The clinical presentation of D-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis
Not a drink yet drunk
Gap, buzz from fermenting funk
Much time in ORs
Slurred speech, stupor, all befall
Carbs bypass to large from small
Link to author
- D-lactate is a stereoisomer of L-Lactate
- L-lactic acid is the main entity involved in lactic acidosis in humans
- Short bowel syndrome eg multi-resection.
- Malabsorption or jejuno-ileal bypass surgery
- Carbs presented to colon are metabolized to D-lactate
- Stupor, inebriation, coma
- Delirium, ataxia, and slurred speech
- Altered mental status, psychosis, or even coma
- ABG: high anion gap metabolic acidosis
- D Lactate not measured by standard lactate assay. If measured D-lactate concentration of >3 mmol/L is used to define the diagnosis
- Intravenous bicarbonate can be used with fluid hydration to correct acidemia. Lactated ringer should be avoided as it contains both D- and L-lactate.
- During an acute episode, enteral carbohydrates should be avoided. Not only will this decrease the D-lactate due to lack of substrate but also the lactate-producing bacteria will starve and die in the absence of a food source
- Carbohydrates can be supplemented parenterally and thiamine supplementation should be considered to cover for the additional pyruvate dehydrogenase activity, especially in the cerebellum.
- Oral antibiotics that are poorly absorbed are most effectively used locally in the gut—these include clindamycin, vancomycin, neomycin, and kanamycin.
- Haemodialysis has been used to rapidly clear D-lactate from the plasma