CORRECT ANSWER IS C
Patient has Anion Gap Metabolic acidosis due to D-lactic acidosis. D-lactate encephalopathy is a rare condition that occurs primarily in individuals who have a history of short bowel syndrome. D-lactic acid accumulation in the blood can cause neurologic symptoms such as delirium, ataxia, and slurred speech and patients often appear to be inebriated or drunk even without any alcohol intake. Diagnosis of D-lactic acidosis is made by special assays for D-lactate. The unabsorbed carbohydrates due to short bowel syndrome acts as a substrate for colonic bacteria and is fermented to form D-lactic acid. High amounts of D-lactate are then absorbed into the circulatory system, resulting in CNS symptoms. Small intestinal bacterial overgrowth (SIBO) occurs commonly in short-bowel syndrome (SBS) and is characterized by a symptom of nutrient malabsorption caused by an increased number in the small intestine. SIBO can cause malabsorption symptoms such as fatty diarrhea, bloating, flatulence due to poor absorption of fats, carbohydrates and proteins. Bile salts, which are normally needed to digest fats, are broken down by the excess bacteria in small intestine, resulting in incomplete digestion of fats causing diarrhea. Patient was started on amitriptyline (for anxiety) and Vicodin (for pain) which can slow down gastrointestinal motility and increase D-lactic acid production and malabsorption symptoms. The acidic pH generated as a result of D-lactate production further propagates production of D-lactic acid, hence giving rise to a vicious cycle. Treatment involves restriction of carbohydrate intake to 100-120 g/day, oral administration of poorly absorbed antibiotics (such as metronidazole, neomycin, or vancomycin) to eliminate colonic microbiota and correcting the acidosis.
Although patient consumed alcohol, it is less likely explain the full constellation of symptoms as noticed in the patient’s clinical history, especially occurrence of symptoms at other times without alcohol intake. Alcohol is metabolized in the liver by alcohol dehydrogenase to acetaldehyde. Alcohol binds strongly to GABA receptors in CNS, activating the inhibitory cascade, which results in sedation, cognitive dysfunction, and decreased coordination. Alcohol poisonings are associated with an increased serum osmolal gap, if the patient presents relatively soon after the ingestion. In this case patient does not have any persistent elevated serum osmolal gap suggesting that alcohol has already been metabolized to end products of acetaldehyde by Alcohol dehydrogenase and subsequently to acetate by aldehyde dehydrogenase. Checking for ethanol is not likely to be positive.
Reference
Ethanol metabolism: The good, the bad, and the ugly – ScienceDirect
D-Lactic Acidosis: An Underrecognized Complication of Short Bowel Syndrome – PMC (nih.gov)
