SESSION TYPE: Critical Care Case Report Posters
PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION: Insulin deficiency or resistance in diabetes mellitus leads to an increased circulating triglyceride (TG) levels which can be responsible for precipitating acute pancreatitis (1). There have been few reported cases of severe hypertriglyceridemia (defined as TG level > 2,000 mg/dL) in diabetic ketoacidosis accompanied by acute pancreatitis in Korea, but none from the United States.
CASE PRESENTATION: 30-year-old male with a history of insulin dependent diabetes mellitus, non compliance presented with complaint of abdominal pain described as constant, sharp, 10/10 in severity, located in epigastric region, associated with nausea and vomiting for one day duration. On physical examination, he was afebrile, BP=129/81 mmHg, pulse=89 bpm and had mild tenderness over the epigastric region. Laboratory examination revealed a white blood cell count 14,500 /µL, sodium 125 meq/L, potassium 4.7 meq/L, chloride 97 meq/L, bicarbonate 19 meq/L, BUN 6 mg/dL, creatinine 0.5 mg/dL, an anion gap of 9. Glucose was 543 mg/dL and lipase was 1055 U/L. Urinalysis showed glucose > 1000 mg/dL, ketones > 80 mg/dL. Patient was admitted to the medical floor for managing pancreatitis. Thereafter fasting lipid profile was obtained and triglycerides were 3354mg/dL. Repeat metabolic panel showed an anion gap of 27 and the patient was transferred to the intensive care unit for diabetic ketoacidosis. Patient was continued on intravenous fluid hydration and insulin drip was started. The anion gap closed the following day but the insulin drip was continued to manage hypertriglyceridemia. Subsequent triglyceride levels were 2289, 1340, 769, 396 mg/dL.
DISCUSSION: The insulin mediated lipoprotein lipase suppression and VLDL production is defective in insulin resistance, leading to increased free fatty acid and VLDL production, which results in increased circulating triglyceride concentrations (2). Lipase in the pancreatic bed breaks the serum triglycerides into toxic free fatty acids which results in pancreatitis (3). Diagnostic clues include lipemic serum; high urine anion gap as compared to normal serum anion gap. Treatment includes insulin therapy with conservative management and rarely some cases require plasma exchange.
CONCLUSIONS: A case of hypertriglyceridemia resulting in acute pancreatitis and diabetic ketoacidosis, managed with aggressive hydration and a continuous insulin infusion, thus leading to a correction of both the acidosis and hypertriglyceridemia.
1) Suk Jae et al. Severe Hypertriglyceridemia in Diabetic Ketoacidosis Accompanied by Acute Pancreatitis. (2010): http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923793/.
2) Kronenberg et al. Williams Textbook of Endocrinology. 11. 2007.
3) TaYamada et al, Textbook of Gastroenterology. 5th; 2. 2008.
DISCLOSURE: The following authors have nothing to disclose: Vibu Varghese, Vipin Mittal, Anery Patel, Muhammad Ali, Mourad Ismail
No Product/Research Disclosure InformationSt. Joseph's Regional Medical Center, Paterson, NJ