Balancing Sedation and Risks: A Case Report on Propofol Infusion Syndrome

Introduction Propofol infusion syndrome (PRIS) is a rare, life-threatening complication of prolonged or high-dose propofol use, marked by lactic acidosis, rhabdomyolysis, hyperlipidemia, and cardiac dysfunction [1]. This report highlights a case of PRIS, focusing on early recognition, diagnostic challenges, and management strategies. Case Presentation A 35 y/o male was admitted to the Neurosurgery Intensive Care Unit (NSICU) with impaired consciousness and respiratory failure following a severe traumatic brain injury. Anamnesis - he had jumped out of a moving car. Upon arrival at the ER, his GCS score was 8. The patient was sedated, intubated, and underwent surgery for bifrontal decompressive craniectomy, ICP sensor placement. Sedation was maintained with propofol (administered for 7 days at doses ranging from 1.7 to 6.4 mg/kg/h) and fentanyl (0.2 mg/h), while norepinephrine was used for arterial pressure and brain perfusion, with ICP initially stable at 13 mmHg. On the 7th day in the NSICU, the patient developed atrial fibrillation, renal dysfunction with rising uremic markers, metabolic acidosis without lactate elevation and hyperkalemia. Laboratory findings revealed significantly elevated creatine kinase, triglycerides, and liver enzymes, raising suspicion of rhabdomyolysis secondary to PRIS (McMahon Rhabdomyolysis Score: 7). Propofol was discontinued, and sedation was switched to ketamine (2.5 mg/kg/h) and midazolam (7.5 mg/h), maintaining ICP between 14–17 mmHg and brain tissue oxygenation at 24 mmHg. Sodium bicarbonate was administered to address acidosis, and treatments for hyperkalemia, rhabdomyolysis, renal failure, and atrial fibrillation were initiated. After stabilised condition he was transfered to the neurosurgery department. Discussion PRIS has an incidence of 1–4.9% and a mortality rate of up to 49% in adults [2–4]. It involves mitochondrial dysfunction, leading to impaired ATP synthesis and cellular hypoxia. Risk factors include high infusion rates, critical illness, and sedation over 48 hours or >4 mg/kg/h [5]. Diagnosis is based on metabolic acidosis, ECG changes, and rhabdomyolysis, with treatment focusing on stopping propofol Conclusions PRIS, a rare but fatal complication of prolonged propofol use, requires prompt recognition and treatment. Vigilance in high-risk cases is vital for better outcomes.