In children, SIADH occurs most often in association with central nervous system (CNS) disorders. Laboratory evidence of SIADH was noted in almost 60% of children presenting with bacterial meningitis. ADH levels in patients with meningitis also were elevated significantly in comparison with normal and febrile controls. The duration and degree of hyponatremia was shown to correlate significantly with the subsequent development of seizures and subdural effusions. A leak of endogenous ADH across inflamed meninges has been suggested to explain these findings, but laboratory markers of inflammation did not show a correlation with arginine vasopressin (AVP) levels. SIADH occurs with other CNS infections, including brain abscesses and encephalitis, and with Rocky Mountain spotted fever, most likely secondary to the hypothalamic involvement from rickettsial vasculitis. Such CNS disturbances as head trauma, perinatal hypoxia, brain tumors, subarachnoid hemorrhage, anatomic defects, and Guillain-Barré syndrome may produce SIADH.

Intrathoracic disturbances are less common causes of SIADH in children. Pulmonary tuberculosis is well recognized, but viral, fungal, bacterial, and mycoplasma pneumonias also have been cited. Disorders that lead to decreased left atrial pressure, such as positive-pressure ventilation or pneumothoraces, can induce an excessive release of ADH by diminishing venous return. This condition is perceived inappropriately by stretch receptors as evidence of decreased circulating blood volume. Levels of ADH probably are elevated by a similar mechanism in status asthmaticus, leading one to reconsider the vigorous use of intravenous fluids often recommended in initial management.