Epidural hematoma

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.

For epidural hematoma limited to the spine, see “Spinal epidural hematoma.”

• Hemorrhage into the intracranial epidural space, which lies between the dura mater and the inner table of the skull or calvarium ^[1][2]

• Incidence: occurs in approx. 10% of patients with moderate to severe traumatic brain injury (TBI) ^[3][4]
• Sex: ♂ > ♀ (4:1)
• Age ^[4]
  • 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.

Inciting event

• Traumatic EDH
  • Head injury (most common; e.g., due to motor vehicle accidents, falls, assault) ^[2]
  • Traumatic removal of epidural catheter (especially in patients taking on anticoagulation medication)
• Nontraumatic EDH (rare) ^[5][6]
  • Infections
  • Coagulopathies
  • Dural vascular malformation
  • Dural metastases

Source of hemorrhage ^[2][7]

• Arterial EDH
  • Source: middle meningeal artery rupture or tear (a branch of the maxillary artery and the most common source of hemorrhage in EDH) ^[2]
  • Sites of rupture ^[2][8]
    • Pterion (most common): the thinnest part of the skull and a site at which the middle meningeal artery lies in close proximity to the skull ^[4]
    • Skull base (foramen spinosum)
• Venous EDH (rare)
  • Source
    • Middle meningeal vein rupture or tear
    • Dural venous sinus injury
    • Rupture of a dural vascular malformation
  • Sites of rupture ^[7]
    • Posterior fossa (injury to the transverse sinus, sigmoid sinus, or confluence of venous sinuses)
    • Middle cranial fossa (sphenoparietal sinus injury)
    • Vertex (superior sagittal sinus injury)

• Head trauma (usually severe) → skull fracture → rupture of middle meningeal artery (most common) → hemorrhage into the epidural space, typically in the temporal or temporoparietal region ^[2][9]
• Venous shunting of blood out from the epidural space and initial asymptomatic compression of the anterior temporal lobe → lucid interval ^[2][10]
• Continued expansion of EDH → increased intracranial pressure → transtentorial uncal herniation (Monro-Kellie principle) which leads to: ^[2]
  • 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, Cushing triad, and either of the following:
    • Compression of ipsilateral cerebral peduncle (more common) → contralateral hemiparesis
    • Compression of the contralateral cerebral peduncle against the contralateral tentorial edge (less common) → ipsilateral hemiparesis (false localizing sign known as Kernohan syndrome)
• Unrelieved brain stem compression → coma and death

The features of EDH depend on the size and location of the hematoma. The majority of patients have an associated skull fracture.

• Classic presentation of EDH ^[2][10]
  1. Initial loss of consciousness immediately following a head injury
  2. Temporary recovery of consciousness with return to normal or near-normal neurological function (lucid interval): in 20–50% of patients with EDH ^[11][12]
  3. Renewed decline in neurological status and onset of symptoms caused by hematoma expansion and mass effect:
     • Contralateral focal neurological deficits
     • Signs of ↑ ICP (e.g., headache, Cushing triad) ^[13]
     • Pupillary abnormalities (sign of uncal herniation) ^[9]
       • Anisocoria with ipsilateral mydriasis (most common)
       • Unilateral or bilateral fixed dilated pupils
       • Potentially contralateral or bilateral mydriasis
     • Signs of cerebral herniation syndromes
     • Coma, death
• Signs of associated skull fractures; (e.g., scalp hematoma, liquorrhea, CSF rhinorrhea, otorrhea, Battle sign, raccoon eyes)
• See also “Clinical features” in “Traumatic brain injury.”

A lucid interval is seen in up to 50% of patients with EDH. ^[11][12]

The majority (70–95%) of patients with EDH have an associated skull fracture. ^[2][8]

Neurological decline following a lucid interval can be rapid (“talk and deteriorate”) and fatal without urgent intervention. ^[14][15]

General principles ^[1][3]

• Follow trauma protocols for patients with traumatic EDH
  • Immediate initiation of neuroprotective measures takes precedence over diagnostics.
  • Diagnostics should not delay transfer to a neurocritical care unit 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. ^[3]
• 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). ^[14][16]

Imaging ^[7][17]

CT head without IV contrast

• Indications: first-line imaging in patients with suspected acute EDH
• Characteristic findings
  • Biconvex (lenticular shaped), sharply demarcated extraaxial lesion
  • Typically hyperdense in appearance ^[7][18][19]
  • Limited by suture lines
  • Common locations
    • Arterial EDH: temporal or temporoparietal region ^[7][9][20]
    • Venous EDH: posterior cranial fossa ^[7]
  • 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 ^[21]

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 ^[7][17]

• Indications
  • Stable patients with suspected small EDH (i.e., normal or near-normal initial CT scan)
  • Follow-up neuroimaging in stable patients with neurological deterioration not explained by CT findings.
  • Difficulty distinguishing EDH from SDH on CT scan
• Characteristic findings
  • Similar to those on CT scan
  • Lesion would appear hypointense on a T2-weighted scan ^[7]

Additional imaging

• Traumatic EDH: See “Diagnostics in TBI.”
• Nontraumatic EDH: Consider angiography if a dural vascular malformation is suspected. ^[22][23]
• Suspected associated cerebral venous sinus thrombosis: Consider venography. ^[7]

Laboratory studies

• Traumatic EDH: See “Diagnostics in TBI” for routine laboratory studies that should be obtained in all patients with TBI.
• Nontraumatic EDH: coagulation panel and additional studies for coagulopathy, if suspected ^[24][25]

See “Overview of intracranial hemorrhage” for a table comparing:

• Epidural hematoma
• Subdural hematoma
• Subarachnoid hemorrhage
• Intracerebral hemorrhage

The differential diagnoses listed here are not exhaustive.

General principles

EDH is a neurosurgical emergency, as hematoma expansion can rapidly lead to brain herniation and death.

• The main aspects of EDH management are:
  • Primary survey with simultaneous initiation of neuroprotective measures (see “Initial management of TBI” for an algorithmic approach)
  • Empiric ICP management
  • Urgent craniotomy and hematoma/clot evacuation
  • Prevention of complications in brain injuries (e.g., anticoagulant reversal to prevent hematoma expansion)
• 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. ^[26][27][28]
• See “Management of moderate and severe TBI” for details on anticoagulant reversal and seizure prophylaxis.

Expect rapid neurological deterioration following a lucid interval and do not delay initiation of therapy and patient transfer to a trauma center or neurocritical care unit. ^[4]

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

Surgery ^[9]

• Indications: Patients fulfilling any or all of these criteria should be operated on urgently. ^[4]
  • 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) ^{[9][29][14][30]}
• Preoperative antibiotic prophylaxis: recommended in all patients to prevent meningitis (e.g., cefazolin ). ^[1][31][32]
• Procedures ^[9]
  • First-line: urgent craniotomy, hematoma evacuation, and ligation of the ruptured blood vessel
  • Emergency temporizing procedure: skull trephination ^[14][33]
    • Indication: suspected or confirmed EDH with GCS ≤ 8 and/or signs of brain herniation or coma in a facility without an on-site neurosurgeon
    • Further management: urgent transfer to a neurocritical care unit for definitive management by a neurosurgeon ^[14]

Skull trephination should only be considered if there is evidence of brain herniation or coma attributable to an EDH and access to definitive neurosurgical care is delayed.

Conservative management

• Indications: Absence of all indications for surgery (see above) ^[9][34][35]
• Procedure
  • Admission to neuro-ICU or ICU ^[36]
  • Frequent GCS monitoring and neurological checks for at least 72 hours ^[3][36]
  • Serial CT scans to monitor for early hematoma expansion ^[37][37][38]
    • If clinically stable: Repeat within 4–6 hours.
    • Clinical deterioration or new neurologic deficits: Repeat immediately.
• Failure of conservative management (EDH progression during observation): Perform craniotomy and hematoma evacuation. ^{[34][36][37][38]}

• In patients with no other associated brain injury, early decompression is associated with good neurological outcomes, including full recovery. ^[30]
• Factors associated with a worse prognosis ^[2][14][39]
  • GCS ≤ 8 at presentation
  • Pupillary abnormalities (especially fixed dilated pupil) at presentation
  • Prolonged period of time between onset of brain herniation and decompressive surgery
  • Age > 75 years ^[40]
  • Large volume EDH causing significant midline shift
  • Associated brain injuries

Every hour of delay from the onset of signs of brain herniation to decompressive surgery worsens the neurological outcome and increases the mortality rate. ^[14]

• ABCDE survey and additional prehospital trauma care as needed (e.g., cervical spine control, analgesics, fluid resuscitation) ^[1][3][41]
• 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. ^[26][42][43]
  • 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. ^[44][45]
• 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
  • Skull trephination before transfer if GCS ≤ 8 and signs of brain herniation attributable to acute EDH are evident
  • Urgent transfer to a neurocritical care unit
• Serial neurological examination and assessment of GCS
• Continuous monitoring of vitals, pulse oximetry, and capnography
• Admit to neuro-ICU.