| Discussion: Epidural hematoma (EDH) is defined as hemorrhage into the potential space between the dura, which is inseparable from cranial periosteum, and the adjacent bone. This topic has recently been heavily covered by the mass media since actress Natasha Richardson's death following an epidural hematoma resulting from a ski accident. Recommendations and guidelines - Epidural hematomas that are greater than 30 cm3 should be surgically evacuated regardless of the patient's Glasgow Coma Scale (GCS) score.
- In patients with a GCS score greater than 8 who do not have a focal deficit, epidural hematomas can be managed nonoperatively (with serial CT and neurologic observation) if they are less than 30 cm3, are less than 15 mm in thickness, and have less than a 5-mm midline shift (MLS).
- It is strongly recommended that patients undergo surgical evacuation as soon as possible if they have an acute EDH in coma (GCS score <9) with anisocoria.
- Although there are insufficient data to support one particular surgical treatment method for EDH, craniotomy has been shown to provide a more complete evacuation.
- Clot thickness, hematoma volume, and MLS on preoperative CT scans have been shown to correspond with outcome.
- In nonoperative patients with EDH, the first follow-up CT scan should be obtained within 6-8 hours after traumatic brain injury (TBI).
- A temporal location of EDH has been shown to be associated with failure of nonoperative management and should therefore lower the threshold for surgery
Less than 20% of patients have the classic clinical presentation of an initial injury with or without a temporary loss of consciousness followed by a lucent phase when they remain conscious as the hematoma enlarges. A fistulous connection between venous channels or extension through the fracture into the subgaleal space with resultant pseudoaneurysm formation may act to decompress the hematoma and halt expansion; however, EDH is considered a neurosurgical emergency in which somnolence, coma, and even herniation can result if it is untreated Almost always associated with preceding head trauma, most intracranial epidural hematomas result from skull fractures and the associated disruption or laceration of the arteries that lie along the inner table of the calvaria between the skull and the dura. The most common site of EDH is the temporoparietal region, where the anterior or posterior division of the middle meningeal artery or its trunk is lacerated. Blood then accumulates at the site of arterial injury, seldom crossing the cranial suture lines because of the tightly adherent periosteum at the suture margins. Dural venous sinus disruption/laceration
Another cause of EDH is disruption of the dural venous sinuses in the dura adjacent to a skull fracture. As many as 30% of EDHs are venous. When due to laceration of a dural venous sinus, EDHs usually occur in the frontal, parieto-occipital, or occipital region because of disruption of the superior sagittal sinus, torcular herophili, or lateral sinuses. The injured dural sinus is commonly stripped away from the adjacent calvaria by the expanding hematoma and occasionally occluded by an intimal tear resulting from the fracture. Because of the generally slow growth of a venous EDH, it may be found incidentally. Presenting symptoms, such as hydrocephalus resulting from mass effect on the cerebellum with a posterior fossa hematoma, may be delayed.8 Calvarial bending in children
In young children, open sutures and compliant bones result in increased calvarial flexibility, which may permit outward bending of the calvaria without fracture. This bending may lead to separation of the periosteum from the inner table of the skull and disruption of perforating arteries or veins, causing an EDH CT: CT may demonstrate the responsible fracture in addition to the hematoma. Epidural hematomas can typically be distinguished from subdural hematomas by their biconvex shape, compared to the crescent-shape of the subdural hematoma. If the epidural hematoma is small, it can be difficult to differentiate from subdural hematoma, and EDH may coexist with this condition. With typical biconvex, elliptical, extra-axial fluid collections, the CT appearance of EDH depends on the source of bleeding, the time elapsed since injury, the severity of hemorrhage, and the degree of clot organization and breakdown. - Acute, or type 1, EDH may contain both a hyperattenuating clot and a swirling lucency. These findings are believed to represent a mixture of active bleeding and the serum remaining after previous clot formation.
- Subacute, or type 2, EDH becomes homogeneously hyperattenuating as active bleeding ceases and organized clot forms.
- Chronic, or type 3, EDH is at least partly hypoattenuating as the clot undergoes breakdown and resorption. Enhancing membrane formation may result from neovascularity and the formation of granulation tissue in the displaced dura during the clot-resorption process.
MRI:
MRI demonstrates a biconvex mass separated from the overlying dura by a thin rim of extruded serum lying between the clot and the dura. This stripe is hyperintense on both T1- and T2-weighted images.Acute epidural hematoma is isointense to minimally hypointense on T1-weighted images and markedly hypointense on T2-weighted images; this appearance corresponds to the deoxyhemoglobin phase. Subacute EDH is hyperintense on T1-weighted images because deoxyhemoglobin is converted to methemoglobin. On T1-weighted images, the dura may be seen as a thin, hypointense stripe that the hematoma displaces inwardly |
EPIDURAL HEMATOMA
