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INFANTS WITH PYLORIC STENOSIS

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).

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.

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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