ODP150 Hypertriglyceridemic Induced Acute Pancreatitis with Diabetic Ketoacidosis Treated with Insulin: A Case Report

INTRODUCTION: Acute pancreatitis due to hypertriglyceridemia with DKA is a unique entity. The diagnosis of acute pancreatitis in DKA is challenging as most patients present with abdominal pain, and elevated amylase, and lipase are quite common in DKA. Hypertriglyceridemia-induced pancreatitis (HTGP) accounts for 1 to 35 percent of all cases of acute pancreatitis. Pancreatitis may occur in DKA with high anion gap metabolic acidosis. Lack of insulin results in lipolysis with release of free fatty acids. Increased free fatty acids presented to the liver, causes increased VLDL, which inhibits lipoprotein lipase in peripheral tissues and results in elevated triglycerides. CASE PRESENTATION: A 29-year-old morbidly obese male with Asperger's syndrome, prediabetes, and hyperlipidemia presented with a 3-day history of sharp, non-radiating, and progressively worsening right upper abdominal pain, associated with nausea, non-bilious vomiting, and shortness of breath. His past medical history was notable for a prior bout of gallstone pancreatitis, for which he underwent a laparoscopic cholecystectomy. On his arrival in the emergency department, he was afebrile, but tachycardic (HR 139), mildly hypertensive (BP 149/98) with a Kussmaul breathing saturating 98% on room air. His lung sounds were clear but diminished and his abdomen was soft but diffusely tender, without peritoneal signs. Initial laboratory tests showed a neutrophilic leukocytosis of 12K, glucose of 867 mg/dL, hyponatremia (corrected 131), ketonuria, with elevated lipase 1,164 U/L. Venous blood gas showed a pH of 7.18 and PCO2 24 mmHg. He also had severe hypertriglyceridemia with a total triglyceride level of > 9,000 mg/dL. His CT abdomen showed peripancreatic inflammation consistent with acute pancreatitis. He was admitted to the ICU, and initially managed with aggressive intravenous fluids and pain control, then was started on an insulin drip for diabetic ketoacidosis and hypertriglyceridemia. His hospital course was notable for the development of acute kidney injury requiring hemodialysis. His triglyceride level gradually decreased and was 396 U/L on hospital day #9. He was discharged on fenofibrate, Lantus 20 units daily and insulin lispro 10 units with meals. CONCLUSION: Hypertriglyceridemia is an uncommon but a well-established cause of acute pancreatitis leading to significant morbidity and mortality. In this case, a prediabetic patient presented with DKA and further investigation revealed HTGP. There is currently a paucity of data to support an optimal treatment for this condition; however, both insulin and plasmapheresis have been successfully employed. Plasmapheresis helps remove plasma lipoproteins and reduces triglyceride more rapidly than insulin and has been recommended for severe cases. In our case, insulin infusion alone significantly reduced the triglyceride level. Presentation: No date and time listed