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LACTIC ACIDOSIS- PART 2

Causes of lactic acidosis:
●Type A lactic acidosis: caused by impaired tissue oxygen delivery, as in-
•anaerobic muscle activity- physical exercise, generalises tonic conic convulsions;
•impaired tissue perfusion- global (shock- hypovolemic, cardiac ir sepsis) or regional (mesenteric ischaemia);
•impaired tissue oxygen delivery or utilization- carbon monoxide poisoning, severe anemia, hypoximia.
●Type B lactic acidosis: not associated with any evidence of impaired oxygen delivery. It may be due to various mechanism-
•Type B1: Associated with disease states- diabetes, hematological malignancies, AIDS, chronic alcoholism, thiamine deficiency;
Diabetic patients may develop lactic acidosis of various etiology.
This type of lactic acidosis is due to decrease activity of pyruvate dehydrogenase.
Increased lactate production by neoplastic cells give rise to lactic acidosis in leukemia and lymphoma.
In chronic alcoholics lactic acidosis develops because of hepatic dysfunction and reduced NAD/NADH ratio.
•Type B2: Associated with drugs/ toxins- metformin, propofol, linezolid, nucleoside reverse transcriptase inhibitors, beta agonists, cyanide, nitroprusside, ethanol in chronic alcoholics, ethylene glycol;
Type B3: Associated with genetic diseases- MELAS syndrome (Mitochondrial encephalomyopathy Lactic acidosis Stoke like syndrome). 
●D lactic acidosis: D lactic acid is a stereoisomer 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 by colonic bacteria as metabolic product of carbohydrate.
D lactic acid is not metabolised 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 end result 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 excrered in urine as sodium and potassium salts. This results in increased urine anion gap, 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.

Diagnosis:
Therefore in a patient with unexplained  high anionic gap metabolic acidosis with above mentioned  predisposing conditions, D lactic acidosis should be strongly considered.  
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 lactobacili. Low carbohydrate diet is also helpful, by diminishing substrate supply in colon.
If D lactic acidosis is caused by propylene glycol, culprit drug should be stopped.
Sodium bi carbonate can be used to tide over, till acidosis is corrected after removal of root cause.

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