In this article, the author describes cranial epidural hematoma primarily as a result of traumatic head injury. It represents a hemorrhage between the dura mater and the inner table of the skull. Focal and global neurologic deficits are common, and the mainstay of treatment is surgical decompression. In this review, he describes the pathophysiology, diagnosis, and management of epidural hematoma. Updates to this article include a review of newer imaging techniques that assist with evaluating the extent of associated brain injury and prognosis in patients with traumatic epidural hematoma.
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• The recognition and surgical treatment of traumatic cranial epidural hematoma has a history dating back thousands of years to the earliest reports of skull trepanation.
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• The modern era of CT scanning beginning in the late 1970s and early 1980s brought early diagnosis and rapid surgical evacuation of epidural hematoma, potentially eliminating fatal outcome unless there is additional traumatic brain injury.
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• The majority of traumatic epidural hematomas evolve rapidly from arterial bleeding and evolve clinically during the initial 24 hours.
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• A subset of adult and pediatric patients with small epidural clot volume and minimal symptoms may be treated nonsurgically with support and close observation and may demonstrate spontaneous resolution.
Historical note and terminology
Hemorrhage into the cranial epidural (or “extradural”) space is 1 of the oldest recognized and most treatable of all neurosurgical disorders. Neolithic man (10,000 to 7000 BC) utilized skull trepanation for a variety of purposes (49). This practice was advanced by the ancient Chinese, Mesopotamians, and pre-Columbian Americans. The Incas were particularly adept at skull trepanation, employing this technique to evacuate traumatic clots. During the mid-5th century BC in ancient Greece, Hippocrates formulated a classification system for head injuries and recommended trepanation for some, recognizing the intimate association between epidural hemorrhage and head trauma. Five centuries later, the writings of Celcus, Galen, and Paulus advocated surgical exploration of the epidural space via rudimentary craniotomies to evacuate fragments of bone, elevate depressed fractures, and drain blood, pus, and other humors (32).
Interest in the surgical treatment of intracranial pathology waned during the Dark Ages, and was not rekindled until the latter portion of the Renaissance. Prominent physicians of the 17th and 18th centuries such as Heister, Pott, and Larry began to correlate the presence of intracranial mass lesions with somatic manifestations such as hemiparesis and aphasia. Heister and Pott advocated the placement of multiple calvarial trephines contralateral to the side of hemiparesis in the unconscious patient, in an effort to localize and decompress a causative epidural mass. From this time forward, epidural hematoma has been recognized as a lesion for which surgical treatment is indicated (32).
Soon after, investigators began to delineate the pathophysiological mechanisms underlying epidural hematoma formation. In 1779, Erichsen proposed that detachment of the dura from the inner calvarial table was requisite for the formation of such a lesion. In 1816, Charles Bell demonstrated that blows to the cranium caused the dura to strip away from the calvarium at the site of impact. He postulated that disruption of a dural artery or venous sinus in the traumatized region allowed blood to accumulate within the epidural pocket; if under sufficient pressure, the hemorrhage would further dissect the dura from the inner table and permit lesion expansion.
Treatment of epidural hemorrhage advanced during the late 19th and early 20th centuries by such neurosurgical pioneers as Victor Horsley, W.H. Jacobson, Harvey Cushing, Hugh Cairns, and Walter Dandy (49). Improvements in surgical anesthesia and an emphasis on antisepsis during this time also contributed to enhanced patient survival. In 1941, Munro and Maltby published the first large series of surgically treated patients with traumatic epidural hematomas (57). Their results indicated that survival correlated directly with level of consciousness immediately prior to operation, a concept that has been verified by many subsequent investigators.
In the following half-century, the principal objective in the management of epidural hemorrhage was to improve patient survival via (1) early diagnosis, (2) rapid treatment, and (3) intensive postoperative care. Initially, positive change was effected through widespread education and training, new additions to the critical care arsenal (particularly mechanical ventilation), and aggressive surgical indications. The patient suspected of harboring an epidural hematoma was subjected to immediate burr-hole exploration at various sites over the calvarium as dictated by the neurologic examination. Radiological investigations, including plain skull films, cerebral angiography, and ventriculography, were considered "unnecessary" and excessively "time consuming" and were, thus, omitted in favor of diagnosis by trepanation. With these aggressive surgical techniques, Jamieson and Yelland reported a major reduction in mortality (15.6% overall, 1.4% if noncomatose) from epidural hemorrhage, justifying their belief in the importance of early diagnosis and treatment of this lesion (36). Later, the advent of reliable neurodiagnostic modalities such as CT played a principal role in improving outcome by facilitating rapid diagnosis, precise anatomical localization, recognition of associated injuries, and identification of subclinical lesions (23). The now-ubiquitous availability of modern imaging techniques coupled with vastly improved pre-hospital care standards, rapid triage systems, and improved postoperative care have allowed the modern neurosurgeon to approach the goal of zero mortality in the treatment of isolated epidural hematoma (10).