Document Type

Conference Proceeding

Publication Date

5-1-2026

Abstract

Introduction: The American Diabetes Association (ADA) recognizes diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) as life-threatening hyperglycemic emergencies that can overlap clinically; approximately 10% of presentations are described as mixed DKA–HHS. Because current guidelines do not define a single “mixed” category, overlap is best understood as concurrent fulfillment of key elements of both syndromes: DKA-type anion-gap metabolic acidosis with ketonemia or ketonuria, together with HHS-type severe hyperglycemia, hyperosmolality, and dehydration. We report an extreme HHS presentation (glucose >2,100 mg/dL) with limited DKA overlap. Case Description: A 34-year-old woman with longstanding type 1 diabetes mellitus managed with an insulin pump, was brought to the emergency department after being found delirious at home following several days of upper respiratory symptoms and poor oral intake. On arrival, she had altered mental status, and her insulin pump was nonfunctional due to a depleted battery. Initial laboratory evaluation showed leukocytosis (WBC 13.8 ×10³/µL) and anemia (hemoglobin ≈9 g/dL). Chemistry demonstrated profound hyperglycemia (>2,100 mg/dL), marked hyperosmolality (406 mOsm/kg), and acute kidney injury (creatinine peak 2.73 mg/dL, improving to ≈1.26–1.33 mg/dL with resuscitation). Ketone testing revealed minimal ketosis (small serum acetone; urine ketones negative). Arterial blood gas revealed pH 7.296, pCO₂ 22.9 mmHg, and bicarbonate 10.9 mmol/L, consistent with a high–anion-gap metabolic acidosis. Lactate was 7.51 mmol/L and improved to 2.18–2.28 mmol/L after volume repletion. She met HHS criteria, including severe hyperglycemia, effective osmolality >320 mOsm/kg, altered mental status, and dehydration with acute kidney injury, with minimal ketones. Although acidemia and low bicarbonate could suggest DKA, the lack of significant ketonemia or ketonuria supported lactic acidosis from hypoperfusion and severe volume depletion as the primary driver of the anion gap, consistent with HHS-dominant physiology with limited DKA overlap. She was transferred to the ICU for protocolized management with aggressive intravenous fluids, intravenous insulin infusion with frequent glucose and electrolyte monitoring, and targeted electrolyte repletion. Insulin was withheld when serum potassium fell below 3.3 mEq/L and resumed only after adequate repletion to reduce the risk of malignant ventricular arrhythmias. Glucose correction was controlled at approximately 60–80 mg/dL per hour to limit rapid osmotic shifts. With ongoing resuscitation, mental status normalized, renal function recovered, and metabolic derangements resolved. She was transitioned to subcutaneous insulin and discharged home in stable condition. Discussion: This case underscores the diagnostic and therapeutic complexity of hyperglycemic crises along the DKA–HHS spectrum. Despite acidemia and markedly reduced bicarbonate, minimal ketosis and absence of progressive ketonemia indicated lactic acidosis—not ketoacidosis—as the principal cause of the high–anion-gap metabolic acidosis, highlighting that acidemia alone should not be equated with DKA. Management should be guided by dominant physiologic derangements rather than rigid labels. Here, extreme hyperosmolality and hypovolemia required aggressive crystalloid resuscitation, potassium-guided insulin therapy, and controlled glucose reduction to minimize complications such as cerebral edema and malignant arrhythmias. Likely precipitants included insulin pump failure with interruption of basal insulin, poor oral intake, and suspected infection. Recognizing an HHS-dominant presentation with DKA-overlap features enabled safe, targeted management and clinical recovery.

Comments

American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter 2026 Resident and Medical Student Day, May 1, 2026, Troy, MI

Download

Included in

Critical Care Commons

Share

COinS