Diabetes insipidus: Difference between revisions
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==Background== | ==Background== | ||
*Characterized as either: | *Characterized as either: | ||
**Central Diabetes Insipidus (DI) | **Central Diabetes Insipidus (or neurogenic DI) | ||
** | ***Deficient secretion of antidiuretic hormone (ADH) | ||
**Nephrogenic DI | |||
***Normal ADH secretion but decreased renal sensitivity to ADH | |||
*Causes [[hypernatremia]] | *Causes [[hypernatremia]] | ||
| Line 12: | Line 14: | ||
**Idiopathic | **Idiopathic | ||
*Nephrogenic DI | *Nephrogenic DI | ||
**Renal disease | **[[renal failure|Renal disease]] | ||
**Drug Induced (e.g [[Lithium]]) | **Drug Induced (e.g [[Lithium]]) | ||
**[[Hypokalemia]] | **[[Hypokalemia]] | ||
**[[Hypercalcemia]] | **[[Hypercalcemia]] | ||
**[[Polycystic kidney disease]] | **[[Polycystic kidney disease]] | ||
**[[ | **[[Sjögren syndrome]] | ||
**[[Amyloidosis]] | **[[Amyloidosis]] | ||
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*[[Hypernatremia]] | *[[Hypernatremia]] | ||
*Decreased urine osmolality | *Decreased urine osmolality | ||
*Dehydration | *[[Dehydration]] | ||
*Irritability | *Irritability | ||
* | *[[Tremor]]s | ||
*[[Ataxia]] | *[[Ataxia]] | ||
*Hyperreflexia | *Hyperreflexia | ||
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**Serum Osm >295 mOsm/L | **Serum Osm >295 mOsm/L | ||
*Record response to 5 units subcutaneous [[vasopressin]] | *Record response to 5 units subcutaneous [[vasopressin]] | ||
**Response to vasopressin is diagnostic of central DI (response is indicated by urine osm >800 mOsm/L) | **Response to [[vasopressin]] is diagnostic of central DI (response is indicated by urine osm >800 mOsm/L) | ||
**No response is diagnostic of nephrogenic DI | **No response is diagnostic of nephrogenic DI | ||
*In adults, onset of central DI usually abrupt whereas onset gradual in nephrogenic DI | |||
==Management== | ==Management== | ||
*Place foley for strict I/Os | |||
*Volume repletion with [[normal saline]] or lactated ringers solution | *Volume repletion with [[normal saline]] or lactated ringers solution | ||
*Patients will be water-deprived | *Patients will be water-deprived | ||
**Calculate water deficit: | **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 | *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 | **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 | ||
Revision as of 13:38, 26 January 2020
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
- 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