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Cerebral salt-wasting syndrome (CSWS), also written cerebral salt wasting syndrome, is a rare endocrine condition featuring a low blood sodium concentration and dehydration in response to injury (trauma) or the presence of tumors in or surrounding the brain. In this condition, the kidney is functioning normally but excreting excessive sodium. [1]
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 associated with subarachnoid hemorrhage (SAH) which may require fluid supplementation rather than restriction to prevent brain damage.
There are several recorded cases of forced ingestion of concentrated salt solution in exorcism rituals leading to death. [11] Mineralcorticoid excess due to a disease state such as Conn's syndrome usually does not lead to hypernatremia unless free water intake is restricted. Salt poisoning is the most common cause in children.
In dystrophic calcification, basophilic calcium salt deposits aggregate, first in the mitochondria, then progressively throughout the cell. [citation needed] These calcifications are an indication of previous microscopic cell injury, occurring in areas of cell necrosis when activated phosphatases bind calcium ions to phospholipids in the membrane.
[17] [18] [19] The following conditions should also be excluded: DI, cerebral salt wasting, pseudohyponatraemia caused by hyperlipidemia or hyperparaproteinemia, SIADH, mineralcorticoid deficiency, salt-wasting nephropathy, nephrotic syndrome, chronic heart failure and cirrhosis.
The fractional excretion of sodium (FE Na) is the percentage of the sodium filtered by the kidney which is excreted in the urine.It is measured in terms of plasma and urine sodium, rather than by the interpretation of urinary sodium concentration alone, as urinary sodium concentrations can vary with water reabsorption.
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.
(The terms "salt-wasting CAH", and "simple virilizing CAH" usually refer to subtypes of this condition.) CAH due to deficiencies of enzymes other than 21-hydroxylase present many of the same management challenges, as 21-hydroxylase deficiency, but some involve mineralocorticoid excess or sex steroid deficiency.