ORF30-03 - The Enigmatic Triangle: Successful Management of Hypertriglyceridemia-Induced Acute Pancreatitis and Diabetic Ketoacidosis with High-Dose Insulin Therapy

Introduction:

The "enigmatic triangle" refers to a rare but dangerous combination of diabetic ketoacidosis (DKA), severe hypertriglyceridemia (SHTG), and acute pancreatitis (AP). These conditions are interconnected through insulin deficiency. This deficiency leads to uncontrolled lipolysis and reduces lipoprotein lipase activity, causing excessive triglyceride buildup. When pancreatic lipase breaks down triglycerides, it produces toxic free fatty acids that harm pancreatic acinar cells, triggering pancreatitis. This report describes successful management of this triad using a focused insulin-based treatment approach.


Case Presentation:

A 53-year-old Filipino woman with poorly controlled type 2 diabetes mellitus came in after 24 hours of severe vomiting and severe epigastric pain. On admission, her blood pressure was low at 87/48 mmHg, and her heart rate was high at 114 beats per minute. Lab tests confirmed DKA, showing a plasma glucose level of 39.7 mmol/L, an arterial pH of 7.37, bicarbonate at 11.6 mmol/L, and an anion gap of 31.3 mEq/L. Her serum triglycerides were extremely high at 4573 mg/dL. A lipase level of 2253 U/L and a C-reactive protein level of 150 mg/L supported the diagnosis of acute pancreatitis. A non-contrast abdominal CT scan showed widespread peripancreatic edema without cholelithiasis, confirming the diagnosis.

Management and

Results:

Initial management focused on aggressive fluid resuscitation with 1500 mL of normal saline in the first hour, followed by a continuous intravenous insulin infusion titrated to reduce glucose by 50-75 mg/dL per hour. The primary therapeutic goal was the activation of LPL to facilitate triglyceride clearance while simultaneously suppressing ketogenesis. Once blood glucose approached 250 mg/dL, dextrose-containing fluids were introduced. This allowed for the continuation of high-dose insulin therapy required to treat the SHTG and AP without risking iatrogenic hypoglycemia. Electrolytes were monitored and corrected as needed. By hospital day 1, the patient showed significant clinical improvement. Triglycerides decreased to 3295 mg/dL and lipase plummeted to 194 U/L. By day 3, triglyceride levels reached 1376 mg/dL, and the patient was successfully transitioned to subcutaneous insulin and a clear liquid diet. By day 5, triglycerides were 599 mg/dL. The patient was discharged on a regimen of fenofibrate, insulin, and strict dietary counseling.


Conclusion:

This case shows that protocol-driven intravenous insulin therapy is an effective first-line treatment for the DKA-SHTG-AP triad. It addresses both blood sugar levels and lipid-related pancreatic injury.