Epidural Hematomas Workup
- Author: Jamie S Ullman, MD; Chief Editor: Brian H Kopell, MD more...
Hematocrit level, chemistries, and coagulation profile (including platelet count) are essential in the assessment of patients with EDH, whether spontaneous or traumatic.
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 required, appropriate factors are administered preoperatively and intraoperatively. Presence of coagulopathy may be associated with worse outcomes.
In adults, EDH rarely causes a significant drop in the 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 can result in hemodynamic instability; therefore, careful and frequent monitoring of the hematocrit level is required.
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 fractures. In children, this rate is less because of greater skull deformability.
CT scanning is the most accurate and sensitive method of diagnosing acute EDH. The findings are characteristic. The space occupied by EDH is limited by the adherence of the dura to the inner table of the skull, especially at the suture lines, contributing to the lenticular or biconvex appearance (see the image below). Hydrocephalus may be present in patients with a large posterior fossa EDH exerting a mass effect and obstructing the fourth ventricle.
Cerebrospinal fluid is not commonly mixed with epidural hematomas; therefore, the hematoma is denser and homogenous. The quantity of hemoglobin in the hematoma determines the amount of radiation absorbed.
The signal density of the hematoma compared with the brain parenchyma changes over time after the injury. The acute phase is hyperdense (ie, bright signal on CT scan). The hematoma then becomes isodense at 2-4 weeks, and then 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.[10, 11, 5]
Another less frequently involved area is the vertex, an area in which confirming the diagnosis on CT scans may be difficult. Vertex epidural hematomas can be mistaken as artifact in traditional axial CT scan sections. Even when correctly detected, the volume and the mass effect may easily be underestimated. In some cases, coronal and sagittal reconstructions can be used to evaluate the hematoma on 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 2009 study by Park et al suggests that routine repeat CT scanning within 24 hours of blunt head trauma may lessen potential neurological deterioration among patients with a GCS of less than 12, epidural hematoma, or multiple lesions, as indicated on initial CT scanning.
Gean et al reported a series of 21 patients with anterior temporal tip epidural hematomas. These lesions were usually 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.
Acute blood on MRIs is isointense, making this modality less suited to detection of hemorrhage in acute trauma. Mass effect, however, can be observed when extant.
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