diseases discussed below can be endemic, but mostly are contracted abroad. Infectious Disease and Foreign Travel Emergencies 159 COMMON IMPORTED DISEASES OF TRAVELLERS MALARIA DIAGNOSIS 1 Falciparum malaria is the most dangerous form of malaria. Cases are imported to Australia from Africa, Asia and Papua New Guinea, but other tropical sources include the western Pacific, Amazon basin and Oceania. (i) Malaria is a potentially fatal infection. Survivors may experience damage to the brain, kidneys, liver, heart, gastrointestinal tract and lungs. (ii) Cerebral malaria is an abrupt onset of encephalopathy with headache that can progress rapidly to confusion, seizures and coma. (iii) Other malaria presentations include an influenza-like illness, diarrhoea and vomiting, jaundice, acute renal failure, acute respiratory distress, postural hypotension or shock, progressive anaemia and thrombocytopenia. (iv) The patient may not look ill in the first few days, but the nonimmune or splenectomized patient may then deteriorate rapidly over a few hours and die. 2 The patient usually presents within 4 weeks of returning from a malarious area with fever, rigors, nausea, vomiting, diarrhoea, and headache. Hepatosplenomegaly is common. 3 Infection may persist for months due to the release of parasites from the hepatic extra-erythrocytic phase in the liver, even after apparently successful treatment. (i) Late onset acute presentation can occur months or even more than a year after return from overseas. (ii) This relapse due to hepatic extra-erythrocytic phase does not occur in falciparum malaria. 4 Send blood for FBC, coagulation profile, ELFTs, two sets of blood cultures and: (i) Request at least two sets of thick and thin blood films for malarial parasites in every patient returning from abroad with fever and with any of the above symptoms or signs. 5 Request an MSU. MANAGEMENT 1 Falciparum malaria is a medical emergency requiring prompt treatment with oral or i.v. artemisinin derivative therapy. (i) Call the senior ED doctor if you suspect falciparum malaria. (ii) Give immediate artesunate 2.4 mg/kg i.v. repeated at 12 and 24 h, then once daily, if there is an altered conscious level, jaundice, 160 Infectious Disease and Foreign Travel Emergencies COMMON IMPORTED DISEASES OF TRAVELLERS oliguria, severe anaemia, hypoglycaemia, vomiting, acidosis or respiratory distress, or if over 2% red cells are parasitized. Admit these severe cases to the ICU (a) give quinine 20 mg/kg up to 1.4 g infused over 4 h if artesunate is not immediately available, with BP, blood sugar and electrocardiographic monitoring. (iii) Admit other less severe patients under the medical team when falciparum malaria is even considered possible, and begin treatment immediately – if necessary before definitive blood results are available (a) give those who can tolerate oral treatment artemetherlumefantrine combination therapy. 2 Refer patients with other types of malaria (P. vivax, P. ovale, P. malariae and P. knowlesi) to the medical team; some may be suitable for treatment as an outpatient. 3 Ask a patient with two sets of negative thick and thin blood films, but a suggestive history, to return for repeat malaria blood films in 48 h or earlier if symptoms persist. (i) Inform the GP of the possibility of malaria by fax and letter. TYPHOID DIAGNOSIS 1 The incubation period is up to 3 weeks following travel to India, Latin America, the Philippines and South-East Asia. There is an initial insidious onset of fever, malaise, headache, anorexia, dry cough, and constipation in the first week. 2 The illness then progresses to abdominal distension and pain associated with diarrhoea, splenomegaly, a relative bradycardia, bronchitis, confusion or coma. (i) The characteristic crop of fine rose-pink macules on the trunk is rare. 3 Send blood for FBC that may show a leucopenia with a relative lymphocytosis. Send ELFTs and two sets of blood cultures in all suspected cases. 4 Request an MSU and a stool culture if diarrhoea is prominent. (i) Blood cultures are positive in up to 90% in the first week. (ii) Stool culture becomes positive in 75% and urine culture in 25% in the second week. Warning: do not diagnose the ’flu in a febrile patient without asking about recent foreign travel and considering malaria. ! Infectious Disease and Foreign Travel Emergencies 161 COMMON IMPORTED DISEASES OF TRAVELLERS MANAGEMENT 1 Commence i.v. rehydration with normal saline or Hartmann’s. 2 Refer all suspected cases to the medical team for azithromycin 1 g i.v. or orally daily for 7 days. (i) Or give ciprofloxacin 400 mg i.v. 12-hourly or ciprofloxacin 500 mg b.d. orally for 7–10 days, if the infection was not acquired in the Indian subcontinent or South-East Asia. DENGUE DIAGNOSIS 1 Dengue occurs after a short 1-week incubation period from infection by one of four serotypes of mosquito-borne flavivirus, particularly in Central or South America and South-East Asia. 2 There is abrupt fever, chills, retro-orbital or frontal headache, myalgia, back pain, lymphadenopathy and rash. (i) The initial rash is a transient, generalized, blanching macular rash in the first 1–2 days. (ii) A secondary maculopapular rash with areas of sparing occurs lasting 1–5 days. (iii) A later haemorrhagic rash may be associated with thrombocytopenia. 3 Dengue haemorrhagic fever (DHF) and dengue shock syndrome occur in repeat infections with a different serotype. 4 Send blood for FBC, coagulation profile, ELFTs, two sets of blood cultures and dengue serology. MANAGEMENT 1 Admit the patient under the medical team for supportive care with i.v. fluids and antipyretic analgesics. 2 Admit patients with DHF or dengue shock syndrome to the ICU. TYPHUS AND SPOTTED FEVERS DIAGNOSIS 1 Typhus includes several diseases caused by Rickettsiae, such as epidemic and murine (endemic) typhus. 2 Scrub typhus is one of the spotted fevers, and is caused by an acute bacterial infection by Orientia tsutsugamushi, transmitted by trombiculid mites (‘chiggers’). Foci of scrub typhus occur in South-East Asia, northern Japan and northern Australia. COMMON IMPORTED DISEASES OF TRAVELLERS 162 Infectious Disease and Foreign Travel Emergencies COMMON IMPORTED DISEASES OF TRAVELLERS (i) Other tick-borne spotted fevers include Rocky Mountain and Mediterranean. 3 Infection is characterized by high fevers, headache, lymphadenopathy and a fine vasculitic maculopapular rash, with a characteristic black eschar at the site of the original chigger bite in scrub typhus. 4 Potential complications include pneumonitis, encephalitis and myocarditis, which usually occur in the late phase of the illness. 5 Send blood for FBC, coagulation profile, ELFTs, blood cultures and serology. (i) Leucopenia and deranged LFTs are common in the early phase of infection. 6 Scrub typhus can be confirmed by PCR assay on ethylenediaminetetraacetic acid (EDTA) blood in its early stages, or serological tests in the later or convalescent stage. MANAGEMENT 1 Give doxycycline 100 mg orally b.d. for 7–10 days. 2 Refer the patient to an infectious disease specialist for exclusion of additional travel-related infections, and follow up. HELMINTH INFECTIONS DIAGNOSIS 1 Schistosomiasis (bilharzia) caused by fresh-water trematodes (flukes) rarely presents acutely, but should be suspected in cases from endemic areas such as Africa, South America, the Middle East and Asia presenting with fever and diarrhoea associated with eosinophilia (Katayama fever). (i) Chronic infection may present up to years later with painless terminal haematuria or obstructive uropathy, portal or pulmonary hypertension and seizures. 2 Roundworm infection (ascariasis) is discovered when the adult worm is passed in the stool, although occasionally allergic pneumonitis, abdominal pain, diarrhoea or urticaria occur. 3 Tapeworm infection usually presents with lassitude, weight loss and anaemia or with disease-specific complications such as seizures in cysticercosis, and mass effects in hydatid disease (Echinococcus). MANAGEMENT 1 Discuss your suspicions with an infectious disease specialist and take advice about which laboratory tests are indicated. Infectious Disease and Foreign Travel Emergencies 163 PANDEMIC INFLUENZA ● A pandemic is a global outbreak of a new type of infection in susceptible individuals, with rapid person-to-person spread and the potential to affect millions. ● International travel is the main reason for the speed of pandemic spread, so international travellers are thus represented among the first cases of a variant of influenza A to be seen in any new location. ● H1N1 influenza 09 was the most common cause of human influenza in 2009, and spread around the world causing additional deaths, especially in young adults. Pregnant women and the morbidly obese were at particular risk. ● In 2010, H1N1 influenza 09 became the principal cause of seasonal influenza. DIAGNOSIS 1 Influenza is an acute illness with an abrupt onset and peak symptoms in the first 24–48 h. (i) These most commonly include sudden fever, chills, headache, dry cough, sore throat and muscle aches. (ii) Diarrhoea can be a presenting complaint. 2 Ask patients presenting with fever or respiratory symptoms specifically about interstate and international travel, or about contact with anyone who has an acute respiratory illness ideally at triage, before entering the ED. (i) Check the status of the current ‘at-risk’ countries at http:// wwwnc.cdc.gov/travel/ or refer to local policy information concerning global infection threats. MANAGEMENT 1 Place a suspected case of influenza in isolation, preferably a negativepressure room, and give him or her a surgical mask to wear. 2 All attending staff must wear a correctly fitted, high-filtration mask (N95), long-sleeved gown, gloves, and full eye protection. 3 Inform the senior ED doctor, the local infectious disease physician, and hospital infection control officer. (i) Call the clinical microbiologist and take FBC, ELFTs, blood cultures and 30 mL serology including for atypical pneumonia. (ii) Send a nose/throat swab and arrange a chest X-ray: (a) alert the radiographer to the infection risk. (iii) A nasopharyngeal aspirate (NPA) has a higher risk to staff and is not recommended. 4 Specialist consultation and local policy will determine further management. 164 Infectious Disease and Foreign Travel Emergencies FURTHER READING Australian Department of Health and Ageing (2008) The Australian Immunisation Handbook, 9th edn. http://immunise.health.gov.au/internet/immunise/ publishing.nsf/Content/Handbook-home (hepatitis B, HIV, rabies). Australian Prescriber. http://www.australianprescriber.com/magazine/29/1/6/8/ (bite injuries). CDC Travellers’ Health. http://wwwnc.cdc.gov/travel/ (travellers’ health). Department of Health. http://www.dh.gov.uk/en/Publichealth/Immunisation/ index.htm Immunisation against infectious diseases 2006 ‘The Green Book’ (immunization). Health Protection Agency. http://www.hpa.org.uk/ (infectious diseases). World Health Organization. http://www.who.int/rabies/human/postexp/en/ index.html/ (rabies). TOXICOLOGY Section V 166 Toxicology Most cases of acute poisoning are acts of deliberate self-harm in the adult, but they are usually accidental in children. All cases are initially managed as medical emergencies and require substance identification, risk assessment, resuscitation, specific and non-specific treatment, and a period of observation. Thereafter, cases will require psychiatric assessment. Remember that an apparently trivial act of self-harm may still indicate serious suicidal intent (see p. 438). DIAGNOSIS 1 Consider acute poisoning in any unconscious patient or one exhibiting bizarre behaviour, or in unexplained metabolic, respiratory or cardiovascular problems. 2 Obtain specific information from the patient, witnesses, and ambulance personnel regarding: (i) Pharmaceutical agent or toxin ingested: (a) remember that two or more drugs are taken in 30% of cases (b) alcohol is a common adjunct. (ii) Quantity of agent ingested (look for empty blister packets or bottles). (iii) Time since ingestion. (iv) History of any toxic effects experienced from the poisoning. (v) Specific events prior to arrival in the emergency department (ED), such as: (a) rapid deterioration in conscious level (b) seizures. (vi) Clinical features on presentation. 3 Corroborate the history in the cooperative patient, but do not be misled, as information supplied may be incomplete or deliberately false. 4 Focus the examination on immediate life threats, identification of clinical signs specific to certain drugs, and obtaining baseline vital signs. (i) Rapidly assess airway patency, respiratory function and conscious level. (ii) Record the pulse, blood pressure, respiratory rate, temperature and blood sugar level, and attach a cardiac monitor and pulse oximeter to the patient (a) hypoglycaemia and hyperthermia are common findings in the collapsed patient with a drug overdose, and are often overlooked. (iii) Look for signs of seizure activity, assess upper and lower limbs for signs of hypertonicity and clonus, and examine the pupils. ACUTE POISONING: GENERAL PRINCIPLES Toxicology 167 ACUTE POISONING: GENERAL PRINCIPLES (iv) Look for clues to the substance taken (‘toxidrome’): (a) dilated pupils: tricyclics, amphetamine, antihistamines, anticholinergic agents (b) pinpoint pupils: opiates, organophosphates (c) nystagmus: alcohol, benzodiazepines, phenytoin (d) hyperventilation: salicylates (e) nasal bleeding or perioral sores: solvent abuse. 5 Gain i.v. access and send blood for FBC, U&Es, LFTs, a paracetamol level in all poisonings, and a salicylate level only if symptomatic of salicylism or when comatose (see p. 172). 6 Perform an arterial blood gas to rapidly determine metabolic acidosis, respiratory function and electrolyte imbalance, if the patient is significantly unwell. (i) Metabolic acidosis is associated with many poisonings including salicylates, methanol, iron and ethylene glycol. 7 Request other specific measurable serum drug levels in ingestion of phenytoin, sodium valproate, digoxin, carbamazepine, iron, methotrexate and theophylline. 8 Perform an electrocardiogram (ECG) to look for tachycardia, bradycardia and potential cardiac conduction abnormalities such as QT prolongation and widening of the QRS complex. 9 Request a chest X-ray (CXR) if clinical signs of aspiration are present. 10 Request an abdominal X-ray (AXR) when potentially radiopaque tablets such as iron or potassium have been ingested. MANAGEMENT 1 Start immediate resuscitation if risk assessment indicates ingestion of a potentially lethal drug, or if the patient is obtunded with signs of cardiorespiratory distress. 2 Unconscious or collapsed patient (i) Clear the airway by extending the head, remove dentures, vomit or blood by a quick sweep round the mouth with a Yankauer suction catheter, and give oxygen via a face mask. (ii) Insert an oropharyngeal Guedel airway if the patient is not breathing or the gag reflex is reduced, and use a bag–valve mask system to ventilate the patient, aiming for an oxygen saturation above 94%. (iii) Call an airway-skilled doctor urgently to pass a cuffed endotracheal tube to protect and maintain the airway and to optimize ventilation. 3 Administer the following without delay: (i) 50% dextrose 50 mL i.v. if the blood sugar level is low. (ii) Naloxone 0.1–0.4 mg i.v. slowly if the pupils are pinpoint, the 168 Toxicology ACUTE POISONING: GENERAL PRINCIPLES respiratory rate is below 10/min and opioid intoxication is suspected (see p. 176) (a) beware that larger doses of naloxone may precipitate opioid withdrawal and severe agitation in an opioid-dependent patient. (iii) Normal saline to treat hypotension and maintain the circulation. If hypotension is secondary to an arrhythmia or myocardial depression, specific drug therapy and inotropic support may be needed. 4 Treat toxic seizures with: (i) Midazolam 0.05–0.1 mg/kg i.v., diazepam 0.1–0.2 mg/kg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. (ii) Second-line treatment such as phenobarbitone (phenobarbital) 10–20 mg/kg i.v. at no faster than 100 mg/min. Phenytoin is contraindicated in the treatment of toxic seizures. 5 Gastrointestinal decontamination This is not routine, and it is only instituted once basic resuscitative and supportive care have been performed and the airway is secure. (i) Activated charcoal: (a) this is used to reduce the absorption of many drugs. Consider in patients presenting within 1 h of taking a potentially toxic overdose of an agent known to be adsorbed to charcoal (b) give 50 g for adults (1 g/kg body weight in children) in 100–200 mL water administered orally or via a nasogastric tube. Warn the patient that charcoal is somewhat unpalatable and will turn the stools black (c) charcoal administration is contraindicated when: – an oral antidote such as methionine is to be given – the patient has an altered level of consciousness or an unprotected airway – the patient has ingested substances not adsorbed to charcoal, such as iron, lithium, alcohols, acid, alkali, petroleum, pesticides or cyanide. (ii) Whole bowel irrigation (WBI): (a) is not used routinely, but may be helpful in poisonings with: – toxic ingestion of agents such as iron, lithium and calciumchannel blockers – sustained-release or enteric-coated medications – ‘body-packers’ who have ingested wrapped illicit drugs (b) is contraindicated in patients with: – an unprotected airway – haemodynamic instability – bowel obstruction, perforation or ileus. Toxicology 169 SPECIFIC POISONS 6 Enhanced elimination Consider for specific poisonings in consultation with the ICU. Obtain additional advice from a Poisons Information Service. (i) Multiple-dose activated charcoal (MDAC): give repeated 25–50 g charcoal every 4 h. This may be useful in severe dapsone, carbamazepine, phenobarbitone (phenobarbital), quinine and theophylline poisoning and possibly salicylate poisoning. (ii) Haemodialysis, charcoal haemoperfusion and urinary pH modification are alternatives in certain severe poisonings. 7 Antidotes These drugs counter the effects of the poison, but only exist for a few specific agents. 8 Admit the patient following ED resuscitation, supportive care, decontamination and antidote administration to the ED observation unit, medical team or ICU, depending on the clinical severity of poisoning. 9 All patients require psychiatric evaluation and management following their medical care. SPECIFIC POISONS Obtain advice as necessary regarding toxic ingestions 24 h a day from the Poisons Information Centre on 13 11 26 in Australia, and in New Zealand on 03 479 7248 (or 0800 764 766 within New Zealand only). Advice in the UK is available from the National Poisons Information Service (NPIS), comprising four individual units (Birmingham, Cardiff, Edinburgh, Newcastle). The NPIS coordinates an internet and telephone service to assist in the diagnosis, treatment and management of all types of poisonings. ● TOXBASE® is an online resource for the routine diagnosis, treatment and management of patients exposed to toxic substances. Use this as the first point of contact for poisons advice. It is available on http://www.toxbase.org/ ● Specialist consultants are available for telephone advice in more complex clinical cases. A 24-h number 0844 892 0111 will direct callers to the relevant local centre in the UK. Warning: gastric lavage is rarely if ever used, and induced emesis is positively contraindicated. ! 170 Toxicology SPECIFIC POISONS PARACETAMOL DIAGNOSIS 1 Paracetamol overdose is common and potentially lethal. 2 Hepatocellular necrosis is the major complication of paracetamol toxicity. Factors that enhance the potential for hepatotoxicity, and therefore morbidity and mortality, include: (i) Late presentation with delayed antidote administration, especially if over 24 h. (ii) Staggered overdose: multiple supra-therapeutic ingestions over a number of days. (iii) Glutathione deficiency in starvation and debilitating illness such as AIDS. (iv) Enzyme-inducing drugs such as carbamazepine, phenobarbitone (phenobarbital), rifampicin or isoniazid. (v) Regular alcohol use. 3 Determine the time since ingestion, total paracetamol consumed and the patient’s weight: (i) Patients who have taken >10 g (20 tablets) or >200 mg/kg over a period of <8 h are considered at risk from severe liver damage. (ii) The greatest risk of hepatotoxicity is related to the extent of delay beyond 8 h until antidote treatment with N-acetylcysteine (NAC) is commenced. (iii) Hepatotoxicity may also occur in patients who take repeated or staggered doses, or sustained-release preparations. 4 The patient is usually asymptomatic, but can present in fulminant hepatic failure with abdominal pain, vomiting, hypoglycaemia, tender hepatomegaly, jaundice and encephalopathy. 5 Gain i.v. access and send bloods for full blood count (FBC), urea and electrolytes (U&Es), liver function tests (LFTs), prothrombin index (PTI) (international normalized ratio [INR]) and a blood sugar level. (i) These bloods become more important if the patient presents over 8 h after ingestion, and are essential if presentation is delayed beyond 24 h or more. (ii) Send a paracetamol level once 4 h or more have elapsed since overdose. MANAGEMENT 1 Resuscitation is rarely required unless the patient is in fulminant hepatic failure. (i) Administer 50% dextrose 50 mL i.v. if the patient is hypoglycaemic. Toxicology 171 SPECIFIC POISONS 2 Review the blood results: (i) Plot the serum paracetamol level on the paracetamol nomogram for all patients presenting between 4 and 24 h after an acute, single ingestion of paracetamol (Fig. 5.1). (a) the treatment nomogram has been simplified from previously, with a single treatment line now for all patients following paracetamol ingestion (b) this line has been lowered by 25% from prior standard lines. (ii) Treat all patients who have a serum paracetamol level above the nomogram treatment line (Fig. 5.1). (iii) A raised PTI (INR) or alanine aminotransferase (ALT) levels >1000 IU/L define significant hepatotoxicity. 3 NAC, the antidote for paracetamol, is highly effective when commenced within 8 h of poisoning. Administer NAC in the following circumstances: (i) Patients presenting within 8 h of ingestion, with a 4–8-h serum paracetamol level above the nomogram treatment line (see Fig. 5.1). 1000 900 800 700 600 500 400 300 200 100 0 160 150 140 130 120 110 100 90 80 70 60 50 40 30 20 10 0 Blood paracetamol concentration (μmol/L) Blood paracetamol concentration (mg/L) Time (hours) 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Figure 5.1 Treatment nomogram for paracetamol poisoning. Treat any patient with a serum paracetamol level above the nomogram treatment line. (Make certain the correct units are used). Reproduced with permission from Daly FFS, Fountain JS, Murray L et al. (2008) Guidelines for the management of paracetamol poisoning in Australia and New Zealand – explanation and elaboration. Medical Journal of Australia 188: 296–301. 172 Toxicology SPECIFIC POISONS (ii) A potentially toxic ingestion of paracetamol (more than 20 tablets or 200 mg/kg) in a patient presenting 8– 24 h after overdose, or if the serum paracetamol level will not be available within 8 h of the original ingestion: (a) commence treatment immediately without waiting for the blood results (b) cease treatment if the serum paracetamol level turns out to be below the relevant treatment line, and the ALT and PTI (INR) are normal. (iii) Patients presenting with deranged ALT and PTI (INR) more than 24 h after acute overdose, or following staggered overdose (a) serum paracetamol levels are difficult to interpret in cases of staggered ingestion. Monitor the PTI (INR) and ALT regularly instead and seek specialist toxicologist advice (see below). 4 Consult a clinical toxicologist for patients presenting with a staggered overdose, with delayed presentation of more than 24 h, and patients with severe liver dysfunction and an elevated PTI (INR). 5 Use the adult infusion protocol for NAC below. (i) Take care with the dose calculation. Read from the drug-insert infusion dosage guide the volume in millilitres of NAC 200 mg/ mL to be added to the 5% dextrose, according to the patient’s weight: (a) 150 mg/kg in 5% dextrose 200 mL i.v. over 15 min. (b) 50 mg/kg in 5% dextrose 500 mL i.v. over 4 h. (c) 100 mg/kg in 5% dextrose 1000 mL i.v. over 16 h. 6 Side effects are mostly from non-allergic anaphylactic reactions, occurring in the first 30 min of administering high-dose NAC. These include nausea, flushing, itching, urticaria, wheeze and hypotension. (i) Stop the infusion. (ii) Give promethazine 12.5–25 mg i.v. and hydrocortisone 200 mg i.v. (iii) Once symptoms have settled, re-commence the initial infusion at a slower rate (e.g. 150 mg/kg over 1 h). SALICYLATES DIAGNOSIS 1 The clinical features of salicylate toxicity following acute ingestion are dose related: (i) Ingested dose <150 mg/kg: usually asymptomatic. (ii) 150–300 mg/kg: moderate symptoms such as tachypnoea, nausea, vomiting and tinnitus (salicylism). Toxicology 173 SPECIFIC POISONS (iii) 300–500 mg/kg: severe toxicity with hyperthermia, marked dehydration, agitation, confusion and an altered level of consciousness, which may lead to coma. (iv) More than 500 mg/kg ingested is associated with pulmonary and cerebral oedema and may be fatal. 2 Gain i.v. access and send bloods for U&Es, blood sugar and a salicylate level. (i) Perform arterial blood gases (ABGs) to detect respiratory alkalosis or a metabolic acidosis in symptomatic patients. MANAGEMENT 1 Call an airway-skilled doctor immediately to pass a cuffed endotracheal tube if the patient is obtunded, unconscious or unable to protect their airway. 2 Commence a normal saline infusion to replace insensible losses associated with hyperthermia, hyperventilation and vomiting. 3 Administer charcoal as soon as possible, even in patients with a delayed presentation, as salicylates cause delayed gastric emptying. Consider repeatdose activated charcoal every 4 h to reduce salicylate absorption in the following situations: (i) Overdose of sustained-release aspirin. (ii) Evidence of continued absorption with rising serum salicylate levels. 4 Urinary alkalinization may reduce salicylate elimination from 20 to 5 h. Consider in patients with signs and symptoms of salicylate toxicity, or a serum salicylate level of >300 mg/L (2.2 mmol/L). (i) Give a bolus of 8.4% sodium bicarbonate 1 mmol/kg (1 mL/kg) i.v. (ii) Follow with an infusion of 8.4% sodium bicarbonate 100 mmol (100 mL) in 5% dextrose solution 1 L, at a rate of 100–250 mL/h. (iii) Titrate this bicarbonate infusion to maintain urinary pH >7.5 and urine output >1 mL/kg per h. 5 Monitor serum electrolytes, salicylate level and urinary pH every 2–4 h. (i) Salicylate level: (a) symptoms occur at 300 mg/L (2.2 mmol/L) (b) significant toxicity occurs at 500 mg/L (3.6 mmol/L) (c) repeat the level at least once. Rising levels indicate continued drug absorption. (ii) Potassium: significant hypokalaemia hinders salicylate elimination so potassium may need to be replaced. 6 Patients with no clinical evidence of salicylate toxicity, normal ABGs and falling serum salicylate levels 4 h apart may be medically cleared, ready for psychiatric review. 174 Toxicology SPECIFIC POISONS 7 Otherwise observe all patients with clinical salicylate toxicity for a minimum of 12 h until they demonstrate resolution of symptoms and a falling serum salicylate level, before considering them medically stable. 8 Consult a clinical toxicologist for patients with salicylate levels >500 mg/L (3.6 mmol/L), severe symptoms or obtunded. (i) Consider haemodialysis for severe poisoning with a metabolic acidosis or a salicylate level >700 mg/L (5.1 mmol/L). TRICYCLIC ANTIDEPRESSANTS DIAGNOSIS 1 Tricyclic antidepressant (TCA) overdose is associated with significant mortality. Ingestion of ≥15–20 mg/kg is potentially fatal. 2 The onset of symptoms is usually rapid, and in large overdoses deterioration occurs within 1–2 h. Significant toxicity is heralded by cardiotoxicity, convulsions and coma. 3 Clinical features include: (i) Anticholinergic: warm dry skin with absent sweating, dilated pupils, urinary retention, sinus tachycardia, and delirium. (ii) Central nervous system (CNS): seizures are usually associated with an altered level of consciousness and rapid development of coma, especially with a large overdose. (iii) Cardiovascular: cardiac arrhythmias are common and occur as a result of sodium-channel blockade. They are often associated with hypotension. 4 Perform an ECG. Look for tachycardia, heart block, junctional rhythms and ventricular tachycardia (VT) including polymorphic VT (torsades de pointes). (i) A QRS interval of >100 ms and right axis deviation indicate cardiotoxicity and is predictive of ventricular arrhythmias. 5 Gain i.v. access and send blood for FBC, U&Es and a paracetamol level and attach a cardiac monitor and pulse oximeter to the patient. 6 Perform an ABG to monitor for hypoxia and acidosis, both of which exacerbate cardiotoxicity. MANAGEMENT 1 Give high-dose oxygen and commence a normal saline infusion. 2 Call an airway-skilled doctor to pass an endotracheal tube in patients with a reduced conscious level, inadequate respiratory effort or convulsions, with or without cardiac arrhythmias. (i) The patient should be hyperventilated to a pH of 7.5, as alkalaemia decreases the risk of cardiotoxicity. Toxicology 175 SPECIFIC POISONS 3 Administer activated charcoal as soon as possible once the airway is secured, to all patients with significant TCA ingestion, even with a delayed presentation. 4 Give a loading dose of 8.4% sodium bicarbonate 1–2 mmol/kg (1–2 mL/kg), followed by an infusion of 20–100 mmol/h (20–100 mL/h) to maintain an arterial pH of between 7.50 and 7.55. (i) Sodium bicarbonate is a specific antidote in TCA poisoning and provides high concentrations of sodium ions, which help reduce cardiotoxicity. (ii) Indications for sodium bicarbonate administration include: (a) cardiac arrhythmia or cardiac arrest (b) widened QRS interval of >120 ms (c) persistent hypotension despite saline or colloid fluid administration. 5 Repeat the ABGs and electrolytes regularly to ensure maintenance of alkalaemia and avoid hypernatraemia. 6 Perform repeated ECGs to monitor for cardiac arrhythmias and to ensure the resolution of any QRS prolongation. 7 Refer patients with significant cardiovascular or CNS toxicity to the intensive care unit (ICU) or coronary care unit (CCU), for ECG monitoring and supportive care. 8 Observe patients with drowsiness alone and non-progressive or absent ECG changes in the ED observation unit, until all clinical signs of sedation or anticholinergic delirium have resolved. BENZODIAZEPINES DIAGNOSIS 1 These are comparatively safe if taken alone. Reported deaths are associated with mixed overdoses with other CNS depressants such as opioids and alcohol. 2 Clinical manifestations include drowsiness, respiratory depression, ataxia and dysarthria. 3 Coma is unusual unless combined with other sedatives or alcohol, or in the elderly. 4 Gain i.v. access and send blood for U&Es and a paracetamol level. No specific investigations are required unless co-ingestion is suspected. Attach a cardiac monitor and pulse oximeter to the patient. 5 Perform a baseline ECG. MANAGEMENT 1 Give high-dose oxygen and nurse in the left lateral position to prevent aspiration, unless the airway is protected. 176 Toxicology SPECIFIC POISONS 2 Administer normal saline to maintain a normal blood pressure (BP). 3 Gastrointestinal decontamination is rarely necessary unless there is co-ingestion or the patient is deeply unconscious, in which case protect the airway first by endotracheal intubation. 4 Admit the patient to the ED observation unit overnight, followed by subsequent psychiatric evaluation. 5 The use of flumazenil, a specific benzodiazepine receptor antagonist, is controversial. It is rarely if ever indicated, and must be discussed with the senior ED doctor. (i) Flumazenil may induce VT, elevate intracranial pressure, precipitate benzodiazepine withdrawal in chronic abusers, and may invoke seizures, particularly with co-ingestion of TCAs. (ii) Potential roles for flumazenil are thus restricted to: (a) reversal of excessive benzodiazepine sedative effect following procedural sedation (b) reversal of respiratory depression and coma in a pure benzodiazepine overdose, to prevent the need for intubation. The difficulty is knowing when no other drugs were ingested. OPIOIDS DIAGNOSIS 1 Opioid drugs include opium alkaloids such as morphine and codeine; semisynthetic opioids such as heroin (diamorphine) and oxycodone and fully synthetic opioids such as pethidine and methadone. 2 Opioids produce euphoria, pinpoint pupils, sedation, respiratory depression and apnoea with increasing doses. 3 Other complications of opioid intoxication include hypotension, convulsions, non-cardiogenic pulmonary oedema and compartment syndrome from prolonged immobility. 4 Perform a thorough examination to evaluate potential complications, and to exclude alternative causes of an altered mental state with bradypnoea such as sepsis, neurotrauma, stroke and metabolic disease (see p. 80). 5 Send bloods for U&Es, blood sugar and serum paracetamol level. Perform an ECG. MANAGEMENT 1 Commence supportive care with oxygen and assisted ventilation. 2 Give naloxone 0.1–0.4 mg i.v. as a bolus or in 0.1 mg increments. Carefully titrate response to achieve improved airway control and adequate ventilation, without precipitating an acute agitated withdrawal state. Toxicology 177 SPECIFIC POISONS (i) Naloxone is a short-acting opioid antagonist that may be administered by the i.m., i.v., s.c. or endotracheal routes. (ii) It is safe and rarely associated with complications, but may cause acute withdrawal and severe agitation in the opioid-dependent individual. (iii) Use it to reverse severe respiratory depression, apnoea and oversedation, or for cases of undifferentiated coma with respiratory depression and pinpoint pupils. 3 Continue to monitor for respiratory depression and hypoxia. Further doses of naloxone or an infusion may be required due to its short half-life. 4 Observe all patients for a period, because re-sedation with respiratory depression may occur as the naloxone wears off. IRON DIAGNOSIS 1 Acute iron overdose is a potentially life-threatening condition, particularly in children who mistake iron tablets for sweets. 2 The clinical course following iron overdose includes: (i) Gastrointestinal toxicity: haemorrhagic gastroenteritis with vomiting, abdominal pain and bloody diarrhoea. Failure to develop significant gastrointestinal symptoms within 6 h of ingestion effectively rules out significant iron poisoning. (ii) Systemic toxicity: hypotension, shock, lethargy, metabolic acidosis, seizures, coma, and acute liver and renal failure. 3 Toxicity is determined by the quantity of elemental iron ingested: (i) <20 mg/kg: usually asymptomatic. (ii) 20–60 mg/kg: gastrointestinal symptoms predominate. (iii) 60–120 mg/kg: systemic toxicity and high lethality. 4 Send blood for FBC, U&Es, LFTs, a serum iron level and venous blood gas (VBG). (i) Serum iron levels peak at 4–6 h after ingestion. (ii) Levels >90 mol/L are associated with systemic toxicity. 5 Request a plain AXR to show residual whole tablets or a concretion, as most iron preparations are radio-opaque. (i) A negative AXR does not rule out ingestion. MANAGEMENT 1 This depends on the initial assessment and clinical manifestations, and the potential amount of elemental iron ingested. 2 Start aggressive fluid resuscitation in patients with signs of gastrointestinal or systemic toxicity, and institute decontamination and chelation measures. 178 Toxicology SPECIFIC POISONS Discuss these with the senior ED doctor or a clinical toxicologist: (i) Decontamination: (a) do not administer charcoal or attempt to induce vomiting (b) perform whole bowel irrigation if there are significant numbers of tablets beyond the pylorus. (ii) Chelation therapy: (a) Start a desferrioxamine infusion at 2 mg/kg per h and increase to a maximum of 15 mg/kg per h in severe cases. 3 Most patients will remain asymptomatic, or develop mild gastrointestinal symptoms only. (i) Give i.v. fluids to replace vomiting and diarrhoea losses, provide supportive care and observe for a minimum of 6 h. 4 Refer all moderate-to-severe cases to the ICU team. DIGOXIN DIAGNOSIS 1 Toxicity occurs from acute overdose or secondary to long-term therapy. Foxglove and oleander ingestion will also cause acute cardiac glycoside poisoning. 2 Acute digoxin overdose in adults is usually intentional. Clinical manifestations include: (i) Nausea and vomiting. (ii) Hyperkalaemia. (iii) Bradycardia and ventricular arrhythmias. 3 Chronic digoxin toxicity occurs particularly in the elderly and may be precipitated by renal impairment, hypokalaemia, hypercalcaemia and drugs such as amiodarone and quinidine. Clinical manifestations include: (i) Nausea, vomiting, diarrhoea. (ii) Sedation, confusion, delirium. (iii) Visual disturbances, such as yellow haloes (xanthopsia). (iv) Cardiac automaticity and a wide range of ventricular and supraventricular arrhythmias. 4 Gain i.v. access and send bloods for U&Es and a serum digoxin level. (i) Therapeutic range for digoxin is 0.5–2.0 ng/mL. (ii) Take serum levels early to confirm poisoning, and repeat in 4 h if acute ingestion is suspected. (iii) The serum digoxin level is most accurate at 6 h post-ingestion. 5 Perform an ECG: (i) Any cardiac arrhythmia may be seen in both acute and chronic ingestions. (ii) The most common arrhythmias are bradycardia, heart block, paroxysmal atrial tachycardia, ventricular ectopics and ventricular tachycardia. Toxicology 179 SPECIFIC POISONS MANAGEMENT 1 Treatment depends on haemodynamic stability, conscious state, and whether it is an acute or chronic intoxication. 2 Gain i.v. access in all patients and start fluid resuscitation for hypotension, continuous cardiac monitoring, and perform regular ECGs. 3 Acute digoxin intoxication (i) Administer oral activated charcoal if presentation is within 1 h of significant overdose. This may be impossible if the patient is vomiting continuously. Repeated administration should not delay other interventions. (ii) Treat hyperkalaemia with a dextrose–insulin infusion (see p. 132) (a) do not use i.v. calcium as this may precipitate asystole. (iii) Administer digoxin-specific antibody fragments (Digibind™) for: (a) cardiac arrest (b) haemodynamic instability with cardiac arrhythmia (c) serum potassium >5.5 mmol/L (d) serum digoxin level >15 nmol/L (11.7 ng/mL) (e) ingested digoxin dose >10 mg (4 mg in a child). (iv) Calculate the number of vials of Digibind™ required from the estimated ingested dose or the serum digoxin concentration, if obtained at least 6 h post acute poisoning (a) Empiric dosing starting with 5–10 vials of Digibind™ will be required if the acutely ingested dose is unknown. (v) Admit all acute poisonings for cardiac monitoring and close observation for a minimum of 12 h. 4 Chronic digoxin intoxication (i) Cease the digoxin medication. (ii) Correct any hypokalaemia with potassium chloride 10 mmol/h i.v., and hypomagnesaemia with magnesium sulphate 10 mmol in 100 mL normal saline i.v. over 30 min. (iii) Administer two vials of digoxin-specific antibody fragments (Digibind™) i.v. over 30 min to symptomatic patients with an altered mental state, cardiac arrhythmia or gastrointestinal symptoms. (iv) Patients usually recover quickly. Admit under the medical team for treatment of any ongoing cardiac instability, renal impairment and electrolyte disturbances. LITHIUM DIAGNOSIS 1 Lithium toxicity may be acute or chronic. Toxicity is associated with significant morbidity and mortality, and an acute overdose of >250 mg/kg (25 g). 180 Toxicology SPECIFIC POISONS 2 Acute overdose (i) Clinical manifestations of acute overdose include: (a) gastrointestinal: anorexia, nausea, vomiting (b) CNS: similar to chronic intoxication, but features develop slowly enough for treatment with i.v. crystalloid therapy. 3 Chronic toxicity (i) This is commonly associated with renal impairment, dehydration, diuretic use and congestive cardiac failure. (ii) Clinical manifestations of chronic toxicity include: (a) CNS: – mild: tremor, hyper-reflexia, ataxia, muscle weakness – moderate: rigidity, hypotension, stupor – severe: myoclonus, coma and convulsions (b) gastrointestinal symptoms are not present in chronic toxicity. 4 Gain i.v. access and send bloods for U&Es, blood sugar and serum lithium level. 5 Perform an ECG. MANAGEMENT 1 Acute overdose (i) Do not administer activated charcoal. (ii) Commence normal saline to correct hypotension, salt and water deficits, and to maintain a urine output >1 mL/kg per h. (iii) Most patients recover quickly with adequate fluid resuscitation. Observe until they have a normal mental status, the serum lithium level is falling and is <2.5 mmol/L. (iv) Consider haemodialysis in a patient with impaired renal function, late presentation, a serum lithium level of >3.5 mmol/L or progressive neurological signs. Contact the ICU. 2 Chronic toxicity (i) Discontinue lithium medications. Commence normal saline to correct hypotension, salt and water deficits, and to maintain a high urine output. (ii) Refer the following patient to ICU for consideration of haemodialysis: (a) neurological abnormalities such as an altered mental state, coma or convulsions (b) serum lithium level of >3.5 mmol/L and significant neurotoxicity. Toxicology 181 SPECIFIC POISONS THEOPHYLLINE DIAGNOSIS 1 Theophylline toxicity may result from acute ingestion or chronic use. Both are associated with significant morbidity and mortality. (i) Chronic ingestion is exacerbated by intercurrent illness or the concomitant administration of drugs that interfere with hepatic metabolism. 2 Clinical manifestations include: (i) Gastrointestinal tract: nausea, abdominal pain, intractable vomiting. (ii) Cardiovascular: sinus tachycardia, hypotension and cardiac arrhythmias. (iii) CNS: anxiety, agitation and insomnia. (iv) Hyperventilation, gastrointestinal bleeding, convulsions, coma and ventricular tachycardia in severe toxicity. 3 Clinical signs of significant toxicity may be delayed by up to 12 h in acute overdose, when sustained-release tablets have been ingested. 4 Gain i.v. access and send bloods for U&Es, LFTs, blood sugar and a theophylline level. (i) Look for hypokalaemia, hypomagnesaemia, hyperglycaemia and metabolic acidosis, particularly in severe acute ingestions. 5 Determine the serum theophylline level. (i) Acute poisoning: (a) toxic symptoms occur with a theophylline level over 25 mg/L (b) levels of 40–60 mg/L are serious, and a level >80 mg/L is potentially fatal. (ii) Chronic toxicity: (a) levels over 20 mg/L cause symptoms, and over 40 mg/L may be life-threatening. 6 Perform an ECG and cardiac monitoring. Cardiac arrhythmias are common and include sinus tachycardia, supraventricular tachycardia, atrial flutter and VT. MANAGEMENT 1 Ensure the airway is secure and administer high-flow oxygen. Correct fluid depletion and hypokalaemia with normal saline and potassium under ECG monitoring. 2 Administer oral activated charcoal in acute overdose, even if presentation is delayed. Give repeat doses at 4-h intervals. 182 Toxicology SPECIFIC POISONS 3 Give high-dose metoclopramide 10–40 mg i.v. for intractable vomiting, or give ondansetron 4–8 mg i.v. if this fails. 4 Give midazolam 0.05–0.1 mg/kg, diazepam 0.1–0.2 mg/kg i.v., or lorazepam 0.07 mg/kg i.v. up to 4 mg for seizures, although endotracheal intubation may be required. 5 Administer a -blocker such as propranolol 1 mg i.v. over 1 min, repeated up to a maximum of 10 mg only in a non-asthmatic patient with supraventricular tachycardia, hypokalaemia and hyperglycaemia. 6 Admit all patients with signs of toxicity for cardiac monitoring. (i) Refer patients with severe toxicity, obtundation and seizures to ICU for haemodialysis or charcoal haemoperfusion. -BLOCKERS DIAGNOSIS 1 Significant -blocker toxicity is associated particularly with propranolol ingestion, coexistent cardiac disease, and in polypharmacy overdose with calcium-channel blockers and TCAs. 2 Clinical evidence of toxicity usually presents within the first 6 h of overdose. Toxicity is associated with: (i) Bradycardia, arrhythmias, hypotension and cardiogenic shock. (ii) Sedation, altered mental status, convulsions and coma. 3 Gain i.v. access and send blood for U&Es and a blood sugar level, as hypoglycaemia may occur, especially with atenolol. Attach a cardiac monitor and pulse oximeter to the patient. 4 Perform an ECG. Look for toxic conduction defects such as atrioventricular block, right bundle branch block, prolongation of the QRS (propranolol) and ventricular arrhythmias (particularly with sotalol). MANAGEMENT 1 Ensure the airway is secure and administer high-flow oxygen. Commence i.v. fluid administration for hypotension. 2 Administer oral activated charcoal as soon as possible. 3 Give atropine 0.6–1.2 mg i.v. for bradycardia, up to a maximum of 0.04 mg/kg. 4 Give glucagon 50–150 g/kg i.v. bolus followed by an infusion at 1–5 mg/h. 5 Titrate an adrenaline (epinephrine) or isoprenaline infusion to maintain organ perfusion in resistant cases. Cardiac pacing may be necessary. 6 Admit all symptomatic patients to coronary care or ICU. 7 Propranolol is potentially the most toxic agent. It acts as a sodium-channel blocker agent similar to TCAs, and should be treated in the same way (see p. 174). Toxicology 183 SPECIFIC POISONS CALCIUM-CHANNEL BLOCKING DRUGS DIAGNOSIS 1 Toxicity is related to underlying cardiac disease, co-ingestants, delay to treatment, increased age, and the specific calcium-channel blocker (CCB) ingested. (i) Sustained-release (SR) verapamil or diltiazem are associated with the majority of significant poisonings. 2 Clinical signs of toxicity usually present within 2 h, but may be delayed up to 8 h with sustained-release preparations. Features include: (i) Gastrointestinal: nausea and vomiting. (ii) Cardiovascular: hypotension, sinus bradycardia and complex cardiac arrhythmias. (iii) CNS: lethargy, slurred speech, confusion, coma and convulsions. 3 Gain i.v. access and send blood for U&Es, LFTs and a blood sugar level. Take an arterial or venous blood gas. (i) Hyperglycaemia and metabolic acidosis are common with significant toxicity. 4 Perform an ECG. Look for toxic conduction defects such as high-grade AV block, complete heart block, and accelerated atrioventricular nodal rhythms. MANAGEMENT 1 Ensure the airway is secure and administer high-flow oxygen. Commence i.v. fluid administration. 2 Administer oral activated charcoal to all patients as soon as possible. More aggressive decontamination, such as whole bowel irrigation, may be required with large ingestions of SR tablets. 3 Give 10% calcium chloride 10 mL i.v. bolus, and repeat up to 30 mL i.v. followed by an infusion. Calcium increases cardiac output and restores perfusion to vital organs. 4 If hypotension and reduced myocardial contractility persist: (i) Commence an adrenaline (epinephrine) infusion at up to 0.5–1.0 g/kg per min, titrated to maintain organ perfusion. (ii) High-dose insulin therapy (0.5–1.0 IU/kg/h), in combination with 50% dextrose infusion to maintain euglycaemia, is effective treatment for severe CCB poisoning. (iii) Discuss management early with a poisons centre clinical toxicologist. 5 Admit the patient to ICU for cardiorespiratory monitoring. 184 Toxicology SPECIFIC POISONS CARBON MONOXIDE DIAGNOSIS 1 Carbon monoxide poisoning is usually associated with the combustion of fuel with an inadequate flue, e.g. a blocked domestic heater, or from the fumes of a car exhaust. It is a colourless odourless gas and the most common poison used for successful suicide in the UK and Australia. 2 Clinical manifestations are directly related to early ABG carboxyhaemoglobin (COHb) concentration levels around the time of exposure. Later COHb levels lack prognostic value: (i) 0–10%: asymptomatic (may be seen in smokers). (ii) 10–25%: throbbing frontal headache, nausea, shortness of breath on exertion. (iii) 25–40%: cognitive impairment, auditory and visual disturbances, dizziness, aggression and psychosis. (iv) 40–50%: confusion, coma and seizures. (v) 50–70%: hypotension, respiratory failure, cardiac arrhythmias and cardiac arrest. (vi) >70%: death. 3 A strong clinical suspicion is important in making the diagnosis. Suspect carbon monoxide toxicity if several members of one household present in a similar fashion. 4 Remember a pulse oximeter does not distinguish between carboxyhaemoglobin and oxyhaemoglobin, so will record misleadingly normal oxygen saturations. (i) Therefore send an ABG sample in all cases. Look for evidence of metabolic acidosis and an elevated carboxyhaemoglobin level. 5 Gain i.v. access and send blood for FBC, U&Es, LFTs, troponin, serum lactate and blood sugar level. Check a -human chorionic gonadotrophin (hCG) pregnancy test in women. 6 Perform an ECG. Look for evidence of cardiac arrhythmias or myocardial ischaemia. 7 Request a CXR and arrange a CT brain scan in a comatose patient. MANAGEMENT 1 Secure the airway and give 100% oxygen by tight-fitting mask with reservoir bag. (i) Call the senior ED doctor and prepare for endotracheal intubation in comatose patients, to protect and maintain the airway and to optimize ventilation with 100% oxygen. 2 Commence fluid resuscitation for hypotension and to correct acid–base disturbances. Hypotension usually responds to fluids, but may require inotropic support. Toxicology 185 SPECIFIC POISONS 3 Give 20% mannitol 0.5–1.0 g/kg (2.5–5 mL/kg) for clinical or radiographic evidence of cerebral oedema. 4 Refer the patient to a hyperbaric oxygen (HBO) unit if the patient was found unconscious, has significant neurological symptoms, or is pregnant. (i) Local referral practices will vary, as the efficacy of HBO is challenged. CYANIDE DIAGNOSIS 1 Cyanide is a metabolic poison associated with a high mortality. 2 Features of toxicity include: (i) Cardiovascular: initial hypertension followed by profound hypotension, bradycardia, arrhythmias, cardiovascular collapse and cardiorespiratory arrest. (ii) CNS: headache, anxiety, sedation, respiratory depression, seizures and coma. 3 Gain i.v. access and send blood for a serum lactate level and ABG analysis. 4 A raised anion gap metabolic acidosis and raised lactate level relate closely to clinical signs of intoxication and the serum cyanide level (which is not available acutely). MANAGEMENT 1 Assess and secure the airway immediately. Give 100% oxygen and commence fluid resuscitation. 2 Call for immediate senior ED doctor help, and/or advice from a clinical toxicologist if time allows. Give the following: (i) Hydroxocobalamin 70 mg/kg up to 5 g i.v. over 30 min or as a bolus in critical cases. Although unlicensed, it is preferred to dicobalt edetate. (ii) Then 25% sodium thiosulphate 12.5 g (50 mL) i.v. at a rate of 2–5 mL/min. Do not mix in the same infusion as the hydroxocobalamin. (iii) Repeat the above within 15 min, if there is no or only partial improvement. 3 Refer a patient with significant toxicity to ICU. CHLOROQUINE DIAGNOSIS 1 Overdose with quinine, chloroquine and hydroxychloroquine is potentially fatal with as little as 2.5–5 g ingested, and is associated with significant morbidity. 186 Toxicology SPECIFIC POISONS 2 Clinical manifestations (‘cinchonism’) are dose related and include: (i) Mild: flushed and sweaty skin, tinnitus, blurred vision, confusion, reversible high-frequency hearing loss, abdominal pain, vertigo, nausea and vomiting. (ii) Severe: hypotension, deafness, blindness, anaphylactic shock, cardiac arrhythmias and cardiac arrest. 3 Gain i.v. access and send blood for FBC, U&Es, LFTs, blood sugar level and -hCG in females. Attach a cardiac monitor and pulse oximeter to the patient. 4 Perform an ECG. Look for QRS and QT prolongation and ventricular arrhythmias. MANAGEMENT 1 Assess and secure the airway and give high-flow oxygen. Commence i.v. fluid resuscitation for hypotension. 2 Give oral activated charcoal to patients presenting within 1 h of overdose. 3 Administer midazolam 0.05–0.1 mg/kg i.v., diazepam 0.1–0.2 mg/kg i.v. or lorazepam 0.07 mg/kg up to 4 mg to treat seizures and agitation, and to reduce the tachycardia. 4 Commence an isoprenaline infusion for torsades de pointes, or arrange for overdrive cardiac pacing for the QT prolongation, because magnesium is contraindicated. 5 There are no specific treatment modalities to reverse blindness and deafness in severe toxicity, other than supportive care. 6 Admit the patient to CCU or ICU. COCAINE DIAGNOSIS 1 Cocaine hydrochloride is a fine white powder, which may be mixed with baking soda to make ‘crack’ (free base cocaine) and smoked. It rapidly reaches the cerebral circulation and has a half-life of 90 min. 2 Complications following cocaine abuse include: (i) Respiratory: dyspnoea, pneumothorax, pneumonitis and thermal airway injury. (ii) Cardiovascular: palpitations, hypertension, aortic dissection, myocardial ischaemia, arrhythmias and cardiac arrest. (iii) Nervous system: agitation, altered mental state, syncope, seizures, focal neurological signs, intracranial haemorrhage and coma. (iv) Hyperthermia. 3 Base the diagnosis on history and clinical suspicion. Monitor the core temperature for hyperthermia. Toxicology 187 SPECIFIC POISONS 4 Gain i.v. access and send blood for FBC, U&Es, LFTs, blood sugar level and troponin as indicated clinically. Attach a cardiac monitor and pulse oxi meter to the patient. 5 Perform an ECG and look for signs of myocardial ischaemia, infarction and cardiac arrhythmias. 6 Request a CXR. MANAGEMENT 1 Assess and secure the airway and give high-flow oxygen. 2 Give midazolam 0.05–0.1 mg/kg i.v., diazepam 0.1–0.2 mg/kg i.v. or lorazepam 0.07 mg/kg up to 4 mg to treat seizures, agitation and to reduce the tachycardia, hypertension and hyperthermia. 3 Treat myocardial ischaemia with sublingual or i.v. nitrates and benzodiazepine sedation. (i) Ideally arrange for percutaneous coronary intervention (angioplasty) if myocardial infarction occurs. (ii) Further i.v. nitrates or sodium nitroprusside may be required to treat hypertension. (iii) Avoid -blockers, which can worsen -adrenergic mediated vasoconstriction. 4 Admit all patients requiring high-dose benzodiazepine therapy and patients with evidence of cardiovascular instability for cardiac monitoring and observation. ORGANOPHOSPHATES DIAGNOSIS 1 Organophosphates are extremely toxic pesticides, which produce acetylcholine excess with muscarinic, nicotinic and CNS effects. 2 They are rapidly absorbed through the skin, bronchi and small intestine if ingested orally. 3 Patients present with degrees of cholinergic crisis, usually within 4 h of ingestion or exposure. Specific manifestations include: (i) Muscarinic: (a) bronchospasm, vomiting, pinpoint pupils, bradycardia and hypotension (b) excessive sweating, lacrimation, salivation, profuse diarrhoea and urination. (iii) Nicotinic: fasciculation, tremor, weakness, muscle paralysis, tachycardia and hypertension. (ii) CNS: initial agitation followed by sedation and altered mental status leading to convulsions and coma. 188 Toxicology SPECIFIC POISONS 4 Gain i.v. access and send blood for FBC, U&Es, LFTs and a plasma cholinesterase level, which is a marker of exposure, but a poor indicator of severity. 5 Perform an ECG to evaluate cardiac arrhythmias. 6 Request a CXR as aspiration pneumonitis is common. MANAGEMENT 1 Instruct all staff to wear a gown and gloves when removing soiled clothing or washing the skin. 2 Give oxygen, and call an airway-skilled doctor to pass an endotracheal tube for severe bronchorrhoea and respiratory failure. 3 Commence a normal saline infusion to manage hypotension and replace losses. 4 Treat seizures with midazolam 0.05–0.1 mg/kg i.v., diazepam 0.1–0.2 mg/kg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. 5 Give atropine 2 mg i.v. repeated until the skin becomes dry, and bronchial secretions are minimal. (i) Massive doses (50–100 mg) may be necessary, but do not rely on pupillary dilatation and tachycardia as indicative end points, as they may not reflect adequate atropinization. 6 Give pralidoxime 2 g (30 mg/kg) i.v. over 15 min and then 1 g every 8 h for the next 48 h, in all moderate-to-severe cases (except for carbamate poisoning). (i) Monitor serial plasma or red cell cholinesterase levels and look for signs of clinical improvement before ceasing treatment. 7 Admit the patient to ICU. PARAQUAT DIAGNOSIS 1 Paraquat is a highly toxic herbicide. Significant oral ingestion is associated with fulminant multi-organ failure. If patients survive this, they develop progressive pulmonary fibrosis, and may die 4–6 weeks later from hypoxaemia. 2 Clinical effects depend on the route of exposure: (i) Skin: localized irritation, erythema, blistering, ulceration. (ii) Eyes: corneal inflammation, oedema, ulceration. Warning: staff treating patients exposed to organophosphates may develop mild headache, eye irritation and pulmonary symptoms secondary to the hydrocarbon solvent and not the organophosphate itself. These resolve with simple analgesia and by removing the staff from the exposure source. ! Toxicology 189 CHEMICAL BURNS (iii) Systemic from oral ingestion: (a) <15 mL of 20% solution: nausea, vomiting and diarrhoea with reversible pulmonary irritation (b) >15 mL of 20% solution: pharyngeal ulceration, hypersalivation, intractable vomiting, haematemesis, severe abdominal pain and bowel perforation. 3 Gain i.v. access and send blood for FBC, U&Es, LFT, coagulation profile and blood sugar level. Request a serum paraquat level. (i) A serum level of >5 mg/L is invariably fatal. 4 A qualitative urine test may be performed by adding 1 mL of 1% sodium dithionite solution to 10 mL of urine. Paraquat ingestion is confirmed if the urine turns blue. 5 Perform an ECG. 6 Request a CXR to look for evidence of mediastinitis, aspiration, pulmonary opacities and abdominal viscus perforation. MANAGEMENT 1 Early gastrointestinal decontamination is paramount. Give activated charcoal 50–100 g immediately orally or via a nasogastric tube. (i) The traditional alternative adsorbing agent 15% aqueous suspension Fuller’s earth (bentonite) 1000 mL is rarely available now. 2 Administer oxygen only if the SaO2 is <90%, as otherwise oxygen enhances pulmonary toxicity. 3 Refer the patient immediately for admission to ICU. CHEMICAL BURNS DIAGNOSIS 1 These occur at home, in schools, in laboratories and in industrial accidents. 2 Most agents are strong acids or alkalis, although occasionally phosphorus and phenol are responsible. 3 Alkali burns are generally more serious than acid as they penetrate deeper. MANAGEMENT 1 Wear gloves to remove any contaminated clothing. Treat by copious irrigation with running water. Continue irrigating for at least 30 min. 2 Do not attempt to neutralize the chemical, as many resultant reactions produce heat and will exacerbate the injury, except in the case of hydrofluoric acid. 190 Toxicology FURTHER READING 3 Hydrofluoric acid burns (i) Neutralize these as follows: (a) convert hydrofluoric acid to the calcium salt by covering the affected area with dressings soaked in 10% calcium gluconate solution, or by rubbing in 2.5% calcium gluconate gel (b) inject s.c. 10% calcium gluconate if the pain and burning persist (c) give i.v. regional treatment with 10% calcium gluconate (similar to a Bier’s block technique) for an extensive limb burn. (ii) Dermal absorption of fluoride ions may result in systemic fluorosis causing hypocalcaemia, hypomagnesaemia, hyperkalaemia and cardiac arrest (a) systemic fluorosis may follow burns affecting as little as 2–5% of body surface area from concentrated 70% hydrofluoric acid (b) seek immediate senior ED doctor help, and give large amounts of i.v. calcium chloride and magnesium sulphate as indicated clinically, and from blood testing. 4 Refer all patients to the surgical team unless the area burnt is minimal and the patient is pain free. 5 Refer patients with systemic fluorosis to ICU. The hyperkalaemia may require haemodialysis. FURTHER READING American Heart Association (2010) Part 12: Cardiac arrest in special situations: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S829–61. European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances. Resuscitation 81: 1400–33. Murray L, Daly F, Little M, Cadogan M (2011) Toxicology Handbook, 2nd edition. Elsevier, Sydney. National Poisons Information Service TOXBASE®. http://www.toxbase.org/ (poisons information). Toxinz. http://www.toxinz.com/ (toxicology first aid and management). TOXINOLOGY EMERGENCIES Section VI 192 Toxinology Emergencies SNAKE BITES Australian snakebite management advice is available from the Poisons Information Centre (24 h) on 13 11 26. There are no endemic venomous snakes in New Zealand, although toxinology advice is still available from the National Poisons Centre on 03 479 7248 (or 0800 764 766 within New Zealand only). Snake bite is exceedingly rare in the UK, but may present in zookeepers and herpetologists, or following a mishap with an exotic pet. Advice on management is always available from the National Poisons Information Service (24 h) on 0844 892 0111 in the UK. ELAPID SNAKE BITES DIAGNOSIS 1 The 10 most venomous snakes in the world are all elapid snakes found in Australia. (i) Elapids have permanently erect front fangs and produce venom containing haemotoxins, neurotoxins and myotoxins (a) major species include brown snake, black snake, taipan, tiger snake and death adder (b) only 5–10% snake bites by a venomous snake lead to severe envenomation. 2 Some bites such as from the tiger snake and black snake may cause immediate local pain, bruising or swelling within hours, although local signs following a snakebite are usually minimal, with fine scratches or small puncture marks only. 3 Look for the following signs that indicate systemic envenomation, although these may be subtle or fluctuate: (i) Non-specific findings such as headache, sweating, nausea, vomiting, abdominal pain, diarrhoea and transient hypotension. (ii) Tissue-specific findings indicating severe envenomation (any one of): (a) haemotoxic effects including asymptomatic venom-induced consumptive coagulopathy (VICC) with undetectable fibrinogen/raised international normalized ratio (INR) >3.0/raised D-dimer (10 times assay cut-off) on laboratory testing, or causing bite- or venepuncture-site oozing, haematemesis, melaena and haematuria (b) thrombotic microangiopathy with raised creatinine with or without renal failure, thrombocytopenia and intravascular haemolysis on blood film (c) neurotoxic effects including ptosis, diplopia, dysphagia and respiratory or distal paralysis Toxinology Emergencies 193 SNAKE BITES (d) myotoxic effects including muscle pain or tenderness with creatine kinase (CK) >1000 U/L, myoglobinuria and renal failure. (iii) Sudden collapse, convulsions and cardiac arrest (especially brown snake). 4 Gain i.v. access and send blood for full blood count (FBC), urea and electrolytes (U&Es), CK and coagulation profile including INR, activated partial thromboplastin time (aPTT) and fibrinogen. Attach a cardiac monitor and pulse oximeter to the patient. 5 Send urine for protein, haemoglobin and myoglobin estimation. 6 Attempt to identify the snake species with a venom detection kit (VDK) analysis from a bite-site swab (carefully taken from a window cut in the pressure-immobilization bandage), or on the urine. (i) Visual inspection and an amateur ‘guess’ at the species is unreliable and misleading, and is a waste of time unless you are a trained herpetologist. 7 Perform an electrocardiogram (ECG), chest radiograph (CXR) and spirometry in significant envenoming. MANAGEMENT 1 Make sure that first aid has been applied to impede the spread of venom through local lymphatics, using the pressure-immobilization technique: (i) Apply a broad firm bandage around the bite site and extend proximally up the limb to cover it completely, as tight as one would bandage a sprained ankle. (ii) Splint the dependent limb and organize for transport to be brought to the patient. (iii) Keep the immobilization bandage in place until the first set of bloods are negative and the patient is asymptomatic, or if envenomed until definitive treatment has been instituted and the patient is systemically improved. 2 Give high-flow oxygen via face mask and watch for any signs of airway compromise. 3 Give antivenom for definite systemic envenomation. Do not use antivenom for a positive VDK result alone, if no other abnormal clinical or laboratory features are present: (i) Indications for antivenom therefore include the presence of any clinical signs, particularly impending respiratory arrest, refractory hypotension, cardiac arrhythmias, renal failure and/or abnormal laboratory findings, including consumption coagulopathy. 194 Toxinology Emergencies SNAKE BITES (ii) Give the appropriate species-specific monovalent antivenom if the snake species has been positively identified on VDK (or by an expert herpetologist). (a) start with two vials (2000 units) in brown snake envenoming, occasionally up to 10 vials (10 000 units) for critical cases (b) give up to two vials (6000 units) for tiger snake envenoming; one or two vials (6000 to 24 000 units) for taipan; and start with one vial for envenoming by black snake (18 000 units) and death adder (6000 units). (iii) Get expert advice urgently if the snake species is still unknown in an envenomed patient (a) tiger snakes are the only terrestrial venomous snake native to Tasmania, simplifying the use of antivenom in that state (b) in the other Australian states, give polyvalent antivenom two to four vials i.v. This is more expensive and carries a greater risk of anaphylaxis. (iv) Give antivenom slowly by i.v. infusion over 30 min after 1 in 10 dilution with normal saline (a) give an undiluted neat bolus of antivenom as a life-saving measure if the patient is in cardiac arrest or has circulatory collapse. (v) Pre-treatment with adrenaline (epinephrine) is unhelpful, but adrenaline must be available as there is the possibility of anaphylaxis to the horse-serum derived antivenom: (a) the risk of an immediate-type hypersensitivity reaction to antivenom is 41% for polyvalent and tiger snake antivenom and 10% to brown snake antivenom, but overall only 5% reactions are severe anaphylaxis. 4 Give tetanus prophylaxis according to the patient’s immune status. 5 Refer all patients with signs of systemic envenomation to ICU or the local toxicology unit. 6 Remove the pressure-immobilization bandage and observe carefully those patients who remain systemically well, with no clinical signs of envenomation and who have normal initial laboratory blood tests. (i) Repeat the laboratory tests 1 h after bandage removal, including INR, aPTT and CK. (a) treat with antivenom if they become abnormal, of if the patient develops any clinical signs of envenoming. (ii) Observe the patient for a further 12 h prior to discharge, with careful clinical examination looking particularly for delayed neurotoxicity or myotoxicity. (iii) Repeat the same laboratory tests including INR, aPTT and CK at 6 h and again at 12 h after bandage removal. If these remain normal and the patient is well, discharge. Toxinology Emergencies 195 SNAKE BITES VIPER (ADDER) SNAKE BITES DIAGNOSIS 1 Snakes of the viper species include the North American rattlesnake, the African rhinoceros viper and the adder, which is the only naturally occurring venomous snake in the UK. 2 Local effects of an adder bite include pain, bruising, swelling and local lymphadenopathy within hours of the bite. However, fewer than 50% of bites are associated with envenomation, and occasionally systemic poisoning may occur with no local reaction. 3 Systemic envenomation causes: (i) Early features including non-allergic anaphylaxis with transient syncope and hypotension, angioedema, urticaria, abdominal pain, vomiting and diarrhoea. (ii) Late features including recurrent or persistent hypotension, ECG changes, spontaneous bleeding, coagulopathy, adult respiratory distress syndrome and acute renal failure. 4 Gain i.v. access, and send blood for FBC, clotting screen, U&Es and liver function tests (LFTs). 5 Perform an ECG and a CXR in severe cases. MANAGEMENT 1 Reassure the patient, apply a firm bandage proximal to the bite, immobilize the dependent limb and transport the patient rapidly to hospital. 2 Treat non-allergic anaphylaxis reactions with oxygen, adrenaline (epinephrine) and fluids (see p. 27). 3 Give European viper venom antiserum for significant adder envenomation: (i) Indications for viper venom antiserum include: (a) hypotension (b) ECG changes (c) vomiting (d) bleeding (e) extending limb swelling within 4 h of the bite. (ii) Add one 10 mL vial to normal saline 5 mL/kg diluent and infuse over 30 min, repeated as indicated. (iii) Have adrenaline (epinephrine) immediately available for anaphylactic reactions to the antivenom. 4 Give tetanus prophylaxis, and refer all patients to the medical team for admission, even in the absence of initial symptoms or signs. 196 Toxinology Emergencies SPIDER BITES The majority of spider bites are associated with local symptoms of pain and erythema. Certain species are associated with significant envenomation, and may be fatal. DIAGNOSIS 1 Latrodectus species includes the red-back (Australia), the black widow (America), and the katipo (New Zealand) spiders. Envenomation is by the female. Clinical features of latrodectism include: (i) Local pain, erythema, sweating, lymphadenopathy and piloerection. (ii) Systemic features such as headache, nausea, vomiting, abdominal pain, generalized sweating and hypotension. 2 Over 40 species of funnel-web spider occur in Australia, with the most significant envenomation by the male Sydney funnel-web spider. Clinical features of funnel-web spider envenomation include: (i) Severe localized pain, with erythema. (ii) Generalized muscle fasciculations, nausea, vomiting, abdominal pain, sweating, lacrimation and salivation. (iii) Initial tachycardia and hypertension progressing to hypotension, pulmonary oedema and finally convulsions and coma. 3 Base the diagnosis on history and clinical examination, as no laboratory tests are helpful. 4 Perform an ECG and request a CXR if funnel-web spider bite is suspected. MANAGEMENT 1 Apply a pressure-immobilization bandage immediately after a funnel-web spider bite to retard the spread of the venom. Never use this in red-back spider envenomation. 2 Otherwise, give general first-aid treatment by applying ice or heat and giving oral analgesia as symptomatic relief. 3 Observe all patients in a monitored resuscitation area, assess and secure the airway, and administer oxygen. Gain i.v. access only if antivenom is indicated. 4 Antivenom administration: (i) Red-back spider antivenom (a) administer red-back spider antivenom to patients with clinical manifestations of systemic toxicity or severe uncontrolled local symptoms (b) give one to two vials (500–1000 units) red-back spider antivenom i.m. Toxinology Emergencies 197 MARINE ENVENOMATION (c) i.v. administration diluted in 100 mL normal saline over 30 min may be used as an alternative, particularly if the initial response to i.m. antivenom by 90 min was poor (d) discuss additional management with a clinical toxicologist if symptoms continue (e) observe all patients given antivenom until symptoms have resolved (f) discharge all the other patients with mild or absent symptoms. Advise them to return if symptoms worsen, as antivenom may work even days after envenoming. (ii) Funnel-web spider antivenom (a) administer funnel-web spider antivenom to patients with clinical manifestations of systemic toxicity or severe uncontrolled local symptoms (b) give two vials (250 units) i.v. slowly (four if severe) and repeat every 15 min until symptoms have resolved (c) refer all patients with persistent local symptoms or significant systemic envenomation to the intensive care unit (ICU) (d) discharge other patients who remain systemically well, with absence of signs of envenoming by 4 h after removal of any first-aid bandage applied. MARINE ENVENOMATION Several hazardous marine animals are found in coastal waters around the world. Warm water immersion is useful symptomatic treatment for injuries from many species of spiny fish, with antivenom therapy available for only a few specific instances. DIAGNOSIS 1 Jellyfish (i) Irukandji syndrome (Australia). This causes mild local pain followed 30–40 min later by severe generalized muscle cramps, back and abdominal pain, hypertension, and pulmonary oedema. It is potentially fatal. (ii) Box jellyfish (Australia). This causes severe local pain and cross-hatched erythematous dermal lesions, associated with cardiovascular and respiratory collapse. It is also potentially fatal. (iii) Bluebottle or Portuguese man-of-war (worldwide). These cause severe local stinging pain, erythema, and elliptical blanched wheals, rarely associated with a muscle pain syndrome and hypotension. 198 Toxinology Emergencies MARINE ENVENOMATION 2 Poisonous fish such as the stonefish, lionfish, bullrout (Australia) or lesser weever (UK): (i) These fish have venomous spines that can cause extreme local pain and oedema. (ii) Systemic effects include diarrhoea, respiratory depression and hypotension. 3 Sea urchins, fire coral (worldwide) (i) Sea urchins cause local erythema and pain from the many tiny spines which may break off and enter a joint cavity or the deep palmar or plantar spaces. (ii) Fire coral causes local burning similar to a jellyfish sting. MANAGEMENT 1 Assess and secure the airway first and provide basic life support to patients with cardiovascular collapse and systemic toxicity. 2 Jellyfish first aid (i) Box jellyfish and Irukandji: rinse jellyfish wounds with seawater, remove adherent tentacles, and prevent further nematocyst discharge with 5% acetic acid (vinegar). (ii) Bluebottle: rinse with seawater (not vinegar), remove adherent tentacles, and immerse the affected area in warm water at 40–45°C without scalding. 3 Jellyfish systemic envenomation (i) Irukandji (a) administer oxygen and give opiate analgesia, e.g. with fentanyl 5 g/kg i.v. every 10 min until pain is controlled (b) commence a glyceryl trinitrate (GTN) infusion if severe hypertension is not controlled with pain management. (ii) Box jellyfish (a) administer oxygen and commence i.v. fluid resuscitation for hypotension. Give morphine 5–10 mg i.v. for severe local pain (b) administer box jellyfish antivenom if the pain is refractory to opiates, the patient is shocked, or in cardiac arrest: – give three vials (60 000 units) diluted 1 in 10 with normal saline i.v. over 30 min or six vials as a bolus in cardiac arrest. 4 Poisonous fish (i) Immerse the affected area in warm water at 40–45°C without scalding. If pain persists, perform a regional block with 2% lignocaine (lidocaine) and give morphine 5–10 mg i.v. (ii) Debride the wound, remove spines and give tetanus prophylaxis according to the patient’s immune status. Toxinology Emergencies 199 BEE AND WASP STINGS (iii) Systemic stonefish envenomation: give one vial (2000 units) of stonefish antivenom i.m. for every two puncture marks visible. 5 Sea urchins and fire coral (i) Relieve pain by immersion in hot water at 40–45°C without scalding or by using a local anaesthetic block, followed by exploration, irrigation and debridement as necessary, and give tetanus prophylaxis. (ii) Give an antibiotic such as doxycycline 100 mg orally once daily for 5 days (not in children or pregnant patients), for deep or necrotic wounds. BEE AND WASP STINGS DIAGNOSIS 1 There are more deaths from anaphylaxis following bee or wasp stings than from all the other venomous bites and stings combined. 2 Local pain predominates and may be followed by a severe anaphylactic reaction causing laryngeal oedema, bronchospasm, hypotension and collapse (see p. 27). MANAGEMENT 1 Remove a bee sting by scraping the sting out with a knife, without squeezing. 2 Anaphylaxis: (i) Assess and secure the airway, give oxygen, gain i.v. access and commence fluid resuscitation for shock. (ii) Give 1 in 1000 adrenaline (epinephrine) 0.3–0.5 mg (0.3–0.5 mL) i.m. early. Give 1 in 10 000 adrenaline (epinephrine) or 1 in 100 000 adrenaline (epinephrine) 0.75–1.5 g/kg, i.e. 50–100 g slowly i.v. if circulatory collapse occurs. 3 Arrange for patients prone to anaphylaxis from bee or wasp stings to carry a pre-filled adrenaline (epinephrine) syringe (EpiPen® or Anapen®) at all times. 200 Toxinology Emergencies FURTHER READING Murray L, Daly F, Little M, Cadogan M (2011) Toxicology Handbook, 2nd edition, Elsevier, Sydney. National Poisons Information Service TOXBASE®. http://www.toxbase.org/ (poisons information). Toxinz. http://www.toxinz.com/ (toxicology first aid and management). University of Adelaide. Clinical Toxinology Resources. http://www.toxinology. com/ ENVIRONMENTAL EMERGENCIES Section VII 202 Environmental Emergencies HEAT, COLD AND DROWNING HEAT ILLNESS Heat illness occurs when the body’s capacity to dissipate heat is exceeded by internal heat production and/or by heat stress from an external source. Heat illness is predisposed to by hot weather, exercise, obesity, fever, lack of physical fitness or acclimatization, skin disease such as psoriasis or eczema, alcohol intake, and drugs such as anticholinergic agents, cocaine and amphetamines. DIAGNOSIS 1 Mild to moderate heat illness Thermoregulatory mechanisms remain intact. (i) Heat cramps (a) pain develops in heavily exercising muscles in hot weather secondary to sodium depletion and dehydration. (ii) Heat exhaustion (a) thirst, cramps, headache, vertigo, anorexia, nausea and vomiting occur (b) the patient is flushed and sweating, with rectal temperature of 38–39°C (c) tachycardia and orthostatic hypotension occur secondary to dehydration. 2 Severe heat illness: Heat stroke Thermoregulatory mechanisms fail and the rectal temperature is over 40.6°C. (i) Classic (non-exertional) heat stroke (CHS): CHS usually occurs in the elderly or very young during a heat wave secondary to high environmental temperatures. (ii) Exertional heat stroke (EHS): EHS is associated with young adults exercising in high temperatures. (iii) Symptoms include headache, vomiting and diarrhoea associated with mental state change progressing to aggressive or bizarre behaviour, collapse, seizures and coma. (iv) Hot dry skin is usual, but profuse sweating occurs in up to 40% of patients with exertional heat stroke. (v) The patient is flushed, tachypnoeic, tachycardic and hypotensive. Muscle rigidity, transient hemiplegia, dilated pupils, disseminated intravascular coagulation (DIC) and multi-organ failure may all occur. Environmental Emergencies 203 HEAT, COLD AND DROWNING (vi) Gain i.v. access and send blood for full blood count (FBC), coagulation profile, urea and electrolytes (U&Es), blood sugar, liver function tests (LFTs), creatinine kinase (CK) and lactate. (vii) Check an arterial blood gas (ABG). Attach an electrocardiographic (ECG) monitor and pulse oximeter to the patient. MANAGEMENT 1 Heat cramps (i) Rest in a cool environment, and replace fluid orally with added salt or give 1 L normal saline iv. (ii) The patient is usually able to go home. 2 Heat exhaustion (i) Rest in a cool environment and give up to 3 L cooled normal saline i.v. (ii) Cool the patient with tepid sponging and fanning. (iii) Admit for observation, particularly when elderly or if orthostatic hypotension persists. 3 Heat stroke (i) Give oxygen and aim for an oxygen saturation above 94%. Call the senior emergency department (ED) doctor for help, and arrange for endotracheal intubation for airway protection. (ii) Commence urgent cooling by tepid sponging, fans and cold packs to the groin and axillae until the temperature is <38.5°C (a) avoid excessive shivering, but do not use chlorpromazine 25 mg i.v. to suppress this due to its multiple side effects (b) antipyretics such as aspirin and paracetamol are also not indicated. (iii) Give 1 L cooled normal saline over 20 min, then give fluid according to the blood pressure, serum sodium level and urine output. (iv) Give midazolam 0.05–0.1 mg/kg up to 10 mg i.v., diazepam 0.1–0.2 mg/kg up to 20 mg i.v., or lorazepam 0.07 mg/kg up to 4 mg i.v. for seizures and/or agitation. (v) Monitor for complications such as hypoglycaemia and give 50% dextrose 50 mL. (vi) Give 8.4% sodium bicarbonate 50 mL plus 20% mannitol 0.5–1.0 g/kg (2.5–5 mL/kg) for rhabdomyolysis, and maintain a urinary output of 1–2 mL/kg per h. (vii) Admit the patient to the intensive care unit (ICU) for sedation, intubation and neuromuscular blockade. 204 Environmental Emergencies HEAT, COLD AND DROWNING OTHER HYPERTHERMIA-RELATED ILLNESS Hyperthermia-related syndromes may be associated with specific drug administration such as anticholinergic agents, serotonin agonists, dopamine antagonists and inhalational anaesthetics. DIAGNOSIS 1 Neuroleptic malignant syndrome (i) Rare but potentially lethal syndrome complicating the use of dopamine antagonist neuroleptic medication such as antipsychotic agents (e.g. chlorpromazine, haloperidol) and some antiemetics (metoclopramide). (ii) It is associated with development of muscle rigidity, bradyreflexia, bradykinesia, altered mental status, extrapyramidal symptoms and hyperthermia. 2 Serotonin syndrome (i) This is a clinical manifestation of excessive stimulation of serotonin receptors in the central nervous system (CNS). (ii) It follows drug combinations with selective serotonin reuptake inhibitors (SSRIs), monoamine-uptake inhibitors, analgesics such as fentanyl or tramadol, antiemetics such as ondansetron, and stimulants such as amphetamine or cocaine. (iii) It has a spectrum of severity ranging from agitation and hyperreflexia through to generalized rigidity, myoclonus, autonomic instability, mental status changes and hyperthermia. 3 Malignant hyperthermia syndrome (i) A rare genetic disorder that develops during or after receiving an inhalational anaesthetic or suxamethonium. (ii) Characterized by muscular rigidity, hypercapnoea, tachycardia, hypertension, mottled diaphoretic skin and agitation. 4 Gain i.v. access and send urgent bloods including FBC, coagulation profile, electrolyte and liver function tests (ELFTs), CK and lactate. Add blood cultures if sepsis is suspected. 5 Check an ABG, perform an ECG, and send a midstream urine (MSU) sample. MANAGEMENT 1 Give high flow oxygen and commence i.v. normal saline. 2 Check the temperature and commence supportive care. (i) Temperature >38.5° is an indication for continuous coretemperature monitoring. (ii) Temperature >39.5° with an altered mental status is an emergency: Environmental Emergencies 205 HEAT, COLD AND DROWNING (a) arrange a senior doctor to perform endotracheal intubation and ventilation with muscle paralysis, to protect the airway and prevent further muscle-generated heat production leading to multiple organ failure, neurological injury and death. 3 Neuroleptic malignant syndrome (i) Give bromocriptine (a dopamine agonist) orally or via a nasogastric tube. Start at 2.5 mg 8-hourly, increasing to 5 mg every 4 h (maximum 30 mg/day) in moderate to severe cases. 4 Serotonin syndrome (i) Give bromocriptine (a dopamine agonist) orally or via a nasogastric tube. Start at 2.5 mg 8-hourly, increasing to 5 mg every 4 h (30 mg/day) in moderate to severe cases. (ii) Add midazolam 0.05–0.1 mg/kg i.v., or diazepam 0.1–0.2 mg/kg i.v. titrated to achieve gentle sedation. 5 Malignant hyperthermia syndrome (i) Administer dantrolene 1 mg/kg i.v. for severe muscle rigidity and hyperthermia. Further doses of 1–2.5 mg/kg (up to a maximum of 10 mg/kg/24 h) may be required. HYPOTHERMIA This is present when the core temperature drops to <35°C (95°F), and occurs when heat loss exceeds the body’s ability to produce and conserve heat. Mild hypothermia is classified as 32–35°C (89.6–95°F), moderate hypothermia as 30–32°C (86–89.6°F), and severe hypothermia as <30°C (86°F). DIAGNOSIS 1 Hypothermia is predisposed by the following: (i) Exposure to low air temperatures, particularly with wind and rain. (ii) Exposure in cold water. (iii) Unconscious patient, or patients who have taken sedative drugs, especially alcohol. (iv) Babies or the elderly with intercurrent illness, e.g. stroke, pneumonia, diabetic ketoacidosis (DKA). (v) Endocrine disorders, such as myxoedema or hypopituitary coma (rare). 2 Clinical manifestations include: (i) Mild hypothermia: poor judgement, lethargy, ataxia, shivering and tachypnoea. (ii) Moderate hypothermia: bradycardia, hypotension, bradypnoea, and confusion. Shivering is absent. 206 Environmental Emergencies HEAT, COLD AND DROWNING (iii) Severe hypothermia: the patient is comatose and may appear dead with an undetectable pulse, absent reflexes, unrecordable blood pressure and fixed pupils. 3 Record the core temperature rectally with a low-reading thermometer. This is more accurate than any tympanic membrane device. 4 Send blood for FBC, U&Es, CK, coagulation profile and blood sugar level. Check serum lipase/amylase, as pancreatitis may be associated. Send ABGs. 5 Perform an ECG. (i) Look for evidence of bradycardia, low-voltage complexes, atrial fibrillation and prolongation of the QT interval. (ii) Osborn ‘J’ waves (a slurred notching of the terminal portion of the QRS complex) may be present at core temperatures of <32°C (a) Osborn waves are not pathognomic and are seen in other conditions such as subarachnoid haemorrhage, head trauma and hypercalcaemia. 6 Request a CXR. MANAGEMENT 1 Mild hypothermia (i) Remove wet clothing and cover the patient in warm blankets and layers of polythene to minimize evaporative, convective and conductive heat loss. (ii) Rehydrate the alert but shivering patient, and give high-energy food and drinks. 2 Moderate and severe hypothermia (core temperature ≤32°C ) (i) Remove wet clothing and cover the patient in warm blankets and layers of polythene to minimize evaporative, convective and conductive heat loss. (ii) Give high-flow, warmed 42–46°C (108–115°F), humidified oxygen. (iii) Give i.v. fluids cautiously through a warming device at 43°C (109°F). Pulmonary oedema may be precipitated by excessive fluid administration. (iv) Use a forced-air re-warming blanket, e.g. Bair Hugger®, and aim for a core temperature rise of 1°C/h in younger patients and 0.5°C per h in the elderly. (v) Take extreme care with any airway manoeuvres such as endotracheal intubation, as this may precipitate ventricular fibrillation (VF) in severe hypothermia. Call the senior ED doctor for help. Environmental Emergencies 207 HEAT, COLD AND DROWNING 3 Cardiac arrest in a hypothermic patient (i) Severe hypothermia (core temperature <30°C) (a) attempt defibrillation once for VF, delivering 150–200 J biphasic or 360 J monophasic (b) standard resuscitation drugs are usually ineffective as the efficacy of adrenaline (epinephrine) and amiodarone are reduced, with an increased circulation time (c) provide aggressive active internal re-warming with warmed 40°C pleural, gastric or peritoneal lavage, aiming for a core temperature rise to at least 33°C (d) extracorporeal blood re-warming is ideal, when available. (ii) Moderate hypothermia (core temperature 30–32°C) (a) attempt defibrillation with one direct current (DC) shock (b) administer standard resuscitation medications, but double the time between doses. (iii) Apply usual resuscitation protocols with core temperatures of ≥33°C. (iv) Continue resuscitation attempts in hypothermic cardiac arrest until the core temperature rises to at least 33°C, or until a senior doctor advises to the contrary (a) this may involve a prolonged period of resuscitation and aggressive measures as outlined. DROWNING DIAGNOSIS 1 Drowning is a common cause of accidental death in Australasia and Europe. It is defined as any process that results in primary respiratory impairment following immersion (face and upper airway), or submersion (whole body) in a liquid medium. 2 The duration of hypoxia is the most important factor that determines outcome and a full neurological recovery. Victims with spontaneous circulation and breathing on arrival at hospital usually have a good outcome. 3 The presence of lung crackles indicates likely inhalation of water, with the risk of hypoxaemia. The initial difference between sea-water (hypertonic) and fresh-water (hypotonic) drowning is of little clinical significance. However, contaminated water such as sewage will require antibiotic prophylaxis. (i) About 15% of drowned victims experience ‘dry drowning’, assumed due to laryngospasm, where little or no fluid is found in the lungs. 4 Consider other more relevant factors: (i) Preceding injury, especially to the cervical spine in a diving accident. 208 Environmental Emergencies SPORTS-DIVING ACCIDENTS (ii) Sudden preceding illness, such as a myocardial infarction, cerebrovascular accident or epileptic seizure that may have led to the drowning. (iii) Alcohol or drug use (a contributing factor in up to 70% of drownings). (iv) Hypothermia. 5 Check FBC, U&Es, blood sugar and ABGs. Attach a cardiac monitor and pulse oximeter to the patient. 6 Perform an ECG and request a CXR. MANAGEMENT 1 Record the rectal temperature and re-warm the patient if the core temperature is low. 2 Commence cardiopulmonary resuscitation if the patient has no detectable cardiac output or is not breathing. (i) Be careful to control the cervical spine if a neck injury is suspected. (ii) Insert a nasogastric tube early to decompress the stomach. Gastric regurgitation is common in up to 85% of patients requiring basic life support. (iii) Continue prolonged resuscitation efforts, which may be successful particularly with drowning in cold water associated with sudden hypothermia. 3 Otherwise, give high-flow oxygen and aim for an oxygen saturation above 94%. 4 Call an airway-skilled doctor to intubate the patient if unconscious or he or she develops respiratory failure with a PaO2 of <75 mmHg (10 kPa) on 50% oxygen, or a rising PaCO2 >56 mmHg (7.5 kPa). 5 Refer all patients to the medical team or ICU for admission. (i) Delayed adult respiratory distress syndrome (ARDS) may develop 6–72 h after submersion, previously referred to as ‘secondary drowning’. (ii) Initiate cerebral protection measures in the comatose patient. Prevent and treat hypoglycaemia, hypotension, seizures and intracranial hypertension. Maintain normocarbia. SPORTS-DIVING ACCIDENTS Dysbarism is the medical complication of exposure to gases at higher than normal atmospheric pressure. It manifests clinically as decompression illness (DCI), which may be further classified by the acuity, evolution, presence or absence of barotrauma and the organs involved. Environmental Emergencies 209 SPORTS-DIVING ACCIDENTS It is most commonly associated with sports-diving accidents with scuba (selfcontained underwater breathing apparatus) diving. DECOMPRESSION ILLNESS Decompression illness (DCI) occurs when inert nitrogen gas forms bubbles within the venous and lymphatic systems, or body tissues, rather than being eliminated by the lungs. DIAGNOSIS 1 Symptoms may occur within minutes of surfacing or up to 48 hours after diving. It is important to look for and treat any patient who presents within hours of a dive as DCI until proven otherwise. 2 Clinical manifestations include: (i) Mild (a) joint pain, ranging from a dull ache to the crippling ‘bends’. Pain usually commences in large joints such as the elbow or shoulder and may migrate (b) unusual fatigue and malaise (c) skin itching, marbling (cutis marmorata), scarlatiniform rashes, painful lymphadenopathy and local oedema. (ii) Serious (a) cardiopulmonary: – ‘the chokes’: retrosternal or pleuritic chest pain, dyspnoea, cough and haemoptysis – may be associated with myocardial infarction, hypotension and cardiac arrhythmia, and progress to respiratory failure (b) central nervous system: – ‘the staggers’: labyrinthine damage with deafness, tinnitus, nystagmus, vertigo and nausea – motor and sensory loss with hemiplegia and paraplegia – personality disorder, seizures and urinary retention. 3 Gain i.v. access and take blood for FBC, U&Es, LFTs, blood sugar level, troponin and CK. The peak CK can be a marker for the severity of acute gas embolism. 4 Perform an ECG and request a CXR in patients with cardiopulmonary symptoms. MANAGEMENT 1 Give the patient 100% oxygen by tight-fitting face mask with reservoir bag. Manage the patient in the supine or left lateral position. 2 Commence normal saline rehydration, avoiding glucose-containing solutions as they may exacerbate CNS injury. 210 Environmental Emergencies SPORTS-DIVING ACCIDENTS 3 Give midazolam 0.05–0.1 mg/kg i.v., diazepam 0.1–0.2 mg/kg i.v. or lorazepam 0.07 mg/kg up to 4 mg i.v. for seizures. (i) These drugs may also be used for severe labyrinthine disturbance after discussion with a hyperbaric medicine unit. 4 Minimize strong analgesics, particularly opiates, as they mask symptoms. 5 Fill the endotracheal tube cuff with saline to avoid changes in volume on recompression if mechanical ventilation is required. 6 Refer every patient, however strange their symptoms, to a hyperbaric medicine unit: (i) Provide information about any dive in the preceding 48 h, including the depth and duration, gas mix, time and duration of symptoms. (ii) Advice on diagnosis and arrangements for treatment are available by telephoning local or national hyperbaric medicine units (a) in a dire emergency ring the police or coastguard, who will have the relevant contact details. (iii) Long-distance retrievals require air transport pressurized to 1 atmosphere. DECOMPRESSION ILLNESS WITH BAROTRAUMA DIAGNOSIS 1 Middle ear barotrauma (i) This is the most common medical disorder associated with diving, almost always occurring on descent. (ii) Symptoms include local pain, bleeding from the ear and conductive hearing loss. (iii) The tympanic membrane appears reddened or may rupture. 2 Inner ear barotrauma (i) This is associated with too rapid descent. (ii) Vertigo, tinnitus and sensorineural deafness occur secondary to rupture of the round or oval windows and an associated perilymph fistula. (iii) It mimics labyrinthine CNS decompression illness. 3 Sinus barotrauma Local pain occurs over the maxillary and frontal sinus, sometimes associated with bleeding. 4 Dental barotrauma Pain occurs in or around fillings or carious teeth and percussion of the involved tooth is painful. Environmental Emergencies 211 SPORTS-DIVING ACCIDENTS 5 Pulmonary barotrauma This is the most serious form of barotrauma that causes: (i) Surgical emphysema, pneumothorax or pneumomediastinum associated with chest pain and dyspnoea. (ii) Arterial gas embolus affecting the: (a) coronary circulation, with cardiac pain, arrhythmia and cardiac arrest (b) cerebral circulation, with sudden onset of neurological symptoms just before or within 5 min of surfacing (without the delay seen in CNS decompression illness) – any neurological symptom or sign from confusion to seizures or coma may occur, and may fluctuate. 6 Gain i.v. access and take blood for FBC, U&Es, LFTs, blood sugar level and cardiac biomarkers. 7 Perform an ECG in patients with cardiopulmonary symptoms, and request a CXR to exclude pneumothorax or pneumomediastinum. MANAGEMENT 1 Middle ear barotrauma (i) Give an analgesic such as paracetamol 500 mg and codeine phosphate 8 mg. (ii) Give amoxicillin 500 mg orally t.d.s. for 5 days if tympanic membrane rupture is present, and refer the patient to the next ENT clinic. (iii) The patient should not dive again until the drum is fully healed. 2 Inner ear barotrauma Discuss immediately with a hyperbaric medicine unit, as labyrinthine CNS decompression illness is possible. 3 Sinus and dental barotrauma Give an analgesic such as paracetamol 500 mg and codeine phosphate 8 mg. 4 Pulmonary barotrauma (i) Give oxygen and insert an intercostal drain if a significant pneumothorax is present (see p. 473) (a) manage a pneumomediastinum and surgical emphysema conservatively. (ii) If arterial gas embolus is suspected: (a) keep the patient horizontal on their left side (not head-down, as this raises intracranial pressure) (b) give 100% oxygen by tight-fitting face mask with reservoir bag (c) commence normal saline rehydration 212 Environmental Emergencies ELECTRICAL BURNS, ELECTROCUTION AND LIGHTNING STRIKE (d) give midazolam 0.05–0.1 mg/kg i.v., diazepam 0.1–0.2 mg/kg, or lorazepam 0.07 mg/kg up to 4 mg i.v. for seizures (e) refer the patient to a hyperbaric medicine unit, even after apparent recovery, as delayed deterioration can occur and recompression may still be required. ELECTRICAL BURNS, ELECTROCUTION AND LIGHTNING STRIKE Factors influencing the severity of electrical injury include whether the current is alternating or direct, the resistance to current flow, voltage, the pathway of current through the patient and the area and duration of skin contact. Skin resistance is decreased by moisture which increases the current and the likelihood of injury. Electrical injury may be considered in four groups: ● Electrical flash burns. ● Low-voltage electrocution. ● High-voltage electrocution. ● Lightning strike. ELECTRICAL FLASH BURNS DIAGNOSIS 1 The external passage of current from the point of contact to the ground is associated with arcing. Electrical energy is converted to heat as electricity traverses the skin associated with brief high temperatures that may ignite clothing. 2 Burns are usually superficial partial-thickness, but they may be deep dermal or even full-thickness. Secondary flame burns may occur if clothing ignites. MANAGEMENT 1 Assess the depth and extent of the burn (see p. 251). 2 Check the eyes for evidence of corneal injury using fluorescein. 3 Dress the areas as for a thermal burn and treat accordingly. LOW-VOLTAGE ELECTROCUTION DIAGNOSIS 1 Injury primarily occurs in the home through faulty electrical equipment or carelessness. Household voltage supply is usually 240 V alternating current (AC). Environmental Emergencies 213 ELECTRICAL BURNS, ELECTROCUTION AND LIGHTNING STRIKE 2 AC is more dangerous than DC and may induce tetanic muscle spasm. The longer the duration of contact, the greater the potential for injury. (i) Gripping the electrical source by hand will prevent release and worsens the injury. 3 Low-voltage electrical injury causes local tissue necrosis with a contact surface burn that is often full-thickness. The underlying thermal tissue damage may be extensive and include blood vessels and muscle. There may be a similar exit (earthing) burn. 4 Arrhythmias (including VF) and unconsciousness may occur if the charge crosses the heart or brain. 5 Attach a cardiac monitor and pulse oximeter to the patient. Perform a 12-lead ECG. 6 Request a computed tomography (CT) head scan if there is coma, confusion or focal neurological signs. MANAGEMENT 1 Manage cardiac or respiratory arrest as for cardiopulmonary resuscitation (see p. 2). 2 Otherwise, give oxygen and aim for an oxygen saturation over 94%. 3 Give i.v. normal saline for any hypotension, aiming for a urine output of 100 mL/h if there is evidence of myoglobinuria (tea-coloured urine with a false-positive urine dipstick test for blood). 4 Treat muscle pain with simple analgesia such as paracetamol 500 mg and codeine phosphate 8 mg. 5 Admit patients with an abnormal ECG or history of arrhythmias for cardiac monitoring. 6 Discharge the patient if there is no history of altered consciousness or cardiac arrhythmia, and the neurological state and ECG are normal, provided there is no significant thermal soft-tissue burn. (i) A lethal delayed cardiac arrhythmia is exceptionally rare in a patient with no initial history of an arrhythmia. HIGH-VOLTAGE ELECTROCUTION DIAGNOSIS 1 These injuries occur from electric shocks sustained from sources >1000 V such as electrical cables and power stations. These are serious injuries, and often fatal. Warning: electrical burns may look deceptively innocent. A white blister or small area of broken skin can cover extensive deep-tissue damage requiring admission to hospital. Always look for the entry and exit wound. ! 214 Environmental Emergencies ELECTRICAL BURNS, ELECTROCUTION AND LIGHTNING STRIKE 2 Injuries are associated with: (i) Electrical flash burns with full-thickness injury at points of electricity entry and exit, or flame burns secondary to clothing ignition. (ii) Extensive tissue damage, deep muscle necrosis, and compartment syndrome requiring fasciotomy and potentially limb amputation. (iii) Tetanic muscle spasm causing long-bone fracture, vertebral crush fracture, muscle tears and joint dislocations. (iv) Indirect injury from a resultant fall. 3 According to the pathway the charge follows, other effects include: (i) Lungs: asphyxia from respiratory paralysis and lung parenchyma burns. (ii) Heart: cardiac arrest or arrhythmia. The most common cardiac arrest rhythm is VF. (iii) Brain and CNS: confusion, coma, cerebral haemorrhage, spinal cord damage and peripheral nerve damage. (iv) Gastrointestinal tract: bowel perforation and intestinal ileus. (v) Kidneys: acute kidney injury secondary to tubular deposition of myoglobin and haemoglobin. (vi) Visceral and connective tissue: immediate damage to nerves, muscle and bone from heat, vascular thrombosis or delayed secondary haemorrhage. (vii) Eyes and ears: dilated pupils, uveitis, vitreous haemorrhage, ruptured eardrum, deafness and the late development of cataracts. 4 Gain i.v. access and send blood for FBC, U&Es, blood sugar, CK, group and save (G&S) and ABGs. Attach a cardiac monitor and pulse oximeter to the patient. 5 Perform an ECG. 6 Request a CXR, pelvic or limb X-rays, and or a CT head and neck scan according to the suspected additional injuries. MANAGEMENT 1 Assess the airway, give oxygen and commence an i.v. infusion ensuring adequate volume replacement guided by the blood pressure and urine output. (i) Fluid requirements are higher than they appear from assessment of the burnt areas alone. Aim for a urine output of 100 mL/h if there is myoglobinuria. 2 Examine for major injuries secondary to falls and treat accordingly. 3 Refer patients to the specialist burns unit or surgical team for admission. Escharotomy, fasciotomy, surgical debridement and limb amputation may all become necessary. Environmental Emergencies 215 ELECTRICAL BURNS, ELECTROCUTION AND LIGHTNING STRIKE LIGHTNING STRIKE DIAGNOSIS 1 Lightning strike can deliver from 300 000 to over 100 000 000 V DC in a few milliseconds, most of which passes over the surface of the body ‘external flashover’. 2 Death is secondary to cardiac or respiratory arrest (as in industrial and domestic electrical injuries). (i) The commonest rhythm in cardiac arrest is asystole, as opposed to VF with a high-voltage injury. (ii) Overall mortality is up to 30%, with 70% of survivors sustaining significant morbidity. 3 Lightning strike can produce a wide range of clinical effects: (i) Full-thickness contact burns usually to the head, neck and shoulders. (ii) Respiratory arrest secondary to thoracic muscle spasm and depressed respiratory drive (a) this may persist even after return of spontaneous circulation, and may lead to secondary hypoxic arrest. (iii) Cardiac arrest secondary to depolarization of the entire myocardium. (iv) Massive autonomic stimulation with hypertension, tachycardia and myocardial necrosis. (v) Neurological deficits ranging from initial loss of consciousness, sensorineural deafness and vestibular dysfunction to peripheral nerve damage, intracerebral haemorrhage, cerebral oedema and transient total body or limb paralysis (keraunoparalysis). (vi) Arborescent, feathery cutaneous burns presenting within the first 6 h post injury, known as Lichtenberg figures or lightning flowers. (vii) Miscellaneous injuries including tympanic membrane rupture, corneal defects, retinal detachment and optic nerve damage. 4 Send bloods for FBC, U&Es, LFTs, CK, blood sugar and G&S. 5 Perform an ECG and request trauma X-rays such as chest and pelvis, and CT scan of the head and cervical spine as indicated clinically. (i) Non-specific ECG changes include QT prolongation and T wave inversion. Warning: do not take fixed dilated pupils as an indicator of death after lightning strike. Full recovery is possible. ! 216 Environmental Emergencies FURTHER READING MANAGEMENT 1 Use standard protocols for VF and asystolic cardiac arrest if there is no pulse or absent respirations (see p. 2). 2 Assess the airway and give high-flow oxygen. Remove smouldering clothing to prevent secondary thermal injury to skin. 3 Perform early endotracheal intubation to prevent airway obstruction secondary to soft tissue oedema associated with head and neck burns. Call for urgent senior ED doctor help. (i) Ventilatory support is also essential to prevent hypoxic cardiac arrest secondary to thoracic muscle paralysis. (ii) Maintain spinal precautions and inline cervical immobilization during endotracheal intubation and physical examination, as there is a risk of unrecognized spinal trauma. 4 Commence an i.v. infusion with normal saline. (i) Ensure adequate volume replacement guided by blood pressure, urine output and the degree of metabolic and respiratory acidosis. (ii) Give vigorous fluid resuscitation to maintain urine output >2 mL/kg per hour to enhance excretion of tissue necrosis by-products such as myoglobin and potassium from extensive rhabdomyolysis. 5 Examine for major injuries secondary to a fall and treat accordingly. 6 Admit all patients. Survivors of the initial lightning strike have an excellent prognosis provided secondary trauma has not occurred. FURTHER READING American Heart Association (2010) Part 12: Cardiac arrest in special situations: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122: S829–61. European Resuscitation Council (2010) European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances. Resuscitation 81: 1400–33. Tip: resuscitate those patients at the scene in cardiac arrest first, the opposite to a mass casualty disaster, where they would be left for dead while other patients with survivable injuries are treated as the priority. ✓ SURGICAL EMERGENCIES Section VIII 218 Surgical Emergencies MULTIPLE INJURIES OVERVIEW The management of every severely injured patient requires a coordinated approach, such as that taught in Advanced Trauma Life Support (ATLS™, American College of Surgeons) and the equivalent Early Management of Severe Trauma (EMST™, Royal Australasian College of Surgeons) courses. This involves a rapid primary survey, resuscitation of vital functions, a detailed secondary survey and the initiation of definitive care. 1 Primary survey Rapid patient assessment to identify life-threatening conditions and establish immediate priorities. 2 Resuscitation phase Optimizes the patient’s respiratory and circulatory status. The response to resuscitation is recorded with comprehensive non-invasive monitoring. (i) Once resuscitation is under way, a trauma series of X-rays is taken, bloods are sent, and additional procedures such as a rapid bedside ultrasound, nasogastric tube insertion and urinary catheterization are performed. 3 Secondary survey Commences after the primary survey is complete and the resuscitation phase well under way: (i) A detailed head-to-toe examination is made. (ii) Special X-rays, repeat ultrasound, computed tomography (CT) scan and angiographic studies are performed as indicated. 4 Definitive care Management of all the injuries identified, including surgery, fracture stabilization, hospital admission or preparation of the patient for transfer, if required. 5 Expect serious injuries in patients presenting with altered physiology, or after the following high-risk mechanisms: (i) Abnormal vital signs: systolic blood pressure <90 mmHg, Glasgow Coma Scale (GCS) score ≤12, respiratory rate <10/min or >30/min. (ii) Motorcyclist or pedestrian struck. (iii) Fall >5 m (15 ft). (iv) Entrapment. (v) High-speed impact, ejection or death of another vehicle occupant. 6 Call senior Emergency Department (ED) staff immediately for any multipleinjury patient, to organize an integrated team response incorporating anaesthetic, intensive care, surgical and orthopaedic colleagues. MULTIPLE INJURIES Surgical Emergencies 219 7 The time-honoured mnemonic for the initial sequence of care is ABCDE (see Table 8.1). IMMEDIATE MANAGEMENT 1 Airway (i) Assess the airway to ascertain patency and identify potential obstruction: (a) clear the airway of loose or broken dentures and suck out any debris (b) insert an oropharyngeal airway if the patient is unconscious (c) give 100% oxygen by tight-fitting mask with reservoir bag (d) aim for an oxygen saturation above 94%. (ii) Intubation (a) a definitive procedure to protect and maintain the airway is indicated if the patient is unconscious, or has a reduced or absent gag reflex (b) take great care to minimize neck movements in the unconscious head injury or suspected neck injury by maintaining in-line manual immobilization during airway assessment and endotracheal intubation (c) rapid sequence induction (RSI) intubation – this is the airway technique of choice, provided the operator is skilled in the technique – confirm correct tube placement using capnography to measure end-tidal carbon dioxide (ETCO2) (see p. 467). (iii) Surgical airway: proceed directly to cricothyrotomy if endotracheal intubation is impossible due to laryngeal injury or severe maxillofacial injury (see p. 469). Table 8.1 Mnemonic for initial sequence of care of the multiply-injured patient during the primary survey and resuscitation phases A Airway maintenance with cervical spine control B Breathing and ventilation C Circulation with haemorrhage control D Disability: brief neurological evaluation E Exposure/environmental control: completely undress the patient, but prevent hypothermia Warning: never attempt RSI unless you have been trained. Use a bag-valve mask technique instead while awaiting help. ! MULTIPLE INJURIES 220 Surgical Emergencies 2 Maintain the integrity of the cervical spine (i) Place the unconscious head injury and the patient with suspected neck injury in a semi-rigid collar. (ii) Minimize head movement. When the patient requires turning, the body should be ‘log-rolled’, holding the head in the neutral position at all times. 3 Breathing and ventilation Look for and treat the following critical conditions: (i) Tension pneumothorax (a) suspect a tension pneumothorax if examination reveals tachycardia, hypotension, unequal chest expansion, absent or decreased breath sounds and distended neck veins (b) insert a wide-bore cannula into the second intercostal space in the mid-clavicular line on the affected side. Following initial decompression, proceed to formal intercostal tube drainage (see p. 471). (ii) Sucking chest wound with open pneumothorax (a) cover with an occlusive dressing such as paraffin gauze under an adhesive film dressing, secured along three sides only. Leave the fourth side open for air to escape (b) proceed to formal intercostal catheter drainage (see p. 473). (iii) Flail chest (a) causes paradoxical movement of part of the chest wall and may necessitate positive-pressure ventilation (b) an associated haemothorax or pneumothorax will require an intercostal catheter chest drain to prevent the development of a tension pneumothorax, if positive-pressure ventilation is used. 4 Circulation with haemorrhage control (i) Apply a bulky sterile dressing to compress any external bleeding point (not a tourniquet, as this increases bleeding by venous congestion). (ii) Monitor the pulse, blood pressure, pulse oximetry and electrocardiogram (ECG). (iii) Establish an i.v. infusion (a) insert two large-bore (14- or 16-gauge) cannulae into the antecubital veins (b) one cannula should be below the diaphragm in mediastinal or neck injuries, e.g. in the femoral vein (c) although a central venous (CVP) line is useful both to administer fluids and to monitor the response to resuscitation, only senior ED staff should perform this to minimize the potential complications of arterial puncture and pneumothorax. See page 476. MULTIPLE INJURIES Surgical Emergencies 221 (iv) Infusion fluid (a) infuse normal saline or Hartmann’s (compound sodium lactate) to correct hypovolaemia (b) remember that in healthy adults the only signs associated with the loss of up to 30% of the circulatory blood volume (1500 mL) may be tachycardia with a narrowed pulse pressure (c) therefore, a consistent fall in systolic blood pressure indicates that at least 30% of the blood volume has already been lost (d) change infusion fluid to blood if 3000 mL of normal saline or Hartmann’s (compound sodium lactate) fail to reverse hypotension. A full cross-match takes 45 min, a type-specific cross-match takes 10 min, and O rhesus-negative blood is available immediately (e) use a blood warmer and macropore blood filter for multiple transfusions – give fresh frozen plasma 8–10 units and platelets after transfusing 8–10 units of blood or more, i.e. in a 1:1 ratio for a ‘massive blood transfusion’. (v) Send blood for haemoglobin, urea and electrolytes (U&Es), liver function tests (LFTs) and blood sugar, and cross-match at least 4 units of blood according to the suspected injuries. Save serum for a drug screen in case alcohol or drug intoxication is subsequently suspected. (vi) Cardiac tamponade (a) consider cardiac tamponade if there is persistent hypotension with distended neck veins that fill on inspiration (Kussmaul’s sign), particularly following penetrating chest trauma (b) arrange an immediate focused ultrasound to look for pericardial fluid (blood) (c) call the surgical and/or cardiothoracic team for an urgent thoracotomy if there is persistent haemodynamic compromise (see p. 237). 5 Disability: brief neurological evaluation (i) Assess the level of consciousness using the GCS (see p. 30). (ii) Examine the eye movements, pupil size, shape and reactivity. (iii) Assess for abnormal tone, weakness and gross sensory loss, or an asymmetrical response to pain if the patient is unconscious. Check the limb reflexes, including the plantar responses. (iv) Examine the face and scalp for injuries. 6 Exposure: completely undress the patient (i) Request a chest radiograph (CXR), pelvic X-ray and lateral cervical spine X-ray, known as the ‘trauma series’. Perform these in the resuscitation bay without interrupting patient care MULTIPLE INJURIES 222 Surgical Emergencies (a) lateral cervical spine X-rays have now largely been replaced by incorporating the cervical spine with CT scanning of the head. (ii) Examine the front of the abdomen, including the perineum, for evidence of blunt or penetrating trauma, e.g. seat-belt bruising or a tyre mark on the skin. Cover any exposed abdominal viscera with saline-soaked packs. (iii) Log-roll the patient and examine the back for evidence of blunt or penetrating trauma. Palpate the spine for deformity and widened interspinous gaps. (iv) Perform a rectal examination to assess the anal sphincter tone, position of the prostate, integrity of the rectal wall, and to check for evidence of internal bleeding. (v) Assess the pelvis by springing to detect instability from major pelvic ring fracture, although this is an unreliable sign. (vi) Look for associated urethral injury. Suspect urethral transection if there is any bleeding from the urethral meatus, a scrotal haematoma or a high-riding prostate (a) do not attempt urethral catheterization if any of these are present (b) otherwise, insert a urethral catheter and measure the urine output, which should be >50 mL/h in the adult, and 1 mL/kg per hour in a child. 7 Pass a large-bore nasogastric tube, or orogastric tube if a basal skull or mid-face fracture is present (see p. 433). (i) This is particularly important in children, who commonly develop acute gastric dilatation following trauma. 8 Splint major limb fractures, cover compound injuries with sterile dressings and check the peripheral pulses. 9 Administer increments of morphine 2.5–5 mg i.v. titrated to analgesic response. The above procedures will save life during the resuscitation phase, and allow a decision on priorities in proceeding to definitive care. Obtain as full a history as possible from ambulance crew, witnesses or relatives, as well as the patient. A useful mnemonic for remembering the components in the history is AMPLE (see Table 8.2). Table 8.2 Mnemonic for components of the history in multiple trauma A Allergies M Medications P Past history, including alcohol and cigarette use L Last meal E Events/environment relating to the injury, including time, speed of impact, initial vital signs, and any change in condition HEAD AND FACIAL INJURIES Surgical Emergencies 223 Make sure an ongoing record is kept of all vital signs and clinical findings, and keep re-examining the patient regularly. FURTHER DIAGNOSIS AND MANAGEMENT OF MULTIPLE INJURIES: DEFINITIVE CARE This is considered under the following headings: ● Head and facial injuries. ● Neck injuries. ● Chest injuries. ● Abdominal and pelvic trauma. ● Additional orthopaedic injuries. HEAD AND FACIAL INJURIES DIAGNOSIS AND MANAGEMENT 1 Scalp (i) Look for lacerations, haematomas, penetrating wounds and foreign bodies. (ii) Palpate for evidence of deformity and fracture. (iii) Assess the level of consciousness if a major head injury is suspected, and manage as described on p. 29. 2 Face (i) Check the integrity of the airway again, and remember the possibility of an unrecognized neck injury. (ii) Look for bruising, swelling or deformity suggesting orbital, nasal, malar or mandibular fractures (see p. 430). (iii) Look for parotid and facial nerve damage in injuries to the face in the area in front of the ear. (iv) Clean and evaluate all facial lacerations. They will require meticulous debridement and formal closure when the patient’s condition is stable, and all serious injuries have been dealt with. 3 Eyes (i) Inspect the eyes for evidence of penetrating or blunt injury. Look for specific conditions such as iris prolapse, hyphaema, lens dislocation and traumatic mydriasis (see p. 415). (ii) Assess the pupil size and reactions, and examine the fundi for evidence of vitreous or retinal haemorrhage and retinal detachment. (iii) Check the visual acuity and eye movements. NECK INJURIES 224 Surgical Emergencies 4 Nose (i) Examine for evidence of blood or cerebrospinal fluid (CSF) leakage suggesting a basal skull fracture (see p. 31). (ii) Palpate for deformity and nasal bone fracture (see p. 401). (iii) Look specifically for a septal haematoma, which, if large, will require incision and drainage to reduce the risk of subsequent cartilage necrosis (see p. 401). 5 Mouth (i) Examine for broken or missing teeth. They may have been inhaled (see p. 429). (ii) Check for dental malocclusion, suggesting maxillary or mandibular fracture (see p. 430). (iii) Assess for nasopharyngeal bleeding, which may be profuse and associated with a basal skull fracture. Look for any tongue lacerations, although they rarely need repairing (see p. 428). 6 Ears (i) Examine for skin and cartilage damage, which will require drainage and suture later. (ii) Consider perforation of the eardrum, although if frank bleeding is seen, do not examine with a speculum to avoid introducing infection: (a) this bleeding may be associated with either a basal skull fracture or damage to the external ear canal (see p. 397). NECK INJURIES CERVICAL SPINE INJURY This should be considered in all patients with localized neck pain or pain on palpation following trauma. It should also be assumed in any unconscious head injury, multiply injured patient, a patient under the influence of alcohol or drugs, and a patient with a locally distracting injury above the clavicles. DIAGNOSIS 1 Ask about local pain or tenderness on palpation if the patient is conscious, and about any associated limb weakness or sensory deficit noticed. 2 Check the vital signs. A cervical or high thoracic cord lesion will cause respiratory difficulty, tachypnoea and abdominal breathing. (i) Loss of sympathetic tone will cause bradycardia, hypotension and hypothermia from vasodilation if the ambient temperature is low. NECK INJURIES Surgical Emergencies 225 3 Palpate for areas of tenderness, swelling or deformity in the neck. Assess for limb tone, weakness, reflex loss and sensory deficit, including loss of perineal sensation and anal tone. 4 Describe any motor weakness found by the myotome and reflex abnormalities: (i) Myotomes in the upper limb. Nerve roots C5 to T1 supply the muscles of the upper limb (see Table 8.3). (ii) Use the Medical Research Council scale to grade muscle weakness, so that the same terminology is used by each doctor examining the patient (see Table 8.4). (iii) Reflexes in the upper limb: assess for the biceps, triceps and supinator upper limb reflexes, which indicate normal or other functioning of certain motor roots (see Table 8.5 for motor roots of the reflexes) Table 8.3 Myotomes in the upper limb and their associated actions Root Action C5 Shoulder abduction C6, C7 Shoulder adduction C5, C6 Elbow flexion C7 Elbow extension C6 Pronation and supination (C6), C7 Wrist flexion C6, (C7) Wrist extension C8 Finger flexion C7 Finger extension T1 Intrinsic hand muscles Table 8.4 Medical Research Council (MRC) scale used to grade muscle weakness Recorded grade Physical finding Grade 0 Complete paralysis Grade 1 A flicker of contraction only Grade 2 Movement possible only if gravity is eliminated Grade 3 Movement against gravity Grade 4 Movement against gravity and resistance Grade 5 Normal power NECK INJURIES 226 Surgical Emergencies (a) use reinforcement (Jendrassik’s manoeuvre) before concluding that a reflex is absent, e.g. ask the patient to clench the teeth hard or hold the knees together when testing a reflex. 5 Describe sensory deficit by dermatomes: (i) Assess sensation by testing pain fibres using pinprick (spinothalamic tracts), and examine fine touch or joint position sense (posterior columns). (ii) Dermatomes C5–T1 supply the upper limb (see Table 8.6). (iii) Dermatomes C4 and T2 are adjacent on the front of the chest at the level of the first and second ribs. 6 The myotomes, reflexes and dermatomes in the leg are described on p. 331. 7 Cervical spine imaging: (i) Lateral cervical spine X-ray: (a) make sure an adequate view is obtained and that all seven cervical vertebrae and the C7/T1 junction are visualized. A swimmer’s view may be required (b) look for appropriate alignment of the cervical spine longitudinal lines. Anterior displacement of >3 mm implies ligament disruption and cervical spine instability (see Fig. 8.1) (c) observe the bony vertebrae for signs of fractures such as wedge and teardrop. Examine the soft-tissue shadows in front of the vertebral bodies (see Fig. 8.1): – the retropharyngeal space should be <5 mm between C1 and C4/C5 Table 8.5 Reflexes in the upper limb Reflex Root Biceps C5, (C6) Supinator (C5), C6 Triceps (C6), C7, C8 Table 8.6 Dermatomes supplying the upper limb Root Dermatomal distribution C5 Outer upper arm C6 Outer forearm C7 Middle finger C8 Inner forearm T1 Inner upper arm NECK INJURIES Surgical Emergencies 227 – the retrotracheal space should be less than the width of one vertebral body in adults between C4/C5 and T1. (ii) Open-mouth odontoid view: examine the odontoid peg and dens of C2, and the lateral masses of C1 for evidence of fracture. (iii) Anteroposterior cervical spine X-ray: look for rotation of the vertebrae, loss of joint space and transverse process fracture. (iv) Cervical spine CT scan: Perform this following plain cervical spine X-rays if bony injury is still suspected, or to further define any cervical fracture and vertebral subluxation seen on those films. CT is particularly useful to evaluate trauma patients with: (a) abnormal plain films (b) suspicious, inadequate or incomplete plain films (c) neurological deficit (d) suspected vascular, airway, oesophageal or other soft-tissue injury (e) head injury requiring CT head scan, particularly if intubated. (a) 1 1 2 2 3 3 4 5 6 (b) Figure 8.1 Cervical spine x-ray in the adult (a) Lateral view: (1) retropharyngeal space (<5 mm), (2) retrotracheal space (less than the width of one vertebral body), (3) anterior longitudinal ligament line, (4) posterior longitudinal ligament line, (5) spinolaminar line, (6) posterior spinal line. Lines 3, 4, 5 and 6 should all be parallel, following the normal gentle lordotic curve of the cervical spine. The spinal cord runs between lines 4 and 5. (b) Anteroposterior view: (1) interspinous line, (2) foramen transversarium line, (3) transverse processes line. Lines 1, 2 and 3 should be straight in the normal neck. NECK INJURIES 228 Surgical Emergencies (v) MRI is more sensitive than CT and plain X-ray for identifying soft-tissue damage such as ligamentous injuries, disc herniation or a haemorrhage causing compression of the spinal cord or cervical nerve roots (a) it is rarely available in the acute situation, but may be arranged subsequently. MANAGEMENT 1 Always apply a semi-rigid collar, minimize head movements in any suspected neck injury, and use laterally placed sandbags taped to the forehead to prevent head rotation. 2 Arrange urgent airway control with orotracheal intubation for the unconscious patient or for respiratory distress. (i) Only an airway-skilled doctor should perform this, usually by a rapid sequence induction (RSI) intubation technique (see p. 467) with in-line manual immobilization to protect the neck from any movement. 3 Restore the circulatory volume if the patient is hypotensive. (i) First look for sources of blood loss before diagnosing neurogenic shock. (ii) Neurogenic shock causes hypotension in a patient with a cervical cord injury due to loss of sympathetic tone with vasodilation and bradycardia. (iii) Place a urinary catheter to monitor urinary output. 4 Severe ligamentous damage with cervical spine instability may occur, with an apparently normal X-ray. (i) This is more likely in children, in whom up to 50% of serious spinal injuries have normal X-rays (SCIWORA – spinal cord injury without radiological abnormality). (ii) Neck hyperextension may cause predominant weakness of the arms in elderly patients with cervical spondylosis, without any associated fracture or dislocation, known as the central cord syndrome. (iii) Arrange an MRI in these circumstances. 5 Refer all suspected cervical spine injuries to the orthopaedic or surgical team and begin pressure-area nursing. 6 The value of high-dose methylprednisolone to improve neurological outcome in patients with complete or incomplete spinal cord damage remains unconvincing and controversial, and has been abandoned in many centres. (i) Start treatment within 8 h of injury, guided by the advice of the regional spinal injuries unit. NECK INJURIES Surgical Emergencies 229 (ii) Infuse methylprednisolone 30 mg/kg over 15 min, followed 45 min later by 5.4 mg/kg per hour for 23 h. AIRWAY INJURY DIAGNOSIS 1 Airway injuries may be penetrating or blunt, isolated, or associated with multiple injuries. 2 Patients may present with a hoarse voice, pain, stridor, cough and/or haemoptysis. 3 Examine for local swelling, subcutaneous emphysema, pneumothorax or haemothorax. 4 Perform anteroposterior and lateral cervical spine X-rays and a CXR. MANAGEMENT 1 Do not leave the patient unattended at any stage. Call for urgent senior ED staff to help. 2 Perform endotracheal intubation or cricothyrotomy, or insert an endotracheal tube directly into a gaping wound in the trachea to maintain patency of the airway. 3 Refer the patient immediately to the surgical team for admission. (i) Arrange a CT scan once the airway has been protected by an endotracheal tube. VASCULAR INJURY IN THE NECK DIAGNOSIS AND MANAGEMENT 1 Vascular injury causes obvious external haemorrhage, or internal bleeding with rapid haematoma formation, which may compromise the airway. 2 Do not attempt to probe or explore any penetrating wounds in the ED. Leave all penetrating objects in situ. 3 The patient will require angiography and panendoscopy with urgent surgical referral to arrange formal wound exploration in theatre. NERVE INJURY IN THE NECK DIAGNOSIS AND MANAGEMENT 1 Damage to the following nerves causes specific signs and symptoms: (i) Recurrent laryngeal branch of the vagus: hoarseness and vocal cord paralysis. (ii) Accessory nerve: loss of function of trapezius and sternomastoid. (iii) Phrenic nerve: loss of diaphragmatic movement. NECK INJURIES 230 Surgical Emergencies (iv) Hypoglossal nerve: deviation of the tongue to the affected side. (v) Cervical sympathetic cord: Horner’s syndrome, with partial ptosis, a constricted pupil, and decreased sweating on the same side of the face. 2 Refer any of these injuries to the surgical team. OESOPHAGEAL INJURY DIAGNOSIS AND MANAGEMENT 1 Oesophageal injury in the neck causes dysphagia, drooling and localized pain, with the development of surgical emphysema. 2 Refer this rare condition to the surgical team for immediate admission. NECK SPRAIN DIAGNOSIS 1 Neck sprain is most commonly associated with hyperextension injuries resulting from sudden deceleration in a motor vehicle collision. (i) The lay term for this mechanism of injury is ‘whiplash’. In practice, neck sprain occurs with other directions of impact, including hyperflexion. 2 The resultant neck pain and stiffness often go unnoticed at the time of injury. Patients typically present 12–24 h later, often with symptoms of headache. 3 The pain may radiate to the shoulders and arms, causing paraesthesiae, but neurological examination does not show any objective deficit. Neck movements are restricted by pain. 4 Cervical spine X-ray may show loss of the normal anterior curvature due to muscle spasm. MANAGEMENT 1 Treat the patient with a non-steroidal anti-inflammatory analgesic drug (NSAID), such as ibuprofen 200–400 mg orally t.d.s. or naproxen 250 mg orally t.d.s., and encourage early mobilization. 2 Refer the patient to the physiotherapy team if the pain fails to settle, for heat treatment and motion exercises. 3 Unfortunately, symptoms may continue for months, and may be exacerbated by further minor injuries. Surgical Emergencies 231 CHEST INJURIES PNEUMOTHORAX DIAGNOSIS 1 Tension pneumothorax (i) This causes severe respiratory distress, tachypnoea and hypotension. There is tracheal deviation away from the affected side, distended neck veins, loss of chest expansion on the affected side, a hyper-resonant percussion note, and diminished or absent breath sounds. (ii) Perform immediate decompression. Use a large-bore i.v. cannula inserted into the second intercostal space in the mid-clavicular line, followed by placement of an intercostal drain (see p. 471). 2 Simple pneumothorax (i) This is caused by blunt or penetrating chest trauma, and penetrating abdominal trauma breaching the diaphragm. (ii) It is surprisingly easy to miss. Examine for subcutaneous emphysema, decreased chest expansion, and quiet breath sounds. (iii) Confirm the diagnosis with an erect CXR to highlight a small apical pneumothorax, provided there is no possibility of spinal injury (a) the supine CXR may, however, appear normal and miss a small pneumothorax lying anteriorly. MANAGEMENT 1 Most cases of traumatic pneumothorax require chest-drain insertion to avoid the subsequent development of tension, particularly if positivepressure ventilation is necessary. 2 Insert an intercostal drain into the fifth or sixth intercostal space in the mid-axillary line (see p. 473). HAEMOTHORAX DIAGNOSIS 1 This results from chest wall damage, penetrating or blunt lung injury and great vessel damage. 2 It causes hypotension, respiratory difficulty with reduced chest expansion, quiet breath sounds and a dull percussion note at the base of the affected lung. 3 Request an erect or semi-erect CXR to identify a fluid level, provided there is no possibility of spinal injury. CHEST INJURIES 232 Surgical Emergencies 4 Look for diffuse ground-glass haziness over one hemithorax if the CXR is taken supine, which is easy to miss. 5 Alternatively, take a lateral decubitus CXR. MANAGEMENT 1 Give high-dose oxygen and commence i.v. fluid, including blood. 2 Insert a large-bore 32- or 36-French gauge intercostal drain in the fifth or sixth intercostal space in the mid-axillary line, using blunt dissection down to and through the pleura (see p. 473). 3 A thoracotomy may be required if bleeding is severe and persists (see p. 238). RIB AND STERNUM FRACTURES DIAGNOSIS 1 These injuries are associated with direct trauma, including from a seat belt. They cause localized pain and tenderness, worse on breathing or springing the chest wall. 2 Associated injury may occur with fractures in the following areas: (i) Clavicle, first and second ribs: damage to the subclavian vessels, aorta, trachea, main bronchus, and spinal cord or brachial plexus. (ii) Sternum: damage to the myocardium, great vessels and upper thoracic spine. (iii) Right lower ribs: damage to the liver and right kidney. (iv) Left lower ribs: damage to the spleen and left kidney. 3 A flail segment with paradoxical chest wall movement from multiple rib fractures in two sites causes hypoxia, mainly from the underlying pulmonary contusion. 4 Perform an ECG to exclude myocardial contusion (see below). 5 Request a CXR to look for the associated complications of pneumothorax, haemothorax and a widened mediastinum, not simply to visualize the fractures. (i) A lateral sternal X-ray is indicated for a suspected sternal fracture. MANAGEMENT 1 Give the patient high-flow oxygen by face mask and aim for an oxygen saturation of 94%. 2 Commence i.v. resuscitation as required, insert an intercostal drain if indicated, and administer adequate analgesia such as increments of morphine 2.5–5 mg i.v. CHEST INJURIES Surgical Emergencies 233 3 Refer the following patients to the surgical team for admission: (i) Pneumothorax, haemothorax. (ii) Fractured sternum with severe pain or ECG abnormalities. (iii) Injury to other thoracic or abdominal organs. (iv) Pre-existing lung disease with poor respiratory reserve. (v) Rib fractures with significant pain. These patients may require a thoracic epidural. 4 Discharge remaining patients with uncomplicated rib fractures or an isolated sternal fracture with a normal ECG and CXR. 5 Provide an analgesic such as paracetamol 500 mg and codeine phosphate 8 mg two tablets orally q.d.s. (i) Recommend regular deep-breathing exercises to prevent atelectasis. (ii) Contact the general practitioner (GP) by fax or letter. 6 Positive-pressure ventilation may be required for deteriorating respiratory function, although an intercostal drain must be inserted first for any pneumothorax, however small. MYOCARDIAL CONTUSION DIAGNOSIS 1 This is due to blunt deceleration injury and is associated with rib fractures, sternal fracture and chest wall contusion. It is difficult to diagnose as there is no agreed gold standard. 2 It may be asymptomatic, but can cause chest pain or rarely cause transient right ventricular dysfunction with distended neck veins, tachycardia and hypotension. 3 Gain i.v. access and send blood for full blood count (FBC), U&Es, cardiac biomarkers and group and save (G&S). (i) Cardiac enzyme changes including creatine kinase (CK) and CKMB isoenzymes are unreliable, non-specific, and do not predict the presence of contusion or its complications. (ii) Troponins are a more reliable indicator of cardiac myocyte damage, but do not quantify the potential risk, and may be falsely normal: (a) in addition they may diagnose antecedent myocardial infarction, if raised. 4 Perform an ECG. (i) Myocardial contusion may result in ventricular conduction abnormalities and malignant arrhythmias. (ii) ECG abnormalities range from sinus tachycardia, atrial fibrillation, bundle branch block and ventricular extrasystoles to non-specific ST and T wave abnormalities or ST elevation. CHEST INJURIES 234 Surgical Emergencies 5 Request a CXR. 6 Organize an echocardiogram, which may show wall motion abnormalities but is most useful to exclude cardiac tamponade or acute valvular rupture. MANAGEMENT 1 Give the patient high-dose oxygen and administer a cautious fluid challenge if hypotensive. 2 Give morphine 2.5–5 mg i.v. with an antiemetic such as metoclopramide 10 mg i.v. for pain. 3 Admit all patients with unstable arrhythmias and haemodynamic instability to the intensive care unit (ICU). (i) Obtain an urgent echocardiogram if hypotension persists and or cardiac tamponade cannot be excluded. 4 Refer a stable patient with ECG abnormalities, age >50 years or pre-existing cardiac disease to a coronary care unit (CCU) for cardiac monitoring if there is evidence of significant blunt myocardial trauma. 5 Discharge home patients <50 years with normal ECG findings, and without a history of cardiac disease with oral analgesia. AORTIC RUPTURE DIAGNOSIS 1 This occurs following high-speed deceleration injury, when the aorta is torn just distal to the left subclavian artery. (i) It is increasingly being recognized in lower-speed injuries including side-impact. 2 Always consider this diagnosis in any deceleration injury >60 k.p.h. (45 m.p.h.) or following a fall from >5 m (15 ft). 3 Only 10–15% of patients with rupture of the thoracic aorta survive to reach hospital. 4 Clinical signs of aortic rupture are subtle or absent and so diagnosis is suspected largely based on the mechanism of injury, or from a history of chest or interscapular pain, unequal blood pressures in each arm, or different femoral and brachial pulse volume, and the initial CXR. 5 Insert two large-bore i.v. cannulae and cross-match 10 units of blood. 6 Perform a CXR and look for the following signs of aortic rupture: (i) Widened mediastinum (≥8 cm on a 1 m supine anteroposterior X-ray): (a) 10% of these patients will have a contained aortic rupture confirmed CHEST INJURIES Surgical Emergencies 235 (b) other causes of a widened mediastinum include a mediastinal haematoma from sternal fracture, lower cervical or thoracic spine fracture, oesophageal injury, local venous oozing and projection artefact. (ii) Blurred aortic outline with obliteration of the aortic knuckle. (iii) Left apical cap of fluid in the pleural space and a left haemothorax. (iv) Depressed left main stem bronchus. (v) Displacement of the trachea to the right. (vi) Displacement of a nasogastric tube in the oesophagus to the right. 7 Look for a cervical, thoracic or sternal fracture clinically and on X-ray, although exclusion of aortic rupture is still necessary irrespective of clinical findings if the CXR is suggestive. 8 Perform a high-speed helical CT angiogram scan of the chest to look for blood contiguous with the aorta, or an abnormal aortic wall indicative of rupture. MANAGEMENT 1 Administer fluid cautiously. (i) Initial hypotension responds to modest fluid replacement in contained aortic rupture. (ii) Take care to avoid over-transfusion or hypertension from poorly controlled pain, etc. 2 Refer the patient urgently to the surgical or vascular team for further evaluation, if the patient has a high-risk mechanism of injury and positive radiographic findings. (i) Urgent thoracotomy and repair are indicated when either of these show a rupture, or endovascular stenting if the expertise is available locally. DIAPHRAGM RUPTURE DIAGNOSIS 1 This may occur from blunt or penetrating chest or abdominal trauma, including crush fracture of the pelvis. Left-sided lesions are more common and allow eventration of the stomach or intestine into the chest. 2 75% of patients with ruptured diaphragm have associated intra-abdominal injuries. 3 It causes difficulty in breathing, and occasionally bowel sounds are audible in the chest. CHEST INJURIES 236 Surgical Emergencies 4 Perform a CXR and look for the following signs seen in diaphragm rupture: (i) Haemothorax, pneumothorax, elevated hemidiaphragm and coils of bowel or a nasogastric tube curled up in the left lower chest. (ii) The diagnosis is often missed, as the CXR appears normal in up to 25% of cases. MANAGEMENT 1 Decompress the stomach with a nasogastric tube. 2 Carefully insert an intercostal drain for an associated haemothorax or pneumothorax, using blunt dissection down to and through the parietal pleura (see p. 473). (i) Never use the trocar introducer to insert the drain. 3 Refer the patient to the surgical team following resuscitation. OESOPHAGEAL RUPTURE DIAGNOSIS 1 This rare injury is most commonly associated with penetrating trauma or following blunt trauma to the upper abdomen. (i) Other causes include instrumentation, swallowing a sharp object, and spontaneous rupture from vomiting (Boerhaave’s syndrome). 2 The patient complains of retrosternal pain, difficulty in swallowing and occasionally haematemesis. Look for cervical subcutaneous emphysema. 3 Establish venous access with a large-bore i.v. cannula. 4 Request a CXR to look for a widened mediastinum with mediastinal air, a left pneumothorax, pleural effusion or haemothorax. These findings in the absence of rib fracture should suggest the possibility of rupture. 5 Request a CT scan to better define air in the mediastinum. MANAGEMENT 1 Administer oxygen and replace fluids. Give morphine 2.5–5 mg i.v. for pain with an antiemetic. 2 Commence broad-spectrum antibiotics if rupture is considered likely, such as gentamicin 5 mg/kg i.v., ampicillin 1 g i.v., and metronidazole 500 mg i.v. 3 Carefully insert an intercostal drain if there is a pleural effusion. Particulate matter in the intercostal tube drainage would confirm the diagnosis. 4 Refer the patient to the surgical team for a Gastrografin swallow and/or oesophagoscopy, followed by surgical repair if feasible. CHEST INJURIES Surgical Emergencies 237 PENETRATING CHEST INJURY DIAGNOSIS 1 Penetrating chest injury may be predicted by wounds: (i) Medial to the nipple line anteriorly or tips of the scapulae posteriorly – high risk of heart or great vessel injury. (ii) Below the fourth intercostal space – injury to the abdominal contents. (iii) Above the umbilicus – injury to the lungs, heart or great vessels. 2 Patients usually present with pain and dyspnoea. However, some patients are surprisingly undistressed. 3 The patient may become hypotensive due to blood loss from a haemothorax, or the development of cardiac tamponade or tension pneumothorax. 4 Gain i.v. access and send bloods. 5 Request a CXR to look for any of the above complications. 6 Arrange an urgent focused bedside ultrasound if cardiac tamponade is suspected, particularly in the presence of a raised JVP. MANAGEMENT 1 Assess and secure the airway, give high-flow oxygen, and perform needle thoracocentesis if required. Commence fluid resuscitation. 2 80% of penetrating chest injuries are managed conservatively with the insertion of an intercostal drain (see p. 473). 3 Injuries involving the heart and great vessels require a thoracotomy, either in the ED or urgently in theatre. 4 Emergency department thoracotomy Patients in cardiac arrest secondary to trauma require an immediate thoracotomy in the resuscitation room: (i) Optimum survival rates are found in patients with: (a) palpable pulse and spontaneous respirations at the scene of the incident (b) elapsed time since cardiac arrest of <10 min (c) penetrating trauma secondary to stab wound or low-velocity bullet. (ii) Conversely traumatic cardiac arrest is nearly always fatal in patients with: (a) blunt chest trauma or a high-velocity bullet wound (b) absence of palpable pulse or respiratory effort at the scene of the incident (c) elapsed time without signs of life >15 min. ABDOMINAL AND PELVIC TRAUMA 238 Surgical Emergencies 5 Operating room thoracotomy Transfer patients with the following injuries immediately to the operating theatre for an urgent thoracotomy: (i) Penetrating cardiac injury. (ii) Massive haemothorax with >1500 mL initial drainage or >200 mL/h for 2–4 h. (iii) Persistent large air leak suggesting tracheobronchial injury. (iv) Cardiac tamponade following trauma. ABDOMINAL AND PELVIC TRAUMA BLUNT ABDOMINAL TRAUMA DIAGNOSIS 1 This should be suspected in the following: (i) Road traffic crash or a fall from a height, particularly if there is evidence of chest, pelvic or long-bone injury (e.g. injuries on either side of the abdomen). (ii) Trauma victims with unexplained hypotension in the absence of obvious external bleeding or a thoracic injury. 2 Ask about referred shoulder-tip pain or localized pain suggesting lower rib, pelvic or thoracolumbar spine injury. 3 Look for the imprint of clothing or tyre marks as indicators of potential intra-abdominal injury. (i) Bruising from a lap seat belt may be associated with duodenal, pancreatic or small bowel injury, and/or fracture-dislocation of the lumbar spine. 4 Examine the chest, as well as the abdomen, pelvic area and perineum including genitalia. Consider a vaginal examination when there are signs of local injury. 5 Log-roll the patient to examine the thoracolumbar spine. Inspect the buttock area and perform a rectal examination. 6 Insert two large-bore i.v. cannulae and send blood for FBC, U&Es, LFTs, blood sugar, lipase/amylase, and cross-match at least 4 units of blood. 7 Request initial radiology including chest, pelvis and thoracolumbar spine X-rays. A plain abdominal film is rarely indicated. (i) Erect CXR: this may demonstrate a thoracic injury or free gas under the diaphragm. Look particularly for lower rib fractures that may be associated with liver, splenic and renal injury. ABDOMINAL AND PELVIC TRAUMA Surgical Emergencies 239 (ii) Pelvis X-ray: a fractured pelvis may be associated with major intra-abdominal or retroperitoneal injuries. (iii) Plain abdominal film is usually of little value, and rarely performed (a) look for loss of the psoas shadow, transverse process fracture, abnormal renal outlines and free gas within the peritoneal cavity on a lateral decubitus view. MANAGEMENT 1 Give high-flow oxygen. Transfuse initially with crystalloid such as normal saline or Hartmann’s (compound sodium lactate), then blood when available. 2 Pass a nasogastric tube to drain the stomach. 3 Insert a urethral catheter to measure the urine output and to look for haematuria. (i) Omit this if a urethral injury is suspected from blood at the meatus, a scrotal haematoma or a high-riding prostate on rectal examination. 4 Consider the need for an immediate laparotomy, call the surgeon if not present and alert theatre. Indications include: (i) Persistent shock. (ii) Rigid, silent abdomen. (iii) Radiological evidence of free gas or ruptured diaphragm. 5 Commonly there are no immediate indications for laparotomy and further investigation is needed: (i) Ultrasound (a) focused assessment by sonography for trauma (FAST) ultrasound is ideal for unstable patients unable to be transferred for CT evaluation (b) it is rapid, repeatable at the bedside, non-invasive and highly sensitive for free intraperitoneal fluid, i.e. blood from a haemoperitoneum. It can also demonstrate cardiac tamponade (c) however, it is operator dependent, and may miss hollow viscus, diaphragmatic and retroperitoneal injuries. (ii) CT scan (a) patients must be stable. CT scanning takes time and the patient must be transported out of the resuscitation room (b) CT provides anatomical information on the intra-abdominal organs injured allowing non-operative management (c) CT also visualizes the retroperitoneum, pelvis and lower chest, although it may still miss hollow viscus and diaphragmatic injuries. ABDOMINAL AND PELVIC TRAUMA 240 Surgical Emergencies (iii) Diagnostic peritoneal lavage (DPL) (a) has largely been entirely superseded by FAST and CT scans (b) may be used when the above are not available, to diagnose a haemoperitoneum with unexplained hypotension, or other suspected abdominal injury or when abdominal examination is: – unreliable, due to coma, intoxication or spinal injury – equivocal, due to fractured lower ribs, pelvis or lumbar spine – impractical in planned extra-abdominal radiographic or surgical procedures. (c) infiltrate local anaesthetic with adrenaline (epinephrine), and then perform open dissection via a mini-laparotomy incision through all the layers of the abdominal wall (d) the procedure is positive if: – 5–10 mL of frank blood or enteric contents are aspirated – peritoneal lavage fluid effluent exits via a chest tube or bladder catheter – laboratory analysis of lavage fluid shows >100 000 red blood cells/mm3. (e) it is highly sensitive for intraperitoneal bleeding although it provides no indication about its source or volume, and misses retroperitoneal injury to the duodenum, pancreas, kidney and pelvis, or a diaphragm rupture. 6 Involve the admitting surgical team at all stages of investigation, as the decision on emergency laparotomy is theirs. PENETRATING ABDOMINAL TRAUMA DIAGNOSIS 1 Penetrating abdominal injury may occur in stab wounds, industrial incidents, road traffic crashes, explosions and gunshot wounds. 2 Gunshot wounds may be divided into three types: (i) High-velocity wound (a) the muzzle velocity of a bullet from a high-velocity rifle is >1000 m/s (b) a small entry wound is associated with gross internal tissue damage from cavitation and a large exit wound. (ii) Low-velocity wound (a) the muzzle velocity from a hand gun reaches 250 m/s (b) the bullet causes local internal damage by perforation and laceration, often passing through several structures. (iii) Shotgun wound (a) usually fatal from a range of <3 m (10 ft), and causes massive superficial internal damage from close range (<7 m) ABDOMINAL AND PELVIC TRAUMA Surgical Emergencies 241 (b) there is scattering of shot if the shotgun is fired from >7 m, perforating structures within the abdomen (c) a shot from >40 m may not even penetrate the peritoneal cavity. 3 An entry wound may be obvious, with evisceration of bowel, or may be difficult to find especially if hidden by a gluteal fold or in the perineum. 4 The most important signs to look for are hypotension and shock. 5 Abdominal examination is often unreliable as abdominal tenderness on examination is absent in up to 50% of patients with acute haemoperitoneum. (i) Positive examination findings include local rigidity and guarding with reduced bowel sounds. 6 Remember that an associated chest injury can occur with any wound above the umbilicus. 7 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, lipase/ amylase and cross-match. 8 Request a CXR to look for associated thoracic injury, and an abdominal X-ray (AXR) to assess for metallic foreign bodies. 9 Test gastric aspirate and urine for blood, although haematuria indicating a urological injury is an unreliable sign. 10 Arrange a CT scan with i.v. contrast particularly if non-operative management is considered. MANAGEMENT 1 Cover any exposed bowel with saline-soaked pads. 2 Give oxygen, and replace fluid initially with normal saline. Titrate analgesic requirements by administering 2.5–5.0 mg morphine i.v. 3 Commence broad-spectrum antibiotics, e.g. gentamicin 5 mg/kg i.v., ampicillin 1 g i.v. and metronidazole 500 mg i.v. Give tetanus prophylaxis. 4 Refer all patients to the surgical team for urgent admission and laparotomy for all gunshot wounds and the vast majority of stab wounds. PELVIC INJURY The major complication of a pelvic fracture is massive blood loss, with up to 3 L or more of concealed haemorrhage, which may continue despite resuscitation. DIAGNOSIS 1 Pelvic injuries usually result from high-energy blunt trauma in road traffic crashes, crush injuries and from falls. 2 Associated bladder, urethral, rectal and vaginal injuries occur, which account for further morbidity. A ruptured diaphragm must also be excluded. 3 There is local pain, tenderness and bruising. Bony instability demonstrated by distracting the iliac crests is an unreliable sign that may increase bleeding. ABDOMINAL AND PELVIC TRAUMA 242 Surgical Emergencies 4 Rectal examination is mandatory to identify rectal or urethral injury. 5 Insert two large-bore i.v. cannulae and send blood for FBC, U&Es, lipase/ amylase, coagulation profile, blood sugar and cross-match at least 6 units of blood. 6 Request a pelvic X-ray in all multi-trauma patients, especially if there is unexplained hypotension. 7 Pelvic fractures associated with the greatest risk of haemorrhage include: (i) Quadripartite ‘butterfly’ fracture of all four pubic rami. (ii) Open-book fracture with diastasis of the symphysis pubis over 2.5 cm. (iii) Vertical shear fracture with hemipelvic disruption, such as the Malgaigne fracture. 8 Arrange a CT scan with i.v. contrast providing the patient is not haemodynamically unstable. MANAGEMENT 1 Give high-flow oxygen. Commence i.v. fluid resuscitation, and change to blood as indicated. 2 Do not attempt to catheterize the bladder if urethral rupture is suspected, but await assistance from an experienced ED doctor, or the surgical team. 3 Fashion a pelvic sling from a sheet secured tightly around the front of the pelvis, or preferably use one of the radiolucent, commercially available pelvic slings. 4 Exclude intraperitoneal bleeding with an early bedside ultrasound (FAST) or failing this a supra-umbilical, open diagnostic peritoneal lavage (DPL), if the patient is too unstable for a CT scan. 5 Call the surgical, orthopaedic and interventional radiology team imme - diately. (i) Control of haemorrhage secondary to pelvic trauma may require external fixation, arterial embolization and/or laparotomy. BLUNT RENAL INJURY DIAGNOSIS 1 These may be associated with injury to the vertebral column, lower ribs, ureters, aorta, inferior vena cava and the abdominal contents. 2 Blunt renal trauma causes haematuria, loin pain and tenderness, and rarely a flank mass may be felt. 3 Hypotension is due to retroperitoneal bleeding or sometimes an associated paralytic ileus. ABDOMINAL AND PELVIC TRAUMA Surgical Emergencies 243 4 Insert a large-bore i.v. cannula and send blood for FBC, U&Es and crossmatch 2–6 units of blood. 5 Request a thoracolumbar spine X-ray to exclude bony trauma. 6 Proceed to radiological imaging of the kidney and ureters. Indications include: (i) Significant deceleration injury with the risk of renal pedicle injury. (ii) Local physical signs. (iii) Macroscopic haematuria. (iv) Microscopic haematuria with shock (systolic blood pressure ≤90 mmHg) at any time. (v) Penetrating proximity trauma (see below). 7 Request a CT scan with i.v. contrast to evaluate suspected renal injury in the presence of any of the above. It has replaced the intravenous pyelogram (IVP). MANAGEMENT 1 Resuscitate the patient with i.v. fluids and exclude associated intraabdominal injuries with ultrasound (FAST) or CT. 2 Refer the patient to the surgical team for admission and observation. Over 85% of blunt renal injuries settle on conservative management with bed rest and analgesia. PENETRATING RENAL INJURY DIAGNOSIS 1 These are rare and usually involve injury to the abdominal contents, ureter or vertebral column. They may be multiple or associated with penetrating anterior truncal injury. 2 There is usually haematuria, localized pain, and tenderness, although significant renal or ureteric injury may be present without haematuria. 3 Ureteric colic can occur from the passage of blood clots. 4 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, and crossmatch 2–4 units. 5 Perform special imaging with a CT scan with i.v. contrast (or an IVP if that is all that is available). (i) These demonstrate the nature of the renal injury and also confirm the presence and normal function of the other kidney. (ii) CT scan gives essential additional information on intra- or retroperitoneal injury. ADDITIONAL ORTHOPAEDIC INJURIES IN MULTIPLE TRAUMA 244 Surgical Emergencies MANAGEMENT 1 Resuscitate the patient with i.v. fluids, commence antibiotics such as gentamicin 5 mg/kg i.v. and ampicillin 1 g i.v. and give tetanus prophylaxis as indicated. 2 Refer the patient to the surgical team for admission. BLADDER AND URETHRAL INJURIES DIAGNOSIS 1 These injuries are more commonly associated with direct blunt trauma to the lower abdomen and with major pelvic fractures. 2 Bladder rupture This may be intraperitoneal or extraperitoneal. (i) Intraperitoneal is associated with shock and peritonism. (ii) Extraperitoneal: (a) causes signs of urine extravasation and local bruising (b) >95% have macroscopic haematuria. 3 Urethral rupture This may occur to the membranous or bulbous urethra. (i) Membranous urethra: (a) associated with difficulty voiding urine and urethral bleeding, which mimics extraperitoneal rupture of the bladder (b) rectal examination reveals a high-riding prostate, often with an underlying boggy haematoma. (ii) Bulbous urethra: (a) caused by a straddle injury (falling astride an object) (b) results in local perineal bruising, pain and meatal bleeding. MANAGEMENT 1 Call for a senior ED doctor and attempt to gently catheterize the bladder, but stop if any resistance at all is encountered. 2 Treat the patient for pain and blood loss, and give antibiotics such as gentamicin 5 mg/kg i.v. and ampicillin 1 g i.v. 3 Refer to the surgical team for an ascending urethrogram or cystogram, before a CT scan of the abdomen with i.v. contrast is performed. ADDITIONAL ORTHOPAEDIC INJURIES IN MULTIPLE TRAUMA Early orthopaedic team involvement is common for pelvic trauma particularly if associated with haemorrhage, as well as for thoracic and lumbosacral spine injury, and limb injury. ADDITIONAL ORTHOPAEDIC INJURIES IN MULTIPLE TRAUMA Surgical Emergencies 245 THORACIC AND LUMBOSACRAL SPINE INJURY DIAGNOSIS 1 This type of injury is caused by blunt trauma from a fall, a direct blow or following a traffic crash. A fractured sternum may accompany a hyperflexion wedge fracture of the upper thoracic spine. 2 Always examine the back in multi-trauma patients. Maintain spinal precautions and carefully log-roll all patients with a suspected spinal injury. 3 Look for bruising, deformity and evidence of penetrating injury. 4 Palpate for localized tenderness and swelling around the vertebral column or for an abnormal gap between the spinous processes suggesting a fracture, or overlying the renal areas suggesting a kidney injury (see p. 242). 5 Perform a careful neurological examination, assessing for sensory deficit and a sensory level, loss of peri-anal sensation, and for motor and reflex loss in the legs (see p. 331 for the dermatomes, myotomes and reflex roots in the legs). (i) The spinal cord ends at the level of the first lumbar vertebra, so any injury distal to this involves the cauda equina only, causing lower motor neuron weakness. 6 Send blood for FBC, U&Es, blood sugar and G&S. 7 Request thoracolumbar spine X-rays in all the following high-risk patients: (i) Fall from 3 m (10 ft). (ii) High-speed motor vehicle crash at over 80 k.p.h. (50 m.p.h.). (iii) Ejection from motor vehicle or motor cycle. (iv) GCS score of ≤8. (v) Neurological deficit. (vi) Back pain or tenderness (may be absent). 8 X-rays may show vertebral body fractures, e.g. a distraction ‘Chance’ fracture or a wedge fracture, transverse process fracture, or a dislocation (particularly between T12/L1, and L4/L5). 9 Request a CT scan for all significant or potentially unstable fractures. MANAGEMENT 1 Treat associated thoracic and abdominal injuries as a priority. Maintain spinal precautions, log-roll the patient and minimize unnecessary movements, as thoracolumbar fractures are commonly unstable. 2 Commence i.v. fluids if there is hypotension from local or retroperitoneal bleeding, or from loss of sympathetic tone in a high thoracic cord injury. 3 Refer the patient to the orthopaedic team. (i) Consider i.v. methylprednisolone for spinal cord damage within 8 h of injury, only after consultation with the regional Spinal Injuries unit (see p. 228). ADDITIONAL ORTHOPAEDIC INJURIES IN MULTIPLE TRAUMA 246 Surgical Emergencies LIMB INJURY The management of limb injuries in the multi-trauma patient does not take precedence over head, thoracic, abdominal or pelvic injuries, even though they may appear more dramatic and attract instant attention. Limb injuries are covered in detail in Section IX, Orthopaedic Emergencies. DIAGNOSIS 1 Look for obvious deformity, swelling, tenderness, abnormal movement or crepitus (if the patient is unconscious). 2 Check the distal pulses, particularly in a supracondylar humeral fracture or a dislocated knee. 3 Remember that closed fractures bleed extensively with little external evidence, and open fractures bleed even more. See Table 8.7 for the amounts of concealed blood loss expected with pelvic and limb injuries in multiple trauma. 4 Note any neurological deficit, e.g. sciatic nerve damage in posterior hip dislocation, or radial nerve damage in humeral shaft fracture. MANAGEMENT 1 Restore any deformity to a normal anatomical alignment. This will reduce the risk of neurovascular compromise and maintain skin integrity, reducing long-term complications. Examples include: (i) Posteriorly dislocated hip, to prevent sciatic nerve damage. (ii) Dislocated knee, to maintain vascular circulation to the distal extremity. (iii) Dislocated ankle, to prevent ischaemic pressure necrosis of the skin overlying the malleolus (see p. 312). 2 Give increments of morphine 2.5–5 mg i.v. for pain with an antiemetic such as metoclopramide 10 mg i.v. 3 Cover compound fractures with a saline-soaked sterile dressing. Give flucloxacillin 2 g i.v. or cefuroxime 1.5 g i.v. and tetanus prophylaxis. 4 Immobilize the fracture using a plaster of Paris backslab, or a specially designed splint such as the Donway™ traction splint for femoral shaft fractures. Table 8.7 Expected concealed blood loss from orthopaedic injuries in multiple trauma Site of closed fracture Predicted blood loss Pelvic ring Up to 6 units or more Femoral shaft 2–4 units Tibial shaft 1–3 units HEAD INJURY Surgical Emergencies 247 (i) Splinting reduces pain, making handling easier; it also reduces blood loss and the risk of neurovascular injury. 5 Obtain urgent vascular and orthopaedic consults if distal ischaemia is present. Otherwise refer the patient when the other major injuries have been stabilized. 6 Traumatic amputation of a limb or digit (i) Control haemorrhage by direct pressure and elevation of the stump. (ii) Consider the possibility of replantation, especially in a clean, sliced wound without crushing (a) preserve the amputated part by wrapping in a saline-soaked sterile dressing (b) seal the wrapped part in a sterile dry plastic bag, and immerse in a container of crushed ice and water (c) give i.v. antibiotics and tetanus prophylaxis as for a compound fracture (d) X-ray the limb and severed part (e) refer the patient to the orthopaedic or plastic surgery team for consideration of microvascular surgery ideally performed within 6 h of injury. HEAD INJURY The diagnosis and management of head injuries is best considered in two groups: ● Severe head injury – see page 29, Section I, Critical Care. ● Conscious head injury. CONSCIOUS HEAD INJURY The aim is to differentiate patients requiring admission from those who could be allowed home. DIAGNOSIS 1 History Enquire about: (i) The nature and speed of impact. (ii) Subsequent loss of consciousness, drowsiness, vomiting or seizures. (iii) The length of post-traumatic amnesia (PTA) from the time of injury to the time of the return of memory for consecutive events. This is often underestimated (a) >10 min PTA is significant. HEAD INJURY 248 Surgical Emergencies (iv) Associated alcohol or drug intoxication. (v) Relevant medical conditions and drug therapy, including warfarin. 2 Examination (i) Record the temperature, pulse, blood pressure and respirations. (ii) Assess higher mental functions, including the level of consciousness, using the GCS score (see p. 30). (iii) Check the pupil size and reactions, eye movements, cranial nerves and the limbs for lateralizing neurological signs. (iv) Examine the scalp for bruising, lacerations or palpable fractures and haematomas. (v) Exclude associated neck or other injuries. 3 Radiological imaging (i) Request three-view cervical spine X-rays, if there is any suggestion of an associated neck injury (a) lateral cervical spine view, with an anteroposterior and openmouth odontoid view (b) make sure C1–C7/T1 are visualized, if necessary by traction on the shoulders (see p. 227). (ii) CT head scan. Request a CT scan of the head as the investigation of choice for the detection of acute, clinically important brain injuries. (iii) Indications for a CT head in the conscious GCS 15 head injury patient following any loss of consciousness or significant anterograde amnesia (PTA) include: (a) drug or alcohol intoxication at time of trauma or evaluation (b) headache or repeated vomiting ≥2 episodes (c) age >60 (d) warfarin (or other bleeding tendency, e.g. chronic liver disease) (e) dangerous mechanism, such as high-speed injury, injury from a sharp or heavy object (f) trauma above the clavicle such as a deep scalp laceration, large haematoma, or skull fracture suspected on palpation (g) seizure or focal neurological sign (h) suspected open skull fracture (i) signs of a basal skull fracture such as cerebrospinal fluid or blood loss from the nose or ear. (iv) Skull X-rays. These really now only have a limited role, if any: (a) detection of non-accidental injury in children (b) when CT scanning services are unavailable, in conjunction with inpatient observation – look for a linear fracture, the double shadow of a depressed fracture, suture diastasis, an air-fluid level in a sinus, a traumatic aerocoele, shift of the pineal or a foreign body. HEAD INJURY Surgical Emergencies 249 MANAGEMENT 1 Avoid giving patients with suspected head injury excessive parenteral analgesia until fully assessed, to allow an appropriate measure of consciousness and to look for other neurological signs. 2 Clean scalp lacerations thoroughly, trim the edges and remove any foreign bodies. Then suture in layers using a monofilament synthetic nonabsorbable material such as nylon or polypropylene. 3 Give tetanus prophylaxis according to the patient’s immune status. 4 Admission (i) Admit patients with a minor head injury and any of the following features to the surgical team for neurological observation: (a) confusion or any other decreased level of consciousness (b) neurological symptoms or signs, including persistent headache or vomiting (c) abnormal CT head scan (d) skull fracture (e) difficulty assessing, e.g. alcohol, drugs, epilepsy (f) other medical condition, e.g. warfarin, coagulation defect (g) significant associated injuries requiring inpatient care. (ii) Make certain all of the above have had radiological imaging, ideally with a CT head scan. Some will be discussed with the neurosurgery team. 5 Discharge (i) Send the following patients with a minor head injury home, provided there is someone with them and home circumstances are suitable: (a) fully conscious and oriented (b) normal CT head scan (c) normal skull X-ray (when CT unavailable) (d) no other significant injuries (e) no seizures or focal neurological signs (f) no persistent headache or vomiting. (ii) Give each patient a standard head injury advice card (a) these cards advise patients to return if complications such as confusion, drowsiness, seizure, visual disturbance, vomiting or persistent headache occur in the subsequent 24 h after discharge. (iii) This still leaves some patients with a minor head injury yet to be dealt with. Admit the following patients to the ED short-stay ward for observation: (a) no one to accompany them (b) poor home circumstances (c) an unreliable history, particularly if they were under the influence of alcohol or drugs (d) other painful injuries, e.g. to the face or nose, etc. BURNS 250 Surgical Emergencies 6 Always remember (i) Look for the cause of any preceding fall in the elderly, such as a transient ischaemic attack, Stokes–Adams attack or other syncopal episode (a) these require diagnosis and management in their own right, in addition to the resultant head injury. (ii) A head injury in a child may be due to non-accidental injury (see p. 372). (iii) Cervical spine injuries are associated with head injuries and appropriate examination and investigation is performed based on clinical grounds. BURNS These are considered in the following categories: ● Major burns. ● Minor burns and scalds. ● Minor burns of the hand. ● Minor burns of the face. ● Bitumen burns. MAJOR BURNS DIAGNOSIS 1 Determine the nature of the fire, how it started, whether there was any explosion, the time of the incident and delay in reaching hospital. 2 Ask if the patient was in an enclosed place and, if so, for how long. Ascertain whether smoke or fumes, which predispose to carbon monoxide and cyanide poisoning, were present and the duration of exposure. 3 Examine for signs of a respiratory burn. (i) Look for burns around the face and neck, burnt nasal hairs, and soot particles in the nose and mouth. (ii) Look for signs of tachypnoea, hoarseness, stridor or wheezing. (iii) Assess for headache and confusion suggesting carbon monoxide poisoning. 4 Consider the possibility of cyanide poisoning from burning plastics and fabrics, especially in patients with: (i) Tachypnoea, respiratory failure, cardiac arrhythmias, hypotension, convulsions and coma. (ii) Severe, persistent, raised anion gap metabolic acidosis with a venous lactate level of >10 mmol/L despite fluid resuscitation (see p. 185). BURNS Surgical Emergencies 251 5 Check for associated injuries, particularly if burns occurred from an explosion, blast injury or high-voltage electrocution. 6 Determine the extent of the burn. (i) Use Wallace’s Rule of Nines in adults, ignoring areas of mere erythema (see Fig. 8.2). (ii) Use comparison with the size of the child’s palm, equal to 1% of body surface area (BSA), when estimating the extent of a burn in children. A child’s head is relatively larger than an adult’s (12–14%) and the legs are relatively smaller (14%). (iii) Or use a body map such as a Lund and Browder chart. Figure 8.2 Wallace’s Rule of Nines in adults, for estimating the percentage of body surface area burned 9% 9% 9% 1% 18% 18% Front 18% Back 18% BURNS 252 Surgical Emergencies 7 Determine the depth of the burn. (i) Full-thickness: the skin is white or brown, dry, leathery, and anaesthetic with no capillary refill. This will require skin grafting. (ii) Partial-thickness (a) deep dermal – the skin is pink or white, feels thickened, does not blanch, and has reduced sensation. This should heal over in about 3 weeks, but some areas may require grafting to avoid leaving a scar (b) superficial – the skin is red and blistered, blanches and is painful. This should heal spontaneously in 10–14 days. (iii) Superficial: erythema, blanching and pain occur, followed by peeling as in sunburn. This should heal rapidly in 5–7 days. 8 Insert two large-bore i.v. cannulae and send blood for FBC, U&Es, CK, blood sugar, G&S and a drug screen if there is suspected alcohol or drug abuse. (i) The cannula may be placed through burned skin if absolutely necessary, or use a cut-down technique if no vein is found. (ii) Avoid central line insertion because there is a high risk of sepsis from this procedure. 9 Check ABGs. An elevated carboxyhaemoglobin level will confirm exposure to carbon monoxide (see p. 184). 10 Monitor the ECG and attach a pulse oximeter to the patient. 11 Request a CXR. MANAGEMENT 1 Confirm the adequacy of the airway and give 100% oxygen by tight-fitting mask with reservoir bag. 2 Give salbutamol 5 mg nebulized for wheeze. 3 Organize for an airway-skilled person to perform urgent endotracheal intubation using an RSI technique with an uncut endotracheal tube in patients with: (i) Significant burns involving the face, tongue and pharynx. (ii) Stridor, hoarseness, respiratory distress or a deteriorating level of consciousness. (iii) Evidence of cyanide toxicity from smoke and fume inhalation. 4 Commence i.v. fluids in any burn >10% BSA in a child or 15% BSA in an adult, or for associated injuries causing hypovolaemia. 5 Determine the rate of fluid administration using the Parkland formula: (i) Give fluid at 4 mL/kg per percentage of BSA burned (a) administer the first 50% in the initial 8 h, and the remaining 50% in the subsequent 16 h. (ii) More rapid fluid replacement may be required to catch up if there has been a delay in reaching hospital. BURNS Surgical Emergencies 253 (iii) Give additional maintenance fluid at 1.0–1.5 mL/kg per hour of normal saline. (iv) The Parkland formula and other fluid resuscitation formulae such as the Muir and Barclay are a guide only. Aim for at least 1 mL/kg per hour urine output. 6 The quantity of fluid is more important than the type. (i) Consider albumin initially in extensive, deep (e.g. electrical) burns, or when resuscitation is delayed. (ii) Otherwise, use a crystalloid solution alone, such as Hartmann’s (compound sodium lactate). 7 Insert a urinary catheter to assess the adequacy of resuscitation, aiming for a urine output of 50 mL per hour in adults, or 1 mL/kg per hour in children <30 kg. 8 Pass a nasogastric tube in patients with burns >20%, who may develop gastric stasis. 9 Give morphine 0.1 mg/kg i.v. with an antiemetic such as metoclopramide 10 mg i.v. Remember that under-transfusion or hypoxia are more common causes of restlessness than pain. 10 Give tetanus prophylaxis to all burn patients (see p. 321). 11 Consider the need for escharotomy in the following: (i) Circumferential, leathery, full-thickness burns that may cause distal ischaemia in limbs or digits by restricting blood flow, and respiratory compromise by constricting chest wall movements. (ii) Ask the surgical team to perform relieving incisions through the burn area. 12 Leave any adherent clothing alone and do not break blisters in the burnt area. Remove constricting articles such as rings, bracelets and watches. (i) Cover the burn with a non-adherent, paraffin-impregnated gauze dressing or plastic cling wrap. Beware of hypothermia in children if wet soaks were left on. (ii) Avoid silver sulfadiazine cream at this stage until the patient has been assessed by the surgical or burns unit team. 13 All full-thickness burns of >1–2% BSA require hospital admission by the surgical team. Refer patients on to a specialist burns unit with: (i) Burns >10% in children and 15% in adults. (ii) Burns of important functional areas, such as the face, hands, feet, perineum and genitalia. (iii) Respiratory burns. (iv) Chemical burns and electrical burns, including lightning injury. 14 Assess all serious burns with care and resuscitate fully before departure, similar to the precautions taken when transferring serious head injuries to a neurosurgical unit. BURNS 254 Surgical Emergencies (i) Remember the risk of sudden respiratory obstruction during transit. (ii) Make sure a senior doctor has assessed the need for endotracheal intubation in any significant respiratory burn, prior to departure. MINOR BURNS AND SCALDS These include full-thickness burns <1% or partial-thickness burns <15% BSA in adults and <10% in children. The aim is to manage them as outpatients, as distinct from patients with major burns, who require admission (see above). INITIAL MANAGEMENT 1 Irrigate the wound immediately with copious running cold water until the pain is relieved. 2 Assess the extent and depth of the burn (see p. 251). In general, superficial partial-thickness burns heal spontaneously, deep dermal partial-thickness burns heal slowly with scar formation; and full-thickness burns do not heal at all, unless <1–2 cm in diameter, when epithelium will cover the area from the edges. Otherwise grafting is required. 3 Clean with sterile saline or an antiseptic such as chlorhexidine. 4 Give adequate analgesia such as paracetamol 500 mg with codeine 8 mg two tablets orally q.d.s. and/or ibuprofen 200–400 mg orally t.d.s. Give children 15 mg/kg of paracetamol elixir. 5 De-roof large blisters that have broken, or aspirate the fluid if the blister is tense. Otherwise leave blisters intact to protect the healing epithelium. 6 Apply silver sulfadiazine cream and cover the burn with a non-adherent paraffin-impregnated gauze dressing. 7 Then apply gauze and an absorbent layer consisting of a cotton-wool and gauze combine pad, overlapping the paraffin-impregnated gauze dressing by 3 cm at either end. 8 Finally, keep the absorbent layer in place with a firm crêpe bandage, again overlapping each end by 3 cm, and seal with adhesive tape. 9 Always elevate the limb using a high-arm sling for arm and hand burns. Tip: burn injuries are always frightening and unexpected, and relatives (particularly the parents of children) may feel guilty and angry. Special counselling and reassurance are helpful from the start to aid coming to terms with the injuries and to allay anxiety, so they are useful as a support to the victim. ✓ BURNS Surgical Emergencies 255 10 Give tetanus prophylaxis and oral analgesics such as paracetamol 500 mg and codeine phosphate 8 mg two tablets q.d.s. to take home. 11 Remember that burns of the perineum, feet or hands in children may be due to non-accidental injury. (i) Suspect this when there has been a delay in seeking treatment and the explanation is tenuous, or there is absence of any evidence of splashing. (ii) Refer the child to the paediatric team for admission if nonaccidental injury is possible, however trivial the burn (see p. 372). FOLLOW-UP MANAGEMENT 1 Review the patient after 24–48 h to clean the affected site, to reassess the condition of the burn, and to ensure that no evidence of secondary infection is present. Re-dress the site, but omit the silver sulfadiazine. 2 Thereafter, change the dressing every 5 days, unless the wound becomes painful, or smells, or the bandage becomes soaked (‘strike through’), when the dressing should be renewed immediately. (i) Leave the paraffin-impregnated gauze in place when changing the dressing, if it has become adherent to the skin, to avoid destroying the delicate new epithelium forming underneath. (ii) Otherwise, replace the paraffin-impregnated gauze, the gauze and cotton-wool absorbent layer, and the crêpe bandage. 3 When the wound is healing and has become epithelialized, leave it exposed or cover it with a dry, non-adherent dressing. 4 Refer burns that have not healed in 10–12 days to a plastic surgery unit for review and consideration for skin grafting. 5 Warn the patient that healed burns will initially be both hypersensitive and photosensitive, will have dry scaly skin, and that there may be depigmentation in dark-skinned races. MINOR BURNS OF THE HAND DIAGNOSIS AND MANAGEMENT These are difficult to dress. 1 Cover the hand with silver sulfadiazine cream and place the hand inside a sterile polythene bag, bandaged over a gauze ring as a seal at the wrist. 2 Elevate the hand and encourage the patient to move the fingers regularly. 3 Give tetanus prophylaxis and analgesia. 4 Replace the silver sulfadiazine cream and bag daily, as turbid fluid collects in the bag. ACUTE ABDOMEN 256 Surgical Emergencies MINOR BURNS OF THE FACE DIAGNOSIS AND MANAGEMENT 1 Leave these alone and exposed to heal in 10 days. A proprietary moisturizing lotion may be used. 2 Exclude corneal damage by staining with fluorescein. 3 Warn the patient that facial swelling may develop the following day. BITUMEN BURNS DIAGNOSIS AND MANAGEMENT 1 Road-laying and roofing accidents are usually responsible. 2 Irrigate the area immediately with cold water. 3 Leave the bitumen alone and cover it with paraffin-impregnated gauze. 4 Await blister formation or re-epithelialization, which will allow the bitumen to drop off. 5 Assess subsequently for the depth of the burn, which is usually partialthickness. ACUTE ABDOMEN The aims are to resuscitate critically ill patients; differentiate those requiring referral to a surgical, gynaecological, urological or medical team; and to determine who can be allowed home. SERIOUSLY ILL PATIENT DIAGNOSIS AND MANAGEMENT 1 Clear the airway, give oxygen, and attach a cardiac monitor and pulse oximeter to the patient. Check the temperature, pulse, blood pressure, respiratory rate and blood sugar level. 2 Obtain a brief history of the onset, duration, nature and character of the pain, prior episodes of pain, relevant previous operations and illnesses, present medication and known drug allergies. 3 Examine the chest and heart, and then lay the patient flat to examine the abdomen, including the femoral pulses. 4 Look for a ruptured abdominal aortic aneurysm (AAA), pancreatitis, inferior myocardial infarction, mesenteric infarction or a ruptured ectopic pregnancy in any shocked patient presenting with sudden acute abdominal pain. 5 Perform a rectal examination. ACUTE ABDOMEN Surgical Emergencies 257 6 Insert one or two large-bore i.v. cannulae and send blood for FBC, U&Es, LFTs, blood sugar and lipase/amylase. Cross-match blood if haemorrhage is suspected. Send blood cultures if pyrexial. Check an arterial or venous blood gas. 7 Commence an i.v. infusion with normal saline. (i) Arrange insertion of a CVP line by an experienced doctor in older patients with pre-existing cardiac disease, to avoid precipitating heart failure from fluid overload. 8 Catheterize the bladder. Test the urine for sugar, blood, protein, bile and urobilinogen, and send for microscopy and culture. (i) Perform a urinary -human chorionic gonadotrophin (hCG) pregnancy test in females of reproductive age. 9 Perform an ECG. 10 Request plain radiology: (i) Erect CXR or lateral decubitus abdominal film if the patient is unable to sit upright, to look for free gas in suspected perforation. (ii) AXR for possible bowel obstruction, volvulus or for abnormal air such as the ‘double-wall sign’ in a perforation. 11 Arrange a focused bedside ultrasound for a suspected AAA or ectopic pregnancy. 12 Insert a nasogastric tube if there is evidence of intestinal obstruction, ileus or peritonitis. 13 Commence broad-spectrum antibiotics such as gentamicin 5 mg/kg, ampicillin 1 g i.v. and metronidazole 500 mg i.v. for generalized peritonitis. 14 Refer the patient immediately to the surgical team. STABLE PATIENT WITH AN ACUTE ABDOMEN DIAGNOSIS AND MANAGEMENT 1 Determine the onset and nature of pain: (i) Explosive and excruciating pain: consider myocardial infarction, ruptured aortic aneurysm, perforated viscus, and biliary or renal colic. (ii) Rapid, severe and constant pain: consider pancreatitis, strangulated bowel, mesenteric infarction and ectopic pregnancy. (iii) Gradual, steady pain: consider cholecystitis, appendicitis, diverticulitis, hepatitis and pelvic inflammatory disease (salpingitis). (iv) Intermittent pain with crescendos: consider mechanical obstruction. 2 Ask about the location and radiation of pain: (i) Central abdominal pain radiating to the back suggests an aortic aneurysm or pancreatitis. (ii) Flank pain radiating to the genitalia suggests ureteric colic, or rarely ruptured aortic aneurysm. ACUTE ABDOMEN 258 Surgical Emergencies (iii) Otherwise pain tends to localize over the organ affected, provided there is peritoneal involvement, with radiation to a shoulder tip if the diaphragm is irritated, e.g. by cholecystitis or a ruptured spleen. 3 Look for associated features such as: (i) Nausea and vomiting: (a) pain tends to precede the nausea and vomiting in the surgical acute abdomen (b) a medical condition such as gastroenteritis or gastritis is more likely if the nausea and vomiting precede the pain. (ii) Fever and rigors: (a) a low-grade pyrexia is usual in appendicitis or diverticulitis (b) a high fever and rigors suggest cholecystitis, cholangitis, diffuse peritonitis, pyelonephritis or acute pelvic inflammatory disease (salpingitis). 4 Check the temperature, pulse, blood pressure and respiratory rate. 5 Inspect for visible peristalsis and distension, palpate for local tenderness, guarding and masses, percuss for free gas, and listen for increased or absent bowel sounds. Examine the hernial orifices, particularly in cases of intestinal obstruction. 6 Perform a rectal examination, external genitalia examination in male patients, and consider a vaginal examination in female patients. 7 Insert an i.v. cannula and send blood for FBC, U&Es, LFTs, blood sugar and lipase/amylase. (i) Their true discriminatory value in differentiating between the various conditions is limited, apart from the lipase/amylase. 8 Test the urine for sugar, blood, protein, bile and urobilinogen, and send for microscopy and culture in suspected UTI. (i) Perform a -hCG pregnancy test in females with abdominal pain. 9 Record an ECG. 10 Plain and special radiology. Only request radiologic investigation for the following specific indications: (i) An erect CXR – to look for evidence of pulmonary disease, a secondary pleural reaction from intra-abdominal disease and free gas under the diaphragm indicating a perforation. (ii) Erect and supine abdomen films – to look at the gas pattern for obstruction or volvulus, splenic shadow, renal outlines and psoas shadows, and for calcification and opacities. (iii) Upper abdominal ultrasound to confirm biliary colic or cholecystitis. (iv) Lower abdominal ultrasound to confirm an AAA or ureteric colic. (v) Pelvic ultrasound – to look for a gynaecological cause (remember to do the -hCG first). (vi) CT scan (a) with i.v. contrast for a suspected aortic aneurysm, provided the patient is haemodynamically stable ACUTE ABDOMEN Surgical Emergencies 259 (b) with i.v. plus or minus oral contrast for difficult diagnoses particularly in the older patient, such as suspected bowel cancer or other complex masses, diverticulitis (c) without contrast to confirm ureteric colic. 11 Give all patients i.v. analgesia as required, such as morphine 2.5–5 mg i.v. with metoclopramide 10 mg i.v. This does not interfere with the surgical diagnosis, which may even be facilitated. 12 Refer all cases to the surgical team if an acute surgical condition is suspected or cannot be excluded. CAUSES OF ACUTE ABDOMINAL PAIN Disorders causing acute abdominal pain may be categorized as intestinal, biliary, vascular, pancreatic, urinary, peritoneal and retroperitoneal, gynaecological and medical. See Table 8.8 for a complete list. Table 8.8 Causes of acute abdominal pain Intestinal disorders Acute appendicitis Intestinal obstruction Intussusception Perforation of a viscus Diverticulitis Inflammatory bowel disease Biliary disorders Biliary colic Acute cholecystitis Vascular disorders Ruptured aortic aneurysm Ischaemic colitis Mesenteric infarction Ruptured spleen Pancreatic disorder Acute pancreatitis Urinary disorders Renal and ureteric colic Pyelonephritis Acute urinary retention Acute epididymo-orchitis Acute testicular torsion Peritoneal/retroperitoneal disorders Primary peritonitis Retroperitoneal haemorrhage Gynaecological disorders Medical disorders ACUTE ABDOMEN 260 Surgical Emergencies ACUTE APPENDICITIS DIAGNOSIS 1 Acute appendicitis causes poorly localized central abdominal pain, worse on coughing or moving, which classically shifts to the right iliac fossa. There is associated anorexia, nausea, vomiting, and diarrhoea or constipation. 2 Low-grade pyrexia, localized abdominal tenderness, rebound and guarding are found. 3 A rectal examination is commonly performed to help diagnose a retrocaecal or pelvic appendix, but really has little true discriminatory value. 4 Always perform a urinalysis to look for glycosuria, white cells, and a -hCG pregnancy test. Even if positive, none of these rules out appendicitis. 5 Gain i.v. access. (i) FBC is frequently performed, but rarely influences decision making alone. 6 Request an ultrasound in females to rule out pelvic pathology, or a CT scan for doubtful cases only. 7 Diagnosis is most difficult in very young, elderly or pregnant patients. MANAGEMENT 1 Commence a normal saline infusion and administer i.v. analgesia. 2 Keep the patient nil by mouth. Give gentamicin 5 mg/kg i.v., ampicillin 1 g i.v. q.d.s. and metronidazole 500 mg i.v. t.d.s. if rupture is suspected with peritonitis. 3 Admit all patients under the surgical team, whether the diagnosis appears clear or is just suspected in an atypical case, such as: (i) Confused elderly patient, infant with diarrhoea, or older child off his or her food, any of whom could have appendicitis. INTESTINAL OBSTRUCTION DIAGNOSIS 1 The causes are many, including adhesions, an obstructed hernia, carcinoma, diverticulitis, volvulus, intussusception, mesenteric infarction, and Crohn’s disease. 2 Intermittent colicky abdominal pain occurs with abdominal distension and vomiting in high obstruction, and constipation with failure to pass flatus in low obstruction. 3 Visible peristalsis may be seen, associated with tinkling bowel sounds and signs of dehydration. ACUTE ABDOMEN Surgical Emergencies 261 4 The pain becomes more continuous and generalized if strangulation occurs (most common with a femoral hernia), associated with tachycardia and signs of shock. 5 Always examine the hernial orifices and perform a rectal examination. 6 Gain i.v. access and send blood for FBC, U&Es, lipase/amylase and blood sugar. 7 Request erect and supine abdominal X-rays and look for the following features: (i) Small bowel obstruction: (a) X-rays show dilated loops of small bowel and a colon devoid of air (b) small bowel is usually central in distribution with regular transverse bands (valvulae conniventes) extending across the entire diameter of the bowel (c) fluid levels, with over five considered significant. Note fluid levels also occur in gastroenteritis. (ii) Large bowel obstruction: (a) X-rays show dilated large bowel, with a peripheral distribution, irregular haustral folds and faecal mass content. MANAGEMENT 1 Commence an infusion of normal saline to correct dehydration from vomiting and fluid loss into the bowel. 2 Pass a nasogastric tube, administer analgesia, and refer the patient to the surgical team. INTUSSUSCEPTION DIAGNOSIS 1 This is caused by telescoping or prolapse of one portion of bowel into an immediately adjacent segment. It usually occurs in children aged 3–18 months and is characterized by intermittent abdominal pain with sudden screaming and pallor, followed by vomiting. 2 Abdominal distension and a mass may be felt, with blood-stained mucus (‘redcurrant jelly’) found on rectal examination in 50%. 3 Send blood for FBC, U&Es and blood sugar. 4 Request erect and supine AXRs, which may be normal in the early stages, or reveal signs of intestinal obstruction. (i) Look for evidence of a soft-tissue mass surrounded by a crescent of air (‘doughnut sign’) or free air from perforation of a viscus. 5 Arrange an abdominal ultrasound, or a contrast or air enema. (i) Both have high degrees of sensitivity, with an enema resulting in therapeutic reduction in 75% of cases. ACUTE ABDOMEN 262 Surgical Emergencies MANAGEMENT 1 Insert an i.v. cannula and commence careful i.v. rehydration with analgesia. 2 Refer immediately to the surgical team. PERFORATION OF A VISCUS DIAGNOSIS 1 Perforation may occur anywhere in the gastrointestinal tract. Common sites are a peptic ulcer, the appendix, or a colonic diverticulum. (i) There may be an antecedent history of alcohol or NSAID ingestion, dyspepsia, or lower abdominal pain, or (ii) Perforation can occur de novo. 2 It presents with severe pain and signs of generalized peritonitis with boardlike rigidity. Shock soon supervenes. 3 Gain i.v. access and send blood for FBC, U&Es, blood sugar and lipase/ amylase. 4 Request an erect CXR to look for gas under the diaphragm, seen in >70% of cases. 5 Arrange a CT scan of the abdomen with i.v. and oral contrast. MANAGEMENT 1 Treat shock with i.v. normal saline, administer i.v. analgesia with morphine in 2.5–5 mg increments and pass a nasogastric tube. 2 Commence broad-spectrum antibiotics such as gentamicin 5 mg/kg once daily, ampicillin 1 g i.v. q.d.s. and metronidazole 500 mg i.v. t.d.s. 3 Refer the patient immediately to the surgical team. DIVERTICULITIS DIAGNOSIS 1 This follows inflammation of one or more colonic diverticulae. 2 It causes lower abdominal pain radiating to the left iliac fossa, and bloody diarrhoea, sometimes with sudden profuse rectal bleeding. 3 Look for a low-grade fever, abdominal tenderness, and guarding on the left with a palpable mass. 4 Complications of perforation, severe bleeding, fistula formation and bowel obstruction may occur. 5 Gain i.v. access and send blood for FBC, U&Es, blood sugar and G&S. 6 Perform an ECG and request an erect CXR if perforation is suspected. 7 Organise a CT scan of the abdomen with i.v. contrast. ACUTE ABDOMEN Surgical Emergencies 263 MANAGEMENT 1 Commence an i.v. infusion to treat dehydration or shock. 2 Refer the patient to the surgical team for analgesia and antibiotics such as gentamicin 5 mg/kg once daily, ampicillin 1 g i.v. q.d.s. and metronidazole 500 mg i.v. t.d.s., or for surgery if bowel obstruction or a pelvic abscess is suspected. INFLAMMATORY BOWEL DISEASE DIAGNOSIS 1 Ulcerative colitis associated with bouts of diarrhoea with blood-stained mucus may present as a fulminating attack with fever, tachycardia and hypotension. 2 Crohn’s disease, associated with recurrent abdominal pain, diarrhoea, malaise and peri-anal fistulae or abscesses, may present acutely with obstruction, perforation or right iliac fossa pain. This can mimic acute appendicitis. 3 Gain i.v. access and send blood for FBC, U&Es, blood sugar, lipase/amylase and blood culture. 4 Request a plain AXR to look particularly for the following: (i) Ulcerative colitis: extensive mucosal ulceration may leave normal mucosal islands (pseudopolyps) visible on plain film. Dilation of the transverse colon >6 cm indicates the presence of a megacolon. Perforation is a serious risk. (ii) Crohn’s disease: free air associated with perforation may be seen. Stenotic regions of small bowel are best visualized with barium follow-through studies, or on colonoscopy. 5 Organize a CT scan of the abdomen with i.v. contrast. MANAGEMENT 1 Commence an i.v. infusion and treat pain with i.v. analgesia. 2 Refer all cases with shock, fever, peritonitis, severe bleeding or an obstructed bowel immediately to the surgical team. 3 Organize urgent gastroenterology advice for a toxic megacolon with fever, tachycardia and hypotension. (i) Start hydrocortisone 200 mg i.v. 6-hourly, and broad-spectrum antibiotics such as gentamicin 5 mg/kg once daily, ampicillin 1 g i.v. q.d.s. and metronidazole 500 mg i.v. t.d.s. ACUTE ABDOMEN 264 Surgical Emergencies BILIARY COLIC DIAGNOSIS 1 This presents with discrete episodes of colicky pain in the right hypochondrium, referred to the scapula. 2 Look for right upper quadrant tenderness on examination. The patient may be jaundiced if the common bile duct is obstructed, with yellow sclera, and bilirubin in the urine. 3 Gain i.v. access and send blood for FBC, U&Es, LFTs and lipase/amylase. 4 Request an upper abdominal ultrasound. MANAGEMENT 1 Treat pain with i.v. analgesia such as morphine 0.1 mg/kg i.v. with an antiemetic such as metoclopramide 10 mg i.v. 2 Refer the patient to the surgical team if the pain is severe or acute cholecystitis is suspected. 3 Otherwise, advise the patient to eat a diet low in saturated fats and refer them to the GP or surgical outpatients for follow-up. ACUTE CHOLECYSTITIS DIAGNOSIS 1 This causes acute, constant right upper quadrant pain referred to the scapula, with anorexia, nausea and vomiting. 2 Look for localized tenderness, with involuntary guarding and rebound tenderness. Painful splinting of respiration on deep inspiration and right upper quadrant palpation is frequent (Murphy’s sign). Fever is common. 3 Occasionally a gall bladder may be palpable in association with jaundice, although more commonly the gall bladder is not felt as it is shrunken and contracted. 4 Gain i.v. access and send blood for FBC, U&Es, blood sugar, LFTs, lipase/ amylase, and blood culture. 5 Request an upper abdominal ultrasound. MANAGEMENT 1 Give analgesia such as morphine 0.1 mg/kg i.v. with an antiemetic such as metoclopramide 10 mg i.v., and commence an i.v. infusion of normal saline. 2 Give gentamicin 5 mg/kg i.v., and ampicillin 1 g i.v. q.d.s. 3 Refer the patient to the surgical team for bed rest, analgesia, antibiotics and cholecystectomy. ACUTE ABDOMEN Surgical Emergencies 265 RUPTURED ABDOMINAL AORTIC ANEURYSM DIAGNOSIS 1 This classically presents with sudden abdominal pain radiating to the back or groin, syncope, collapse or unexplained shock. Tachycardia and hypotension occur in 50% of cases. 2 Feel for a tender mass with expansile pulsation on examination, or a vague fullness with discomfort to the left of the umbilicus. 3 Always consider this diagnosis in men >45 years in particular, even when only one feature of the ‘classic triad’ of abdominal or back pain, shock, and a pulsatile or tender abdominal mass is present. (i) Also consider a ruptured AAA first in the older patient with apparent ‘ureteric colic’. 4 Gain large-bore i.v. access in both arms and send blood for FBC, U&Es, blood sugar, lipase/amylase and cross-match up to 10 units of blood. 5 Catheterize the bladder. 6 Record the ECG because ischaemic heart disease is usually associated with or exacerbated by the hypotension. 7 Request a CXR if there is time. 8 Perform a rapid bedside ultrasound scan to confirm the presence of an abdominal aneurysm if the patient is haemodynamically unstable and the diagnosis is uncertain. 9 Or proceed directly to theatre if the patient is moribund. 10 Only request a CT scan if the patient is haemodynamically stable. Remember to modify the dose of i.v. contrast depending on the renal function. MANAGEMENT 1 Give the patient high-flow oxygen by face mask and commence a slow i.v. infusion. (i) Only give minimal amounts of normal saline or Hartmann’s (compound sodium lactate), aiming for a systolic blood pressure of no more than 90–100 mmHg (i.e. minimal volume or hypotense resuscitation). (ii) Avoid giving massive fluid volumes, as this leads to coagulopathy, hypothermia, increases the bleeding and causes a higher mortality. 2 Refer the patient urgently to the vascular surgical team for immediate laparotomy. (i) Contact the duty anaesthetist, alert theatre, and inform ICU. ACUTE ABDOMEN 266 Surgical Emergencies ISCHAEMIC COLITIS DIAGNOSIS 1 This usually occurs in an elderly patient with recurrent abdominal pain, progressing to episodes of bloody diarrhoea or intestinal obstruction from stricture formation. 2 Gain i.v. access and send blood for FBC, coagulation profile, electrolyte and liver function tests (ELFTs), blood sugar, lipase/amylase, lactate and G&S. 3 Record an ECG. 4 Request a plain AXR that may reveal ‘thumb-printing’ of the colonic wall, or proximal colon dilation, intramural gas, and the most ominous sign of gas within the portal vein. 5 Arrange a CT scan with i.v. contrast that may show free fluid and colonicwall oedema or air, although many of the features are non-specific. MANAGEMENT 1 Commence an i.v. infusion of normal saline. 2 Give analgesia and keep the patient nil by mouth. 3 Refer the patient to the surgical team. MESENTERIC INFARCTION DIAGNOSIS 1 This may be due to embolism from atrial fibrillation or a myocardial infarction, or due to arterial or venous thrombosis, or arterial occlusion such as following an aortic dissection. 2 There is sudden onset of severe, diffuse abdominal pain, usually in an elderly patient, associated with vomiting and bloody diarrhoea. 3 Abdominal examination reveals distension, generalized tenderness, absent bowel sounds and fresh rectal blood. 4 Gain i.v. access and send blood for FBC, U&Es, LFTs, lipase/amylase, blood sugar and cross-match 2–4 units of blood. Send a lactate as a marker of lactic acidosis. 5 Record the ECG. MANAGEMENT 1 Commence an i.v. infusion of normal saline or Hartmann’s (compound sodium lactate) to treat shock. 2 Refer the patient to the surgical team, who will determine the need for angiography to confirm the diagnosis. However, the prognosis is poor. ACUTE ABDOMEN Surgical Emergencies 267 RUPTURED SPLEEN DIAGNOSIS 1 Left lower rib injuries following blunt trauma are associated with splenic damage in up to 20% of cases. Occasionally, trivial injury to an already enlarged spleen from glandular fever, malaria or leukaemia can cause rupture. 2 The timing of the splenic rupture may be: (i) Acute: causing tachycardia, hypotension and abdominal tenderness with pain referred to the left shoulder. (ii) Delayed: occurring up to 2 weeks or more after an episode of trauma. Initial localized discomfort and referred shoulder-tip pain give way to signs of intra-abdominal haemorrhage. 3 Gain large-bore i.v. access and send blood for a FBC and cross-match 6 units of blood for an acutely ruptured spleen. 4 Request a CXR to look for fractured left lower ribs and a basal pleural effusion, especially in delayed splenic rupture. (i) AXR is unhelpful, as features are non-specific such as a displaced stomach bubble to the right and an enlarged soft-tissue shadow in the splenic area. 5 Arrange an urgent upper abdominal ultrasound if the patient is unstable, or a CT scan with i.v. contrast if the patient is stable. MANAGEMENT 1 Commence an infusion of normal saline and refer the patient immediately to the surgical team. ACUTE PANCREATITIS DIAGNOSIS 1 Predisposing factors include alcohol abuse, gallstones, viruses such as mumps, Epstein–Barr virus and cytomegalovirus, trauma, ischaemia or vasculitis, and following endoscopic retrograde cholangiopancreatography (ERCP). 2 Acute pancreatitis presents with sudden, severe abdominal pain radiating to the back, that is eased by sitting forward, associated with repeated vomiting or retching. 3 Vital signs may reveal a low-grade fever and tachycardia with hypotension. 4 Look for epigastric tenderness, guarding and decreased or absent bowel sounds on abdominal examination. 5 Insert a large-bore i.v. cannula and send blood for FBC, U&Es, LFTs, blood sugar, calcium, lipase/amylase and G&S. Check an arterial blood gas. ACUTE ABDOMEN 268 Surgical Emergencies 6 Record the ECG, which may show diffuse T wave inversion, in the absence of myocardial ischaemia. 7 Request an erect CXR to exclude viscus perforation or lobar pneumonia as a cause of the pain. 8 Perform a CT scan of the abdomen in severe cases that provides both diagnostic and prognostic information. MANAGEMENT 1 Commence an i.v. infusion of normal saline and pass a nasogastric tube. Give morphine 5–10 mg i.v. with an antiemetic such as metoclopramide 10 mg i.v. 2 Refer the patient to the surgical team. 3 Admit patients with hypoxia, shock, metabolic acidosis, hypocalcaemia or renal impairment to ICU. RENAL AND URETERIC COLIC DIAGNOSIS 1 Renal and ureteric calculi may cause pain, haematuria, hydronephrosis or infection. 2 Symptoms are caused by obstruction of one or more calyces, the renal pelvis or ureter. 3 Characteristically these include sudden, severe colicky pain radiating from the loin to the genitalia, restlessness, vomiting and sweating. There may also be urinary frequency and haematuria. 4 Look for loin tenderness in the costovertebral angle, and remember to consider a possible ruptured abdominal aortic aneurysm in men >45 years, especially with a first episode of renal colic, and/or if haematuria is absent (see p. 265). 5 Gain i.v. access and send blood for FBC, U&Es, LFTs, lipase/amylase, calcium and uric acid. 6 Perform a bedside urinalysis for macroscopic or microscopic haematuria, which occurs in 90%. (i) Send a formal midstream urine (MSU) for microscopy and culture. 7 Request a plain AXR KUB (kidneys, ureters, bladder), as most renal calculi are radio-opaque. This is of greatest value in subsequently tracking the course of a calculus. 8 Request a non-contrast abdominal CT scan of the renal tract in all patients >40 years with acute flank pain, to rule out other retroperitoneal pathology at the same time. ACUTE ABDOMEN Surgical Emergencies 269 (i) CT can determine the presence of calculi, their size, degree of ureteric obstruction and exclude other important differential diagnoses, particularly an AAA. 9 Alternatively request a renal ultrasound, particularly in a younger patient or for recurrent colic. 10 An IVP is best reserved for post complex urological surgery only. MANAGEMENT 1 Start analgesia: (i) Give morphine 0.1 mg/kg i.v. with an antiemetic such as metoclopramide 10 mg i.v. particularly if the pain is intense and incapacitating. (ii) Alternatively, use diclofenac 75 mg i.m. or indomethacin (indometacin) 100 mg p.r. (iii) NSAIDs are as effective as opiates, but are not controlled drugs, and will also discourage those who are simply ‘seeking’ narcotics. 2 Admit patients with resistant pain, a stone >6 mm in diameter with an obstructed kidney (these are unlikely to pass spontaneously), or any evidence of infection. (i) An infected obstructed kidney is a urological emergency needing immediate drainage. (ii) Call the urology team urgently for percutaneous nephrostomy insertion. 3 Discharge the remainder to their GP or urology outpatients for follow-up, and recommend a reduced sodium and low-protein diet that decreases the likelihood of recurrent calcium-based stones. PYELONEPHRITIS DIAGNOSIS 1 Typically symptom onset is rapid and characterized by frequency, dysuria, malaise, nausea, vomiting and sometimes rigors. 2 Raised temperature, renal-angle tenderness, and vague low abdominal pain are found. 3 Dipstick urinalysis shows blood, protein and nitrites. 4 Insert an i.v. cannula and send blood for FBC, U&Es, blood sugar and blood cultures in any patient who is significantly ill. 5 Send an MSU to look for bacteria, leucocytes and red blood cells on microscopy and for culture. ACUTE ABDOMEN 270 Surgical Emergencies MANAGEMENT 1 Significantly ill patients. (i) Includes those with vomiting, dehydration, or prostration; those who are pregnant, very young or old; and those who are known to have urinary tract abnormalities, e.g. a duplex system, horseshoe kidney or renal/ureteric stones. (ii) Commence i.v. fluids. Give gentamicin 5 mg/kg i.v. and ampicillin 2 g i.v. q.d.s. (iii) Refer these patients to the medical team for admission. 2 Otherwise, if the symptoms are mild, commence an oral antibiotic depending on local prescribing policy, such as cephalexin 500 mg q.d.s, or amoxicillin 875 mg with clavulanic acid 125 mg one tablet b.d., or trimethoprim 300 mg once daily, all for 10 days. 3 Return the patient to the GP with a letter requesting the GP to organize a repeat urine culture after the completion of a full antibiotic course, to ensure that the infection has been eradicated. 4 Arrange a renal ultrasound in any male with a proven urinary tract infection, or in females with recurrent pyelonephritis and refer to urology outpatients for follow-up. ACUTE URINARY RETENTION DIAGNOSIS 1 Predisposing factors include prostatic hypertrophy, urethral stricture, pelvic neoplasm, anticholinergic drugs, pregnancy, local painful condition such as genital herpes and faecal loading in the elderly. 2 Occasionally, retention is due to a neurogenic cause such as multiple sclerosis. 3 The enlarged bladder is easily palpable, dull to percussion and is usually painful, although in the semiconscious patient it may manifest as restlessness. 4 Always perform a rectal examination, and assess perineal sensation and leg reflexes in every patient. 5 Send blood for FBC, ELFTs and blood sugar. MANAGEMENT 1 Carefully pass a urethral catheter as a strict aseptic procedure, and send a specimen of urine for microscopy and culture (see p. 484). 2 Refer the patient to the surgical team or gynaecology as appropriate. ACUTE ABDOMEN Surgical Emergencies 271 ACUTE EPIDIDYMO-ORCHITIS DIAGNOSIS 1 This occurs in sexually active men with a preceding history of urethritis, or following urinary tract infection or instrumentation including catheterization. 2 Pain begins gradually and is usually localized to the epididymis or testis, associated with a low-grade fever. 3 Send a FBC to look for a neutrophilia and request a urine microscopy to look for leucocytes. MANAGEMENT 1 Never diagnose epididymo-orchitis in a patient <25 years old without considering testicular torsion first (see below). 2 Give the patient a scrotal support if torsion has been excluded, analgesics such as paracetamol 500 mg and codeine phosphate 8 mg two tablets q.d.s., and an antibiotic. 3 The choice of antibiotic depends on the suspected aetiology: (i) Sexually acquired epididymo-orchitis Give ceftriaxone 500 mg i.v. daily for 3 days, plus azithromycin 1 g orally once, plus either another 1 g orally 1 week later or doxycycline 100 mg orally b.d. for 14 days (a) arrange follow-up in a genitourinary medicine clinic, and partner treatment. (ii) Bacterial cystitis with epididymo-orchitis Give cephalexin 500 mg b.d., or amoxicillin 875 mg with clavulanic acid 125 mg one tablet b.d., or trimethoprim 300 mg once daily, all for 14 days and refer to the urology clinic. ACUTE TESTICULAR TORSION DIAGNOSIS 1 Suspect this diagnosis in any male under 25 years with sudden pain in a testicle, which may radiate to the lower abdomen. There may be associated nausea and vomiting. 2 The testicle lies horizontally and high in the scrotum, and is very tender. There may be a small hydrocoele. 3 Urinalysis is typically negative and the blood white cell count normal. MANAGEMENT 1 Always refer every suspected case urgently to the urology team, as the testicle becomes non-viable after 6 h of torsion. ACUTE ABDOMEN 272 Surgical Emergencies (i) Still refer the patient for surgery even if >6 h have elapsed, as orchidopexy is required on the other side to prevent subsequent torsion there. 2 Only arrange scrotal ultrasound if the diagnosis is in doubt, or the history is prolonged to assess blood supply and to look for an alternative diagnosis. This must never delay urgent urological assessment. PRIMARY PERITONITIS DIAGNOSIS AND MANAGEMENT 1 Primary bacterial peritonitis occurs almost exclusively in patients with ascites, particularly due to cirrhosis or the nephrotic syndrome. 2 Look for fever, abdominal pain and tenderness. 3 Send blood for FBC, U&Es, LFTs, blood sugar and blood cultures. Check a urinalysis. 4 Refer the patient to the medical team for a diagnostic peritoneal tap and culture, to exclude Mycobacterium tuberculosis and to distinguish bacterial peritonitis from familial Mediterranean fever. RETROPERITONEAL HAEMORRHAGE DIAGNOSIS 1 This may occur following trauma to the pelvis, kidney or back, or from aortic aneurysm rupture, or from trivial trauma – even spontaneously in those with a bleeding tendency or on anticoagulants. 2 It presents with hypovolaemic shock following trauma, in the absence of an obvious external or internal thoracic or abdominal source for haemorrhage. A paralytic ileus may develop. 3 Insert a wide-bore i.v. cannula and send blood for FBC, coagulation profile, ELFTs, blood sugar, lipase/amylase and cross-match blood according to the degree of shock. (i) Check the urine for blood. 4 Request a CT scan of the abdomen with i.v. contrast to localize the bleeding. (i) Plain abdominal X-ray is unhelpful. It may show loss of the psoas shadow or possibly fractures of the vertebral transverse processes in traumatic cases, but a CT is indicated. MANAGEMENT 1 Commence an infusion of normal saline. 2 Refer to the surgical team for admission. ACUTE ABDOMEN Surgical Emergencies 273 GYNAECOLOGICAL CAUSES The following causes are discussed in Section XII, Obstetric and Gynaecological Emergencies. ● Ruptured ectopic pregnancy (see p. 377). ● Pelvic inflammatory disease (acute salpingitis) (see p. 379). ● Ruptured ovarian cyst (see p. 380). ● Torsion of an ovarian tumour (see p. 380). ● Endometriosis (see p. 381). MEDICAL DISORDERS PRESENTING WITH ACUTE ABDOMINAL PAIN It is rare for non-surgical disorders causing acute abdominal pain to present without other symptoms or signs suggesting their true medical origin. Always remember diabetic ketoacidosis (DKA), and perform a urinalysis in every patient with abdominal pain. DKA is suggested by finding glycosuria and ketonuria (see p. 78). DIAGNOSIS Medical disorders presenting with acute abdominal pain include: 1 Thoracic origin (i) Myocardial infarction, pericarditis. (ii) Pulmonary embolus, pleurisy, pneumonia. (iii) Aortic dissection. 2 Abdominal origin (i) Hepatic congestion from hepatitis or right heart failure. (ii) Infection, including gastroenteritis, pyelonephritis and primary peritonitis. (iii) Intestinal ischaemia from atheroma or sickle cell disease, vasculitis and Henoch–Schönlein purpura. (iv) Irritable bowel syndrome. 3 Endocrine and metabolic origin (i) Diabetic ketoacidosis. (ii) Hypercalcaemia – ‘stones, bones and abdominal groans’. (iii) Addison’s disease. (iv) Lead poisoning, paracetamol or iron poisoning. (v) Porphyria (acute intermittent). Warning: constipation, particularly in the elderly, should be regarded as a symptom and not a diagnosis. Other significant underlying conditions such as a bowel obstruction, diverticulitis, urinary or other sepsis, colon cancer, hypercalcaemia or neurological disease must be actively excluded. ! FURTHER READING 274 Surgical Emergencies 4 Neurogenic origin (i) Herpes zoster. (ii) Radiculitis from spinal cord degeneration or malignancy. (iii) Tabes dorsalis. 5 Thoracolumbar spine origin Collapsed vertebra due to osteoporosis, neoplasm or infection, e.g. tuberculosis (see p. 332). 6 Psychiatric Münchausen’s syndrome or ‘hospital hopper’: (i) Be suspicious of a patient presenting with acute abdominal pain or renal colic, who usually does not live locally, and with no GP, who may have multiple abdominal scars from operations ‘at another hospital’. (ii) Their aim is to gain narcotic analgesia or hospital admission by feigning illness. (iii) Ask for a previous hospital number or admission details, so you can ‘go and verify their story’. (iv) Seek advice from the senior ED doctor. 7 Take a careful history in every case, do a thorough examination, and send blood for FBC, U&Es, LFTs, blood sugar and lipase/amylase. 8 Request a urinalysis, perform an ECG and request a CXR and AXR to avoid missing the more serious diagnoses. MANAGEMENT 1 Discuss the case with the senior ED doctor. Admit the patient as appropriate according to the underlying diagnosis. FURTHER READING National Institute for Health and Clinical Excellence, NHS UK. http://www.nice. org.uk/Guidance/CG/Published National Institute of Clinical Studies (Australia). http://www.nhmrc.gov.au/nics/ index.htm Scottish Intercollegiate Guidelines Network. http://www.sign.ac.uk/ Trauma.org http://www.trauma.org/ (trauma education and management). ORTHOPAEDIC EMERGENCIES Section IX

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