Extradural Haematoma

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Extradural haematoma (EDH) is defined as an acute bleed between the dura mater and the inner surface of the skull. This then causes increased intracranial pressure, which puts vital brain structures at risk.

Patients most commonly affected by extradural haematomas (EDH) are adult males between 20-30 years old. This is because they are more likely to experience a traumatic injury.



An extradural haematoma is most commonly caused by skull trauma in the temporoparietal area, usually following falls, assaults or sporting injuries. An EDH is found with a skull fracture in 75% of cases.

The pterion, an anatomical landmark, is located in this area. It is vulnerable to trauma as it is the fusion point between the parietal, frontal, sphenoid and temporal bones.

The middle meningeal artery is involved in 75% of EDH as it lies underneath the pterion, which leads to a high risk of arterial rupture.

EDH can also occur secondary to the rupture of a vein, particularly if the middle meningeal vein or dural sinuses are involved.

Rarely, EDH can occur secondary to arteriovenous abnormalities or other systemic bleeding disorders.

Diagram showing the bones of the skull with the pterion marked in red
Figure 1: A diagram showing the bones of the skull with the pterion marked in red 2


As the volume of blood leaking from the damaged blood vessel into the extradural space increases, it begins to strip the outer layer of the meninges, the dura mater, away from the skull.

This often leads to the “lemon” shaped-bleed, which is seen on CT and MRI imaging.

If the extradural haematoma continues to increase in size, the pressure inside the cranium (intracranial pressure) also increases.

Without treatment, this increased pressure can cause damage to the brain through a midline shift (displacement of the brain) and tentorial herniation (see figure 2).

A rising level of intracranial pressure (ICP) will eventually lead to brainstem death.

Diagram showing the different types of brain herniation
Figure 2: Diagram showing the different types of brain herniation 5


Clinical presentation

This section has been split into different sections: first, a summary of the typical history of EDH and then a more detailed stage-by-stage look at a typical patient presentation.

History overview

  • History of head trauma
  • Immediate fluctuating level of consciousness following the trauma before appearing lucid (i.e. conscious)
  • Rapid deterioration some time following regaining consciousness


Stage-by-stage presentation

Early signs

Severe headache:

  • Occurs after the initial impact and can persist


Initial loss or fluctuance in consciousness:

  • May present vaguely as tiredness or confusion


Period of lucidity after initial loss of consciousness:

  • Usually lasts between 6 and 8 hours
  • May last for days depending on the speed of the haematoma growth


Late signs

Rapid deterioration and loss of consciousness:

  • GCS score will begin to drop as intracranial pressure rises and the brainstem begins to herniate



  • Focal neurological deficits become apparent in the eyes
  • This is due to compression of the cranial nerves
  • For example, CNIII (oculomotor nerve) palsy may result in fixed dilation of the ipsilateral pupil. This is colloquially known as a “blown pupil”.


Muscle weakness:

  • Hemiparesis typically begins on the contralateral side to the EDH due to compression of the ipsilateral motor cortex.
  • Hemiparesis may become bilateral as the ICP increases and the brainstem becomes compressed.
  • Ipsilateral hemiparesis can also occur through Kernohan’s phenomenon (extensive midline shift of the brain due to mass effect from the growing extradural haematoma). 7


Upper motor neuron signs:

  • Positive Babinski’s sign (upgoing toes), hyperreflexia and spasticity (hypertonia).
  • These signs are not specific to EDH, which is why taking a good history is important!

Cushing’s triad:

  • A physiological response to critically high ICP
  • This is characterised by bradycardia, hypertension and deep/irregular breathing


Persisting unconsciousness:

  • Deep coma and very low GCS



  • Often by respiratory arrest
  • The respiratory centres in the brainstem become so compressed that they are unable to function.



Non-contrast CT

  • First line investigation
  • Must be ordered urgently if an EDH is suspected
  • Will show characteristic bi-convex mass within the skull if there is an EDH is present (“lemon-shaped” as opposed to the typical “banana-shape” of subdural haemorrhages)
  • This characteristic lemon shape occurs as because the dura attaches to the skull more tightly across the suture lines and the pressure of the haematoma is not enough to overcome these sutures. As a result, the haematoma expands medially.
  • Secondary features on CT head can include midline shift and brain stem herniation, both of which are indications for early surgical intervention.


Non-contrast CT Scan of an Extradural Haematoma
Figure 3: Non-contrast CT Scan of an extradural haematoma, which shows midline shift 8


  • Has little benefit over CT and is not preferred as it takes longer and is not suitable for urgent scanning.
  • May, however, be used post-operatively if the patient is unexpectedly unwell as it can reveal underlying brain contusions, diffuse axonal injury or ischaemia.
  • It may be useful in differentiating between extradural and subdural haemorrhages through looking at the displaced dura.



  • Not a first line investigation because a CT head is more sensitive at detecting fractures.
  • However, a skull fracture found on X-ray is always an indication for an immediate CT head.
Non-contrast CT showing an EDH with a skull fracture marked by the arrow
Figure 4: A non-contrast CT showing an EDH with a skull fracture marked by the arrow 9


  • May be performed when assessing a non-traumatic aetiology (e.g arteriovenous malformation)
  • Used very rarely


Lumbar punctures are absolutely contraindicated for extradural haematomas, as they result in a drop in CSF pressure, which may speed up brain herniation.



Immediate management

  • ABCDE approach to assessment and management
  • If appropriate, this will include high flow oxygen, C-spine protection, and intubation/ventilation
  • The above management applies to all trauma patients
  • The patient needs to be urgently referred to the neurosurgical team in order to give them the best chance of recovery


Surgical management

  • Objectives of the operation are decompression, haemostasis, and prevention of a re-bleed
  • Urgent decompression/evacuation is done to relieve the pressure on essential brain structures
  • This is done via a burr hole into the skull at the point where the haematoma is thickest
  • The haematoma can then be evacuated to help relieve the pressure
  • A craniectomy may be done to enable the surgeons to stop the cause of the bleeding. This would involve taking a piece of skull (a bone flap) away to give them access to the vasculature.
  • Ligation, or cauterisation, of any bleeding vessels, can then be performed if appropriate.


Medical management

  • Diuretics: mannitol is typically used to help decrease ICP, through an osmotic effect
  • Anti-convulsants: these help to prevent post-traumatic seizures
  • Prophylactic antibiotics: these are used to reduce the risk of secondary meningitis following any open skull fracture
  • Barbiturates: these CNS depressants may be used to help reduce ICP and to protect the brain from anoxia (absence of oxygen) and ischaemia


Post-operative management

  • Patients will receive close observation during their recovery period, with regular neurological observations (including GCS)
  • The aim is to prevent any secondary insults (e.g oedema, ischaemia or infection)
  • ICP monitoring and repeat CT scans are useful for detecting early clinical deterioration
  • Medical management methods mentioned above are often used alongside surgical management, once the primary surgery has been performed



Most people with an extradural haematoma, even if relatively large, have very good outcomes if they receive evacuation surgery early.

The outcome is significantly better when compared to other forms of traumatic brain injury (TBI) where prognosis is generally poor.

However, prognosis worsens significantly if surgical intervention is delayed. This is why it is essential that a diagnosis is made early.

Clinical features associated with a poorer prognosis:

  • Low GCS
  • Lack of lucid interval
  • Pupil abnormalities
  • Decerebrate rigidity (exaggerated extensor posture of all extremities which occurs after a midbrain injury)
  • Other existing types of brain injury




  • Can be associated with skull fractures



  • Often occurs adjacent to the haematoma
  • Can also arise in the areas supplied by an injured/ruptured artery


Post-traumatic epilepsy

  • Seizures post-trauma can cause further brain damage
  • Epilepsy may remain long-term as a result of the brain damage


Cognitive impairment

  • Due to direct brain tissue insults at the time of the injury and damage occurring secondary to raised intracranial pressure



  • Due to direct brain tissue insults at the time of the injury and damage occurring secondary to raised intracranial pressure (e.g. motor cortex and cerebral peduncle)



  • Excessive accumulation of fluid in the brain secondary to obstruction of cerebrospinal fluid drainage
  • Hydrocephalus increases ICP, which can cause further damage to brain tissue


Brainstem injury

  • Due to increased ICP, leading to brainstem herniation (see Figure 2)
  • This often results in permanent brainstem injury or death


Edited by

Samantha Strickland

Hull York Medical Student


Reviewed by

Mr Konstantinos Lilimpakis

Neurosurgical Clinical Fellow



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  2. Edited image originally from Mariana Ruiz Villarrea. Published online 2007 Jan 4. Available here: [LINK] [Accessed 15th November 2018]
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  6. Image by Hellerhoff. Published online 2009 Nov 1. Available here: [LINK] [Accessed 15th November 2018]
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