Hyponatremia and Intravascular Volume Contraction

Hyponatremia occurs in up to one-third of patients following SAH. Although originally attributed to the syndrome of inappropriate secretion of antidiuretic hormone, the picture is more complex. Disturbances of humoral and neural regulation of sodium, intravascular volume, and water in SAH lead to intravascular volume contraction and hyponatremia, sometimes referred to as cerebral salt wasting. When administered the usual 2 to 3 L of fluids per day, up to half of patients develop intravascular volume contraction. The important clinical consequences include a higher rate of symptoms in patients with angiographic vasospasm and an increase in the number of delayed ischemic deficits that progress to infarction.

Levels of several circulating natriuretic factors are elevated following SAH, yet antidi-uretic hormone levels remain elevated during hyponatremia. Administration of large volumes of isotonic fluids can prevent volume contraction and appears to limit the severity of the hypo-natremia. Hyponatremia can frequently be managed with restriction of all free water by giving only isotonic or hypertonic intravenous fluids (1.25-3.0% saline), minimizing oral liquids, and using concentrated enteral feedings.

Two randomized, controlled trials have evaluated the ability of the mineralocorticoid fludrocortisone to correct hyponatremia and fluid balance. One (75) found that it helped correct the negative sodium balance but not volume contraction or hyponatremia; the second

(76) reported a reduced need for fluids and improved sodium levels with fludrocortisone.

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