How do you differentiate and manage SIADH (Syndrome of Inappropriate Antidiuretic Hormone) versus cerebral salt wasting?

Differentiating and Managing SIADH vs Cerebral Salt Wasting

Key Diagnostic Distinction: Volume Status Assessment

The critical difference between SIADH and cerebral salt wasting (CSW) is volume status: SIADH presents with euvolemia while CSW presents with hypovolemia, and this distinction is essential because their treatments are diametrically opposed—fluid restriction for SIADH versus aggressive volume and sodium replacement for CSW. 1, 2

Clinical Assessment of Volume Status

Physical examination findings to identify hypovolemia in CSW:

• Orthostatic hypotension and tachycardia 1, 3
• Dry mucous membranes and decreased skin turgor 1, 3
• Central venous pressure (CVP) <6 cm H₂O in CSW versus 6-10 cm H₂O in SIADH 3, 4
• Unquenchable thirst (suggests CSW or polydipsia, not SIADH) 3

Physical examination findings suggesting euvolemia in SIADH:

• No edema, no orthostatic hypotension 5
• Normal skin turgor and moist mucous membranes 5
• Absence of clinical signs of hypovolemia or hypervolemia 5

Laboratory Differentiation

Both conditions share similar laboratory features:

• Serum sodium <135 mEq/L with hypoosmolality 1, 5
• Urine sodium >20 mEq/L (often >40 mEq/L) 1, 5, 4
• Inappropriately high urine osmolality (>500 mosm/kg) relative to serum osmolality 1, 5, 3
• Serum uric acid <4 mg/dL (73-100% positive predictive value for SIADH, though may include CSW patients) 1, 5

Key distinguishing feature:

• Improvement of hypouricemia and increased fractional excretion of uric acid after correction of hyponatremia occurs in SIADH but not in CSW 4

Common Diagnostic Pitfall

The most critical error is misdiagnosing CSW as SIADH and treating with fluid restriction, which worsens outcomes by exacerbating volume depletion in an already hypovolemic patient. 1, 5, 2 This is particularly dangerous in neurosurgical patients with subarachnoid hemorrhage at risk for vasospasm, where fluid restriction can precipitate cerebral ischemia 1, 5, 6.

Management Algorithms

SIADH Management

For mild/asymptomatic SIADH (sodium 120-135 mEq/L):

• Fluid restriction to 1 L/day as cornerstone therapy 1, 5
• If no response, add oral sodium chloride 100 mEq three times daily 1
• Consider demeclocycline, lithium, or diuretics for resistant cases 1, 5

For severe symptomatic SIADH (sodium <120 mEq/L with seizures, confusion, coma):

• Transfer to ICU for close monitoring 5
• Administer 3% hypertonic saline with goal to correct 6 mmol/L over 6 hours or until symptoms resolve 1, 5
• Monitor serum sodium every 2 hours initially 5
• Never exceed total correction of 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 1, 5

Cerebral Salt Wasting Management

For mild to moderate CSW:

• Volume and sodium replacement with isotonic (0.9%) saline, NOT fluid restriction 1, 7, 2
• Aggressive volume resuscitation with crystalloid or colloid agents 8
• Oral sodium supplementation as tolerated 1

For severe symptomatic CSW:

• ICU admission with close monitoring 1
• 3% hypertonic saline administration (may require substantial volumes for prolonged periods) 1, 7
• Fludrocortisone 0.1-0.2 mg daily to reduce renal sodium losses 1, 7, 8
• Hydrocortisone may prevent natriuresis in subarachnoid hemorrhage patients 1, 8
• Monitor serum sodium every 2-4 hours during active correction 1
• Maintain correction rate ≤8 mmol/L in 24 hours 1, 7

Special Considerations for Neurosurgical Patients

In patients with subarachnoid hemorrhage or other CNS disease:

• CSW is more common than SIADH in this population 1, 6
• Avoid fluid restriction in patients at risk for vasospasm 1, 5
• Hypertonic saline increases regional cerebral blood flow and brain tissue oxygen 8
• Fludrocortisone may be considered to prevent vasospasm 1, 5

Pathophysiologic Mechanisms

SIADH pathophysiology:

• Inappropriate ADH secretion causes renal water retention 5, 4
• Results in volume-expanded euvolemic state 4, 2
• Physiologic natriuresis occurs to maintain fluid balance despite euvolemia 4

CSW pathophysiology:

• Excess secretion of natriuretic peptides or loss of sympathetic stimulation to kidney 8
• Tubular defect in sodium transport causes renal salt wasting 7, 8
• Results in contracted extracellular volume and negative sodium balance 4, 2
• Volume depletion is followed by secondary water loss 4

Monitoring During Treatment

For both conditions during active correction:

• Check serum sodium every 2 hours for severe symptoms, every 4 hours after symptom resolution 1
• Watch for signs of osmotic demyelination syndrome (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) typically occurring 2-7 days after rapid correction 1
• If overcorrection occurs (>8 mmol/L in 24 hours), immediately switch to D5W and consider desmopressin 1

Prevalence and Clinical Context

Recent evidence suggests RSW (renal salt wasting, the broader term for CSW) is much more common than previously recognized, occurring in 38% of hyponatremic patients in general hospital wards, with 87% having no evidence of cerebral disease 6. This challenges the traditional view that CSW only occurs in neurosurgical patients and emphasizes the importance of considering this diagnosis broadly 6, 8.