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Acidosis, Metabolic, Increased Anion Gap

For further information, see CMDT Part 21-17: Metabolic Acidosis

For further information, see CMDT Part 21-18: Increased Anion Gap Acidosis (Increased Unmeasured Anions)

Key Features

Essentials of Diagnosis

  • Decreased HCO3– with acidemia

  • Classified into increased anion gap acidosis and normal anion gap acidosis

  • Lactic acidosis, ketoacidosis, and toxins produce metabolic acidoses with the largest anion gaps

  • Normal anion gap acidosis is mainly caused by gastrointestinal HCO3– loss or RTA. Urinary anion gap may help distinguish between these causes

General Considerations

  • Calculation of the anion gap is useful in determining the cause of the metabolic acidosis

  • Normochloremic (increased anion gap) metabolic acidosis

    • Generally results from addition to the blood 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, diabetic ketoacidosis (DKA), and acidosis of unknown etiology

    • Uremia creates 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.
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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.

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  

Methylene glycol

Ethylene glycol

 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 ...

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