A 38-year-old obese woman received halothane for laparoscopic cholecystectomy six weeks ago. She is re-exposed to halothane for a second procedure. On postoperative day 8 she develops fever, a transient rash, peripheral eosinophilia and jaundice. AST is 1450 U/L with INR 2.1. The most likely mechanism of her liver injury is:

• A Immune-mediated massive hepatocellular necrosis against trifluoroacetylated liver proteins ✓
• B Direct dose-dependent centrilobular necrosis from reduced hepatic blood flow
• C Obstruction of the common bile duct by sludge formed during fasting
• D Reactivation of latent hepatitis B following surgical stress

Explanation

Type II halothane hepatitis is rare, occurs mainly after repeated exposure, and is more frequent in obese middle-aged women. Oxidative metabolism forms trifluoroacetylated hepatocyte proteins that act as haptens, triggering an antibody-mediated fulminant necrosis with fever, rash, eosinophilia and a latency of days to weeks. Direct dose-related injury is type I, which is mild, asymptomatic and self-limiting.

Reference: Morgan and Mikhail's Clinical Anesthesiology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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