Management of sodium abnormalities in patients with CNS disease

The CNS plays an integral role in the neuroendocrine regulation of sodium and water homeostasis. Therefore, disturbances of this function are common in patients with CNS disease. The body's sodium and water content are tightly regulated in order to maintain normal osmolality and intravascular volume. Complex neural, humoral, and renal mechanisms integrate information regarding osmolality, intravascular volume, blood pressure, and intake of sodium and water. They act to modify intake and excretion of sodium and water and vascular tone. Most sodium abnormalities in patients with CNS disease result from altered water excretion secondary to disturbed release of antidiuretic hormone (ADH). Insufficient release is seen with lesions in or near the optic chiasm and pituitary gland and results in diabetes insipidus (DI). DI is common following surgery or trauma in this region and care must be exercised in treating these patients because of the potentially variable and transient nature of the disturbance. The syndrome of inappropriate release of ADH is seen in a wide variety of CNS disorders and produces a dilutional hyponatremia. Symptomatic hyponatremia should be managed aggressively with diuretics and hypertonic saline followed by fluid restriction. However, very rapid correction or overcorrection should be avoided. In some patients, especially those with acute subarachnoid hemorrhage, disturbed sodium regulation appears to contribute to hyponatremia. Patients with subarachnoid hemorrhage and hyponatremia should not be fluid restricted, because of the risk of exacerbating vasospasm, but treated with large volumes of isotonic saline.