Serum Anion Gap in Metabolic Acidosis

Abstract

METABOLIC ACIDOSIS, DEFINED AS A pathophysiologic state characterized by an arterial pH <7.35 in the absence of an elevated partial pressure of carbon dioxide in arterial blood (PaCO2), is a common finding in the critically ill neonate. It is the result of excess acid production, decreased renal excretion of acid, or increased loss of base.1,2In the neonatal period, metabolic acidosis is most often the result of shock or severe liver or kidney failure. In rare cases, however, it may be a discrete finding suggestive of an inborn error affecting acid production or renal acid excretion.3Left untreated, this acidosis can disturb many cell functions, potentially resulting in respiratory distress, pulmonary vasoconstriction, right ventricular dysfunction, tachycardia, myocardial depression, increased intracranial pressure, hyperkalemia, insulin resistance, decreased affinity of oxygen for hemoglobin, abdominal distention, or vomiting.4Although the most common treatment for acidosis is to “correct” it with bicarbonate (HCO3−), this therapy is not without its potential adverse effects. Therefore, correction of the underlying cause is considered to be the most important therapeutic measure in the management of metabolic acidosis.3,5Calculation of the anion gap is a useful and inexpensive tool with which to develop a differential diagnosis for metabolic acidosis in the neonate. This column examines the usefulness and limitations of calculating the serum anion gap.