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.