Subdural Hematoma (SDH) 

Definition

Subdural hematoma (SDH) = collection of blood between dura mater and arachnoid mater, usually due to rupture of bridging veins.

 Pathophysiology

 Basic Mechanism

• Bridging veins connect cortex → dural sinuses
• Sudden acceleration–deceleration injury
  → Vein stretching → rupture → slow venous bleed

 Key Concepts

1. Low-pressure venous bleed

• Slower than epidural hematoma (arterial)
• Symptoms may be delayed

2. Spreading pattern

• Blood spreads widely over hemisphere
• Crosses suture lines (unlike epidural)
• Limited by falx cerebri → does NOT cross midline

3. ICP effects

• Gradual rise in ICP → cerebral edema + mass effect
• Can lead to herniation syndromes

 Types of SDH 

1. Acute SDH (<72 hours)

• Severe trauma
• Rapid neurological deterioration
• Often associated with:
• Cerebral contusion
• Diffuse axonal injury (DAI)

2. Subacute SDH (3–21 days)

• Blood becomes isodense
• Diagnosis becomes tricky on CT

3. Chronic SDH (>21 days)

• Seen in elderly/alcoholics
• Liquefied hematoma
• Minimal trauma may cause it

 Risk Factors

 Structural

• Brain atrophy (elderly)
• Previous neurosurgery

 Hematological

• Anticoagulants (warfarin, DOACs)
• Antiplatelets
• Coagulopathy (liver disease, uremia)

 Others

• Alcoholism
• Recurrent falls
• Seizure disorders

 Clinical Features

 Acute SDH

• ↓ GCS (rapid)
• Headache
• Vomiting
• Focal deficits (hemiparesis)
• Seizures
• Signs of raised ICP:
• Papilledema (late)
• Cushing triad

Chronic SDH 

• Insidious onset
• Elderly patient + trivial trauma history
• Symptoms:
• Cognitive decline (mimics dementia)
• Personality changes
• Gait disturbance
• Headache
• Mild hemiparesis

 Diagnosis

 CT Scan (Investigation of Choice)

Findings:

• Crescent-shaped hyperdensity (acute)
• Crosses sutures
• Mass effect:
• Midline shift
• Ventricular compression

 Density Evolution 

 MRI (Better for subacute/chronic)

• Detects isodense SDH
• Shows membranes

 Complications

• Raised ICP
• Brain herniation:
• Uncal herniation → CN III palsy
• Seizures
• Rebleeding
• Chronic SDH formation

 Herniation Syndromes 

• Uncal herniation:
• Ipsilateral dilated pupil
• Contralateral hemiplegia
• Central herniation
• Tonsillar herniation → death

 Management 

 1. Initial Stabilization (ATLS PROTOCOL)

• Airway protection (GCS ≤8 → intubation)
• Maintain:
• SpO₂ >94%
• SBP >100–110 mmHg
• Avoid:
• Hypoxia
• Hypotension (double insult)

 2. Medical Management (ICP CONTROL)

– Head elevation (30°)

– Sedation + analgesia

– Osmotherapy:

• Mannitol (0.25–1 g/kg)
• Hypertonic saline (3%)

– Ventilation

• Target PaCO₂: 35–40 mmHg
• Temporary hyperventilation if herniation

– Seizure prophylaxis

• Levetiracetam / phenytoin

 3. Reversal of Anticoagulation

• Warfarin → PCC + Vitamin K
• DOACs → specific antidotes (idarucizumab, andexanet)
• Platelets if antiplatelet + surgery planned

 4. Surgical Management 

 Indications 

Operate if:

• Thickness >10 mm
  OR
• Midline shift >5 mm
  OR
• GCS drop ≥2 points
  OR
• Pupillary asymmetry
  OR
• ICP >20 mmHg

 Surgical Options

1. Burr hole drainage

• Chronic SDH
• Most common procedure

2. Craniotomy

• Acute SDH
• Clotted blood removal

3. Decompressive craniectomy

• Severe cerebral edema

 Acute SDH Severity Predictors

• GCS at presentation (most important)
• Age
• Pupillary response
• Midline shift

 SDH vs Epidural Hematoma

 Special Scenarios

– Elderly with chronic SDH

• Often bilateral
• Minimal symptoms
• Treat with burr hole

– Anticoagulated patients

• High mortality
• Early reversal critical

– Pediatric SDH

• Consider non-accidental injury (abuse)

 Prognosis

• Acute SDH mortality: 40–60%
• Chronic SDH: good prognosis if treated early