accomplished slowly because overly rapid volume correction can cause cerebral edema, seizures, and death If the child is not hypotensive, or once the hypotension and perfusion have been corrected, free water replacement is done over 48 hours Calculations of appropriate fluids must include maintenance requirements, replacement needs, and ongoing urinary losses (see Chapter 22 Dehydration ) If DI is strongly suspected on the basis of discrepant serum and urine osmolality, Desmopressin (DDAVP®) (10 μg intranasally or 0.2 to 0.4 mCg/kg subcutaneously) may be a useful adjunct to IV fluid therapy If desmopressin is not available or cannot be used for some reason, other antidiuretic agents are available Aqueous vasopressin (Pitressin® ) may be administered as a continuous IV infusion starting at 2.5 mU/kg/hr and slowly (every 15 to 30 minutes) increasing the rate by increments of 2.5 milliunits (maximum 10 mU/kg/hr) to decrease urine output to less than mL/kg/hr Desmopressin and vasopressin act rapidly to promote tubular resorption of free H2 O; clinically, this response should be apparent as decreased urinary output, when being measured with a bladder catheter, and should demonstrate increased urine osmolality within 15 minutes of administration Once the patient has responded, however, extreme care must be used in subsequent fluid management because the patient can no longer excrete excess water Therefore, baseline IV fluid administration must be restricted to L/m2 of body surface area per day (or roughly two-thirds maintenance fluids) using a low sodium infusate, such as 5% dextrose with one-fourth normal saline (0.23%), in addition to the fluid designed to replete the initial estimated free water deficit over 48 hours Failure to respond to either form of ADH suggests the possibility of tubular unresponsiveness to ADH (nephrogenic DI); however, more commonly, failure to respond results from improper administration of the medication or use of desmopressin that has lost its potency Because of these factors, if cessation of diuresis is not noted within hours of administration of the first dose, a second dose from a different bottle of desmopressin should be tried The use of an ADH agonist generally simplifies management by reducing the quantity of fluid that must be infused; however, careful monitoring of input and output remains essential Children who fail to respond to desmopressin are likely to have nephrogenic DI and must be managed acutely with fluid therapy alone Hypercalcemia and renal failure are the most common causes of nephrogenic DI Paradoxically, the thiazide diuretics have proven to be useful in the chronic control of nephrogenic DI The child should be closely observed for changes in level of consciousness, pulse rate, and blood pressure Fluid input and output should be meticulously monitored Serum osmolality and [Na+ ] should be determined every to hours until the rate of their decline can be determined Urine osmolality should be measured every to hours to determine the responsiveness of the renal tubule to DDAVP Because large volumes of dextrose-containing fluids are used, the blood glucose should also be followed closely If the blood glucose exceeds 150 mg/dL, the concentration of dextrose in the infusate should be decreased Clinical Indications for Discharge or Admission Clinically significant electrolyte derangements or the inability to maintain hydration status are indications for admission in well-appearing child Children with intact thirst mechanism who are able to tolerate PO can be discharged with plan for close outpatient follow-up SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION Goals of Treatment The goals of treatment in a child with syndrome of inappropriate antidiuretic hormone (SIADH) are to raise the serum sodium and improve the neurologic status of the patient; secondarily, causes of SIADH should be identified CLINICAL PEARLS AND PITFALLS Most patients are asymptomatic from SIADH until the serum sodium