Case Presentation:
A 58‐year‐old Caucasian woman presented to the emergency department with mental status change since eight weeks. The changes included episodes of confusion, slurred speech, unsteady gait, short call memory impairment, and visual and auditory hallucinations. She had visited a local hospital for her complaints, where she had been diagnosed with anion gap metabolic acidosis of unknown etiology. She had been seeing a psychiatrist and was prescribed citalopram and risperidone. Her past surgical history consisted of intestinal bypass surgery in 1975 for obesity. Psychiatric history was unremarkable. She reported chronic diarrhea since her surgery and denied taking any new medications in the past several months. She did not smoke or drink alcohol and denied any recreational drug use. S. Bicarbonate was 19 mmol/L. TSH, B12 levels, folate levels, and urine tox screen were normal. Serum lactate and pyruvate levels were normal. Her cerebral MRI showed no acute ischemic events. EEG was unremarkable. D‐LDH levels were elevated at 0.36 mmol/L establishing the diagnosis of D‐lactic acidosis. She was treated with oral sodium bicarb and metronidazole.
Discussion:
Lactic acidosis can be divided into typea A, B, and a rare type D. Lactic acidosis (type D) occurs in patients with jejunoileal bypass or short bowel syndrome. It results from metabolism of carbohydrates in the colon to D‐lactic acid, which is absorbed into systemic circulation. Since D‐lactate is not recognized by L‐lactate dehydrogenase, acidemia persists. D‐lactate is slowly metabolized in humans. Overgrowth of gram‐positive anaerobes (i.e. Lactobacilli) that produce D‐lactate is often noted. Normally, only small amounts of glucose and starch are delivered to the colon. With small bowel bypass, delivery of these substrates to colon is markedly enhanced. Patients with short bowel syndrome frequently demonstrate a chronically elevated serum concentration of D‐lactate, not sufficient to induce symptoms. In some patients, carbohydrate loading leads to symptomatic D‐lactic acidosis. These patients' typical presentation includes episodic metabolic acidosis, characteristic neurologic abnormalities including confusion, cerebellar ataxia, slurred speech and loss of memory. Normal serum lactate and ketone concentrations are noted. An elevated D‐LDH is considered confirmatory of the diagnosis.
Conclusion:
The signs and symptoms described above are similar to prior case reports. However, the onset of symptoms approximately thirty years after intestinal surgery is unique and never previously reported, to our knowledge. This diagnosis should be considered in patients with history of intestinal surgery associated with anion gap metabolic acidosis and neuropsychiatric manifestations. As described, symptoms can be delayed and hospital physicians should be aware of such atypical clinical presentations
Author Disclosure Block:
A. Aneja, None; M.R. Bakhru, None; A. Kumar, None.