Anion Gap (Elevated) Differential Diagnosis
Normal Anion Gap: 8 - 12 +/- 2
- Associations: Acute ingestion +/- liver damage (rising AST/ALT) +/- metabolic acidosis
- Pathophysiology: Acetaminophen metabolite, oxoproline and pyroglutamic acid.
- Associations: History of alcohol abuse + normal glucose + ketones in urine
- Pathophysiology: Multifactorial: Decreases in insulin, increases in glucagon, impaired NADH to NAD+ ratios from alcohol metabolism and volume depletion with vomiting.
- Associations: Glucose levels > 250 mg/dL +/- abdominal pain +/- nausea & vomiting + ketones in the urine + serum bicarbonate < 18
- Pathophysiology: Insufficient presence of insulin that results in the abnormal breakdown of fatty acids that generate ketoacids.
- Associations: Ingestion of antifreeze + inebriation +/- metabolic acidosis +/- acute renal impairment
- Pathophysiology: Ethylene glycol gets metabolized to eventually for glycolic acid and oxalic acid.
- Associations: Iron ingestion or hemochromatosis or repeated blood transfusions
- Pathophysiology: Results in liver damage.
- Associations: History of tuberculosis (latent or active)
- Pathophysiology: Due to functional deficiencies in pyridoxine (vitamin B6) that can serve as a co-factor in metabolic reactions. This leads to a metabolic acidosis.
- Associations: Numerous medical conditions or drugs containing propylene glycol (lorazepam; phenytoin)
- Pathophysiology: Lactic acid formation is a byproduct of another underlying problem that prevents its metabolism or prevent pyruvate from entering the Krebs cycle.
- Associations: Type 2 diabetes +/- impaired renal function
- Pathophysiology: Impairs lactate metabolism in the liver.
- Associations: Reports of ingestion +/- metabolic acidosis +/- changes in vision
- Pathophysiology: Methanol is metabolized to formic acid.
- Associations: Reports of ingestion (though no longer used)
- Pathophysiology: Metabolized to acetaldehyde.
- Associations: Reports of ingestion/Suicide Attempt (or) elderly patient on chronic aspirin +/- mixed acid/base disorder
- Pathophysiology: Initially stimulates the medullary center in the brain and causes increased respirations leading to respiratory alkalosis. Then shifts to a metabolic acidosis and uncoupling of cellular respiration.
Alcoholic Ketoacidosis (AKA)
Diabetic Ketoacidosis (DKA)
Ethylene Glycol (Antifreeze; Toxic Alcohol)
Lactic Acidosis (from Cyanide or Hydrogen Sulfide)
Metformin or Phenformin
Salicylates (Aspirin; Salicyclic Acid)