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 ||Download (.pdf)
Table S-1 Causes of SIADH
|Infection||Infection:||Bronchogenic carcinoma||Increased water|
|-meningitis||-bacterial||Adenocarcinoma of:||Permeability of nephron:|
|Subarachnoid hemorrhage||-viral||Carcinoma of:||-oxytocin|
|Hypoxia-ischemia||-tuberculosis||-ureter||Promote ADH release:|
|Intraventricular||Decreased left atrial||-prostate||-nicotine |
|Hemorrhage of newborn|| pressure:||Thymoma ||-barbiturates |
|Cerebrovascular accident||-atelectasis||Lymphoma||-carbamazepine |
|Psychosis (dipsogenic)||-PDA ligation||Mesothelioma||-diuretics|
|Guillain-Barré syndrome||Cystic fibrosis||Hemophagocytic syndrome
|Vasculitis||Hyaline membrane of||-vincristine |
|VA shunt obstruction||newborn||-vinblastine |
|Inhibit prostaglandin synthesis |
|Potentiate ADH action|
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 ...