SIADH is observed frequently with a variety of cerebral lesions that do not involve the hypothalamus directly (infarct, tumor, hemorrhage, meningitis, encephalitis) and with many types of local hypothalamic diseases (trauma, surgery, vascular lesions). In most cases, it tends to be a transient feature of the underlying illness. The acute dysautonomia of Guillain-Barré syndrome is a common neurologic cause of SIADH; it is ostensibly the result of the neuropathy affecting the afferent nerves from volume receptors in the right atrium and jugular veins. Of interest, hyponatremia is particularly likely to occur in such patients on positive-pressure ventilation because increased thoracic pressure provides an additional stimulus to SIADH. Acute porphyric episodes have the same effect. Neoplasms, particularly small cell tumors, and inflammatory lesions of the lung such as sarcoidosis may elaborate an ADH-like substance and produce this syndrome. Certain drugs—such as carbamazepine, chlorpromazine, chlorothiazide, chlorpropamide, clofibrate, nonsteroidal anti-inflammatory agents, and vincristine—also stimulate ADH release and may lead to hyponatremia. In some cases, no cause or associated disease is apparent.
A fall in serum sodium to 125 mEq/L usually has few 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 If hyponatremia has been of several days or more duration, the rapid restitution of serum sodium to normal or above-normal levels carries a risk of producing osmotic demyelination (also called central pontine myelinolysis; see Chap. 40). 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/d and to verify the desired urinary loss of water by checking the patient’s weight and serum sodium until it reaches approximately 130 mEq/L. If there is drowsiness, confusion, or seizures that cannot be confidently attributed to the underlying neurologic illness, or if the serum sodium is in the range of 100 to 115 mEq/L, isotonic or 3 percent NaCl should be infused over 3 to 4 h and furosemide 20 to 40 mg administered to prevent fluid overload. In order to avoid osmotic demyelination, a safe clinical rule is to raise the serum sodium by no more than 12 mEq/L in the first 24 h and by no more than 20 mEq/L in 48 h.
A moderate reduction in the serum sodium concentration is a common finding 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. Later it was erroneously identified as SIADH, until the pathophysiological understanding of this disorder subsequently returned to the concept of natriuresis rather than water retention caused by ADH secretion. As Nelson and colleagues demonstrated many years ago, neurosurgical patients with hyponatremia have a reduction in blood volume, suggesting sodium loss rather than water retention. This distinction has important clinical implications because fluid restriction, which is used to treat SIADH, can have disastrous results when a patient has volume depletion associated with salt wasting.