Riad Akkari, MD
Critical Care Fellow
George Washington University
Laurel, MD
Disclosure information not submitted.
Joseph Devlin, MD
Surgical resident
George washington University, United States
Disclosure information not submitted.
Robert Markie, RN
ECMO Coordinator
George Washington University Hospital, United States
Disclosure information not submitted.
David Yamane, BS, MD
Assistant Professor of Emergency Medicine, Anesthesiology, and Critical Care Medicine
George Washington University Hospital, United States
Disclosure information not submitted.
Mustafa Al-mashat, MD
Assistant professor
George Washington University, United States
Disclosure information not submitted.
Title: Fatty ECMO: A case of propofol-induced membrane lung failure
Introduction: Propofol is commonly used in the intensive care unit for sedation in ventilated patients. Prolonged use of propofol in high concentrations can complicate propofol infusion syndrome and can also contribute to lipemia which can cause pancreatitis and severe metabolic acidosis. We describe a case of lipemia leading to membrane lung (ML) dysfunction during extracorporeal membrane oxygenation (ECMO) and worsening hypoxemia.
Description: A 25-year-old man who presented poly-trauma after a 30-foot fall with multiple orthopedic traumas to the lower extremities whose hospital course was complicated by acute respiratory distress syndrome in the setting of presumed fat emboli along with multi-organism pneumonia, leading to refractory hypoxemia requiring paralytic therapy and increasing amounts of sedation while intubated, that eventually required further support with venovenous ECMO support. He continued to require a high concentration of prolonged propofol infusion. Our patient remained to have hypoxemia complicating his status despite support, and eventually had pre- and post-oxygenator blood gas checked, which revealed poor oxygenation though had no visual signs of thrombosis, and so the decision was made to exchange the lung membrane which revealed the significant evidence of lipemia that was noted and visualized with cessation of flow. The lipemia and fat collections were thought to be secondary to the hypertriglyceridemia from propofol infusion and hence was discontinued, with improved triglyceride level and improved oxygenation post ML exchange.
Discussion: Propofol-induced hypertriglyceridemia is a possible cause of membrane lung failure that can contribute to refractory hypoxemia despite ECMO support. Our patient had no clinical signs of developing propofol infusion syndrome and had only a moderate increase in triglyceride levels (686mg/dL), but had contributed to a significant oxygenator membrane dysfunction and hypoxia, with no discernible increase in pump power or decrease in pump flow was observed; that can be hard to identify unless keeping a high index of suspicion. Prolonged use of propofol would require close monitoring along with the possible need for frequent oxygenator change.