Hyponatremia in the syndrome of inappropriate antidiuretic hormone secretion (SIADH) results from ADH-induced retention of ingested or infused water. Although water excretion is impaired, sodium handling is intact since there is no abnormality in volume-regulating mechanisms such as the renin-angiotensin-aldosterone system or atrial natriuretic peptide .
The treatment of hyponatremia due to SIADH (including the reset osmostat variant) will be reviewed here. The choice of therapy of SIADH is dependent upon a number of factors including the degree of hyponatremia, the presence or absence of symptoms, and, to some degree, the urine osmolality.
The pathogenesis and etiology of the SIADH and a general review of the treatment of hyponatremia due to a variety of causes are discussed separately. (See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)" and "Overview of the treatment of hyponatremia in adults".)
To understand the approach to therapy of hyponatremia in SIADH, it is worthwhile to briefly review the pathogenesis of hyponatremia in this disorder. Among patients with SIADH, the combination of water retention and secondary solute (sodium plus potassium) loss accounts for essentially all of the reduction in serum sodium [2,3].
These changes occur in the following sequence [3,4]: