A patient with a 3-day-old 40% TBSA burn is given succinylcholine for rapid sequence intubation. Thirty seconds later, the cardiac monitor shows peaked T waves followed by ventricular fibrillation. The mechanism responsible is:
- A Histamine release causing vasovagal reaction
- B Succinylcholine-induced rhabdomyolysis releasing myoglobin
- C Upregulation of extra-junctional acetylcholine receptors releasing massive potassium ✓
- D Phase II block causing prolonged depolarisation of cardiac muscle
Explanation
Thermal burns, denervation, prolonged immobility, and other muscle injuries cause proliferation of immature (fetal-type) extrajunctional nicotinic acetylcholine receptors across the entire muscle membrane. Succinylcholine depolarises all these receptors simultaneously, causing massive efflux of intracellular potassium into plasma, potentially raising serum K+ by 5–10 mEq/L acutely and precipitating lethal hyperkalaemic dysrhythmias. This risk persists from approximately 24–72 hours post-injury until healing is complete (up to 1–2 years). Succinylcholine does not directly act on cardiac muscle; phase II block is a neuromuscular junction phenomenon.
Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.
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