Introduction
Epidural hemorrhage (EDH) is an easily treated form of head injury that is often associated with a good prognosis. In rare instances, such hemorrhages can be spontaneous. Advances in contemporary CT imaging have made confirmation of an EDH diagnosis rapid and accurate.
Problem
EDH occurs in the potential space between the dura and the cranium. Epi is Greek for over or upon. An EDH can also be referred to as extradural (outside of the dura).
EDH results from interruption of dural vessels, including branches of the middle meningeal arteries, veins, dural venous sinuses, and skull vessels. Continued bleeding and growth can result in intracranial hypertension.
An image depicting epidural hemorrhage can be seen below.
CT scan of an acute left-sided epidural hematoma. Note the typical convex or lens-shaped appearance. The hematoma takes this shape as the dura strips from the undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular system is present. This hemorrhage requires immediate surgical evacuation.
Frequency
As many as 10-20% of all patients with head injuries are estimated to have EDH, the incidence of which is proportionate to age in the pediatric population. Approximately 17% of previously conscious patients who deteriorate into coma following a trauma have EDH.
Etiology
Trauma is the typical cause of EDH. The trauma frequently is a blunt impact to the head from an assault, fall, or other accident. Dystocia, forceps delivery, and excessive skull moulding through the birth canal have been implicated in EDH in newborns.1
Pathophysiology
Unlike the subdural hematoma, cerebral contusion, or diffuse axonal injury of the brain, EDH is not generated secondary to head motion or acceleration. EDH is mainly caused by structural disruption of the dural and skull vessels commonly associated with calvarial fractures. Laceration of the middle meningeal artery and its accompanying dural sinuses is the most common etiology.
In the posterior fossa, disruption of dural venous sinuses (eg, transverse or sigmoid sinus) by fracture may lead to EDH. Disruption of the superior sagittal sinus may cause vertex EDH. Other non-arterial sources of epidural hemorrhage include venous lakes, diploic veins, arachnoid granulations, and the petrosal sinuses.
A small number of epidural hematomas have been reported in the absence of trauma. The etiologies include infectious diseases of the skull, vascular malformations of the dura mater, and metastasis to the skull. Spontaneous EDH can also develop in patients with coagulopathies associated with other primary medical problems (eg, end-stage liver disease, chronic alcoholism, other disease states associated with dysfunctional platelets).
Presentation
Most epidural hematomas are traumatic in origin, often involving a blunt impact to the head. Patients may have external evidence of head injuries such as scalp lacerations, cephalohematoma, or contusions. Systemic injuries may also be present. Depending on the force of impact, patients may present with no loss of consciousness, brief loss of consciousness, or prolonged loss of consciousness.
The classic lucid interval occurs in 20-50% of patients with EDH. Initially, the concussive force that caused the head injury results in an alteration of consciousness. After recovering consciousness, the EDH continues to expand until the mass effect of the hemorrhage itself results in increased intracranial pressure, a decreased level of consciousness, and a possible herniation syndrome.
With severe intracranial hypertension, a Cushing response may occur. The classic Cushing triad involves systemic hypertension, bradycardia, and respiratory depression. This response usually occurs when cerebral, particularly brainstem, perfusion is compromised by increased intracranial pressure. Antihypertensive therapy during this time may lead to critical cerebral ischemia and cell death.2 Evacuation of the mass lesion alleviates the Cushing response.
Neurological assessment is essential. Attention should be paid to the level of consciousness, motor activity, eye opening, verbal output, pupillary reactivity and size, and lateralizing signs such as hemiparesis or plegia. The Glasgow Coma Score (GCS) is essential in assessing the current clinical condition. The GCS has been positively correlated with outcome. In awake patients with a mass lesion, the pronator drift phenomenon might help to assess clinical significance. Drifting of the extremity when the patient is asked to hold both arms outstretched with palms facing upward indicates subtle but significant mass effect.
Indications
The diagnosis and indications for treatment of EDH are discussed in the following sections.
Relevant Anatomy
Below the skull bone lies the dura mater, which overlies the leptomeningeal structures, the arachnoid, and the pia mater, which, in turn, overlie the brain. The dura mater consists of 2 layers, with the outer layer serving as a periosteal layer for the inner surface of the skull.
As a person ages, the dura becomes more adherent to the skull, reducing the frequency of EDH formation. In infancy, the skull is more pliable and less likely to fracture. EDH can form when the dura is stripped from the skull during impact.
The dura is most adherent to the sutures, which connect the various bones of the skull. The major sutures are the coronal sutures (frontal and parietal bones), the sagittal sutures (both parietal bones), and the lambdoid sutures (parietal and occipital bones). EDH rarely extends beyond the sutures.
The region most commonly involved with EDH is the temporal region (70-80%). In the temporal region, the bone is relatively thin and the middle meningeal artery is close to the inner table of the skull. The incidence of EDH in the temporal region is lower in pediatric patients because the middle meningeal artery has not yet formed a groove within the inner table of the skull.3 EDH occurs in the frontal, occipital, and posterior fossa regions with approximately equal frequency. EDH occurs less frequently in the vertex or parasagittal areas.
According to a recent anatomical study by Fishpool et al, the middle meningeal artery is accompanied by 2 dural sinuses that are situated along each side of the vessel.4 Therefore, laceration of this artery is likely to cause a mixture of arterial and venous bleeding.
Contraindications
EDH, when not treated by careful observation or surgery, may result in eventual cerebral herniation and brainstem compression, with cerebral infarction or death as a consequence. Therefore, recognition of EDH is extremely important.
More on Epidural Hemorrhage |
 Overview: Epidural Hemorrhage |
| Workup: Epidural Hemorrhage |
| Treatment: Epidural Hemorrhage |
| Follow-up: Epidural Hemorrhage |
| Multimedia: Epidural Hemorrhage |
| References |
| Further Reading |
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References
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Miller DJ, Steinmetz M, McCutcheon IE. Vertex epidural hematoma: surgical versus conservative management: two case reports and review of the literature. Neurosurgery. Sep 1999;45(3):621-4; discussion 624-5. [Medline].
Fishpool SJ, Suren N, Roncaroli F, Ellis H. Middle meningeal artery hemorrhage: an incorrect name. Clin Anat. May 2007;20(4):371-5. [Medline].
Al-Nakshabandi NA. The swirl sign. Radiology. Feb 2001;218(2):433. [Medline].
Arrese I, Lobato RD, Gomez PA, Nunez AP. Hyperacute epidural haematoma isodense with the brain on computed tomography. Acta Neurochir (Wien). 146(2):193-194. [Medline].
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[Guideline] Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW. Surgical management of acute epidural hematomas. Neurosurgery. Mar 2006;58(3 Suppl):S7-15; discussion Si-iv. [Medline].
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Liu JT, Tyan YS, Lee YK, Wang JT. Emergency management of epidural haematoma through burr hole evacuation and drainage. A preliminary report. Acta Neurochir (Wien). Mar 2006;148(3):313-7; discussion 317. [Medline].
Suzuki S, Endo M, Kurata A, et al. Efficacy of endovascular surgery for the treatment of acute epidural hematomas. AJNR Am J Neuroradiol. Aug 2004;25(7):1177-80. [Medline].
Berker M, Cataltepe O, Ozcan OE. Traumatic epidural haematoma of the posterior fossa in childhood: 16 new cases and a review of the literature. Br J Neurosurg. 17(3):226-229. [Medline].
Bozbuga M, Izgi N, Polat G. Posterior fossa epidural hematomas: observations on a series of 73 cases. Neurosurg Rev. 1999;22(1):34-40. [Medline].
Chesnut RM, Servadei F. Surgical treatment of post-traumatic mass lesions. In: Marion DW, ed. Traumatic Brain Injury. 1999:81-99.
Kelly DF, Nikas DL, Becker DP. Diagnosis and treatment of moderate and severe head injuries in adults. In: Youmans JR, ed. Neurological Surgery. 1996;3:1643-1645.
Lee EJ, Hung YC, Wang LC. Factors influencing the functional outcome of patients with acute epidural hematomas: analysis of 200 patients undergoing surgery. J Trauma. 45(5):946-952. [Medline].
Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological Surgery. 4th ed. 1996:1549-1594.
Lobato RD, Rivas JJ, Gomez PA. Head-injured patients who talk and deteriorate into coma. Analysis of 211 cases studied with computerized tomography. J Neurosurg. 75(2):256-261. [Medline].
Radulovic D, Janosevic V, Djurovic B, Slavik E. Traumatic delayed epidural hematoma. Zentralbl Neurochir. May 2006;67(2):76-80. [Medline].
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Servadei F, Nanni A, Nasi MT. Evolving brain lesions in the first 12 hours after head injury: analysis of 37 comatose patients. Neurosurgery. 37(5):899-906; discussion 906-907. [Medline].
Further Reading
Clinical guidelines
Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, Servadei F, Walters BC, Wilberger JE, Surgical Management of Traumatic Brain Injury Author Group. Surgical management of acute epidural hematomas. Neurosurgery 2006 Mar;58(3 Suppl):S2-7-S2-15. 10
Keywords
epidural hemorrhage, EDH, epidural hematoma, extradural hematoma, extraaxial hematoma, extraaxial collection, extra-axial hematoma, extra-axial collection, extradural hemorrhage, extraaxial hemorrhage, extra-axial hemorrhage, blunt head trauma, head trauma, acute epidural hematoma
