Epidural Hematomas

Epidural hematoma 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 elevation of intracranial pressure, which may be detected in a clinical setting by observing ipsilateral pupil dilation (secondary to uncal herniation and oculomotor nerve compression), as well as elevated blood pressure, slowed heart rate, and irregular breathing. This triad is known as the “Cushing reflex.” These findings may indicate the need for immediate intracranial intervention to prevent central nervous system depression and death.[1]

(An image depicting epidural hemorrhage is shown below.)

Epidural hematoma 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.

Unlike subdural hematoma, cerebral contusion, or diffuse axonal injury of the brain, EDH is not generated secondary to head motion or acceleration. 

In the posterior fossa, disruption of dural venous sinuses (eg, transverse sinus, sigmoid sinus) by fracture may lead to EDH. Disruption of the superior sagittal sinus may cause vertex EDH. Other nonarterial 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 because of disruption of the sphenoparietal sinus.[8]

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.[9]

A small number of epidural hematomas have been reported in the absence of trauma. Etiologies include infectious disease of the skull, vascular malformation of the dura mater, and metastasis to the skull.

Spontaneous EDH can also occur in patients with coagulopathies associated with other primary medical problems (eg, end-stage liver disease, chronic alcoholism, other disease states associated with dysfunctional platelets).

As many as 2% of all head-injured patients and 15% of those with fatal head injuries are estimated to have EDH; incidence is proportionate to age in the pediatric population. Approximately 17% of previously conscious patients who deteriorate into coma following a trauma have EDH.[10]

Males are more often affected than females. Furthermore, the incidence is higher among adolescents and young adults. The mean age of affected patients is 20 to 30 years, and EDH is rare after 50 to 60 years of age. As an individual's age advances, the dura mater becomes more adherent to the overlying bone. This decreases the chance that a hematoma can develop in the space between the cranium and the dura.[1]

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; the outer layer serves 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 is less likely to fracture. Epidural hematoma can form when the dura is stripped from the skull during impact.

The dura is most adherent to the sutures that connect various bones of the skull. Major sutures include coronal sutures (frontal and parietal bones), sagittal sutures (both parietal bones), and lambdoid sutures (parietal and occipital bones). Epidural hematoma 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 among pediatric patients because the middle meningeal artery has not yet formed a groove within the inner table of the skull.[11] Epidural hematoma occurs in frontal, occipital, and posterior fossa regions with approximately equal frequency. It occurs less frequently in the vertex and in parasagittal areas.

An anatomic study found that the middle meningeal artery is accompanied by 2 dural sinuses that are situated along each side of the vessel.[12] Laceration of this artery is likely to cause a mixture of arterial and venous bleeding.

Factors that may influence outcomes of patients with EDS include the following:

• Patient age
• Time lapsed between injury and treatment
• Immediate coma or lucid interval
• Presence of pupillary abnormalities
• GCS/motor score, on arrival
• CT findings (ie, hematoma volume, degree of midline shift, signs of active hematoma bleeding, associated intradural lesions) ^[1]

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 consciousness is recovered, 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.[13]  Evacuation of the mass lesion alleviates the Cushing response.

Neurologic assessment is essential. Attention should be paid to level of consciousness, motor activity, eye opening, verbal output, pupillary reactivity and size, and lateralizing signs such as hemiparesis or plegia. The Glasgow Coma Scale 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.

Symptomatic postoperative EDH is rare, with an incidence of 0.10-0.69%. Many studies have reported advanced age, preoperative or postoperative coagulopathy, and multilevel laminectomy as risk factors. Symptomatic postoperative epidural hematomas usually present within the first 24-48 hours after surgery but can present later. Patients first report a marked increase in axial pain, followed by radicular symptoms in the extremities, then motor weakness and sphincter dysfunction. Magnetic resonance imaging (MRI) should be conducted, and if it confirms a compressive hematoma, surgical evacuation should be carried out as quickly as possible. The prognosis for neurologic improvement after evacuation depends on the time delay and the degree of neurologic impairment before evacuation.[14]

Several case reports have described emergency hematoma evacuation after epidural steroid injection. Spinal epidural hematoma is a rare condition that can rapidly lead to severe neurologic deficits. The pathophysiology of this development remains unclear.[15]

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

Laboratory studies such as international normalized ratio (INR), partial thromboplastin time (PTT), thromboplastin time (PT), and liver function test (LFT) may be obtained to assess for increased bleeding risk or underlying coagulopathies.[1]

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 surgery is required, appropriate factors are administered preoperatively and intraoperatively. The presence of coagulopathy may be associated with worse outcomes.[16]

In adults, EDH rarely causes a significant drop in 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 may lead to hemodynamic instability; therefore, careful and frequent monitoring of the hematocrit level is required.

Advances in contemporary computed tomography (CT) imaging have made confirmation of an EDH diagnosis rapid and accurate. Although EDH is relatively uncommon (approximately 2% of all patients with head injuries and < 10% of those who are comatose), it should always be considered in evaluation of a serious head injury.

Radiography

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 fracture. In children, this rate is less because of greater skull deformability.

CT scanning

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

(See the image below.)

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

Signal density of the hematoma compared with the brain parenchyma changes over time after injury. The acute phase is hyperdense (ie, bright signal on CT scan). The hematoma becomes isodense at 2-4 weeks; 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, 17, 18]

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

(See the images below.)

Approximately 10-50% of EDH cases are associated with other intracranial lesions. These lesions include subdural hematomas, cerebral contusions, and intracerebral hematomas. 

A case report of a rare case of spontaneous resolution of EDH describes a 20-year-old male with a history of a fall from height for whom initial scan showed a large EDH requiring surgical evacuation. Subsequent scans showed near-complete resolution, changing the management approach from surgical to conservative. Study authors state that rare cases like this should always be kept in mind, and the importance of a repeat scan should never be disregarded.[19]

Gean et al reported a series of 21 patients with anterior temporal tip epidural hematoma.[8] These lesions usually were 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

Brain magnetic resonance imaging (MRI) is more sensitive than CT scanning, particularly when one is assessing for EDH in the vertex. Magnetic resonance imaging should be conducted when high clinical suspicion for EDH accompanies a negative initial head CT scan.[1]

For suspected spinal EDH, spinal MRI is the preferred imaging modality, as it affords higher resolution than spinal CT.[1]

Diagnosis of symptomatic postoperative EDH requires correlation of clinical signs and symptoms with a compressive hematoma on MRI. Patient reports of a marked increase in axial pain, followed by radicular symptoms in the extremities and then motor weakness and sphincter dysfunction, should be investigated by an MRI obtained emergently; if a compressive hematoma is confirmed, surgical evacuation should be carried out as quickly as possible.[14]

Acute blood on MRI is isointense, making this modality not well suited to detection of hemorrhage in acute trauma. However, mass effect may be observed.[9]

Angiography

When EDH located in the vertex is evaluated, the healthcare professional should look for the presence of a dural arteriovenous fistula that may have arisen from the middle meningeal artery. Angiography may be required to fully evaluate the presence of such a lesion.[1]

The treatment approach for patients with EDH depends on various factors. Adverse effects on brain tissue are mainly the result of mass effect causing structural distortion, life-threatening brain herniation, and increased intracranial pressure. Treatment options for these patients are (1) immediate surgical intervention and (2) initial, conservative, close clinical observation with possible delayed evacuation. Note that EDH tends to expand in volume rapidly, and patients require very close observation if the conservative route is taken.

A case report of a 31-year-old male patient who underwent a left craniotomy for acute EDH followed by successful postoperative embolization for an expanding right-sided EDH revealed that endovascular exploration and possible follow-up treatment can be justified in patients with EDH who do not have a clear surgical indication.[20]

Early follow-up scanning should be performed 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 if the patient develops anisocoria or a neurologic deficit, surgery is indicated. Middle meningeal artery embolization has been described in the early stages of EDH, especially when angiographic dye extravasation has been observed.

Not all cases of acute EDH require immediate surgical evacuation.[21, 22] If a lesion is small and the patient is in good neurologic condition, observing the patient with frequent neurologic examinations is reasonable. One subset of this entity, acute anterior temporal tip EDH, runs a benign course, which usually can be followed by imaging and observation. The likely venous origin of this condition contributes to slow expansion and eventual tamponade of the bleeding source.[8]

In a retrospective review over a 5-year period of patients with EDH 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.[23]

Conservative management is often left to clinical judgment. The Brain Trauma Foundation (BTF) Guidelines for the Management of Severe Head Injury recommends that patients who exhibit an EDH that measures less than 30 mL, is less than 15 mm thick, and has less than 5-mm midline shift, with no focal neurologic deficit and with GCS greater than 8, can be treated nonoperatively.[24]  These traumatic brain injury (TBI) guidelines have been expanded, refined, and made increasingly more rigorous in conjunction with new clinical evidence and evolving methodologic standards. Perhaps the greatest limitation of TBI guidelines is the lack of high-quality clinical research, as well as of novel diagnostics and treatments, on which substantially new recommendations can be based.[25]

A population-based study examined effects on patient outcomes when clinicians adhered to BTF guidelines for intracranial pressure monitoring while treating patients with severe TBI. Study authors reported that greater adherence to these guidelines was associated with higher mortality rates (OR 2.01, 95% CI, 1.56-2.59; P< 0.001), greater morbidity, and increased intensive care unit and hospital lengths of stay (P< 0.001), leading them to conclude that current BTF criteria for insertion of ICP monitors may fail to identify patients likely to benefit.[26]

Temporal hematomas, if they are large or expanding, may lead to uncal herniation and rapid deterioration. Epidural hematoma in the posterior fossa, which is frequently related to interruption of the lateral venous sinus, often requires prompt evacuation because of the limited space available compared with the supratentorial compartment.[27]

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

(See the images below.)

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

Drilling of exploratory burr holes is currently reserved for the following circumstances:

• Definitive localizing signs and clinical evidence of intracranial hypertension in patients who are unable to tolerate a CT scan because of severe hemodynamic instability

• Immediate surgical intervention for systemic injuries

Reports have described burr holes with negative pressure drainage as a primary mode of EDH treatment in select patients (ie, patients awaiting transfer to a higher-level trauma facility, or patients with hemorrhage of nonarterial origin).[28]  However, despite these reports, craniotomy remains the standard treatment.

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, which are often used for intracranial surgery, are not routinely applied because they may propagate existing skull fractures.

Occipital or posterior fossa EDH requires positioning in the lateral, semi-prone, or prone position. Three-point head clamps are then applied with care to achieve stable head fixation.

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

Surgical treatment of EDH involves opening the calvaria over the site of hemorrhage. The EDH, whcih is readily apparent after elevation of the bone flap, 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 by head-of-the-bed elevation, with care taken to avoid venous air embolism. The utmost care should be taken when depressed bone fragments on or near the dural venous sinuses are elevated. 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 with clinical signs of intracranial hypertension, a small incision is made in an area considered to be over the hematoma. A rapid burr hole is created, and the epidural is partially evacuated. This maneuver often provides 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 ultrasonography is sometimes helpful in identifying such lesions. Occasionally, the bone flap (decompressive craniectomy) may not be reattached to the skull and instead is stored in a freezer, discarded, or preserved in the abdominal fat layer. This occurs when significant intracerebral swelling or injury is noted on initial CT scan or is encountered during the operation, or when intractable intracranial hypertension develops during the postoperative period. Such decompression can allow for further brain expansion.

Patients usually are treated in the intensive care unit or in a monitored setting until their condition improves. Associated intracranial or systemic injuries are managed as needed. Depending on their neurologic condition and on 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 facilitate evaluation for delayed hematoma.

Many of the complications associated with EDH occur when pressure 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, most often in the pons.

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

Drifting of the extremity when the patient is asked to hold both arms outstretched with palms facing upward indicates subtle but significant mass effect.

Epidural hematoma is an emergent neurosurgical disease that can be managed with close clinical and radiographic observation or by 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 burr hole evacuation with negative pressure may need to be further investigated.[28] In addition, endovascular approaches may be a new avenue for investigation. 

A case report of a 31-year-old male patient who underwent a left craniotomy for acute EDH followed by successful postoperative embolization for an expanding right-sided EDH revealed that endovascular exploration and possible follow-up treatment can be justified in patients with EDH who do not have a clear surgical indication.[20]

The Brain Trauma Foundation (BTF) Guidelines for the Management of Severe Head Injury were the first clinical practice guidelines published by any surgical specialty. These guidelines, which were provided in 2007, have earned a reputation for rigor and have been widely adopted around the world. Implementation of these guidelines has been associated with a 50% reduction in mortality and reduced costs of patient care. Since the time of publication, these traumatic brain injury (TBI) guidelines have been expanded, refined, and made increasingly more rigorous in conjunction with new clinical evidence and evolving methodologic standards.[25]

Planned changes to future TBI guidelines are intended to increase their utility and positive impact in an evolving medical landscape. Perhaps the greatest limitation of TBI guidelines is the lack of high-quality clinical research, as well as novel diagnostics and treatments, on which to based substantially new recommendations.[25]