In patients with a subdural hematoma, how does serum sodium change (e.g., hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting) and what is the recommended management?

Sodium Disturbances in Subdural Hematoma

Subdural hematoma commonly causes hyponatremia through cerebral salt wasting (CSW) or syndrome of inappropriate antidiuretic hormone secretion (SIADH), with CSW being more prevalent in neurosurgical patients and requiring fundamentally opposite treatment from SIADH.

Pathophysiology and Mechanisms

Subdural hematomas affect sodium homeostasis through two primary mechanisms that produce hyponatremia:

• Cerebral salt wasting occurs more frequently than SIADH in neurosurgical patients with subdural hematomas, characterized by excessive natriuretic peptide secretion causing renal sodium loss and volume depletion 1, 2, 3
• SIADH can develop even with small chronic subdural hematomas that do not require surgical intervention, producing hyponatremia through inappropriate ADH secretion despite low plasma osmolality 4
• Both conditions can occur sequentially in the same patient, with CSW appearing initially followed by SIADH during recovery, requiring vigilant reassessment of volume status 5

The incidence varies by hematoma characteristics:

• Acute subdural hematomas are recognized risk factors for post-traumatic seizures and associated electrolyte disturbances 1
• Chronic subdural hematomas may present with hyponatremia as the primary clinical manifestation, even when the hematoma itself is small and asymptomatic 4

Critical Diagnostic Distinction: CSW versus SIADH

Volume status assessment is the decisive diagnostic factor that determines completely opposite treatment approaches 2, 3:

Cerebral Salt Wasting (Hypovolemic)

• Clinical hypovolemia with orthostatic hypotension, tachycardia, dry mucous membranes, decreased skin turgor, flat neck veins, and central venous pressure <6 cm H₂O 2, 3
• Urine sodium >20 mmol/L despite volume depletion (inappropriately elevated) 2, 3
• High urine osmolality relative to serum osmolality with evidence of ongoing natriuresis 2
• Elevated atrial natriuretic hormone (ANH) levels, potentially reaching 277 pg/ml (normal 25-77 pg/ml) 6
• Normal or low ADH levels in pure CSW 6

SIADH (Euvolemic)

• Euvolemic state with no edema, no orthostatic hypotension, normal skin turgor, and moist mucous membranes 2
• Urine sodium >20-40 mmol/L with urine osmolality >300 mOsm/kg 2
• Elevated or inappropriately normal ADH levels despite hypo-osmolality 4
• Normal renal, thyroid, and adrenal function 2

Physical examination alone has poor diagnostic accuracy (sensitivity 41.1%, specificity 80%), necessitating integration of laboratory data and central venous pressure measurements when available 2.

Management Based on Etiology

Treatment of Cerebral Salt Wasting

Aggressive volume and sodium replacement is the cornerstone of CSW management, with fluid restriction being absolutely contraindicated 2, 3:

Severe Symptomatic Hyponatremia (Sodium <120 mmol/L or Neurological Symptoms)

• Administer 3% hypertonic saline with initial goal to correct 6 mmol/L over 6 hours or until severe symptoms resolve, checking serum sodium every 2 hours during correction 2, 3
• Total correction must not exceed 8 mmol/L in any 24-hour period to prevent osmotic demyelination syndrome 2, 3
• ICU admission is required for close monitoring during active correction 2

Moderate CSW (Sodium 120-130 mmol/L)

• Isotonic saline (0.9% NaCl) at 50-100 mL/kg/day for volume resuscitation to restore intravascular volume 3
• Target central venous pressure of 8-12 cm H₂O to confirm adequate volume repletion 3

Adjunctive Pharmacologic Therapy

• Fludrocortisone 0.1-0.2 mg daily should be strongly considered to reduce ongoing renal sodium losses, particularly in severe or refractory cases 1, 2, 3
• Hydrocortisone may prevent natriuresis in patients with subdural hematoma, with studies showing 0% incidence of hyponatremia versus 43% in controls 1, 3

Treatment of SIADH

Fluid restriction is the primary treatment for SIADH, representing the opposite approach from CSW 2:

Mild to Moderate SIADH (Sodium 125-134 mmol/L)

• Fluid restriction to ≤1 L/day (or <800 mL/day for refractory cases) as first-line therapy 2
• Add oral sodium chloride 100 mEq three times daily if no response to fluid restriction alone 2

Severe Symptomatic SIADH

• 3% hypertonic saline targeting correction of 6 mmol/L over 6 hours, with maximum 8 mmol/L in 24 hours 2
• Pharmacologic options for resistant cases include urea, loop diuretics, demeclocycline, and lithium 2

Monitoring Requirements

Intensive sodium monitoring is essential during active treatment 2, 3:

• Check serum sodium every 2 hours during initial correction of severe symptoms, then every 4 hours after symptom resolution 2, 3
• Monitor daily weights, fluid balance, and urine output to assess volume status 3
• Track urine sodium concentration to gauge ongoing renal losses 3
• Watch for signs of osmotic demyelination syndrome (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) typically occurring 2-7 days after rapid correction 2

Special Considerations for Subdural Hematoma Patients

Surgical Timing and Electrolyte Management

• Large subdural hematomas requiring neurosurgical intervention are more commonly associated with SIADH in the literature, though CSW remains more prevalent overall 4
• Small chronic subdural hematomas not requiring surgery can still produce clinically significant SIADH requiring medical management 4
• Prophylactic use of normal saline rather than hypotonic solutions is recommended postoperatively to avoid sodium balance problems 6

Seizure Prophylaxis Considerations

• Chronic subdural hematoma is a recognized risk factor for post-traumatic seizures, and antiepileptic prophylaxis may be considered 1
• If antiepileptic drugs are used, levetiracetam should be preferred to phenytoin due to higher tolerance and fewer side effects 1
• Phenytoin has been associated with worse cognitive outcomes and should be avoided when possible 1

Critical Pitfalls to Avoid

Misdiagnosing CSW as SIADH and applying fluid restriction can precipitate cerebral ischemia and worsen outcomes, representing a potentially fatal error 2, 3:

• Using fluid restriction in CSW worsens hypovolemia and increases risk of cerebral ischemia 2, 3
• Failing to distinguish between CSW and SIADH leads to inappropriate treatment with potentially catastrophic consequences 2, 3
• Correcting sodium faster than 8 mmol/L in 24 hours risks osmotic demyelination syndrome regardless of etiology 2, 3
• Inadequate monitoring during active correction can result in overcorrection 2, 3
• Ignoring the possibility of sequential occurrence of both CSW and SIADH in the same patient 5

Prognosis and Outcomes

• Hyponatremia following subdural hematoma is associated with longer hospital stays (15.7 vs. 9.6 days in eunatremic patients, p<0.001) 7
• CSW and SIADH have similar mortality rates when appropriately managed 7
• Hypernatremia, if it develops, is an independent risk factor for increased mortality and poor outcomes 8
• Moderate fluid restriction appears effective for long-term management after stabilization of serum sodium in SIADH cases 4