Approach to increased anion gap metabolic acidosis

An approach to the assessment of increased anion gap acidosis is summarized in Table,...?.


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Table 2 Diagnosis of increased anion gap metabolic acidosis

Table 2 Diagnosis of increased anion gap metabolic acidosis

Ketoacidosis can be diagnosed by measurement of ketones in serum and urine; blood glucose should also be measured. Ketoacidosis generates both acetone and b-hydroxybutyrate. However, only acetone is detected when measuring urine and serum ketones. If both acetone and b-hydroxybutyrate are present, increased ketone levels are detected. If only b-hydroxybutyrate is present, ketone levels are normal. In conditions of tissue hypoxia, the major ketone is b-hydroxybutyrate, not acetone. Therefore, in a patient who has both diabetic ketoacidosis and tissue hypoxia (e.g. in the setting of concomitant shock), serum ketones may be normal and the diagnosis of diabetic ketoacidosis may be missed. Lactic acidosis may occur in conjunction with diabetic ketoacidosis.

Uremia is detected by elevated urea and creatinine. However, severe protein depletion suppresses these levels, hepatic disease impairs urea formation, and blood in the gastrointestinal tract raises urea concentration. Salicylate poisoning can be recognized by increased serum salicylate levels.

Alcohol poisoning which causes increased anion gap acidosis (methanol and ethylene glycol) also increases the osmole gap. With increased anion gap acidosis, the osmole gap (Halperin jnd GoJdsteiniiin1988; EmmMïM..M 1992) should always be assessed as follows:

osmole jwp — (measured osmolirity) — (2[Na"*]+ |qrca] + Iglucosej + [ethanalj)

where the osmole gap is expressed in milliosmoles per liter and [Na+], [urea], [glucose], and [ethanol] are in millimoles per liter. The normal osmole gap is less than 10 mosmol/l. Methanol and ethylene glycol poisoning (but not ethanol intoxication) increase the osmole gap. Other clues to the specific form of alcohol poisoning include the presence of dilated pupils with decreased light reflex (methanol), hyperemia of the optic disk and retinal edema (methanol), and oxalate crystalluria (ethylene glycol).

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