Metabolic alkalosis is characterized by a rise in the plasma bicarbonate concentration, and causes include hydrogen loss from the gastrointestinal tract or kidneys, volume contraction around a relatively constant amount of extracellular bicarbonate (contraction alkalosis), and the administration of bicarbonate Given the renal capacity to excrete excess bicarbonate, clinical circumstances must be present that impair bicarbonate excretion in order to develop this disorder Therefore, when approaching the patient with metabolic alkalosis, identification of both the inciting cause and the clinical factors allowing persistence of the disorder must be pursued Although there are many causes ( Table 100.12 ), metabolic alkalosis in children most commonly results from diuretic therapy and hydrogen ion loss from gastrointestinal secretions Loop and thiazide diuretics increase distal delivery of both sodium and water and predispose to volume contraction, thereby stimulating aldosterone secretion and enhancing hydrogen ion secretion into the tubular lumen Gastrointestinal causes of metabolic alkalosis include vomiting or nasogastric suction Gastric secretions have high concentrations of hydrogen chloride and a lesser amount of potassium chloride (5 to 10 mEq/L), and gastric losses will predispose to the development of metabolic alkalosis In normal subjects, the renal capacity to excrete bicarbonate prevents the development of metabolic alkalosis The persistence of metabolic alkalosis implies a limitation of renal bicarbonate excretion, and the most common perpetuating cause is effective circulating volume depletion In addition to volume depletion, chloride depletion will also limit renal bicarbonate excretion and is associated with gastric fluid loss and diuretic therapy Low renal tubular concentration of chloride favors both bicarbonate reabsorption and decreases bicarbonate excretion Hypokalemia also directly increases bicarbonate reabsorption, which is in part due to intracellular acidosis induced by the entry of hydrogen ions into the cell in exchange for potassium movement out of the cell Intracellular acidosis induces renal acid excretion and promotes net bicarbonate reabsorption