Cerebral Salt Wasting: Definition and Clinical Overview
Cerebral salt wasting (CSW) is a hypovolemic hyponatremia syndrome characterized by excessive renal sodium loss, extracellular volume depletion, and inappropriately high urinary sodium concentration (typically >20 mmol/L) occurring in the setting of central nervous system pathology. 1, 2
Pathophysiology
CSW results from excessive secretion of natriuretic peptides, which causes hyponatremia through inappropriate natriuresis and may provoke volume contraction 1. This mechanism fundamentally differs from SIADH, where water retention causes dilutional hyponatremia in a euvolemic state 2.
Clinical Presentation
The hallmark features of CSW include:
- Hyponatremia (serum sodium <135 mmol/L) 1, 2
- Evidence of extracellular volume depletion including hypotension, tachycardia, dry mucous membranes, and poor skin turgor 1, 2
- Inappropriately high urinary sodium concentration (typically >20 mmol/L) despite clinical hypovolemia 1, 2
- High urine osmolality relative to serum osmolality 1, 2
- Low serum uric acid concentration 3
Associated Conditions
CSW is more common in patients with:
- Poor clinical grade subarachnoid hemorrhage 1, 2
- Ruptured anterior communicating artery aneurysms 1, 2
- Hydrocephalus 1, 2
- Traumatic brain injury 4, 3
- Bacterial meningitis 5
- Post-neurosurgical states 5
- Cerebral tumors or lesions 6
Critical Distinction from SIADH
Distinguishing CSW from SIADH is absolutely essential because the treatments are diametrically opposed. 1, 2, 7
Key differentiating features:
- Volume status: CSW presents with hypovolemia (orthostatic hypotension, tachycardia, dry mucous membranes), while SIADH is euvolemic (no edema, normal blood pressure, moist mucous membranes) 1, 2
- Central venous pressure: CSW typically has CVP <6 cm H₂O versus SIADH with CVP 6-10 cm H₂O 2
- Clinical context: Both can occur with CNS pathology, but CSW more commonly follows acute brain injury 1, 2
Treatment Principles
CSW requires aggressive volume and sodium replacement—fluid restriction will worsen outcomes and potentially precipitate cerebral ischemia. 1, 2, 7
Primary treatment approach:
- Isotonic saline (0.9% NaCl) for initial volume resuscitation 7
- 3% hypertonic saline for severe symptomatic hyponatremia (sodium <120 mmol/L), with goal to correct 6 mmol/L over 6 hours 1, 7
- Maximum correction rate: Never exceed 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 1, 2, 7
Adjunctive pharmacotherapy:
- Fludrocortisone (mineralocorticoid) has demonstrated substantial benefit in managing CSW and should be strongly considered, especially when sodium losses persist despite aggressive saline replacement 7, 4, 8
- Hydrocortisone may be used to prevent natriuresis in subarachnoid hemorrhage patients 1, 2, 7
Monitoring Requirements
- Serum sodium every 2 hours during active correction, then every 4 hours after symptom resolution 1, 7
- Daily weights and fluid balance to assess volume status 7
- Urine sodium concentration to gauge ongoing renal losses 7
- Watch for osmotic demyelination syndrome signs (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) typically occurring 2-7 days after rapid correction 1
Common Pitfalls
- Using fluid restriction in CSW worsens outcomes and can precipitate cerebral ischemia—this is the treatment for SIADH, not CSW 1, 2, 7
- Failing to distinguish CSW from SIADH leads to inappropriate treatment with potentially catastrophic consequences 1, 2, 7
- Correcting sodium too rapidly (>8 mmol/L in 24 hours) risks osmotic demyelination syndrome 1, 2, 7
- Inadequate monitoring during active correction 1, 7
Clinical Significance
CSW may be an independent risk factor for poor outcomes in patients with neurological disorders 1. In subarachnoid hemorrhage patients at risk for vasospasm, maintaining normovolemia or slight hypervolemia is critical, and fluid restriction is absolutely contraindicated 1, 2, 7.