SIADH results from a failure of the negative feedback system that regulates the release and inhibition of ADH. This results in excessive ADH, which disables patients with SIADH from excreting dilute urine even during periods of subnormal serum osmolality. Fluid is retained excessively, and they can experience dilutional hyponatremia.
Etiology
SIADH is often nonendocrine in origin. For example, the syndrome may occur in patients with bronchogenic carcinoma in which malignant lung cells synthesize and release ADH. SIADH has also occurred in patients with disorders of the lungs, and malignant tumors that affect other organs.
Disorders of the central nervous system (head injury, brain surgery, brain tumor, infection) are believed to produce SIADH through direct stimulation of the pituitary gland. Some medications (e.g., vincristine, phenothiazines, tricyclic antidepressants, thiazide diuretics) and nicotine have been implicated in SIADH through direct stimulation or decreased sensitivity of renal tubules to circulating ADH.
Management
- Medical: SIADH is generally self-limiting. Treatment is focused on the underlying cause, if possible, and restricting fluid intake.
- Restrict fluid intake. Extracellular fluid volume contracts and serum sodium concentration gradually increases to normal.
- Diuretic agents such as furosemide can be used along with fluid restriction.
- Correct severe hyponatremia with the use of hypertonic saline (3% NaCl) via IV.
- Antidiuretic hormone antagonists such as Tolvaptan (drug of choice) and tetracyclines (Demeclocycline) have off-label uses for ADH antagonists.
- Nursing:
- Close monitoring of intake and output.
- Continuous examination: daily weight, urine and blood chemistries, and neurologic status.
- Patient Education: explanations of procedures and treatments.
- Safe environment is required; hyponatremia can alter the level of consciousness.