Pediatric emergency medicine trisk 1894 1894
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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 <125 mEq/L.
SIADH is present in a high proportion of patients with bacterial meningitis (50%),
positive pressure ventilation (20%), and Rocky Mountain spotted fever (70%).
There are numerous relatively benign causes of SIADH, including fever, nausea,
pain, pneumonia, and a wide range of physiologic stressors.
For severe lethargy, seizure, or coma administer 3% saline emergently (3 mL/kg
every 10 to 20 minutes as needed) and consider furosemide with a normal saline
infusion.
For asymptomatic or mildly symptomatic patients, treat with rigorous fluid restriction and
consider a vasopressin receptor antagonist if recurrent.
Current Evidence
Excessive secretion of ADH accompanying normal or low plasma osmolality or [Na+ ] is
inappropriate because it further depresses the plasma osmolality and [Na+ ]. The overall
incidence of the SIADH secretion in childhood is unknown, but it is common in certain
disease states. Normal ADH secretion is stimulated by hypertonicity of the fluid surrounding
the hypothalamic osmoreceptors, volume receptors in the right atrium, and ill-defined nervous
impulses from higher cortical centers. Disorders of the CNS ( Table 89.8 ) may cause
excessive ADH secretion by producing either a local disturbance of the hypothalamic
osmoreceptors or some undetermined nervous stimuli. Many intrathoracic conditions are
associated with SIADH, probably due to the vestigial ability of the lung to produce ADH.
Physical and emotional stress, severe pain, and nausea are also potent stimuli of ADH
secretion. Excessive secretion of ADH leads to water retention by the collecting tubules of the
kidneys, a mechanism mediated by insertion of water channels into the luminal membrane of
the collecting duct and allowing water reabsorption along the medullary concentration
gradient. The retained water expands the intravascular compartment, dilutes all plasma
constituents, and lowers the plasma osmolality.
