A normal anion gap is 3 to 11. A decrease in the albuminconcentration of 1 g/dL decreases the anion gap by roughly 4mEq/L. Similarly, albeit less commonly, an increase in unmeasured cations, such as calcium, potassium, or magnesium, decreases the anion gap. Conversely, a decrease in unmeasuredcations is a rare cause of an increased anion gap. Because ofthese variables, the broad range of a normal anion gap, and other factors, the presence of a normal or increased anion gapis not always reliable in differentiating the causes of a metabolicacidosis, especially when the metabolic acidosis is mild. Somepatients have more than one explanation for their metabolic acidosis, such as a child with diarrhea and lactic acidosis secondaryto hypoperfusion. The anion gap should not be interpreted indogmatic isolation; consideration of other laboratory abnormalities and the clinical history improves its diagnostic utility.
The most effective therapeutic approach for patients with a metabolic acidosis is correction of the underlying disorder, if possible. The administration of insulin in diabetic ketoacidosis or restoration of adequate perfusion in lactic acidosis from shock eventually results in normalization of acid-base balance. The use of bicarbonate therapy is indicated when the underlying disorder is irreparable; examples include RTA and chronic renal failure. In salicylate poisoning, alkali administration increases renal clearance of salicylate and decreases the amount of salicylate in brain cells. Short-term base therapy is often necessary in other poisonings and inborn errors of metabolism.
The causes of a metabolic alkalosis are divided into two categories based on the urinary chloride (Table 37-3). The alkalosis in patients with a low urinary chloride is maintained by volume depletion. They are called chloride responsive because volume repletion with fluid containing sodium chloride and potassium chloride is necessary to correct the metabolic alkalosis. Emesis, which causes loss of hydrochloride and volume depletion, is the most common cause of a metabolic alkalosis. Diuretic use increases chloride excretion in the urine. Consequently, while a patient is receiving diuretics, the urinary chloride is typically high (>20 mEq/L). After the diuretic effect resolves, the urinary chloride is low (<15 mEq/L), because of appropriate renal chloride retention in response to volume depletion. Categorization of diuretics based on urinary chloride depends on the timing of the measurement. The metabolic alkalosis from diuretics is clearly chloride responsive; it corrects only after adequate volume repletion. This is the rationale for including it among the chloride-responsive causes of a metabolic alkalosis.
The chloride-resistant causes of metabolic alkalosis can be subdivided based on blood pressure. Patients with the rare disorders that cause a metabolic alkalosis and hypertension either have increased aldosterone or act as if they have increased aldosterone. Patients with Bartter syndrome or Gitelman syndrome (Chapter 36) have metabolic alkalosis, hypokalemia, and normal blood pressure secondary to renal tubular defects that cause continuous urinary losses of chloride.
The symptoms in patients with a metabolic alkalosis often are related to the underlying disease and associated electrolyte disturbances. Hypokalemia is often present, and occasionally severe, in the diseases that cause a metabolic alkalosis (see Chapter 36). Children with chloride-responsive causes of metabolic alkalosis often have symptoms related to volume depletion (see Chapter 33). In contrast, children with chloride-unresponsive causes may have symptoms related to hypertension. Severe alkalemia may cause arrhythmias, hypoxia secondary to hypoventilation, or decreased cardiac output.