Epidural Hemorrhage Treatment & Management

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.^{[8, 9]} If a lesion is small and the patient is in good neurological condition, observing the patient with frequent neurological examinations is reasonable.

Although conservative management is often left to clinical judgment, the recently published "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.^[10] 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.

According to the "Guidelines for the Management of Traumatic Brain Injury,"^[10] EDH with volume greater than 30 mL should undergo surgical evacuation, regardless of GCS.^[10] 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).

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).^{[11, 12]} However, despite these reports, craniotomy remains the standard.

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.

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.

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.

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.

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.^{[11, 12]} 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.^[13] This therapy was reserved for patients who demonstrated contrast dye extravasation on CT scans. The desired result was achieved in all 9 patients.