Abstract: PUB160
Diagnostic Puzzle: Concurrent D-Lactic and Renal Tubular Acidosis in Short-Bowel Syndrome
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Ahmed, Waqar, United Health Services Hospitals Inc, Binghamton, New York, United States
- Siddiqi, Mahwash, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
- Irshad, Maheen, United Health Services Hospitals Inc, Binghamton, New York, United States
- Jayaraman, Venkatesh, United Health Services Hospitals Inc, Binghamton, New York, United States
- Quasem, Mohammad A., United Health Services Hospitals Inc, Binghamton, New York, United States
- Farooq, Umar, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
Introduction
D-lactic acidosis is rare and is a known complication of Short bowel syndrome (SBS), although it can be difficult to diagnose and treat. Renal tubular acidosis (RTA), particularly due to tubular dysfunction, might further complicate therapy, especially when co-existing with D-lactic acidemia. This case highlights the diagnostic and therapeutic challenges in a patient presenting with SBS who developed mixed metabolic acidosis due to concurrent distal RTA and D-lactic acidosis.
Case Description
A 57-year-old female with a past medical history of prothrombin gene mutation complicated with superior mesenteric vein thrombosis status post small bowel resection, short bowel syndrome with chronic diarrhea, cirrhosis, presented to the emergency room for altered mental status and frequent falls. Diagnosis was confirmed with serum D-lactate levels and urinary studies. She was found to have high anion-gap metabolic acidosis and normal L-lactate levels, which we routinely check in the lab. All other workup was negative. Considering her history of short bowel syndrome, D-lactate level was checked, and it was elevated, causing high-anion-gap metabolic acidosis. But she was also found to have hyperchloremic non-anion gap metabolic acidosis. In that case urine anion gap should be negative, but our patient had a positive urine anion gap (Urine Na 166, urine potassium 21, and urine chloride 71).She was managed with Rifaximin, reduced carbohydrate intake, bicarb, and potassium supplementation.
Discussion
This case demonstrates the diagnostic complexities of having both D-lactic acidosis and distal renal tubular acidosis (RTA) in a patient with short bowel syndrome. D-lactic acidosis, an uncommon complication of SBS, is caused by bacterial fermentation of unabsorbed carbohydrates and is characterized by significant anion gap metabolic acidosis as well as neurologic symptoms. The patient's normal L-lactate and increased D-lactate levels validated the diagnosis.
Hyperchloremic non-anion gap metabolic acidosis, hypokalemia, nephrolithiasis, and a positive urine anion gap all point to coexisting distal RTA. The combination of both disorders resulted in a mixed acid-base imbalance, complicating diagnosis and treatment.