Epidural Hematomas 

Updated: Apr 13, 2016
Author: Jamie S Ullman, MD, FACS; Chief Editor: Brian H Kopell, MD 



Epidural hematoma (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. Although epidural hematomas are relatively uncommon (approximately 2% of all patients with head injuries and < 10% of those who are comatose), they should always be considered in evaluation of a serious head injury. Patients with epidural hematomas who meet surgical criteria and receive prompt surgical intervention can have an excellent prognosis if there is limited underlying primary brain damage from the traumatic event.[1]


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. 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.


As many as 2% of all head-injured patients and 15% of those with fatal 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.[31]

Using the Nationwide Inpatient Sample (NIS), a retrospective analysis was performed of all cases of EDH in the United States. A total of 5189 admissions were identified, and in-hospital mortality and complication rate were determined to be 3.5% and 2.9%, respectively.[2]


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.[3]


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. Anterior temporal tip epidural hematomas have been postulated to form due disruption of the sphenoparietal sinus.[4]

Posterior fossa epidural hemorrhage can mimic a sinus thrombus by compressing and displacing the sinuses. It is important to recognize this possibility, because treatment of a suspected thrombus with anticoagulation can worsen epidural hemorrhage.[5]

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).


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.[6] 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 (see the Glasgow Coma Scale calculator). 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.


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.[7] 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.[8] Therefore, laceration of this artery is likely to cause a mixture of arterial and venous bleeding.


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.



Laboratory Studies

Hematocrit level, chemistries, and coagulation profile (including platelet count) are essential in the assessment of patients with EDH, whether spontaneous or traumatic.

Severe head injury can cause release of tissue thromboplastins, which can result in disseminated intravascular coagulation. Prior knowledge of coagulopathy is required if surgery is to be undertaken. If required, appropriate factors are administered preoperatively and intraoperatively. Presence of coagulopathy may be associated with worse outcomes.[9]

In adults, EDH rarely causes a significant drop in the hematocrit level within the rigid skull cavity. In infants, whose blood volume is already limited, epidural bleeding within an expansile cranium with open sutures can result in significant blood loss. Such bleeding can result in hemodynamic instability; therefore, careful and frequent monitoring of the hematocrit level is required.

Imaging Studies


Skull radiographs often reveal a fracture crossing the vascular shadow of the middle meningeal artery branches. An occipital, frontal, or vertex fracture also might be observed.

The presence of a fracture does not necessarily guarantee the existence of EDH. However, more than 90% of EDH cases are associated with skull fractures. In children, this rate is less because of greater skull deformability.

CT scanning

CT scanning is the most accurate and sensitive method of diagnosing acute EDH. The findings are characteristic. The space occupied by EDH is limited by the adherence of the dura to the inner table of the skull, especially at the suture lines, contributing to the lenticular or biconvex appearance (see the image below). Hydrocephalus may be present in patients with a large posterior fossa EDH exerting a mass effect and obstructing the fourth ventricle.

CT scan of an acute left-sided epidural hematoma. 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.

Cerebrospinal fluid is not commonly mixed with epidural hematomas; therefore, the hematoma is denser and homogenous. The quantity of hemoglobin in the hematoma determines the amount of radiation absorbed.

The signal density of the hematoma compared with the brain parenchyma changes over time after the injury. The acute phase is hyperdense (ie, bright signal on CT scan). The hematoma then becomes isodense at 2-4 weeks, and then it becomes hypodense (ie, dark signal) thereafter. Hyperacute blood may be observed as isodense or low-density areas, possibly indicating ongoing hemorrhage or a low serum hemoglobin level.[10, 11, 5]

Another less frequently involved area is the vertex, an area in which confirming the diagnosis on CT scans may be difficult. Vertex epidural hematomas can be mistaken as artifact in traditional axial CT scan sections. Even when correctly detected, the volume and the mass effect may easily be underestimated. In some cases, coronal and sagittal reconstructions can be used to evaluate the hematoma on coronal planes (see the images below).

Axial CT scan that demonstrates a large vertex, bi Axial CT scan that demonstrates a large vertex, bifrontoparietal epidural hemorrhage (EDH). Air bubbles are within the hematoma.
CT bone window image of same patient in Media file CT bone window image of same patient in Media file 2 that demonstrates a large midline fracture.
Coronal CT scan reconstruction that further clarif Coronal CT scan reconstruction that further clarifies the thickness and mass effect associated with this vertex epidural hemorrhage (EDH).
Sagittal CT scan reconstruction that further defin Sagittal CT scan reconstruction that further defines the anterior-posterior extent of the vertex epidural hemorrhage (EDH).

Approximately 10-50% of EDH cases are associated with other intracranial lesions. These lesions include subdural hematomas, cerebral contusions, and intracerebral hematomas. A 2009 study by Park et al suggests that routine repeat CT scanning within 24 hours of blunt head trauma may lessen potential neurological deterioration among patients with a GCS of less than 12, epidural hematoma, or multiple lesions, as indicated on initial CT scanning.[12]

Gean et al reported a series of 21 patients with anterior temporal tip epidural hematomas.[4] These lesions were usually limited by the orbital fissure medially and by the sphenotemporal suture laterally and were confined to the anterior temporal fossa without expansion on subsequent imaging.


Acute blood on MRIs is isointense, making this modality less suited to detection of hemorrhage in acute trauma. Mass effect, however, can be observed when extant.[5]



Medical Therapy

Treatment of the epidural hematoma depends on various factors. The adverse effect on brain tissue is mainly from mass effect causing structural distortion, life-threatening brain herniation, and increased intracranial pressure.

The 2 treatment options for these patients are (1) immediate surgical intervention and (2) initial, conservative, close clinical observation with possible delayed evacuation. Note that EDHs tend to expand in volume more rapidly than subdural hematomas, and patients require very close observation if the conservative route is taken.

Not all cases of acute EDH require immediate surgical evacuation.[13, 14] If a lesion is small and the patient is in good neurological condition, observing the patient with frequent neurological examinations is reasonable. Acute anterior temporal tip EDH are one subset of this entity which runs a benign course and can usually be followed with imaging and observation. The likely venous origin of these EDH contributes to slow expansion and eventual tamponade of the bleeding source.[4]

In a retrospective review over a 5-year period of EDH patients who were initially triaged for conservative management, only 11.2% required surgery. Statistical comparison showed that younger age and coagulopathy were the only significant factors for conversion to surgery.[15]

Although conservative management is often left to clinical judgment, the "Guidelines for the Surgical Management of Traumatic Brain Injury" recommended that patients who exhibit an EDH that is less than 30 mL, less than 15-mm thick, and less than 5-mm midline shift, without a focal neurological deficit and GCS greater than 8 can be treated nonoperatively.[16] Early follow-up scanning should be used to assess a further increase in hematoma size prior to deterioration. Delayed epidural formation has been reported. If a rapid size increase is noted and/or the patient develops anisocoria or a neurological deficit, then surgery is indicated. Middle meningeal artery embolization has been described in the early stages of EDH, especially when angiographic dye extravasation has been observed (see Future and Controversies).

When treating patients with spontaneous EDH, the underlying primary disease process must be addressed in addition to the fundamental principles discussed above.

Surgical Therapy

According to the "Guidelines for the Management of Traumatic Brain Injury,"[16] EDH with volume greater than 30 mL should undergo surgical evacuation, regardless of GCS.[16] This criterion becomes especially important when the EDH exhibits thickness of 15 mm or more, and a midline shift beyond 5 mm. Most patients with such an EDH experience a worsening of the conscious state and/or exhibit lateralizing signs.

Location is also an important factor in the surgical decision. Temporal hematomas, if they are large or expanding, may lead to uncal herniation and more rapid deterioration. EDH in the posterior fossa, which is often related to interruption of the lateral venous sinus, often requires prompt evacuation because of the limited space available compared with the supratentorial compartment (see the images below).[17]

CT image of a pre-adolescent male with a left post CT image of a pre-adolescent male with a left posterior fossa epidural hemorrhage (EDH). Such hemorrhages need to be watched carefully, and the surgical team should have a low threshold for surgical intervention because this region has less room to accommodate mass lesions.
Bone window of the same patient as Media file 6 th Bone window of the same patient as Media file 6 that reveals a diastasis (separation) of the left mastoid suture.

Before the advent of CT scanning, drilling exploratory burholes was commonplace, especially when the patient demonstrated lateralizing signs or rapid deterioration. Currently, with fast-scan techniques, this type of exploration is rarely required.

Currently, drilling exploratory burholes is reserved for the following patients:

  • Patients with definitive localizing signs and clinical evidence of intracranial hypertension who are unable to tolerate a CT scan because of severe hemodynamic instability

  • Patients who require immediate surgical intervention for systemic injuries

Reports have emerged that discuss burholes with negative pressure drainage as a primary mode of EDH treatment in select patients (ie, those patients awaiting transfer to a higher level trauma facility or patients with hemorrhages of nonarterial origin; see Future and Controversies).[18] However, despite these reports, craniotomy remains the standard.

Preoperative Details

Patients are brought to the operating room as quickly as possible after CT scanning. The body is supine, and the head is placed on a donut or horseshoe head holder. Three-point head clamps that are often used for intracranial surgery are not routinely used by the authors because they may propagate existing skull fractures.

Occipital or posterior fossa EDH requires positioning in the lateral, semiprone, or prone position. Three-point head clamps are then used for stable head fixation and are applied with care.

If the cervical spine is not adequately cleared for fracture or instability in patients with trauma, a hard cervical collar is kept in place.

Intraoperative Details

Surgical treatment of epidural hematomas involves opening the calvaria over the site of the hemorrhage. The EDH is readily apparent after elevating the bone flap, and it is removed. Coagulation of bleeding dural vessels is usually performed. Epidural tack-up sutures are placed from the dura to the craniotomy bone edge and to the center of the craniotomy flap to tamponade epidural bleeding from areas beyond the craniotomy edges and to prevent recurrence. Dural venous sinus bleeding is controlled with tamponade by gelatin sponges and cotton strips and head-of-the-bed elevation, taking care to avoid venous air embolism. The utmost care should be taken when elevating depressed bone fragments on or near the dural venous sinuses. If present, the Cushing response remains untreated until it resolves spontaneously as the mass effect is relieved.

If the patient presents with a dilated pupil or clinical signs of intracranial hypertension, a small incision is first made in an area considered to be over the hematoma. A rapid burhole is made, and the epidural is partially evacuated. This maneuver often allows for some initial pressure relief until the entire epidural blood clot can be evacuated.

If other significant intracranial injuries (eg, subdural hematoma, intracerebral hematoma) are apparent after imaging or upon direct visualization, they are surgically evacuated as needed. Intraoperative ultrasound is sometimes helpful in identifying such lesions. Occasionally, the bone flap (decompressive craniectomy) may not be reattached to the skull and is instead stored in a freezer, discarded, or preserved in the abdominal fat layer. This occurs when significant intracerebral swelling or injury is noted on the initial CT scan or encountered during the operation or if intractable intracranial hypertension develops in the postoperative period. Such decompression can allow for further brain expansion.

Postoperative Details

Patients are usually treated in the ICU or a monitored setting until they improve. Associated intracranial or systemic injuries are managed as needed. Depending on their neurological condition and radiographic findings, some patients may require intracranial pressure monitoring.


Follow-up CT scans are performed to determine the extent of clot evacuation. These scans can also help evaluate for delayed hematomas.


Many of the complications from EDH occur when the pressure they exert results in significant brain shifting. When the brain is subject to subfalcine herniation, the anterior and posterior cerebral arteries may occlude, resulting in cerebral infarction.

Downward herniation of the brain stem can result in Duret hemorrhages within the brainstem, mostly in the pons.

Transtentorial herniation may result in an ipsilateral cranial nerve III palsy, which often takes many months to resolve once the pressure is relieved. Cranial nerve III palsy manifests as ptosis, pupillary dilation, and the inability to move the eye in medial, upward, and downward directions.

In children younger than 3 years, a skull fracture may result in a leptomeningeal cyst or a growing fracture. These cysts are believed to occur when brain pulsation and growth do not allow the fracture to heal, thus expanding a dural tear and enlarging the edge of the fracture. Patients with a leptomeningeal cyst usually develop a pulsatile scalp mass.

Outcome and Prognosis

Although the ultimate goal is to achieve 0% mortality and 100% good functional outcomes, the overall mortality in most series of patients with EDH ranges from 9.4-33%, averaging approximately 10%. In general, the preoperative motor examination, the Glasgow Coma Scale score, and pupillary reactivity are significantly correlated to the functional outcome of patients with acute epidural hematomas when they survive. Because many isolated epidural hematomas do not involve underlying structural brain damage, the overall outcome is excellent if prompt surgical evacuation is undertaken.

Future and Controversies

Epidural hematoma is an emergent neurosurgical disease that can be managed with close clinical and radiographic observation or surgical evacuation. Most cases involve skull fractures over the lateral convexities of the hemispheres, with rupture of middle meningeal artery branches. Prompt diagnosis and appropriate management have resulted in low mortality and excellent functional outcomes.

With growing interest and experience in minimally invasive techniques, the value of burhole evacuation with negative pressure may need to be further investigated.[18] In addition, endovascular approaches may be a new avenue for investigation. In 2004, Suzuki et al reported on 9 patients undergoing embolization of the middle meningeal artery during the early stages of epidural hematoma formation to arrest further expansion. This therapy was reserved for patients who demonstrated contrast dye extravasation on CT scans. The desired result was achieved in all 9 patients.