100 Cases in Emergency Medicine and Critical Care PDF

100 Cases in Emergency Medicine and Critical Care http://taylorandfrancis.com  100 Cases in Emergency Medicine and Critical Care Eamon Shamil MBBS MRes MRCS DOHNS, AFHEA Specialist Registrar in ENT – Head & Neck Surgery Guy’s and St Thomas...

100 Cases in Emergency Medicine and Critical Care http://taylorandfrancis.com  100 Cases in Emergency Medicine and Critical Care Eamon Shamil MBBS MRes MRCS DOHNS, AFHEA Specialist Registrar in ENT – Head & Neck Surgery Guy’s and St Thomas’ NHS Foundation Trust, London, UK Praful Ravi MA MB BChir MRCP Resident in Internal Medicine, Mayo Clinic, Rochester, MN, USA Dipak Mistry MBBS BSc DTM&H FRCEM Consultant in Emergency Medicine, University College London Hospital NHS Foundation Trust, London, UK 100 Cases Series Editor: Janice Rymer Professor of Obstetrics & Gynaecology and Dean of Student Affairs, King’s College London School of Medicine, London, UK Boca Raton London New York CRC Press is an imprint of the Taylor & Francis Group, an informa business CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2018 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Printed on acid-free paper International Standard Book Number-13: 978-1-139-03547-8 (Paperback) International Standard Book Number-13: 978-1-138-57253-9 (Hardback) This book contains information obtained from authentic and highly regarded sources. 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Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com  To Mum, Dad, Dania, and Adam for their unconditional love. To Mohsan, Shah, and Praful for their endless support. And to my patients and teachers, who have drawn me closer to humanity. Eamon Shamil To my parents, patients and teachers. Praful Ravi To my wife, Snehal, for her endless support. Dipak Mistry http://taylorandfrancis.com CONTENTS Contributors xi Introduction xiii Critical Care Case 1: Respiratory distress in a tracheostomy patient 1 Case 2: Nutrition 5 Case 3: Shortness of breath and painful swallowing 9 Case 4: Collapse while hiking 13 Case 5: Fever, headache and a rash 17 Case 6: Nausea and vomiting in a diabetic 19 Case 7: Stung by a bee 23 Case 8: A bad chest infection 27 Case 9: Head-on motor vehicle collision 31 Case 10: Intravenous fluid resuscitation 35 Case 11: Found unconscious in a house fire 37 Case 12: Painful, spreading rash 41 Case 13: Submersion 45 Case 14: Crushing central chest pain 49 Internal Medicine Case 15: Short of breath and tight in the chest 53 Case 16: A productive cough 57 Case 17: A collapse at work 61 Case 18: Dysuria and weakness 63 Case 19: Leg swelling, shortness of breath and weight gain 67 Case 20: Chest pain in a patient with sickle cell anaemia 71 Case 21: Fever, rash and weakness 75 Case 22: Rectal bleeding with a high INR 77 Case 23: Back pain, weakness and unsteadiness 81 Case 24: Feeling unwell while on chemotherapy 83 Case 25: Productive cough and shortness of breath 87 Case 26: Vomiting, abdominal pain and feeling faint 89 Case 27: Seizure and urinary incontinence 91 Case 28: Chest pain in a young woman 95 Case 29: Faint in an elderly woman 99 Case 30: An abnormal ECG 103 Case 31: Fever in a returning traveller 107 Case 32: Loose stool in the returned traveller 111 vii  Contents Mental Health and Overdose Case 33: Unconscious John Doe 115 Case 34: An unresponsive teenager 119 Case 35: Deteriorating overdose 125 Case 36: Attempted suicide 129 Neurology and Neurosurgery Case 37: Back pain at the gym 133 Case 38: Passed out during boxing 137 Case 39: Headache, vomiting and confusion 141 Case 40: Motor vehicle accident 143 Case 41: Slurred speech and weakness 147 Case 42: A sudden fall while cooking 151 Case 43: Neck pain after a road traffic accident 153 Trauma and Orthopaedics Case 44: My back hurts 155 Case 45: My shoulder popped out 159 Case 46: Fall on the bus 163 Case 47: Motorbike RTC 165 Case 48: Fall onto outstretched hand (FOOSH) 167 Case 49: Painful hand after a night out 171 Case 50: Cat bite 173 Case 51: Pelvic injury in a motorcycle accident 177 Case 52: Unable to stand after a fall 181 Case 53: Twisted my knee skiing 185 Case 54: Fall in a shop 187 Case 55: I hurt my ankle on the dance floor 191 Case 56: Fall whilst walking the dog 195 General Surgery and Urology Case 57: Upper abdominal pain 199 Case 58: Gripping abdominal pain and vomiting 203 Case 59: My ribs hurt 207 Case 60: Severe epigastric pain 211 Case 61: Left iliac fossa pain with fever 213 Case 62: Acute severe leg pain 217 Case 63: Abdominal pain and nausea 219 Case 64: Epigastric pain and nausea 223 viii  Contents Case 65: A 68-year-old man with loin to groin pain 227 Case 66: Right flank pain moving to the groin 231 Case 67: Testicular pain after playing football 235 ENT, Ophthalmology and Maxillofacial Surgery Case 68: Recurrent nosebleeds in a child 237 Case 69: Worsening ear pain 241 Case 70: Chicken bone impaction 243 Case 71: Ear pain with discharge and facial weakness 245 Case 72: Post-tonsillectomy bleed 247 Case 73: A swollen eyelid 249 Case 74: Red eye and photosensitivity 253 Case 75: Painful red eye 257 Case 76: Visual loss with orbital trauma 261 Case 77: Difficulty opening the mouth 265 Paediatrics Case 78: Cough and difficulty breathing in an infant 269 Case 79: A child with stridor and a barking cough 271 Case 80: A child with fever of unknown origin 273 Case 81: My son has the ‘runs’ 277 Case 82: A child with lower abdominal pain 281 Case 83: A child acutely short of breath 283 Case 84: A child with difficulty feeding 287 Case 85: A child with head injury 291 Case 86: The child with prolonged cough and vomiting 293 Case 87: A child with a prolonged fit 297 Obstetrics and Gynaecology Case 88: Vomiting in pregnancy 301 Case 89: Abdominal pain in early pregnancy 305 Case 90: Bleeding in early pregnancy 309 Case 91: Pelvic pain 313 Case 92: Abdominal pain and vaginal discharge 317 Case 93: Vulval swelling 321 Case 94: Fertility associated problems 325 Case 95: Headache in pregnancy 329 Case 96: Breathlessness in pregnancy 333 Case 97: Postpartum palpitations 337 ix  Contents Medicolegal Case 98: Consenting a patient in the ED 341 Case 99: A missed fracture 345 Case 100: A serious prescription error 349 Appendix: Laboratory test normal values 353 Index 355 x CONTRIBUTORS Mental Health and Overdose, Ophthalmology, Maxillofacial Dr Mohsan M. Malik BSc, MBBS Specialist Trainee in Ophthalmology The Royal London Hospital Barts Health NHS Trust London, UK Obstetrics and Gynaecology Dr Hannan Al-Lamee MPhil, MBChB Specialist Trainee in Obstetric and Gynaecology Imperial College Healthcare NHS Trust London, UK Paediatrics Dr Noor Kafil-Hussain BSc, MBBS, MRCPCH Specialist Trainee in Paediatric Medicine London Deanery London, UK Neurology and Neurosurgery Dr Vin Shen Ban MB BChir, MRCS, MSc, AFHEA Resident in Neurological Surgery University of Texas Southwestern Medical School Dallas, Texas xi http://taylorandfrancis.com INTRODUCTION Emergency Medicine and Critical Care are difficult specialties and they can be quite daunt- ing for new physicians. The modern Emergency Medicine physician has to take a focused history, which can often be incomplete due to the patient’s care being spread over several hos- pitals, examining the patient, arranging rational investigations and then treating the patient. This is often combined with seeing multiple patients simultaneously as well as time pressure. Similarly, in Critical Care, there is the challenge of having to very rapidly assess unwell or deteriorating patients and initiating a suitable management strategy. This book has been written for medical students, doctors and nurse practitioners. One of the best methods of learning is case-based learning. This book presents a hundred such ‘cases’ or ‘patients’ which have been arranged by system. Each case has been written to stand alone so that you may dip in and out or read sections at a time. Detail on treatment has been deliberately rationalised as the focus of each case is to recognise the initial presentation, the underlying pathophysiology, and to understand broad treatment principles. We would encourage you to look at your local guidelines and to use each case as a springboard for further reading. We hope that this book will make your experience of Emergency Medicine and Critical Care more enjoyable and provide you with a solid foundation in the safe management of patients in this setting, an essential component of any career choice in medicine. Eamon Shamil Praful Ravi Dipak Mistry xiii http://taylorandfrancis.com CRITICAL CARE CASE 1: RESPIRATORY DISTRESS IN A TRACHEOSTOMY PATIENT History An 84-year-old patient is brought into the resuscitation area of the Emergency Department by a blue-light ambulance. He is in obvious respiratory distress and has a tracheostomy sec- ondary to advanced laryngeal cancer. Examination On examination, he is cyanotic and visibly tired with a respiratory rate of 28. His oxygen saturation is 84% on room air, blood pressure 94/51, pulse 120 and temperature 36.4°C. Questions 1. What are the indications for a tracheostomy? 2. How do you manage a patient with a tracheostomy in respiratory distress? 3. What is the standard care for a tracheostomy patient? 1  100 Cases in Emergency Medicine and Critical Care DISCUSSION A tracheostomy refers to a stoma between the skin and the trachea. It means that air bypasses the upper aerodigestive tract. This removes the natural mechanisms of voice production (larynx) and humidification (nasal cavity). Patients are more prone to chest infections from mucus accumulating in the lungs. Tracheostomy emergencies may be encountered in the Emergency Department, Intensive Care Unit or the ward. Indications for a tracheostomy include the following: Weaning patients from prolonged mechanical ventilation is the commonest indi- cation in ICU. The tracheostomy reduces dead space and the work of breathing compared to an endotracheal tube. The TracMan study in the United Kingdom has shown that there is no difference in hospital length of stay, antibiotic use or mortal- ity between early (day 1–4 ICU admission) or late (day 10 or later) tracheostomy. Emergency airway compromise – e.g. supraglottitis, laryngeal neoplasm, vocal cord palsy, trauma, foreign body, oedema from burns and severe anaphylaxis. In preparation for major head and neck surgery. To manage excess trachea–bronchial secretions – e.g. in neuromuscular disorders where cough and swallow is impaired. If a patient with a tracheostomy is in respiratory distress Call for urgent help from both an anaesthetist and an ENT surgeon and have a difficult airway trolley at the bedside. Apply oxygen (15 L/min) via a non-rebreather mask to the face and tracheostomy site. Use humidified oxygen if available. Look, listen and feel for breath- ing at the mouth and tracheostomy site. Remove the speaking valve and inner tracheostomy tube, and then insert a suction catheter to remove secretions that may be causing the block- age. If suction does not help, deflate the tracheostomy cuff so air can pass from the mouth into the lungs. Look, listen and feel for breathing and use waveform capnography to moni- tor end-tidal CO2. If the patient is not improving and is NOT in imminent danger, then a fibreoptic endoscope can be inserted into the tracheostomy to inspect for displacement or obstruction. If a single lumen tracheostomy is blocked and suction and cuff deflation does not provide adequate ventilation, remove the tracheostomy and insert a new tube of the same or smaller size whilst holding the stoma open with tracheal dilators. If you cannot insert a new trache- ostomy tube, insert a bougie into the stoma or railroad a tube over a fibreoptic endoscope to allow insertion under direct vision. If you are unable to unblock or change the tracheostomy tube, then perform bag-valve mask ventilation via the nose and mouth with a deflated tracheostomy cuff and cover stoma with gauze and tape to prevent air leak. If this does not work, then try to bag-valve-mask ventilate over the tracheostomy stoma after closing the patient’s mouth and nose. If the patient has normal anatomy (i.e. no airway obstruction from a tumour or infection), then think about oral intubation or bougie-guided stoma intubation. In contrast, laryngectomy patients have an end stoma and cannot be oxygenated by the mouth or nose unlike tracheostomy patients. If passing a suction catheter does not unblock a lar- yngectomy tube/stoma, then remove the laryngectomy tube from the stoma and look, listen and feel or apply waveform capnography to assess patency. If the stoma is not patent, apply a 2  Case 1: Respiratory distress in a tracheostomy patient paediatric facemask to the stoma and ventilate. A secondary attempt can be made to intubate the laryngectomy stoma with a small tracheostomy tube or cuffed endotracheal tube. A fibre- optic endoscope can be used to railroad the endotracheal tube in the correct position. Post-tracheostomy care should be conducted by an appropriately trained nurse or trained patient/carer and includes Humidified oxygen with regular suctioning Bedside spare tracheostomy tube, introducer and tracheal dilators Pen and paper for patient to communicate Tracheostomy change after 7 days to allow speaking valve application and formation of a stoma tract Patient and family education Key Points Indications for a tracheostomy include the following: weaning patients from pro- longed mechanical ventilation, emergency airway compromise, in preparation for major head and neck surgery and managing excess trachea–bronchial secretions When facing a tracheostomy patient in respiratory distress, think of the three C’s: 1. Cuff – Put the cuff down so the patient can breathe around it. 2. Cannula – Change the inner cannula. 3. Catheter – Insert a suction catheter into the tracheostomy. 3 http://taylorandfrancis.com  CASE 2: NUTRITION History A 54-year-old man has been admitted into the Intensive Care Unit with severe gallstone pancreatitis, complicated by acute kidney injury and acute respiratory distress syndrome (ARDS). He is currently intubated and ventilated, and requires haemofiltration. He will likely require a prolonged hospital admission. The intensive care consultant asks you to ‘take care of his nutrition’. Questions 1. What are the causes of nutritional disturbance? 2. How can nutrition be assessed? 3. What are the options for optimising nutrition? Name some complications. 5  100 Cases in Emergency Medicine and Critical Care DISCUSSION Nutrition is an important part of every patient’s care and should be optimised with the help of a dietician, in parallel with treating his or her underlying pathology. It should be assessed soon after admission as it is estimated that around a quarter of hospital inpatients are inade­ quately nourished. This may be due to increased nutritional requirements (e.g. in sepsis or post-operatively), nutritional losses (e.g. malabsorption, vomiting, diarrhoea) or reduced intake (e.g. sedated patients). Signs of malnutrition include a body mass index (BMI) under 20 kg/m2, dehydration, reduced tricep skin fold (fat) and indices such as reduced mid-arm circumference (lean muscle) or grip strength. Low serum albumin is sometimes quoted as a marker of malnutrition, but this is not an accurate marker in the early stages as it has a long half-life and may be affected by other factors including stress. The body’s predominant sources of energy are fat (approximately 9.3 kcal/g of energy), ­glucose (4.1 kcal/g) and protein (4.1 kcal/g). The recommended daily intake of protein is around 1 g/kg; nitrogen 0.15 g/kg; calories 30 kcal/kg/day. A patient’s basal energy expendi- ture is doubled in head injuries and burns. The major nutrient of the small bowel is amino acid glutamine, which improves the intestinal barrier thereby reducing microbe entry. The fatty acid butyrate is the major source of energy for cells of the large bowel (colonocytes). There are two options for nutrition, namely enteral (through the gut) and parenteral (intrave- nous). Enteral feeding can be administered by different routes including oral, nasogastric (NG) tube, nasojejunal (NJ) tube and percutaneous endoscopic gastrostomy (PEG)/jejunostomy (PEJ). Enteral nutrition is generally preferred to parenteral nutrition as it keeps the gut bar- rier healthy, reduces bacterial translocation and has less electrolyte and glucose disturbances. Feeding through the mouth is the ideal scenario as it is safe and provides adequate nutrition. Before abandoning oral intake, patients should be tested on semi-solid or puree diets and reassessed for risk of aspiration (e.g. in stroke). When comparing NG and NJ tube feeding, NG tubes are advantageous in terms of being larger in diameter and less likely to block, whereas NJ tubes are better if a patient is at risk of lung aspiration as they bypass the stomach. NJ tubes are also used in pancreatitis as they bypass the duodenum and pancreatic duct, which reduces pancreatic enzyme release that would have exacerbated pancreatic inflammation. NG/NJ feeds should be built up gradually, and if the patient experiences diarrhoea or distention, the feed can be slowed down. Patients on a feed should undergo initially daily blood tests for re-feeding syndrome, which causes deficiencies in potassium, phosphate and magnesium. Total parenteral nutrition (TPN) is composed of lipids (30% of calories), protein (20% of ­calories) and carbohydrates (50% of calories in the form of dextrose), as well as water, electro- lytes, vitamins and minerals. TPN is indicated in patients who have inadequate gastrointes- tinal absorption (short bowel syndrome), or where bowel rest is needed (e.g. gastrointestinal fistula or bowel obstruction). The disadvantage of TPN compared to enteral nutrition is that it is more expensive, contributes to gut atrophy if prolonged and exacerbates the acute phase response. Other complications of TPN include intravenous line infection or insertion com- plication, re-feeding syndrome, fatty liver, electrolyte and glucose imbalance and acalculous cholecystitis. 6  Case 2: Nutrition Key Points Nutrition should be optimised in all patients, in parallel with treating their underly- ing pathology. A dietician should be involved especially where critical care input or prolonged inpatient stay is predicted. There are two types of nutrition, enteral and parenteral. If it is safe and provides adequate nutrition, oral intake is the preferred option. NG/NJ/TPN feeding all have complications including re-feeding syndrome, which can cause hypophosphatemia, hypokalaemia and hypomagnesaemia. 7 http://taylorandfrancis.com  CASE 3: SHORTNESS OF BREATH AND PAINFUL SWALLOWING History A 48-year-old man presents with shortness of breath, painful swallowing and hoarseness. This is on a background of a worsening sore throat for the past 3 days. He has not been on antibiotics. The patient experiences sore throats several times per year, but never this severe. He does not have any other medical problems and does not take regular medications. He doesn’t smoke or drink alcohol, and he works in the supermarket, but has been off work since yesterday. Examination There is obvious inspiratory stridor heard from the end of the bed. The patient is sitting upright with an extended neck on the edge of the bed. He is drooling, sweating and strug- gling to speak. His vital signs are as follows: temperature of 38.8°C, respiratory rate of 28, oxygen saturation of 96% on room air, pulse of 107 beats per minute, blood pressure of 100/64 mmHg. He has bilateral non-tender cervical lymphadenopathy. His oropharynx demonstrates bilat- erally enlarged grade 3 tonsils with white exudate. There is pooled saliva in the oral cavity. Flexible fibreoptic naso-pharyngo-laryngoscopy demonstrates a normal nasal cavity and naso­­ pharynx. However, there is marked inflammation of the supraglottis including a cherry- coloured epiglottis and oedematous aryepiglottic folds. The vocal cords are not swollen and fully mobile. Questions 1. What is the diagnosis? 2. What investigations are appropriate? 3. How would you manage this patient? Which teams would you involve, and what is the major concern? 9  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient has supraglottitis. This is a life-threatening emergency with risk of upper airway obstruction. This is caused by an infection of the supraglottis, which is the upper part of the larynx, above the vocal cords, including the epiglottis. It is important to appreciate that halving the radius of the airway will increase its resistance by 16 times (Poiseuille’s equation), and hearing stridor means there is around 75% airway obstruction. Supraglottitis, which includes acute epiglottitis, is bimodal, with presentations most com- mon in children under 10 years old and adults between 40 and 50 years old. Classically the causative organism in children is Haemophilus influenzae type B, but since the advent of its vaccination, the incidence has reduced in children. The infection is now twice as com- mon in adults, even if they have been vaccinated. The most common organisms are now Group A Streptococcus, Staphylococcus aureus, Klebsiella pneumoniae and beta-haemolytic Streptococci. Viruses such as HSV-1 and fungi including candida are an important cause in immunocompromised patients. Sore throat and odynophagia occur in the majority of patients. Other signs include drooling, dysphonia, fever, dyspnoea and stridor. In adults, the disease has more of a gradual onset, with a background of sore throat for 1–2 days, whereas in children, the disease progresses more acutely. In children, the disease may be confused with croup (laryngotracheobronchitis). To distin- guish these clinically, epiglottitis tends to be associated with drooling, whereas croup has a predominant cough. Other diagnoses to consider in adults and children include tonsillitis, deep neck space infection, such as retro- or para-pharyngeal abscess, and foreign body in the upper aerodigestive tract. In adults, an advanced laryngeal cancer may also have a similar presentation. Investigations such as venepuncture and examination of the mouth should be deferred in children, as upsetting the child may precipitate airway obstruction. Adults are more toler- ant to investigations and should include an arterial blood gas, intravenous cannulation and drawing of blood for blood cultures, a full blood count and electrolyte testing. Radiographic imaging including x-rays should be avoided in the acute setting. The use of bedside naso- pharyngo-laryngoscopy allows direct visualization of the pathology. This patient should be initially assessed and managed in the resuscitation area by a senior emergency medicine doctor. After a quick assessment, prompt involvement of a multidisci- plinary team should take place. This should include a senior anaesthetist, ENT surgeon and intensive care doctors. Airway resuscitation and temporizing measures include the following: Sit upright. 15 L/min oxygen via a non-rebreather mask to keep oxygen saturations above 94%. Nebulised adrenaline (5 mL 1:1000) to reduce tissue oedema and inflammation. IV or intramuscular corticosteroids (e.g. 8 mg dexamethasone IV) to reduce tissue oedema and inflammation. Broad-spectrum IV antibiotics as per local microbiology guidelines (e.g. ceftriaxone and metronidazole) to combat the infective process. 10  Case 3: Shortness of breath and painful swallowing Ensure there is an emergency airway trolley at the bedside including a needle crico- thyroidotomy and surgical cricothyroidotomy set. If there is Heliox, ask for it (79% helium, 21% oxygen) as this has a lower density and higher laminar flow than air, which can buy time in an acute scenario. A joint anaesthetic–ENT airway assessment should take place in an area with access to emer- gency airway resuscitation equipment, ideally in the operating theatre. This should include fibreoptic flexible nasopharyngo-laryngoscopy. The patient should be warned of the possibil- ity of a tracheostomy and ideally sign a written consent form prior to any intervention. A discussion should take place between all members of the team to plan for possible com- plications. Best practice would be to have the ENT surgeon scrubbed and ready to perform an emergency tracheostomy while the anaesthetist attempts intubation either under direct vision or by video laryngoscopy/fibreoptic scopes. If this fails, an ENT surgeon may attempt rigid bronchoscopy, surgical cricothyroidotomy or tracheostomy. If intubation is likely to fail due to the amount of airway obstruction and poor visualization of the glottis, then a local anaesthetic tracheostomy should be performed. Management of epiglottitis in children differs. Oxygen or nebulisers may be wafted over their mouth, but IV antibiotics and steroids should be deferred if they may upset the child. The priority is to transfer the child, accompanied by a parent, to the operating theatre for assess- ment and management. Postoperatively, the patient should be managed in the intensive care unit with regular IV antibiotics and steroids. After around 48 hours, extubation may be attempted if there are signs of improvement. Daily assessment of the supraglottic area should take place with flex- ible nasendoscopy. Key Points Supraglottitis is a life-threatening airway emergency that usually presents with odynophagia, dysphonia and dyspnoea on the background of a sore throat. It can affect children and adults. Multidisciplinary management in the resuscitation area of the Emergency Depart­ ment or in theatres is required. The team should include an emergency physician, anaesthetist, ENT surgeon and an intensivist. Emergency airway management prior to definitive control by endotracheal intu- bation or tracheostomy should include 15 L/min oxygen through non-rebreather mask, nebulised adrenaline, intravenous steroids and broad-spectrum antibiotics. 11 http://taylorandfrancis.com  CASE 4: COLLAPSE WHILE HIKING History A 55-year-old man is brought to the Emergency Department after collapsing while hiking with his son. Bystander CPR was performed for 5 minutes before the paramedics arrived and continued resuscitation. The rhythm was ventricular fibrillation (VF), and a total of 8 shocks were delivered before return of spontaneous circulation. He has a history of hypertension and type 2 diabetes, controlled with medications. He is a smoker, but there is no family history of sudden cardiac death. Examination Vital signs: temperature of 37.5°C, blood pressure of 105/55, heart rate of 95 and regular. He is intubated, ventilated and sedated with fentanyl and propofol. Physical examination is notable for normal heart sounds and bilateral breath sounds. GCS is 3/15. Investigations Hb 14.6, WCC 15.3, PLT 275, Cr 95. Arterial blood gas: pH 7.15 pO2 22.5, pCO2 4, HCO3 20, lactate 7.5. A chest radiograph shows appropriate positioning of the endotracheal tube. An ECG shows Q waves in the anterior leads. Questions 1. Describe the general principles of post-resuscitation care. Should therapeutic hypo- thermia be initiated? 2. Is there any role for coronary revascularisation (i.e. angiography) in this patient? 3. How can this patient’s prognosis be assessed? 13  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient presents with an out of hospital cardiac arrest (OHCA) with successful resus- citation after a relatively prolonged period. The main aims of management in OHCA are to minimise secondary neurologic injury, to appropriately support cardiac function and to look for a cause. Post-resuscitation care should proceed along an ‘ABCDE’ approach, and since most patients will have a low Glasgow Coma Score, the airway should be protected with intubation and mechanical ventilation as has occurred in this case. In addition to assessing for signs of cir- culatory shock (cool peripheries, mottled skin), it is also important to look for signs that are suggestive of the underlying cause (e.g. heart murmur, rigid abdomen). A basic neurologic assessment to calculate the GCS pre-intubation is necessary as this correlates with neurologic outcomes and provides a baseline for future comparison. Key initial investigations that should be performed include an electrocardiogram (to look for cardiac ischaemia), bedside ultrasonography (looking for pulmonary embolism, assess for ventricular function, fluid status or abdominal aortic aneurysm) and a chest radiograph. Additional blood tests, including an arterial blood gas and renal function, are important as they may point towards the underlying cause. D-dimer and troponin will often be elevated and need careful evaluation in the clinical context. Current recommendations state that patients with shockable OHCA should be cooled to pre- vent secondary brain injury. This is termed therapeutic hypothermia. It is suggested that patients with non-shockable OHCA are cooled too. Core body temperature should be low- ered to between 32 and 36°C by removing clothes and infusing cooled saline or by using external cooling jackets. The aim is to reduce secondary brain injury by decreasing cellular metabolism. The role for coronary angiography in OHCA has not been completely defined, and there is variation in practice across treatment centres. Emergent coronary angiography is indicated in patients with ECG findings of ST elevation myocardial infarction (i.e. ST elevation, new left bundle branch block) and is typically performed urgently in patients in whom a cardiac cause is suspected. In this patient, given the presence of a VF arrest and anterior Q-waves on the electrocardiogram, you should liaise with the local cardiology service. In large cities, patients may be taken directly to cardiology centres bypassing the ED in patients with a VF/ VT arrest and return of spontaneous circulation (ROSC). After successful resuscitation from an OHCA, only 10% of patients will survive to discharge, and many of these individuals will have significant neurologic disability. Prognostication is difficult, but negative prognostic factors include delayed initiation of CPR, PEA or asys- tolic arrests, older age and persistent coma. Absent corneal or pupillary reflexes at 24 hours, absent visual evoked potentials and elevated serum neuron-specific enolase (NSE) are poor prognostic markers. 14  Case 4: Collapse while hiking Key Points Out of hospital cardiac arrest is an important and common cause of mortality in developed countries. Post-resuscitation care should proceed in an ‘ABCDE’ manner, with the aim to minimise brain injury and support cardiac function. Therapeutic hypothermia is recommended for all patients with a shockable OHCA and suggested for non-shockable cases. Coronary angiography and reperfusion therapy should be considered in those patients thought to have an underlying cardiac cause. Prognosis after out of hospital cardiac arrest is generally poor. 15 http://taylorandfrancis.com  CASE 5: FEVER, HEADACHE AND A RASH History A 20-year-old student is brought to the Emergency Department after his room-mate noticed that he did not attend a class tutorial and found him in a semi-conscious state. He had been feeling generally unwell for the past 2–3 days after fresher’s week and complained of a head- ache. He has no other past medical history and only takes anti-histamines as needed for hayfever. Examination Vital signs: temperature of 39.4°C, heart rate of 100 and regular, blood pressure of 95/60, respiratory rate of 16, 95% O2 saturation on air. Physical examination reveals a pale man who intermittently follows commands. GCS is 12/15 (Eyes 3, Verbal 4, Motor 5). There is a purpuric rash on his arms and legs, and bleeding from his gums. Neurologic examination is notable for neck stiffness. Cardiorespiratory examina- tion is unremarkable. Questions 1. What is the diagnosis, and what complication is the patient likely suffering from? 2. What investigations need to be performed immediately? 3. What empiric treatment should the patient receive in the Emergency Department? 17  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient presents with fever, reduced level of consciousness and evidence of meningism on examination, which are classic for bacterial meningitis. This is a condition that is fatal unless promptly recognised and treated. The two most common pathogens causing bacte- rial meningitis are Streptococcus pneumoniae and Neisseria meningitidis. In this patient, the latter is the likely cause due to the presence of the petechial rash seen with meningococcal disease; additionally, bleeding from the gums suggests disseminated intravascular coagula- tion (DIC), which is associated with meningococcal sepsis. Meningococcal meningitis has a high mortality, with 10%–15% of patients dying of the dis- ease despite appropriate therapy. Therefore, the role of the Emergency Department physi- cian is crucial in initiating treatment. Sick patients should be assessed and treated along the standard ‘ABCDE’ approach, and antibiotics given early after drawing baseline blood tests and blood cultures. Ceftriaxone and vancomycin will provide broad spectrum cover and are first-line empiric therapy. If the diagnosis is uncertain and encephalitis is suspected, add an antiviral agent (i.e. aciclovir). Aside from antibiotics, good supportive care with intravenous fluid and vasopressors as well as supplemental titrated oxygen is key. There is no specific treatment for DIC except treating the underlying infection, although there is limited evidence that protein C concentrate may improve coagulopathy but not mortality. Dexamethasone has been shown to be beneficial in pneumococcal meningitis by reducing neurological complications but has no clear benefit in meningococcal infection. A lumbar puncture should be performed after a CT head. CSF fluid analysis may show organ- isms such as Gram-negative diplococci (Neisseria meningitidis), and the white cell count will be elevated (neutrophilic predominance) together with elevated CSF protein and low CSF glucose. PCR studies may be performed to give a rapid diagnosis of the causative organism. Another key aspect of managing this patient involves gathering a history of contact exposure as antibiotic prophylaxis is required in close contacts (‘kissing contacts’). Anyone with pro- longed (i.e. >8 hours) and close contact with the patient as well as those directly exposed to the patient’s oral secretions will need chemoprophylaxis. The choice of agent may vary according to local guidelines, but a single dose of either ciprofloxacin, rifampicin or ceftriaxone is com- monly used. The public health department will need to be informed in confirmed meningitis cases as it is a ‘notifiable’ disease and can help with contact tracing and prophylaxis. Key Points Patients presenting a fever and headache should be considered at risk for meningitis. Meningococcal meningitis is a rapidly fatal disease and must be recognised and treated promptly. Empiric antibiotic therapy for suspected meningitis comprises of ceftriaxone and vancomycin, and blood and cerebrospinal fluid cultures should be obtained to help tailor therapy towards the pathogen. The public health department must be contacted as this is a ‘notifiable’ disease. 18  CASE 6: NAUSEA AND VOMITING IN A DIABETIC History A 27-year-old man presents to the Emergency Department with a 1-day history of nausea, vomiting and feeling generally unwell. He reports pain over his right lower leg and some red- ness overlying the area. He has a history of type 1 diabetes and is on a ‘basal-bolus’ regime comprising of daily glargine and mealtime novorapid. He does not check his blood sugars frequently and does not recall when he last took insulin. Examination Vital signs: temperature of 37.6°C, blood pressure of 90/60, heart rate of 100 and regular, respiratory rate of 24, 96% O2 saturation on air. His peripheries are cool and capillary refill time is 2 s; JVP is not visible and mucous mem- branes are dry. Cardiorespiratory examination is unremarkable and abdominal palpation reveals generalised tenderness. There is an erythematous area on his right shin with associ- ated warmth and tenderness to touch. Neurologic examination is normal. Investigations Hb 15.6, WCC 16.7 (neutrophils 13.5), PLT 210, Na 132, K 3.4, Cl 98, Ur 11.5, Cr 80. Venous blood gas shows: pH 7.15, pO2 12.4, pCO2 4.1, HCO3 16, glucose 28, lactate 4.7. Questions 1. What is the diagnosis, and the likely precipitating factor in this case? 2. What further investigations should be performed in the Emergency Department? 3. What are the initial steps in the management of this patient? How should the patient be monitored? 19  100 Cases in Emergency Medicine and Critical Care DISCUSSION The most important diagnosis to exclude in any patient with type 1 diabetes who is unwell is diabetic ketoacidosis (DKA), whereby insulin deficiency leads to impaired glucose utilisation by cells and the production of ketone bodies leading to a metabolic acidosis. DKA usually develops over a 24-hour period, and the symptoms seen in this patient (nausea and vomit- ing) are a common manifestation. Additionally, the elevated respiratory rate seen is likely a compensatory response to metabolic acidosis (Kussmaul breathing). Common precipitating factors in DKA include infection, lack of compliance with insulin therapy and intercurrent illness. Infection and acute illness promote a stress response with production of counter- regulatory hormones (e.g. glucagon, adrenaline) and lead to relative insulin deficiency. In this case, the patient appears to be suffering from a concurrent right leg cellulitis. The initial evaluation of DKA includes measuring electrolytes, serum glucose and a venous blood gas. Additionally, urinalysis should be performed to look for urine ketones – many centres can also measure serum ketones to confirm the diagnosis. An electrocardiogram should be performed given the presence of mild hypokalaemia in this patient. Further investigations should be directed at identifying the potential precipitating cause (e.g. chest radiograph and urine culture, swab of any purulent material expressed from the leg). It would also be reasonable to check an HbA1C if none has been performed recently to deter- mine glycaemic control. DKA is a medical emergency and carries a low, but not insignificant, mortality risk. Initial assessment and management should follow the standard ‘ABCDE’ approach. The first step in treating DKA is to replace the fluid deficit, which can be up to several litres. This patient shows signs of hypovolaemic shock and therefore 1 L boluses of isotonic fluid (0.9% saline) should be given with monitoring of haemodynamic response. Once his blood pressure improves and tachycardia settles, fluid replacement should continue as per local protocol, normally as a reducing regime of intravenous fluid. Potassium replacement is required given that insu- lin therapy will lead to intracellular movement of potassium out of the vascular space, with 20–30 mmol added to each litre of saline administered. Intravenous insulin (actrapid) is the second major component of DKA treatment and serves to turn off the ketogenic switch. It should be commenced at a fixed rate of 0.1 units/kg/hour, equating to 7 units/hour in a 70 kg individual. Adjunctive therapy in DKA includes admin- istration of bicarbonate (typically only if pH < 6.9), although there is limited evidence for its benefit, as well as treatment of the underlying cause (e.g. antibiotics for cellulitis). Once initial treatment is begun, patients require careful monitoring, ideally in a high depen- dency care setting. The rate of fluid administration needs to be tailored according to haemo- dynamic parameters, and serum glucose and potassium should be checked frequently (hourly to begin with). Once glucose falls to below 10–12 mmol/L, the rate of the insulin infusion may be reduced, although each hospital may have its own protocol. Venous (or arterial) pH should also be checked regularly together with urine or serum ketones, as the resolution of ketoacidosis is an indicator that subcutaneous insulin can be commenced, providing the patient can eat, with overlap of intravenous insulin for 1–2 hours. Patients with a low GCS and who do not show immediate improvement with initial resuscita- tion should have a CT scan of the head to look for cerebral oedema. They may need intubation to protect their airway and for ventilatory control prior to scan. Cerebral oedema is more 20  Case 6: Nausea and vomiting in a diabetic commonly seen in children but may also occur in adults. The aetiology is not clear but it may be related to severely acidotic states and fluid shifts associated with rehydration. Key Points Always consider diabetic ketoacidosis (DKA) in any diabetic patient who is unwell. Check serum electrolytes, glucose, urine ketones and serum ketones, as well as a venous blood gas in patients with suspected DKA. Fluid replacement, potassium repletion and intravenous insulin are the mainstays of the early management of DKA. 21 http://taylorandfrancis.com  CASE 7: STUNG BY A BEE History A 17-year-old man is brought to the Emergency Department by his mother after he was stung by an insect. He had been playing football at the local park when his mother thought she saw a bee near his leg. He is feeling nauseous and reports a rash on his leg that is spreading to the rest of his body. He complains that his throat feels itchy and feels like he is having palpita- tions. He has a history of asthma. Examination Vital signs: temperature of 36.8°C, blood pressure of 85/60, heart rate of 110 and regular, respiratory rate of 24, 95% O2 saturation on air. General examination reveals a blotchy, erythematous rash on his right leg that is spreading upwards towards his trunk, as well as swelling of his lips and tongue. Cardiac examination is unremarkable, and auscultation of the chest is notable for mild expiratory wheeze. Questions 1. What is the diagnosis? Briefly describe its pathophysiology. 2. How would you manage the patient? 3. Assuming he responds appropriately to treatment, does the patient need to be admitted? Is any follow-up required? 23  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient is suffering from anaphylaxis, which is an acute-onset potentially life-threatening allergic or hypersensitivity reaction. The diagnosis of anaphylaxis can be made when any one of the following is present: i. Acute onset illness that involves the skin and/or mucosa, with either respiratory compromise or hypotension ii. Two or more of the following that occur quickly after exposure to a known allergen for a patient: involvement of the skin/mucosa, hypotension, respiratory compromise or persistent gastrointestinal symptoms iii. Hypotension after exposure to a known allergen for a patient (defined as systolic BP 94% and large- bore intravenous cannulae placed, along with initiation of a fluid bolus. The most important treatment in anaphylaxis is adrenaline. The normal dose is 0.5 mg (0.5 mL of 1:1000 solution) in adults, and it is usually administered intramuscularly into the outer thigh. The dose may be repeated at an interval of 3–5 minutes should there be no response. Adjunctive treatments include bronchodilators (salbutamol 5 mg nebulised), anti-histamines (chlorpheniramine 10 mg IV) and steroids (hydrocortisone 200 mg IV), as well as fluid boluses titrated to blood pressure. In non-responders, intravenous adrenaline may be given in 50 μg boluses, but this should only be given by senior ED, anaesthetic or intensive care physicians due to the danger of precipitating cardiac ischaemia. Take care to remove the sus- pected source of anaphylaxis if possible such as a retained insect sting as in this case or other potential sources like colloid solution or blood products. Anyone who has had a severe reaction or required multiple doses of adrenaline should be admitted for observation for a biphasic reaction. Those with a single dose of adrenaline may be discharged after 6 hours if they are symptom free. At discharge, patients should be pre- scribed an adrenaline auto-injector (‘Epipen’, usual dose 0.3 mg) and consider once daily oral prednisolone for up to 3 days. Follow-up should also be arranged with an allergy specialist, who may arrange further testing to identify the allergen and initiate preventive therapy. UK guidelines suggest mast cell tryptase should be measured on arrival and subsequent sam- ples at 2 and 12 hours. It may be particularly helpful when patients suffer from an allergic reaction in unusual circumstances (e.g. when under general anaesthetic) or to confirm the diagnosis when features are atypical such as isolated angioedema. Blood testing should not, however, delay treatment, which should be based on clinical grounds. 24  Case 7: Stung by a bee Key Points Always think of anaphylaxis when seeing patients with skin/mucosal symptoms, respiratory difficulty and/or hypotension, especially after exposure to a potential allergen. Adrenaline 0.5 mg IM is the first-line treatment. Any patient with an anaphylactic reaction must at least be observed for several hours in case of biphasic reaction, and any patient with a severe reaction should be admitted. 25 http://taylorandfrancis.com  CASE 8: A BAD CHEST INFECTION History A 55-year-old man presents with a 3-day history of a productive cough and shortness of breath. He has a history of chronic obstructive pulmonary disease (COPD) with frequent exacerbations but no previous intensive care admissions. He is a current smoker and type 2 diabetic, and takes inhaled tiotropium and subcutaneous glargine daily. Examination Vital signs: weight of 90 kg, temperature of 38.5°C, blood pressure of 85/50, heart rate of 105 and regular, respiratory rate of 25, 94% O2 saturation on 4 L/min. Physical examination is notable for coarse crackles and bronchial breathing at the right lower lung fields. Investigations Hb 16, WCC 18.5 (neutrophils 15), PLT 200, Ur 8, Cr 135, lactate 3.5. Blood and sputum cultures are pending. A chest radiograph shows opacification of the right base. He is given a 500 mL fluid bolus, a urinary catheter is inserted and empiric broad- spectrum antibiotics (vancomycin and piperacillin-tazobactam) are commenced. He is transferred to the Intensive Care Unit (ICU) for further management, where a central line and arterial line are placed. Questions 1. What would be the initial goals of therapy in the ICU in the first few hours of admis- sion, and what parameters should be monitored to assess response to treatment? 2. After 6 hours, he has received 6 L of intravenous fluid and his blood pressure remains 85/50, urine output is 30 mL/hour and lactate has increased to 4.5. What is the term given to this condition, and outline of the next steps in management? 3. How should his diabetes be managed while he is critically ill? 27  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient presents with symptoms and signs suggestive of sepsis, likely arising from a chest infection. He is febrile, hypotensive, tachycardic and hypoxic, and has an elevated white blood cell count and lactate, all indicators of a dysregulated inflammatory reaction to infec- tion which defines a sepsis syndrome. The initial resuscitation provided to the patient is appropriate and is discussed fully in another case (‘Dysuria and weakness’, Case 18, page 63). The goal of initial resuscitation is to restore perfusion and prevent or limit organ dysfunction. The term ‘early goal-directed therapy’ (EGDT) refers to the administration of intravenous fluid within the first 6 hours of presentation that uses various physiologic targets to direct fluid management. These targets or goals include i. Mean arterial blood pressure (MAP) ≥65 mmHg ii. Urine output ≥0.5 mL/kg/hour iii. Central venous pressure (CVP) of 8–12 mmHg iv. Central venous oxyhaemoglobin saturation (ScvO2) ≥70% v. Clearance of lactate While randomised evidence on the benefit of using such targets in a protocol-based man- ner is conflicting, it is standard practice in most centres. In particular, targeting CVP 8–12 mmHg, MAP ≥65 mmHg and urine output ≥0.5 mL/kg/hour are commonly used in the ICU setting, and achieved via the administration of fluid boluses with continuous mea- surement of these parameters to ensure that the rate of fluid administration can be adjusted accordingly. In this case, reassessment after 6 hours reveals that the patient’s MAP is 62 mmHg, urine out- put is 10 mmol/L) is associated with poor outcomes and may arise due to the stress response to infection or as a result of coexisting diabetes. In these circumstances, a continuous insulin infusion or intermittent short-acting insulin (e.g. actrapid) is used as they can be adjusted easily and reduce the risk of hypoglycaemia. Generally, a blood glucose target of 7.5–10 mmol/L is used to titrate the insulin infusion rate, as intensive insulin therapy increases the risk of hypoglycaemia, which may lead to increased mortality. 28  Case 8: A bad chest infection Key Points Early goal-directed therapy utilises various physiologic parameters, including MAP ≥65 mmHg and urine output ≥0.5 mL/kg/hour, to guide fluid management within the first 6 hours of a diagnosis of sepsis. Septic shock, which is defined by refractory hypotension despite adequate fluid administration, requires the use of vasopressor and inotropic agents such as nor- adrenaline to maintain perfusion. Hyperglycaemia is common in critical illness, particularly in diabetic patients, and is usually managed with a continuous insulin infusion to maintain a blood glucose target of 7.5–10 mmol/L. 29 http://taylorandfrancis.com  CASE 9: HEAD-ON MOTOR VEHICLE COLLISION History A 35-year-old male is brought in by ambulance. He was the driver of a vehicle involved in a head-on collision with another vehicle. Both vehicles were travelling at 50 miles per hour and the patient was restrained by a seatbelt. On arrival to the resuscitation area of the Emergency Department, he is confused and disori- entated, unable to confirm his name or age. He is tachypnoeic with a respiratory rate of 32, 97% O2 saturation on 15 L/min oxygen via a non-rebreather mask, heart rate of 130, blood pressure of 91/49 and temperature of 35.8°C. In the ambulance, he received 1 L of 0.9% normal saline and 1 unit of Group O Rhesus- negative packed red cells. Despite this, his respiratory rate, heart rate and level of confusion have worsened. Examination He is maintaining his airway and is working hard to breathe, with an obvious strap mark on his chest secondary to his seatbelt. His chest expansion is symmetrical with reduced breath sounds in the bases of both lungs. His heart sounds are muffled with marked engorgement of the external jugular veins in the neck. The remainder of his examination is unremarkable with no injury to the head, spine, abdomen or limbs. A portable chest radiograph shows a possible widened mediastinum, increased cardiac shadow and numerous bilateral rib fractures. The lung fields are opacified bilaterally. The patient’s vital signs improve slightly but remain unstable. The patient is taken to theatre for an emergency thoracotomy. Questions 1. What is the underlying diagnosis? 2. Define shock. What are its signs? 3. How do you manage shock in the haemorrhaging patient? 31  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient has sustained blunt trauma that has caused cardiac tamponade, bilateral hae- mothoraces and hypovolaemic shock. Shock refers to inadequate organ perfusion and tissue oxygenation. The commonest cause in an injured patient is hypovolaemic shock due to blood loss, but other causes include cardiogenic shock due to myocardial dysfunction, neurogenic shock due to sympathetic dysfunction or obstructive shock due to obstruction of the great vessels or heart. It is easy to recognise shock if you think about the results of inadequate organ perfusion. Early signs include tachycardia, which is the body’s way of attempting to preserve cardiac reserve and cool peripheries or reduced capillary refill time due to peripheral vasocon- striction. This is caused by catecholamine and vasoactive hormone release, which result in increased diastolic blood pressure and reduced pulse pressure. For this reason, measuring pulse pressure rather than systolic blood pressure allows earlier detection of hypovolaemic shock, as the body can lose up to 30% of its blood volume before a drop in systolic blood pressure is appreciated. Brain hypoperfusion initially causes anxiety and later confusion. In summary, tachycardia, cool skin and reduced pulse pressure are early signs of shock until proven otherwise. It is important to realise that large volumes of blood loss may only cause a minimal drop in haemoglobin or haematocrit levels in the acute setting. More commonly, you will see an elevated lactate level and negative base excess on the venous blood gas, which corresponds to vasoconstriction and cellular hypoxia. Do not wait for a trauma patient to develop hypo- tension before starting fluid replacement therapy. The goal is to maintain organ perfusion and tissue oxygenation. Start with a crystalloid fluid bolus of 20 mL/kg for children or 1 L in adults. Ensure the crystalloid fluid is warmed in order to prevent hypothermia. In those who have sustained significant blood loss, consider early transfusion of packed red cells and activation of the major haemorrhage protocol. Current trauma guidelines suggest that a degree of hypotension may be tolerated in certain circumstances. This is termed ‘balanced resuscitation’ or ‘permissive hypotension’. The prin- ciple behind this is to stabilise any clots that may have formed as these as thought to be the most stable. Aggressive blood pressure rises may risk disrupting the ‘first clot’ and exacerbate blood loss. This is still a developing field and local guidelines should be followed. In any hypotensive trauma patient, seek senior help early to help guide management as decisions can be complex and experience in this setting is an asset. To assess response to fluid resuscitation, monitor level of consciousness, improvement in tachycardia and skin temperature or capillary refill time (as mentioned earlier, these are good early signs of shock). Urine output measurement is also a useful marker (>0.5 mL/kg/hour for adults). The response to initial fluid resuscitation is key to determining subsequent management. Three possibilities exist: 1. The haemodynamically normal patient with adequate tissue oxygenation and nor- mal vital signs after fluid resuscitation. This patient is a rapid responder to fluid therapy and likely lost 10%–20% of their blood volume. 2. The haemodynamically stable patient with improved but persistently abnormal vital signs (tachycardia and oliguria) following fluid therapy. This patient is under- resuscitated and has transiently responded to fluids. Their tissue oxygenation may 32  Case 9: Head-on motor vehicle collision respond to further fluid therapy, but if it does not, they will require definitive surgi- cal management. They have likely lost 20%–40% of their blood volume and may lose more. 3. The haemodynamically unstable patient who continues to deteriorate despite aggressive fluid resuscitation. In this scenario, emergency surgical management as well as ongoing blood replacement may be required. Depending on the urgency of the blood transfusion, the following products are available. Type O Rhesus negative packed red cells are used for the exsanguinating patient, where there is no time to wait for cross-matching. Type-specific blood compatible with ABO and Rhesus blood types takes 10–20 minutes to obtain from the laboratory and is useful for transient responders. Fully cross-matched blood is the most preferable product and takes around 1 hour to obtain from the laboratory. Aside from administering a blood transfusion (packed red cells), do not neglect transfus- ing the patient with platelets, fresh frozen plasma and cryoprecipitate. Large volume blood loss consumes coagulation factors and precipitates a coagulopathy in around 30% of severely injured patients. Within 1 hour of presentation, ensure a full clotting screen has performed to allow early detection of these. The focus of treatment is to identify and treat the cause of bleeding. Adjuncts in the trauma setting include focused assessment sonography in trauma (FAST), as well as radiographic imaging of the chest, pelvis and long bones of the limbs. It is now accepted practice to per- form CT scanning from the head to the thigh in a major trauma scenario. This is a fast and accurate way of detecting life-threatening injuries, allowing appropriate medical and surgi- cal intervention. Ensure that the patient is haemodynamically stable before transfer to the CT scanner as transfer times may be prolonged and deterioration whilst en route or in the scanner is difficult to deal with. Key Points Shock refers to inadequate organ perfusion and tissue oxygenation. Its signs include tachycardia, reduced pulse pressure and cool peripheries. Management of hypovolaemic shock should include warm crystalloid fluid resus- citation with early consideration of a blood transfusion to restore the oxygen- carrying capacity of the intravascular volume. The cause of the hypovolaemic shock should be identified and addressed whilst resuscitation is ongoing. Ultrasonography, radiographs and CT scanning can be considered if the patient is stable enough. 33 http://taylorandfrancis.com  CASE 10: INTRAVENOUS FLUID RESUSCITATION History A 48-year-old male was the driver in a head-on collision between two cars travelling at 45 miles per hour. He has an open tibial fracture and a distended and bruised abdomen. During the pri- mary survey in the Emergency Department, it is noted that he is hypotensive and tachycardic. A decision is made to initiate fluid resuscitation. Questions 1. What is the content of 0.9% saline and Hartmann’s solution? 2. How is water distributed in the body? 3. How is 1 L of crystalloid fluid distributed in the body? How is 1 L of 5% dextrose solution distributed in the body? How is 1 L of blood distributed in the body? 35  100 Cases in Emergency Medicine and Critical Care DISCUSSION Intravenous fluids can be divided into crystalloids and colloids. Crystalloids are made up of water-soluble molecules (e.g. saline solution, Hartmann’s solution). Colloid fluids contain insoluble molecules (e.g. Gelofusin, which contains gelatin). Saline solution (0.9% sodium chloride) contains both sodium (154 mmol/L) and chloride (154 mmol/L). Hartmann’s solution contains the following: sodium 131 mmol/L, chloride 111 mmol/L, potassium 5 mmol/L, calcium 2 mmol/L and bicarbonate 29 mmol/L (which is sup- plied in the form of lactate, which is then metabolised to bicarbonate). Sixty percent percent of the human body mass is composed of water, of which two-thirds lies in the intracellular compartment and one-third lies in the extracellular compartment. The extracellular compartment is further subdivided into interstitial fluid (75%) and intravascu- lar fluid (25%). Thus, a 70 kg human will have 42 L of total body water (60% of mass), of which 28 L (two-thirds) is intracellular and 14 L (one-third) is extracellular. Of the extracellular water, 10.5 L (75%) is interstitial and 3.5 L (25%) is intravascular fluid. To calculate what volume of 1 L of crystalloid such as saline 0.9% or Hartmann’s solu­ tion enters the intravascular space, the above principles apply. The sodium content of both of these fluids is similar to plasma, which means the entire 1 L of fluid will be distrib- uted amongst the extracellular compartment. Thus, 750 mL (75%) will be interstitial, and 250 mL (25%) will be intravascular. Five percent of dextrose or glucose solutions are distrib- uted relative to total body water, so that 666.6 mL is intracellular and 333.3 mL is extracel- lular. Of the extracellular fluid, 250 mL is interstitial and 83.3 mL is intravascular. Of note, when administering a blood transfusion, all of the content is distributed in the intravascular space, making it ideal for hypotensive resuscitation. The disadvantage of using colloids such as Gelofusin is that they contain insoluble pro- teins that can cause bleeding disorders, interfere with blood cross-matching and may lead to anaphylaxis. Although colloids provide more initial intravascular expansion, it is now accepted that there is no significant difference in reducing mortality when using crystalloids or colloids for fluid resuscitation. This was demonstrated in the Saline versus Albumin Fluid Evaluation (SAFE) Study (2004), which showed that albumin (colloid) and saline (crystalloid) should be considered clinically equivalent treatments for intravascular volume resuscitation in a heterogeneous population of patients in the Intensive Care Unit. Further studies on fluid resuscitation of patients with traumatic brain injury have shown that colloids are associated with a higher mortality than crystalloids. Key Points When resuscitating a hypotensive patient, using 1 L of crystalloid will equate to 250 mL of intravascular fluid; using 1 L of dextrose 5% will equate to less than 100 mL of intravascular fluid; and using 1 L of blood will equate to 1 L of intravascular fluid. Advanced Trauma Life Support (ATLS) guidelines and the SAFE study recommend crystalloid instead of colloid fluid resuscitation. Crystalloids are cheaper and do not exhibit the same disadvantages (blood clotting disorders and anaphylaxis) as colloids. 36  CASE 11: FOUND UNCONSCIOUS IN A HOUSE FIRE History A 48-year-old man is brought into the Emergency Department resuscitation area. He was found unconscious in a burning house. The mechanism of the fire and duration of exposure are unknown. Examination Assessment reveals a singeing of the nasal hairs, carbon-stained saliva, oropharyngeal oedema and extensive deep partial thickness burns to the face and neck and full thickness burns to the chest and upper limbs. His oxygen saturation is 88% on air, with a respiratory rate of 22 with limited chest expansion, pulse of 107, blood pressure – no reading obtainable. Questions 1. How do you classify thermal burns? 2. How would you manage this patient? 3. What are the concerns when it comes to electrical burns? 37  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient has severe thermal burns and is at high risk of complications of smoke inhala- tion. These include airway obstruction, restrictive chest expansion, carbon monoxide poi- soning, hypovolaemic shock (as burns cause increased capillary permeability and loss of intravascular fluid), compartment syndrome and rhabdomyolysis. First-degree burns affect the epidermis and are equivalent to sunburn. They heal without scarring. Partial thickness burns are classified into superficial (affecting the papillary dermis) and deep (affecting the reticular dermis). Superficial partial thickness burns are pink, painful and blanch. They are generally wet and hypersensitive even to air current. They form blisters but do not scar and take around 2 weeks to heal. Deep partial thickness burns are painless and insensate, and do not blanch. They have fixed staining due to capillary thrombosis and take 4–6 weeks to heal because there is a smaller concentration of pilosebaceous glands from which epidermal cells originate. Tetanus prophylaxis should be considered in all burns patients. Superficial and deep thick- ness partial burns are treated with agents that chemically debride non-viable tissue, have antibacterial properties and moisture the tissue. The wound should be kept clean and undergo regular review by specialist nurses and plastic surgeons. Full thickness burns can appear white or black and are painless. They affect layers deeper than the dermis and require debridement and superficial thickness skin grafting (autograft down to the dermal layer). Generally, burns patients are not given prophylactic systemic antibiotics but benefit more from topical antibiotics, as eschar that contains bacteria is avascular. Other complications to look out for in burns patients include pneumonia, electrolyte (hyperkalaemia) disturbances, acute kidney injury and acute stress gastric ulcers (Curling’s ulcer). Burns management begins with airway assessment and definitive securement. Look for signs of smoke inhalation such as oropharyngeal oedema or carbon deposits, voice changes, singeing of the eyebrows or nasal hairs as well as obvious burns to the face, neck and chest. Bronchoscopy is the gold standard diagnostic method to evaluate the effect of smoke inhala- tion on the lungs. Respiratory failure can occur from physical airway obstruction due to pha- ryngeal oedema and carbon monoxide poisoning, which may manifest as nausea, headache or confusion. If there is no spinal injury, keep the patient elevated at 30 degrees to reduce head and neck oedema. All patients with burns should be administered with 15 L/min of oxy- gen through a non-rebreather mask with consideration of early orotracheal intubation. High concentration oxygen speeds up the dissociation of carbon monoxide with haemoglobin. Usually, the carbon monoxide–haemoglobin (carboxyhaemoglobin, HbCO) compound’s half-life is around 4 hours on room air, but this is reduced to less than 1 hour with supple- mentary high concentration oxygen. A carboxyhaemoglobin level >60% is associated with very high mortality rates. Obtain baseline arterial blood gas (ABG) analysis and carboxyhae- moglobin levels; do not be reassured by a normal PaO2 on an ABG as this is not an accurate predictor of carbon monoxide poisoning. A baseline chest radiograph is also important to track changes in pulmonary function with time. If there are circumferential burns to the chest that restrict the chest wall movement, an emergency chest wall escharotomy may be indicated. Burn severity is based on the depth of the burn and the total body surface area (BSA). In adults, the BSA can be estimated using the ‘rule of nines’ or by using the palmar surface including the fingers of a patient’s hand to represent approximately 1% of the BSA. Knowing this is important when it comes to fluid resuscitation. 38  Case 11: Found unconscious in a house fire The initial fluid resuscitation for burns patients is extremely important to counter hypovo- laemic shock. It is permissible to place an intravenous cannula through burnt skin, and this is often necessary in extensive injuries. Formulas differ between centres, but the Brooke and Parkland formulae are the commonest. The Brooke formula uses 2 mL and the Parkland formula 4 mL in the equation below: total fluid in 24 hours = 2 – 4 mL × weight (kg) × total burn surface area (%) Half of the fluid is given in the first 8 hours from the time of the injury (not the time of pre- sentation to the ED) and the other half over the remaining 16 hours. The choice of fluid is generally Hartmann’s solution. For example, a 70 kg man with 30% total BSA burns requires (2 to 4) × 70 × 30 = 4200 – 8400 mL of Hartmann’s over 24 hours. The patient’s hourly urinary output should be kept above 0.5 mL/kg/hour for adults, with fluid rate adjusted accordingly. Blood pressure and pulse readings are sometimes difficult to record due to the burns, so urine output becomes an accurate measure of response to fluid resuscitation. There should be a low threshold for considering myoglobinuria or rhabdomyolysis, which also requires aggressive fluid resuscitation and/or sodium bicarbonate infusion. Alkali burns are more harmful than acidic. They have a longer lasting effect because the body cannot buffer alkali. Electrical burns cause more destruction than the external burn may suggest. They are associated with internal destruction, as the path of least resistance is nerves and blood vessels. They can also cause arrhythmias and an electrocardiogram should be performed. Key Points Early high concentration oxygen administration helps to prevent and treat hypoxia and carbon monoxide poisoning. Early definitive management of the patient’s airway (with orotracheal intubation if necessary) is crucial if there are signs of burns in the nose, oropharynx, face or neck. Airway compromise can rapidly develop in these patients. Aggressive fluid resuscitation helps to prevent and treat hypovolaemic shock and rhabdomyolysis. 39 http://taylorandfrancis.com  CASE 12: PAINFUL, SPREADING RASH History An 18-year-old woman attends the Emergency Department with her mother with a history of painful ulcers in her mouth and skin peeling. She reports it starting as a small lip ulcer, but has progressed rapidly and has become increasingly painful, especially when eating or drinking. She has recently returned from holiday and spent a lot of time sun bathing and partying. However, in the past few days, she reports having a fever at times, sore throat and muscle ache. She denies any unprotected sexual intercourse or illicit drug use. She suffers from epilepsy for which she used to use sodium valproate; however, it was recently changed to lamotrigine. She has no allergies and admits to binge drinking during her holiday. Examination Vital signs: temperature of 36.6°C, blood pressure of 112/58, heart rate of 105 and regular, respiratory rate of 20, 98% oxygen saturations on air. The patient has a fair skin type. There are widespread red papules that appear to have erupted on the face and chest. You also note marked blistering and ulcers on the lips and gums. Questions 1. What is the likely diagnosis? 2. How would you classify the severity of this patient’s condition? 3. What are the possible triggers for this condition? 4. What are the complications of this condition? 41  100 Cases in Emergency Medicine and Critical Care DISCUSSION Steven Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered to be part of a continuous spectrum of a life-threatening mucocutaneous reaction. SJS is defined as epidermal loss of 30% epidermal loss is charac- terised as severe TEN syndrome, with an overlap syndrome between 10% and 30%. SJS/TEN is rare in the United Kingdom, with an estimated incidence of around 1–2 cases per million with an increased incidence in HLA-B75 positive patients. Differentials include other bullous and infective disorders such as erythema multiforme, pemphigus vulgaris, pemphigoid syndromes, IgA bullous dermatosis, Staphyloccal scalded skin syndrome (SSSS) and necrotising fasciitis. SJS/TEN is an acute, potentially life-threatening mucocutaneous disorder characterised by progressive dermal loss and inflammation of mucosal surface. When left untreated, it can result in multi-organ failure. SJS is associated with mortality 90%. Age >40 years Associated malignancy Heart rate >120 Urea >10 mmol/L Initial >10% epidermal loss Serum bicarbonate 14 mmol/L Immediate management should focus on managing the causative agent (Table 12.1). Blood investigations should include full blood count, ESR, C-reactive protein, renal function, elec- trolytes (including magnesium, phosphate and bicarbonate), glucose, liver function test, coagulation study and mycoplasma serology should be done. Clinical photography is useful in monitoring mucocutaneous involvement. Initially manage the large fluid loss from epidermal loss with intravenous fluid resuscita- tion. Analgesia should be given and titrated as per individual needs. Patient with severe eat- ing difficulties due to oral involvement should have nasogastric tube inserted and feeding 42  Case 12: Painful, spreading rash Table 12.1 Common causes for SJS/TEN Drugs Infection Other Carbamazepine Viral Haematological malignancy Lamotrigine Herpes simplex virus (HSV) Autoimmune disorders Phenytoin Adenovirus Physical injury or tattoos, Allopurinol Coxsackie radiotherapy Sulphur-containing Epstein Barr virus (EBV) Idiopathic antibiotics Cytomegalovirus (CMV) Sulphasalazine Bacterial NSAIDS Mycoplasma Streptoccocus Proteus Fungal Histoplasmosis initiated. Similarly, consider early catheterisation in urological involvement and it will aid in fluid balance monitoring. Wounds are often difficult to manage without general anaesthesia or potent analgesia such as opioids or ketamine. However, regular warm saline irrigation can be performed with greasy emollient cover and topical antibiotics (as per local guidelines). Patients with SJS/TEN should be referred to intensive or high dependency care units for spe- cialist nursing. Intensive monitoring and management is required to manage further acute complications and multi-organ failure. Key Points SJS/TEN is rare but life-threatening, analogous to burn injury. Early supportive therapy with fluid and wound management is important for best outcomes. SCORETEN should be calculated on all patients to predict mortality. Multidisciplinary management is required due to multi-system involvement and the wide range of complications – dermatology, critical care, dietician, pharmacist, specialist nurses, ophthalmology and urology. 43 http://taylorandfrancis.com  CASE 13: SUBMERSION History A 19-year-old man has been brought into the Emergency Department as a ‘cardiac arrest call’. He appeared to be heavily intoxicated and was seen to be wandering along the canal path late in the evening. Passers-by saw him floating in the water and rescued him. It is thought he was submerged for around 10 minutes in very cold water. There were no signs of life on scene and bystander CPR was started. He has been brought into the ED by a full paramedic crew in cardiac arrest with ongoing CPR. The paramedic crew tell you they have not performed DC cardioversion or given any drugs. Total downtime is now 25 minutes. Examination During a pulse check, assessment is as follows: A: The patient has a supraglottic airway device inserted and is being ventilated. B: There are coarse crackles throughout both lung fields and saturations are unrecord- able on high flow oxygen. C: There is no palpable pulse and the patient is in asystole. There is an intra-osseous needle inserted into the left proximal humerus. D: The GCS is 3/15 and both pupils are fixed at 5 mm. E: Core temperature is 29°C and there are no external signs of injury. Investigations Arterial blood gas: pH 7.015, pO2 35, pCO2 13, HCO3 16, BE-10, lactate 9.6, glucose 17. Questions 1. How are you going to manage this patient? 2. What are the recommendations for DC cardioversion and administration of drugs? 3. When should you consider stopping CPR? 45  100 Cases in Emergency Medicine and Critical Care DISCUSSION This man has suffered a submersion injury and should be managed along Advanced Life Support (ALS) guidelines. CPR should be continued whilst the paramedics hand the patient over to the receiving ED team, and at the end of the 2-minute CPR cycle, a brief initial assessment should be per- formed when directed by the team leader. This should be completed in less than 10 seconds and CPR resumed if there is no palpable pulse or signs of life. Ventilation may be carried out via several methods. The simplest is via a bag-valve-mask connected to high flow oxygen. If there are trained practitioners, this should be changed to either a supraglottic device (i-gel®, LMA) or preferably endotracheal intubation as soon as possible. In cases of submersion, this is advan- tageous as it allows increased positive end expiratory pressure (PEEP), which will recruit ­collapsed or flooded alveoli. Once this has been established, it is recommended to switch to continuous chest compressions at 100 per minute and ventilation at a rate of 10–12 breaths per minute. There is often concern for concurrent cervical spine injury in these cases, and it may add a layer of complexity into management. Without evidence of diving or head injury, the incidence is around 0.5%, and spinal precautions are not required in every case. During the resuscitation attempt potentially reversible causes of cardiac arrest should be sought and corrected. They are hypoxia, hypothermia, hypovolaemia, hypo- or hyperkalae- mia (and other electrolytes), tension pneumothorax, tamponade, toxins and thromboembo- lism (4Hs and 4Ts). This patient is complex and has several potential reversible causes. The submersion injury will almost certainly cause pulmonary oedema by flooding the lungs with contaminated water and mixing with surfactant. Endotracheal intubation and warmed high flow oxygen are keys to reversing hypoxia here. The alcohol ingestion combined with the prolonged submersion means that the patient may be hypovolaemic. Warmed 0.9% saline or other cystalloid solution should be used to resuscitate the patient. Arterial or venous blood gas testing should be performed as soon as practically possible as it will help to identify any correctible electrolyte disturbances. Heavy alcohol consumption will contribute to a metabolic acidosis as well as cellular hypoxia from the cardiac arrest but should improve with fluid administration. Sodium bicarbonate (8.4%) may be considered for extreme metabolic acidosis in those that fail to improve with fluid resuscitation. The core temperature was noted to be 29°C, and efforts should be made to rewarm the patient in the ED. Possible options include warmed intravenous fluids, removal of cold wet clothes and forced warm air induction (Baire® hugger). Advanced warming techniques such as bladder lavage, peritoneal lavage or ECMO may be employed if available. Arrhythmias due to the sudden temperature change may be a contributing cause and if pres- ent should be managed per ALS guidelines. Below 30°C, up to three attempts should be made for DC cardioversion and drugs (adrenaline, amiodarone) withheld until core temperature is >30°C. The interval between drug doses should be doubled until core temperature is >34°C. How long should you continue? There are no fixed criteria but current guidelines suggest that many factors should be considered – the age of the patient, submersion time, temperature of the water and co-morbidities. Younger patients submerged in very cold water (34°C before making final decisions. Mechanical chest compression devices (e.g. LUCAS ®, AutoPulse®) should be considered where prolonged CPR is anticipated as they prevent team fatigue and ideally should be deployed on arrival to the ED. Key Points The incidence of cervical spine injury in submersion cases is low. The team should be prepared for prolonged CPR. Drug doses and DC cardioversion thresholds are altered according to core temperature. The patient should be warmed to 34°C and all reversible causes corrected before consideration of cessation of CPR. 47 http://taylorandfrancis.com  CASE 14: CRUSHING CENTRAL CHEST PAIN History A 62-year-old man is brought to the Emergency Department as a ‘priority call’ after he developed chest pain. One hour ago, while he was doing some gardening, he started to expe- rience sudden onset, severe central chest pain that did not radiate anywhere. He had associ- ated nausea and sweating, but did not vomit. He has never experienced similar pain in the past. His medical history is notable for type 2 diabetes and hypertension, and there is no family history of cardiac disease. He is a current smoker, but denies any drug use. Examination Vital signs: temperature of 36.5°C, heart rate of 75 and regular, blood pressure of 100/60, respiratory rate of 20, 94% O2 saturation on air. Physical examination reveals a diaphoretic individual in moderate pain. Radial pulses are equal bilaterally, and cardiorespiratory and abdominal are unremarkable. JVP is not elevated and he has no evidence of peripheral oedema. Investigations An electrocardiogram (ECG) is shown below. I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 II Questions 1. What does the ECG show, and what is the diagnosis? 2. What are the next steps in management that must be performed in the Emergency Department? 3. Would management change if he had presented 3 hours after development of symptoms? 49  100 Cases in Emergency Medicine and Critical Care DISCUSSION This patient has significant cardiac risk factors (smoking, diabetes and hypertension) and presents with acute cardiac-sounding chest pain. Based on the presentation, the treating phy- sician must consider myocardial ischaemia or infarction as the most important diagnosis to exclude, and a 12-lead ECG must be obtained immediately in all such patients. Often, the paramedics will have performed a 12 lead ECG, and this must be interpreted if available. In this case, the ECG shows ST elevation in the inferior leads (II, III and F) as well as recip- rocal ST depression in the anterior and lateral leads. This finding, together with the history, is concerning for an ST-elevation myocardial infarction (STEMI), which is a medical emer- gency. The finding of ECG changes in leads II, III and aVF points towards inferior or poste- rior wall ischaemia/infarction. The initial steps to managing this patient should proceed along the ‘ABCDE’ approach. Supplemental oxygen was traditionally provided even to non-hypoxic patients, but recent evidence suggests it does not provide any benefit and may even harm such individuals. Given the presence of hypotension and possible right ventricular involvement and the absence of signs to suggest pulmonary oedema, an intravenous fluid bolus (250–500 mL) should be administered. Concomitantly, basic blood tests including a full blood count, electrolytes, coagulation screen and troponin must be performed. A chest radiograph is also useful to look for pulmonary oedema, estimate the heart size and exclude thoracic dissection. Pain should be controlled, with morphine being preferred due to its potency and rapid onset of action, and nitrate should also be used, dependent on blood pressure. The most important goal of the acute management of STEMI is coronary reperfusion, which may be achieved either by percutaneous coronary intervention (PCI) or use of fibrinolytic agents (thrombolysis). PCI is the preferred strategy if it can be delivered within 120 minutes of first medical contact (and ideally within 90 minutes), and would be the best option in this individual. Hospitals may have a STEMI alert/paging system to enable deployment of the primary PCI team, and this should be activated. Prior to PCI, antiplatelet therapy should be administered with a loading dose of aspirin (300 mg) as well as a second anti-platelet agent (e.g. ticagrelor 180 mg or clopidogrel 300 mg). If there is a delay in presentation to the Emergency Department (e.g. 3 hours after symptom onset), PCI is still the preferred option providing it can be delivered within 120 minutes of first patient contact (i.e. door to balloon time). Only if there is an anticipated delay in provi- sion of PCI of >2 hours from first patient contact (e.g. if the patient initially presents to a dis- trict hospital without primary PCI capabilities and requires transfer to another centre, with an expected travel time >2 hours) should fibrinolysis be chosen as the reperfusion strategy. This is because several randomised trials have shown that PCI provides improved short- and long-term survival outcomes compared to fibrinolysis, providing it can be performed within the appropriate time frame. 50  Case 14: Crushing central chest pain Key Points >1 mm ST elevation in anatomically contiguous lead locations should raise suspi- cion for ST-elevation myocardial infarction (STEMI). Any patient with a suspected STEMI should be considered for emergent coronary reperfusion via percutaneous coronary intervention (PCI). Prior to PCI, dual anti-platelet therapy, with aspirin 300 mg and either clopidogrel 300 mg or ticagrelor 180 mg, should be administered. The alternative to PCI is thrombolysis, but PCI is preferred providing it can be per- formed within 120 minutes of first patient contact. 51 http://taylorandfrancis.com INTERNAL MEDICINE CASE 15: SHORT OF BREATH AND TIGHT IN THE CHEST History A 20-year-old woman is brought in as a ‘priority call’ to the Emergency Department. She has become increasingly short of breath over the last few hours and complains of a ‘tight’ feeling in her chest. She has a history of asthma managed with regular use of inhaled beclometha- sone and salbutamol as needed. Today, she has used her salbutamol inhaler on multiple occa- sions, but it has provided minimal relief. She has never previously been admitted to hospital with an asthma attack and has no other medical comorbidities. Examination Vital signs: temperature of 36.0°C, blood pressure of 110/60, heart rate of 120 and regular, respiratory rate of 25, 94% O2 saturations on air. Physical examination reveals an anxious-appearing slim female who has difficulty complet- ing sentences in one full breath. Respiratory examination is notable for widespread expira- tory wheeze. Investigations An arterial blood gas performed on arrival (with the patient breathing room air) shows pH 7.43, pO2 8.2, pCO2 4.0, HCO3 22. Peak