ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: PO1491

Starvation Ketoacidosis in a Patient with Muscular Dystrophy

Session Information

Category: Trainee Case Report

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Srour, Khaled, Henry Ford Hospital, Detroit, Michigan, United States
  • Khan, Bilal Shahzad Azam, Henry Ford Hospital, Detroit, Michigan, United States
  • Novak, James E., Henry Ford Hospital, Detroit, Michigan, United States

Patients with muscular dystrophy have low muscle mass; thus, they have lower glycogen stores and are more prone to develop ketoacidosis with minimal stress or decreased oral intake. Here we present a rare presentation of ketoacidosis in a patient with muscular dystrophy with concurrent ketoacidosis and hyperchloremic metabolic acidosis who was treated successfully with lactated Ringer’s (LR) and dextrose (D5W).

Case Description

A 48 year old woman with a history of muscular dystrophy and chronic, ventilator dependent respiratory failure was referred to our hospital for evaluation of granulation tissue in her trachea. Body mass index was 18 kg/m 2 . Laboratory data on admission were significant for sodium of 132 meq /L, potassium of 4.5 meq /L chloride 114 mEq/L, bicarbonate 12 mEq/L, creatinine < 0.1 mg/d, and pH 7.23 (venous blood gas) consistent with non anion gap metabolic acidosis. The following day, laboratory data showed sodium 137 mEq/L, chloride 113 mEq/L, bicarbonate 8 mEq/L, and pH 7.29. The calculated anion gap was 16 mEq/L with albumin 4.2 g/ dL. The urine anion gap was 30 mmol/L. Serum β hydroxybutyrate (BHB) was elevated at 6.6 mmol/L. Because of muscular dystrophy with decreased oral intake, the patient’s anion gap metabolic acidosis was attributed to starvation ketoacidosis. The non anion gap metabolic acidosis was attributed to renal tubular acidosis. LR and D5W solutions were administered to treat non anion gap and anion gap metabolic acidosis (starvation ketoacidosis), respectively. After 1-2 days, BHB decreased and electrolytes normalized.


Few cases have been reported regarding ketoacidosis in patients with muscular dystrophy, and all of these were treated with dextrose and 0.9% saline. In our case, we used LR and D5W due to concurrent non anion gap and anion gap metabolic acidosis, as 0.9% saline administration was projected to worsen the hyperchloremic acidosis.
Anion gap metabolic acidosis in patients with muscular dystrophy and without diabetes should raise suspicion for starvation ketoacidosis requiring D5W. LR should be substituted for 0.9% saline in patients with concurrent hyperchloremic acidosis.