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be taken in the acute stages to replace the uid lost in the urine, but not to the point of water intoxication These problems can be avoided by matching the amount of intravenous uids to the urinary volume and by evaluating serum and urine osmolalities every 8 to 12 h For patients with partial preservation of ADH function, chlorpropamide, clo brate, or carbamazepine can be used to stimulate release of the hormone Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion As mentioned, blood volume and osmolality are normally maintained within narrow limits by the secretion of ADH and the thirst mechanism A reduction in osmolality of even 1 percent stimulates osmoreceptors in the hypothalamus to decrease ADH and to suppress thirst and drinking; increased osmolality and reduced blood volume do the opposite Normally, blood osmolality is about 282 mmol/kg and is maintained within a very narrow range Release of ADH begins when it reaches 287 mmol/kg (osmotic threshold) At this point, plasma ADH levels are 2 pg/mL and increase rapidly as the osmolality rises The response of ADH secretion to hyperosmolality is not the same for all plasma solutes; in contrast to hypernatremia, for example, hyperosmolality induced by elevations in urea nitrogen or endogenous glucose produce minimal or no elevations in ADH Derangement of this delicately regulated mechanism, taking the form of dilutional hyponatremia and water retention without edema, is observed under a variety of clinical circumstances in which the plasma ADH is above normal or inappropriately normal despite plasma hypo-osmolality The term inappropriate secretion of antidiuretic hormone (SIADH) was applied to this syndrome by Schwartz and Bartter because of its similarity to that produced in animals by the chronic administration of ADH The same syndrome can arise from ectopic production of the hormone by tumor tissue In such cases, the thirst mechanism is not inhibited by decreased osmolality, and continued drinking further increases blood volume and reduces its solute concentration; ADH levels are found to be persistently elevated The physiologic hallmarks of this condition are a concentrated urine, usually with an osmolality above 300 mosm/L, and low serum osmolality and sodium concentrations Because of the dilutional effects, urea nitrogen and uric acid are reduced in the blood and serve as markers for excessive total body water Tissue edema is not seen because sodium excretion in the urine is maintained by suppression of the renin-angiotensin system and by an increase in atrial natriuretic peptide secretion (see below) SIADH is observed frequently with a variety of cerebral lesions (infarct, tumor, hemorrhage, meningitis, encephalitis) that do not involve the hypothalamus directly and with many types of local hypothalamic disease (trauma, surgery, vascular lesions) In most cases it tends to be a transient feature of the underlying illness The acute dysautonomia of Guillain-Barre syndrome is a common cause of SIADH, and hyponatremia is particularly likely to occur in such patients being ventilated mechanically The increased thoracic pressure induced by positive-pressure ventilation promotes SIADH in susceptible patients Acute porphyric episodes have the same effect Neoplasms, particularly oat-cell tumors and sometimes in ammatory lesions of the lung, may elaborate an ADH-like substance, and certain drugs such as carbamazepine, chlorpromazine, chlorothiazide, chlorpropamide, clo brate, nonsteroidal antiin ammatory 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 no apparent
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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
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