Intracranial epidural hematoma in adults

INTRODUCTION — Subdural hematoma (SDH) and epidural hematoma (EDH) are characterized by bleeding into the spaces surrounding the brain or spinal cord.

●SDHs form between the dura and the arachnoid membranes.

●EDHs arise in the potential space between the dura and the skull.

Clinical issues related to intracranial EDH in adults will be reviewed here. A rapid overview summarizes the clinical features, evaluation, and management of EDH in adults (table 1).

EDH in children and SDH are discussed separately:

●(See "Intracranial epidural hematoma in children".)

●(See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis".)

EPIDEMIOLOGY AND ETIOLOGY — EDH is an uncommon but serious complication of head injury. While the exact incidence is unknown, it is found in 1 to 4 percent of traumatic head injury cases and 5 to 15 percent of autopsy series [1,2].

The incidence of EDH is highest among adolescents and young adults. In observational studies, the mean age of patients with EDH is between 20 and 30 years of age [2]. EDH is rare in patients older than 50 to 60 years of age.

Most cases of EDH are due to head trauma caused by traffic accidents, falls, and assaults. Skull fractures are present in 75 to 95 percent of patients [3].

In the setting of closed head injury, the linear translation of acceleration along the diameter of the skull in the lateral direction can produce injury to veins, arteries, or brain parenchyma, resulting in subdural hematoma (SDH), EDH, or coup-countercoup contusions [4]. In addition, thalamic lesions and secondary brainstem injury may develop as a consequence of the mass effect produced by a large EDH or SDH.

Key differences between SDH and EDH are readily demonstrable by unenhanced computed tomography (CT) of the head. EDH does not cross sutural margins but does cross dural attachments because it is located in the potential space between dura and skull. As a result, EDH characteristically has a lens-shaped appearance. In comparison, SDH can cross sutural margins but is limited by dural attachments and therefore appears as a crescent-shaped extra-axial lesion.

EDH in adults is most commonly (approximately 85 percent of cases) due to arterial injury [1,2,5]. The major cause of arterial injury is trauma to the skull base with associated tearing of the middle meningeal artery as it courses through the foramen spinosum, resulting in hemorrhage over the cerebral convexity in the middle cranial fossa. In addition, EDH is occasionally found in the anterior cranial fossa, owing to rupture of the anterior meningeal artery, and rarely due to a dural arteriovenous fistula at the vertex [6].

In approximately 15 percent of cases, injury to one of the dural sinuses or the confluence of sinuses in the posterior cranial fossa proves to be the source of hemorrhage [1].

Nontraumatic acute EDH is rare. Potential etiologies include:

●Infection, coagulopathy, congenital anomalies, vascular malformations of the dura, and hemorrhagic tumors [7,8]

●Complication of neurosurgical procedures

●Epidural abscess, leading to pressure necrosis of meningeal vessels [9]

●Pregnancy, sickle cell disease, systemic lupus erythematosus, open heart surgery, Paget disease of the skull, and hemodialysis [8,10-14]

Postulated mechanisms of EDH during hemodialysis include fluctuations of intracranial pressure, heparin administration, hypertension in the presence of anticoagulation, and uremic platelet dysfunction [11,15].

CLINICAL MANIFESTATIONS — As with subdural hematoma (SDH), the initial presentation of EDH has a spectrum of manifestations. Severe head trauma may result in EDH with coma, while a lesser injury may produce EDH with only momentary loss of consciousness.

In some patients with acute EDH and transient loss of consciousness, there is a so-called "lucid interval" with recovery of consciousness, followed by deterioration over a period of hours due to continued arterial bleeding and hematoma expansion [16]. This deterioration is typically associated with symptoms such as headache, vomiting, drowsiness, confusion, aphasia, seizures, and hemiparesis [2,17].

In a systematic review, a lucid interval followed by deterioration was observed in 456 of 963 patients (47 percent) who had surgery for EDH [2]. A similar sequence can be seen with EDH due to venous bleeding, with the exception that the neurologic decline is typically slower, occurring over days to weeks [17].

In any of the above settings, unchecked hematoma expansion leads to elevated intracranial pressure and clinical signs, such as an ipsilateral dilated pupil (due to uncal herniation with compression of the oculomotor nerve) or the Cushing reflex (ie, hypertension, bradycardia, and respiratory depression/irregularity). Such events will culminate in brain herniation and death unless immediate decompression is undertaken.

Approximately 7 to 14 percent of traumatic intracranial EDHs occur in the posterior fossa [18]. Such patients may present with elevated intracranial pressure due to venous sinus obstruction [19]. In some instances, cortical blindness is observed secondary to bioccipital dysfunction [20].

DIAGNOSTIC EVALUATION — In the setting of acute head trauma, imaging serves a key role in both diagnosis and appropriate initial treatment [21,22]. In addition to EDH, head trauma is a major cause of a variety of other central nervous system lesions including subdural hematoma (SDH), subarachnoid hemorrhage, cerebral contusion, diffuse brain swelling, and laceration [2,17]. Any of these injuries may coexist in a given patient following trauma, and their clinical manifestations can be difficult to distinguish. However, it is important to identify the specific nature of the lesion during initial evaluation, since potentially life-saving treatment will differ with the lesion.

Lumbar puncture is contraindicated in cases where a space-occupying lesion such as EDH is suspected, due to the risk of herniation.

Head CT — Computed tomography of the head is the most widely used imaging study for acute head trauma owing to its speed, relative simplicity, and widespread availability [21]. Most EDHs are identifiable on CT.

Findings — Epidural blood produces a lens-shaped or biconvex pattern on head CT because its collection is limited by firm dural attachments at the cranial sutures (image 1) [1,22].

Occasionally, heterogeneous foci of lower attenuation appear within an acute EDH. This finding of a mixed-density blood clot (or swirl sign) indicates active extravasation of blood and represents an indication for immediate surgical evaluation [4].

Of note, acute EDH may not be apparent on initial head CT in up to 8 percent of cases [23]. Several issues may be associated with a nondiagnostic head CT, including:

●Severe anemia, which lowers the density of the hemorrhage

●Severe hypotension, which reduces the rate of arterial extravasation

●Early scanning after trauma, before enough blood has accumulated to be visible on imaging

●Venous bleeding with slow accumulation of blood

Hematoma volume estimation — Hematoma volume influences management decisions in adult patients with acute EDH because it correlates with outcome. The hematoma volume can be estimated quickly from the head CT scan by using the formula ABC/2, which approximates the volume of an ellipsoid. This formula was originally used to estimate intracerebral hemorrhage volume but can be applied to EDH as well [2].

The formula is calculated using the centimeter scale on the CT images as follows [24]:

●A is the greatest hemorrhage diameter on the CT slice with the largest area of hemorrhage

●B is the largest diameter 90 degrees to A on the same CT slice

●C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness in centimeters

To calculate C, each CT slice with hemorrhage is visually compared with the CT slice with the largest hemorrhage [24]. An individual hemorrhage slice is counted as one full slice for determining C if the hemorrhage area is >75 percent of the area on the slice with the largest hemorrhage. A slice is counted as one-half if the hemorrhage area is approximately 25 to 75 percent of the area on the largest hemorrhage slice. The slice is not counted if the area is <25 percent of the largest hemorrhage slice.

Brain MRI — Although head CT is more widely used, brain magnetic resonance imaging is more sensitive than head CT for the detection of intracranial bleeding (image 2) [25]. MRI is especially useful in the diagnosis EDH at the vertex [26]. In most centers, MRI is typically used an adjunct to CT in the evaluation of acute head trauma when there is a strong suspicion for EDH or SDH (ie, suppressed level of consciousness or focal neurologic deficit in the setting of trauma) despite no clear evidence of hematoma by CT.

The MRI signal appearance of EDH can evolve over time in a manner similar to that observed in parenchymal hematoma [17]. However, the timing of MRI signal progression in EDH is more variable and less well studied than with intracerebral hemorrhage.

●In the hyperacute phase (within hours of onset), the clot may be isointense or hyperintense on T2-weighted images. Signal heterogeneity within the clot may reflect active bleeding.

●The acute clot may be hypointense on T2-weighted images due to the presence of deoxyhemoglobin. On T2*-weighted (gradient recall echo or susceptibility-weighted) images, blood is typically hypointense.

●Over subsequent weeks, deoxyhemoglobin degrades to methemoglobin, which appears hyperintense on both T1- and T2-weighted images.

●At several months, only hemosiderin remains, and the clot again becomes hypointense on the T1-weighted images.

Angiography — Under unusual conditions, cerebral angiography is indicated for the evaluation of EDH. As an example, EDH located at the vertex can originate from a dural arteriovenous fistula of the middle meningeal artery. In this setting, angiography is necessary to fully evaluate the possibility of an underlying vascular lesion [6,27].

MANAGEMENT — Acute symptomatic EDH is a neurologic emergency that often requires surgical treatment to prevent irreversible brain injury and death caused by hematoma expansion, elevated intracranial pressure, and brain herniation. Select patients who present in good clinical condition with small-volume EDH can be managed nonoperatively as long as they remain stable. Close observation and serial brain imaging is an important aspect of nonoperative management, since hematoma enlargement and neurologic deterioration requiring surgery may occur in such patients.

Glucocorticoid therapy is not indicated following head injury including EDH as it has been associated with increased acute mortality. This issue is discussed separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Glucocorticoids'.)

Reversing anticoagulation — Coexistent anticoagulation in patients with either traumatic or spontaneous EDH is not uncommon and must be reversed before surgical intervention. In addition, we reverse anticoagulation for most patients who are managed nonoperatively. However, the potential benefit of reversing anticoagulation (a reduced risk of hematoma enlargement) must be weighed against the risk related to the underlying need for anticoagulation in this group (eg, atrial fibrillation, mechanical heart valve, etc).

Effective reversal of the effects of anticoagulation therapy varies by agent. Our preferred strategy for patients with EDH is similar to that recommended for patients with other forms of intracranial hemorrhage. (See "Reversal of anticoagulation in intracranial hemorrhage".)

●Warfarin – We use 4-factor prothrombin complex concentrate (PCC) along with vitamin K 10 mg by slow intravenous infusion (table 2). We use fresh frozen plasma (FFP) if PCC is not available. The goal of therapy should be an INR in the normal range (ie, <1.2 in most laboratories). (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Warfarin'.)

●Dabigatran – We use idarucizumab or a 4-factor PCC if idarucizumab is unavailable (table 3). (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Dabigatran'.)

●Direct factor Xa inhibitors (eg, apixaban, edoxaban, rivaroxaban) – We use either andexanet alfa or a 4-factor PCC (table 3). (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Apixaban, edoxaban, and rivaroxaban'.)

●Heparin and low molecular weight heparins – Protamine sulfate reverses the effects of heparins. The dose varies by the type of heparin used and the time elapsed since the last dose. Andexanet alfa may be used for patients taking low molecular weight heparin. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Unfractionated heparin' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'LMW heparin'.)

Deciding who needs surgery — Most patients with large or symptomatic EDH require emergent surgical hematoma evacuation to prevent irreversible brain injury or death caused by hematoma expansion, elevated intracranial pressure, and brain herniation. Criteria for surgery established by an expert panel in 2006 include patients with EDH and any of the following features [2]:

●Focal signs or symptoms attributable to the acute EDH

●Coma (Glasgow Coma Scale [GCS] score <9) and pupillary abnormalities due to acute EDH

●Large hematoma volume (>30 cm³ [>30 mL])

●Hematoma growth causing elevated intracranial pressure or neurologic deterioration

For patients with acute EDH who are awake and have no focal neurologic deficits, we suggest management based upon the size of the hematoma and the degree of midline shift, in agreement with guidelines [2]. Patients with a small hematoma (hematoma volume <30 cm³ and clot thickness <15 mm and midline shift <5 mm on brain imaging) are managed nonoperatively with close observation. Those not meeting these criteria are managed surgically.

Surgical techniques — Craniotomy with hematoma evacuation is the mainstay of surgical treatment of symptomatic acute EDH. When indicated, identification and ligation of the bleeding vessel must be undertaken. However, there are few data comparing different surgical techniques. Burr hole evacuation (trephination) has been used for acute EDH and may be lifesaving if access to neurosurgical expertise is limited or likely to be delayed [28]. Open craniotomy affords a more complete evacuation of the hematoma [2]. Craniectomy may be performed in selected cases when the EDH is associated with significant underlying cerebral edema or midline shift. An endovascular approach with middle meningeal artery embolization has been used to stabilize bleeding and avoid open surgery for some patients with small EDH [29].

Timing of surgery — The available evidence, though limited, suggests that surgery should be performed within one to two hours after head trauma or the onset of neurologic deterioration for comatose patients with acute EDH and signs of brain herniation. One series of patients with acute EDH compared surgery within two hours after onset of coma (n = 18) with later surgery (n = 16). Patients who had early evacuation had a significantly lower mortality rate (17 versus 56 percent) and higher rate of good recovery (67 versus 13 percent) [30]. Another series of adults with acute EDH and admission GCS score <8 included 10 patients who developed new anisocoria after admission [31]. Five patients had craniotomy more than 90 minutes after onset of anisocoria, and all of these patients died. Another five patients had craniotomy within 70 minutes after anisocoria onset, and all survived with either good recovery or moderate disability.

Nonoperative management — We recommend close observation to monitor for neurologic deterioration or hematoma enlargement for all patients with small or mildly symptomatic EDH who are managed nonoperatively. (See 'Deciding who needs surgery' above.)

●Serial clinical examinations – We monitor patients with EDH in an inpatient setting with neurosurgical expertise [2]. Neurologic assessments including the GCS score (table 4) should be performed every one to two hours for at least the first 24 hours after presentation. The frequency of examinations may be subsequently reduced for patients with stable imaging and clinical findings.

●Repeat head CT – We obtain surveillance repeat head CT scan no later than six to eight hours after initial imaging, in agreement with guidelines [2]. In addition, urgent repeat head CT is warranted for all patients with neurologic deterioration.

EDH expansion is likeliest in the first 36 hours after injury and may precede neurologic deterioration when expansion is mild or when severe initial impairment on neurologic examination limits the ability to assess for clinical deterioration. In a retrospective study of 160 adult patients with EDH who were managed nonoperatively, hematoma expansion on follow-up head CT was observed in 23 percent [32]. The mean time to enlargement after injury was eight hours, and enlargement occurred within 36 hours after injury in all cases where it was observed. Another retrospective study evaluated patients who had two head CT scans in the first 24 hours after traumatic brain injury, with a mean time to follow-up scan of seven hours [33]. Early hemorrhage expansion was seen in 22 percent of patients with EDH.

Progressive hematoma enlargement of small EDHs over several weeks has also been reported in patients followed by serial CT [17]. Calcification and ossification of persistent EDH has been reported and would suggest a need for surgical evacuation of EDHs that do not spontaneously absorb over the course of serial follow-up examinations, even if the patient's clinical condition is good [34].

No randomized trials have compared surgery with conservative management for patients with EDH, but retrospective data suggest that stable patients with EDH who have small hematomas and mild symptoms can be managed nonoperatively [35-37]. In one case series, 80 patients with acute EDH were selected for nonoperative management on the basis of a GCS score >8, an EDH volume <30 mL (<30 cm³), and clot thickness <20 mm [37]. Subsequent surgical evacuation for neurologic deterioration and hematoma enlargement occurred in five patients, one of whom died and four had a good outcome. In another series of 74 patients with traumatic EDH and good initial clinical status (GCS score >12) who were managed nonoperatively, neurologic deterioration occurred in 14 patients (19 percent), prompting delayed surgery [38]. Patients requiring surgery were more likely to have EDH volume >30 mL, clot thickness >15 mm, and midline shift >5 mm than those who did not have surgery. All patients in this series achieved a good outcome.

Intracranial pressure — Patients with EDH may develop elevated intracranial pressure requiring urgent intervention. Definitive therapy is usually hematoma evacuation; medical resuscitation techniques include head elevation, hyperventilation, and osmotic diuresis with intravenous mannitol or hypertonic saline. The management of elevated intracranial pressure is reviewed elsewhere. (See "Evaluation and management of elevated intracranial pressure in adults".)

PROGNOSIS — Data regarding outcome after EDH are mainly from observational studies. In surgical series, mortality after EDH in adults and children is approximately 10 and 5 percent, respectively [2]. The full range of outcomes is illustrated by the following studies:

●In a study that prospectively collected data for 107 consecutive patients with EDH, the overall mortality was 5 percent, and there were no deaths among patients with a Glasgow Coma Scale (GCS) score ≥8 who underwent hematoma evacuation [39]. At six months after injury, a good recovery was observed in 89 percent of the cohort.

●In a retrospective review of 139 adult patients with EDH admitted to an intensive care unit, 46 percent had a good recovery, 31 percent were moderately disabled, 10 percent were severely disabled, 4 percent were persistently vegetative, and 9 percent died [40].

Prognostic indicators — In observational studies, the following variables have been associated with unfavorable outcome from EDH [2]:

●Low GCS score on admission or before surgery [39,41-44]. The GCS grades coma severity according to three categories of responsiveness: best eye opening, best verbal, and best motor response. The GCS is scored between 3 and 15, with higher scores indicating better performance (table 4).

●Presence of pupillary abnormalities, particularly contralateral or bilateral unreactive pupils [31,42,43,45,46].

●Older age [43].

●Coagulopathy or leukocytosis at admission [44].

●Longer time interval between neurologic deterioration and surgery [30,31].

●Postoperative elevated intracranial pressure [40,46].

In addition, several studies have identified head CT findings that correlate with poor outcome:

●Hematoma volume >30 to 150 cm³ [42,45]

●Presence of midline shift >10 to 12 mm [42]

●Mixed-density blood clot, indicating acute bleeding [45]

●Presence of associated intracranial lesions such as contusions, intracerebral hemorrhage, subarachnoid hemorrhage, and diffuse brain swelling [30,42,43,45]

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)

SUMMARY AND RECOMMENDATIONS

●Rapid overview – A rapid overview summarizes the clinical features, evaluation, and management of EDH in adults (table 1).

●Definition and etiology – Epidural hematoma (EDH) is caused by bleeding in the potential space between the dura and the skull, usually as a consequence of traumatic injury. Nontraumatic acute EDH is rare. The source of blood in EDH is most often arterial, but 15 percent of cases are due to venous bleeding. (See 'Epidemiology and etiology' above.)

●Clinical features – Clinical manifestations of EDH are highly variable and include altered consciousness, headache, vomiting, drowsiness, confusion, aphasia, seizures, and hemiparesis. Some patients with acute EDH and transient loss of consciousness have a "lucid interval" with recovery of consciousness, followed by deterioration due to hematoma enlargement. (See 'Clinical manifestations' above.)

●Imaging diagnosis – Head CT is a fast and accurate method for the detection of acute intracranial hemorrhage (image 1). Epidural blood produces a lens-shaped pattern on head CT. Brain MRI has a higher sensitivity than CT and can be useful when diagnostic uncertainty exists. (See 'Diagnostic evaluation' above.)

●Management

•Reverse anticoagulation – Coexistent anticoagulation must be reversed before surgical intervention for patients with either traumatic or spontaneous EDH. In addition, we reverse anticoagulation for most patients who are managed nonoperatively (table 2 and table 3). However, the potential benefit of reversing anticoagulation to prevent EDH expansion must be weighed against the risk related to the underlying need for anticoagulation in this group. (See 'Reversing anticoagulation' above.)

•Surgery for most patients – Urgent surgical hematoma evacuation is required for patients with EDH that is large (ie, >30 mL) or causing focal or progressive neurologic deficits to prevent irreversible brain injury or death caused by hematoma expansion, elevated intracranial pressure, and brain herniation. In addition, we recommend surgical evacuation for patients with coma or early signs of brain herniation on imaging, given the potential for recovery (Grade 1C). Other patients with smaller EDH and milder symptoms may be managed nonoperatively with close observation. (See 'Management' above and 'Deciding who needs surgery' above.)

•Nonoperative surveillance – We recommend close observation to monitor for neurologic deterioration or hematoma enlargement for all patients with small or mildly symptomatic EDH who are managed nonoperatively. (See 'Nonoperative management' above.)

-We monitor patients with EDH in an inpatient setting with neurosurgical expertise. Neurologic assessments including the Glasgow Coma Scale (GCS) score (table 4) should be performed every one to two hours for at least the first 24 hours after presentation. The frequency of examinations may be subsequently reduced for patients with stable imaging and clinical findings.

-We obtain surveillance repeat head CT scan no later than six to eight hours after initial imaging. In addition, urgent repeat head CT is warranted for all patients with neurologic deterioration.

●Prognosis – The majority of patients have a good recovery with appropriate management of EDH, but mortality in adults and children is approximately 10 and 5 percent, respectively. Factors associated with poor prognosis include the severe neurologic deficits, the presence of pupillary abnormalities, larger hematoma volume or degree of midline brain shift, and coexisting trauma or coagulation disorders. (See 'Prognosis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges David Brock, MD, CIP, who contributed to an earlier version of this topic review.