SUN-604 - Fatal Diabetic Ketoacidosis with Concurrent Acute Pancreatitis Presenting as Out-of-Hospital Cardiac Arrest

Introduction:
Diabetic ketoacidosis (DKA) is a life-threatening hyperglycemic emergency that may rapidly progress to circulatory collapse from profound metabolic derangement and electrolyte shifts. Common precipitants include infection, medication nonadherence, and physiologic stress. Acute pancreatitis is an uncommon but recognized precipitant. We report fatal DKA with concurrent acute pancreatitis presenting as an out-of-hospital cardiac arrest.

Case Description:
A 22-year-old male with autism and no prior diabetic history presented to the hospital after a cardiac arrest. His father reported several days of malaise and diarrhea and found the patient with agonal respirations on the morning of presentation. Emergency medical services found him to be pulseless. Return of spontaneous circulation was achieved approximately 20 minutes after emergency department arrival.

Initial studies showed potassium 4.3 mmol/L (3.4–5.1), bicarbonate 18 mmol/L (21–32), glucose 812 mg/dL (70–99), creatinine 3.27 mg/dL (0.67–1.17), lipase 5568 units/L (15–77), beta-hydroxybutyrate 5.2 mmol/L (0–0.3), lactic acid 9.6 mmol/L (0–2), and anion gap of 23. Venous blood gas demonstrated severe acidemia with pH < 6.96 and pCO2 35. He was treated with insulin infusion, vasopressor support, and aggressive intravenous fluids and admitted to the intensive care unit. Computed tomography (CT) of the head demonstrated extensive global hypoxic ischemic injury with increased intracranial pressure. Abdominal CT revealed inflammatory changes around the pancreatic head and uncinate process concerning for acute pancreatitis. Formal neurologic testing conducted 72 hours later confirmed neurologic brain death.

Discussion:
This case highlights an uncommon and devastating presentation of severe DKA in a patient with no prior documented history of diabetes mellitus as out-of-hospital arrest. Severe acidemia, profound volume depletion, and total-body potassium deficit likely contributed to circulatory collapse despite a normal initial serum potassium concentration. This case emphasizes the need for early recognition of DKA symptoms and awareness that acute pancreatitis may coexist with, and possibly precipitate, severe DKA.
Severe acidemia may further worsen hemodynamic instability by impairing myocardial contractility and catecholamine response. Although severe DKA is well known and described, patients first presenting with cardiac arrest leading to hypoxic-ischemic brain injury is rare, particularly in the setting of acute pancreatitis. This case underscores the importance of early recognition of DKA symptoms and the potential for rapid deterioration in the setting of severe metabolic derangements. Furthermore, it emphasizes the need for heightened vigilance in patients with developmental disabilities, in whom early symptoms may not be as readily apparent.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*