SUN-626 - From Ketoacidosis to Catastrophe: A Triad of DKA, Necrotizing Pancreatitis, and Pulmonary Embolism

Introduction
Diabetic ketoacidosis (DKA) may occur across the diabetes spectrum, including atypical phenotypes, with rare complications of severe inflammatory and thrombotic events. We report recurrent DKA complicated by necrotizing pancreatitis and pulmonary embolism (PE) in the setting of high-risk psychiatric medications.

Case
A 25-year-old African-American woman with bipolar disorder and schizophrenia on olanzapine and valproic acid, type 2 diabetes (T2DM), obesity, and recurrent DKA presented five days after being discharged with altered mental status after insulin nonadherence. She was hypothermic, tachycardic, and hypotensive with glucose >1200 mg/dL, AG 36, VBG pH 7.08/HCO₃⁻ 12.5 mmol/L (24-30), lactate 4.9 mmol/L (0.5-2.2), Cr 4.4 mg/dL (0.6-1.2), and WBC 16.4×10³/µL (4-10), consistent with DKA; she was treated with insulin infusion, IV fluids, and broad-spectrum antibiotics.

She subsequently developed fever and abdominal pain. CT A/P showed pancreatic body/tail hypoattenuation consistent with necrotizing pancreatitis, with labs reporting lipase 682 U/L (22-51), triglycerides 96 mg/dL (20-140), and segmental PE. She was treated with heparin drip, meropenem, and bowel rest. A peripancreatic collection seen in the course was drained under image guidance, yielding sterile inflammatory fluid with radiographic resolution. Autoimmune workup from her prior admission showed diabetes without islet autoantibodies and low but detectable C-peptide, and she was transitioned from insulin infusion to a basal-bolus regimen. After stabilization, she was discharged on basal-bolus insulin therapy, apixaban, and her psychiatric medications, with close multidisciplinary follow-up.

Discussion
The incidence of necrotizing pancreatitis during recurrent severe DKA is not well established in the medical literature. Diagnosis should also prompt evaluation for secondary causes, including medication-associated pancreatitis, like in our patient who was receiving valproate, olanzapine, and haloperidol. Pancreatitis may be idiosyncratic and occur independent of triglyceride elevation, so normal triglycerides do not exclude a drug-related contribution. Negative islet autoantibodies with detectable C-peptide support ketosis-prone T2DM, a phenotype more prevalent in African-American patients, while pancreatic necrosis raises concern for evolving pancreatogenic (type 3c) diabetes requiring longitudinal monitoring after pancreatitis. Concomitant PE underscores the prothrombotic risk of severe hyperglycemic crises and a low threshold to evaluate for venous thromboembolism when clinically suspected.

Conclusion: Although most cases of DKA are associated with acute pancreatitis, necrotizing pancreatitis and thrombotic pathologies should be considered in the cases of recurrent DKA, with earlier recognition leading to decreased morbidity and mortality.

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