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clinical effects, although signs of an associated neurologic disease, such as a previous stroke or a subdural hematoma, may worsen Sodium levels of less than 120 meq/L are attended by nausea and vomiting, inattentiveness, drowsiness, stupor, and generalized seizures There may be asterixis As is characteristic of most metabolic encephalopathies, the more rapid the decline of the serum sodium, the more likely there will be accompanying neurologic symptoms Treatment of SIADH The rapid restitution of serum sodium to normal or above-normal levels carries a risk of producing central pontine myelinolysis (see page 973) Our usual procedure in patients with serum sodium concentrations of 117 to 125 meq/L is to slowly correct the sodium concentration by restricting water to 400 to 800 mL/day and to verify the desired urinary loss of water by checking the patient s weight and serum sodium until it reaches the lower range of 130 meq/L If there is drowsiness, confusion, or seizures that cannot be con dently attributed to the underlying neurologic illness or if the serum sodium is in the range of 100 to 115 meq/L, isotonic or 3% NaCl should be infused over 3 to 4 h and furosemide 20 to 40 mg administered to prevent uid overload A safe clinical rule is to raise the serum sodium by no more than 12 meq/L in the rst 24 h and by no more than 20 meq/L in 48 h in order to prevent myelinolysis Neurogenic (Cerebral) Salt Wasting A moderate reduction in the serum sodium concentration is a common nding in patients with acute intracranial diseases and postoperatively in neurosurgical patients Originally it was described as a cerebral salt-wasting syndrome by Peters and colleagues and later was erroneously identi ed with the then newly described Schwartz-Bartter syndrome of SIADH In recent years it has again come to be recognized as being due to natriuresis and not to water retention caused by ADH secretion Later, as Nelson and colleagues demonstrated, neurosurgical patients with hyponatremia and ostensibly with SIADH showed, instead, a reduction in blood volume, suggesting sodium loss rather than water retention This distinction has important clinical implications, because the use of uid restriction with the intention to treat SIADH can have disastrous results if a state of volume contraction exists from salt wasting One leading hypothesis concerning the mechanism of hyponatremia in these cases is secretion of another oligopeptide, atrial natriuretic factor (ANF), that is found mainly in the walls of the cardiac atria but also in neurons surrounding the third ventricle in the anteroventral hypothalamic region Physiologically, ANF activity opposes that of ADH in the kidney tubules and also has a potent inhibitory effect on ADH release from the hypothalamus; ie, it causes a natriuresis (see review by Samson) ANF, like some other neural peptides, is secreted in bursts, and the natriuresis is evident only if total urinary sodium content is measured over many hours or days The role of ANF in causing the hyponatremia that follows subarachnoid hemorrhage is controversial (see Wijdicks et al and Diringer et al for opposing views), but it is our experience that the hyponatremia in this condition is the result mainly of salt loss, not water retention Because uid restriction after subarachnoid hemorrhage may precipitate cerebral ischemia from vasospasm, the proper approach is to maintain intravascular volume with intravenous uids and to correct hyponatremia by infusion of normal saline In addition to head trauma, salt wasting has also been reported with cerebral tumors, after pituitary surgery, and in the dysautonomia of Guillain-Barre syndrome, conditions that have also been associated at times with SIADH As already stated, in each of these.

disorders, should the patient be hyponatremic, it is desirable to determine the intravascular volume and the urine sodium output before instituting treatment Other Disturbances of ADH and Thirst Conditions have been described in which the osmoreceptor control of ADH and of thirst appear to be dissociated As reported by Hayes and coworkers, one of our colleagues patients repeatedly developed severe hypernatremia (levels as high as 180 to 190 meq/L), at which time he became confused and stuporous Although the patient was able to initiate a release of ADH, his thirst mechanism was nonfunctional Only when the patient was compelled to drink water at regular intervals did his serum sodium fall Robertson and others have described similar cases with abnormalities of thirst These have been reported under the title of central or essential hypernatremia

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