Arterial bleeding between skull and dura, classically from middle meningeal artery injury.
Also known as: EDH, extradural hematoma, epidural hemorrhage
Overview
Collection of blood in the potential space between the inner table of the skull and the dura mater, typically from arterial bleeding after temporal bone fracture lacerating the middle meningeal artery. Less commonly from venous bleeding (dural sinus injury) or skull base fractures.
Epidemiology
1-4% of traumatic head injuries. Most common in young adults (mean age ~20-30); rare in elderly (dura tightly adherent) and infants (skull deformable, fewer fractures). Male predominance.
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Head trauma — usually blunt impact to the temporal region
Motor vehicle collision, assault, sports injury (boxing, contact sports)
Falls
Coagulopathy or anticoagulant use (smaller-impact injuries can produce EDH)
Pathophysiology
A fracture across the pterion (where the temporal bone meets the sphenoid wing) lacerates the middle meningeal artery, causing arterial blood to dissect the dura away from the inner skull. Because the dura is tightly adherent at suture lines, the hematoma cannot cross them, producing the classic lens-shaped (biconvex) appearance. The high-pressure arterial source allows rapid expansion and herniation if not evacuated promptly.
Clinical presentation
Symptoms
Head trauma with brief loss of consciousness
Classic 'lucid interval' (minutes to hours of normal mentation) followed by rapid neurologic deterioration in ~20-50%
Headache, vomiting, confusion progressing to coma
Contralateral hemiparesis from midline shift
Many present with persistent decreased LOC from initial trauma; lucid interval not always present
Signs / physical exam
Decreased GCS, often worsening over minutes-hours
Ipsilateral fixed and dilated pupil (uncal herniation compressing CN III)
Emergency neurosurgical evacuation via craniotomy for hematomas >30 mL, thickness >15 mm, midline shift >5 mm, GCS ≤8, or pupillary asymmetry
Surgical outcomes are excellent if surgery occurs BEFORE herniation
Second-line / adjunct
Small, asymptomatic EDH (<30 mL, <15 mm thick, no shift, GCS >8): close observation with serial CT and neuro exams in ICU
Seizure prophylaxis (short-course levetiracetam or phenytoin) commonly used in severe TBI
DVT prophylaxis (mechanical immediately; chemical typically delayed 24-72 h after intracranial bleed)
ICU monitoring with ICP monitor if GCS ≤8 and abnormal CT
Complications
Uncal herniation, brainstem compression, death (if untreated)
Permanent neurologic deficits despite evacuation
Seizures (early or late post-traumatic epilepsy)
Hydrocephalus
Post-concussive syndrome
Recurrent or residual hematoma requiring re-operation
PANCE pearls
Classic boards triad: temporal blow + lucid interval + rapid deterioration. Time-critical: surgery before herniation = good outcome.
Lens shape that does NOT cross sutures = epidural. Crescent that DOES cross sutures = subdural.
Middle meningeal artery is the most common source, but venous EDHs (less rapid) occur from dural sinus or diploic vein injury — often in posterior fossa or anterior frontal locations.
Pediatric EDH is often venous, slower to expand, and may lack lucid interval. Maintain high suspicion.
Posterior fossa EDH can compress the brainstem rapidly — low threshold for surgery even with smaller volumes.
References
Brain Trauma Foundation 2017 — Guidelines for the Management of Severe Traumatic Brain Injury (Carney et al., Neurosurgery 2017)
Surgical Guidelines — Surgical Management of Acute Epidural Hematomas (Bullock et al., Neurosurgery 2006)
ACS TQIP — ACS TQIP Best Practices in the Management of TBI (American College of Surgeons, 2015)
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