S3411 Diabetic Ketoacidosis, Hypertriglyceridemia, and Acute Pancreatitis: A Rare but Potentially Fatal Triad Complicated by Pancreatic Pseudocyst

Introduction: High triglyceride induced acute pancreatitis (HTGP) is a well-known cause of acute pancreatitis (AP), with severity correlating to hypertriglyceridemia. Concurrent HTGP and DKA in a patient without prior diabetes is rare. We present a case of high TG levels exceeding 5,000 mg/dL, new-onset concurrent DKA complicated by AP and a pancreatic pseudocyst. Case Description/Methods: A 33-year-old obese (body mass index 33) man with no medical history presented with 3-day of worsening, intermittent 10/10 epigastric pain, with multiple episodes of non-bloody, non-bilious emesis. He also reported polydipsia and nocturia (>20 voids/night). On examination, he was tachycardia (HR 122), afebrile, and in moderate distress. Abdominal exam revealed epigastric tenderness without rebound or guarding. Initial laboratory studies: WBC: 27.4K, bicarbonate: <4, anion gap: 20, glucose: 399, Ca: 8.5, Creatine: 1.71, lipase 193, TG >5680, cholesterol: 569, unable to detect LDH, β-hydroxybutyrate: 6.93, HbA1c: 11%, osmolarity: 315. ABG pH: 7.06, CO2: 12, O2: 112, bicarbonate: 3.3, lactate 2.8. Contrast-enhanced computed tomography showed acute pancreatitis with peripancreatic inflammation, diffuse hepatic steatosis, and a 10.8 × 9.7 cm low-attenuation lesion in the pancreatic tail consistent with a pseudocyst. The patient was diagnosed with HTGP and DKA and admitted to the intensive care unit. He received aggressive intravenous hydration, an insulin infusion per DKA protocol, and serial monitoring of complete metabolic profile (q4 hr) and TG (q12 hr). Empiric antibiotics and opioid analgesia were initiated. Plasmapheresis was considered but deferred as TG values decreased to 2,840, then 1,354 on day 2, and 451 mg/dL on day 3, with closure of the anion gap and bicarbonate rising to 18. Surgical and IR teams recommended outpatient pseudocyst follow-up. A post-DKA C-peptide of 1.1 ng/mL suggested underlying T2DM. On hospital day 6, repeat computed tomography: a markedly reduced pseudocyst (1.1 × 1.0 cm), despite worsening peripancreatic inflammation with increased free fluid. Lipase decreased to 126 U/L. Upon clinical improvement, the patient was discharged on a basal-bolus insulin, fenofibrate, atorvastatin, and a strict low-fat diet. Discussion: Pancreatic pseudocysts usually develop more than 4 weeks after acute pancreatitis. Per AGA guidelines, most resolve spontaneously with conservative management. In our case, a pseudocyst formed during the acute phase but regressed as inflammation subsided without intervention. Broad-spectrum antibiotics were administered because walled-off necrosis could not be excluded.