You are in: eMedicine Specialties > Neurosurgery > Trauma Epidural HemorrhageArticle Last Updated: Dec 11, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Jamie S Ullman, MD, Associate Professor, Department of Neurosurgery, Mount Sinai School of Medicine; Director, Department of Neurosurgery, Elmhurst Hospital Center Jamie S Ullman is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, and Congress of Neurological Surgeons Coauthor(s): Anthony Sin, MD, Staff Physician, Department of Neurosurgery, Louisiana State University Editors: Michael G Nosko, MD, PhD, Chief, Division of Neurosurgery, Director of Neurovascular Surgery, Medical Director of Neuroscience Unit, Associate Professor, Department of Surgery, University of Medicine and Dentistry at New Jersey; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Ryszard M Pluta, MD, PhD, Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences at Warsaw, Poland; Senior Researcher, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH; Herbert H Engelhard III, MD, PhD, Director, UIC Neuro-Oncology Program, Chief, Division of Neuro-Oncology, Associate Professor, Department of Neurosurgery, University of Illinois at Chicago; Allen R Wyler, MD, Medical Director, Northstar Neuroscience, Inc Author and Editor Disclosure Synonyms and related keywords: epidural hemorrhage, EDH, epidural hematoma, extradural hematoma, extraaxial hematoma, extraaxial collection, extra-axial hematoma, extra-axial collection, extradural hemorrhage, extraaxial hemorrhage, extra-axial hemorrhage, blunt head trauma, head trauma, acute epidural hematoma INTRODUCTIONSection 2 of 12
  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. ProblemEDH 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. FrequencyAs 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.{{Ref1} Approximately 17% of previously conscious patients who deteriorate into coma following a trauma have EDH. EtiologyTrauma 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.2 PathophysiologyUnlike 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. 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). ClinicalMost 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.3 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. 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. INDICATIONSSection 3 of 12
The diagnosis and indications for treatment of EDH are discussed in the following sections. RELEVANT ANATOMYSection 4 of 12
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. CONTRAINDICATIONSSection 5 of 12
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. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
TREATMENTSection 7 of 12
Medical therapyTreatment 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. When treating patients with spontaneous EDH, the underlying primary disease process must be addressed in addition to the fundamental principles discussed above. Surgical therapyAccording 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. 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:
Preoperative detailsPatients 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 detailsSurgical 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 detailsPatients 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-upFollow-up CT scans are performed to determine the extent of clot evacuation. These scans can also help evaluate for delayed hematomas. COMPLICATIONSSection 8 of 12
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 PROGNOSISSection 9 of 12
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 CONTROVERSIESSection 10 of 12
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. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Article Last Updated: Dec 11, 2007 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
