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D-lactic acidosis or D-lactate encephalopathy
🧪 D-lactic acidosis presents with recurrent episodes of encephalopathy and high-anion gap metabolic acidosis, particularly in patients with short bowel syndromes.
📌 About
- 🌀 D-lactate is a stereoisomer of the usual L-lactate.
- Only L-lactic acid is normally produced and metabolised in humans.
- Accumulation of D-lactate leads to neurotoxicity and acidosis.
🧬 Aetiology
- Short bowel syndrome (e.g. multiple resections).
- Malabsorption or jejuno-ileal bypass surgery.
- Excess carbohydrates reaching the colon → fermentation by gut bacteria → overproduction of D-lactate.
🧠 Clinical Features
- Stupor, delirium, ataxia, slurred speech.
- Episodes of inebriation-like behaviour, sometimes mistaken for intoxication.
- Can progress to psychosis or coma if untreated.
- Symptoms often episodic, triggered by high-carbohydrate intake.
🔎 Investigations
- ABG: High anion gap metabolic acidosis.
- Standard lactate assays only measure L-lactate ❌.
- Special assay required: D-lactate concentration >3 mmol/L confirms diagnosis ✅.
💊 Management
- IV fluids + sodium bicarbonate to correct acidaemia (❌ avoid lactated Ringer’s as it contains both D- and L-lactate).
- During acute episodes: restrict enteral carbohydrates → starves lactate-producing bacteria.
- Parenteral carbohydrate nutrition if required, with thiamine supplementation (prevents Wernicke-like syndromes by supporting pyruvate metabolism).
- Gut-acting antibiotics (poorly absorbed): clindamycin, vancomycin, neomycin, kanamycin.
- Haemodialysis: can rapidly clear D-lactate in severe cases.
📚 References
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