Cerebral Salt Wasting Syndrome: Diagnosis and Treatment
Distinguishing CSW from SIADH: The Critical First Step
The single most important factor in diagnosing cerebral salt wasting (CSW) is determining extracellular fluid volume status—CSW presents with true hypovolemia while SIADH presents with euvolemia, and this distinction dictates opposite treatment strategies. 1, 2, 3
Clinical Assessment of Volume Status
Look for these specific hypovolemic signs in CSW:
- Orthostatic hypotension and tachycardia 1, 2
- Dry mucous membranes and decreased skin turgor 1, 2
- Flat neck veins 1
- Central venous pressure <6 cm H₂O (if available) 1, 2
In contrast, SIADH shows euvolemia:
- No orthostatic changes 4, 2
- Normal skin turgor and moist mucous membranes 4
- Central venous pressure 6-10 cm H₂O 4
Laboratory Findings (Identical in Both Conditions)
Both CSW and SIADH present with:
- Serum sodium <135 mmol/L (investigate when <131 mmol/L) 1, 2
- Inappropriately high urine sodium (typically >20 mmol/L despite volume depletion in CSW) 1, 5, 3, 6
- High urine osmolality relative to serum osmolality 1, 3
- Low serum uric acid (<4 mg/dL) 1, 6
The laboratory values cannot distinguish between CSW and SIADH—only volume status assessment can. 7, 3, 8
Treatment of Cerebral Salt Wasting
Severe Symptomatic Hyponatremia (Seizures, Altered Mental Status)
For severe symptoms, immediately administer 3% hypertonic saline with a target correction of 6 mmol/L over 6 hours or until symptoms resolve, with ICU admission and serum sodium monitoring every 2 hours. 1, 2, 5
Critical correction limits:
- Maximum 8 mmol/L correction in any 24-hour period 1, 2, 5
- High-risk patients (liver disease, alcoholism, malnutrition) require even slower correction at 4-6 mmol/L per day 1, 2
Non-Severe CSW: Volume and Sodium Replacement
The cornerstone of CSW treatment is aggressive volume and sodium replacement—fluid restriction must never be used as it worsens outcomes and can precipitate cerebral ischemia. 1, 2, 5, 3
Fluid replacement strategy:
- Isotonic saline (0.9% NaCl) at 50-100 mL/kg/day for volume repletion 1, 5, 3
- Hypertonic saline (3%) for severe cases or when large sodium deficits exist 5, 3, 6
- Target central venous pressure of 8-12 cm H₂O to confirm adequate volume repletion 1
Adjunctive Pharmacologic Therapy: Fludrocortisone
Fludrocortisone (0.1-0.2 mg daily) is recommended as adjunctive therapy in severe or refractory CSW to reduce renal sodium losses. 1, 2, 5, 6
Evidence for fludrocortisone:
- Reduces the volume of hypertonic saline required 5
- Helps maintain serum sodium levels once corrected 5
- Particularly beneficial in subarachnoid hemorrhage patients at risk for vasospasm 1, 2
Hydrocortisone may also prevent natriuresis in subarachnoid hemorrhage patients. 1, 2
Special Considerations in Subarachnoid Hemorrhage
In SAH patients at risk for vasospasm, hyponatremia should be managed with volume expansion, never fluid restriction, to prevent cerebral ischemia. 1, 2
CSW is more common than SIADH in neurosurgical patients, particularly those with:
Common Pitfalls and How to Avoid Them
Pitfall #1: Misdiagnosing CSW as SIADH
Physical examination alone has poor accuracy (sensitivity 41%, specificity 80%) for volume assessment—incorporate CVP measurements and overall clinical context. 1
If volume status is uncertain in a neurosurgical patient, err on the side of treating as CSW with volume expansion rather than fluid restriction, especially in SAH patients at risk for vasospasm. 2, 8
Pitfall #2: Using Fluid Restriction in CSW
Applying fluid restriction to CSW (the treatment for SIADH) markedly worsens hypovolemia, increases cerebral ischemia risk, and can be fatal. 1, 2, 7
Pitfall #3: Overcorrecting Sodium Too Rapidly
Never correct chronic hyponatremia faster than 8 mmol/L in 24 hours—this causes osmotic demyelination syndrome (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis appearing 2-7 days after correction). 1, 2
Pitfall #4: Delaying Treatment While Awaiting ADH Levels
Do not postpone treatment while awaiting ADH or natriuretic peptide levels—evidence does not support this delay, and clinical assessment of volume status is more useful. 1, 2
Monitoring Protocol
During active correction:
- Serum sodium every 2 hours for severe symptoms 1, 2
- Serum sodium every 4 hours after symptom resolution 1
- Serial orthostatic vital signs and volume status assessment 1
- Urine output and urinary sodium concentration to guide ongoing replacement 1
Watch for osmotic demyelination syndrome signs 2-7 days after correction. 1, 2
Pathophysiology: Why CSW Occurs
CSW is produced by excessive secretion of natriuretic peptides (BNP and ANP), causing hyponatremia through excessive natriuresis and subsequent volume contraction. 1, 8
CSW may be an independent risk factor for poor neurological outcomes in patients with CNS disorders. 1