Continues Renal Replacement Therapy as a Cause of Euglycemic Diabetic Ketoacidosis
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
- Abu Farsak, Hisham Neyazi, Hamilton Medical Center, Dalton, Georgia, United States
- Kabir, Purnima, Hamilton Medical Center, Dalton, Georgia, United States
- Salem, Saba, Hamilton Medical Center, Dalton, Georgia, United States
Ketoacidosis occurs when absolute or relative insulin deficiency inhibits the ability of glucose to enter cells for utilization as metabolic fuel, the result being that the liver rapidly breaks down fat into ketones to employ as a fuel source. The overproduction of ketones ensues, causing them to accumulate in the blood and urine and turn the blood acidic. Ketoacidosis is not commonly recognized as a cause for anion gap metabolic acidosis in patients who are on continuous renal replacement therapy (CRRT).
We present a case for a patient with acute kidney injury who developed euglycemic diabetic ketoacidosis (EDKA) on CRRT.
A 78 year-old Caucasian female patient with past medical history significant for diabetes mellitus type 2, chronic kidney disease stage 3, and dementia, who was admitted to the ICU for altered mental status secondary to septic shock presumed secondary to urinary tract infection. Patient was intubated for airway protection. She became hypotensive after intubation and required vasopressors continuously. Patient started to develop oliguric acute kidney injury which required CRRT initiation for hyperkalemia and volume removal after 5 days of her hospitalization.
Three days after starting CRRT, her serum bicarbonate level was 14 mEq/L, her anion gap worsened to 22 mEq/L. Her lactate level was normal. Her blood glucose levels were 100-220 mg/dL since admission. Uremia was unlikely with normal serum urea and close-to-normal creatinine while on CRRT. She was not on any drugs known to cause metabolic acidosis. Ketoacidosis was suspected and confirmed by high serum b-hydroxybutyrate level.
She was started on glucose and insulin infusions. After 24 hours, her bicarbonate improved to 26 mEq/L, with a significant decrease in b-hydroxybutyrate level.
EDKA is diagnosed in patients with normoglycemia, wide anion gap metabolic acidosis, and ketonemia. CRRT theoretically may be complicated with EDKA because of potentially compromised caloric intake and increased metabolic demands and stress from underlying critical illness, which may lead to a decrease in endogenous insulin production and a simultaneous increase in glucagon levels, which subsequently leads to lipolysis and ketogenesis.
CRRT is an under-recognized etiology of euglycemic DKA which requires early recognition and treatment to avoid catastrophic outcomes.