Epidural hematoma

Last updated: September 11, 2023

Summarytoggle arrow icon

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.”

Definitiontoggle arrow icon

Epidemiologytoggle arrow icon

  • 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.

Etiologytoggle arrow icon

Inciting event

Source of hemorrhage [2][7]

Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

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

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]

Diagnosticstoggle arrow icon

General principles [1][3]

  • Follow trauma protocols for patients with traumatic EDH
  • 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
    • 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

Additional imaging

Laboratory studies

Differential diagnosestoggle arrow icon

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

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

General principles

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

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]

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]

Prognosistoggle arrow icon

  • 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]

Acute management checklisttoggle arrow icon

Referencestoggle arrow icon

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