Cerebral Salt Wasting

History

  • Hsitorical Recognition: first recognized in 1950

Etiology


Physiology

  • Likely Mediated by Brain Natriuretic Peptide (BNP) and Ouabain-Like Peptide
    • Results in increased urine sodium (>25 nmol/L), high urine osmolarity, polyuria, and clinical hypovolemia (the aspect of clinical hypovolemia distinguishes it from SIADH)

Diagnosis

  • Urine Sodium: increased (usually >25 nmol/L)
  • Urine Osmolarity: high

Clinical Manifestations

Cardiovascular Adverse Effects

  • Hypovolemia (see Hypovolemic Shock, [[Hypovolemic Shock]]): presence of hypovolemia distinguishes cerebral salt wasting from SIADH

Renal Adverse Effects

Other Adverse Effects

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References

  • A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians. 1950;63:57-64 [MEDLINE]
  • Cerebral salt wasting syndrome: a review. Neurosurgery. 1996 Jan;38(1):152-60 [MEDLINE]
  • Hyponatremia in acute brain disease: the cerebral salt wasting syndrome. Eur J Intern Med. 2002 Feb;13(1):9-14 [MEDLINE]
  • Cerebral salt wasting: pathophysiology, diagnosis, and treatment. Neurosurg Clin N Am. 2010 Apr;21(2):339-52. doi: 10.1016/j.nec.2009.10.011 [MEDLINE]