Treatment of Cerebral Salt Wasting
Cerebral salt wasting (CSW) requires aggressive volume and sodium replacement with isotonic or hypertonic saline, NOT fluid restriction, which can worsen outcomes and increase the risk of cerebral ischemia. 1, 2
Distinguishing CSW from SIADH
The critical first step is determining extracellular fluid volume status, as CSW and SIADH require fundamentally opposite treatments 3:
- CSW: Hypovolemia with clinical signs of volume depletion (hypotension, tachycardia, dry mucous membranes, CVP <6 cm H₂O) 1, 3
- SIADH: Euvolemia with no edema, normal skin turgor, moist mucous membranes, CVP 6-10 cm H₂O 3
- Both conditions show inappropriately high urinary sodium (>20 mmol/L) and high urine osmolality (>500 mOsm/kg) 3, 4
Common pitfall: Using fluid restriction in CSW instead of SIADH worsens outcomes and can precipitate cerebral ischemia, particularly in subarachnoid hemorrhage patients 1, 2, 3
Treatment Algorithm Based on Symptom Severity
Severe Symptomatic CSW (seizures, altered mental status, Na <120 mmol/L)
- Transfer to ICU for close monitoring 1, 2
- Administer 3% hypertonic saline with goal to correct 6 mmol/L over 6 hours or until severe symptoms resolve 1, 2, 3
- Add fludrocortisone 0.1-0.4 mg daily to reduce renal sodium losses 1, 5, 6
- Monitor serum sodium every 2 hours initially 1, 2
- Maximum correction: 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 1, 2, 3
Mild to Moderate CSW (Na 120-131 mmol/L, minimal symptoms)
- Isotonic saline (0.9% NaCl) at 60-100 mL/h for volume repletion 1, 2
- Oral sodium chloride 100 mEq three times daily if patient can tolerate oral intake 1
- Consider fludrocortisone 0.1-0.2 mg daily for persistent sodium wasting 5, 6, 4
- Monitor serum sodium every 4 hours initially, then daily 1
Fludrocortisone Use in CSW
Fludrocortisone is particularly valuable in CSW as it reduces renal sodium losses and decreases the volume of hypertonic saline required 5, 6:
- Starting dose: 0.1-0.2 mg daily 6, 4
- Duration: Typically 4-125 days depending on resolution of underlying neurological condition 6
- Monitor for complications: Hypokalemia (most common), hypertension requiring dose reduction 6
- Fludrocortisone enables weaning of hypertonic fluids and stabilization of serum electrolytes 5, 6
Special Considerations for Neurosurgical Patients
Subarachnoid Hemorrhage (SAH)
- Never use fluid restriction in SAH patients at risk for vasospasm 1, 3
- CSW is more common in patients with poor clinical grade, ruptured anterior communicating artery aneurysms, and hydrocephalus 4
- Fluid restriction in SAH patients with hyponatremia resulted in cerebral infarction in 21 of 26 patients (81%) in one retrospective analysis 1
- Consider hydrocortisone to prevent natriuresis in SAH patients 1, 3
Post-Neurosurgery and Traumatic Brain Injury
- CSW can occur after any neurosurgical procedure or traumatic brain injury 5, 7
- Substantial volumes of hypertonic saline may be required for prolonged periods 5
- High index of suspicion required as diagnosis can be challenging 5, 7
Monitoring Requirements
- Daily weights and strict intake/output monitoring 1
- Serum sodium: Every 2 hours for severe symptoms, every 4 hours after symptom resolution, then daily 1, 2
- Urine sodium and osmolality to confirm ongoing renal losses 4
- Watch for osmotic demyelination syndrome (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) typically 2-7 days after rapid correction 2, 3
Calculating Sodium Deficit
Use the formula: Desired increase in Na (mEq/L) × (0.5 × ideal body weight in kg) 1
This conservative calculation helps determine the appropriate amount of sodium supplementation needed while avoiding overcorrection 1
Key Pathophysiological Distinction
CSW is produced by excessive secretion of natriuretic peptides causing hyponatremia through excessive natriuresis and volume contraction 4. This is fundamentally different from SIADH, where the problem is water retention with euvolemia 3. The hallmarks of substantial CSW are hyponatremia, reduced volume status, and inappropriately high renal sodium loss 5, 4.