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SIADH is characterized by: (1) hyponatremia; (2) decreased osmolality (< 280 mosm/kg) with inappropriately increased urine osmolality (> 150 mosm/kg); (3) absence of cardiac, renal, or liver disease; (4) normal thyroid and adrenal function (see 26); and (5) urine sodium usually over 20 mEq/L The mechanisms that regulate sodium excretion in response to increases in ECF volume, such as suppression of the sympathetic nervous and renin angiotensin systems and increased secretion of atrial natriuretic factor, are preserved and account for the increase in urinary sodium Other changes frequently seen in SIADH include low blood urea nitrogen (BUN) (< 10 mg/dL) and hypouricemia (< 4 mg/ dL), which are not only dilutional but result from increased urea and uric acid clearances in response to the volumeexpanded state A high BUN suggests a volume-contracted state, which excludes a diagnosis of SIADH
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b 09% saline In asymptomatic patients whose serum sodium is less than 120 mEq/L, 09% saline with furosemide may be used Urinary sodium and potassium losses are replaced as above c Demeclocycline Demeclocycline (300 600 mg twice daily) is useful for patients who cannot adhere to water restriction or need additional therapy; it inhibits the effect of ADH on the distal tubule Onset of action may require 1 week, and concentrating may be permanently impaired Therapy with demeclocycline in patients with cirrhosis appears to increase the risk of renal failure d Fludrocortisone Hyponatremia occurring as part of the cerebral salt-wasting syndrome can be treated with fludrocortisone e Selective renal vasopressin V2 antagonists For hospitalized patients with euvolemic SIADH, conivaptan is given as an intravenous loading dose of 20 mg delivered over 30 minutes, then as 20 mg continuously over 24 hours Subsequent infusions may be administered every 1 3 days at 20 40 mg/d by continuous infusion Mozavaptan is another intravenous agent in this class approved in Japan, but not yet in the United States; it is used to treat paraneoplastic SIADH Results of recent clinical trials of an oral selective V2 antagonist, tolvaptan, are promising
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A Hypovolemic Hypotonic Hyponatremia
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Treatment consists of replacement of lost volume with isotonic or half-normal (045%) saline or lactated Ringer s infusion The rate of correction must be adjusted to prevent permanent cerebral damage (see below)
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B Euvolemic Hypotonic Hyponatremia
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1 Symptomatic hyponatremia Symptomatic hyponatremia is usually seen in patients with serum sodium levels less than 120 mEq/L If there are central nervous system symptoms, hyponatremia should be rapidly treated at any level of serum sodium concentration a Rate and degree of correction Central pontine myelinolysis may occur from osmotically induced demyelination due to overly rapid correction of serum sodium (an increase of more than 1 mEq/L/h, or 25 mEq/L within the first day of therapy) Hypoxic anoxic episodes during hyponatremia may contribute to the demyelination A reasonable approach is to increase the serum sodium concentration by no more than 1 2 mEq/L/h and not more than 25 30 mEq/L in the first 2 days; the rate should be reduced to 05 1 mEq/L/h as soon as neurologic symptoms improve The initial goal is to achieve a serum sodium concentration of 125 130 mEq/L, guarding against overcorrection b Saline plus furosemide Hypertonic (eg, 3%) saline with furosemide is indicated for symptomatic hyponatremic patients If 3% saline without a diuretic is administered to a patient with SIADH, the serum sodium concentration increases temporarily, but euvolemic patients excrete the excess sodium If furosemide (05 1 mg/kg intravenously) is added, however, the kidney cannot concentrate urine even in the presence of high levels of ADH Infusion of 3% saline is accompanied by excretion of isotonic urine with a net loss of free water The sodium concentration of 3% saline is 513 mEq/L To determine how much 3% saline to administer, a spot urinary Na+ is determined after a furosemide diuresis has begun The excreted Na+ is replaced with 3% saline, empirically begun at 1 2 mL/ kg/h and then adjusted based on urinary output and urinary sodium For example, after administration of furosemide, urine volume may be 400 mL/h and sodium plus potassium excretion 100 mEq/L The excreted Na+ plus K+ is 40 mEq/h, which is replaced with 78 mL/h of 3% saline (40 mEq/h divided by 513 mEq/L) Free water loss is about 1% of total body water Therefore, an approximately 1% rise in plasma sodium concentration (1 15 mEq/L/h) can be expected Measurements of plasma sodium should be done approximately every 4 hours and the patient observed closely 2 Asymptomatic hyponatremia In asymptomatic hyponatremia, the correction rate of hyponatremia need be no more than 05 mEq/L/h No specific treatment is needed for patients with reset osmostats a Water restriction Water intake should be restricted to 05 1 L/d A gradual increase of serum sodium will occur over days
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