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Toxicology – Causes of Anion Gap Metabolic Acidosis
Alcohol (Ethanol)
Ethanol intoxication may lead to hypoglycemia, lactic acidosis, and alcoholic ketoacidosis, all of which contribute to an increased anion gap.
Aspirin (Salicylates)
Salicylate toxicity should be suspected in patients with anion gap metabolic acidosis and altered mental status. It typically produces a mixed disorder with metabolic acidosis and respiratory alkalosis due to direct stimulation of the respiratory center. It also increases renal loss of bicarbonate and potassium while promoting lactic and pyruvic acid formation.
Methanol
Methanol poisoning results in a high anion gap and hyperosmolar metabolic acidosis due to accumulation of formic acid, a toxic metabolite.
Ethylene Glycol
Commonly found in antifreeze, ethylene glycol is metabolized into glycolic, glyoxylic, and oxalic acids, producing a severe high anion gap metabolic acidosis.
Metformin
Metformin toxicity can lead to lactic acidosis by increasing production of lactate and other metabolic intermediates, particularly in patients with renal impairment or after contrast exposure.
Diabetic Ketoacidosis (DKA)
DKA occurs due to insulin deficiency, resulting in increased fatty acid metabolism and accumulation of ketoacids such as acetoacetate and β-hydroxybutyrate. Starvation and alcoholic ketosis can produce similar effects.
Uremia
Advanced kidney failure leads to accumulation of nitrogenous waste products and acids such as sulfuric and phosphoric acid, causing an anion gap metabolic acidosis.
Lactic Acidosis
Lactic acid accumulation from anaerobic metabolism is a common cause of anion gap acidosis and may result from hypoxia, hypoperfusion, toxins, or metabolic disorders.
Toluene
Toluene exposure, often through inhalation of solvents, increases production of organic acids such as benzoic and hippuric acid and may also cause renal tubular acidosis with chronic use.
Carbamazepine
Overdose of this antiepileptic drug can lead to metabolic acidosis along with hyperglycemia, ketonuria, altered mental status, seizures, and coma.
Isoniazid (INH)
Isoniazid toxicity can result in lactic acidosis, often accompanied by seizures and altered mental status.
Iron
Iron overdose contributes to metabolic acidosis through hypovolemia, hypotension, and the release of hydrogen ions during its metabolic conversion.
Paraldehyde
This older sedative-hypnotic agent, historically used for seizures, can contribute to anion gap metabolic acidosis in toxic exposures.
Alcohol (Ethanol)
Ethanol intoxication may lead to hypoglycemia, lactic acidosis, and alcoholic ketoacidosis, all of which contribute to an increased anion gap.
Aspirin (Salicylates)
Salicylate toxicity should be suspected in patients with anion gap metabolic acidosis and altered mental status. It typically produces a mixed disorder with metabolic acidosis and respiratory alkalosis due to direct stimulation of the respiratory center. It also increases renal loss of bicarbonate and potassium while promoting lactic and pyruvic acid formation.
Methanol
Methanol poisoning results in a high anion gap and hyperosmolar metabolic acidosis due to accumulation of formic acid, a toxic metabolite.
Ethylene Glycol
Commonly found in antifreeze, ethylene glycol is metabolized into glycolic, glyoxylic, and oxalic acids, producing a severe high anion gap metabolic acidosis.
Metformin
Metformin toxicity can lead to lactic acidosis by increasing production of lactate and other metabolic intermediates, particularly in patients with renal impairment or after contrast exposure.
Diabetic Ketoacidosis (DKA)
DKA occurs due to insulin deficiency, resulting in increased fatty acid metabolism and accumulation of ketoacids such as acetoacetate and β-hydroxybutyrate. Starvation and alcoholic ketosis can produce similar effects.
Uremia
Advanced kidney failure leads to accumulation of nitrogenous waste products and acids such as sulfuric and phosphoric acid, causing an anion gap metabolic acidosis.
Lactic Acidosis
Lactic acid accumulation from anaerobic metabolism is a common cause of anion gap acidosis and may result from hypoxia, hypoperfusion, toxins, or metabolic disorders.
Toluene
Toluene exposure, often through inhalation of solvents, increases production of organic acids such as benzoic and hippuric acid and may also cause renal tubular acidosis with chronic use.
Carbamazepine
Overdose of this antiepileptic drug can lead to metabolic acidosis along with hyperglycemia, ketonuria, altered mental status, seizures, and coma.
Isoniazid (INH)
Isoniazid toxicity can result in lactic acidosis, often accompanied by seizures and altered mental status.
Iron
Iron overdose contributes to metabolic acidosis through hypovolemia, hypotension, and the release of hydrogen ions during its metabolic conversion.
Paraldehyde
This older sedative-hypnotic agent, historically used for seizures, can contribute to anion gap metabolic acidosis in toxic exposures.
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