Skip to Main Content

21-17: Increased Anion Gap Acidosis

Nayan Arora; J. Ashley Jefferson

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.
View Table||Download (.pdf)
Table 21–13. Common causes and therapy for increased anion gap metabolic acidosis.
Cause Treatment
Lactic acidosis Therapy aimed at correcting the underlying cause. Treatment of type A requires improving perfusion and matching oxygen consumption with fluids, packed red cells, vasopressors, and inotropes as needed. Treatment of type B generally requires removal of the offending agent or supplementing key cofactors of anaerobic metabolism.
D-Lactic acidosis Sodium bicarbonate may be administered in the setting of severe acidemia. Specific antimicrobial agents (metronidazole, neomycin) can be utilized in patients with short gut syndrome. A low carbohydrate diet can be effective by decreasing substrate delivery to the distal colon. Fecal transplant has been utilized successfully in patients unresponsive to conventional therapies.

Ketoacidosis

Diabetes mellitus

Starvation

Alcoholic

 Therapy involves correction of the state of insulin deficiency and glucagon excess. In diabetic ketoacidosis, this requires administration of exogenous insulin, generally with a continuous infusion. In starvation and alcoholic ketoacidosis, dextrose-containing fluids will stimulate endogenous insulin release. In all groups, correction of volume depletion with isotonic fluids as well as judicious repletion of electrolytes (particularly potassium and phosphorous) are imperative.
Kidney failure Supplemental alkali therapy (sodium bicarbonate or sodium citrate). Hemodialysis when necessary.
Ingestions

Ethylene glycol

Methanol

 See Chapter 38.
Salicylic acid See Chapter 38.
Pyroglutamic acid (5-Oxoproline) Therapy is directed at the underlying cause. Generally requires withdrawal of the offending agent (acetaminophen) and sodium bicarbonate therapy for severe acidemia. N-acetylcysteine may be effective in restoring glutathione stores.

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, ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.

This site uses cookies to provide, maintain and improve your experience. MH Privacy Center Close