Abstract: SA-PO0609
Hiding in Plain Sight: The Silent Case of Euglycemic Diabetic Ketoacidosis in an Anuric Patient on CRRT
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Jan, Muneeb Ullah, The University of Tennessee Health Science Center Department of Medicine, Memphis, Tennessee, United States
- Gyamlani, Geeta G., VA Memphis Healthcare System, Memphis, Tennessee, United States
- Khaliq, Muhammad, The University of Tennessee Health Science Center Department of Medicine, Memphis, Tennessee, United States
- Rafaey, Wania, The University of Tennessee Health Science Center Department of Medicine, Memphis, Tennessee, United States
- Rustom, David S., The University of Tennessee Health Science Center Department of Medicine, Memphis, Tennessee, United States
- Adeboye, Adedamola M., VA Memphis Healthcare System, Memphis, Tennessee, United States
- Naseer, Adnan, VA Memphis Healthcare System, Memphis, Tennessee, United States
Introduction
High anion gap metabolic acidosis (HAGMA) is a life-threatening condition that requires prompt identification of its underlying etiology. HAGMA due to euglycemic diabetic ketoacidosis (EUDKA) is rare. EUDKA is defined by elevated serum and urine ketones with a serum glucose level below 250 mg/dL. Its occurrence in patients on continuous renal replacement therapy (CRRT) is particularly uncommon. However, EUDKA may be more common than recognized when glucose free CRRT fluids are used in critically ill patients with poor nutritional intake or relative insulin deficiency.We present a case of persistent HAGMA in an anuric patient on CRRT, ultimately attributed to EUDKA.
Case Description
A 78-year-old man with type 2 diabetes mellitus, hypertension, and stage IV chronic kidney disease (CKD) admitted to ICU for septic shock from Pasteurella multocida. He became anuric, required vasopressor support and was started on glucose-free CRRT. Although his overall condition improved and his metabolic labs normalized, he continued to have a persistent HAGMA, with AG ranging between 20 and 22 mEq/L and a delta-delta ratio of 0.03. This continued to worsen despite increasing CRRT effluent dose. Uremia, toxins, and medication related causes were ruled out, and his blood glucose stayed normal throughout, with no prior or current exposure to SGLT2 inhibitors. A markedly elevated serum beta hydroxybutyrate level (82 mg/dL/7.9 mmol/L) confirmed euglycemic DKA. After initiating intravenous dextrose and insulin, both the anion gap and ketone levels quickly returned to normal.
Discussion
In critically ill, septic diabetic patients who are anuric and receiving glucose free CRRT, the development of an unexplained HAGMA may be driven directly by the glucose free CRRT or may worsen an underlying episode of EUDKA. Because these patients cannot produce urine, urine ketone testing is not possible, making serum beta hydroxybutyrate the only dependable marker of ketoacidosis. Glucose free CRRT solutions can create a carbohydrate depleted state, which can trigger lipolysis and ketogenesis even in the absence of SGLT2 inhibitor use. Importantly, this form of EUDKA typically resolves quickly with intravenous dextrose and insulin.