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Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion
M L Cannon1, S S Glazier, L A Bauman
1Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA. mlcannon@wfubmc.edu
Insights
A pediatric patient experienced fatal metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion for sedation. This case highlights the risks of using propofol for extended sedation in children.
Area of Science:
- Pediatric Critical Care Medicine
- Neurocritical Care
- Clinical Pharmacology
Background:
- Severe closed head injury management in pediatric patients often requires prolonged sedation.
- Continuous propofol infusion is a common strategy for sedation in pediatric intensive care units (PICUs).
Observation:
- A 13-year-old girl with a severe head injury received a continuous propofol infusion (100 microg/kg/min) for 4 days.
- The patient developed severe metabolic acidosis, rhabdomyolysis, acute renal failure, and cardiovascular collapse.
- Despite maximal therapy, the patient's condition rapidly deteriorated, leading to multisystem organ failure.
Findings:
- The patient exhibited severe high anion gap/low lactate metabolic acidosis unresponsive to treatment.
- Rhabdomyolysis led to acute renal failure, and myocardial dysfunction presented with wide QRS complexes.
- Death occurred due to myocardial collapse secondary to severe metabolic acidosis and organ failure.
Implications:
- This case underscores the potential for severe adverse events, including metabolic acidosis and cardiovascular collapse, associated with prolonged propofol infusions in pediatric patients.
- Alternative pharmacological agents should be considered for long-term sedation in pediatric populations to mitigate these risks.
- Further research into the safe duration and dosage of propofol in pediatric critical care is warranted.
Abstract:
The authors present the hospital course of a 13-year-old girl with a closed head injury who received a prolonged infusion of propofol for sedation and, subsequently, died as a result of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse. The patient had been treated for 4 days at a referring hospital for a severe closed head injury sustained in a fall from a bicycle. During treatment for elevations of intracranial pressure, she received a continuous propofol infusion (100 microg/kg/min). The patient began to exhibit severe high anion gap/low lactate metabolic acidosis, and was transferred to the pediatric intensive care unit at the authors' institution. On arrival there, the patient's Glasgow Coma Scale score was 3 and this remained unchanged during her brief stay. The severe metabolic acidosis was unresponsive to maximum therapy. Acute renal failure ensued as a result of rhabdomyolysis, and myocardial dysfunction with bizarre, wide QRS complexes developed without hyperkalemia. The patient died of myocardial collapse with severe metabolic acidosis and multisystem organ failure (involving renal, hepatic, and cardiac systems) approximately 15 hours after admission to the authors' institution. This patient represents another case of severe metabolic acidosis, rhabdomyolysis, and cardiovascular collapse observed after a prolonged propofol infusion in a pediatric patient. The authors suggest selection of other pharmacological agents for long-term sedation in pediatric patients.
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