Pediatric emergency medicine trisk 2883 2883
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alkalosis, the conservation of chloride is intact, and a urine chloride
concentration less than 25 mEq/L would be consistent with volume
depletion. A urine chloride concentration greater than 40 mEq/L in the
setting of metabolic alkalosis would be consistent with disorders such as
primary mineralocorticoid excess, Bartter syndrome, Gitelman syndrome,
or continued diuretic therapy.
The treatment of metabolic alkalosis is supportive, and reversible
underlying causes should be addressed. The focus of therapy should aim at
restoring adequate circulating volume and correcting chloride and
potassium deficits. Providing isotonic sodium chloride will restore
intravascular volume, remove the stimulus for sodium retention, and
increase distal chloride delivery. Once these results have been achieved,
there will be decreased bicarbonate reabsorption, increased bicarbonate
excretion, and correction of the metabolic alkalosis. Potassium chloride
should be provided if depletion is suspected with close monitoring to avoid
excessive replacement. Though the extracellular concentration of potassium
may be low during metabolic alkalosis due to transcellular shift to the
intracellular space, true potassium depletion may be present. Potassium can
be lost due to impaired renal absorption from diuretic therapy, aldosterone
effect associated with volume depletion, and obligatory wasting of cations
(Na+ and K+ ) associated with bicarbonate excretion. In patients with
metabolic alkalosis and edematous states, providing sodium chloride may
be hazardous. Therapy should take into account the underlying condition
and planned in concert with appropriate subspecialty care if possible.
ACUTE KIDNEY INJURY
CLINICAL PEARLS AND PITFALLS
