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A gap metabolic acidosis is secondary to the addition of acid, either exogenous or endogenous. The major causes are lactic acidosis, ketoacidosis, kidney disease, and ingestions (Table 21–12). A useful mnemonic for the differential diagnosis of increased anion gap metabolic acidosis is GOLDMARK (glycols [ethylene glycol and propylene glycol], oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, and ketoacidosis) (Table 21–13).

Table 21–13.Common causes and therapy for increased anion gap metabolic acidosis.

A. Lactic Acidosis

Lactic acidosis is a common cause of metabolic acidosis, producing an elevated anion gap and decreased serum pH when present without other acid-base disturbances. Lactate is formed from pyruvate in anaerobic glycolysis. Normally, lactate levels remain low (1 mEq/L) because of metabolism of lactate principally by the liver through gluconeogenesis or oxidation via the Krebs cycle. In lactic acidosis, lactate levels are at least 4–5 mEq/L but commonly significantly higher. There are three types of lactic acidosis.

Type A (hypoxic) lactic acidosis is most common, resulting from tissue hypoxia, usually from septic, cardiogenic, or hemorrhagic shock; mesenteric ischemia; respiratory failure; and carbon monoxide poisoning. These conditions increase peripheral lactic acid production and decrease hepatic metabolism of lactate as liver perfusion declines.

Type B lactic acidosis is secondary to impaired mitochondrial oxygen utilization and may be due to metabolic causes (eg, diabetes mellitus, liver disease, kidney disease, thiamine deficiency, ...

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