A 32-year-old male with a family history of malignant hyperthermia presents for elective laparoscopic cholecystectomy. Regarding the clinical features and management of MH, all of the following statements are true EXCEPT:

Explanation

## Clinical Features and Management of Malignant Hyperthermia **Key Point:** In an "all EXCEPT" question, the FALSE statement is the correct answer. Option C contains a factual inaccuracy: hyperkalemia in MH is **primarily due to rhabdomyolysis and muscle cell destruction** (massive potassium efflux from lysed muscle cells), not merely "continued depolarization." While succinylcholine-induced depolarization contributes early, the dominant mechanism of severe hyperkalemia in a full MH crisis is rhabdomyolysis-driven cell lysis. ### Why Option C is FALSE (the EXCEPT answer) **Mechanism of Hyperkalemia in MH:** 1. Uncontrolled calcium release from the sarcoplasmic reticulum → sustained muscle contraction 2. Massive ATP consumption → muscle cell energy failure 3. **Rhabdomyolysis** (muscle cell destruction) → large-scale potassium efflux from lysed cells 4. This is the **primary** driver of the severe hyperkalemia (K⁺ can exceed 9 mEq/L) seen in MH crisis 5. Continued depolarization alone (as stated in Option C) is a secondary/contributing mechanism, not the primary one **Reference:** Miller's Anesthesia (9th ed.) and Barash Clinical Anesthesia both attribute the severe hyperkalemia of MH primarily to rhabdomyolysis, not to continued depolarization per se. ### Why the Other Options Are TRUE (and thus NOT the answer) | Option | Statement | Verdict | |--------|-----------|---------| | **A** | Masseter muscle rigidity after succinylcholine is an early sign of MH | **TRUE** — MMR is a recognized early warning sign per Barash/Miller; requires immediate vigilance | | **B** | Dantrolene blocks calcium release via ryanodine receptor (RYR1) | **TRUE** — Classic mechanism; dantrolene binds RYR1 to prevent Ca²⁺ release | | **D** | MH-susceptible patients can safely receive propofol and non-depolarizing NMBs | **TRUE** — Triggering agents are volatile halogenated anesthetics and succinylcholine only | ### Dantrolene Mechanism **Clinical Pearl:** Dantrolene sodium: - Blocks calcium release from the sarcoplasmic reticulum via the **ryanodine receptor (RYR1)** - Reduces intracellular calcium → decreases sustained muscle contraction and thermogenesis - Dose: **2.5 mg/kg IV bolus**, repeat every 5 minutes up to **10 mg/kg** if crisis continues ### Safe Anesthetic Technique for MH-Susceptible Patients **Mnemonic: SAFE** - **S** = Succinylcholine — AVOID - **A** = All volatile halogenated agents — AVOID - **F** = Fast IV induction with propofol/etomidate — SAFE - **E** = Everything else (non-depolarizing NMBs, nitrous oxide, local anesthetics) — SAFE **High-Yield:** The earliest and most sensitive sign of MH is **unexplained rise in end-tidal CO₂ (ETCO₂)**, followed by tachycardia. Fever is a late sign. Masseter rigidity after succinylcholine is an early warning that mandates heightened vigilance and preparation for MH management. **Reference:** Miller's Anesthesia, 9th ed., Chapter on Malignant Hyperthermia; Barash Clinical Anesthesia, 8th ed.