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This was not "salt wasting"; it was a physiologic response to an expanded intravascular volume. Vasopressin-ADH administration to normal humans was shown to result in water retention and urinary loss of electrolytes (primarily sodium) in other studies at the time. [24] The term "cerebral salt wasting" (CSW) was coined by Cort in 1954.
SIADH is less common than appropriate release of ADH. While it should be considered in a differential, other causes should be considered as well. [15] Cerebral salt wasting syndrome (CSWS) also presents with hyponatremia, there are signs of dehydration for which reason the management is diametrically opposed to SIADH. Importantly CSWS can be ...
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Hypoosmolar hyponatremia is a condition where hyponatremia is associated with a low plasma osmolality. [1] The term "hypotonic hyponatremia" is also sometimes used.[2]When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states: low volume, normal volume, or high volume.
If the patient presents with acute hyponatraemia (low sodium levels due to overhydration) caused by psychogenic polydipsia, treatment usually involves administration of intravenous hypertonic (3%) saline until the serum sodium levels stabilise to within a normal range, even if the patient becomes asymptomatic. [30]
I thought the core differentiating feature between SIADH and increased secretion of ADH due to other causes (CHF, cirrhosis, and nephrotic syndrome) was that in SIADH euvolemia is maintained while in the latter hypervolemia is seen. (The article says "Maintained hypervolemia" under "Diagnosis" Pradyumna k m 14:52, 2 September 2010 (UTC)
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Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. [4] It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. [3] [8] Symptoms can be absent, mild or severe.