Kidney Week

Abstract: SA-PO509

A Case of Cocaine-Induced Euglycemic Diabetic Ketoacidosis

Session Information

• Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
  October 26, 2024 | Location: Exhibit Hall, 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

• Moghaddam, Amir, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States

Amir Moghaddam, MD

• Shareef, Zan, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States

Zan Shareef, MD

• Liu, Song, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States

Song Liu, MD

• Teixeira, J. Pedro, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States

J. Pedro Teixeira, MD, FASN

Introduction

Severe anion gap metabolic acidosis (AGMA) may be life-threatening and often requires specific therapy, but prompt diagnosis may be challenging. We present a case of euglycemic diabetic ketoacidosis (euDKA) likely triggered by cocaine use.

Case Description

A 69-year-old man with diabetes, hypertension, and polysubstance use presents after being found unresponsive by his son. He is intubated for airway protection and is found to have acute kidney injury and severe acidosis with creatinine 3.5 mg/dL, BUN 75 mg/dL, pH 7.13, pCO2 35 mmHg, bicarbonate 10 mEq/L, anion gap 26 mEq/L, lactate 2.0 mmol/L, negative toxic alcohol panel, and serum glucose 66-191 mg/dL. Urinalysis reveals ketonuria and serum beta-hydroxybutyrate is 3.2 mmol/L. Urine drug screen is positive for cocaine. Despite treatment with IV dextrose and IV bicarbonate for >24 h, anion gap remains >20 (Figure). Nephrology is consulted and recommends IV insulin with dextrose which results in normalization of his anion gap within 24 h, at which point his mental status improves sufficiently for extubation.

Discussion

The severity of the AGMA, lack of response to dextrose alone, need for insulin, and glucose consistently <200 mg/dL all strongly suggest euDKA in this case rather than starvation ketosis or classic DKA. Though increasingly identified in patients taking sodium-glucose cotransporter-2 inhibitors, euDKA may be triggered by stressful events such as pregnancy, surgery, or pancreatitis. A classic trigger of DKA, cocaine stimulates counterregulatory hormones like epinephrine and cortisol which normally raise blood glucose, inhibits insulin secretion, and stimulates breakdown of free fatty acids into ketones. One study found 14% of DKA cases to be related to cocaine. However, cocaine may less commonly trigger euDKA via suppression of feeding centers that results in oral intake poor enough to prevent hyperglycemia. Given the specific therapy required, nephrologists and intensivists alike must recognize cocaine-induced euDKA as a potential cause of unexplained severe AGMA.