Diabetes insipidus

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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
  • 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) = ((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