High AG metabolic acidosis is explained by eight mechanisms
MUDPILES as shown in the table. High
anion gap in these conditions is due to consumption of bicarbonate in buffering
excess acid.
Determination of osmolal gap in the
presence of high anion gap acidosis, will help in determining the source of
unmeasured anion.Methanol: It is metabolized by
liver to formaldehyde and formic acid. Accumulation of this acid leads to
metabolic acidosis with high anion gap and clinical symptoms of blindness.
Methanol as well as other alcohol will also increase the plasma osmolality.
Urea of renal failure: Due the loss
of renal tubular mass there is decreased ammonia formation, decreased hydrogen
ion excretion and bicarbonate reabsorption.
Diabetes or ketoacidosis: These
ketoacids accumulate and represent unmeasured anions. Accumulation of these
ketone bodies cause decreased in bicarbonate, a normal or low Cl-
and high AG.
Isoniazid, Iron, or Ischemia (three
I’s): These all lead to lactic acidosis. Isoniazid and Iron are hepatotoxic and
lead to impaired lactate clearance. Ischemia lead to anaerobic glycolysis
producing lactate.
Lactic acidosis: Physiologically it
exists as lactate and is mainly produced by muscle cells (mainly during
exercise) and erythrocytes during anaerobic glycolysis or any other conditions
that lead to hypoxia. It is normally metabolized by the liver. Increase in
lactate >2 mmol/L with associated increase in H+ is considered
lactic acidosis. Alcoholism can also cause lactic acidosis as it prevents
gluconeogenesis from lactate in liver, because oxidation of ethanol to
acetaldehyde competes for the NAD+ that is necessary for conversion
of lactate to pyruvate.
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