Subdural Haemorrhage (SDH)

1. Clinical Overview

Definition and Importance

Subdural haemorrhage (SDH) is a collection of blood in the subdural space - the potential space between the dura mater and the arachnoid mater. This pathology represents one of the most important neurosurgical emergencies and has distinct presentations depending on the time course of development. [1,2]

SDH is predominantly a venous bleed caused by rupture of bridging veins that traverse the subdural space, connecting the cerebral cortex to the dural venous sinuses. On neuroimaging, it characteristically appears as a crescentic (crescent moon or banana-shaped) collection that conforms to the contour of the brain surface. [3]

The clinical significance of SDH cannot be overstated:

• Acute SDH carries mortality rates of 50-90%, making it one of the deadliest consequences of traumatic brain injury. [4]
• Chronic SDH is increasingly common in aging populations (incidence ~20 per 100,000 in those > 70 years), and represents a treatable cause of neurological decline in elderly patients. [5,6]
• Misdiagnosis is common, particularly in chronic presentations where symptoms mimic dementia, stroke, or psychiatric conditions.

Key Classification

SDH is classified by time from injury to symptom onset:

The Clinical Challenge

The "Great Imitator" - Chronic SDH presents insidiously in elderly patients with vague confusion, gait disturbance, or personality change, often weeks after a forgotten "minor bump." These patients are frequently misdiagnosed with dementia, depression, or stroke. The key principle: always image a confused elderly patient with any history of head trauma, no matter how trivial. [7]

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2. Epidemiology

Incidence and Prevalence

Acute Subdural Haemorrhage:

• Occurs in 10-20% of all traumatic brain injuries (TBI). [8]
• Annual incidence: approximately 5-29 per 100,000 population. [9]
• Peak incidence in young adults (road traffic accidents, assaults) and elderly (falls).
• Male:female ratio approximately 2-3:1. [10]

Chronic Subdural Haematoma:

• Incidence increases markedly with age:
  • less than 60 years: 1-2 per 100,000
  • 60-70 years: 8 per 100,000

  • 70 years: 20-58 per 100,000. [5,6]

• Projected to become the most common neurosurgical condition requiring surgery in elderly by 2030 due to aging populations. [11]

Risk Factors

Key Insight: The combination of brain atrophy (increases distance bridging veins must span) + anticoagulation (promotes bleeding) + frequent falls explains why chronic alcoholics and elderly patients are at dramatically elevated risk. [12]

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3. Anatomical Basis and Pathophysiology

Meningeal Anatomy

Understanding the meningeal layers is fundamental to differentiating intracranial haemorrhages:

From outer to inner:

1. Skull bone
2. Dura mater (tough outer layer, periosteal + meningeal layers)
3. Subdural space (potential space) ← SDH occurs here
4. Arachnoid mater
5. Subarachnoid space (contains CSF and vessels)
6. Pia mater (adherent to brain surface)
7. Cerebral cortex

The Bridging Vein Mechanism

Bridging veins are delicate vessels that drain blood from the superficial cerebral cortex across the subdural space into the superior sagittal sinus and other dural venous sinuses.

Pathophysiology of rupture:

1. Trauma causes differential movement between brain and skull
2. Acceleration-deceleration forces create shear stress on bridging veins
3. Brain's inertia causes it to lag behind the skull movement
4. Veins tear at the point of maximum stress (usually cortical surface or sinus entry point)
5. Venous blood (low pressure) leaks slowly into subdural space

Why elderly are vulnerable:

• Brain atrophy (↓ brain volume) means bridging veins are already stretched taut
• Less brain bulk means more space for blood to accumulate before causing symptoms
• Minor trauma (e.g., bump on door frame) sufficient to tear already-tensioned veins. [13]

Evolution of the Haematoma

Acute Phase (less than 3 days)

• Fresh blood with intact red blood cells
• Hyperdense (bright/white) on CT (protein content)
• Often associated with underlying brain injury (contusions, diffuse axonal injury)
• Mass effect causes immediate raised ICP

Subacute Phase (3 days - 3 weeks)

• Red blood cell lysis releases haemoglobin
• Clot liquefaction begins
• Isodense (same density as brain) on CT - diagnostic pitfall!
• Must look for secondary signs: sulcal effacement, midline shift, ventricular compression

Chronic Phase (> 3 weeks)

• Blood fully liquefied ("motor oil" appearance at surgery)
• Hypodense (dark/black) on CT (similar to CSF)
• Haematoma membrane forms:
  • Outer membrane (from dura)
  • Inner membrane (from arachnoid)
  • Contains fragile neovascularization. [14]

Expansion mechanism (chronic SDH): Traditional "osmotic gradient" theory has been largely replaced by understanding that:

• Repeated micro-bleeds from fragile membrane vessels cause gradual expansion
• Inflammatory mediators and fibrinolysis prevent clot organization
• Collection acts as space-occupying lesion, creating mass effect. [15]

Associated Brain Injury

Acute SDH vs Chronic SDH - Critical Difference:

Acute SDH:

• Usually accompanies severe primary brain injury (contusions, lacerations, diffuse axonal injury)
• High-velocity trauma (RTA, fall from height)
• Poor prognosis due to underlying brain damage, not just the blood collection
• Mortality 50-90% even with surgery. [4]

Chronic SDH:

• Often NO significant primary brain injury
• Low-velocity trauma (minor bump, fall from standing)
• Good prognosis because brain parenchyma intact
• Mortality less than 10% with treatment. [16]

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4. Clinical Presentation

Acute Subdural Haemorrhage

Typical Scenario: Young male involved in high-speed RTA, found with GCS 6 at scene.

History:

• Major trauma mechanism (RTA, fall from height, assault)
• May have brief lucid interval (20% of cases) but much less common than in extradural haemorrhage
• Rapid neurological deterioration

Symptoms:

• Severe headache
• Vomiting
• Rapid loss of consciousness
• Seizures (10% at presentation)

Signs:

• Decreased GCS (typically ≤8)
• Anisocoria - unilateral pupil dilatation indicates uncal herniation (ipsilateral to haematoma)
• Hemiparesis - contralateral to haematoma (or ipsilateral if Kernohan's notch phenomenon)
• Cushing's triad (late sign of raised ICP):
  • Hypertension
  • Bradycardia
  • Irregular respirations
• Decerebrate/decorticate posturing

Chronic Subdural Haematoma

Typical Scenario: 78-year-old man on warfarin for AF, presents with 3-week history of confusion and unsteadiness. Daughter recalls he "bumped his head on a cupboard" 6 weeks ago but seemed fine at the time.

History:

• Trivial trauma 4-12 weeks ago (patient or family may not recall)
• Insidious onset of symptoms
• Fluctuating course - good days and bad days
• Risk factors: elderly, anticoagulation, alcohol, prior head injury

Symptoms - The "Triad" (only 25-50% have all three):

1. Headache - gradual onset, worse in mornings, not severe
2. Confusion/cognitive decline - "not quite right," memory problems
3. Gait disturbance - unsteadiness, falls

Additional symptoms:

• Personality change, apathy
• Urinary incontinence (mimics normal pressure hydrocephalus)
• Speech disturbance
• Visual changes
• Seizures (5-15%)

Signs:

• Fluctuating GCS or cognitive impairment
• Mild hemiparesis (often subtle)
• Primitive reflexes - grasp, pout
• Papilloedema (if chronically raised ICP)
• Skull examination - may reveal evidence of trauma

Subacute Presentation

Intermediate features between acute and chronic, often presenting with:

• Persistent headache after trauma
• Progressive drowsiness
• Focal neurological deficits developing days after injury

Special Presentations

Infants (Non-Accidental Injury):

• Irritability, poor feeding, vomiting
• Bulging fontanelle
• Increased head circumference
• Retinal haemorrhages (suggest shaking injury)
• Requires urgent safeguarding assessment. [17]

Posterior Fossa SDH:

• Rare but important
• Presents with cerebellar signs, cranial nerve palsies
• High risk of rapid deterioration due to small posterior fossa volume

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5. Differential Diagnosis

Key Differentials to Consider

Clinical Differentiation: Acute vs Chronic SDH

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6. Investigations

CT Head (Non-Contrast) - GOLD STANDARD

When to scan - indications for urgent CT:

• Any GCS less than 15 at 2 hours post-injury
• Suspected skull fracture
• Post-traumatic seizure
• Focal neurological deficit

• 1 episode of vomiting

• Loss of consciousness or amnesia + risk factors (age > 65, anticoagulation, dangerous mechanism)

Acute SDH appearance:

• Shape: Crescentic/concave inner margin (conforms to brain surface)
• Density: Hyperdense (bright/white) - denser than brain parenchyma
• Distribution: Crosses suture lines (unlike extradural)
• Does NOT cross: Midline (limited by falx cerebri) or tentorium
• Common locations: Cerebral convexities, along falx, over tentorium

Chronic SDH appearance:

• Hypodense (dark/black) - similar density to CSF
• Often bilateral (30-40% of cases)
• May have acute-on-chronic appearance: mixed density with fresh hyperdense blood within hypodense collection

Subacute SDH (The Pitfall):

• Isodense - same density as brain tissue
• Collection may be invisible
• Look for secondary signs:
  • Sulcal effacement (smooth cortical surface)
  • Midline shift
  • Ventricular compression
  • Loss of grey-white differentiation
• Consider MRI if high clinical suspicion but CT negative

Key measurements to document:

• Thickness of haematoma (measure at maximal point)
• Midline shift (distance from septum pellucidum to midline)
• Presence/absence of mass effect
• Associated injuries: Skull fracture, brain contusions, subarachnoid blood

MRI Brain

Indications:

• Subacute phase when CT equivocal (isodense SDH)
• Better detection of small subdurals
• Assessment of underlying brain injury
• Dating of haematoma (different signal characteristics at different ages)
• Posterior fossa subdural (better visualization)

Typical findings:

• Acute: Isointense on T1, hypointense on T2
• Subacute: Hyperintense on T1 and T2
• Chronic: Hypointense on T1, hyperintense on T2
• Membrane enhancement with gadolinium in chronic SDH

Coagulation Studies - ESSENTIAL

Must check before any intervention:

• INR - target less than 1.4 for surgery
• APTT - assesses intrinsic pathway and heparin effect
• Platelet count - target > 75-100 × 10⁹/L
• DOAC levels if applicable (dabigatran, rivaroxaban, apixaban, edoxaban)
• Liver function - coagulopathy risk
• Thromboelastography (TEG/ROTEM) - some centres use for rapid assessment

Additional Investigations

Routine bloodwork:

• FBC (anaemia from blood loss, thrombocytopenia)
• U&E (renal function for contrast studies)
• Glucose (hypoglycaemia can mimic neurological emergency)
• Group and Save/Crossmatch (may need transfusion)

In specific contexts:

• Toxicology screen - if altered consciousness without clear cause
• Skeletal survey (infants) - if non-accidental injury suspected
• Retinal examination (ophthalmology) - shaken baby syndrome
• CT angiography - if concern about vascular injury
• Chest/pelvis X-ray - polytrauma assessment

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7. Classification and Risk Stratification

Acute Subdural Haemorrhage - Surgical Criteria

Brain Trauma Foundation Guidelines: [18]

Indications for SURGERY:

1. Thickness > 10mm on CT, OR
2. Midline shift > 5mm, OR
3. GCS drop ≥2 points from time of injury to admission, OR
4. Pupillary abnormalities (asymmetry, fixed/dilated), OR
5. ICP > 20 mmHg (if monitor in situ)

Conservative management possible if:

• Thickness less than 10mm AND
• Midline shift less than 5mm AND
• GCS stable AND
• No signs of raised ICP AND
• Reliable for neurological monitoring

Chronic Subdural Haematoma - Treatment Criteria

Indications for SURGERY:

1. Symptomatic (headache, confusion, weakness), OR
2. Midline shift > 10mm, OR
3. Neurological deterioration, OR
4. Thickness > 10mm even if asymptomatic (some neurosurgeons)

Conservative management if:

• Asymptomatic AND
• Small collection (less than 10mm) AND
• Minimal mass effect AND
• Patient can be monitored reliably

Conservative management with serial imaging may fail in 30-50% - watch for deterioration. [19]

Prognostic Scoring Systems

Acute SDH - Corticosteroid Randomisation After Significant Head Injury (CRASH) Score:

• Age
• GCS
• Pupil reactivity
• Major extracranial injury
• CT findings (subarachnoid blood, petechial haemorrhages, midline shift)
• Predicts mortality and unfavourable outcome

Chronic SDH - Nakaguchi Classification (Imaging):

• Homogeneous: Uniform hypodensity - low recurrence risk
• Laminar: Layering of different densities - intermediate risk
• Separated: Membranes visible - intermediate risk
• Trabecular: Multiple septations - high recurrence risk

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8. Management

Acute Subdural Haemorrhage

Initial Resuscitation (Pre-Hospital and Emergency Department)

ABCDE Approach with Neuroprotection:

A - Airway:

• GCS ≤8: Intubate (protects airway, controls ventilation, prevents aspiration)
• Rapid sequence induction with neuroprotective strategy
• Avoid hypoxia (target SpO₂ > 95%)

B - Breathing:

• Avoid hypoxia (secondary brain injury) - target PaO₂ > 13 kPa
• Avoid hypercapnia initially (raises ICP) - target PaCO₂ 4.5-5.0 kPa
• Judicious hyperventilation only if signs of herniation (temporary measure, target PaCO₂ 4.0-4.5 kPa)

C - Circulation:

• Maintain cerebral perfusion pressure (CPP) = MAP - ICP
• Target CPP > 60 mmHg
• Avoid hypotension (SBP less than 90 mmHg doubles mortality)
• Fluid resuscitation: isotonic crystalloids (0.9% saline)
• Avoid hypotonic fluids (worsen cerebral oedema)

D - Disability:

• GCS assessment and serial monitoring
• Pupil examination (size, reactivity, symmetry)
• Blood glucose - correct hypoglycaemia immediately

E - Exposure:

• Prevent hypothermia (coagulopathy) but also avoid hyperthermia (worsens outcome)
• Full trauma survey (C-spine immobilization if appropriate mechanism)

Neuroprotective Measures

Head positioning:

• Head-up 30° (improves venous drainage, reduces ICP)
• Midline head position (avoid neck rotation/flexion that impedes venous return)

Seizure prophylaxis:

• Levetiracetam 500mg BD or Phenytoin 15-20mg/kg loading dose
• Evidence supports prophylaxis for 7 days in acute TBI with SDH [20]
• Reduces early post-traumatic seizures (within 7 days)
• No proven benefit beyond 7 days for late seizures

Osmotic therapy (if signs of raised ICP/herniation):

• Mannitol 0.25-1g/kg IV (rapid effect, lasts 2-6 hours)
  • Watch for rebound ICP rise
  • Monitor serum osmolality (keep less than 320 mOsm/L)
• Hypertonic saline 3-5% (alternative, may be superior)
  • Longer duration of action
  • Does not cause osmotic diuresis

Temperature management:

• Target normothermia (36.5-37.5°C)
• Treat fever aggressively (↑ cerebral metabolic demand)

Glucose control:

• Avoid hypo- and hyperglycaemia
• Target 6-10 mmol/L

Anticoagulation Reversal - TIME-CRITICAL

Warfarin:

• Prothrombin Complex Concentrate (PCC - Octaplex/Beriplex) 25-50 units/kg IV + Vitamin K 10mg IV
• Target INR less than 1.4 (ideally less than 1.2)
• Check INR 30 minutes post-PCC
• Do NOT wait for Vitamin K to work (takes 12-24 hours) - give PCC immediately

DOACs (Dabigatran, Rivaroxaban, Apixaban, Edoxaban):

• Dabigatran: Idarucizumab 5g IV (specific reversal agent)
• Factor Xa inhibitors (Rivaroxaban, Apixaban, Edoxaban): Andexanet alfa (if available) or PCC 50 units/kg
• If specific reversal unavailable: supportive care, PCC, consider haemodialysis for dabigatran

Antiplatelet agents:

• No specific reversal for aspirin/clopidogrel
• Platelet transfusion controversial (may worsen bleeding in some studies)
• Consider Desmopressin (DDAVP) 0.3 mcg/kg IV (improves platelet function)
• Tranexamic acid 1g IV - evidence from CRASH-2 trial for TBI [21]

Heparin/LMWH:

• Protamine sulfate 1mg per 100 units of heparin (partial reversal of LMWH)

Surgical Management - Acute SDH

Craniotomy (Decompressive Craniectomy):

Technique:

1. Large trauma flap (frontotemporoparietal)
2. Dura opened in cruciate or stellate fashion
3. Clot evacuation (acute clot is solid, cannot be washed out)
4. Haemostasis - identify bleeding points
5. Duraplasty if dural closure tight
6. Bone flap:
   • Replaced if minimal brain swelling
   • Removed (craniectomy) if significant swelling - left out to allow brain expansion
   • Stored in abdominal wall subcutaneous pocket or bone bank (replaced weeks later when swelling resolved)

ICP monitoring:

• Intraparenchymal bolt or External ventricular drain (EVD) inserted intraoperatively
• Target ICP less than 20 mmHg

Post-operative care:

• Neurosurgical ICU admission
• Serial GCS and pupils (hourly initially)
• Repeat CT head at 24 hours or if deterioration
• ICP monitoring and CPP-targeted therapy
• DVT prophylaxis (mechanical initially, then pharmacological once haemostasis secure)

Conservative Management (Selected Cases)

Strict criteria:

• Small SDH (less than 10mm, less than 5mm shift)
• GCS 13-15 and stable
• No pupillary abnormalities
• Reliable for neurological observation

Protocol:

• Neurosurgical unit admission (or high-dependency unit with neurosurgery on-site)
• Hourly GCS and pupils for 24 hours, then reduce frequency if stable
• Repeat CT at 12-24 hours and as clinically indicated
• LOW threshold for surgical intervention if any deterioration

Chronic Subdural Haematoma

Anticoagulation Management

Pre-operative:

• STOP anticoagulation (discuss with haematology/cardiology regarding stroke/VTE risk)
• Reverse as per acute management if urgent surgery needed
• Warfarin: stop 5 days pre-op, bridge with LMWH if high thromboembolic risk
• DOACs: stop 24-48 hours pre-op depending on renal function

Post-operative:

• Restart timing controversial:
  • "Low thromboembolic risk: restart 7-14 days post-op"
  • "High risk (mechanical valve, recent VTE): restart earlier (48-72 hours) after imaging confirms no rebleeding"
• Multidisciplinary discussion essential

Surgical Management - Burr Hole Drainage

Indications:

• Symptomatic chronic SDH
• Asymptomatic with > 10mm thickness or > 10mm shift (some centres)

Technique (Standard Approach):

1. GA or local anaesthesia (many done under LA + sedation in elderly)
2. Positioning: Supine or lateral, head-up
3. Incision: 3-4cm linear incision
4. Burr hole(s): 1 or 2 holes (frontal and parietal most common)
   • Single burr hole vs double: double may reduce recurrence but not definitively proven [22]
5. Dura opened with cruciate incision
6. Drainage: Dark, "motor oil" fluid gushes out
7. Irrigation: Warm saline irrigation until clear (500-1000ml)
8. Subdural drain inserted and tunneled subcutaneously
9. Closure: Watertight closure

Post-operative:

• Head flat for 24-48 hours (controversial, but traditional teaching to allow brain re-expansion)
• Drain left 24-48 hours (removed when drainage less than 30ml/day)
• Mobilize after drain removal
• Repeat CT before discharge to confirm resolution

Alternative techniques:

• Twist drill craniostomy (TDC): Smaller hole, bedside procedure possible, higher recurrence rates [23]
• Craniotomy: Reserved for organized/calcified chronic SDH not amenable to burr holes
• Middle meningeal artery embolization (MMAE): Emerging technique, reduces neovascularization and recurrence [24]

Conservative Management (Selected Chronic SDH)

Indications:

• Asymptomatic small collections
• High surgical risk patients who are stable
• Patient choice after informed discussion

Monitoring:

• Serial CT (2 weeks, 6 weeks, 3 months)
• Clinical review
• Clear instructions to return if symptoms develop

Spontaneous resolution rates: 30-40% of small asymptomatic chronic SDH resolve without intervention

Medical adjuncts (emerging evidence):

• Dexamethasone 4-8mg daily for 2-4 weeks: conflicting evidence, may reduce recurrence [25]
• Atorvastatin 20mg daily: anti-inflammatory effects, some evidence for reducing recurrence [26]
• Tranexamic acid 500mg TDS: antifibrinolytic, under investigation

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9. Complications

Immediate/Early Complications

Late Complications

Post-traumatic epilepsy:

• Risk 5-20% depending on severity of initial injury
• Higher with penetrating injury, early seizures, prolonged coma
• May require long-term antiepileptic medication

Cognitive impairment:

• Acute SDH: severe cognitive deficits common in survivors (underlying brain injury)
• Chronic SDH: most return to baseline if treated early, but some residual deficits

Chronic headache:

• Post-traumatic headache syndrome
• May persist months to years

Subdural hygroma:

• CSF collection in subdural space
• May form after SDH evacuation
• Usually asymptomatic and resolves spontaneously

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10. Prognosis and Outcomes

Acute Subdural Haemorrhage

Overall mortality: 50-90% [4]

Prognostic factors:

Poor prognosis indicators:

• Age > 65 years
• GCS less than 9 at presentation
• Fixed dilated pupils
• Significant midline shift (> 10mm)
• Associated injuries (diffuse axonal injury, contusions)
• Delay to surgery (> 4 hours from injury)
• Hypotension (SBP less than 90mmHg)
• Hypoxia
• Coagulopathy

Better prognosis:

• Younger age
• Higher admission GCS (13-15)
• Reactive pupils
• Early evacuation
• Isolated SDH without underlying brain injury (rare in acute setting)

Functional outcomes (survivors):

• Good recovery (independent): 20-30%
• Moderate disability: 20-30%
• Severe disability/vegetative: 20-30%
• Mortality: 50-90%

Chronic Subdural Haematoma

Overall mortality: 5-10% (with treatment) [16]

Prognosis generally EXCELLENT if:

• Diagnosed and treated promptly
• Pre-morbid cognitive function normal
• No significant comorbidities

Functional outcomes:

• Complete resolution of symptoms: 70-80%
• Partial improvement: 10-20%
• No improvement/deterioration: 5-10%

Recurrence rate: 10-20% [22]

Factors associated with recurrence:

• Bilateral SDH
• Trabecular/separated type on CT (complex internal architecture)
• Failure to use subdural drain (Santarius trial showed drain reduces recurrence) [27]
• Continued anticoagulation
• Brain atrophy
• Chronic alcoholism

Natural history without treatment:

• 30-40% may resolve spontaneously if small and asymptomatic
• 50-70% progress and require intervention
• Risk of acute deterioration from rebleeding

Return to Activities

After chronic SDH surgery:

• Return to normal activities: 6-8 weeks typically
• Driving: May resume when symptoms resolved and cleared by neurosurgeon (usually 4-6 weeks, check DVLA guidelines)
• Anticoagulation: Restart per protocol (see management section)
• Contact sports: Avoid for 3-6 months minimum

After acute SDH:

• Prolonged rehabilitation often needed
• Return to activities highly variable depending on severity of injury and residual deficits

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11. Prevention and Special Considerations

Primary Prevention

Falls prevention in elderly:

• Home safety assessment (remove trip hazards, install handrails)
• Medication review (reduce sedatives, optimize Parkinson's/epilepsy treatment)
• Visual and hearing assessment
• Physiotherapy for strength and balance
• Treat osteoporosis (reduce fracture risk from falls)

Trauma prevention:

• Seat belt and helmet use
• Alcohol reduction programs
• Violence reduction initiatives

Anticoagulation Decisions

Key question: Should anticoagulation be restarted after SDH?

High thromboembolic risk (favours restarting):

• Mechanical heart valve (especially mitral position)
• Recent VTE (less than 3 months)
• Atrial fibrillation with CHA₂DS₂-VASc ≥4

High bleeding risk (favours not restarting):

• Recurrent SDH despite surgery
• Underlying cerebral amyloid angiopathy
• Severe brain atrophy
• Falls risk

Alternative strategies:

• Left atrial appendage occlusion device (Watchman) for AF patients
• DOACs may have lower intracranial bleeding risk than warfarin [28]
• Antiplatelet monotherapy (aspirin alone) instead of dual therapy

MDT discussion involving neurosurgery, haematology, cardiology essential

Non-Accidental Injury in Infants

Red flags for NAI:

• Subdural haemorrhage (especially bilateral) in infant
• Retinal haemorrhages (ophthalmology exam mandatory)
• Metaphyseal fractures (high specificity for abuse)
• Inconsistent history or injury not explained by developmental stage
• Delayed presentation
• Multiple injuries of different ages

Action:

• Safeguarding referral to local authority
• Paediatric consultation
• Skeletal survey (full radiographic survey for fractures)
• Document thoroughly (may be legal proceedings)

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12. Evidence Base and Guidelines

Key Guidelines

Landmark Evidence

1. Santarius Trial (Lancet 2009) [27]

• RCT comparing burr hole drainage with vs without subdural drain
• Result: Drain placement significantly reduced recurrence (9% vs 24%) and mortality
• Impact: Subdural drain now standard of care in chronic SDH surgery

2. CRASH Trial (Lancet 2004) [21]

• Large RCT of corticosteroids in TBI (including acute SDH)
• Result: Steroids INCREASED mortality - do NOT use
• Impact: Changed practice from steroid use to avoidance in acute TBI

3. STITCH Trial (Lancet 2005)

• Surgical vs conservative management of intracerebral haemorrhage
• Informed similar decision-making for SDH management

4. MRC CRASH-3 Trial (Lancet 2019) [21]

• Tranexamic acid in TBI
• Result: Benefit in mild-moderate TBI (GCS 9-15) if given within 3 hours
• Impact: Many centres now give TXA 1g in SDH with ongoing bleeding

5. Middle Meningeal Artery Embolization Studies (2020-2024) [24]

• Emerging technique: Endovascular embolization of MMA to reduce chronic SDH neovascularization
• Result: Reduced recurrence rates vs surgery alone in some studies
• Impact: May become adjunct or alternative to surgery

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13. Examination Focus

High-Yield Exam Topics

Radiology Stations:

1. "Describe this CT head"

• identify crescentic hyperdensity, crossing sutures, NOT crossing midline

2. Differentiate acute SDH (crescent) from extradural (lens shape)
3. Recognize isodense subacute SDH (look for midline shift as clue)
4. Identify acute-on-chronic SDH (mixed density)

Viva Questions:

Opening statement for SDH: "Subdural haemorrhage is a collection of blood in the subdural space, between the dura and arachnoid mater, classically caused by rupture of bridging veins. It has a crescentic appearance on CT imaging and crosses suture lines but not the midline. The clinical presentation and prognosis differ markedly between acute and chronic forms."

Common questions:

1. "What is the mechanism of bridging vein injury?"

   • Acceleration-deceleration forces cause differential movement between brain and skull, shearing delicate veins at cortical surface or sinus entry point. Elderly with brain atrophy have stretched veins vulnerable to rupture from minor trauma.

2. "What are the surgical indications for acute SDH?"

   • Brain Trauma Foundation criteria: thickness > 10mm, midline shift > 5mm, GCS drop ≥2 points, or pupillary abnormalities. [18]

3. "Why is prognosis poor in acute SDH?"

   • Not primarily due to the blood collection itself, but the associated severe primary brain injury (contusions, diffuse axonal injury) from high-velocity trauma. Mortality 50-90% despite surgery.

4. "How do you manage anticoagulation in a patient with chronic SDH?"

   • Urgent reversal pre-operatively (PCC for warfarin, idarucizumab for dabigatran, etc.). Post-operatively, multidisciplinary discussion balancing thromboembolic risk vs rebleeding. Generally restart cautiously at 7-14 days if low thromboembolic risk, earlier if high risk (e.g., mechanical valve).

5. "What did the Santarius trial show?"

   • RCT demonstrating subdural drain placement after burr hole evacuation of chronic SDH significantly reduces recurrence (9% vs 24%) and mortality. Now standard practice. [27]

6. "Describe the operation for chronic SDH."

   • Burr hole drainage: one or two burr holes (frontal/parietal), dura opened, dark 'motor oil' fluid evacuated, irrigation with warm saline until clear, subdural drain left in situ for 24-48 hours, head flat post-op to allow brain re-expansion.

Anatomy Viva Points

"Describe the layers of the meninges from outer to inner:"

• Skull bone
• Dura mater (two layers: periosteal and meningeal)
• Subdural space (potential space)
• Arachnoid mater
• Subarachnoid space (contains CSF and cerebral vessels)
• Pia mater (adherent to brain)

"What are bridging veins?"

• Veins draining superficial cerebral cortex that traverse the subdural space to enter dural venous sinuses (especially superior sagittal sinus). Vulnerable to shearing in trauma.

"Describe uncal herniation:"

• Medial temporal lobe (uncus) herniates through tentorial notch due to supratentorial mass effect. Compresses:
  1. Oculomotor nerve (CN III): → ipsilateral pupil dilatation (parasympathetic fibres on periphery compressed first)
  2. Cerebral peduncle: → contralateral hemiparesis
  3. Posterior cerebral artery: → occipital lobe infarction
  4. Midbrain: → Reduced consciousness, Cushing's triad

"What is Kernohan's notch?"

• False localizing sign: lateral brain herniation compresses contralateral cerebral peduncle against tentorial edge, causing ipsilateral hemiparesis (same side as lesion rather than opposite).

Common Mistakes (How to Fail)

❌ Confusing acute SDH with extradural haemorrhage:

• SDH: Crescent, venous, crosses sutures, fluctuating course
• EDH: Lens/lentiform, arterial, limited by sutures, lucid interval

❌ Missing isodense subacute SDH on CT:

• Remember to look for secondary signs: midline shift, sulcal effacement, ventricular compression

❌ Saying acute SDH has good prognosis:

• Prognosis is POOR (50-90% mortality) due to associated brain injury
• CHRONIC SDH has GOOD prognosis (less than 10% mortality)

❌ Recommending steroids in acute TBI/SDH:

• CRASH trial showed HARM - never give steroids in acute TBI

❌ Not reversing anticoagulation urgently:

• Time-critical: give PCC + Vitamin K for warfarin immediately, don't wait for INR to drift down

❌ Forgetting subdural drain in chronic SDH:

• Santarius trial evidence: drains reduce recurrence - must mention

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14. Patient and Layperson Explanation

What is a subdural haemorrhage?

It is bleeding on the surface of the brain, in a narrow space underneath the tough outer covering called the dura. The blood presses on the brain and can cause symptoms.

Why did it happen?

There are thin veins called "bridging veins" that connect the surface of your brain to the veins in the skull lining. When the head is hit or shaken, these delicate veins can tear and bleed.

In older people, the brain naturally shrinks a little with age, which stretches these veins tight like elastic bands. This means even a small bump (like hitting your head on a cupboard door) can be enough to tear them and cause slow bleeding.

In younger people, it usually takes a much bigger impact (like a car accident or bad fall) to cause this type of bleeding.

Why did symptoms take weeks to appear?

Because the bleeding is from a vein (low pressure), it happens very slowly. The blood builds up gradually over weeks, like a slow leak. Eventually, there's enough blood pressing on the brain to cause symptoms like confusion, headaches, or unsteadiness.

How is it treated?

For chronic (slow-building) bleeds:

• We make a small hole in the skull (about the size of a 50p coin) - this is called a "burr hole"
• The old blood, which looks like dark motor oil, drains out through the hole
• We wash the area with fluid until it's clean
• A small drain tube is left in for 1-2 days to let any remaining fluid out
• The brain then gradually expands back to fill the space
• Most people make a full recovery

For acute (fresh) bleeds:

• A larger operation called a craniotomy is needed
• A section of skull is temporarily removed to take pressure off the brain
• The blood clot is removed
• This is a bigger operation with more risk, as there's usually more serious brain injury

Will I fully recover?

Chronic subdural: Most people (70-80%) return to their normal selves, especially if treated promptly.

Acute subdural: Recovery is more variable and depends on how badly the brain was injured initially. Some people recover well, but many have lasting effects.

Can it come back?

Yes, there's about a 10-20% chance it comes back after treatment. We monitor you with scans and check-ups. If symptoms return, come back to hospital immediately.

What about my blood thinners?

This is an important discussion. Blood thinners (like warfarin) increase bleeding risk, but they're often needed for other conditions like stroke prevention or blood clots. Your doctors will work together to decide the safest plan - when to stop them for the operation, and when (or if) to restart them afterwards.

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15. References

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21. CRASH-3 trial collaborators. Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial. Lancet. 2019;394(10210):1713-1723. doi:10.1016/S0140-6736(19)32233-0

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25. Hutchinson PJ, Edlmann E, Bulters D, et al. Trial of Dexamethasone for Chronic Subdural Hematoma. N Engl J Med. 2020;383(27):2616-2627. doi:10.1056/NEJMoa2020473

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27. Santarius T, Kirkpatrick PJ, Ganesan D, et al. Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. Lancet. 2009;374(9695):1067-1073. doi:10.1016/S0140-6736(09)61115-6

28. Ruff CT, Giugliano RP, Braunwald E, et al. Comparison of the efficacy and safety of new oral anticoagulants with warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials. Lancet. 2014;383(9921):955-962. doi:10.1016/S0140-6736(13)62343-0

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and follow local guidelines and protocols.