Etiology
Normally, the anion gap (AG) ranges from approximately 3 to 12 mEq/L.[6] An increase in AG usually implies the existence of organic acidosis. Based on this concept, metabolic acidosis can be classified into normal AG and increased AG metabolic acidosis.
1. Normal AG
Bicarbonate (HCO₃-) is lost or diluted, an anion is not generated, and electroneutrality is preserved by reciprocal increases in serum chloride concentration.
Also referred to as hyperchloremic metabolic acidosis.
Commonly caused by GI or renal loss of HCO₃-.
GI causes include diarrhea, GI drainage and fistulas, surgical urinary diversion of bowel, and intake of chloride-containing anion-exchange resins.
Renal causes include renal tubular acidosis, carbonic anhydrase inhibitors, hypoaldosteronism, and use of potassium-sparing diuretics.
Other causes include addition of acid by total parenteral nutrition, ingestion of elemental sulfur, or addition of hydrogen chloride (HCl) or other related chemicals such as ammonium chloride.
2. Increased AG
An organic acid consumes HCO₃-, and the anion that is produced is often retained in extracellular fluid and serum.
Serum chloride concentration does not increase.
Caused by diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, kidney disease, or ingestion of methanol, ethanol, ethylene glycol, propylene glycol (diluent in lorazepam), 5-oxoproline (toxic levels may occur in patients with chronic ingestion of acetaminophen), salicylic acid, paraldehyde, phenformin, metformin, iron, isoniazid, hydrogen sulfide, carbon monoxide, toluene, or ethylene glycol.[7][8][9] [ Anion Gap Opens in new window ] [ Anion Gap in Hypoalbumin States Opens in new window ]
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