Pediatric emergency medicine trisk 2881 2881
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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.
