What is Cerebral Salt Wasting?
Cerebral salt wasting (CSW) is a syndrome of hypovolemic hyponatremia caused by excessive renal sodium loss (natriuresis) and diuresis that occurs in patients with central nervous system pathology. 1
Pathophysiology
CSW results from inappropriate natriuresis leading to volume contraction in the presence of cerebral pathology. 2 The underlying mechanisms involve abnormal elevations in circulating natriuretic peptides, particularly atrial natriuretic factor and C-type natriuretic peptides, though the precise pathways have not been completely delineated. 1, 3
The excessive renal sodium loss leads to:
- Hypovolemia (volume depletion) 1
- Hyponatremia (low serum sodium) 2
- Inappropriately high urinary sodium concentration (typically >20 mmol/L) 4
- High urine osmolality relative to serum osmolality 4
Clinical Presentation
CSW typically occurs in patients with specific neurological conditions, including:
- Subarachnoid hemorrhage (particularly with ruptured anterior communicating artery aneurysms) 4, 5
- Head injury 3
- Bacterial meningitis 6
- Post-neurosurgical patients 6
- Various brain insults 3
Patients present with:
- Clinically significant hyponatremia 2
- Evidence of extracellular volume depletion (hypotension, tachycardia, dry mucous membranes) 4
- Hyponatremic seizures (in severe cases) 2
- Increased diuresis and natriuresis 3
CSW is more common in patients with poor clinical grade, ruptured anterior communicating artery aneurysms, and hydrocephalus. 4
Critical Diagnostic Distinction from SIADH
The most critical aspect of CSW diagnosis is distinguishing it from SIADH, as the treatments are diametrically opposed. 4, 1
Key Differentiating Features:
Volume Status (the crucial distinguishing factor):
- CSW: Hypovolemic with clinical signs of volume depletion; CVP typically <6 cm H₂O 4, 1
- SIADH: Euvolemic; CVP 6-10 cm H₂O 4
Shared Features (cannot distinguish between the two):
- Both have hyponatremia 1
- Both have inappropriately high urine sodium (>20 mmol/L) 4, 1
- Both have high urine osmolality relative to serum 4, 1
Treatment Principles
CSW requires volume and sodium replacement, NOT fluid restriction—this is the opposite of SIADH treatment. 4, 6, 1
Treatment Approach:
Volume and Sodium Replacement:
- Isotonic or hypertonic saline based on severity 4, 1
- Aggressive volume resuscitation with crystalloid or colloid agents to reduce cerebral ischemia risk 4
- For severe symptoms: 3% hypertonic saline with goal to correct 6 mmol/L over 6 hours 7
Adjunctive Mineralocorticoid Therapy:
- Fludrocortisone (0.1-0.2 mg daily) has demonstrated substantial benefit in managing CSW and should be strongly considered 7, 2, 5
- Hydrocortisone may be used to prevent natriuresis in subarachnoid hemorrhage patients 7, 4
Critical Safety Limits:
- Total sodium correction must not exceed 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 7, 4
- Monitor serum sodium every 2 hours initially during active correction 7
Common Pitfalls
- Using fluid restriction in CSW worsens outcomes and can precipitate cerebral ischemia 7, 4, 5
- Misdiagnosing CSW as SIADH leads to inappropriate fluid restriction with potentially catastrophic consequences 4, 5
- Correcting sodium too rapidly (>8 mmol/L in 24 hours) risks osmotic demyelination syndrome 7, 4
- Inadequate monitoring during active correction 7
Clinical Significance
CSW may be an independent risk factor for poor outcome in patients with neurological disorders. 4 In subarachnoid hemorrhage patients at risk of vasospasm, hyponatremia should NOT be treated with fluid restriction, as maintenance of normovolemia or slight hypervolemia is required to prevent vasospasm-related cerebral ischemia. 7