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    Subjects/Anesthesia/Muscle Relaxants — Depolarising and Non-depolarising
    Muscle Relaxants — Depolarising and Non-depolarising
    hard
    syringe Anesthesia

    A 35-year-old male patient is scheduled for emergency laparotomy following a stab wound to the abdomen. Induction is planned with propofol and a muscle relaxant. The patient has a history of severe burns 6 months ago affecting 40% of his body surface area, now in the healing phase. During intubation, after administration of succinylcholine 1.5 mg/kg IV, the patient develops severe hyperkalemia (K⁺ 7.2 mEq/L), peaked T waves on ECG, and cardiac arrhythmias. What is the most likely explanation for this complication?

    A. Succinylcholine causes direct myocardial sensitization to potassium in all patients
    B. Upregulation of extrajunctional acetylcholine receptors in denervated or damaged muscle following thermal injury leads to exaggerated potassium efflux
    C. The patient has underlying chronic kidney disease causing baseline hyperkalemia
    D. Propofol interaction with succinylcholine increases potassium release from muscle

    Explanation

    ## Pathophysiology of Succinylcholine-Induced Hyperkalemia in Burn Patients **Key Point:** Succinylcholine causes a transient rise in serum potassium in all patients (0.5–1.0 mEq/L), but life-threatening hyperkalemia occurs in patients with conditions causing upregulation of extrajunctional (non-junctional) acetylcholine receptors. ### Mechanism in Burn Injury 1. **Thermal injury** causes muscle necrosis and denervation-like changes 2. **Extrajunctional AChR proliferation** occurs across the entire muscle membrane (normally present only at the neuromuscular junction) 3. **Succinylcholine depolarization** activates these widespread receptors 4. **Massive K⁺ efflux** from muscle cytoplasm → severe hyperkalemia within seconds ### Timeline of Risk - **Onset:** 24 hours post-injury - **Peak risk:** 7–10 days post-injury - **Duration:** Up to 6–12 months (as in this case) **Clinical Pearl:** Even 6 months after burn injury, extrajunctional receptors may persist, making succinylcholine dangerous. ### Conditions Associated with Exaggerated K⁺ Release | Condition | Mechanism | Risk Window | |-----------|-----------|-------------| | Thermal burns | Muscle necrosis + denervation | Days to months | | Crush injury | Rhabdomyolysis | Days to weeks | | Spinal cord injury | Denervation | Weeks to months | | Prolonged immobilization | Disuse atrophy | Variable | | Muscular dystrophy | Abnormal AChR distribution | Lifelong | | Sepsis | Inflammatory muscle damage | Variable | **High-Yield:** The rise in K⁺ is **independent of dose** once extrajunctional receptors are present — even small doses of succinylcholine can trigger dangerous hyperkalemia. ### Clinical Presentation - Peaked T waves on ECG (earliest sign) - Bradycardia or tachycardia - Ventricular fibrillation (if K⁺ > 8 mEq/L) - Muscle fasciculations followed by paralysis ## Management 1. **Immediate:** Hyperventilation (↓ K⁺), IV calcium gluconate (membrane stabilization), insulin + dextrose, sodium bicarbonate 2. **Prevention:** Avoid succinylcholine in burn patients; use non-depolarising agents (rocuronium, vecuronium) [cite:Stoelting's Pharmacology in Anesthesia Ch 8]

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