Serum pH is typically acidemic, but the pH may be normal or even alkalemic early in the course of the illness. In one study, 15 percent of patients were alkalemic, 30
percent had normal pH, and 55 percent had acidemia.1 The degree of acidosis is typically less than that seen in patients with diabetic ketoacidosis. If the acidosis is mild and the patient also has a primary respiratory alkalosis (i.e., due to fever, sepsis, or alcohol withdrawal), then the pH may be normal or even alkalemic. Similarly, contraction metabolic alkalosis may mask the presence of a concurrent wide anion-gap acidosis and result in a "normal" or even elevated [HCO3 -], rendering the pH normal or alkalemic. Since volume loss, whether due to poor volume intake or vomiting, is virtually always present in AKA, some degree of metabolic alkalosis is sure to exist.
Without routine evaluation of the anion gap in every patient at risk for AKA, the diagnosis can be easily missed. An anion gap greater than the patient's baseline (or greater than 15 in any case) signifies the presence of a wide anion-gap acidosis regardless of the actual [HCO3 -] concentration or the pH, even if the patient is alkalemic. For example, a common serum chemistry result in a patient with AKA may be along the following lines: [Na+], 145, [Cl], 95, [K+], 4.1, and [HCO3-], 25. In this example, the anion gap (25, excluding K+) is elevated by at least 10, yet the [HCO3-] and electrolyte levels are normal. The only explanation is that a mixed acid-base abnormality of approximately equal but opposing magnitudes exists. Arterial blood-gas determination is not needed to arrive at the correct diagnosis for this relatively complicated acid-base disturbance. (For a more detailed discussion, the reader is referred to Chap.2.1, "Acid-Base Disorders.")
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