Abstract: SA-PO0608
Euglycemic Ketoacidosis During CRRT: A Rare but Important Cause of Refractory Metabolic Acidosis
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
- Bhandari, Sanjeev, New York City Health and Hospitals Jacobi, New York, New York, United States
- Rodriguez, Marcos Alejandro, New York City Health and Hospitals Jacobi, New York, New York, United States
- Varma, Nidhi, New York City Health and Hospitals Jacobi, New York, New York, United States
Introduction
Euglycemic ketoacidosis (EKA) is a rare but significant complication in critically ill patients on continuous renal replacement therapy (CRRT), characterized by ketonemia, high anion gap metabolic acidosis (HAGMA), and euglycemia. Inadequate caloric intake combined with continuous clearance of glucose and nutrients by CRRT can shift metabolism toward ketogenesis. We report a case of EKA during CRRT for AKI from septic shock.
Case Description
An 86-year-old woman with hypertension, type 2 diabetes, and severe aortic stenosis presented with acute abdominal pain and vomiting. She was tachycardic and tachypneic with peritoneal signs. Labs revealed AKI, HAGMA, and lactic acidosis; imaging confirmed bowel perforation. She required dual vasopressors and underwent right hemicolectomy with ileostomy, revealing fecal peritonitis. Postoperatively, she remained intubated and vasopressor-dependent with septic shock.
CVVHDF was initiated on postoperative day 1 at 25 mL/kg/h, using PrismaSol (glucose-containing) as replacement fluid and Phoxillum (glucose-free) as dialysate. Blood glucose was managed with intermittent dextrose pushes; no continuous dextrose, enteral, or parenteral nutrition was provided. By day 7, persistent HAGMA was noted despite improving lactate and uremia (Table 1). No citrate anticoagulation or HAGMA-causing medications were used. Serum beta-hydroxybutyrate was elevated at 6.6 mmol/L, confirming EKA. Dextrose infusion and total parenteral nutrition were initiated with bolus insulin, and HAGMA resolved the following day.
Discussion
EKA is an underdiagnosed complication of CRRT presenting as refractory HAGMA despite adequate solute clearance. Inadequate caloric intake and continuous extracorporeal nutrient removal shift hepatic metabolism toward lipolysis and ketogenesis. Escalating CRRT dose to manage persistent acidosis may paradoxically worsen the condition by increasing nutrient losses. Prompt treatment with dextrose and nutritional support rapidly resolves the ketoacidosis.