Epidural Hemorrhage

Author: Jamie S Ullman, MD; Chief Editor: Ryszard M Pluta, MD, PhD

Background
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.
Epidemiology
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. Anterior temporal tip epidural hematomas
have been postulated to form due disruption of the sphenoparietal sinus.[3]
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.[4] 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.

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.[5] 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. [7] 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.
Laboratory Studies

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

o 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.[8]
o 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

Radiography
o 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.
o 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
o 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

o obstructing the fourth ventricle. 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.
o 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.
o 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.[9, 10]
o 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, bifrontoparietal epidural

hemorrhage (EDH). Air bubbles are within the hematoma.

CT bone window image of same patient in Media file 2 that demonstrates a

large midline fracture.

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 defines the anterior-posterior

extent of the vertex epidural hemorrhage (EDH).
o 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.[11]
o Gean et al reported a series of 21 patients with anterior temporal tip epidural
hematomas.[3] 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.

MRI: 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.

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. [12, 13] 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.[3]
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.[14]
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,"[14] EDH with
volume greater than 30 mL should undergo surgical evacuation, regardless of GCS. [14] 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).

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 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).[15] 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
Follow-up CT scans are performed to determine the extent of clot evacuation. These scans
can also help evaluate for delayed hematomas.
Complications
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.[15] 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.

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