Management of Cerebral Salt Wasting Symptoms
Cerebral salt wasting (CSW) requires aggressive volume and sodium replacement with isotonic or hypertonic saline, and fludrocortisone should be strongly considered as adjunctive therapy—fluid restriction is contraindicated and will worsen outcomes. 1
Critical First Step: Distinguish CSW from SIADH
The treatment approaches are diametrically opposed, making accurate diagnosis essential before initiating therapy 1:
CSW characteristics:
- Hypovolemia with clinical signs: hypotension, tachycardia, dry mucous membranes, flat neck veins 2
- Central venous pressure <6 cm H₂O 2
- Inappropriately high urinary sodium (>20 mmol/L) despite volume depletion 1, 2
- High urine osmolality (>500 mOsm/kg) 2
SIADH characteristics:
- Euvolemia: no edema, normal skin turgor, moist mucous membranes 2
- Central venous pressure 6-10 cm H₂O 2
- Urine sodium >20-40 mmol/L 2
Treatment Algorithm Based on Symptom Severity
Severe Symptomatic CSW (seizures, altered mental status, coma)
Immediate actions:
- Transfer to ICU for close monitoring 2
- Administer 3% hypertonic saline with initial goal to correct 6 mmol/L over 6 hours or until severe symptoms resolve 1, 2
- Add fludrocortisone 0.1-0.4 mg daily to reduce ongoing renal sodium losses 2, 3, 4
- Monitor serum sodium every 2 hours during active correction 1
Mild to Moderate CSW
Initial management:
- Isotonic saline (0.9% NaCl) at 60-100 mL/h for volume repletion 2
- Alternatively, oral sodium chloride 100 mEq three times daily if patient can tolerate oral intake 2
- Consider fludrocortisone 0.1-0.2 mg daily, especially when sodium losses persist despite aggressive saline replacement 1, 5
Critical Correction Rate Limits
Total sodium correction must not exceed 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 1, 6. After correcting 6 mmol/L in the first 6 hours for severe symptoms, only 2 mmol/L additional correction is allowed in the next 18 hours 1.
Fludrocortisone as Adjunctive Therapy
Fludrocortisone has demonstrated substantial benefit in managing CSW and should be strongly considered 1, 3, 4:
- Dosing: 0.1-0.4 mg daily 2, 7
- Mechanism: Reduces renal sodium losses through mineralocorticoid activity 2, 5
- Benefits: Enables weaning of hypertonic fluids, stabilizes serum electrolytes, reduces volume of saline required 3, 4
- Monitoring for side effects: Hypokalemia (most common), hypertension requiring dose reduction 4
- Duration: May be required for 4-125 days depending on underlying pathology 4
Special Considerations for Subarachnoid Hemorrhage
- Never use fluid restriction in SAH patients at risk of vasospasm—this can precipitate cerebral ischemia and infarction 1, 2
- Maintenance of normovolemia or slight hypervolemia is required to prevent vasospasm-related cerebral ischemia 1
- Hypertonic saline increases regional cerebral blood flow, brain tissue oxygen, and pH in high-grade SAH 1
- Consider hydrocortisone to prevent natriuresis in SAH patients 1, 2
Monitoring Requirements
During active treatment:
- Serum sodium every 2 hours initially during severe symptoms 1, 2
- Every 4 hours after severe symptoms resolve 1
- Daily once stabilized 2
- Daily weights and strict intake/output monitoring 2
- Track urine sodium concentration to gauge ongoing renal losses 1
Watch for osmotic demyelination syndrome typically occurring 2-7 days after rapid correction: dysarthria, dysphagia, oculomotor dysfunction, quadriparesis 1
Calculating Sodium Requirements
Use the formula: Desired increase in Na (mEq/L) × (0.5 × ideal body weight in kg) 2
Common Pitfalls to Avoid
- Using fluid restriction in CSW worsens outcomes and can precipitate cerebral ischemia 1, 6, 2
- Failing to distinguish CSW from SIADH leads to inappropriate treatment with potentially catastrophic consequences 1, 6
- Inadequate monitoring during active correction can result in overcorrection and osmotic demyelination syndrome 1
- Correcting sodium too rapidly (>8 mmol/L in 24 hours) risks osmotic demyelination syndrome 1, 6