Intracranial epidural hematoma (EDH) refers to bleeding between the dura mater and the calvarium. Most cases of EDH are traumatic, resulting from a head injury with an associated skull fracture that ruptures or tears the middle meningeal artery, which lies in close proximity to the skull and dura mater. EDH is more common in individuals 20–30 years of age, as the dura mater is not yet densely adherent to the calvarium at this age. The classic manifestation of EDH is an initial loss of consciousness, followed by a lucid interval in which the patient gains normal or near-normal consciousness, followed by rapid neurological decline. An ipsilateral dilated pupil (anisocoria) and contralateral hemiparesis are manifestations of transtentorial uncal herniation and signal imminent neurological decline. Neuroprotective measures to prevent secondary brain injury take precedence over diagnostic tests. Diagnosis is confirmed on a noncontrast CT head, on which EDH appears as a biconvex, hyperdense lesion, typically in the temporal or temporoparietal region. Surgical decompression with craniotomy is indicated in patients with large EDH, GCS ≤ 8, and evidence of neurological deterioration. Small, asymptomatic EDH in patients with GCS > 8 can be managed conservatively with close observation and serial CT scanning. The prognosis depends on several factors, including the GCS at presentation, size of the EDH, and, crucially, the time from the onset of brain herniation to decompressive surgery. Early intervention in patients with signs of brain herniation is associated with good neurological outcomes and lower mortality rates.
- Incidence: occurs in approx. 10% of patients with moderate to severe traumatic brain injury (TBI) 
- Sex: ♂ > ♀ (4:1)
- Most commonly seen in individuals between 20–30 years
- Uncommon in individuals older than 50 years of age
Epidemiological data refers to the US, unless otherwise specified.
- Head injury (most common; e.g., due to motor vehicle accidents, falls, assault) 
- Traumatic removal of epidural catheter (especially in patients taking on anticoagulation medication)
- Nontraumatic EDH (rare) 
Source of hemorrhage 
- Source: middle meningeal artery rupture or tear (a branch of the maxillary artery and the most common source of hemorrhage in EDH) 
- Sites of rupture 
Venous EDH (rare)
- Sites of rupture 
- Head trauma (usually severe) → skull fracture → rupture of middle meningeal artery (most common) → hemorrhage into the , typically in the temporal or temporoparietal region 
- Venous shunting of blood out from the epidural space and initial asymptomatic compression of the anterior temporal lobe → lucid interval 
Continued expansion of EDH → increased intracranial pressure → transtentorial uncal herniation (Monro-Kellie principle) which leads to: 
- Compression of the ipsilateral oculomotor nerve and loss of parasympathetic supply to the pupillary sphincter → ipsilateral dilated pupil (anisocoria)
- Compression of the brain stem → rapid neurological decline, , and either of the following:
- Unrelieved brain stem compression → coma and death
Classic presentation of EDH 
- Initial loss of consciousness immediately following a head injury
- Temporary recovery of consciousness with return to normal or near-normal neurological function (lucid interval): in 20–50% of patients with EDH 
- Renewed decline in neurological status and onset of symptoms caused by hematoma expansion and mass effect:
- Signs of associated skull fractures; (e.g., scalp hematoma, , , , , )
- See also “Clinical features” in “Traumatic brain injury.”
A lucid interval is seen in up to 50% of patients with EDH. 
The majority (70–95%) of patients with EDH have an associated skull fracture. 
Neurological decline following a lucid interval can be rapid (“talk and deteriorate”) and fatal without urgent intervention. 
General principles 
- Follow trauma protocols for patients with traumatic EDH
- Immediate initiation of takes precedence over diagnostics.
- Diagnostics should not delay transfer to a if needed.
- See “Initial management of TBI” for details.
- CT head without IV contrast is the first-line imaging modality for all patients with suspected EDH.
- Imaging should not delay transfer for neurosurgical care in patients who already meet the criteria for intervention. 
- In cases of rapidly declining neurological status or evidence of brain herniation, consider emergency temporizing surgery even in the absence of confirmatory imaging (see “Definitive management of EDH” below). 
CT head without IV contrast
- Indications: first-line imaging in patients with suspected acute EDH
- Biconvex (lenticular shaped), sharply demarcated
- Typically hyperdense in appearance 
- Limited by suture lines
- Common locations
- Arterial EDH: temporal or temporoparietal region 
- Venous EDH: posterior cranial fossa 
- Evidence of skull fracture, if present
- Initial CT scan may be normal in patients with delayed EDH and small lesions can quickly expand in size 
Noncontrast CT of the head is essential for diagnosing epidural hematoma.
The initial CT scan may be normal if the bleed is slow (e.g., small arterial EDH in the middle cranial fossa, venous EDH). Neuroimaging should be repeated if there are any signs of clinical deterioration in patients with neuroimaging that is initially normal.
MRI head without IV contrast 
- Characteristic findings
- Traumatic EDH: See “Diagnostics in TBI.”
- Nontraumatic EDH: Consider angiography if a dural vascular malformation is suspected. 
- Suspected associated cerebral venous sinus thrombosis: Consider venography. 
- The main aspects of EDH management are:
- Conservative management with close observation and serial CT scans can be considered for a small, asymptomatic EDH.
- Consider skull trephination (burr hole surgery) as a temporizing procedure in patients with neurological deterioration if neurosurgical expertise is not immediately available.
- Minimize the duration of time between the onset of neurological decline and surgical clot evacuation.
- When to restart anticoagulation and antithrombotic therapy should be decided on an individual basis. 
- See “Management of moderate and severe TBI” for details on anticoagulant reversal and seizure prophylaxis.
All patients with EDH require emergency neurosurgical consultation. If a neurosurgeon is not available on site, then transfer for definitive care is indicated.
Definitive management of EDH
Indications: Patients fulfilling any or all of these criteria should be operated on urgently. 
- EDH volume > 30 mL (30 cm3) regardless of GCS
- EDH thickness > 15 mm
- Midline shift > 5 mm
- GCS ≤ 8
- Focal neurological deficit
- Evidence of neurological deterioration: pupillary abnormalities, signs of brain herniation
- Associated brain injuries (e.g. SDH, depressed skull fracture) that meet surgical criteria
- Timing: as soon as possible (preferably within 2 hours of loss of consciousness in patients with neurological deterioration and/or GCS ≤ 8) 
- Preoperative antibiotic prophylaxis: recommended in all patients to prevent meningitis (e.g., Cefazolin ). 
- First-line: urgent craniotomy, hematoma evacuation, and ligation of the ruptured blood vessel
- Emergency temporizing procedure: 
- Indications: Absence of all indications for surgery (see above) 
- Failure of conservative management (EDH progression during observation): Perform craniotomy and hematoma evacuation. 
- In patients with no other associated brain injury, early decompression is associated with good neurological outcomes, including full recovery. 
- Factors associated with a worse prognosis 
- ABCDE survey and additional prehospital trauma care as needed (e.g., cervical spine control, analgesics, fluid resuscitation) 
- Immediate initiation of neuroprotective measures (see “Acute management checklist for neuroprotective measures”)
- Rapid neurological examination, including assessment of severity (see “GCS”)
- Assess for signs of increased ICP and initiate ICP management as needed.
- Administer tranexamic acid if GCS 9–13 and < 3 hours have elapsed since injury.
- Assess for other life-threatening or limb-threatening injuries.
- Initiate measures for prevention of complications in brain injuries.
- Stop further doses of antithrombotic agents.
- Patients on anticoagulants: Administer anticoagulant reversal. 
- Patients on antiplatelet therapy : If neurosurgery or an invasive procedure is planned, consider platelet transfusion in patients with a platelet count < 80,000–100,000/μL. 
- Emergency neurosurgery consult for consideration of surgical intervention
- Neurosurgical expertise available on site: urgent surgery for patients meeting criteria for operative intervention
- Neurosurgical expertise not available on site
- Serial neurological examination and assessment of GCS
- Continuous monitoring of vitals, pulse oximetry, and capnography
- Admit to neuro-ICU.