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INFANTS WITH PYLORIC STENOSIS
The excess loss of Cl depletes extracellular chloride
and with the luminal loss of Hydrogen ions produces a metabolic
alkalosis. The kidney tries to initially maintain blood pH by
excreting an alkaline urine. HCO3 is excreted with Na and K until
the overall volume deficit triggers an expansion of the extracellular
volume rather than maintenance of pH. Na is resorbed, but K is
lost via an aldosterone mediated mechanism and this leads to
excretion of H ion resulting in "paradoxical aciduria"
in an alkalotic patient.
|| Nowhere is the importance of understanding
physiology to provide appropriate fluid management more evident
that in the management of an infant with pyloric stenosis. Pure
gastric losses result in volume depletion and specific losses
of Na(60-100mEq/L), Cl(130-150mEq/L), K(10-15mEq/L).
Fluid repletion begins with an assessment of severity of dehydration
and measurement of serum electrolytes. The primary ions lost
are Na and Cl (most of the K is lost in advanced pyloric stenosis
via the kidney rather than from the emesis). Replacement is 0.9NS
along with dextrose. Once a urine output has been established
it is safe to provide KCl. in those infants who are not particularly
dehydrated, provide them with .9NS as a baseline infusion rather
than boluses and even if there are no serum electrolyte changes,
provide Na and Cl via0.45NS because you know by definition that
these were lost to some extent. Adequate fluid resuscitation
has occurred when the patient is well perfused (skin color, turgor,
cap refill, U/O) and serum electrolytes are normalized, the key
indicators based on the physiology of this disease being Cl >100
and HCO <30.
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