Although intracranial epidural hematomas are relatively uncommon (less than 1% of all patients with head injuries and fewer than 10% of those who are comatose), they should always be considered in evaluation of a serious head injury.
The condition is present in one to three percent of head injuries.
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).
Spontaneous (nontraumatic) acute epidural hematoma is a rare and poorly understood complication of sickle cell disease.
see also Intracranial chronic epidural hematoma.
In the era before computerized tomography (CT), extradural hematomas were usually diagnosed by invasive and less accurate techniques, such as cerebral angiography, pneumoencephalography, or exploratory burr holes. Thus, the philosophy for immediate and universal evacuation to avoid the inevitability of brain stem compression is understandable. However, with the advent of CT, an increasing number of patients receive imaging despite minimal neurologic findings. In some cases, an EDH may be identified and the surgeon must decide whether to recommend surgical intervention 4).
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% 5).
With modern surgical and anaesthesia techniques, the mortality rate of epidural hematomas has been reduced to almost 0% in non-comatose patients 6).
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.
125 patients (75% of all EDH) were included. The mean age was 39.1 years. The brain injury was mild in 62.4% of the sample and severe in 14.4%. Only 11.2% of the patients required surgery. Statistical comparison showed that younger age (p< 0.0001) and coagulopathy (p=0.009) were the only significant factors for conversion to surgery. There was no difference in outcomes between patients who had EDHP and those who did not.
Most traumatic EDH are not surgical at presentation. The rate of conversion to surgery is low. Significant predictors of EDHP are coagulopathy and younger age. These patients need closer observation because of a higher risk of EDHP. Outcome of surgical conversion was similar to successful conservative management 7).
In a retrospective cohort study, the Washington State Trauma Registry was queried from 1995 to 2012 for patients with extra-axial hemorrhage and head Abbreviated Injury Scale score of 3 to 5. Data were linked to the state-wide death registry to analyze long-term mortality. The primary outcome was inpatient mortality. Secondary outcomes included 6- and 12-month mortality and modified Functional Independence Measure at discharge. Multivariable analyses were completed for all outcomes.
A total of 22974 patients met inclusion criteria. Over the study period, surgical intervention for severe TBI declined from 36% to 7%. There was a decline in case fatality from 22% to 12%. In 2012, the relative risk of inpatient mortality was 23% lower compared with 1995 (adjusted mortality risk ratio, 0.77; 95% confidence interval, 0.63-0.94). Changes in 6- and 12-month adjusted mortality and modified Functional Independence Measure were not statistically significant.
The decline in surgical intervention for severe TBI caused by extra-axial hemorrhage in Washington State was ubiquitous across regional, demographic, and injury characteristic strata. There was concurrently a reduction in inpatient mortality in this population. Functional status and long-term mortality, however, have remained the same. Future studies are needed to better identify modifiable risk factors for improvement in functional status and long-term mortality in this population 8).
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 9)