Nonoperative Management of Acute Epidural Hematoma Diagnosed by CT: The Neuroradiologist’s Role

As computerized tomography (CT) becomes commonplace in the management of head injuries, clinically silent or unsuspected intracranial pathology is recognized with increasing frequency. Contusions, subarachnoid hemorrhage, and small subdural hematomata in patients who have no neurologic deficits are not uncommon. These lesions do not usually dictate operative intervention unless clinical deterioration occurs, so that their discovery serves mainly to make the already watchful eye more vigilant. Considerably less agreement exists among neurosurgeons regarding the treatment of asymptomatic or mildly symptomatic epidural hematomas (EDH). A number of reports of conservatively managed EDH, suggests that some of these lesions may resolve spontaneously and without sequelae. On the other hand, since the surgical management of EDH is relatively simple and has a very low morbidity, many neurosurgeons recommend immediate evacuation rather than placing patients at risk for deterioration. In the present paper, Hamilton and Wallace describe and analyze their experience with EDHs in order to delineate clinical and CT criteria for conservative management of these lesions ( 1 ). The authors conduct a retrospective analysis of 48 patients with EDH, seen at their center over the past 5 years. Eighteen of these patients were managed conservatively; the remainder underwent suPgery at presentation. The two groups were compared with respect to clinical condition, size, and location of the EDH, radiographic characteristics, and the outcome of the treatment each received. The natural history of epidural hematomas is at the center of this discussion. Epidural hematomas can be caused by a variety of mechanisms (laceration of the middle meningeal artery, venous oozing from overlying fracture, laceration of dural venous sinus), and their natural history is likely to be equally varied. When reporting the history of a conservatively managed case, therefore, it is important to have an accurate assessment of the patient's condition at presentation, the location (and proposed mechanism) of the EDH, as well as its size and the time of its discovery. The authors present a number of interesting findings in their study; still, their conclusions can be considered only preliminary, as not all facets of the natural history are addressed. Also, the retrospective nature of this study introduces an element of bias to its conclusions. Hamilton and Wallace carefully analyze the existence and location of skull fractures in their cases, in an effort to compare the probable mechanisms of EDH formation . They find no statistical difference between the groups, suggesting that hematomas caused by laceration of the middle meningeal artery or a major venous sinus are no more likely to produce rapid deterioration than those caused by venous oozing. This finding may be a function of the retrospective nature of this study; it has not been the experience in prospective series (2). The timing of EDH discovery is crucial, since the likelihood that a hematoma will remain silent increases the longer the lesion has been asymptomatic. The authors do not address this issue in the current series. Also, if we assume that patientc were seen shortly after injury, no statement can be made regarding the natural history of subacute or chronic hematomas. Hamilton and Wallace compare the average sizes of the EDHs carefully and, not surprisingly, find that the operated patients had larger hematomas. Since such measurements do not necessarily reflect the brain 's compliance, their use in conjunction with midline shift is more informative, as in this paper. The fact that the "presence of lucent areas within the hematoma likely indicates active bleeding and suggests the need for