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SIADH is an acronym that stands for: Syndrome of Inappropriate of AntiDiuretic Hormone Secretion. The most common cause of euvolemic hyponatremia characterized by hypokalemic, hypochloremic, metabolic alkalosis, and normotensive, hyperreninemic hyperaldosteronism. A state of positive water balance rather than sodium depletion is present. Numerous etiologies have been associated with this manifestation (see the Table S-1).

Table S-1 Causes of SIADH

Schwartz-Bartter Syndrome; Aldosteronism-Normal Blood Pressure Syndrome; Juxtaglomerular Hyperplasia Syndrome.

First reported in 1957 by William Benjamin Schwartz, American cardiologist, and Frederic Crosby Bartter, American physician. They described two adult patients with bronchial carcinoma who developed persistent hyponatremia, hypoosmolality, and urinary loss of sodium and chloride.

Overproduction of vasopressin from the hypothalamus leads to water retention, urinary sodium loss, and hyponatremia. Results in resultant volume expansion promoting urine flow rate, thus limiting further water retention.

Clinical features and biochemical (low serum sodium levels and low serum osmolality, increased urine sodium content and osmolality, suppression of plasma renin activity, normal/high serum aldosterone level, high plasma antidiuretic hormone and atrial natriuretic hormone levels). Conditions known to be associated with antidiuretic hormone secretion (normal renal, liver, adrenal, thyroid, and cardiac functions) must be excluded.

Symptoms, when present, are caused by acute loss of sodium and are often masked by or mistaken as manifestations of the primary problem (anorexia, confusion, headache, muscle weakness, vomiting, convulsions, and coma). Chronic hyponatremia, lasting longer than 2 to 5 days, usually has minimal or no symptoms. Vascular volume is normal or mildly increased, and peripheral edema is very rare. Blood pressure is normal, even with postural changes; urine output is usually low.

Hyponatremia may contribute to delayed awakening and postoperative confusion, and potentiates the action of neuromuscular blockers. Symptomatic hyponatremia (serum sodium levels <120 mmol/L) should be corrected slowly at a rate of <1 mmol/L/h until a serum level of approximately 130 mmol/L is reached. Rapid correction of long-standing (>2 days) advanced hyponatremia (<110 mmol/L) to normal levels within less than 20 hours ...

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