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Rapid cardiovascular collapse with severe metabolic derangement during propofol sedation should raise concern for propofol infusion syndrome (PRIS).A 21-year-old man with previous traumatic brain injury presented with refractory status epilepticus requiring mechanical ventilation and prolonged propofol sedation.Following four days of infusion, he developed abrupt bradycardia, cardiogenic shock, severe highanion-gap metabolic acidosis, rhabdomyolysis, acute kidney injury, hypertriglyceridemia, and significant left ventricular dysfunction.The combination of prolonged propofol exposure and rapidly evolving multiorgan failure was considered consistent with PRIS.Propofol was discontinued immediately.Management included administration of multiple vasoactive infusions, sodium bicarbonate, calcium chloride, dual high-effluent continuous renal replacement therapy via two dialysis circuits, high-dose euglycemic insulin, and enteral L-carnitine.Hemodynamic improvement occurred within approximately six hours, followed by recovery of cardiac and renal function.He was discharged from the intensive care unit on day 30 and later returned home after rehabilitation without dialysis dependence.This case highlights the importance of early recognition of PRIS and rapid escalation of individualized organ support in severe presentations, while acknowledging that the contribution of individual adjunctive therapies cannot be determined from a single case.
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Power et al. (2026) studied this question.
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