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:
*Causes hypernatremia.
**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===
*Central DI
**Cancer
**Pituitary surgery
**[[Head trauma]]
**Idiopathic
*Nephrogenic DI
**[[renal failure|Renal disease]]
**Drug Induced (e.g [[Lithium]])
**[[Hypokalemia]]
**[[Hypercalcemia]]
**[[Polycystic kidney disease]]
**[[Sjögren syndrome]]
**[[Amyloidosis]]


==Clinical Features==
==Clinical Features==
*Hypernatremia
*[[Hypernatremia]]
*Decreased urine osmolality
*Decreased urine osmolality
*Dehydration
*[[Dehydration]]
*Irritability
*Irritability
*Tremors
*[[Tremor]]s
*Ataxia
*[[Ataxia]]
*Hyperreflexia
*Hyperreflexia
*Spasms
*Spasms
*Seizures
*[[Seizures]]
*death
*Death


==Causes==
*Central DI
**cancer
**Pituitary surgery
**Idiopathic
*Nephrogenic DI
**Renal disease
**Drug Induced (e.g Lithium)
==Differential Diagnosis==
==Differential Diagnosis==
{{Hypernatremia causes}}


==Diagnosis==
==Evaluation==
*Measure serum and urine sodium while patient is water-deprived.  Lack of response to water deprivation is diagnostic.  Serum Osm >295 mOsm/L
*Urine specific gravity < 1.010
*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. 
*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==
==Management==
*Volume repletion with normal saline or lactated ringers solution
*Place foley for strict I/Os
*Patients will be water-deprived.
*Volume repletion with [[normal saline]] or lactated ringers solution
**Calculate water deficit: [Water deficit (in Liters) = ((Measured sodium/Normal sodium)-1)]
*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<ref>Bichet DG et al. Treatment of nephrogenic diabetes insipidus. UpToDate. Jan 7, 2016. http://www.uptodate.com/contents/treatment-of-nephrogenic-diabetes-insipidus#H10</ref>
**Low-salt, low-protein diet
**[[Hydrochlorothiazide]] 25mg BID
**[[Indomethacin]] has greater effect at reducing urine output than ibuprofen


*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. 
==Disposition==
==Disposition==
*Admission for further workup and/or volume replacement
*Nephrology follow up


==See Also==
==See Also==
*[[Hypernatremia]]


==External Links==
==External Links==
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==References==
==References==
<references/>
<references/>
Tintinalli, Judith.  Tintinalli's Emegency MEdicine 7th edition.  Pages 120-121
 
[[Category:Endocrinology]][[Category:FEN]]

Latest revision as of 00:17, 28 February 2022

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
  • Causes hypernatremia

Causes

Clinical Features

Differential Diagnosis

Hypernatremia

Water loss:

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

Disposition

  • Admission for further workup and/or volume replacement
  • Nephrology follow up

See Also

External Links

References

  1. ↑ Bichet DG et al. Treatment of nephrogenic diabetes insipidus. UpToDate. Jan 7, 2016. http://www.uptodate.com/contents/treatment-of-nephrogenic-diabetes-insipidus#H10
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