History

• Hsitorical Recognition: first recognized in 1950

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Etiology

• Brain Tumor
• Head Trauma (see Head Trauma, [[Head Trauma]])
• Hemorrhagic Cerebrovascular Accident (CVA) (see Hemorrhagic Cerebrovascular Accident, [[Hemorrhagic Cerebrovascular Accident]])
• Subarachnoid Hemorrhage (SAH) (see Subarachnoid Hemorrhage, [[Subarachnoid Hemorrhage]])
• Other Neurologic Disorders

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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)

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Diagnosis

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

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Clinical Manifestations

Cardiovascular Adverse Effects

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

Renal Adverse Effects

• Hyponatremia (see Hyponatremia, [[Hyponatremia]])
• Polyuria (see Polyuria, [[Polyuria]])

Other Adverse Effects

• xxx

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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]