FRCEM Single Best Answer

A large AAA (≥5.5 cm) in a haemodynamically stable patient with symptoms (syncope, abdominal pain) represents a symptomatic or contained rupture until proven otherwise and requires urgent CT aortography. This defines the anatomy (infrarenal versus juxtarenal, neck morphology, iliac involvement) needed to plan EVAR or open repair. NICE NG156 (2020) recommends CT aortography as the definitive imaging modality for anatomical planning in stable patients with suspected rAAA or symptomatic AAA. Duplex ultrasound confirms AAA size but cannot provide the anatomical detail required for operative planning.

A blood glucose of 2.1 mmol/L represents significant hypoglycaemia - an immediately reversible cause of confusion, agitation and neurological impairment. Hypoglycaemia also impairs shivering thermogenesis, meaning it may perpetuate the hypothermia itself. All other listed contributors (missed levodopa, alcohol-related Wernicke's encephalopathy, sepsis, myxoedema coma) are plausible concurrent concerns but none are as immediately life-threatening and rapidly correctable as hypoglycaemia at this glucose level. The Resuscitation Council UK 2025 reversible-causes framework and NICE CKS guidance on hypoglycaemia both support immediate glucose correction as the first priority in any deteriorating patient with a critically low blood glucose.

Domperidone is a recognised QT-prolonging agent and its use is associated with TdP, particularly in younger patients and at higher doses. Stopping the culprit drug is the immediate priority once the patient is haemodynamically stable. The QTc of 510 ms mandates cardiology review and admission for monitoring, but the single most important reversible intervention is removing the precipitant. Electrolytes are within acceptable range, so urgent electrolyte replacement is not the priority here. Empirical IV magnesium is indicated for active TdP, not for a self-terminated episode with normal magnesium. Beta-blockade without specialist input is inappropriate in this acute setting without a confirmed congenital LQTS diagnosis. (NICE guidance on domperidone safety; MHRA Drug Safety Update 2014; RCEM Learning, Long QT Syndrome module.)

In moderate-to-severe hypothermia (core temperature below 30°C) with a perfusing rhythm and inadequate response to passive rewarming, active internal (core) rewarming should be escalated. Warmed humidified oxygen, warmed IV fluids via a central route, and bladder irrigation with warm saline are recognised active internal rewarming techniques. Intraosseous access should be used if peripheral IV access fails, allowing delivery of warmed fluids without delay. Warmed intravenous fluids (38-42°C) are a first-line active internal rewarming measure when passive rewarming is insufficient. ECMO is reserved for cardiac arrest or refractory haemodynamic instability unresponsive to other measures. (Resuscitation Council UK 2025 guidelines - Special Circumstances: Hypothermia.)

This presentation is malignant hyperthermia (MH), a pharmacogenetic skeletal muscle disorder triggered by volatile anaesthetic agents and/or suxamethonium. Uncontrolled calcium release from the sarcoplasmic reticulum via mutated ryanodine receptors (RYR1) drives a hypermetabolic crisis. The combination of masseter spasm, generalised rigidity, rapidly rising temperature and markedly elevated end-tidal CO2 in the anaesthetic context is diagnostic. Dantrolene sodium - a ryanodine receptor antagonist that inhibits sarcoplasmic calcium release - is the only disease-specific antidote. The triggering agent must be ceased immediately and dantrolene given at 2.5 mg/kg IV bolus, repeated until rigidity and hyperthermia resolve. Per the Association of Anaesthetists (AAGBI/AAoA) MH guidelines, dantrolene must be available in all anaesthetic environments and is the only intervention that addresses the underlying mechanism.

Osborn (J) waves are the defining ECG feature of hypothermia, appearing as a positive deflection at the J-point (the junction of the QRS and ST segment), most prominent in leads V4-V6 and the inferior leads. Amplitude increases as core temperature falls. Recognising them prevents misinterpretation as STEMI and averts inappropriate cath-lab activation. Additional ECG changes in hypothermia include sinus bradycardia, PR prolongation, QT prolongation, QRS widening, atrial fibrillation, and - as temperature approaches 28°C - ventricular fibrillation. Sources: LITFL ECG Library - Hypothermia; Resuscitation Council UK 2025 Guidelines (Special Circumstances - Hypothermia).

The LEMON mnemonic (Look externally, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility) is the validated pre-intubation assessment tool endorsed by RCEM and DAS guidance for ED use. In a patient with a suspected cervical spine injury requiring MILS, neck mobility is severely restricted by both the injury and the mandatory immobilisation technique. Restricted neck mobility prevents optimal head and neck positioning (sniffing position) required for alignment of the oral, pharyngeal and laryngeal axes, the single factor most directly predicting laryngoscopic difficulty in this scenario. Other LEMON components (mouth opening, thyromental distance, Mallampati class) may be normal.

ACE inhibitor-induced angioedema is bradykinin-mediated, not IgE- or mast-cell-mediated. ACE normally degrades bradykinin; inhibition causes bradykinin accumulation, increasing vascular permeability particularly in the face, lips, tongue, and larynx. Serum tryptase will be normal, distinguishing this from anaphylaxis. Antihistamines and corticosteroids have limited efficacy because the reaction is histamine-independent. The ACE inhibitor must be permanently discontinued. Close observation for laryngeal involvement is the safety priority. Adrenaline should be given if airway compromise develops. Icatibant (bradykinin B2 receptor antagonist) is a specialist option for severe or refractory cases but is not routine first-line ED treatment for a mild, haemodynamically stable presentation. Source: NICE CKS Anaphylaxis; Resuscitation Council UK Anaphylaxis Guideline 2025.

This is Red Man Syndrome, caused by direct non-immunological mast-cell degranulation from rapid vancomycin infusion. The flushing-predominant distribution (face, neck, upper chest), absence of urticaria, angioedema, and bronchospasm, and precise temporal relationship to the infusion distinguish it from IgE-mediated anaphylaxis. Immediate management is to stop or slow the infusion and administer IV chlorphenamine to address histamine-mediated symptoms. Adrenaline is not indicated when true anaphylaxis can be confidently excluded on clinical grounds. Future doses may be tolerated by extending the infusion time to over 90 minutes with antihistamine premedication. (Resuscitation Council UK Anaphylaxis Guidelines 2025; BNF vancomycin monograph.)