Sandbox:Vindhya: Difference between revisions

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|Cerebral salt wasting syndrome
|Cerebral salt wasting syndrome
|d, C/RSW is caused by natriuresis, which is followed by volume depletion and negative sodium balance . e kidneys are unable to conserve sodium leading to variable degrees of reduction in extracellular volume (ECV) depending the extent of the defect in sodium transport and salt intake. In addition, the patient must also have a normally functioning kidney and hypothalamic–pituitary–adrenal axis in order to be diagnosed as C/RSW
| C/RSW is caused by natriuresis, which is followed by volume depletion and negative sodium balance . The  Kidneys are unable to conserve sodium leading to variable degrees of reduction in extracellular volume (ECV) depending the extent of the defect in sodium transport and salt intake. In addition, the patient must also have a normally functioning kidney and hypothalamic–pituitary–adrenal axis in order to be diagnosed as C/RSW
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Revision as of 18:36, 1 August 2017


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Differential diagnosis

Disease pathophysiology diagnosis theraupetic goals
SIADH SIADH is a disease categorized as hypo-osmolar hyponatremia; small amount of volume expansion is caused by excess of renal water reabsorption through inappropriate antidiuretic hormone (ADH) secretion .
Cerebral salt wasting syndrome C/RSW is caused by natriuresis, which is followed by volume depletion and negative sodium balance . The Kidneys are unable to conserve sodium leading to variable degrees of reduction in extracellular volume (ECV) depending the extent of the defect in sodium transport and salt intake. In addition, the patient must also have a normally functioning kidney and hypothalamic–pituitary–adrenal axis in order to be diagnosed as C/RSW
  • Signs and symptoms:

In patients with SIADH there is too much water in the blood,this leads to low sodium in the body.

Hyponatremia is the most common manifestation. The symptoms are based on level of sodium.(hyponatremia: sodium level below 135meq/l)

When symptoms do occur, they may include any of the following:

  • headache
  • altered mental status
  • frequent falls
  • neurological manifestations such as lethargy, confusion...

in severe cases,seizures and coma may result.


Diagnostic criteria of SIADH:

  • Na<135mmol/litre
  • decreased effective serum osmolality<275mosm/kg
  • urine osmolality>100mosm/kg
  • presence of underlying disorders;CNS,pulmonary,malignancies,medications
  • normal adrenal and thyroid function
  • urine Na concentration>40mmol/l,unless taking diuretics,(or) on a severe salt restriction.
  • absence of edematous diseases(such as heart failure,nephrotic syndrome, liver cirrhosis)

Agents and means used in the treatment of SIADH.

Indirect modalities:

  • treatment of underlying pathology
  • salt restriction
  • Hyper-tonic saline
  • Loop diuretics
  • Urea
  • Demecloclycline, lithium
  • Hemodialysis, CVVH(continuous veno-venous hemofiltration), SLED(slow, low-efficiency daily dialysis).

Direct modalities:

"Vaptan drugs": block action of vasopressin at it's receptors,(V1A,V1B,V2)

Prognosis:Patients with SIADH have different characteristics and a different prognosis according to SIADH etiology. Serum sodium concentration at short-term follow-up is predictive of long-term survival. These findings might have diagnostic and treatment-related implications.