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HIGH ANIONIC GAP METABOLIC ACIDOSIS- UNCOMMON CAUSES- 1: D LACTIC ACIDOSIS

 "Life is struggle, not against sin, 
  not against money or power, 
  but against hydrogen ion"
                             - H.L. Mencken

D lactic acid is a stereo-isomer of L lactic acid. L lactic acid is the principle isomer produced by human and is responsible for usual lactic acidosis. D lactate is produced in small amount in humans, by colonic bacteria, as metabolic product of carbohydrate.

D lactic acid is not metabolized by lactate dehydrogenase (which converts L lactate to pyruvate), therefore D lactate is slowly eliminated from body in urine and faeces. 

D lactate accumulates in three clinical settings-
1. Short bowel syndrome,
2. Propylene glycol toxicity,
3. Diabetes ketoacidosis.

In short bowel syndrome, overgrowth of colonic gram positive anaerobes, like lactobacili, produce D lactate. Increased delivery of glucose and other carbohydrates to colon after resection of small bowel, leads to overproduction of D lactate by the colonic microflora.

D lactate is one of the end product of propylene glycol metabolism in body. Propylene glycol is present as solvent in several commonly used intravenous medications like lorazapam and diazepam.

In diabetic ketoacidosis, D lactate is derived from methylglyoxal, a metabolite of both acetone and dihydroxyacetone phosphate.

D lactic acidosis is characterised by both high anionic and normal anionic gap metabolic acidosis. 

Non anionic gap (hyperchloremic) metabolic acidosis is due to, free excretion of  D lactate in urine and faeces, without elimination of accompanying hydrogen ion. 

D lactate is excreted in urine as sodium and potassium salts. This results in increased urine anion gap (urine Na+K-Cl), giving false impression of renal tubular acidosis as the cause, of hyperchloremic acidosis.

Hyperchloremic acidosis leads to renal excretion of hydrogen ion, in the form of NH4Cl, which causes increased urinary osmolality. 

Thus increased urinary anionic gap as well as osmolality, distinguishes hyperchloremic acidosis, of D lactic acidosis, from renal tubular acidosis.

Therefore in a patient with unexplained  high anionic gap metabolic acidosis, with above mentioned  predisposing conditions, D lactic acidosis should be strongly considered.   

In patients with short bowel syndrome it presents as episodic high anionic gap metabolic acidosis, usually occurring after carbohydrate rich meal and associated neurological abnormality like confusion,  cerebellar ataxia and slurred speech. 

Standard enzymatic laboratory assays for lactate don't detect D lactate. Therefore special enzymatic essays should be used.

TREATMENT: In short bowel syndrome, oral antimicrobial (metronidazole, vancomycin, neomycin) may decrease the colonic microbial burden and decrease D lactate production. However antimicrobial use may occasionally precipitate D lactic acidosis by causing overgrowth of bacteria. 

Low carbohydrate diet is also helpful, by diminishing substrate supply in colon.

If D lactic acidosis is caused by propylene glycol, culprit drug infusion should be stopped.

Sodium bicarbonate may be used to tide over, till acidosis is corrected by elimination of root cause.

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