Case Presentation:

A 39 year old man with type 2 diabetes, known hypertriglyceridemia with past episodes of pancreatitis presented to the Emergency Room with severe, diffuse abdominal pain for two days. Despite an outpatient medication regimen that included Gemfibrozil, Atorvastatin, Niacin and Lovaza his initial trigyleceride level was 8169 mg/dL with a lipase level of 1357 U/L and a diffusely tender abdomen on physical exam.  Concominant metabolic derangements included hyperglycemia of 364mg/dL with ketonuria and a serum anion gap of 22. After receiving a bolus of normal saline followed by a continuous saline infusion at 150 cc/hr and analgesic medication the patient was admitted to the Medical Intensive Care Unit for hypertriglyceride induced pancreatitis (APACHE II Score:6, Ranson’s Score:4) and mild diabetic ketoacidosis.

His Intensive Care Unit course included two rounds of plasmapheresis and an continuous insulin infusion. After the first plasmapheresis the triglyceride level decreased to 3620 mg/dL (a 55% decrease) and following the second round the triglycerides were 357 (a 95% decrease). The patient was transitioned to a basal bolus insulin regimen and to the General Medicine floors on hospital day two when his anion gap had closed, his glucose levels were well controlled and his triglyceride levels were 357 mg/dL. A CAT scan of the abdomen and pelvis performed on the second day of admission revealed acute interstitial edematous pancreatitis with peripancreatic fluid and ascites but no necrosis. The remainder of his hospital course was uncomplicated.


Hypertriglyceridemia is the third most common cause of pancreatitis following alcohol and gallstones.  Very severe hypertriglyceridemia, defined as a serum triglyceride level greater than 2000 mg/dL, places a patient at an especially high risk for acute pancreatitis.  Current management strategies for hypertriglyceridemia include conventional treatment (intravenous fluids and analgesia), oral lipid lowering medications, insulin therapy, heparin and lastly apheresis. Randomized control trials comparing these treatment modalities are lacking. This case is unique in that both insulin therapy – necessitated by the mild diabetic keotacidosis, and plasmapheresis were employed simultaneously with a rapid lowering of the triglyceride level and an excellent patient outcome.    


In a patient with severe hypertriglyceridemia causing pancreatitis and mild diabetic ketoacidosis simultaneous insulin therapy and plasmapheresis lead to a rapid improvement in cholesterol levels. Future research is needed as combined plasmapheresis and insulin therapy may be more beneficial than monotherapy with insulin or apheresis alone for the treatment of hypertriglyceride induced pancreatitis.