Short Bowel Syndrome (Short Gut Syndrome)


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Clinical Manifestations

## References

Antibiotic-Induced D-Lactic Acidosis

Boris E. Coronado, MD; Steven M. Opal, MD; and David C. Yoburn, MD
[+] Article and Author Information
Ann Intern Med. 1995;122(11):839-842. doi:10.7326/0003-4819-122-11-199506010-00005
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Objective: To describe a case of oral antibiotic-induced D-lactic acidosis in a patient with enteric overgrowth of Lactobacillus acidophilus.

Design: Single case study.

Setting: University-affiliated community hospital.

Intervention: Oral carbohydrate challenge test with 4000 kcal/d.

Main Results: A patient had several episodes of D-lactic acidosis after receiving oral antibiotics. Stool cultures yielded Lactobacillus acidophilus resistant to the implicated agents. Provocative challenge with dietary carbohydrate alone, in the absence of antibiotics, failed to reproduce the syndrome.

Conclusions: Oral antibiotics may induce D-lactic acidosis in patients with the short-bowel syndrome by promoting the overgrowth of resistant D-lactate-producing organisms. Interactions between carbohydrate intake and antibiotic use are likely determinants in the development of this syndrome. Periodic use of stool cultures with antimicrobial susceptibility testing may assist in the management of these patients by optimizing the selection of antimicrobial agents.

D-Lactic Acidosis
Craig Petersen, RD, CNSD
University of California, Davis, Medical Center and Nutrishare, Inc., Sacramento, California
Correspondence: Craig Petersen, RD, CNSD, University of California, Davis, Medical Center, Nutrition Services, 2315 Stockton Blvd, Sacramento, CA 95817. Electronic mail may be sent to

Nutr Clin Pract December 2005 vol. 20no. 6 634-645

D-Lactic acidosis, also referred to as D-lactate encephalopathy, is a rare neurologic syndrome that occurs in individuals with short bowel syndrome or following jejuno-ileal bypass surgery. Symptoms typically present after the ingestion of high-carbohydrate feedings. Neurologic symptoms include altered mental status, slurred speech, and ataxia, with patients often appearing drunk. Onset of neurologic symptoms is accompanied by metabolic acidosis and elevation of plasma D-lactate concentration. In these patients, malabsorbed carbohydrate is fermented by an abnormal bacterial flora in the colon, which produces excessive amounts of D-lactate. High amounts of D-lactate are absorbed into the circulation, resulting in an elevated concentration of D-lactate in the blood. Development of neurologic symptoms has been attributed to D-lactate, but it is unclear if this is the cause or whether other factors are responsible. This review examines the pathophysiology of the production and accumulation of D-lactate while exploring the potential factors contributing to the development of neurologic manifestations. Methods of diagnosis and treatment are reviewed. Areas requiring further investigation are identified.