Overview
Pathophysiology
SIADH is commonly triggered by central nervous system disorders such as stroke, traumatic brain injury, subarachnoid hemorrhage, meningitis, and encephalitis, where brain inflam...
SIADH is commonly triggered by central nervous system disorders such as stroke, traumatic brain injury, subarachnoid hemorrhage, meningitis, and encephalitis, where brain inflammation or injury stimulates excess ADH release. Pulmonary diseases including pneumonia, tuberculosis, lung abscess, and positive pressure ventilation also promote ADH secretion through unclear mechanisms; notably, small cell lung cancer produces ectopic ADH and represents the most frequent paraneoplastic cause of SIADH. Management of SIADH centers on fluid restriction, typically limiting total fluid intake to 800-1000 mL per day, encompassing all intravenous fluids, medications, and oral intake. In cases of severe or symptomatic hyponatremia, such as seizures or coma, administration of 3% hypertonic saline is required, carefully titrated to raise serum sodium no faster than 8-10 mEq/L within 24 hours to avoid osmotic demyelination syndrome. Correction of the underlying cause is essential, including discontinuation of offending medications like SSRIs and carbamazepine, treatment of infections such as pneumonia, or tumor removal in small cell lung cancer. For refractory SIADH, tolvaptan, a vasopressin V2 receptor antagonist, may be used to induce aquaresis without sodium loss; initiation requires hospitalization due to...
