A patient receiving a prolonged propofol infusion (>48 h at >4 mg/kg/h) for ICU sedation develops metabolic acidosis, rhabdomyolysis, lipemic serum, and bradyarrhythmia resistant to atropine. The most likely diagnosis and its pathophysiological basis is:

• A Lipid overload syndrome; exogenous lipid accumulation in hepatocytes causing steatohepatitis
• B Hypertriglyceridaemia-induced pancreatitis with secondary myopathy
• C Serotonin syndrome from propofol-induced serotonin release at 5-HT3 receptors
• D Propofol infusion syndrome; mitochondrial respiratory chain dysfunction causing failure of fatty acid oxidation ✓

Explanation

Propofol infusion syndrome (PRIS) is characterised by severe metabolic acidosis, rhabdomyolysis, cardiac failure (often right bundle-branch block or ST changes), renal failure, and lipaemic plasma. The mechanism is inhibition of mitochondrial respiratory chain complexes I and IV and impairment of beta-oxidation of free fatty acids; cells switch to anaerobic metabolism producing lactic acidosis. The bradyarrhythmia is often atropine-resistant because it is due to myocardial dysfunction rather than vagotonia. Risk factors include high dose (>4 mg/kg/h), long duration (>48 h), catecholamines, and carbohydrate depletion.

Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.

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Written and medically reviewed by the StethoPrep medical team.