Acid–base disorders are common in hospitalized and critically ill children. More specifically, metabolic acidosis is perhaps the most common acid–base disorder seen in children with illness. Patients with a metabolic acidosis have a low serum bicarbonate level with or without a correlating change in serum carbon dioxide levels. Normal serum pH is between 7.35 and 7.45; therefore, an acidosis is a pH of 7.35. The metabolic acidosis itself is only a sign of an underlying illness or problem that needs to be corrected for the acidosis to be treated. The three basic mechanisms causing metabolic acidosis are loss of bicarbonate from the body, impaired ability to excrete acid by the kidney, and addition of exogenous or endogenous acid to the body. Types of metabolic acidosis are divided into two main categories: with an anion gap and without an anion gap. The anion gap is calculated by subtracting the serum chloride plus the serum bicarbonate from the serum sodium value. A normal anion gap is ≤16. Serum albumin and phosphorus levels also can affect the anion gap but are generally not accounted for unless extremely abnormal.

Metabolic acidosis without an anion gap has two major causes in pediatrics. Diarrhea is the most common, causing a loss of bicarbonate from the body. If diarrhea persists, it can also lead to a lactic acidosis secondary to volume loss and hypoperfusion. The second cause of nonanion gap metabolic acidosis is renal tubular acidosis, which occurs in three forms: distal (type I), proximal (type II), and hyperkalemic (type IV).

Metabolic acidosis with an anion gap has several causes including methanol poisoning, renal failure/uremia, diabetic ketoacidosis, inborn errors of metabolism, lactic acidosis, ethanol or ethylene glycol poisoning, and salicylate poisoning. The basic dogma in treating an anion gap metabolic acidosis is to treat the underlying cause. Acidosis is thought to have a deleterious effect on cellular function and hemodynamics, such as depressed responsiveness of adrenergic receptors to circulating catecholamines, leading to decreased cardiac output. Other detrimental effects of severe academia (pH <7.2) include but are not limited to insulin resistance, increased free radical formation, increased protein degradation, gut barrier dysfunction,
and potentially hemodynamically significant serum electrolyte disturbances, such as serum calcium and potassium. Some types of metabolic acidosis have specific treatments, such as insulin and fluids for patients with diabetic ketoacidosis. Insulin helps convert ketone bodies (acetoacetic acid and β-hydroxybutyrate) formed via increased beta oxidation of fatty acids during insulin-deficient states into bicarbonate, correcting the acidosis. Fluid helps correct intravascular volume depletion caused by glucosuria-mediated diuresis. Similarly, treatment of distal renal tubular acidosis with sodium bicarbonate helps buffer the academia secondary to the kidney’s impaired ability to secrete acid into the urine. Treatment of lactic acidosis is not quite as straightforward.