Diabetes insipidus: Difference between revisions
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==Background== | ==Background== | ||
*Characterized as either central Diabetes Insipidus (DI) or nephrogenic DI [Decreased production of anti-diuretic hormone (ADH) or decreased renal sensitivity to ADH] | *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 | *Causes hypernatremia | ||
===Causes=== | ===Causes=== | ||
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**Cancer | **Cancer | ||
**Pituitary surgery | **Pituitary surgery | ||
**Head trauma | **[[Head trauma]] | ||
**Idiopathic | **Idiopathic | ||
*Nephrogenic DI | *Nephrogenic DI | ||
**Renal disease | **Renal disease | ||
**Drug Induced (e.g Lithium) | **Drug Induced (e.g [[Lithium]]) | ||
**Hypokalemia | **Hypokalemia | ||
**Hypercalcemia | **[[Hypercalcemia]] | ||
**[[Polycystic kidney disease]] | **[[Polycystic kidney disease]] | ||
**[[Sjogren's]] | **[[Sjogren's]] | ||
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*Spasms | *Spasms | ||
*[[Seizures]] | *[[Seizures]] | ||
* | *Death | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
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==Diagnosis== | ==Diagnosis== | ||
*Measure serum and urine sodium while patient is water-deprived | *Measure serum and urine sodium while patient is water-deprived | ||
**Lack of response to water deprivation is diagnostic | **Lack of response to water deprivation is diagnostic | ||
**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 | ||
==Management== | ==Management== | ||
*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: [Water deficit (in Liters) = ((Measured sodium/Normal sodium)-1)] | **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 | *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 | ||
**If pt acutely hypernatremic, idiogenic osmoles have not had time to build up in brain tissue and rapid correction of hypernatremia would not develop cerebral edema | **If pt acutely hypernatremic, idiogenic osmoles have not had time to build up in brain tissue and rapid correction of hypernatremia would not develop cerebral edema | ||
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==References== | ==References== | ||
<references/> | <references/> | ||
[[Category:Endo]] | [[Category:Endo]] | ||
Revision as of 18:27, 19 February 2016
Background
- 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
Causes
- Central DI
- Cancer
- Pituitary surgery
- Head trauma
- Idiopathic
- Nephrogenic DI
- Renal disease
- Drug Induced (e.g Lithium)
- Hypokalemia
- Hypercalcemia
- Polycystic kidney disease
- Sjogren's
- 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)
Diagnosis
- 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
Management
- 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 pt 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 f/u
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