With metabolic acidosis, the anion gap can be increased or normal. An increase in circulating acids will consume and replace bicarbonate ion, increasing the anion gap. The causes include an increase in circulating lactic acid secondary to anaerobic glycolysis, such as that seen under conditions of poor tissue perfusion; increased ketoacids, as with cases of severe diabetes or starvation; exogenous toxins; and renal dysfunction, which leads to increased circulating sulfates and phosphates (37). The diagnosis can be established via a thorough history and measurement of serum lactate (normal <2 mmol/L), serum glucose, and renal function parameters. Metabolic acidosis in the face of a normal anion gap is usually the result of an imbalance of the ions chloride and bicarbonate, which occurs under conditions leading to excess chloride and decreased bicarbonate. Hyperchloremic acidosis can be seen in patients who underwent saline loading. Bicarbonate loss will be seen in patients with small bowel fistulas, new ileostomies, severe diarrhea, or renal tubular acidosis. In patients with marked extracellular volume expansion, which often occurs postoperatively, the relative decrease in serum sodium and bicarbonate will result in a mild acidosis. A summary of the various causes of metabolic acidosis is shown in Table 22.4.
The treatment of metabolic acidosis depends on the cause. In patients with lactic acidosis, restoration of tissue perfusion is imperative. This state can be accomplished through cardiovascular and pulmonary support as needed, oxygen therapy, and aggressive treatment of systemic
Table 22.4 Causes of Metabolic Acidosis
Adapted from Narins RG, Lazarus MJ. Renal system. In: Vandam LD, ed. To make the patient ready for anesthesia: medical care of the surgical patient, 2nd ed. Menlo Park, CA: Addison Wesley, 1984:67–114.
Table 22.5 Acid-Base Disorders and Their Treatment
NaHCl, sodium hydrochloride.
infection wherever appropriate. Ketosis from diabetes can be corrected gradually with insulin therapy. Ketosis resulting from chronic starvation or from lack of caloric support postoperatively can be corrected with nutrition. In patients with normal anion gap acidosis, bicarbonate lost from the gastrointestinal tract should be replaced, excess chloride administration can be curtailed, and, where necessary, a loop diuretic can be used to induce renal clearance of chloride. Dilutional acidosis can be corrected with mild ﬂuid restriction.
Bicarbonates should not be given unless serum pH is lower than 7.2 or severe cardiac complications secondary to acidosis are present. Close monitoring of serum potassium levels is mandatory. Under states of acidosis, potassium will exit the cell and enter the circulation. The patient with a normal potassium concentration and metabolic acidosis is actually depleted of intracellular potassium. Treatment of the acidosis without potassium replacement will result in severe hypokalemia with its associated risks. A summary of the various acid-base abnormalities and associated therapies is shown in Table 22.5.