A51-45 Severe Hypertriglyceridemia-induced Acute Pancreatitis: A Case of Multi-organ Dysfunction and the Uncertain Role of Plasmapheresis

Abstract Introduction Hypertriglyceridemia-associated acute pancreatitis (HTG-AP) is a well-established and prevalent cause of acute pancreatitis (AP). Current management centers around lowering serum triglyceride (TG) levels quickly to prevent systemic inflammation and ischemia. Guidelines recommend starting with conservative management including pain control, intravenous fluids, and insulin prior to alternative therapies such as plasmapheresis. In cases that are refractory to conservative management, there is a lack of consensus for the specific criteria and timing for plasmapheresis initiation, and much variation exists between institutions and societies. Despite current management, patients with HTG-AP remain at higher risk for severe disease, including organ failure and systemic complications, as compared to other etiologies of AP. Case Presentation A 40-year-old male with history of occasional alcohol use presented with acute epigastric pain. Imaging and laboratory findings were significant for acute pancreatitis with undetectably high hypertriglyceridemia and metabolic acidosis. Initial management included admission to the intensive care unit for insulin infusion, but serum TG levels remained markedly elevated. Subsequently, plasmapheresis was performed with rapid lowering of serum TGs. Despite this, the patient developed hemorrhagic pancreatitis and pseudocyst formation leading to a prolonged ICU course with multiorgan dysfunction. This included respiratory failure requiring intubation and then ventilator associated pneumonia. He later developed renal failure and acalculous cholecystitis. Ultimately, he underwent cystogastrostomy for pseudocyst drainage and was weaned to tracheostomy collar. Discussion This case highlights the increased risk of severe complications and organ failure in HTG-AP. Current guidelines emphasize the need for rapid lowering of TG levels to limit the development of systemic inflammation and organ ischemia. Some studies show that plasmapheresis can lower TGs more rapidly than insulin therapy, and certain approaches suggest starting directly with plasmapheresis in patients with signs of significant inflammation. Other guidelines, including those from the endocrine society explicitly recommend against plasmapheresis as first line therapy in HTG-AP. Limited randomized control trials (RCTs) have shown no clear benefit of plasmapheresis over conservative management in terms of morbidity or mortality reduction, which has been attributed to damage being done prior to initiation of therapy. In cases like ours where TGs remain elevated refractory to insulin, clinicians are left to subjectively decide when to initiate plasmapheresis, and patients are left vulnerable to poor outcomes with higher TGs for extended time. Further RCTs should be done to delineate the true benefit of rapidly lowering TGs and the benefit of using plasmapheresis as first line therapy. This abstract is funded by: None