Fig. 12.1 Head tilt, chin lift. Reproduced from Wikimedia commons. Image is in public domain.
Emergency medicine (EM) deals mostly with acute injuries and illnesses that affect patients of all age groups with a full spectrum of undifferentiated physical and behavioural disorders. During your time in this medical specialty you will gain knowledge and skills required for the prevention, diagnosis, and management of such emergent presentations along with an understanding of pre-hospital EM.
EM as it is currently known started as a specialty in the UK in 1952 and Mr Maurice Ellis at Leeds General Infirmary was the first consultant. It was initially called the Casualty Surgeons Association. Rotating through an EM placement can be a daunting task for most medical students. High patient volume, acuity, and varied pathology pose an interesting challenge during the time spent in the ED. The EM placement is unparalleled. You will gain a wide variety of medical experience and procedural skills you will not get anywhere else, from suturing to assisting in cardiac arrests. All in a day’s work!
1. Always think ABCDE: with every patient you see, especially in majors and the resuscitation room, think:
• Airway: is it open? Is it maintainable?
• Breathing: is the respiratory rate and depth normal? Is the air entry equal on both sides of the chest?
• Circulation: are the BP and pulse normal? Is the patient adequately perfused?
• Disability: what is the GCS score? What is the blood glucose?
• Exposure: expose the patient for adequate examination.
2. Know your limitations: you will come across clinical problems and situations you have never been confronted with in the past. The sign of a safe doctor is someone who asks for help early to provide optimal patient care in a timely manner. Always do the right thing, at the right time, to the right patient, in the right place.
3. Listen to your patient: the majority of your diagnoses are clear from the history. If you take a good history, you will get the diagnosis. A good, relevant history is not always time-consuming.
4. Examine the patient properly: a good examination will give you more information about the patient’s condition than state-of-the-art investigations. If a patient complains of pain in a limb, be systematic and examine the entire limb and compare it to the normal side.
5. Anticipate the worst: exclude the life-threatening problems first. If discharging a patient ask yourself: ‘If this patient is discharged home and they die, have I thought of every potentially life-threatening problem, and have I done my best to exclude them?’ If you cannot answer this question with a resounding ‘yes’ then ask for senior help. Examples:
• Has a pregnancy test been done in a fertile woman with abdominal pain to exclude ectopic pregnancy?
• Has a patient with pleuritic chest pain had ABG and D-dimer tests to exclude a pulmonary embolus (PE)?
• Has a patient with a head injury who is fit for discharge gone home with an adult who can keep an eye on him/her to exclude worsening intracranial haemorrhage?
6. Be punctual: arrive on time for lectures and shop floor sessions. The ED runs on a shift system and the clinicians who are imparting valuable knowledge are very busy.
7. Be courteous and professional: to patients, colleagues, and other teams. Otherwise you will find yourself dealing with complaints from people you are working with.
8. Keep a good clinical record: write a clear history, important negative findings, the investigations you want to request, and your management plan. Write legibly in black ink and present succinctly. Your written record will be followed by nurses and other teams to uphold patient safety. Your record may also be used in a court of law in case patient safety has been compromised.
9. Attend the ED teaching: this is compulsory and subsidized. It is vital that you attend these sessions as you are taught topics which are not always covered in textbooks. You will also learn how things are done in your hospital as local policies and protocols differ.
10. Enjoy the placement: EM is one of the most exciting, varied, and interesting placements you will do. You will be on a steep learning curve but will be well supported if you maintain your enthusiasm and willingness to participate. If you do not take the initiative to participate and show your enthusiasm, you will quickly be ignored since it is a busy department. If you show a willingness to learn, then every member of staff will go the extra mile to make you comfortable, guide, and teach you for as long as you wish. Have the guts to do some nights and learn!
Deals with the assessment and treatment of patients, based on the MIST list: Mechanism of injury, Injuries sustained or suspected, Signs (vitals), symptoms, and Treatment received. Treatment priorities of a severely injured patient must be established in a logical and sequential fashion.
Receiving and treating a severely injured patient can lead to anxiety which provokes memory loss. Therefore, one can overcome anxiety and memory loss if one develops a system for doing a rapid primary survey, resuscitation, detailed secondary survey, followed up by definitive care. This process constitutes the ABCDEs of trauma care and identifies life-threatening conditions according to the following sequence:
1. Airway maintenance with cervical spine protection.
3. Circulation with haemorrhage control.
4. Disability and neurological status.
5. Exposure/Environmental control: completely undress the patient, but prevent hypothermia.
A quick (10 sec) assessment of the ABCDE in a trauma patient can be conducted by talking to the patient and asking about basic information (name and what happened). An appropriate response (ability to speak clearly) suggests that there is no major ABC issues and the brain is adequately perfused. The aim of the primary survey is to deal with the life-threatening conditions as they are identified A–E!
• A non-patent airway is rapidly fatal but can often be easily resolved. Think of the airway as a pipe that can be blocked (vomit/foreign body/tongue), swollen (anaphylaxis/burns), or externally compressed (haematoma/tumour/abscess).
• Ascertain patency: open, look, suck secretions, and remove visible foreign bodies. There will be no sound from a totally obstructed airway but signs of a partially obstructed airway include stridor (usually inspiratory), stertor (snoring), and gurgling (fluid). Note facial, mandibular, or tracheal/laryngeal fractures that can obstruct the airway.
• Airway opening manoeuvres: chin lift or jaw thrust (usually reserved for C-spine injury) (see Fig. 12.1 and Fig. 12.2).
• Then protect cervical spine using the trinity of devices (appropriately sized cervical collar, head blocks, and tape) if no ongoing airway concerns.
• Turning an unconscious patient on their side (into the recovery position) can help prevent aspiration of vomit or airway obstruction by the tongue (not if C-spine injury suspected—then clinical team has to log-roll vomiting patient).
Fig. 12.1 Head tilt, chin lift. Reproduced from Wikimedia commons. Image is in public domain.
Fig. 12.2 Jaw thrust, in case C-spine injury suspected. Reproduced from Wikimedia commons. Image is in public domain.
Honours
Prior to application of a cervical collar check the following:
• Look: distended neck veins and neck wounds or bruising.
• Feel: tracheal position, laryngeal crepitus, surgical emphysema and cervical spine tenderness.
Adequately expose the patient’s neck and chest. Inspect, palpate, percuss, and auscultate. The life-threatening chest injuries should be identified during the primary survey and may require immediate attention for ventilatory efforts to be effective (see Table 12.1). These can be remembered by the pneumonic ‘ATOM FC’ and ensure a CXR has been requested.
Table 12.1 Indications for definitive airway
| Airway protection | Ventilation and oxygenation |
| Facial injuries | Inadequate respiratory efforts: tachycardia/hypoxia/cyanosis/hypercarbia |
| Obstruction: stridor, haematoma, laryngeal/tracheal injury | Severe haemorrhaging and need for volume resuscitation |
| Aspiration risk: bleeding, vomiting | Closed head injury requiring hyperventilation |
| Unconscious or low GCS score (usually <8) | Apnoea: paralysis, unconsciousness |
• Airway obstruction/laryngotracheal injury
Tachypnoea, chest wall recession, stridor, grunting, and use of accessory muscles suggest 
work of breathing.
Chest expansion, reduced breath sounds, and O2 saturations suggest reduced efficacy of breathing.
HR or HR, cyanosis, or confusion or reduced level of consciousness would suggest secondary effects on hypoxia on the various organ systems. If there is spontaneous respiratory effort but signs of work of breathing or reduced efficacy or effect, then provide high-flow O2 via a non-rebreather mask (80% O2 with a 15 L/min flow rate). A standard mask without the reservoir bag (Hudson’s mask) provides 50% O2 with a 15 L/min flow rate.
If trained in the use of a self-inflating Ambu® bag and mask, oxygenate and ventilate the patient. With a good mask seal around the mouth and nose, up to 95% O2 with a 15 L/min flow rate can be achieved.
Check pulse rate/HR, central capillary refill time (on the sternum, normal <2 sec), and BP. Gain vascular access and send appropriate bloods. Get a venous blood gas to check for Hb, K+, Ca2+, and glucose. Get a 12-lead ECG. Prolonged capillary refill time and low BP could suggest that the patient is in shock! Shock, syncope, myocardial ischaemia on the ECG (new ST segment or T-wave changes), or heart failure (clammy skin, shortness of breath, lung crackles on auscultation, raised JVP, pitting pedal oedema) in the presence of a brady- or tachycardia suggest adverse features. Rapid and accurate assessment of an injured patient’s haemodynamic status (pulse, BP, skin colour, and level of consciousness) is essential. Tachycardia is often the first sign of circulatory compromise. An injured patient who is cool and tachycardic is in shock until proven otherwise. Shock is defined as inadequate tissue perfusion and oxygenation. Two types include (1) haemorrhagic which is the commonest and (2) non-haemorrhagic (i.e. tension pneumothorax, cardiac tamponade, neurogenic, and septic).
There are four classes of haemorrhage, as listed in Table 12.2.
Table 12.2 Severity of shock
| Parameter | Class | |||
| 1 | 2 | 3 | 4 | |
| Blood loss (mL) | <750 | 750–1500 | 1500–2000 | >2000 |
| Blood loss (%) | <15 | 15–30 | 30–40 | >40 |
| Pulse rate (bpm) | <100 | 100–120 | 120–140 | >140 |
| Systolic BP |
|
|
|
|
| Pulse pressure |
|
|
|
|
| Respiratory rate (breaths/min) | 12–20 | 20–30 | 30–40 | >35 |
| Urine output (mL/hour) | >30 | 20–30 | 5–15 | |
| Fluid replacement | C | C | C + B | C + B |
B, blood; C, crystalloid.
1. Identify external haemorrhage during the primary survey and control it by direct manual pressure, binders for pelvic trauma, reduction and splintage of long bone fractures, and tourniquets for extremity trauma
2. Replace volume loss: crystalloids = 1–2 L in adults or 10 mL/kg boluses in children and/or blood and blood products (2 units of blood in adults or 15 mL/kg of blood as 5 mL/kg boluses in children). For massive haemorrhage replace with 4 units of RBC, 4 fresh frozen plasma, 1 platelet, and 2 cryoprecipitate (if fibrinogen <1.5 g/L) aiming for:
• Prothrombin time ratio: <1.5
3. Vascular access—short and fat does the trick: size 14 (orange or brown colour cap) or a 16 gauge (grey colour).
• Consider tranexamic acid in bleeding trauma patients as soon as possible. If treatment is not given until 3 hours or later after injury, it is less effective and could even be harmful according to the CRASH-2 trial (Lancet)
• Check acid–base balance via ABGs or Venous blood gases.
• Base deficit and lactate are useful in determining the presence and severity of shock.
Top tips
• Trauma aphorism—do not let the obvious (severed or mangled limb) distract you from the occult (tension pneumothorax/cardiac tamponade).
• If tension pneumothorax has been excluded, hypotension following trauma is secondary to hypovolaemia until proven otherwise.
• Beta-adrenergic blocking medications may dampen the shock response (i.e. patient remains bradycardic despite the blood loss).
• Bradycardia with hypotension following trauma 
consider neurogenic shock.
• Standard four views: pericardial, right upper quadrant (RUQ), left upper quadrant (LUQ), and suprapubic.
• Helpful to rule in haemo/haemopneumo/pneumothorax, cardiac tamponade, and haemoperitoneum but it is not a rule out!
• Clinical diagnosis is difficult as clinical examination and conventional signs of peritoneal irritation are unreliable. Assume that abdominal trauma exists unless proven otherwise. Early imaging has become a standard of care.
• Management of abdominal injuries may include (1) non-operative, (2) damage control surgery, and (3) interventional radiology.
• Largest and strongest osteoligamentous body structure and disruption usually due to high-energy (2000–10,000 N).
• Suspect in high-velocity road traffic collisions (RTCs), fall from heights, or crush injury.
• Mechanisms of injury: AP/lateral compression vs vertical shear.
• Management: do not spring the pelvis. Apply a pelvic binder in the primary survey. Look out for signs specific for pelvic and urethral injury including:
• unstable or pelvic tenderness
• high-riding prostrate on digital rectal exam
• request a pelvic X-ray for fractures.
Neurological dysfunction can arise out of direct cerebral injury or secondary to reduced oxygenation and/or perfusion. It is examined through:
• level of consciousness (GCS): hypoglycaemia, alcohol, narcotics, and drugs can alter GCS
• level of spinal cord injury level if present
ICP = mean arterial pressure (MAP) − cerebral perfusion pressure (CPP)
• Resting ICP is 10 mmHg. Pressures >20 mmHg sustained and refractory to treatment have poorer outcomes.
• Features of ICP include headache, N&V, GCS score, mydriasis, ophthalmoplegia, focal neurology, and papilloedema.
• Discuss with the on-call neurosurgeon and consider mannitol (osmotic diuretic) or 3% hypertonic saline and controlled hyperventilation.
• Transfer to a neurosurgical centre with neurological ITU.
• Barbiturate induced coma is also an option if the above-listed measures fail.
• Hypothermia (cooling the brain to 35°C) and decompressive craniectomies have been tried to control the ICP.
Table 12.3 Indications of CT imaging
| Head | Neck |
| GCS score <13 | |
| Focal neurological deficit | |
| Suspected open/depressed/basal skull fracture | Intubation |
| Post-traumatic seizure | Cervical midline tenderness |
| >1 episodes of vomiting | Inadequate X-rays |
| Risk factors: >65 years, high-energy injury (RTC) | |
| Risk factors: warfarin, coagulopathy, >30 min retrograde amnesia | |
Completely undress the patient to facilitate a thorough examination and assessment following which the patient should be covered with warm blankets or an external warming device and warm IV fluids to prevent hypothermia.
Bedside portable CXRs and pelvic X-rays can be taken at the end of the primary survey (Table 12.3). Major trauma CT examination consists of (1) head and C-spine, (2) thorax, (3) abdomen and pelvis, and (4) any other sites of injuries. The following mechanisms of injury suggest the need for a major trauma CT:
• Crush injury to thorax/abdomen
The secondary survey does not begin until the primary survey is completed, resuscitative efforts are underway, and the normalization of vital functions has been demonstrated. The secondary survey constitutes a complete history and a head-to-toe physical evaluation of the trauma patient, including reassessment of all vital signs.
• Events/Environment related to the injury: each body region is completely examined (literally a finger/probe in every orifice).
FBC, clotting screen, electrolytes, ABG (pH, PO2, PCO2, Hb, lactate, base excess, creatinine, glucose), group and save, and cross-match. Consider amylase/lipase in abdominal trauma, paracetamol/salicylates if history of self-harm, and troponin in chest trauma, chest pain/collapse prior to trauma, or ECG changes noted on the monitor.
A sudden stop in effective blood circulation due to failure of the heart to contract effectively or at all. The patients are unconsciousness and there are no signs of life such as breathing or movement. Unless CPR is started, the person may die or suffer permanent brain and other organ damage. CPR involves chest compression (external cardiac massage) and rescue breathing. This is often termed basic life support (BLS) (Figs 12.3–12.5).
1. Place the heel of one hand in the centre of the patient’s chest; then place your other hand on top, interlocking your fingers.
2. Position yourself over the patient’s chest, keeping your arms straight.
3. Use your body weight to compress the chest approximately one-third of the depth of the chest.
4. After each compression allow your hands to recoil.
Fig. 12.3 Chest compressions. Reproduced from Wyatt, J. et al, Oxford Handbook of Emergency Medicine (4 ed.) 2012, Oxford University Press.
Fig. 12.4 Infant CPR. Reproduced from Wyatt, J. et al, Oxford Handbook of Emergency Medicine (4 ed.) 2012, Oxford University Press.
• If alone, compress the sternum with the tips of two fingers.
• If more, use the encircling technique place thumbs flat, side by side, on the lower sternum, with the tips pointing towards the infant’s head spread the rest of both hands, with the fingers together, to encircle the lower part of the infant’s rib cage with the tips of the fingers supporting the infant’s back press down on the lower sternum with your two thumbs to depress it at least one-third of the depth of the infant’s chest.
• Place the heel of one hand over the lower half of the sternum and give compressions and breaths at a ratio of 15:2.
The aetiology of cardiac arrest in adults can be broadly classified as cardiac and non-cardiac:
Fig. 12.5 Causes of cardiac arrest.
Coronary artery disease is the leading cause of cardiac arrest in adults.
Trauma is the leading cause of non-ischaemic cardiac arrests.
Ventricular fibrillation (VF): chaotic electrical activity of the heart which makes the heart quiver (fibrillate) and stops it from pumping blood. See Fig 12.6.
Fig 12.6 VF. Reproduced from Fiona Creed and Christine Spiers, Care of the Acutely Ill Adult 2010, Oxford University Press.
Ventricular tachycardia (VT): see Fig 12.7.
Fig 12.7 VT. Reproduced with permission from Reproduced from Fiona Creed and Christine Spiers, Care of the Acutely Ill Adult 2010, Oxford University Press.
Asystole (flatline): no cardiac electrical activity, the heart does not contract and hence there is no blood flow (i.e. cardiac output). See Fig. 12.8.
Fig. 12.8 Asystole. Reproduced from Fiona Creed and Christine Spiers, Care of the Acutely Ill Adult 2010, Oxford University Press
Pulseless electrical activity (PEA): lack of palpable pulse in the presence of organized cardiac electrical activity. PEA has previously been referred to as electromechanical dissociation (EMD). See Fig. 12.9.
Fig. 12.9 PEA. Reproduced from Fiona Creed and Christine Spiers, Care of the Acutely Ill Adult 2010, Oxford University Press
Potentially reversible and treatable causes of cardiac arrest are remembered as the 4 H’s and 4 T’s (Table 12.4)
Table 12.4 Reversible causes of cardiac arrest
| 4 Hs | 4 Ts |
| 1. Hypovolaemia | 1. Toxins |
| 2. Hypoxia | 2. Tamponade (cardiac) |
| 3. Hyperkalaemia or Hypokalaemia | 3. Tension pneumothorax |
| 4. Hypothermia | 4. Thromboembolism |
• Listen at the nose and mouth for breath sounds.
• Feel for air movement on your cheek.
If a shockable rhythm (VF, pulseless VT, or tachycardia with adverse features) is evidence on ECG monitor, this requires a delivery of current through electrodes attached to the chest wall.
Follow ALS and paediatric ALS algorithms for drugs used in cardiac arrest (see Fig. 12.10, Fig. 12.11, and Table 12.15).
| Adrenaline | |
| Cardiac arrest (IV) | 1 mg (1:10,000) |
| As soon as in asystolic cardiac arrest | |
| After third shock in VF/VT arrest | |
| Anaphylaxis (IM) | 0.5 mg (1:1000) |
| Amiodarone after third shock | |
| Pulseless VT and VF (IV) | 300 mg |
| Broad complex tachycardia | 300 mg (10–20 min if adverse features) 300 mg (20–60 min if stable) |
| Bicarbonate | 50 mL of 8.4% solution |
| Hyperkalaemia | |
| Tricyclic overdose | |
| Severe acidosis (pH <7.1 and base excess −10) | |
| Calcium | 10 mL of 10% CaCl2 |
| Hyperkalaemia, hypocalcaemia | |
| Ca2+ channel blocker or Mg2+ overdose | |
| Magnesium | |
| Torsades de pointes (form of VF) | 2 g |
| Adrenaline | |
| Cardiac arrest (IV) | 0.1 mg/kg (1:10,000) |
| As soon as in asystolic cardiac arrest | |
| After third shock in VF/VT arrest | |
| Anaphylaxis (IM) | |
| >12 years of age | 0.5 mg (1:1000) |
| 6–12 years of age | 0.3 mg (1:1000) |
| <6 years of age | 0.15 mg (1:1000) |
| Amiodarone after third shock | |
| Pulseless VT & VF (IV) | 5 mg/kg |
| Bicarbonate | 1 mL/kg of 8.4% solution |
| Calcium | 0.3 mL/kg of 10% calcium gluconate |
| Hyperkalaemia, hypocalcaemia | |
| Glucose | 2 mL/kg of 10% solution |
| Magnesium | 25–50 mg/kg |
| in Torsades de pointes (form of VF) |
Check GCS, pupil size and reactivity, posture, tone of all four limbs, and plantar reflexes.
Remove the patient’s clothes and check for clues as to the cause of the arrest such as rashes (septicaemia, anaphylaxis), injuries, rectal/vaginal bleeding, or melaena. Measure temperature and cover the patient with a blanket to prevent hypothermia and for dignity.
Do relevant blood tests including ABGs, 12-lead ECG, CXR, and other X-rays if injury suspected.
• 0–12 months = 0.5 × age in months + 4.
• 1–5 years = 2 × age in years + 8.
• 6–12 years = 3 × age in years + 7.
• Internal diameter (mm) = (age/4) + 4.
• Length (oral) (cm) = (age/2) + 12.
• Length (nasal) (cm) = (age/2) + 15.
• Fluid bolus = 20 mL/kg (aliquots of 10 mL/kg in trauma).
• Lorazepam = 0.1 mg/kg (maximum of 4 mg).
Fig. 12.10 Adult ALS. Reproduced with permission from Resuscitation Council (UK) 2015, www.resus.org.uk/resuscitation-guidelines/adult-advanced-life-support/.
A severe systemic allergic reaction. The diagnosis is not always obvious but is highly likely if there is:
• sudden onset and rapid progression of symptoms
• life-threatening airway/breathing/circulation problems
• skin/mucosal changes (flushing, urticaria, angio-oedema).
• Stings, foods (nuts, shellfish)
A therapeutics exam may ask you to administer adrenaline to a patient with anaphylaxis, simulated by an orange with a cannula in it. Do not be so pleased with yourself at remembering the correct dose (500 mcg, i.e. 0.5 mL of 1:1000 for an adult) that you forget it is an intramuscular and not IV injection (as in cardiac arrest situations). This is given in the mid-anterolateral thigh. (See Fig. 12.12.)
To confirm diagnosis, blood is sent for [mast cell tryptase]:
Before discharge the patient should:
• be advised to avoid the trigger (if known)
• be shown how to use an adrenaline auto-injector (EpiPen®)
• have prednisolone and chlorphenamine until allergic symptoms subside
• be referred to immunology clinic follow-up for further testing and prevention.
This is an infrequent cause of cardiac arrest, but remains a leading cause in victims <40 years old. It is also a common cause of non-traumatic coma.
• Accidental: commonly seen in children and in the elderly population.
• Non-accidental injury (NAI): fabricated illness.
• Agents: chemical, biological, radiological and nuclear incidents can occur secondary to industrial accidents or due to terrorism.
Fig. 12.11 Paediatric ALS. Reproduced with permission from Resuscitation Council (UK) 2015 www.resus.org.uk/resuscitation-guidelines/paediatric-advanced-life-support/.
Table 12.5 Normal paediatric observations (ILCOR 2010 (APLS) resuscitation guidelines)
| Age (years) | Heart rate (bpm) | Respiratory rate (breaths/min) | Systolic BP 50th centile | Systolic BP 5th centile |
| <1 | 110–160 | 30–40 | 80–90 | 65–75 |
| 1–2 | 100–150 | 25–35 | 85–95 | 70–75 |
| 2–5 | 95–140 | 25–30 | 85–100 | 70–80 |
| 5–12 | 80–120 | 20–25 | 90–110 | 80–90 |
| >12 | 60–100 | 15–20 | 100–120 | 90–105 |
Fig. 12.12 Treating anaphylaxis. Reproduced with permission from Resuscitation Council (UK) 2015 www.resus.org.uk/anaphylaxis/emergency-treatment-of-anaphylactic-reactions/.
• Supportive care based on preventing cardiorespiratory arrest (correcting hypoxia, hypotension, acid/base, and electrolyte disorders).
• Limiting drug absorption and facilitate drug elimination.
• Specific antidotes according to ToxBase (www.toxbase.org) and National Poisons Information Service on +44 844 892 0111.
• There is a high incidence of pulmonary aspiration of gastric contents after poisoning in unconscious patients who cannot protect their airway.
• Patient examination may give diagnostic clues such as odours, needle puncture marks, pinpoint pupils, tablet residues, signs of corrosion in the mouth, or blisters associated with prolonged coma.
• Measure temperature as hypo- or hyperthermia may occur after a drug overdose.
• Charcoal is made from coal, wood, or other substances. It becomes ‘activated’ when high temperatures combine with a gas or activating agent to expand its surface area.
• Absorbs certain drugs but its efficacy decreases over time.
• Multiple doses may be beneficial in life-threatening poisoning with carbamazepine, dapsone, phenobarbital, quinine, and theophylline.
• Not useful in cyanide, lithium, iron, alcohol, and strong acids or alkali poisonings.
• Gastric lavage followed by activated charcoal therapy is useful only within 1 hour of ingesting the poison. Generally, this should be carried out after tracheal intubation.
• Whole-bowel irrigation by cleansing the GI tract by oral or NG tube with a polyethylene glycol solution.
• Laxatives or emetics are not recommended
• Urine alkalinization (urine pH >7.5) by giving IV sodium bicarbonate in moderate to severe salicylate poisoning.
• Consider haemodialysis—methanol, ethylene glycol, salicylates, and lithium.
• Charcoal haemoperfusion for intoxication with carbamazepine, phenobarbital, phenytoin, or theophylline.
• Use lipid emulsion (Intralipid®) for cardiac arrest caused by local anaesthetic toxicity.
• Benzodiazepines: flumazenil. Caution in epileptics, in patients dependent on benzodiazepines can cause convulsions.
• Cyanide: amyl nitrite, sodium nitrite, sodium thiosulfate, hydroxocobalamin.
• Digoxin: Fab antibodies (digoxin-specific).
• Organophosphate insecticides: atropine (high dose).
• Opioids: naloxone if signs of respiratory depression/coma.
• Paracetamol: N-acetylcysteine (glutathione precursor) (see Fig. 12.13).
Fig. 12.13 Paracetamol poisoning nomogram. Reproduced with permission from Keith Allman, Emergencies in Anaesthesia (2 ed.), 2009, Oxford University Press.
• Most common drug in overdose.
• Just 150 mg/kg or 12 g can be fatal.
• N-acetylcysteine side effects: flushing, wheeze, hypotension, and anaphylaxis.
• Alternative to N-acetylcysteine is methionine PO (<12 hours).
• Classic triad: (1) miosis, (2) hypoventilation, and (3) coma.
• May also present with bradycardia, hypotension, hypothermia, and bowel sounds.
N&V, diarrhoea, abdominal cramps, mydriasis, tachycardia.
Mydriasis, tachycardia, hypertension, hyperthermia, increased respiratory rate, diaphoresis, tremor, agitation, anxiety, hallucinations, confusion, seizures.
Patients with chronic alcohol problems often attend the ED. This is usually a short visit as they tend to refuse admission. Reasons for visits may be:
• fall and head injury leading to subdural haematoma
Occurs in around 10% of chronic alcohol misusers but fatal in up to 20% if inappropriately managed. Only 10% of patients present with a triad of (1) ataxia, (2) confusion, and (3) ophthalmoplegia. Many of these symptoms may be mistaken for alcohol intoxication so Wernicke’s encephalopathy is frequently underdiagnosed. Prevented by giving IV vitamins such as Pabrinex®.
The vast majority of patients have gastroenteritis. However, it could be the presenting complaint for many other conditions. Differential include appendicitis, femoral hernia, intestinal obstruction (initial phase), pneumonia, myocardial infarction, and ectopic pregnancy. Gastroenteritis ought to be the confirmed after excluding all other sinister differentials. Isolate patients with D&V in case of an infective cause. Admit for resuscitation if unable to tolerate oral fluids or dehydrated.
Is a common presenting symptom in the ED. It is extremely important to take a detailed history:
• A sudden onset (thunderclap) headache would suggest SAH.
• Fever with headache—consider meningitis.
• If the headache had occurred previously, it may suggest a more benign cause, but it may be a sentinel bleed (SAH).
• Aura would suggest migraine.
• Pain around the eye may be a cluster headache or in the older patient acute glaucoma.
• Painful blindness may be optic neuritis.
Clinical evidence of infection plus systemic response indicated by two or more of the following (SIRS criteria):
• Hyper- (>38°C) or hypothermia (<36°C).
• Tachypnoea (respiratory rate >20/min or PCO2 <4.16 kPa).
• WCC >12 × 109 or <4 × 109 or 'left shift' 10% immature band forms.
Sepsis associated with organ dysfunction:
Severe sepsis with hypotension (systolic BP <90 mmHg or MAP <65 mmHg) unresponsive to intravascular volume replacement (20–30 mL/kg) or lactate ≥4.
• Sepsis with multiorgan failure: >80%.
A combination of intravascular volume depletion, peripheral vasodilatation, myocardial depression, and metabolism lead to an imbalance between systemic oxygen delivery and oxygen demand resulting in global tissue hypoxia or shock. Global tissue hypoxia is the key development preceding multi-organ failure and death. EGDT has been shown to significantly improve the mortality rate in patients with severe sepsis or septic shock. It reduces mortality rate from 46% to 30%, (p <0.009). Numbers needed to treat is 7 (to save one life).
2. Move patient to the resuscitation room and involve a senior.
3. Find focus of sepsis. Order CXR and urinalysis. Look for other foci (e.g. meningococcal rash, necrotizing fasciitis, cellulitis, etc.).
4. Blood tests. FBC, U&E, LFT, bone profile, troponin, CRP, random cortisol, clotting screen, group and save/crossmatch, blood cultures (before antibiotics).
5. Urinalysis. If positive for a UTI, send for MC&S. If patient has pneumonia, send a urine sample to microbiology for pneumococcal and Legionella antigen screen.
6. Antibiotics. Give appropriate antibiotics within 1 hour of arrival (ideally within 30 min).
7. Steroids. If patient is in septic shock that is not responsive to vasopressors, give hydrocortisone 50 mg IV.
8. Exclusion criteria. CVA, ACS, pulmonary oedema, status asthmaticus, cardiac arrhythmia, GI bleeds, seizures, trauma.
9. Give OXYGEN. Insert (1) central line, (2) arterial line, (3) urinary catheter
10. Monitor vital signs. BP, HR, respiratory rate, temperature, GCS. Start cardiac monitor, also get an ECG and pulse oximetry.
• Follow protocol: consider infusion charts for noradrenaline and dopexamine to maintain adequate perfusion.
• Monitor glucose: aim for glucose <8.3 mmol/L (start insulin infusion if necessary).
Timing of antibiotic treatment in septic shock is vital. A retrospective study of patients admitted to ITU with septic shock suggests that administration of antibiotics within the first 30 min of documented hypotension was associated with an 82.7% survival rate. Administration in the second 30 min was associated with 77.2% survival. The aggregate survival rate for the first hour is 79.9%. Each hour delay in the first 6 hours was associated with a 7.6% increase in mortality, resulting in a mortality rate of 42% if given at 6 hours following first drop in BP.1
Lactate may be raised for several reasons. For instance, an alcoholic with liver impairment may have a high lactate due to clearance. When starting EGDT based on a lactate, do so on an arterial lactate. A venous lactate may be raised due to a tight tourniquet.
It is crucial to provide optimal oxygen therapy to the acutely breathless patient. Oxygen may be delivered by well-fitted face mask with a non-rebreathing reservoir bag, Venturi mask, or nasal prongs (see Fig. 12.14).
• Oxygen is a drug and must be prescribed.
• Oxygen therapy should continue during other treatments such as nebulized therapy.
• Venturi masks should always be used in patients at risk of hypercapnia due to chronic respiratory failure.
• A well-fitted mask with a non-rebreathing reservoir bag should be used to deliver high-concentration oxygen to patients who require it.
• Patients should have continuous monitoring of pulse oximetry.
• The only role for nasal prongs in emergency treatment is to give supplementary low-flow oxygen therapy to patients with known hypercapnic COPD during bronchodilator treatment with an air-driven nebulizer.
These masks can deliver an accurate percentage of O2, ranging from 24% to 60% (see Table 12.6).
Table 12.6 Venturi masks
| Venturi valve | 24% (blue) | 28% (white) | 35% (yellow) | 40% (red) | 60% (green) |
| O2flow (L/min) | 2 | 4 | 8 | 10 | 15 |
These consist of a length of tubing with two prongs, which fit into the nostrils (see Table 12.7).
Table 12.7 Nasal cannulae
| L/min | % O2 |
| 1 | 24% |
| 2 | 28% |
| 3 | 32% |
| 4 | 36% |
• Maximum 4 L/min as it can cause nasal mucosal drying and does not increase FiO2.
• Nasal cannulae should be used to deliver O2 to patients having nebulized medication if the driving gas is air.
• Prevent the airway becoming dry and any secretions becoming tenacious and therefore difficult to clear.
• Warming inspired gases increases their ability to hold water.
To achieve rapid and complete healing of skin and soft tissue structures producing optimal functional and cosmetic results.
Life before limb! Wound care is part of the secondary survey.
How the injury was caused gives clues to which structures and to what extent tissue will be injured. Then likely complications can be predicted and measures taken to avoid them.
• Incised wounds (glass/knife) are associated with minimal skin damage and rarely become infected or leave ugly scars. However, tissue may be divided down to bone so tendon, nerve, and vessel damage must be looked for. Exploration under anaesthesia with the use of a tourniquet is advised, particularly in children unable to cooperate with examination.
• Crushing tissue devitalizes it so the laceration may be stellate and some tissue may need to be excised to prevent necrosis and infection. Dirt may have been forced into tissue.
• Shearing forces rip skin away from blood supply, and careful examination and monitoring is required to identify ischaemic skin which initially looks viable, or compartment syndrome. This commonly happens to young pedestrians when a car tyre rolls over their limb.
• Punch injuries to hands need to be considered as human bites if skin is broken by a tooth/teeth. These often extend into the joint and septic arthritis can occur.
• How (mechanism)? When (degree of bacterial contamination/proliferation already occurred)? Where (what kind of foreign body or pathogen to expect)? Who (in case of bite from human or animal)?
• Medical history and drug allergies (diabetes, corticosteroids, immunosuppressants).
• Vaccination (tetanus and hepatitis B status).
• Occupation, hobbies, and hand dominance.
• Pre and post anaesthesia (analgesia can be given immediately if required, but nerve function must be assessed and documented prior to local anaesthetic or sedation).
• Circulation (of the skin and distal structures).
• Nerve injury: check sensory and motor function and sweating. Remember nerves and vessels run together in bundles.
• Tendons, ligaments, and ducts (?any visible).
• Plain radiograph for fracture, air, or foreign body (glass, metal, or tooth). All wounds sustained from a foreign body, especially broken glass, must have imaging since they can usually be identified.
• Bloods and cultures if septic.
• Wound swab if pus, blood, or exudate present.
• Irrigate with copious warm saline and antiseptics.
• Debride devitalized tissue and remove dirt and foreign bodies.
• Close wound if appropriate or possible.
• Dress wound with non-adherent dressing (Mepitel® or Jelonet®) and self-adhesive dressing or gauze and crepe bandage to provide a moist, occluded healing environment and relieve pain.
• Elevate limbs, especially hands, to relieve swelling.
• Consider antibiotic use, tetanus, and boosters for blood-borne viruses.
• Heavily contaminated wounds which cannot be cleaned thoroughly: penicillin (erythromycin if allergic) and anaerobic cover depending upon contaminant as well as tetanus.
• Human/animal bites: co-amoxiclav and tetanus.
• Open fracture: IV benzylpenicillin and flucloxacillin (or cefotaxime).
• Minor (e.g. phalangeal injuries): nil but clean under local anaesthetic.
• penetrating wounds of hand or finger involving nerve, tendons, or vascular damage
Use non-absorbable interrupted sutures on skin. Absorbable sutures are for mucosal surfaces and deep closure, but this is not required in most wounds. An approximate guide for size and time before removal:
Use on clean, uncomplicated wounds (i.e. skin only, parallel to Langer’s lines) which oppose neatly with little tension. Hold wound edges together and apply the glue to the surface, do not sandwich it between tissue edges. Wait for it to dry before releasing wound. Wear gloves in case the glue trickles and sticks your finger to the patient. Be very careful in the region of the eye; position the patient so that any excess runs away from the eye.
Use on superficial wounds (skin only) in areas where the skin is not subject to much tension spreading the wound (e.g. the volar surface of the wrist as compared to the anterior thigh). Apply with no tension to prevent blisters forming. Wounds which bleed actively will probably be too wet for wound closure strips to stick, and the dressing used should be dry otherwise it will cause the strips to move. Use wide strips as the tension is more evenly distributed. Never use circumferential closure strips on digits/penis. Do not cover a flap laceration completely in closure strips as at early review they would need to be removed in order to assess viability.
Honours
The following wounds should not be sutured, closed with closure strips, or glued (i.e. where there is potential for wound infection):
• Dehisced wounds without a senior review.
Reference
1. Kumar A, Roberts D, Wood KE, et al. (2006). Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 34(6):1589–96.
Is a harsh, vibratory sound produced by turbulent airflow through a partially obstructed airway. Stridor is a conspicuous symptom of an underlying pathology causing an airway obstruction which could be life-threatening. Stridor can be inspiratory, expiratory, or biphasic (obstruction at the level of the glottis or subglottis).
Honours
1. Obstruction that is worse when the child is ‘awake’ suggests laryngeal, tracheal, or bronchial cause. Obstruction that is worse when the child is ‘asleep’ suggests a pharyngeal cause.
2. Inspiratory stridor suggests that the obstruction is ‘extrathoracic’ (larynx/nasopharynx). Expiratory stridor suggests that the obstruction is ‘intrathoracic’ (trachea and bronchus).
• Birth: choanal atresia, laryngeal web, vascular ring, vocal cord paralysis.
• 4–6 weeks: laryngo/tracheomalacia.
• 6 months–3 years: croup (peak incidence at 2 years of age, can occur in older children).
• 1–4 years: foreign body aspiration (peak incidence at 1–2 years of age, can occur in older children).
• 2–16 years: epiglottitis and retropharyngeal abscess (peak incidence at 3 years of age), bacterial tracheitis, peritonsillar abscess (peak incidence at 8 years of age).
• Any age: angio-oedema and laryngeal trauma.
Croup is the most common cause of acute stridor while laryngomalacia is most common cause of chronic stridor in children. Consider laryngotracheal stenosis (secondary to endotracheal intubation) in low-birth-weight infants. Stridor aggravated during feeding could suggest external compression of the trachea. If the airway is severely compromised, it has to be secured prior to any investigations. Exhaustion (quiet and shallow breathing) or silent chest on auscultation, cyanosis, saturation <85% on air, and hypotension are pre-terminal signs call the paediatric arrest team along with the on-call ENT and paediatric anaesthetist.
All children will require high-flow oxygen but arm yourself with nebulized adrenaline, antibiotics, and steroids.
AP and lateral radiographs of the neck and chest are useful in the evaluation of a child with stridor. Flexible fibreoptic nasolaryngoscopy aids visualization of the nasal passages, naso/hypopharynx, and supraglottic larynx. It can be performed in a child who is awake. Fibreoptic and rigid bronchoscopy aids visualization below the glottis and the latter in removal of foreign bodies and with tissue diagnosis. Contrast-enhanced CT helps to identify the causes of extrinsic compression of the airway.
Is characterized by the sudden onset of respiratory distress associated with coughing, gagging, or stridor, a possible history of eating or playing with small items prior to the onset of symptoms, and in the absence of other signs of illness. When a foreign body enters a child’s airway, they tend to cough with a view to expel the foreign body. A spontaneous cough is safe and much more effective than any manoeuvre (back slaps, chest thrust, or Heimlich) a rescuer performs.
Choking can lead to asphyxiation and rapid deterioration if the cough is absent or ineffective and the object obstructs the airway completely (see Table 12.8). If a child becomes unconscious and a foreign body is visible on opening the mouth, make a single attempt to remove it with a finger sweep. Beware of pushing the foreign body deeper inside.
Table 12.8 Signs of ineffective vs effective coughing
| Ineffective coughing | Effective cough
• Crying or verbal response to questions |
Deliver up to five sharp back blows with the heel of one hand in the middle of the back between the shoulder blades.
Back blows are more effective if the child is positioned head down. If this is not possible, support the child in a forward-leaning position and deliver the back blows from behind.
If back blows fail to dislodge the object, and the child is still conscious, use chest thrusts for infants or abdominal thrusts for children.
Do not use abdominal thrusts (Heimlich manoeuvre) for infants.
Identify the landmark for chest compression (lower sternum approximately a finger’s breadth above the xiphisternum). Deliver up to five chest thrusts which are similar to chest compressions, but sharper in nature and delivered at a slower rate.
Stand or kneel behind the child. Place your arms under the child’s arms and encircle their torso. Clench your fist and place it between the umbilicus and xiphisternum. Grasp this hand with your other hand and pull sharply inwards and upwards. Repeat up to four more times. Ensure that pressure is not applied to the xiphoid process or the lower rib cage as this may cause abdominal trauma.
Child abuse is defined as any act of omission or commission by a parent or caregiver that would endanger or impair a child’s or young person’s physical or emotional well-being, or that which is judged by the values of the community and professionals. Younger children are at the greatest risk as they are non-verbal and defenceless.
• Psychiatric illness in parents
• Parent(s) victims of child abuse
Delay in seeking medical attention, vague or changing history, history or mechanism inconsistent with the degree of injury or type of injury sustained, injuries inappropriate for the developmental age, multiple ED attendances, self-inflicted injuries including repeated foreign body ingestion, alleged assault.
Abnormal parental or caregiver behaviour, abnormal interaction between the caregiver/parent and the child, multiple injuries at various stages of healing, specific injuries (pattern of bruising from belts, sticks, clusters or multiple bruises of uniform shape, cigarette or rope or immersion burns, oral and genital injuries), bruising in non-ambulant children, bruising in unusual sites (medial aspect of the arms or thighs), sexual abuse.
Unusual fracture pattern and skeletal injuries (bucket handle tear, spiral fracture in a non-ambulant child, multiple healing fractures), retinal haemorrhages on fundoscopy, subdural bleeds on CT scans.
If there are NAI concerns during the history, examination, or investigation stage, please refer to the paediatric registrar/consultant and paediatric ED sister for a more thorough, sensitive, and holistic approach to the case. They will liaise with social services, designated doctor for safe guarding, and the police as deemed necessary. It is your and everyone’s responsibility to flag up vulnerable patients and cases of potential NAI. Never assume that someone else will always pick it up.1
Honours
If NAI is suspected, the child is likely to be admitted for further investigations including a skeletal survey. Give consideration to the siblings who may also be at risk.
Reference
1. Royal College of Paediatrics and Child Health (RCPCH) Child Protection Companion. 
www.rcpch.ac.uk/resources/about-child-protection-companion
