What is cerebral salt wasting (CSW)?

Cerebral Salt Wasting (CSW)

Cerebral salt wasting is a syndrome of hyponatremia and extracellular volume depletion caused by excessive renal sodium losses in patients with central nervous system disease or injury. 1, 2

Pathophysiology

CSW results from excessive secretion of natriuretic peptides, particularly atrial natriuretic hormone (ANH), which causes inappropriate renal sodium wasting despite hypovolemia. 1, 3 This leads to:

• Excessive natriuresis (urinary sodium typically >20 mmol/L) 2, 4
• Volume contraction with true extracellular fluid depletion 1, 4
• Hyponatremia as a consequence of both sodium loss and secondary water retention 1, 2

The elevated ANH levels can reach as high as 277 pg/ml (normal 25-77 pg/ml), driving the pathologic sodium wasting. 3

Clinical Context

CSW typically occurs in patients with:

• Traumatic brain injury 5, 6, 7
• Subarachnoid hemorrhage 1, 4
• Neurosurgical procedures (including cranial vault remodeling) 3
• Brain tumors 2
• Other intracranial pathology 2, 6

CSW is more common than SIADH in neurosurgical patients, making it a critical diagnosis to consider in this population. 1, 2

Key Diagnostic Features

The hallmark laboratory findings include:

• Hyponatremia (serum sodium <135 mmol/L) 1, 2
• Markedly elevated urine sodium (>20 mmol/L, often much higher) 2, 4
• Inappropriately concentrated urine relative to serum osmolality 2
• Elevated fractional excretion of sodium (can be >6%) 2
• Low serum uric acid 6
• Increased urine output (>1 cc/kg/h) 3

Critical Distinction from SIADH

The fundamental difference between CSW and SIADH is volume status—CSW presents with hypovolemia while SIADH presents with euvolemia. 2, 4 This distinction is absolutely critical because the treatments are opposite. 1, 4

CSW characteristics:

• Hypovolemia with clinical signs: hypotension, tachycardia, dry mucous membranes, decreased skin turgor 4, 6
• Central venous pressure <6 cm H₂O 2, 4
• Requires volume and sodium replacement 1, 4

SIADH characteristics:

• Euvolemia: no edema, normal skin turgor, moist mucous membranes 4
• Central venous pressure 6-10 cm H₂O 4
• Requires fluid restriction 1, 4

Physical examination alone has poor accuracy (sensitivity 41.1%, specificity 80%) for determining volume status, so invasive CVP monitoring may be needed in unclear cases. 2

Treatment Approach

Fluid restriction in CSW worsens outcomes and increases the risk of cerebral ischemia—this is the opposite of SIADH management. 1, 4

For Severe Symptomatic CSW:

• Transfer to ICU for close monitoring 4
• 3% hypertonic saline to correct 6 mmol/L over 6 hours or until severe symptoms resolve 1, 4
• Fludrocortisone 0.1-0.4 mg daily to reduce renal sodium losses 4, 5, 7
• Maximum correction: 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 1, 4

For Mild to Moderate CSW:

• Isotonic saline (0.9% NaCl) at 60-100 mL/h for volume repletion 4
• Oral sodium chloride 100 mEq three times daily if patient can tolerate oral intake 4
• Substantial volumes of hypertonic saline may be required for prolonged periods 5

Special Considerations for Subarachnoid Hemorrhage:

Never use fluid restriction in SAH patients at risk for vasospasm, as this can result in cerebral infarction. 1, 4 Consider hydrocortisone to prevent natriuresis in these patients. 1, 4

Monitoring Requirements

• Serum sodium every 2 hours for severe symptoms 4
• Serum sodium every 4 hours after symptom resolution 4
• Daily weights and strict intake/output monitoring 4
• Watch for osmotic demyelination syndrome 2-7 days after rapid correction 4

Common Pitfalls

• Misdiagnosing CSW as SIADH and treating with fluid restriction, which worsens outcomes 1, 4
• Failing to recognize the high index of suspicion required for CSW diagnosis 5
• Underestimating sodium replacement needs—substantial volumes may be required 5
• Not considering fludrocortisone early enough in refractory cases 5, 7