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Extradural haematoma (EDH) is defined as an acute haemorrhage between the dura mater and the inner surface of the skull. An EDH can cause compression of local brain structures and a rise in intracranial pressure. If intracranial pressure continues to rise, cerebellar herniation may occur leading to brainstem death.
Patients most commonly affected by extradural haematomas (EDH) are adult males between the ages of 20-30.
An extradural haematoma is most commonly caused by skull trauma in the temporoparietal region, typically following a fall, assault or sporting injury. An EDH is associated with a skull fracture in 75% of cases.
The pterion is an anatomical landmark where the parietal, frontal, sphenoid and temporal bones fuse. The pterion is particularly vulnerable to fracture as the bone at this location is relatively thin. The middle meningeal artery (MMA) also lies underneath the pterion and therefore fracture at this location can result in rupture of the MMA. As a result, the middle meningeal artery is involved in 75% of extradural haematomas.
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 bleeding disorders.
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 haematoma, which is visible 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 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.
Typical symptoms of EDH include:
Nausea and vomiting
Loss of consciousness (typically immediately after a head injury) followed by a period of lucidity
Progressively decreasing level of consciousness (typically developing several hours after the initial injury)
Typical clinical signs of EDH include:
Tenderness of the skull (in the context of injury)
Cranial nerve deficits (e.g. oculomotor nerve palsy causing fixed dilation of the ipsilateral pupil)
Motor or sensory deficits of the upper and/or lower limbs (e.g. hemiparesis, paraesthesia)
Hyperreflexia and spasticity
Upgoing plantars (Babinski’s sign)
Cushing’s triad: a physiological response to raised intracranial pressure including bradycardia, hypertension and deep/irregular breathing.
Bedside investigations which may be relevant include:
Capillary blood glucose: to rule out hypoglycaemia as a cause of reduced GCS
ECG: to rule out heart block as a cause of bradycardia
Relevant blood tests may include:
FBC: to identify anaemia which may need correction
U&Es: to rule out electrolyte abnormalities which may contribute to a reduced GCS
CRP: if considering co-existing infection
Coagulation: to rule out underlying coagulopathy
Group and save: to allow transfusion of blood products, particularly relevant if the patient needs to go to theatre
A CT head is the gold standard investigation in cases of suspected intracranial bleeding. This investigation should be requested urgently if intracranial bleeding is suspected.
The primary feature on CT head in the context of EDH is a bi-convex “lemon-shaped” mass (rather than the typical “banana-shape” associated with subdural haemorrhages). This characteristic lemon shape develops due to the haematoma expanding medially due to being unable to expand past the points at which the dura is tightly bound to the suture lines of the skull.
Secondary features on CT head can include midline shift and brainstem herniation, both of which are indications for early surgical intervention.
MRI head has little benefit over CT and takes much longer to perform the scan, making it less ideal in the acute context.
MRI can be used in the sub-acute setting to assess for evidence of underlying cerebral contusions, ischaemia or diffuse axonal injury.
Skull X-ray is not typically used in the investigation of EDH however if a skull fracture is noted on a skull X-ray a CT head should be performed urgently to assess for evidence of EDH.
Cerebral angiography may be used in the sub-acute setting to assess for an underlying arteriovenous malformation which may be the cause of the EDH (e.g. if there was no history of trauma).
Stabilising the patient
Initial management of a patient with a suspected EDH should follow an ABCDE approachto ensure the patient is stable before considering further management options.
Correction of coagulation studies
All patients on anticoagulation will require reversal agents to prevent further bleeding and extension of the EDH haematoma. If a patient is anticoagulated with warfarin, Beriplex is commonly used to quickly replace vitamin-K dependent clotting factors and normalise the INR. Haematology typically guides the anticoagulation reversal.
Patients who are found to have a coagulopathy (e.g. prolonged PT, thrombocytopenia) need to be discussed with haematology for advice on appropriate treatments (e.g. fresh-frozen plasma, platelet transfusion).
Prophylactic antibiotics may be administered, particularly in the context of an open skull fracture to reduce the risk of intracranial infection.
Patients presenting with acute EDH are at an increased risk of developing seizures and therefore may be temporarily commenced on anticonvulsant medication to prevent seizures (e.g. levetiracetam, phenytoin).
Agents to reduce ICP
Mannitol may be used intravenously to help temporarily decrease ICP (via an osmotic effect) prior to surgical management.
Barbiturates may be used to help reduce ICP and to protect the brain from anoxia.
The choice of definitive management differs depending on the location, age, size and clinical features of the bleed.
Conservative management may be appropriate if the bleed is verysmall with minimal mass effect (i.e. midline shift).
Burr hole craniotomy
Burr hole craniotomy is often performed to manage acute EDH allowing evacuation of the haematoma.
A trauma craniotomy is typically used in the context of acute EDH with significant mass effect to both evacuate blood, treat the cause of bleeding (e.g. ligation of a vessel) and reduce intracranial pressure.
If there is a large bleed and/or a lot of associated cerebral oedema a hemicraniectomy (also known as a decompressive craniectomy) may be performed in an attempt to prevent brain stem herniation and death due to rising intracranial pressure.
Patients require close observation during the post-operative period, including regular neurological observations. 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 signs of clinical deterioration.
Most patients with an extradural haematoma, even if relatively large, have a good prognosis if they receive early evacuation of the haematoma. However, prognosis worsens significantly if surgical intervention is delayed.
Clinical features associated with a poorer prognosis include:
Low GCS at presentation
No history of a lucid interval
Pre-existing brain injury
Complications of EDH include:
Infection: due to skull fracture or as a result of operative intervention
Cerebral ischaemia: typically occurs adjacent to the haematoma
Hydrocephalus due to obstruction of the ventricles
Brainstem injury: due to significantly raised ICP
Extradural haematoma (EDH) is defined as an acute haemorrhage between the dura mater and the inner surface of the skull.
An extradural haematoma is most commonly caused by skull trauma in the temporoparietal region, typically following a fall, assault or sporting injury.
Typical symptoms of EDH include headache, nausea/vomiting, confusion and reduced level of consciousness.
Typical clinical signs of EDH include confusion, cranial nerve deficits, motor or sensory deficits of the limbs, hyperreflexia, spasticity, upgoing plantars and Cushing’s triad.
The key investigation in EDH is a CT head to identify the bleed and inform pre-operative planning.
Management of EDH involves initially stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.
The prognosis of EDH is good if treated rapidly but poor if surgical management is delayed.
Complications include infection, cerebral ischaemia, seizures, hydrocephalus and hemiparesis.
Mr Konstantinos Lilimpakis
Neurosurgical Clinical Fellow
Hull York Medical Student
Edited image originally from Mariana Ruiz Villarrea. Published online 2007 Jan 4. Available here: [LINK] [Accessed 15th November 2018]
Rengachary SS (ed.), Ellenbogen RG (ed.). Principles of Neurosurgery, 2nd Edition. Elsevier; 2005
Image by Richard Millard. Published online 2009 Sept 16. Available here: [LINK] [Accessed 15th November 2018]
Kernohan Phenomenon. Available here: [LINK] [Accessed 19th October 2018]
Extradural Haemorrhage. Case courtesy of Dr Sandeep Bhuta, Radiopaedia.org. From the case rID: 4458. [Accessed 18th June 2018]
Image by Hellerhoff. Published online 2009 Nov 1. Available here: [LINK] [Accessed 15th November 2018]