High Anion Gap Metabolic Acidosis
The serum anion gap is calculated as [Na+] - ([Cl-] + [HCO3-]). An elevated anion gap indicates unmeasured endogenous or exogenous organic anions consuming bicarbonate buffers in the blood.
The serum anion gap is calculated as [Na+] - ([Cl-] + [HCO3-]). An elevated anion gap indicates unmeasured endogenous or exogenous organic anions consuming bicarbonate buffers in the blood.
Metabolized by alcohol dehydrogenase to toxic formic acid; causes retinal damage, 'snowfield' blindness, and putaminal necrosis.
Decreased glomerular excretion of organic acids, sulfate, and phosphate.
Insulin deficiency and glucagon excess drive beta-oxidation and production of beta-hydroxybutyrate and acetoacetate.
Solvent in IV lorazepam/phenytoin; metabolized to lactic acid. Or chronic acetaminophen-induced pyroglutamic acidosis.
Direct mitochondrial poison causing shock, hypoperfusion, and uncoupling of oxidative phosphorylation.
Type A (tissue hypoperfusion, sepsis, cardiogenic shock) or Type B (metformin toxicity, cyanide, liver failure).
Antifreeze poisoning metabolized to glycolic and oxalic acid; leads to acute tubular necrosis and calcium oxalate monohydrate envelope crystals in urine.
Early respiratory alkalosis (direct medullary stimulation) followed by mixed high anion gap metabolic acidosis (uncouples oxidative phosphorylation).