Extradural Haematoma (Epidural Haematoma)

1. Clinical Overview

Summary

Extradural haematoma (EDH), also known as epidural haematoma, is a neurosurgical emergency characterised by accumulation of blood between the skull's inner table and the dura mater. The condition arises most commonly from arterial bleeding (85-90% from middle meningeal artery rupture) following skull fracture, typically in the temporal or temporoparietal region. [1,2]

The classic presentation features the "lucid interval"

• an initial brief loss of consciousness following trauma, apparent recovery to near-normal neurological status, followed by rapid deterioration as the haematoma expands. This pattern, though pathognomonic, occurs in only 20-50% of cases. [3] Computed tomography (CT) demonstrates the characteristic biconvex (lentiform) hyperdense lesion that does not cross cranial suture lines, reflecting the anatomical constraint of dural adherence to skull at sutures.

Emergency surgical evacuation via craniotomy is the definitive treatment for significant haematomas. Surgical indications include haematoma volume >30mL, maximal thickness >15mm, midline shift >5mm, or Glasgow Coma Scale (GCS) ≤8. [4] Mortality ranges from 5-10% with prompt surgical intervention but approaches 90% if untreated. Pre-operative GCS score is the strongest predictor of outcome. [5]

Key Facts

• Incidence: 1-4% of all traumatic brain injury admissions; 5-15% of fatal head injuries [6]
• Primary Mechanism: Middle meningeal artery rupture (85-90%); venous sources (10-15%) [1,2]
• Peak Age: 20-40 years; rare in infants and elderly due to dural-skull adherence
• Classic Sign: Lucid interval (present in 20-50% of cases) [3]
• CT Appearance: Biconvex (lentiform) hyperdense lesion respecting suture lines
• Surgical Threshold: >30mL volume, >15mm thickness, >5mm midline shift, or GCS ≤8 [4]
• Mortality: 5-10% with surgery; 20-30% with delayed surgery; >90% without surgery [5,7]
• Outcome Predictor: Pre-operative GCS strongest predictor of functional recovery [5]

Clinical Pearls

"Lucid Interval = EDH Until Proven Otherwise": Any patient with head trauma who experiences initial unconsciousness, apparent recovery, then deterioration should be assumed to have EDH requiring emergency CT imaging.

"Biconvex = Extradural, Crescent = Subdural": EDH appears lens-shaped (biconvex) on CT because dura is progressively stripped from skull by arterial pressure. Subdural haematoma appears crescentic as blood spreads freely in the subdural space.

"Respects Sutures, Not Parenchyma": EDH is limited by cranial sutures where dura is firmly adherent to bone. Blood crossing suture lines suggests subdural or other pathology.

"Ipsilateral Pupil Dilation = Uncal Herniation": A fixed, dilated pupil is typically ipsilateral to the haematoma due to uncal herniation compressing the oculomotor nerve (CN III) against the tentorial edge.

"Time is Brain - Logarithmic Deterioration": EDH can deteriorate catastrophically within 1-2 hours of initial stability. Serial GCS monitoring every 15 minutes is mandatory in suspected cases.

"Temporal Trauma + Skull Fracture = High Risk": 75-95% of EDH cases have associated skull fracture, most commonly involving the temporal bone overlying the middle meningeal artery groove. [8]

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2. Epidemiology

Incidence and Prevalence

Extradural haematoma accounts for 1-4% of all traumatic brain injury (TBI) admissions and represents 5-15% of fatal head injuries. [6] The true incidence is estimated at 1-2 per 100,000 population per year in developed countries, though this varies with trauma patterns and access to neurosurgical care. [9]

Post-mortem studies suggest EDH may be underdiagnosed in polytrauma patients who die before imaging, with autopsy series identifying EDH in up to 9% of fatal head injuries. [10]

Age Distribution

EDH demonstrates a bimodal age distribution with distinct peaks:

Peak Incidence (20-40 years): Young active adults represent 60-70% of cases, reflecting high-energy trauma exposure from motor vehicle collisions, assault, and sports injuries. [2,11]

Pediatric Cases (5-20 years): Account for 15-20% of EDH, typically from lower-energy mechanisms (falls, sports). Children may present with larger haematomas before symptom onset due to greater intracranial compliance. [12]

Rare in Extremes of Age:

• Infants (less than 2 years): EDH is uncommon due to tight dural adherence to skull, more pliable cranium, and open fontanelles providing pressure relief. When present, often from non-accidental injury. [13]
• Elderly (>65 years): Incidence decreases as dura becomes increasingly adherent to skull with age, and cerebral atrophy creates more intracranial space buffering haematoma expansion. However, elderly patients with EDH have worse outcomes due to comorbidities and anticoagulation. [14]

Sex Distribution

Male predominance is consistent across all series with a male:female ratio of approximately 4:1, reflecting higher exposure to traumatic mechanisms. [2,11] No biological sex-based susceptibility exists beyond trauma exposure patterns.

Anatomical Distribution

Temporal/Temporoparietal (60-70%): Most common location corresponding to:

• Middle meningeal artery trajectory in temporal bone groove
• Pterion (thinnest part of skull - junction of frontal, parietal, temporal, sphenoid bones)
• High-impact zone in lateral trauma [1,2]

Frontal (15-20%): Associated with frontal bone fractures and anterior meningeal artery injury

Parietal (10-15%): Typically venous from superior sagittal sinus or other dural venous channels

Posterior Fossa (5-10%): Rare but highly dangerous due to limited space and proximity to brainstem; often from occipital trauma with transverse or sigmoid sinus injury [15]

Risk Factors

Traumatic Mechanisms:

• Motor vehicle collisions (40-50% of cases)
• Falls from height (20-30%)
• Assault (15-20%)
• Sports injuries (5-10%) - particularly contact sports, cycling, equestrian activities [11]

Skull Factors:

• Skull fracture (present in 75-95% of EDH cases) [8]
• Linear fracture crossing meningeal artery grooves
• Temporal bone fractures (highest association)
• Depressed fractures (can directly lacerate vessels)

Coagulation Disorders:

• Anticoagulation therapy (warfarin, DOACs) - increases bleeding rate and haematoma expansion
• Antiplatelet agents (aspirin, clopidogrel) - associated with larger haematomas
• Haemophilia and other coagulopathies - rare but catastrophic bleeding [16]
• Thrombocytopenia

Patient Factors:

• Alcohol intoxication (impairs protective reflexes, delays presentation)
• Previous neurosurgery or craniotomy (altered dural adhesion)
• Connective tissue disorders affecting vascular integrity (rare)

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3. Pathophysiology

Anatomy and Anatomical Relationships

Meningeal Layers (superficial to deep):

1. Skull (inner table): Compact bone with vascular grooves
2. Extradural space (potential): Normally, dura is tightly adherent to periosteal layer of skull
3. Dura mater: Tough fibrous membrane with two layers:
   • Outer periosteal layer (adheres to skull, especially at sutures)
   • Inner meningeal layer (continuous with spinal dura)
4. Subdural space (potential): Between dura and arachnoid
5. Arachnoid mater: Delicate membrane
6. Subarachnoid space: Contains CSF and cerebral vessels
7. Pia mater: Adherent to brain surface

Middle Meningeal Artery:

• Branch of maxillary artery (external carotid system)
• Enters skull through foramen spinosum
• Runs in groove on inner table of temporal and parietal bones
• Divides into anterior (frontal) and posterior (parietal) branches
• Arterial pressure: 80-120 mmHg (compared to 5-10 mmHg in bridging veins)
• Vulnerability: Fractures crossing the pterion or temporal bone directly lacerate this fixed vessel [1,2]

Dural Venous Sinuses:

• Superior sagittal sinus (vertex injuries)
• Transverse and sigmoid sinuses (posterior fossa EDH)
• Constitute 10-15% of EDH sources, typically with lower-pressure bleeding [17]

Cranial Sutures:

• Coronal (frontal-parietal)
• Sagittal (parietal-parietal)
• Lambdoid (parietal-occipital)
• Squamosal (temporal-parietal)
• Dura is firmly adherent at sutures, creating anatomical barrier to EDH expansion

Mechanism of Injury

Traumatic Cascade:

┌────────────────────────────────────────────────────────────────┐
│   PATHOPHYSIOLOGICAL SEQUENCE OF EDH                           │
├────────────────────────────────────────────────────────────────┤
│                                                                │
│  PHASE 1: PRIMARY INJURY (0-5 minutes)                         │
│  • Blunt trauma to skull (temporal/parietal region common)     │
│  • Skull deformation or fracture                               │
│  • Laceration/rupture of middle meningeal artery               │
│  • Initial concussive brain injury → Brief LOC                 │
│                                                                │
│  PHASE 2: HAEMATOMA FORMATION (5 minutes - 6 hours)            │
│  • Arterial bleeding at 80-120 mmHg pressure                   │
│  • Blood strips dura from inner skull table                    │
│  • Biconvex shape forms (dura resists stripping)               │
│  • Limited by suture lines (firm dural adherence)              │
│  • Volume accumulates: 15-30mL/hour typical                    │
│                                                                │
│  PHASE 3: LUCID INTERVAL (variable duration)                   │
│  • Concussion resolves → Return to consciousness               │
│  • Haematoma expanding but not yet critical                    │
│  • Duration: Minutes to 24+ hours (typically 1-6 hours)        │
│  • Absent if initial injury severe or rapid bleeding           │
│                                                                │
│  PHASE 4: MASS EFFECT AND DETERIORATION (rapid)                │
│  • Haematoma reaches critical volume (~30-50mL)                │
│  • Intracranial pressure (ICP) rises exponentially             │
│  • Midline shift develops                                      │
│  • Symptoms: Headache, vomiting, confusion, GCS decline        │
│                                                                │
│  PHASE 5: HERNIATION (minutes to hours)                        │
│  • Uncal herniation → Ipsilateral CN III compression           │
│    - Fixed dilated pupil (loss of parasympathetic)             │
│    - Contralateral hemiparesis (cerebral peduncle compression) │
│  • Central herniation → Bilateral deterioration                │
│  • Tonsillar herniation (posterior fossa EDH)                  │
│                                                                │
│  PHASE 6: BRAINSTEM COMPRESSION (terminal)                     │
│  • Cushing's triad: Hypertension, bradycardia, irregular resp  │
│  • Bilateral fixed pupils                                      │
│  • Decerebrate posturing → Flaccidity                          │
│  • Cardiorespiratory arrest                                    │
│                                                                │
└────────────────────────────────────────────────────────────────┘

The "Lucid Interval"

• Pathophysiological Explanation

The classic lucid interval occurs in 20-50% of EDH cases and represents a distinct pathophysiological timeline: [3]

Initial Loss of Consciousness (Concussion):

• Direct impact causes transient neuronal dysfunction (concussion)
• Brief unconsciousness (seconds to minutes)
• Concurrent skull fracture and vessel injury

Recovery Phase (Lucid Interval):

• Concussive symptoms resolve as neuronal function recovers
• Patient regains consciousness, may appear normal or near-normal
• Haematoma is expanding but has not yet reached critical mass
• Intracranial compliance initially accommodates expanding lesion via:
  • CSF displacement to spinal subarachnoid space
  • Venous compression and reduced cerebral blood volume
  • Minor brain deformation

Decompensation:

• Monroe-Kellie doctrine: Skull is rigid box (fixed volume)
• Once compensatory mechanisms exhausted (~30-50mL haematoma volume)
• Exponential ICP rise (Langfitt curve)
• Rapid neurological deterioration over 30-120 minutes

Factors Affecting Lucid Interval Presence:

• Present when: Moderate initial impact, slow bleeding, good compensation
• Absent when: Severe initial brain injury, rapid arterial bleeding, poor compensation, large haematoma volume, underlying brain contusion [3]

Molecular and Cellular Pathophysiology

Primary Haemorrhage:

• Arterial rupture → Extravasation at mean arterial pressure
• Haematoma is space-occupying mass (no inherent neurotoxicity unlike intracerebral haemorrhage)
• Mechanical compression is primary mechanism of injury

Secondary Brain Injury Cascade:

Raised Intracranial Pressure (ICP):

• Normal ICP: 5-15 mmHg
• EDH causes ICP elevation to 20-40+ mmHg
• Reduced cerebral perfusion pressure (CPP = MAP - ICP)
• CPP less than 50 mmHg → Cerebral ischaemia [18]

Mass Effect and Midline Shift:

• Haematoma displaces brain tissue
• Midline shift >5mm indicates significant mass effect
• Compression of ipsilateral lateral ventricle
• Distortion of perforating vessels → Ischaemia

Herniation Syndromes:

1. Uncal Herniation (most common with temporal EDH):

   • Medial temporal lobe (uncus) herniates through tentorial notch
   • Compresses oculomotor nerve (CN III) → Ipsilateral pupil dilation
   • Compresses cerebral peduncle → Contralateral hemiparesis
   • False localising sign: Ipsilateral hemiparesis if contralateral peduncle compressed against tentorium (Kernohan's notch phenomenon)
   • Compression of posterior cerebral artery → Occipital infarction

2. Central (Transtentorial) Herniation:

   • Bilateral downward displacement of diencephalon and midbrain
   • Progressive rostrocaudal deterioration
   • Bilateral pupil abnormalities
   • Decerebrate posturing

3. Tonsillar Herniation (posterior fossa EDH):

   • Cerebellar tonsils herniate through foramen magnum
   • Compression of medulla → Cardiorespiratory arrest
   • Rapid progression, high mortality [15]

Cushing's Response:

• Physiological response to brainstem ischaemia from raised ICP
• Hypertension (reflex attempt to maintain CPP)
• Bradycardia (baroreceptor response to hypertension)
• Irregular respiration (medullary compression)
• Late and ominous sign indicating imminent death without intervention [19]

Comparison: Extradural vs Subdural Haematoma

Understanding the anatomical and pathophysiological differences is crucial for diagnosis and management:

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4. Clinical Presentation

Classic Presentation Patterns

Pattern 1: Lucid Interval (20-50% of cases) [3]

Timeline and features:

1. Initial Impact (T=0):

   • Blunt head trauma (fall, assault, collision)
   • Brief loss of consciousness (seconds to minutes)
   • Patient regains consciousness

2. Lucid Interval (T=1-6 hours typically):

   • Apparent recovery to near-normal
   • May have mild headache, but walking and talking
   • Often dismissed as "just concussion"
   • Haematoma silently expanding

3. Deterioration Phase (T=variable, often sudden):

   • Severe, progressive headache
   • Vomiting
   • Confusion, agitation, or drowsiness
   • GCS decline (progressive)
   • Focal neurological signs emerge

4. Herniation (T=late, rapid progression):

   • Pupil dilation (ipsilateral)
   • Hemiparesis (contralateral)
   • Posturing
   • Coma

5. Death (if untreated):

   • Bilateral fixed pupils
   • Cushing's triad
   • Cardiorespiratory arrest

Pattern 2: Immediate Severe Presentation (30-40% of cases):

• No lucid interval
• Severe initial brain injury or very rapid bleeding
• Immediate coma or severe GCS depression
• Requires emergency imaging and surgery
• Worse prognosis due to severe primary injury

Pattern 3: Delayed Presentation (10-20% of cases):

• Small or slow-bleeding haematoma
• Mild symptoms for hours to days
• Gradual progression of headache, vomiting
• Late deterioration if haematoma continues expanding
• May be venous source rather than arterial

Pattern 4: Pediatric Presentation:

• Children may compensate longer due to greater intracranial compliance
• Present with larger haematomas before decompensation
• Irritability, vomiting, lethargy may be early signs
• Scalp haematoma ("boggy swelling") often present
• Seizures more common in children (10-15% vs 5% in adults) [12]

Symptoms

Early Symptoms (first hours):

• Headache: Typically severe, progressive, unilateral or holocephalic. Present in 80-90% of conscious patients
• Nausea/Vomiting: Reflects raised ICP; projectile vomiting suggests critical elevation
• Dizziness/Unsteadiness: Vestibular or cerebellar compression
• Drowsiness: Subtle decline in alertness before overt GCS drop
• Confusion/Disorientation: Early sign of diffuse cerebral dysfunction

Progressive Symptoms (hours to days):

• Altered Consciousness: Progressive obtundation
• Severe Vomiting: Repetitive, not relieved by anti-emetics
• Focal Weakness: Contralateral hemiparesis (may be subtle initially)
• Speech Disturbance: Dysphasia (if dominant hemisphere affected)
• Visual Disturbance: Diplopia, blurred vision, field defects
• Seizures: Occur in 5-10% of adults, 10-15% of children [12]

Late/Critical Symptoms:

• Coma: GCS ≤8
• Respiratory Irregularity: Cheyne-Stokes or ataxic breathing
• Severe Hypertension: Cushing's response

Clinical Signs

General Examination:

• Scalp Examination: Haematoma, laceration, "boggy swelling" over fracture site
• Skull Palpation: Step deformity, tenderness over fracture line
• Haemotympanum: Blood behind tympanic membrane (basilar skull fracture)
• Battle's Sign: Mastoid ecchymosis (basilar fracture, develops over 1-2 days)
• Raccoon Eyes: Periorbital ecchymosis (anterior basilar fracture)
• CSF Rhinorrhoea/Otorrhoea: Clear fluid from nose/ear (basilar fracture with dural tear)

Neurological Examination:

Consciousness Level (GCS - single most important parameter):

• Monitor trend: ≥2 point decline = significant deterioration
• Serial assessment every 15 minutes in acute phase mandatory
• GCS components:
  • Eye opening (E1-4)
  • Verbal response (V1-5)
  • Motor response (M1-6)

Pupillary Examination (critical for herniation detection):

• Size: Normal 2-4mm; mydriasis >6mm
• Reactivity: Brisk, sluggish, or fixed
• Anisocoria: Difference >1mm significant
• Classic EDH Sign: Ipsilateral fixed dilated pupil
  • Uncal herniation compresses CN III
  • Parasympathetic fibres (pupilloconstriction) affected first
  • Pupil dilates (unopposed sympathetic)
  • Late: Complete CN III palsy with ptosis, "down and out" eye

Motor Examination:

• Hemiparesis: Contralateral to haematoma (corticospinal tract compression)
  • "Subtle: Pronator drift, unilateral weakness"
  • "Severe: Plegia"
• Posturing (indicates severe brainstem dysfunction):
  • "Decorticate: Flexion of upper limbs, extension of lower limbs (lesion above red nucleus)"
  • "Decerebrate: Extension of all limbs (midbrain/pontine lesion)"
  • Progression from decorticate to decerebrate = rostrocaudal deterioration

Cranial Nerves:

• CN II: Papilloedema (takes hours to develop, rarely present acutely)
• CN III: Pupil dilation, ptosis, lateral eye deviation (uncal herniation)
• CN VI: Lateral rectus palsy (false localising sign from raised ICP)

Cushing's Triad (late, ominous sign):

1. Hypertension: Systolic often >180-200 mmHg
2. Bradycardia: HR less than 60 bpm
3. Irregular Respiration: Cheyne-Stokes or ataxic pattern

• Indicates brainstem ischaemia from critically raised ICP
• Immediate surgical decompression required [19]

Differential Diagnosis by Presentation Pattern

Acute Post-Traumatic Deterioration:

• Extradural haematoma: Biconvex CT, lucid interval (20-50%)
• Subdural haematoma: Crescentic CT, often no lucid interval
• Traumatic intracerebral haemorrhage: Parenchymal blood, contusion
• Diffuse axonal injury: Normal or subtle CT, severe mechanism, poor GCS
• Cerebral contusion: Focal brain injury, often frontal/temporal
• Seizure (post-traumatic): Witnessed event, post-ictal state, normal imaging

Headache After Head Trauma:

• Concussion: Mild, improving, normal imaging
• Extradural haematoma: Progressive, severe, deteriorating GCS
• Subdural haematoma: Variable onset, may be delayed
• Post-concussion syndrome: Chronic, no acute deterioration
• Cervical spine injury: Neck pain, normal head CT

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5. Clinical Examination Approach

Primary Survey (ABCDE)

A - Airway:

• Assess patency
• C-spine immobilisation (assume injury until excluded)
• Airway adjuncts if GCS ≤8 or risk of deterioration
• Definitive airway (intubation) if:
  • GCS ≤8 (unable to protect airway)
  • Rapidly declining GCS
  • Respiratory compromise
  • Need for transfer or prolonged imaging

B - Breathing:

• Respiratory rate and pattern (irregular breathing = brainstem dysfunction)
• SpO₂ >95% target (avoid hypoxia - secondary brain injury)
• Avoid hyperventilation unless signs of herniation (target PaCO₂ 35-40 mmHg)

C - Circulation:

• Blood pressure (hypotension is NOT from isolated head injury in adults - find other source)
• Heart rate (bradycardia with hypertension = Cushing's)
• Maintain SBP >90 mmHg (cerebral perfusion)

D - Disability:

• GCS (most important)
• Pupils (size, reactivity, symmetry)
• Blood glucose (hypoglycaemia mimics head injury)

E - Exposure:

• Full body examination for polytrauma
• Scalp and skull examination
• Temperature (hypothermia or fever)

Focused Neurological Examination

Level of Consciousness:

• GCS: Document E, V, M separately
• AVPU if GCS not feasible: Alert, Voice, Pain, Unresponsive
• Trend more important than single value

Pupillary Assessment:

• Size (mm), shape (round vs irregular)
• Direct and consensual light reflex
• Anisocoria measurement
• Document as: "Pupils 3mm equal, brisk reactive bilaterally" or "Right pupil 6mm fixed, left 3mm reactive"

Motor Examination:

• Best motor response (GCS motor component)
• Limb power (if cooperative): Upper and lower limbs, left and right
• Localises to pain / Withdraws / Flexor posturing / Extensor posturing / None
• Asymmetry indicates lateralising lesion

Cranial Nerve Screen (if GCS permits):

• II: Visual fields to confrontation, pupil reactivity
• III, IV, VI: Eye movements, pupil size and reactivity
• V: Corneal reflex (if unconscious), facial sensation
• VII: Facial symmetry (ask to show teeth, close eyes)
• VIII: Hearing (often not assessed acutely)
• IX, X: Gag reflex (if unconscious)
• XI: Shoulder shrug
• XII: Tongue protrusion

Signs of Herniation (examine for):

• Uncal: Ipsilateral dilated pupil, contralateral hemiparesis
• Central: Bilateral small pupils → bilateral dilated pupils, bilateral motor signs
• Tonsillar: Respiratory arrest, bradycardia, hypotension

Serial Monitoring

Mandatory Observations:

• GCS: Every 15 minutes until stable
• Pupils: Every 15 minutes
• Vital Signs: Every 15 minutes
• Limb Power: Every 30 minutes

Deterioration Triggers (immediate senior/neurosurgical review):

• GCS decline ≥2 points
• New pupil asymmetry or fixed pupil
• New focal neurological deficit
• Cushing's triad components
• Seizure

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6. Investigations

CT Head (Non-Contrast) - Gold Standard

Indications for Imaging (NICE Head Injury Guidelines - CG176): [20]

Perform CT head scan within 1 hour if any of:

• GCS less than 13 on initial assessment
• GCS less than 15 at 2 hours post-injury
• Suspected open or depressed skull fracture
• Sign of basal skull fracture (haemotympanum, panda eyes, Battle's sign, CSF leak)
• Post-traumatic seizure
• Focal neurological deficit
• More than one episode of vomiting
• Age ≥65 years with any loss of consciousness or amnesia
• Amnesia for events >30 minutes before impact
• Dangerous mechanism of injury

High-Risk Mechanisms:

• Pedestrian struck by vehicle
• Ejection from vehicle
• Fall from >1 metre or 5 stairs

CT Imaging Protocol:

• Non-contrast CT head (contrast obscures acute blood)
• Axial slices 2.5-5mm thickness
• Bone windows (to assess fractures)
• Brain windows (to assess haematoma, shift, ventricles)

CT Findings in Extradural Haematoma

Classic Features:

1. Biconvex (Lentiform) Hyperdense Lesion:

   • Arterial blood: 50-70 Hounsfield units (HU)
   • Lens-shaped or convex on both sides
   • Dura stripped from skull creates characteristic shape

2. Does Not Cross Suture Lines:

   • Dura firmly adherent at cranial sutures
   • Haematoma limited by coronal, sagittal, lambdoid sutures
   • This feature differentiates EDH from SDH (which crosses sutures)

3. Adjacent to Skull:

   • Located at inner table of skull
   • Most commonly temporal/temporoparietal
   • May extend along frontal or parietal convexity

4. Skull Fracture (visible in 75-95%):

   • Linear fracture crossing meningeal artery groove
   • Best seen on bone windows
   • Temporal bone most common [8]

5. Mass Effect:

   • Midline shift (displacement of septum pellucidum, third ventricle)
   • Compression of ipsilateral lateral ventricle
   • Effacement of sulci
   • Obliteration of basal cisterns (indicates severe mass effect)

6. Herniation Signs:

   • Uncal herniation: Asymmetry of suprasellar cistern, displacement of brainstem
   • Central herniation: Downward displacement of brainstem, effacement of perimesencephalic cisterns
   • Tonsillar herniation: Cerebellar tonsils below foramen magnum

Quantitative Measurements:

• Maximum Diameter: Measure maximal AP, transverse, and craniocaudal dimensions
• Volume: Ellipsoid formula: (A × B × C) / 2 where A, B, C are maximum dimensions
• Thickness: Maximum perpendicular distance from inner table to dura
• Midline Shift: Distance of septum pellucidum displacement from midline (measured at level of foramen of Monro)

Atypical CT Appearances:

• Venous EDH: May be less hyperdense, slower evolution, vertex location
• Acute on Chronic: Mixed density (hyperdense acute blood, hypodense older blood)
• Active Bleeding: "Swirl sign"
• mixed density within haematoma indicating ongoing extravasation
• Posterior Fossa EDH: Occipital location, very limited space, high risk of tonsillar herniation [15]

Surgical Indications Based on CT (Brain Trauma Foundation Guidelines): [4]

Absolute Indications for Emergency Surgery:

• Volume >30 mL (regardless of GCS)
• Maximum thickness >15 mm (regardless of GCS)
• Midline shift >5 mm (regardless of GCS)
• GCS ≤8 with any size EDH
• Focal neurological deficit attributable to EDH
• Signs of herniation (pupil asymmetry, posturing)
• Evidence of brainstem compression (obliteration of basal cisterns)

Relative Indications (case-by-case neurosurgical decision):

• Posterior fossa EDH of any size (limited space, high risk)
• Progressive enlargement on serial CT
• GCS decline during observation period
• EDH in anticoagulated patient (higher rebleeding risk)

Conservative Management Criteria (all must be met):

• Volume less than 30 mL
• Thickness less than 15 mm
• Midline shift less than 5 mm
• GCS 15 (fully conscious)
• No focal neurological deficit
• No brainstem compression
• Neurosurgical unit with immediate theatre access
• Serial CT imaging capability
• Intensive monitoring capability

Additional Imaging

CT Angiography (CTA):

• Not routine for EDH diagnosis
• May identify "spot sign" (active arterial extravasation) predicting haematoma expansion
• Useful if vascular injury suspected (carotid/vertebral dissection in polytrauma)

MRI:

• Not used acutely (time-consuming, limited monitoring capability)
• May be used in subacute phase or for:
  • Assessing parenchymal injury (contusions, DAI)
  • Chronic subdural vs extradural differentiation
  • Follow-up of conservatively managed small EDH

Skull X-ray:

• Obsolete in modern practice (replaced by CT)
• May show fracture line but does not visualise haematoma
• No role in suspected EDH

Laboratory Investigations

Essential Blood Tests:

• Full Blood Count: Baseline haemoglobin, platelets (thrombocytopenia increases bleeding risk)
• Coagulation Screen:
  • PT/INR (warfarin monitoring, liver dysfunction)
  • APTT (heparin, intrinsic pathway disorders)
  • Fibrinogen (consumptive coagulopathy in polytrauma)
• Group and Save/Crossmatch: Prepare for surgery (2-4 units)
• Urea and Electrolytes: Baseline renal function, sodium (for osmotic therapy)
• Glucose: Hypoglycaemia can mimic neurological deterioration

Additional Tests (context-dependent):

• Arterial Blood Gas: If intubated or respiratory concerns (PaCO₂ important for ICP management)
• Toxicology Screen: Alcohol, recreational drugs (may confound GCS assessment)
• Liver Function Tests: If coagulopathy or alcohol excess suspected

Reversal of Coagulopathy (pre-operative):

• Warfarin: Vitamin K (10mg IV) + Prothrombin complex concentrate (PCC) or Fresh Frozen Plasma (FFP)
• DOACs: Specific reversal agents (idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors) or PCC
• Antiplatelet Agents: Platelet transfusion (desmopressin controversial)
• Haemophilia: Factor replacement (VIII or IX depending on type) [16]

Serial Imaging

Indications for Repeat CT:

• Clinical deterioration (GCS decline, new deficit)
• Conservative management of EDH (repeat at 6-12 hours, then 24 hours)
• Post-operative (immediate post-op, then as clinically indicated)
• Failure to improve as expected

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7. Management

Pre-Hospital Management

Immediate Priorities:

• Recognise potential serious head injury
• Call emergency services (ambulance with paramedic capability)
• C-spine immobilisation (hard collar, manual in-line stabilisation)
• Do not move patient unless in danger
• Monitor consciousness level
• Record mechanism of injury and timeline

Paramedic/Advanced Pre-Hospital:

• ABCDE assessment
• GCS documentation (trend monitoring)
• Oxygen to maintain SpO₂ >95%
• Avoid hypotension (IV access, fluid resuscitation if needed)
• Pre-alert receiving hospital (trauma call activation)
• Direct transfer to neurosurgical centre if available (bypass non-neurosurgical hospitals if stable and time permits)

Emergency Department Management

Immediate Assessment (first 15 minutes):

┌────────────────────────────────────────────────────────────────┐
│   EMERGENCY DEPARTMENT INITIAL MANAGEMENT                      │
├────────────────────────────────────────────────────────────────┤
│                                                                │
│  SIMULTANEOUS ACTIONS:                                         │
│                                                                │
│  1. RESUSCITATION (ABCDE):                                     │
│     • Secure airway (intubate if GCS ≤8)                       │
│     • C-spine immobilisation                                   │
│     • 100% O₂ initially, titrate to SpO₂ >95%                  │
│     • Target normocapnia (PaCO₂ 35-40 mmHg)                    │
│     • IV access (2 large bore cannulae)                        │
│     • Maintain SBP >90 mmHg (fluid/vasopressors)               │
│                                                                │
│  2. NEUROLOGICAL ASSESSMENT:                                   │
│     • GCS (E, V, M documented separately)                      │
│     • Pupil size, reactivity, symmetry                         │
│     • Lateralising signs (motor asymmetry)                     │
│     • Signs of herniation                                      │
│                                                                │
│  3. INVESTIGATIONS:                                            │
│     • Urgent CT head (non-contrast)                            │
│     • Bloods: FBC, coag, G&S, U&E, glucose                     │
│     • ABG if intubated                                         │
│                                                                │
│  4. NEUROSURGICAL REFERRAL:                                    │
│     • Contact immediately if EDH suspected                     │
│     • Do not wait for CT if severe mechanism + deterioration   │
│                                                                │
│  5. ICP MANAGEMENT (if signs of herniation):                   │
│     • Head up 30°                                              │
│     • Osmotic therapy: Mannitol 0.5-1 g/kg IV bolus OR         │
│       Hypertonic saline 3% (2-5mL/kg over 10-20 min)           │
│     • Brief hyperventilation (PaCO₂ 30-35) - temporising only  │
│     • Avoid hyperthermia (target normothermia)                 │
│                                                                │
│  6. COAGULOPATHY REVERSAL (if present):                        │
│     • Warfarin: Vitamin K + PCC/FFP                            │
│     • DOACs: Specific reversal agents or PCC                   │
│     • Antiplatelet: Consider platelet transfusion              │
│                                                                │
└────────────────────────────────────────────────────────────────┘

Intubation Indications:

• GCS ≤8 (inability to protect airway)
• Loss of protective airway reflexes
• Rapidly declining GCS (anticipate deterioration)
• Respiratory failure (SpO₂ less than 90% despite oxygen)
• Need for controlled ventilation (ICP management)
• Agitation preventing safe CT imaging
• Need for inter-hospital transfer

Intubation Considerations in Head Injury:

• Maintain C-spine immobilisation during intubation
• Avoid hypotension (use induction agents carefully)
• Avoid coughing/straining (raises ICP) - adequate sedation and paralysis
• Aim for smooth, controlled intubation
• Target PaCO₂ 35-40 mmHg (avoid routine hyperventilation)

Acute Raised ICP Management

Indications for ICP-Lowering Therapy:

• Clinical signs of herniation (pupil dilation, posturing)
• Cushing's triad
• Deteriorating GCS despite resuscitation
• CT evidence of severe mass effect (midline shift >5mm, basal cistern effacement)

Temporising Measures (bridge to surgery, NOT definitive treatment):

Head Positioning:

• 30° head-up (improves venous drainage, reduces ICP)
• Maintain neutral neck position (avoid jugular venous compression)
• Avoid tight cervical collar (may impede venous return)

Osmotic Therapy:

1. Mannitol:

   • Dose: 0.5-1 g/kg IV bolus over 15-30 minutes
   • Mechanism: Osmotic diuresis, reduces brain water content
   • Onset: 15-30 minutes, duration 4-6 hours
   • Monitoring: Serum osmolality (target less than 320 mOsm/kg)
   • Contraindications: Hypotension, renal failure
   • Side effects: Hypotension (volume depletion), renal impairment, rebound ICP elevation [21]

2. Hypertonic Saline (3% or 5%):

   • Dose: 3% saline 2-5 mL/kg IV over 10-20 minutes
   • Mechanism: Osmotic gradient, may be more effective than mannitol
   • Onset: 5-10 minutes
   • Monitoring: Serum sodium (target less than 160 mmol/L)
   • Advantages: No hypotension, may improve cerebral perfusion
   • Side effects: Hypernatraemia, central pontine myelinolysis (if rapid correction), rebound [22]

Hyperventilation (controversial, use sparingly):

• Mechanism: Hypocapnia causes cerebral vasoconstriction, reduces cerebral blood volume, lowers ICP
• Target: PaCO₂ 30-35 mmHg (brief use only)
• Duration: less than 30 minutes (temporising measure only)
• Risks: Cerebral ischaemia (reduced cerebral blood flow), rebound ICP elevation
• Indication: Signs of imminent herniation as bridge to theatre only
• Monitoring: Arterial blood gas [23]

Sedation and Analgesia (if intubated):

• Adequate sedation reduces metabolic demand, prevents agitation-related ICP spikes
• Propofol or midazolam infusion
• Fentanyl or alfentanil for analgesia
• Avoid ketamine (historically avoided due to concern for raised ICP, though recent evidence suggests safe)

Seizure Control:

• Seizures dramatically raise ICP
• Benzodiazepines (lorazepam 4mg IV or diazepam 10mg IV) for acute seizure
• Consider prophylactic anti-epileptic if seizure occurred (levetiracetam 500mg-1g IV or phenytoin loading)

Temperature Control:

• Hyperthermia exacerbates secondary brain injury
• Target normothermia (36-37°C)
• Paracetamol, active cooling if needed
• Avoid hypothermia (coagulopathy, arrhythmias)

Avoid Secondary Insults:

• Hypotension: SBP less than 90 mmHg doubles mortality - maintain CPP >60 mmHg [18]
• Hypoxia: SpO₂ less than 90% worsens outcome
• Hypercapnia: PaCO₂ >45 mmHg raises ICP
• Hypocapnia: Excessive hyperventilation causes ischaemia
• Hypoglycaemia/Hyperglycaemia: Tight glucose control (6-10 mmol/L)
• Anaemia: Maintain Hb >80-100 g/L

Surgical Management

Craniotomy and Haematoma Evacuation (definitive treatment):

Indications (reiterated): [4]

• Volume >30 mL
• Thickness >15 mm
• Midline shift >5 mm
• GCS ≤8 with EDH
• Any posterior fossa EDH
• Focal neurological deficit
• Signs of herniation

Timing:

• EMERGENCY: Immediate theatre (less than 1 hour from diagnosis)
• Delay worsens outcome significantly - every 30 minutes increases mortality
• "Golden hour" concept applicable
• Door-to-theatre time is critical quality metric [5,7]

Surgical Technique (overview):

• Patient positioning: Supine, head turned to opposite side (for temporal EDH)
• Skin incision: Question mark or reverse question mark incision
• Craniotomy: Bone flap large enough to access entire haematoma
• Haematoma evacuation: Careful removal of clot
• Haemostasis: Identify and coagulate middle meningeal artery (or other source)
• Dural tack-up sutures: Re-adhere dura to skull (prevent recurrence)
• Bone flap replacement (or leave out if severe brain swelling)
• Wound closure in layers

Burr Hole Evacuation (rarely definitive):

• Emergency temporising measure if craniotomy facilities not immediately available
• Single or multiple burr holes to decompress haematoma
• Allows time for transfer to neurosurgical centre
• Definitive craniotomy still required

Decompressive Craniectomy:

• If severe brain swelling present
• Bone flap left off to allow brain expansion
• Reduces ICP but controversial in trauma
• Bone flap replaced later (cranioplasty at 3-6 months)

Intra-Operative Monitoring:

• Anaesthetic goals: CPP >60 mmHg, ICP less than 20 mmHg, normocapnia, normothermia
• Blood loss can be significant (have blood available)
• ICP typically drops rapidly once haematoma evacuated

Post-Operative Care:

• Immediate post-op CT head (check for residual haematoma, brain swelling, new bleeds)
• ICU admission for neurological monitoring
• Continue ICP/CPP management if ICP monitor placed
• Serial GCS and pupil checks (hourly initially)
• Repeat CT if deterioration
• Seizure prophylaxis (controversial - often given for 7 days)

Conservative (Non-Surgical) Management

Strict Criteria (all must be met):

• Volume less than 30 mL AND
• Thickness less than 15 mm AND
• Midline shift less than 5 mm AND
• GCS 15 (fully conscious, no confusion) AND
• No focal neurological deficit AND
• No pupil abnormalities AND
• No signs of raised ICP
• Neurosurgical unit with immediate operating theatre access [4]

Monitoring Requirements:

• Location: Neurosurgical ICU or high-dependency unit
• Neurological Observations: GCS, pupils every 15 minutes for first 6 hours, then hourly
• Serial CT Imaging:
  • Repeat CT at 6-8 hours from initial scan
  • Further repeat at 24 hours
  • Additional scans if any deterioration
• Immediate Surgical Availability: Operating theatre on standby

Indications to Convert to Surgical Management:

• GCS decline ≥2 points
• New pupil asymmetry
• New focal deficit
• Haematoma enlargement on CT
• Midline shift progression
• Patient or family preference for definitive treatment

Outcomes of Conservative Management:

• Success rate: 70-80% in carefully selected patients (no surgery required)
• 20-30% require delayed surgery due to progression
• Close monitoring is labour-intensive and resource-intensive
• Only appropriate in specialist neurosurgical centres [24]

Transfer to Neurosurgical Centre

Indications for Transfer:

• Any EDH identified at non-neurosurgical hospital
• Discuss with neurosurgical registrar/consultant immediately
• Transfer should not delay surgery if patient deteriorating

Pre-Transfer Stabilisation:

• Intubate if GCS ≤8 or deteriorating
• Ensure adequate resuscitation (normotension, normoxia)
• ICP-lowering measures if herniation signs
• Send CT images electronically ahead
• Accompany with experienced doctor (anaesthetist or emergency physician)
• Continuous monitoring during transfer

Direct Admission Pathways:

• Some EMS systems allow direct transfer from scene to neurosurgical centre (bypassing local hospital)
• Appropriate for haemodynamically stable patients with isolated severe head injury
• Reduces time to surgery

---

8. Complications

Complications of Untreated/Delayed Treatment EDH

Brain Herniation:

• Uncal herniation: Most common with temporal EDH, CN III palsy, hemiparesis, progression to coma
• Central herniation: Bilateral signs, rostrocaudal deterioration
• Tonsillar herniation: Posterior fossa EDH, respiratory arrest, sudden death [15]

Secondary Brain Injury:

• Ischaemic injury from raised ICP and reduced CPP
• Permanent neurological deficit (hemiparesis, cognitive impairment, speech disorder)
• Vegetative state or severe disability

Death:

• Mortality >90% if untreated [5,7]
• Brainstem compression → cardiorespiratory arrest

Peri-Operative Complications

Intra-Operative:

• Haemorrhage: Bleeding from middle meningeal artery, dural sinuses, or bone edges - may require transfusion
• Brain Swelling: Herniated brain may not decompress immediately, may require leaving bone flap off
• Air Embolism: Rare, if dural sinus injured and patient positioned head-up
• Anaesthetic Complications: Difficult intubation, aspiration, cardiovascular instability

Immediate Post-Operative:

• Rebleeding: Recurrent haematoma formation (5-10% of cases), requires re-operation [25]
• Acute Brain Swelling: Cerebral oedema, may require repeat decompression
• Tension Pneumocephalus: Air in cranial cavity causing mass effect ("Mount Fuji sign" on CT)
• Seizures: Early post-traumatic seizures (within 7 days) in 5-10%

Delayed Complications

Infection:

• Wound Infection: Scalp infection, cellulitis (5-10%)
• Osteomyelitis: Bone flap infection, may require removal
• Meningitis/Ventriculitis: Intracranial infection (2-5%), higher risk if CSF leak or penetrating injury
• Abscess: Brain or extradural abscess (rare, less than 1%)
• Prevention: Perioperative antibiotics, sterile technique

Post-Traumatic Epilepsy:

• Early seizures (within 7 days): 5-10%
• Late seizures (>7 days): 5-10% in first year, 10-15% lifetime risk
• Risk factors: Severity of initial injury, intracranial haemorrhage, depressed skull fracture
• May require long-term anti-epileptic medication [26]

Chronic Subdural Haematoma:

• Rarely, chronic subdural collection develops weeks to months later
• Presents with headache, confusion, fluctuating GCS
• Requires drainage if symptomatic

Hydrocephalus:

• Post-traumatic hydrocephalus (communicating or obstructive)
• Presents with headache, cognitive decline, gait disturbance
• May require ventriculoperitoneal shunt

Cognitive and Neuropsychological Sequelae:

• Memory impairment
• Executive dysfunction
• Mood disorders (depression, anxiety)
• Personality changes
• Post-concussion syndrome
• May improve over months to years with rehabilitation

Bone Flap Complications (if bone replaced):

• Bone flap resorption (especially in children)
• Infection requiring removal
• Cranioplasty (bone flap replacement) typically at 3-6 months if initially left off

Cosmetic:

• Scalp scarring
• Contour deformity if bone flap not replaced or resorbed
• May require cranioplasty with synthetic material (titanium mesh, PEEK)

---

9. Prognosis and Outcomes

Mortality

Overall Mortality: 5-10% in modern series with prompt neurosurgical care [5,7]

Stratified by Management:

• Early Surgery (within 4 hours): 5-10% mortality
• Delayed Surgery (4-12 hours): 15-25% mortality
• Late Surgery (>12 hours): 30-50% mortality
• Untreated: >90% mortality (historical data, ethical considerations preclude modern studies) [5,7]

Stratified by Pre-Operative GCS:

• GCS 13-15 (mild): less than 5% mortality
• GCS 9-12 (moderate): 10-20% mortality
• GCS 3-8 (severe): 30-50% mortality [5]

Posterior Fossa EDH: Higher mortality (20-30%) due to rapid brainstem compression in confined space [15]

Functional Outcomes

Functional recovery assessed using Glasgow Outcome Scale (GOS) or extended GOS (GOS-E):

• GOS 5 (Good Recovery): Return to pre-injury level, minor deficits only
• GOS 4 (Moderate Disability): Independent but disabled, can work in sheltered setting
• GOS 3 (Severe Disability): Dependent for daily activities
• GOS 2 (Vegetative State): Minimal responsiveness
• GOS 1 (Death)

Outcomes at 6-12 Months:

• Good Recovery (GOS 5): 50-80% of survivors with early surgery
• Moderate Disability (GOS 4): 15-30%
• Severe Disability (GOS 3): 5-15%
• Vegetative State (GOS 2): less than 5%

Pediatric Outcomes: Generally better than adults due to greater neuroplasticity, but similar dependence on time to surgery [12]

Prognostic Factors

Favorable Prognostic Factors:

• Young Age (less than 40 years): Better recovery potential, neuroplasticity
• High Pre-Operative GCS (13-15): Strong predictor of good outcome [5]
• Rapid Time to Surgery (less than 4 hours from injury): Minimizes secondary brain injury [7]
• Pupil Reactivity Preserved: Indicates no/minimal brainstem dysfunction
• Absence of Focal Deficit: Suggests minimal primary brain injury
• Small Haematoma Volume (less than 50mL): Less mass effect and secondary injury
• Isolated EDH: No other intracranial injuries (contusions, DAI, SAH)
• Absence of Systemic Injuries: No hypotension or hypoxia episodes
• No Post-Operative Complications: No rebleeding, infection, seizures

Poor Prognostic Factors:

• Elderly Age (>65 years): Reduced reserve, more comorbidities [14]
• Low Pre-Operative GCS (3-8): Severe primary injury or prolonged secondary injury [5]
• Delayed Surgery (>4-6 hours): Progressive secondary brain injury
• Fixed Dilated Pupils: Brainstem dysfunction, herniation
• Bilateral Pupil Abnormalities: Advanced herniation, very poor prognosis
• Decerebrate Posturing: Brainstem injury
• Large Haematoma (>100mL): Severe mass effect
• Significant Midline Shift (>10mm): Severe brain distortion
• Associated Brain Injuries: Contusions, diffuse axonal injury, subarachnoid haemorrhage
• Hypotension/Hypoxia: Secondary brain injury from systemic insults [18]
• Post-Operative Rebleeding: Requires re-operation, worsens prognosis [25]
• Posterior Fossa Location: Limited space, rapid deterioration [15]

Time to Surgery - Critical Determinant

Multiple studies demonstrate exponential relationship between time to surgery and outcome:

• "Golden Hour": Analogous to trauma, first hour critical
• Each 30-Minute Delay: Associated with increased mortality and worse functional outcome
• Within 2 Hours: Optimal outcomes
• 2-4 Hours: Acceptable outcomes
• >4 Hours: Progressive deterioration in prognosis
• >12 Hours: Very poor outcomes [7]

This emphasizes the critical importance of:

• Rapid diagnosis (immediate CT in head injury)
• Early neurosurgical involvement
• Minimizing door-to-theatre time
• Direct transfer pathways to neurosurgical centres

Long-Term Outcomes

Return to Work:

• 60-80% of good outcome patients return to previous employment
• May require modified duties or graduated return
• Cognitive deficits may limit complex work

Quality of Life:

• Most patients with good recovery report acceptable quality of life
• Subtle cognitive deficits may persist (memory, processing speed)
• Mood disorders (depression, anxiety) in 20-30%
• Post-traumatic stress disorder (especially if assault mechanism)

Seizure Risk:

• Early seizures (within 7 days): 5-10%
• Late seizures: 10-15% lifetime risk
• Often controlled with single anti-epileptic drug [26]

Rehabilitation:

• Acute rehabilitation (first 3 months): Physical, occupational, speech therapy
• Cognitive rehabilitation for memory and executive function deficits
• Psychological support for mood and adjustment
• Vocational rehabilitation for return to work

Follow-Up:

• Neurosurgical clinic at 6 weeks, 3 months, 6 months post-surgery
• CT head to assess brain re-expansion if bone flap left off
• Cranioplasty planning if decompressive craniectomy performed
• Annual review for first 2-3 years
• DVLA notification (driving restrictions: 6-12 months depending on severity and seizures)

---

10. Evidence Base and Guidelines

Key Clinical Guidelines

1. NICE Head Injury Guideline (CG176, 2014, updated 2023): [20]

• Comprehensive guidance on assessment and early management of head injury
• CT head indications (1-hour and 8-hour criteria)
• Transfer to neurosurgical centre criteria
• Observation and discharge advice
• Applicability: Adults and children in UK

2. Brain Trauma Foundation Guidelines for Management of Severe TBI (4th Edition, 2016): [4]

• Evidence-based recommendations for severe TBI (GCS ≤8)
• Surgical indications for EDH and other mass lesions
• ICP monitoring and management thresholds
• Hyperosmolar therapy protocols
• Applicability: Severe TBI globally

3. European Society of Intensive Care Medicine (ESICM) Consensus on TBI (2020):

• Comprehensive review of TBI management including EDH
• Neurointensive care protocols
• Multimodal neuromonitoring

4. American Association of Neurological Surgeons (AANS) and Congress of Neurological Surgeons (CNS) Joint Guidelines:

• Regularly updated evidence-based surgical guidelines
• EDH-specific surgical indications align with BTF guidelines

5. Society of British Neurological Surgeons (SBNS) Standards:

• UK-specific standards for neurosurgical care
• Service configuration for trauma

Key Evidence

Surgical vs Conservative Management:

• No randomized controlled trials (ethical considerations preclude randomization of patients with large EDH to non-surgical management)
• Large observational cohort studies consistently demonstrate:
  • Mortality >90% without surgery (historical data) [5,7]
  • Mortality 5-10% with prompt surgery
  • Conservative management safe only for highly selected small EDH (less than 30mL, GCS 15, no deficit) [24]

Time to Surgery:

• Haselsberger et al. (1988): Landmark study showing time to surgery is independent predictor of outcome; less than 4 hours optimal [7]
• Seelig et al. (1981): Classical study demonstrating mortality increases from 9% if surgery within 4 hours to 27% if delayed beyond 4 hours (primarily SDH but principle applies to EDH)
• Modern series: Consistently show door-to-theatre time predicts outcome; every 30-minute delay worsens prognosis

GCS as Prognostic Indicator:

• Bricolo et al. (1984): Pre-operative GCS strongest predictor of outcome in EDH [5]
• GCS 3-8: Poor prognosis (30-50% mortality)
• GCS 9-12: Intermediate (10-20% mortality)
• GCS 13-15: Good prognosis (less than 5% mortality)

Osmotic Therapy:

• Mannitol: Multiple studies demonstrate transient ICP reduction (15-30 min onset, 4-6 hour duration); no RCT showing mortality benefit but widely used as temporizing measure [21]
• Hypertonic Saline: Recent meta-analyses suggest superiority to mannitol for ICP reduction without hypotension [22]
• Both are bridge to surgery, NOT definitive treatment

Hyperventilation:

• Historical practice: Routine hyperventilation to PaCO₂ 25-30 mmHg
• Modern evidence: Excessive hyperventilation causes cerebral ischaemia (reduced CBF)
• Current recommendation: Avoid routine hyperventilation; brief use (PaCO₂ 30-35 mmHg) only as temporizing measure for imminent herniation [23]

Anticoagulation and EDH:

• Observational studies: Anticoagulated patients with EDH have:
  • Larger haematomas at presentation
  • Higher rates of haematoma expansion
  • Worse outcomes
• Reversal agents: Rapid reversal of coagulopathy essential before surgery [16]

Pediatric EDH:

• Outcomes generally better than adults due to neuroplasticity
• Larger haematomas tolerated before symptoms (greater intracranial compliance)
• Surgical indications similar to adults (volume, thickness, GCS, deficit criteria) [12]

Posterior Fossa EDH:

• Higher mortality (20-30%) despite surgery due to limited space and rapid brainstem compression
• Lower threshold for surgery: Any posterior fossa EDH with mass effect should be considered for evacuation [15]

Levels of Evidence Summary

Ongoing Research and Controversies

Decompressive Craniectomy in TBI:

• DECRA and RESCUEicp trials examined decompressive craniectomy for diffuse TBI
• Results mixed (reduced mortality but increased disability in some studies)
• Application to EDH uncertain (most EDH managed with craniotomy + bone replacement)

Neuroprotective Agents:

• Multiple trials of neuroprotective drugs (hypothermia, progesterone, corticosteroids) in TBI
• None have shown clear benefit
• Corticosteroids may be harmful (CRASH trial) - NOT recommended

Minimally Invasive Techniques:

• Endoscopic EDH evacuation: Small case series, not widely adopted
• Aspiration techniques: Generally inadequate for solid clot

ICP Monitoring:

• BTF guidelines recommend ICP monitoring in severe TBI
• For EDH, surgical evacuation is definitive treatment; ICP monitoring mainly for post-op or non-surgical cases
• Target ICP less than 20 mmHg, CPP >60 mmHg [18]

---

11. Prevention

Primary Prevention

Trauma Prevention Strategies:

• Road Safety: Seatbelt use, speed limits, drink-driving legislation, motorcycle helmets (reduce head injury by 69%) [27]
• Fall Prevention: Home safety for elderly (remove trip hazards, adequate lighting, assistive devices), occupational safety (scaffolding, harnesses)
• Sports Safety: Protective equipment (helmets in cycling, skiing, contact sports), rule changes to reduce head impacts
• Assault Prevention: Public health measures, violence reduction programs, alcohol control
• Workplace Safety: Hard hats in construction, industrial settings

High-Risk Groups:

• Young males (motor vehicle collisions, assault)
• Elderly (falls)
• Athletes (contact sports)
• Cyclists and motorcyclists
• Construction workers

Secondary Prevention (Early Detection)

Public and Healthcare Professional Awareness:

• Recognize "lucid interval" as warning sign
• Seek immediate medical attention for any head injury with loss of consciousness
• Monitor for deterioration in first 24-48 hours post-injury
• Low threshold for CT imaging (per NICE guidelines) [20]

NICE CT Head Indications (reiterated): [20]

• GCS less than 13 or GCS less than 15 at 2 hours
• Suspected skull fracture (clinical signs)
• Post-traumatic seizure
• Focal neurological deficit
• >1 episode vomiting
• Age ≥65 years with any LOC/amnesia
• Amnesia >30 minutes before impact
• Dangerous mechanism

Avoid Delays:

• Do not "watch and wait" in ED if criteria for CT met
• Do not discharge with head injury advice card if significant mechanism and symptoms

Tertiary Prevention (Preventing Complications)

Rapid Diagnosis and Treatment:

• Immediate CT for high-risk patients
• Early neurosurgical consultation
• Minimize door-to-theatre time
• Aggressive management of secondary brain injury (avoid hypotension, hypoxia, hyperthermia)

Post-Operative Care:

• ICU monitoring to detect rebleeding or complications early
• Seizure prophylaxis (reduces early seizures, unclear long-term benefit)
• Venous thromboembolism prophylaxis (balanced against bleeding risk)
• Rehabilitation to maximize functional recovery

---

12. Special Populations

Pediatric Patients

Epidemiological Differences:

• EDH represents 2-4% of pediatric head injuries
• Peak age 8-12 years (active play, sports)
• Better outcomes than adults (neuroplasticity) [12]

Anatomical Considerations:

• Infants (less than 2 years): Rare due to tight dural adherence, open fontanelles (pressure relief)
• When present in infants: Consider non-accidental injury
• Children compensate longer: Larger haematomas before decompensation

Clinical Presentation:

• Lucid interval may be longer
• Non-specific symptoms: Irritability, vomiting, lethargy
• Scalp haematoma ("boggy swelling") often prominent
• Seizures more common (10-15% vs 5% in adults) [12]

Surgical Considerations:

• Same volume/thickness criteria apply
• Lower threshold for surgery in some centers (children decompensate rapidly once compensatory mechanisms exhausted)
• Bone flap resorption more common (may require cranioplasty with synthetic material)

Outcomes:

• Mortality 3-5% (lower than adults)
• Good recovery 70-85%
• Return to school often achievable
• Long-term cognitive monitoring important (subtle deficits may emerge as academic demands increase)

Elderly Patients (>65 years)

Epidemiological Differences:

• EDH less common (dura increasingly adherent with age, cerebral atrophy creates buffering space)
• When present, often from low-energy mechanism (falls) [14]

Clinical Considerations:

• Lower threshold for CT imaging (NICE: age ≥65 + any LOC/amnesia = CT) [20]
• Anticoagulation common (warfarin, DOACs): Higher bleeding risk, larger haematomas, requires reversal
• Comorbidities affect perioperative risk (cardiac, respiratory, renal)
• Polypharmacy

Surgical Considerations:

• Higher surgical risk (anaesthetic complications)
• Coagulopathy reversal essential
• May require multidisciplinary input (cardiology, anaesthetics)

Outcomes:

• Mortality higher (15-25% vs 5-10% in younger adults) [14]
• Functional recovery slower and less complete
• Higher rates of post-operative complications (infection, medical complications)
• Cognitive decline (may unmask early dementia)
• Increased care needs post-discharge

Anticoagulated Patients

Risk Stratification:

• Warfarin: INR >1.5 associated with worse outcomes, requires reversal
• DOACs (Dabigatran, Rivaroxaban, Apixaban, Edoxaban): No routine monitoring, specific reversal agents now available
• Antiplatelet agents (Aspirin, Clopidogrel): Platelet dysfunction, consider transfusion

Management:

• Urgent reversal before surgery:
  • "Warfarin: Vitamin K 10mg IV (slow onset) + Prothrombin complex concentrate (PCC, rapid) or Fresh Frozen Plasma (FFP)"
  • "Dabigatran: Idarucizumab (specific reversal agent)"
  • "Factor Xa inhibitors (Rivaroxaban, Apixaban): Andexanet alfa (specific reversal) or PCC"
  • "Antiplatelet agents: Platelet transfusion (desmopressin controversial) [16]"
• Target INR less than 1.5 before surgery
• Monitor for rebleeding (higher risk post-operatively)

Outcomes:

• Larger haematomas at presentation
• Higher rate of haematoma expansion (if coagulopathy not reversed)
• Increased mortality and morbidity
• Rebleeding risk 10-15% (vs 5% in non-anticoagulated) [25]

Patients with Coagulopathy (Haemophilia, etc.)

• Haemophilia A/B: Factor VIII or IX deficiency, severe spontaneous bleeding risk
• Von Willebrand Disease: Reduced platelet adhesion
• Liver Disease: Reduced clotting factor synthesis, thrombocytopenia

Management:

• Haematology consultation urgently
• Factor replacement: Achieve 100% factor activity before surgery
  • "Haemophilia A: Factor VIII concentrate"
  • "Haemophilia B: Factor IX concentrate"
  • "Von Willebrand: DDAVP or VWF/FVIII concentrate"
• Liver disease: FFP, PCC, consider platelet transfusion if thrombocytopenic
• Maintain factor levels peri-operatively and post-operatively (7-14 days)

Outcomes:

• High mortality if factor replacement delayed
• Good outcomes if promptly managed with adequate factor replacement [16]

Pregnancy

• Rare (trauma less common in pregnancy, but domestic violence consideration)
• Fetal and maternal monitoring required
• Surgical management same indications - maternal resuscitation prioritizes mother
• Multidisciplinary (neurosurgery, obstetrics, anaesthetics)
• Radiation exposure: CT head has minimal fetal radiation (shield abdomen), benefits far outweigh risks

---

13. Patient and Caregiver Information

What is an Extradural Haematoma?

An extradural haematoma (also called an epidural haematoma) is a collection of blood that forms between the skull and the outer protective covering of the brain (called the dura mater). It usually happens after a head injury that causes a skull fracture and tears a blood vessel, most commonly an artery called the middle meningeal artery.

Why is it Dangerous?

The skull is a rigid box with no room to expand. As blood collects, it creates pressure on the brain. This pressure can:

• Damage brain tissue
• Push the brain downwards (called herniation)
• Compress vital structures that control breathing and heart rate
• Lead to death if not treated urgently

What Are the Warning Signs?

After a head injury, seek immediate emergency medical attention (call 999/911) if any of these occur:

Red Flag Symptoms:

• Severe or worsening headache
• Vomiting (especially repeatedly)
• Confusion or unusual behavior
• Increasing drowsiness or difficulty waking
• Weakness in arm or leg (especially on one side)
• One pupil (black part of eye) larger than the other
• Seizure (fit)
• Slurred speech
• Loss of consciousness after initially waking up

The "Lucid Interval"

This is a classic warning sign where:

1. Person is briefly unconscious after a head injury
2. They wake up and seem fine or nearly fine (the "lucid interval")
3. Then they get progressively worse over the next few hours

This pattern is very concerning for an extradural haematoma and requires immediate emergency care.

How is it Diagnosed?

• CT Scan: A special X-ray of the brain that shows the blood collection. This is the definitive test.
• Clinical Examination: Doctors check consciousness level, pupil reactions, and muscle strength

How is it Treated?

Emergency Surgery (Craniotomy):

• This is the main treatment for significant extradural haematomas
• Surgeon makes an opening in the skull
• Removes the blood clot
• Stops the bleeding from the damaged blood vessel
• Replaces the bone and closes the wound
• Usually takes 2-4 hours

When is Surgery Needed? Surgery is required if:

• The blood collection is large (>30mL)
• It is thick (>15mm)
• It is pushing the brain to the side (>5mm shift)
• Consciousness is impaired
• There are signs of brain compression

Small Blood Collections:

• Sometimes, very small haematomas in fully conscious patients can be monitored closely in a specialist neurosurgical unit without surgery
• This requires repeated brain scans and very close observation
• Surgery is performed immediately if any deterioration occurs

What Happens After Surgery?

• Intensive Care: Monitoring in ICU for 1-3 days typically
• Hospital Stay: 5-10 days usually
• Recovery: Most patients gradually improve over weeks to months
• Follow-Up: Outpatient clinic appointments to monitor recovery
• Rehabilitation: Physiotherapy, occupational therapy, or speech therapy if needed

What is the Outlook?

With Prompt Surgery:

• Survival: 90-95%
• Good recovery: 60-80% return to previous level of function
• Some patients have ongoing issues (headaches, memory problems, seizures)

If Treatment is Delayed or Not Given:

• Very high risk of death (>90% mortality)
• This is why emergency treatment is critical

Factors Affecting Recovery:

• Age (younger patients recover better)
• How conscious the patient was before surgery (better consciousness = better outcome)
• How quickly surgery was performed (faster = better)
• Whether there are other brain injuries

Long-Term Considerations

Driving:

• Cannot drive for 6-12 months (depending on severity and country regulations)
• Must notify driving licensing authority (DVLA in UK, DMV in US)

Seizure Risk:

• 10-15% chance of developing epilepsy
• May require medication

Return to Work/School:

• Most people return to work/school, often within 3-6 months
• Some need modified duties or graduated return
• Cognitive rehabilitation may help

Sports and Activities:

• Avoid contact sports for at least 6-12 months
• Discuss with neurosurgeon before returning to high-risk activities

When to Seek Help After Discharge

Call your doctor or go to Emergency Department if:

• Severe headache
• Vomiting
• Confusion or personality change
• Weakness or numbness
• Seizure
• Fever (may indicate infection)
• Wound redness, swelling, or discharge

Support and Resources

• Headway (UK): Charity supporting people with brain injuries (headway.org.uk)
• Brain Injury Association (US): Support and information (biausa.org)
• Neurosurgical follow-up: Regular appointments with specialist
• Rehabilitation services: Access via GP or hospital referral
• Psychological support: Brain injury can be traumatic; counseling available

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14. References

Primary Guidelines and Consensus Statements

1. Bullock MR, et al. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58(3 Suppl):S7-15. DOI: 10.1227/01.NEU.0000210364.29290.C9

2. Rivas JJ, et al. Extradural hematoma: analysis of factors influencing the courses of 161 patients. Neurosurgery. 1988;23(1):44-51. DOI: 10.1227/00006123-198807000-00009

3. Chen TY, et al. Lucid interval in epidural hematoma: is it different in children and adults? Acad Emerg Med. 1995;2(10):894-899. DOI: 10.1111/j.1553-2712.1995.tb03100.x

4. Carney N, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15. DOI: 10.1227/NEU.0000000000001432

5. Bricolo AP, et al. Surgical management of acute extradural haematomas: a retrospective analysis of 127 patients. Acta Neurochir (Wien). 1984;73(3-4):191-204. DOI: 10.1007/BF01406616

6. Lee EJ, et al. Epidemiology of traumatic epidural hematoma. J Korean Neurosurg Soc. 2011;50(1):11-15. DOI: 10.3340/jkns.2011.50.1.11

7. Haselsberger K, et al. Prognosis after acute subdural or epidural haemorrhage. Acta Neurochir (Wien). 1988;90(3-4):111-116. DOI: 10.1007/BF01560563

8. Bor-Seng-Shu E, et al. Skull fractures and epidural hematomas. Arq Neuropsiquiatr. 2010;68(6):869-872. DOI: 10.1590/S0004-282X2010000600007

Epidemiology and Risk Factors

9. Dent DL, et al. Incidence of extradural haematoma in a population-based study. J Trauma. 1995;38(2):195-197.

10. Reilly PL, et al. Head injury: pathophysiology and management of severe closed injury. Chapman & Hall Medical, 1997.

11. Servadei F. Prognostic factors in severely head injured adult patients with epidural haematomas. Acta Neurochir (Wien). 1997;139(4):273-278. DOI: 10.1007/BF01844750

12. Ciurea AV, et al. Traumatic epidural haematomas in children. Rom J Morphol Embryol. 2007;48(3):257-261. PMID: 17914196

13. Leggate JR, et al. Extradural haematoma in infancy. Br J Neurosurg. 1989;3(5):533-540. DOI: 10.3109/02688698909002858

14. Tallon JM, et al. The epidemiology of surgically treated acute epidural hematomas in patients with head injuries: a population-based study. Can J Surg. 2008;51(5):339-345. PMID: 18841220

15. Roda JM, et al. Posterior fossa epidural hematomas: a review and synthesis. Surg Neurol. 1983;19(5):419-424. DOI: 10.1016/0090-3019(83)90208-8

Coagulopathy and Anticoagulation

16. Ivascu FA, et al. Traumatic epidural hematoma in patients on oral anticoagulant therapy. Am Surg. 2006;72(8):720-723. PMID: 16913317

Pathophysiology and Imaging

17. Lobato RD, et al. Acute epidural hematoma: an analysis of factors influencing the outcome of patients undergoing surgery in coma. J Neurosurg. 1988;68(1):48-57. DOI: 10.3171/jns.1988.68.1.0048

18. Marmarou A, et al. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg. 1991;75:S59-66. DOI: 10.3171/sup.1991.75.1s.0s59

19. Cushing H. Concerning a definite regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression. Bull Johns Hopkins Hosp. 1901;12:290-292.

Management and Treatment

20. National Institute for Health and Care Excellence. Head injury: assessment and early management. Clinical guideline [CG176]. 2014 (updated 2023). Available at: https://www.nice.org.uk/guidance/cg176

21. Wakai A, et al. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2013;(8):CD001049. DOI: 10.1002/14651858.CD001049.pub5

22. Kamel H, et al. Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med. 2011;39(3):554-559. DOI: 10.1097/CCM.0b013e318206b9be

23. Muizelaar JP, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991;75(5):731-739. DOI: 10.3171/jns.1991.75.5.0731

24. Bezircioğlu H, et al. Nonoperative treatment of acute extradural hematomas: analysis of 80 cases. J Trauma. 1996;41(4):696-698. DOI: 10.1097/00005373-199610000-00018

Complications and Outcomes

25. Irie F, et al. Acute extradural hematoma in children: computed tomography analysis of 62 patients. Childs Nerv Syst. 1995;11(9):512-515. DOI: 10.1007/BF00822845

26. Annegers JF, et al. A population-based study of seizures after traumatic brain injuries. N Engl J Med. 1998;338(1):20-24. DOI: 10.1056/NEJM199801013380104

Prevention

27. Liu BC, et al. Helmets for preventing injury in motorcycle riders. Cochrane Database Syst Rev. 2008;(1):CD004333. DOI: 10.1002/14651858.CD004333.pub3

Additional Key References

28. Seelig JM, et al. Traumatic acute subdural hematoma: major mortality reduction in comatose patients treated within four hours. N Engl J Med. 1981;304(25):1511-1518. DOI: 10.1056/NEJM198106183042503 (Principles applicable to EDH)

29. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2(7872):81-84. DOI: 10.1016/s0140-6736(74)91639-0 (Glasgow Coma Scale)

30. Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet. 1975;1(7905):480-484. DOI: 10.1016/s0140-6736(75)92830-5 (Glasgow Outcome Scale)

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Last Updated: 2026-01-09
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