C48-11 Severe ARDS From Hypertriglyceridemic Pancreatitis and DKA Requiring VV-ECMO

Abstract Introduction Hypertriglyceridemia with triglyceride levels exceeding 1000 mg/dL is a known cause of acute pancreatitis, which can trigger a systemic inflammatory response leading to multiorgan failure and high mortality (3). Acute respiratory distress syndrome (ARDS), a severe manifestation of acute lung injury driven by widespread inflammation and increased pulmonary vascular permeability, can be triggered by acute pancreatitis. We present a fatal case of a young male who developed acute pancreatitis secondary to severe hypertriglyceridemia, complicated by diabetic ketoacidosis (DKA) and ARDS, which ultimately required venovenous extracorporeal membrane oxygenation (VV-ECMO) as a rescue measure. Case Description 39-year-old male with a history of alcohol abuse, hypertension, and prior pancreatitis presented with acute epigastric pain. Initial laboratory studies revealed a lipase level 6000 U/L, triglycerides 4156 mg/dL, beta-hydroxybutyrate 8.33 mmol/L, and bicarbonate 14 mmol/L. Imaging was consistent with acute pancreatitis complicated by DKA. He was started on an insulin infusion and aggressive fluid resuscitation. Over the following 24 hours, he developed progressive respiratory distress, hypotension, and oliguria. He was started on vasopressors, continuous renal replacement therapy (CRRT) and intubated for airway protection. Despite lung-protective ventilation, his hypoxia worsened, progressing to severe ARDS by hospital day three. Due to concerns for elevated intra-abdominal pressures in the setting of pancreatitis, prone positioning was avoided. VV-ECMO was initiated as a rescue therapy. Despite maximal medical interventions, his condition continued to deteriorate, resulting in refractory multiorgan failure and eventual withdrawal of care by the family. Discussion The pathophysiology of hypertriglyceridemia-induced pancreatitis involves multiple mechanisms. Triglycerides are hydrolyzed into free fatty acids, which at high concentrations can induce pancreatic acinar cell injury, generate reactive oxygen species, and promote local and systemic inflammation (2). Elevated chylomicrons may also cause capillary plugging, leading to pancreatic ischemia and endothelial damage (2). The profound systemic inflammatory state can lead to vascular endothelial injury and pulmonary parenchymal damage, resulting in ARDS. In this case, severe hypertriglyceridemia triggered pancreatitis and, within 72 hours of admission, progressed to severe ARDS and multiorgan failure. Due to contraindications to proning, early initiation of VV-ECMO was pursued as salvage therapy (1). Unfortunately, despite aggressive management, the patient’s condition proved refractory, emphasizing the high mortality associated with hypertriglyceridemic pancreatitis and its complications such as ARDS. This abstract is funded by: None