Differentiating Cerebral Salt Wasting from SIADH
The key distinction between cerebral salt wasting (CSW) and SIADH lies in volume status: CSW presents with hypovolemia requiring aggressive sodium and volume replacement, while SIADH presents with euvolemia requiring fluid restriction. 1
Critical Diagnostic Features
Volume Status Assessment (Most Important Differentiator)
CSW characteristics:
- Clinical hypovolemia with orthostatic hypotension, tachycardia, dry mucous membranes, and decreased skin turgor 1, 2
- Central venous pressure (CVP) <6 cm H₂O 2
- Evidence of extracellular fluid volume depletion 1
- Unquenchable thirst may be present 2
SIADH characteristics:
- Euvolemic state with no edema, no orthostatic hypotension, normal skin turgor, and moist mucous membranes 3
- CVP 6-10 cm H₂O 2
- Absence of clinical signs of hypovolemia or hypervolemia 3
Laboratory Differentiation
Both conditions share similar findings that make differentiation challenging:
- Serum sodium <135 mmol/L 1, 3
- Urine sodium >20 mmol/L (inappropriately high) 1, 3
- Urine osmolality >500 mosm/kg (inappropriately concentrated) 3, 2
- Serum uric acid <4 mg/dL (73-100% positive predictive value for SIADH, though may include CSW) 1
Key distinguishing feature - 24-hour urine collection:
- CSW: Urinary sodium excretion 394 ± 369 mmol/24 hours with urine volume 2,603 ± 996 mL/24 hours (markedly elevated) 4
- SIADH: Urinary sodium excretion only 51 ± 25 mmol/24 hours with urine volume 745 ± 298 mL/24 hours (significantly lower than CSW) 4
Fractional Excretion of Urate (FEurate)
FEurate can help differentiate these conditions, though specific cutoff values require clinical correlation with volume status 5, 6
Clinical Context
CSW is more common than traditionally recognized:
- More prevalent in neurosurgical patients, particularly those with subarachnoid hemorrhage, poor clinical grade, ruptured anterior communicating artery aneurysms, and hydrocephalus 1, 2
- Associated with higher rates of cerebral ischemia and worse outcomes at 3 months in subarachnoid hemorrhage patients 2
- Can occur in patients without cerebral disease, warranting consideration of "renal salt wasting" as a broader diagnostic category 5, 6
SIADH common causes:
- Malignancy (particularly small cell lung cancer affecting 1-5% of patients), CNS disorders, pulmonary disease 3, 2
- Medications including chemotherapeutic agents (cisplatin, vinca alkaloids), antidepressants, carbamazepine, NSAIDs, and opioids 3
Treatment Implications (Diametrically Opposed)
CSW management:
- Volume and sodium replacement with isotonic or hypertonic saline (NOT fluid restriction) 1, 3
- Severe symptoms require ICU admission with 3% hypertonic saline and fludrocortisone 1, 7
- Substantial volumes of hypertonic saline may be required for prolonged periods 7
- Fludrocortisone reduces hypertonic saline requirements and helps maintain sodium levels 1, 7
SIADH management:
- Fluid restriction to 1 L/day for mild/asymptomatic cases 1, 3
- 3% hypertonic saline with careful monitoring for severe symptomatic cases 1, 3
- Add oral sodium chloride 100 mEq three times daily if no response to fluid restriction 1
Critical Pitfall to Avoid
Using fluid restriction in CSW worsens outcomes and can be life-threatening. 1, 3 This is the most dangerous error in management, as CSW requires the opposite approach—aggressive volume and sodium replacement. In neurosurgical patients, particularly those with subarachnoid hemorrhage at risk for vasospasm, fluid restriction should never be used 1, 3
Correction Rate (Same for Both Conditions)
Maximum correction of 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome, with more cautious correction (4-6 mmol/L per day) in high-risk patients with advanced liver disease, alcoholism, or malnutrition 1, 3