Diabetes insipidus
Background
- Characterized as either:
- Central Diabetes Insipidus (or neurogenic DI)
- Deficient secretion of antidiuretic hormone (ADH)
- Nephrogenic DI
- Normal ADH secretion but decreased renal sensitivity to ADH
- Central Diabetes Insipidus (or neurogenic DI)
- Causes hypernatremia
Causes
- Central DI
- Cancer
- Pituitary surgery
- Head trauma
- Idiopathic
- Nephrogenic DI
- Renal disease
- Drug Induced (e.g Lithium)
- Hypokalemia
- Hypercalcemia
- Polycystic kidney disease
- Sjögren syndrome
- Amyloidosis
Clinical Features
- Hypernatremia
- Decreased urine osmolality
- Dehydration
- Irritability
- Tremors
- Ataxia
- Hyperreflexia
- Spasms
- Seizures
- Death
Differential Diagnosis
Hypernatremia
Water loss:
- Decreased Intake
- Water loss > Na loss
- Central DI
- Head Trauma
- CVA
- Tumor
- Meningitis
- Nephrogenic DI
- Thyrotoxicosis
Sodium gain:
- Increased intake
- Na intake
- NaBicarb
- Incorrect preparation of infant formula
- Renal Na retention (secondary to poor perfusion)
Evaluation
- Urine specific gravity < 1.010
- 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
- In adults, onset of central DI usually abrupt whereas onset gradual in nephrogenic DI
Management
- Place foley for strict I/Os
- Volume repletion with normal saline or lactated ringers solution
- Patients will be water-deprived
- Calculate water deficit: Water deficit (in Liters) = [(Body weight(kg)x0.6)x((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 acutely hypernatremic, idiogenic osmoles have not had time to build up in brain tissue and rapid correction of hypernatremia would not develop cerebral edema
- Nephrogenic diabetes insipidus[1]
- Low-salt, low-protein diet
- Hydrochlorothiazide 25mg BID
- Indomethacin has greater effect at reducing urine output than ibuprofen
Disposition
- Admission for further workup and/or volume replacement
- Nephrology follow up
See Also
External Links
References
- ↑ Bichet DG et al. Treatment of nephrogenic diabetes insipidus. UpToDate. Jan 7, 2016. http://www.uptodate.com/contents/treatment-of-nephrogenic-diabetes-insipidus#H10