Extradural haematoma (EDH), also known as an epidural haematoma, is a collection of blood that forms between the inner surface of the skull and outer layer of the dura, which is called the endosteal layer. They are usually associated with a history of head trauma and frequently associated skull fracture. The source of bleeding is usually arterial, most commonly from a torn middle meningeal artery.
EDHs are typically biconvex in shape and can cause a mass effect with herniation. They are usually limited by cranial sutures, but not by venous sinuses. Both CT and MRI are suitable to evaluate EDHs. When the blood clot is evacuated promptly (or treated conservatively when small), the prognosis of EDHs is generally good.
Typically extradural haematomas are seen in young patients who have sustained head trauma, usually with an associated skull fracture.
Unlike subdural haemorrhages, in which a history of head trauma is often difficult to clearly identify, extradural haemorrhages usually are precipitated by clearly defined head trauma.
A typical presentation is of a young patient involved in a head strike (either during sport or a result of a motor vehicle accident) who may or may not lose consciousness transiently. Following the injury, they regain a normal level of consciousness (lucid interval), but usually have an ongoing and often severe headache. Over the next few hours, they gradually lose consciousness.
Due to the long cisternal course of the sixth cranial nerve (abducens nerve, CN VI), it is often involved as downward herniation begins, usually on the side of the haemorrhage and can, in an emergency, guide exploratory burrholes.
See the article: EDH v SDH
The source of bleeding is typically from a torn meningeal artery, usually the middle meningeal artery (75%7). An associated skull fracture is present in ~75% of cases 3. Pain (often severe headache) is caused by the stripping of dura from the bone by the expanding haemorrhage. The posterior fossa is a rare location for traumatic injury, in general, including EDH 3-4.
Occasionally, an EDH can form due to venous blood, typically a torn sinus with an associated fracture: see venous extradural haemorrhage.
Young patients being affected is not only a result of the prevalent demographics of patients with head injury but also relates to the changes that occur in the dura in older patients, as the dura is much more adherent to the inner surface of the skull.
It is important to realise that in the setting of sutural diastasis extradural haematomas can cross sutures, as the continuation of the parietal (periosteal) component of the dura through the suture - which usually limits spread - is likely also to be disrupted.
EDHs are generally unilateral in more than 95% of cases, however, bilateral or multiple EDHs are reported.
- >95% are supratentorial
- temporoparietal: 60%
- frontal: 20%
- parieto-occipital: 20%
- <5% are located infratentorially in posterior fossa 4
Special locations to consider, particularly those related to venous extradural bleeding, include:
- vertex EDH (which displaces the superior sagittal sinus) 6
- anterior middle cranial fossa 7
- likely venous bleeding (sphenoparietal sinus)
- do not cause midline shift or herniation
- rarely grow
- can be managed conservatively
The morphology of extradural haematomas is best understood by reviewing their relationship to the bone and dura. An extradural haematoma is actually a subperiosteal haematoma located on the inside of the skull, between inner table of the skull and parietal layer of the dura mater (which is the periosteum). As a result, EDHs are usually limited in their extent by the cranial sutures, as the periosteum crosses through the suture continuous with the outer periosteal layer. This is therefore helpful in distinguishing EDHs from subdural haematomas, which are not limited by sutures.
Extradural haemorrhages can, however, cross and elevate venous sinuses as long as there is no suture there; after all a venous sinus is located between the parietal and visceral layer of the dura.
Unfortunately, these rules are not foolproof and not infrequently extradural hematomas do cross sutures. One series found up to 11% of EDHs in children cross sutures 5. This occurs in many scenarios:
- skull fracture crosses the suture 5
- sutural diastasis 5
- vertex extradural haematomas, usually due to venous extradural haemorrhage, often cross the midline elevating the superior sagittal sinus 6
In almost all cases, extradural haematomas are seen on CT scans of the brain. They are typically bi-convex (or lentiform) in shape, and most frequently beneath the squamous part of the temporal bone. EDHs are hyperdense, somewhat heterogeneous, and sharply demarcated. Depending on their size, secondary features of mass effect (e.g. midline shift, subfalcine herniation, uncal herniation) may be present.
When acute bleeding is occurring at the time of CT scanning the non-clotted fresh blood is typically less hyperdense, and a swirl sign may be evident 1.
Postcontrast extravasation may be seen rarely in case of acute EDH and peripheral enhancement due to granulation and neovascularisation can be seen in chronic EDH.
MRI can clearly demonstrate the displaced dura that appears as a hypointense line on T1 and T2 sequences which is helpful in distinguishing it from a subdural haematoma.
Acute EDH appears isointense on T1 and shows variable intensities from hypo- to hyperintense on a T2 sequence. Early subacute EDH appears hypointense on T2 while late subacute and chronic EDH are hyperintense on both T1 and T2 sequences.
Intravenous contrast may demonstrate displaced or occluded venous sinus in case of venous origin of EDH.
It can be used to evaluate nontraumatic cause (i.e. AVM) of EDH. Rarely angiography can demonstrate middle meningeal artery laceration and contrast extravasation from middle meningeal artery into paired middle meningeal veins known as "tram track sign".
Treatment and prognosis
Prognosis, even with a relatively large haematoma, is in general quite good, as long as the clot is evacuated promptly. A smaller haematoma without mass effect or swirl sign can be treated conservatively 2, sometimes resulting in calcification of the dura.
Occasionally late complications are encountered, usually relating to the injured meningeal vessel. They include:
With large haematomas, there is rarely significant confusion as to the correct diagnosis. In smaller lesions, especially when there is associated parenchymal injury (e.g. cerebral contusions, traumatic subarachnoid blood, concurrent subdural haematoma) the diagnosis can be more challenging.
Differential considerations include:
- 1. Al-Nakshabandi NA. The swirl sign. Radiology. 2001;218 (2): 433. Radiology (full text) - Pubmed citation
- 2. Sullivan TP, Jarvik JG, Cohen WA. Follow-up of conservatively managed epidural hematomas: implications for timing of repeat CT. AJNR Am J Neuroradiol. 1999;20 (1): 107-13. AJNR Am J Neuroradiol (full text) - Pubmed citation
- 3. Irie F, Le Brocque R, Kenardy J et-al. Epidemiology of traumatic epidural hematoma in young age. J Trauma. 2011;71 (4): 847-53. doi:10.1097/TA.0b013e3182032c9a - Pubmed citation
- 4. Takeuchi S, Wada K, Takasato Y et-al. Traumatic hematoma of the posterior fossa. Acta Neurochir. Suppl. 2013;118: 135-8. doi:10.1007/978-3-7091-1434-6_24 - Pubmed citation
- 5. Huisman TA, Tschirch FT. Epidural hematoma in children: do cranial sutures act as a barrier?. J Neuroradiol. 2009;36 (2): 93-7. doi:10.1016/j.neurad.2008.06.003 - Pubmed citation
- 6. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology. Lippincott Williams & Wilkins. (2007) ISBN:0781761352. Read it at Google Books - Find it at Amazon
- 7. Gean AD, Fischbein NJ, Purcell DD et-al. Benign anterior temporal epidural hematoma: indolent lesion with a characteristic CT imaging appearance after blunt head trauma. Radiology. 2010;257 (1): 212-8. doi:10.1148/radiol.10092075 - Pubmed citation
Stroke and intracranial haemorrhage
stroke and intracranial haemorrhage
- general discussions
- scoring and classification systems
- by region
- hemispheric infarcts
- frontal lobe infarct
- parietal lobe infarct
- temporal lobe infarct
- occipital lobe infarct
- internal capsule infarct
- ataxic hemiparesis syndrome: MCA perforators or basilar artery perforators
- lacunar infarct
- thalamic infarct
- striatocapsular infarct
- cerebellar infarct
- midbrain infarct
- Brissaud-Sicard syndrome
- facial colliculus syndrome
- Gasperini syndrome: basilar artery or AICA
- inferior medial pontine syndrome (Foville syndrome): basilar artery
- lateral pontine syndrome (Marie-Foix syndrome): basilar artery or AICA
- locked-in syndrome: basilar artery
- Millard-Gubler syndrome: basilar artery
- Raymond syndrome: basilar artery
- medullary infarct
- acute spinal cord ischaemia syndrome
- hemispheric infarcts
- by vascular territory
- anterior cerebral artery infarct
- anterior choroidal artery infarct
- anterior inferior cerebellar artery infarct
- basilar artery infarct
- middle cerebral artery infarct
- posterior cerebral artery infarct
- posterior inferior cerebellar artery infarct
- superior cerebellar artery infarct
- treatment options
- by region or type
- basal ganglia haemorrhage
- cerebellar haemorrhage
- cerebral contusions
- cerebral microhaemorrhage
- haemorrhagic venous infarct
- haemorrhagic transformation of an ischaemic infarct
- hypertensive intracranial haemorrhage
- intraventricular haemorrhage (IVH)
- lobar haemorrhage
- pontine haemorrhage
- extra-axial haemorrhage
- extradural versus subdural haemorrhage
- extradural haemorrhage (EDH)
- intralaminar dural haemorrhage
- subdural haemorrhage (SDH)
- subarachnoid haemorrhage (SAH)
- intra-axial haemorrhage
- ischaemic stroke