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Abstract: SA-PO501

Persistent Euglycemic Ketoacidosis During Continuous Renal Replacement Therapy Despite IV Insulin Infusion

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Ajiboye, Oyintayo, Emory University School of Medicine, Atlanta, Georgia, United States
  • Amarapurkar, Pooja D., Emory University School of Medicine, Atlanta, Georgia, United States
  • Connor, Michael J., Emory University School of Medicine, Atlanta, Georgia, United States

Euglycemic diabetic ketoacidosis (DKA) is an uncommon, known complication of continuous renal replacement therapy (CRRT) when using dextrose-free CRRT solutions with insulin-dependent diabetics at higher risk. Typically, CRRT-related euglycemic DKA resolves with increased insulin & dextrose exposure. Here we describe a case of euglycemic DKA which did not resolve with insulin administration & only improved after stopping CRRT.

Case Description

73-year-old female with CKD 3aA1, insulin-dependent diabetes, & lung adenocarcinoma admitted for septic shock from empyema & post-obstructive pneumonia, respiratory failure, & anion-gap metabolic acidosis secondary to lactic acidosis & DKA with initial Beta-hydroxybutyrate (BHB) 1.7 mmol/L & glucose 727 mg/dl. She was placed on vasopressors, antibiotics, & an insulin infusion. However, she progressed to anuric acute kidney injury requiring CRRT using our standard phosphorus-containing, dextrose-free solution which improved the metabolic acidosis. Subsequently, developed recurrent anion-gap metabolic acidosis on CRRT day 3 & evaluation revealed recurrence of elevated BHB to 1.38 mmol/L which steadily increased to 5.9 mmol/L on CRRT day 6 despite increased insulin infusion & escalating exposure to IV & enteral dextrose with bicarbonate levels remaining 14-21meq/L & glucose 142-229 mg/dl on insulin infusion at peak > 5 units/hour. CRRT was stopped on day 6 due to persistent euglycemic DKA with rapid normalization of serum bicarbonate & decrease BHB to 0.78 mmol/L over 12 hours.


CRRT with dextrose-free solutions results in net glucose loss leading to lower serum glucose levels & decreased insulin requirements in ICU patients. In a patient with impaired endogenous insulin production, this decreased insulin exposure can precipitate ketogenesis leading to euglycemic DKA. In prior case descriptions & our local experience, CRRT-related euglycemic DKA typically resolves with increased insulin dose facilitated by a deliberate increase in exogenous dextrose sources. However, in this case, the DKA did not resolve despite a significant increase in hourly insulin dose & only improved with cessation CRRT. Clinicians should be cognizant of, and alert to, euglycemic DKA as a complication of dextrose-free CRRT solutions. CRRT cessation or change to dextrose-containing solutions may be required when conservative management fails.