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Extradural Haemorrhage (EDH)

Emergency Neurological Life Support Traumatic Brain Injury Protocol Version 6.0. Last updated: Dec 2024.

NICE Guideline [NG232] Head injury: assessment and early management. Published: May 2023.

Extradural Haemorrhage (EDH)

Extradural haemorrhage (EDH), also known as epidural haemorrhage, is an acute extra-axial intracranial haemorrhage occurring between the skull and dura.

This updated UKMLA guide to EDH is based on ENLS guideline, which covers: causes, risk factors, symptoms, diagnosis, and management.

Definition and Anatomy

Intracranial haemorrhage is a broad term referring to any bleeding within the skull (cranial vault). It can be categorised into:

Extra-axial haemorrhage = bleeding outside the brain parenchyma Intra-axial haemorrhage = bleeding within the brain parenchyma
Which includes:
  • Extradural haemorrhage (EDH)
  • Subdural haemorrhage (SDH)
  • Subarachnoid haemorrhage (SAH)
Which includes:
  • Intracerebral haemorrhage
  • Intraventricular haemorrhage

There are 3 layers of the meninges, from superficial to deep:

  • Dura
  • Arachnoid
  • Pia

Extra-axial haemorrhages are named according to where bleeding occurs in relation to these layers:

  • Extradural haemorrhage (EDH) = bleeding outside the dura, between the skull and dura
  • Subdural haemorrhage (SDH) = bleeding under the dura, between the dura and arachnoid
  • Subarachnoid haemorrhage (SAH) = bleeding under the arachnoid, between the arachnoid and pia

Overview of Intracranial Extra-Axial Haemorrhage

The 3 main extra-axial haemorrhages:

Haemorrhage type Location Typical cause / source Classic CT appearance High-yield clinical presentation
Extradural haemorrhage (EDH) Between the skull and dura Middle meningeal artery Biconvex / lens-shaped hyperdense mass Head injury followed by a possible lucid interval, then rapid deterioration
Subdural haemorrhage (SDH) Between the dura and arachnoid Bridging veins Crescent-shaped mass (hyperdense in acute; hypodense in chronic) Confusion, focal neurology, reduced GCS, esp. in elderly, alcohol excess, anticoagulation use
Subarachnoid haemorrhage (SAH) Between the arachnoid and pia Ruptured aneurysm Hyperdense signal in the sulci, fissures, or basal cisterns Thunderclap headache, meningism, reduced GCS

Causes

Primary cause: blunt head trauma, usually as part of a traumatic brain injury [Ref]

  • Most common mechanism: temporal bone fracture (classically at the pterion) → laceration of the middle meningeal artery
  • Less commonly, bleeding may arise from the anterior meningeal artery
  • Venous bleeding accounts for up to 10% of cases (usually when a dural venous sinus or diploic veins are injured)

Non-traumatic cases are rare, potential causes include coagulopathies, bleeding disorders, AV malformation, AV fistulas, haemorrhagic tumours, severe craniofacial infections [Ref]

Risk Factors

[Ref]

  • Adolescents and young adults (mean age: 20-30 y/o)
  • Males
  • Individuals who are involved in high-impact activities or at higher risk of road-traffic accidents
  • Use of anticoagulants and antiplatelets

Clinical Features

Small EDHs can be asymptomatic [Ref]

Classic presentation (only seen in ~14-21% of patients): [Ref]

  1. Initial loss of consciousness immediately after the head trauma
  2. “Lucid interval” – transient period of complete recovery
  3. Rapid neurological deterioration

Other symptoms: [Ref]

  • Worsening headache
  • Nausea and vomiting
  • Focal or generalised seizures

Complications

If the haemorrhage continues to enlarge, it can cause progressive elevation in ICP and can lead to uncal herniation, which can cause: [Ref]

  • Ipsilateral fixed, dilated pupil or asymmetrical pupils (due to CN III compression)
  • Contralateral upper motor neuron lesion signs
  • Cushing reflex – triad of ↑ BP (or wide pulse pressure) + bradycardia + irregular breathing (Cheyne-Stokes breathing)

A very large EDH may rarely cause the Kernohan notch phenomenon, a false localising sign where the patient develops ipsilateral motor weakness relative to the haematoma. This occurs when severe mass effect pushes the brain across the midline, compressing the opposite cerebral peduncle against the tentorial edge. [Ref]

Assessment and Management

Since most EDHs result from blunt head trauma / traumatic brain injury, initial assessment and management should follow a standard TBI approach.

1. Standard TBI Assessment and Management

A-E primary survey and management (to be started pre-hospitally and continued in the hospital):

Component Assessment and investigations Management
A & B – Airway and breathing
  • Assess airway patency
  • Monitor oxygen saturation
  • Secure the airway
  • Rapid-sequence intubation if post-resuscitation GCS is 8 or less
  • Maintain oxygenation (≥94%)
  • Target normal ventilation
C – Circulation
  • Monitor BP
  • FAST exam to check for internal bleeding
  • Clotting studies (PT/aPTT/INR, platelet, fibrinogen)
  • Obtain IV or IO access
  • Avoid hypotension
  • Maintain systolic BP ≥100-110 mmHg
  • Correct any coagulopathies
    • If on warfarin → IV vitamin K + PCC
    • If on apixaban / rivaroxaban → andexanet alfa
    • If on dabigatran → idarucizumab
    • If on heparin → protamine sulfate
    • If patient on antiplatelets → platelet transfusion +/- desmopressin
D – Disability
  • Calculate GCS
  • Assess pupil (size, shape and reactivity)
  • Cervical collar and maintain strict spinal immobilisation until cervical spine stability can be established
E – Exposure
  • Expose the patient properly to assess for traumatic injuries
  • Maintain normothermia
  • Avoid prolonged exposure as it can result in hypothermia

2. EDH Investigation and Diagnosis

Indications for Urgent CT Head

Non-contrast CT head is the 1st line investigation for suspected EDH. It should be performed urgently once the primary survey is complete, and the patient is stable enough for imaging.

Perform a non-contrast CT head within 1 hour if ANY of the following are present (based on NICE NG232):

  • GCS ≤12 on initial assessment
  • GCS <15 at 2 hours after injury
  • Suspected open / depressed skull fracture
  • Signs of basal skull fracture
  • Post-traumatic seizure
  • Focal neurological deficit
  • >1 vomiting episode

See the Head Injury in Adults article for other indications of CT.

CT Findings of EDH

Classic CT findings: biconvex or lens-shaped (lentiform) hyperdense mass

  • Location: extra-axial (on the edge of the skull)
  • Hyperdense = bright white on non-contrast CT
  • Memory aid: EDH can look like a “lemon” on CT.

Remember: suspected EDH (or general head injury / TBI) should be first investigated with a non-contrast CT head.

Acute blood already appears bright/white on CT, so contrast is not needed initially. Giving contrast can also make blood vessels and enhancing structures appear bright, which may obscure or mimic acute haemorrhage.

Other radiographic features:

  • Associated skull fractures (esp. temporal bone)
  • The haemorrhage rarely crosses the cranial suture lines – as the dura is firmly attached at the cranial sutures
  • “Swirl sign” – a relatively darker (hypodense) region within the bright (hyperdense) haemorrhage – indicates active uncoagulated bleeding and is associated with worse outcomes (larger volume, higher risk of expansion)

3. EDH Management

If EDH is suspected / diagnosed, patient should be referred to neurosurgery for assessment and management.

EDH-Specific Management

There are 2 main definitive management options:

Management approach Indications Description [Ref]
Operative (neurosurgical) ANY of the following:
  • Haemorrhage volume >30 cm3
  • Haemorrhage thickness >15 mm
  • Midline shift that is >5 mm
  • GCS ≤8
Standard procedure: craniotomy with haematoma evacuation

Burr hole evacuation is a temporary emergency procedure used only when definitive management (a full craniotomy) is unavailable

Non-operative (conservative) Consider if none of the above (indications for surgery) is present No active treatment

Goal: allow the body to naturally reabsorb the blood

Closed observation is necessary to ensure the bleed does NOT expand:

  • Close clinical observation (serial neurological examination and charting)
  • Radiological surveillance (follow-up non-contrast CT head typically performed 6 hours after initial scan)

Complication / Other Management

Clinical aspect / complication Management
ICP monitoring Insertion of an ICP monitor is indicated with ANY of the following:
  • Abnormal CT + GCS ≤8
  • Normal CT + GCS ≤8 + at least 2 of the following
    • >40 y/o
    • Motor posturing
    • Systolic BP <90 mmHg
Raised ICP If monitored, ICP >22 mmHg requires prompt treatment:
  • Initial steps
    • Elevate the bed to 30 degrees
    • Optimise sedation and analgesia
  • Hyperosmolar therapy (mannitol or hypertonic saline)
  • Consider temporary hyperventilation
Seizure prophylaxis Cortical irritation from the blood increases the risk of seizures

Levetiracetam is the preferred medication

Do NOT routinely perform or give the following:

  • Corticosteroids
  • Prophylactic hypothermia
  • Prophylactic hyperventilation (in the absence of signs of raised ICP and brain herniation)

References

Related Articles

Head Injury in Adults

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