Revision as of 14:57, 21 January 2016 by Bassomar (Created page with "==Background== *Characterized as either central Diabetes Insipidus (DI) or nephrogenic DI [Decreased production of anti-diuretic hormone (ADH) or decreased renal sensitivity t...")
- Characterized as either central Diabetes Insipidus (DI) or nephrogenic DI [Decreased production of anti-diuretic hormone (ADH) or decreased renal sensitivity to ADH].
- Causes hypernatremia.
- Decreased urine osmolality
- Central DI
- Pituitary surgery
- Nephrogenic DI
- Renal disease
- Drug Induced (e.g Lithium)
- Measure serum and urine sodium while patient is water-deprived. Lack of response to water deprivation is diagnostic. Serum Osm >295 mOsm/L
- Record response to 5 units subcutaneous vasopressin. Response to vasopressin is diagnostic of central DI (response is indicated by urine osm >800 mOsm/L). No response is diagnostic of nephrogenic DI.
- Volume repletion with normal saline or lactated ringers solution
- Patients will be water-deprived.
- Calculate water deficit: [Water deficit (in Liters) = ((Measured sodium/Normal sodium)-1)]
- Serum sodium should not decrease by more than 10-15 mEq/L per day in chronic cases of hypernatremia.
- Over-aggressive reduction of serum sodium may result in cerebral edema secondary to presence of idiogenic osmoles the build up in brain cells when exposed to chronic hypernatremia. If patient is acutely hypernatremic, idiogenic osmoles have not had time to build up in brain tissue and rapid correction of hypernatremia would not develop cerebral edema.
Tintinalli, Judith. Tintinalli's Emegency MEdicine 7th edition. Pages 120-121