Normochloremic metabolic acidosis generally results from addition of organic acids such as lactate, acetoacetate, beta-hydroxybutyrate, and exogenous toxins. Other anions such as isocitrate, alpha-ketoglutarate, malate, and D-lactate may contribute to the anion gap of lactic acidosis, DKA, and acidosis of unknown etiology. Uremia causes an increased anion gap metabolic acidosis from unexcreted organic acids and anions (Table 21–13).
Table 21–13.Common causes and therapy for increased anion gap metabolic acidosis. |Favorite 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. 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. |
|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 || |
|Initial treatment requires rapid stabilization of the patient’s airway and circulation as needed. Sodium bicarbonate should be given to address systemic acidosis by bolus and subsequently continuous infusion therapy to maintain a pH > 7.35. Fomepizole (or less commonly ethanol) can be given to inhibit alcohol dehydrogenase. Fomepizole is loaded at 15 mg/kg intravenously, followed by 10 mg/kg every 12 hours. Hemodialysis is the most effective method for removing parent alcohols and their toxic metabolites. Hemodialysis should be initiated early in patients with an elevated anion gap metabolic acidosis or end organ damage in the setting of known ingestion. |
|Salicylic acid ||Activated charcoal may be administered to awake or intubated patients within 2 hours of ingestion. Sodium bicarbonate should be initiated by bolus followed by continuous infusion to target a urine pH of 7.5 or higher. Supplemental glucose should be administered to all patients with alteration in mental status. Hemodialysis is effective in removing salicylate and generally reserved for severe cases or marked elevations in salicylate concentration. |
|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. |