Cerebral Salt Wasting
Both SIADH and CSW present with hyponatraemia and high urine sodium.
🔑 Key difference = Volume status:
- CSW → Hypovolaemic 💧
- SIADH → Euvolaemic/Hypervolaemic ⚖️
🧠 About
- Cerebral Salt Wasting (CSW) is a condition in which cerebral injury leads to inappropriate renal sodium loss.
- This sodium loss causes water loss → hypovolaemia + hyponatraemia.
- SIADH differs because the patient is euvolaemic or hypervolaemic → here, management is fluid restriction, not replacement.
- Clinical importance: misdiagnosis can worsen hyponatraemia — e.g. fluid restriction in CSW can be dangerous ❌.
⚠️ Aetiology
- Increased release of cerebral natriuretic peptides after CNS injury.
- Sympathetic dysfunction affecting renal sodium handling.
- Common triggers: Subarachnoid haemorrhage (SAH), traumatic brain injury, intracranial surgery, meningitis, encephalitis.
👩⚕️ Clinical Features
- Often occurs in patients with head injury or SAH.
- Polyuria (>2.5 L/day).
- Features of volume depletion:
- Hypotension
- Tachycardia
- Dehydrated mucous membranes
- Contrast: SIADH patients look euvolaemic.
🧪 Investigations
- Serum sodium: Low (<134 mmol/L).
- Serum osmolality: Low.
- Urine osmolality: Raised (inappropriately concentrated).
- Urine sodium: >20 mmol/L (usually higher than SIADH).
- Urine output: Often >2500 mL/day.
📊 CSW vs SIADH (Key Differences)
| Feature |
CSW |
SIADH |
| Volume Status |
Hypovolaemic 💧 (dehydrated) |
Euvolaemic / Hypervolaemic ⚖️ |
| Urine Sodium |
High (>40 mmol/L, often very high) |
High (>20 mmol/L but not extreme) |
| Urine Output |
Polyuria (often >2.5 L/day) |
Normal or low |
| Main Mechanism |
Renal salt wasting due to CNS natriuretic peptides |
Excess ADH secretion → water retention |
| Management |
Replace fluids + sodium (0.9% saline or hypertonic 3% NaCl) + fludrocortisone if refractory |
Fluid restriction ± demeclocycline / vasopressin antagonists |
💊 Management
- CSW: Treat with fluid + sodium replacement (opposite of SIADH!).
- Options:
- IV 0.9% saline or 3% hypertonic saline for severe cases.
- Fludrocortisone may be used to reduce natriuresis.
- SIADH: Managed by fluid restriction — highlighting the danger of misdiagnosis.
📚 References
Cases — Cerebral Salt Wasting (CSW)
- Case 1 — Post-Subarachnoid Haemorrhage 🧠:
A 54-year-old woman admitted with aneurysmal subarachnoid haemorrhage develops hyponatraemia (Na⁺ 122 mmol/L) on day 5. She is confused, tachycardic, hypotensive (BP 90/60), with high urine sodium and high urine output.
Diagnosis: Cerebral salt wasting secondary to SAH.
Management: IV normal saline (or hypertonic if severe), fludrocortisone; avoid fluid restriction (would worsen hypovolaemia).
- Case 2 — Traumatic Brain Injury 🚑:
A 38-year-old man with severe head injury develops progressive hyponatraemia (Na⁺ 118 mmol/L). He has polyuria, postural hypotension, and tachycardia. Urine sodium high (>40 mmol/L), serum uric acid low.
Diagnosis: Cerebral salt wasting following TBI.
Management: Volume and sodium replacement (saline, hypertonic if needed), mineralocorticoids; monitor fluid balance and electrolytes closely.
Teaching Commentary 🧠
Cerebral salt wasting is characterised by renal loss of sodium + water → hypovolaemic hyponatraemia.
- Occurs after CNS insults (SAH, TBI, neurosurgery, infections).
- Key distinction from SIADH: both cause hyponatraemia with high urine sodium, but
- CSW = hypovolaemia (low BP, tachycardia, dehydration).
- SIADH = euvolaemia/hypervolaemia.
- Management: Sodium + volume replacement, fludrocortisone in resistant cases. Fluid restriction is contraindicated (unlike SIADH).
