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Anaesthesia · Malignant hyperthermia
Sample itemA 20-year-old man is anaesthetised with sevoflurane and suxamethonium. Soon afterwards he develops masseter spasm, tachycardia, a rapidly climbing end-tidal CO2 and a rising core temperature. Blood gas shows mixed acidosis and potassium is high. Which diagnosis fits, and which gene product is abnormal?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Malignant hyperthermia, with an abnormal ryanodine receptor
Malignant hyperthermia is a pharmacogenetic crisis of skeletal muscle triggered by volatile agents and suxamethonium, caused by a defect in the ryanodine receptor releasing calcium uncontrollably. It causes hypercarbia, rigidity, hyperkalaemia and hyperthermia. Treatment is to stop triggers, give dantrolene and cool the patient.
Option by option
A. Neuroleptic malignant syndrome, with dopamine receptor blockade
Neuroleptic malignant syndrome follows antipsychotic use and develops over days, not within minutes of induction.
B. Malignant hyperthermia, with an abnormal ryanodine receptor (correct)
Correct. Volatile agent plus suxamethonium, rising CO2 and masseter spasm indicate this ryanodine receptor disorder.
C. Thyroid storm, with excess thyroid hormone
Thyroid storm occurs in thyrotoxic patients and is not triggered by suxamethonium and volatile agents.
D. Serotonin syndrome, with excess 5-HT activity
Serotonin syndrome follows serotonergic drugs and causes clonus and hyperreflexia rather than a rising CO2 with masseter spasm.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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