A102-07 Clogged by Lipids: A Rare Presentation of Hypertriglyceridemia-Related Membrane Lung Dysfunction

Abstract Introduction The deleterious effects of high serum lipid content on the membrane lung (ML) during extracorporeal membrane oxygenation (ECMO) are poorly documented, and the threshold of lipemia-induced membrane failure is not well described. Here, we present the case of a patient on Veno-Venous Extracorporeal Membrane Oxygenation (VV ECMO) who developed severe hypertriglyceridemia and, as a result, developed ML failure, shown by impaired gas exchange and high transmembrane pressures. Case A 47-year-old man with no past medical history presented for worsening dyspnea and was found to have interstitial lung disease and diffuse subcutaneous emphysema secondary to anti-MDA5 dermatomyositis. His course was complicated by worsening hypoxia requiring intubation and mechanical ventilation, VV ECMO, and ultimately Veno-Arterial-Venous Extracorporeal Membrane Oxygenation (VAV ECMO) given worsening shock. Furthermore, the patient developed worsening renal failure and required hemodialysis. After clinical improvement, the arterial limb was removed following a successful ramp-down. Soon thereafter, the VV ECMO circuit demonstrated persistently low flows and rising transmembrane pressures. A transesophageal echocardiogram (TEE) revealed non-occlusive echodensities in the drainage cannula. Despite troubleshooting, flow remained suboptimal, prompting a circuit exchange. Following replacement, circuit flows immediately normalized. Laboratory evaluation during this episode revealed markedly elevated triglycerides (2,613 mg/dL) with grossly lipemic, turbid plasma that interfered with routine assays (Figure 1). The patient was not on propofol or other lipid-based therapies, suggesting acute, unexplained hypertriglyceridemia as the cause of membrane lung failure. The critical illness stress response could have been a contributing factor to the severe hypertriglyceridemia observed in this patient. Discussion Severe hypertriglyceridemia (serum triglycerides 1000 mg/dL) can cause multiple complications, including significantly increasing the plasma viscosity, impairing capillary blood flow, and even inducing tissue ischemia. In this case, profound lipemia likely caused ECMO membrane dysfunction, as evidenced by elevated transmembrane pressures and low circuit flows that resolved following circuit exchange. The exact etiology of the hypertriglyceridemia remains uncertain.This case highlights the importance of considering hyperlipidemia as a reversible cause of membrane lung failure. Early recognition and routine monitoring of serum triglyceride levels during ECMO, especially in patients receiving prolonged support or parenteral nutrition, may prevent catastrophic circuit failure. This abstract is funded by: None