The desired volume of normal saline can then be determined by keeping in mind that its sodium concentration is 154 mEq/L and that of 3 percent (hypertonic) saline solution is 513 mEq/L. If hypertonic saline is administered, it is usually necessary to simultaneously reduce intravascular volume with furosemide, beginning with a dose of 0.5 mg/kg intravenously, and to increase the dosage until a diuresis is obtained. (As a rule of thumb, 300 to 500 mL of 3 percent saline, infused rapidly intravenously, will increase the serum sodium concentration by about 1 mEq/L/h for 4 h.) Guidelines to prevent an overly rapid correction of Na are elaborated further on in relation to central pontine myelinolysis (no more rapidly than 10 mmol/L in the first 24 h). Although the syndrome of SIADH is usually self-limiting, it may continue for weeks or months, depending on the type of associated brain disease.
Not all patients with neurologic disorders who manifest hyponatremia have SIADH. Diuretic excess, adrenal insufficiency, and salt wasting also produce hypovolemic hyponatremia as a result of natriuresis. When renal salt wasting is seen in the context of a central neurologic disorder, the process has been termed “cerebral salt wasting” (Nelson et al). Sodium loss in these circumstances is attributable to the production by the heart or brain of a potent polypeptide natriuretic factor. As discussed in Chap. 33, under “Subarachnoid Hemorrhage,” the distinction between SIADH and cerebral salt wasting is of more than theoretical importance, insofar as fluid restriction to correct hyponatremia may be dangerous in patients with salt wasting, particularly in those with vasospasm after ruptured intracranial aneurysms.
Arieff emphasized the hazards of postoperative hyponatremia in a series of 15 patients, all of them women, in whom severe hyponatremia followed elective surgery. About 48 h after these patients had recovered from anesthesia, their serum Na fell markedly, at which point generalized seizures occurred, followed by respiratory arrest. We are more familiar with acutely developing hyponatremia in the context of prostate surgery, where large amounts of hypotonic fluids are routinely administered both intravenously and intravascularly. A similar syndrome is known in instances of overly zealous fluid resuscitation in children with diabetic ketoacidosis. The mechanisms of neurologic deterioration in all of these cases is likely to be brain edema.
An important consideration in the management of severe hyponatremia, as mentioned earlier, is the rapidity with which the abnormality is corrected and the danger of provoking central pontine myelinolysis and related brainstem, cerebellar, and cerebral lesions (extrapontine myelinolysis; osmotic demyelination). These issues are considered below, in the section “Central Pontine Myelinolysis.”
Hypernatremia (Na >155 mEq/L) and dehydration are observed in diabetes insipidus, the neurologic causes of which include head trauma with damage to the pituitary stalk (Chap. 26), and in nonketotic diabetic coma, protracted diarrhea in infants, and the deprivation of fluid intake in the stuporous patient. The last condition is usually associated with a brain lesion that impairs consciousness. Exceptionally, in patients with chronic hydrocephalus, the hypothalamic thirst center is rendered inactive and severe hypernatremia, stupor, and coma may follow a failure to drink. In hypernatremia from any cause, the brain volume is manifestly reduced. Retraction of the cerebral cortex from the dura has been known to rupture a bridging vein and cause a subdural hematoma.