Sandbox:Vindhya
| Disease | Features |
|---|---|
| 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. 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, neurologic manifestations such as lethargy and confusion. In severe cases , seizures and coma may result.
Diagnostic criteria of SIADH include:
|
| Cerebral salt wasting
Cerebral salt wasting is defined as the renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. |
|
| Adrenal insufficiency | |
| Hypopituitarism | |
| Hypothyroidism | |
| Psychogenic polydipsia |
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
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.