Intracranial acute epidural hematoma
Epidemiology
Incidence of epidural hematoma (EDH): 1% of head trauma admissions (which is ≈ 50% the incidence of acute subdurals). Ratio of male:female = 4:1. Usually occurs in young adults, and is rare before age 2 yrs or after age 60 (perhaps because the dura is more adherent to the inner table in these groups).
Etiology
Dogma was that a temporoparietal skull fracture disrupts the middle meningeal artery as it exits its bony groove to enter the skull at the pterion, causing arterial bleeding that gradually dissects the dura from the inner table resulting in a delayed deterioration. Alternate hypothesis: dissection of the dura from the inner table occurs first, followed by bleeding into the space thus created. Source of bleeding: 85%=arterial bleeding (the middle meningeal artery is the most common source of middle fossa EDHs). Many of the remainder of cases are due to bleeding from middle me- ningeal vein or dural sinus. 70% occur laterally over the hemispheres with their epicenter at the pterion, the rest occur in the frontal, occipital, and posterior fossa (5–10% each).
Epidural hematoma often has a traumatic origin and in most of cases is caused by a medial meningeal artery lesion. The blood collection grows rapidly in the epidural space, compressing the underlying brain parenchyma. Several observations on EDH have shown that clots confined to the temporal fossa produce uncal herniation more rapidly and with a smaller critical volume than clots located elsewhere 1).
Ford and McLaurin demonstrated that EDH achieves nearly full size within a very brief period following the injury, suggesting that physical and chemical effects other than increasing size may be the cause of neurologic deterioration in untreated cases. Several authors emphasized the effects of cerebral edema, hypoxia, and/or impaired cerebrospinal fluid (CSF) drainage as causing the deleterious effects of the hematoma 2) 3).
Classification
see Bilateral intracranial acute epidural hematoma.
Spontaneous (nontraumatic) acute epidural hematoma is a rare and poorly understood complication of sickle cell disease.
Diagnosis
Treatment
Outcome
The mortality rates range from 1.2 to 33%.
The mortality rate associated with this condition has improved radically since the time of Rose and Carless, who in 1927 reported mortality rates of 86% 4).
With modern surgical and anaesthesia techniques, the mortality rate of epidural hematomas has been reduced to almost 0% in non-comatose patients 5).
The surgical intervention for severe traumatic brain injury (TBI) caused by extra-axial hemorrhage has declined in recent decades. The effect of this change on patient outcomes is unknown.
Patients with epidural hematomas who meet surgical criteria and receive prompt surgical intervention can have an excellent prognosis, presumably owing to limited underlying primary brain damage from the traumatic event.
Case series
Case reports
A 30-year old man arrived at the Emergency Department after a traumatic brain injury. General examination revealed severe headache, no motor or sensory disturbances, and no clinical signs of intracranial hypertension. A CT scan documented a significant left fronto-parietal epidural hematoma, which was considered suitable for surgical evacuation. The patient refused surgery. Following CT scan revealed a minimal increase in the size of the hematoma and of midline shift. The neurologic examination maintained stable and the patient continued to refuse the surgical treatment. Next follow up CT scans demonstrated a progressive resorption of hematoma.
This report an unusual case of a remarkable epidural hematoma managed conservatively with a favorable clinical outcome. This case report is intended to rather add to the growing knowledge regarding the best management for this serious and acute pathology 6).