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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Question 1NeurologyMedium
A 20-year-old man is struck in the temporal area and briefly loses consciousness. He then becomes lucid before rapidly deteriorating. CT shows a biconvex extra-axial hematoma. Which of the following best explains the bleeding source?
AMiddle meningeal artery rupture
BCerebral contusion hemorrhage
CLenticulostriate artery rupture
DBridging vein tearing
EBerry aneurysm rupture
Reveal answer & full explanation
Correct answer: A — Middle meningeal artery rupture
AMiddle meningeal artery rupture✓
BCerebral contusion hemorrhage
CLenticulostriate artery rupture
DBridging vein tearing
EBerry aneurysm rupture
Why Middle meningeal artery rupture is correct
Epidural hematoma classically follows a temporal bone fracture that lacerates the middle meningeal artery beneath the pterion.
Arterial pressure strips the dura off the skull, producing the lens-shaped (biconvex) collection that does not cross suture lines.
The lucid interval then rapid decline reflects expanding arterial bleeding with herniation.
Why the others are wrong
Bridging vein tearing — Venous bridging-vein tears cause a crescent-shaped subdural hematoma that crosses sutures; choosing it confuses the two extra-axial collections (right-test-wrong-shape).
Berry aneurysm rupture — A ruptured saccular aneurysm causes subarachnoid blood in the basal cisterns and a thunderclap headache, not a trauma-driven biconvex clot (buzzword-match on "rupture").
Lenticulostriate artery rupture — Lenticulostriate vessels bleed into the basal ganglia parenchyma in hypertensive hemorrhage, an intra-axial bleed, not an extra-axial lens-shaped clot (vascular-word trap).
Cerebral contusion hemorrhage — a temporal blow often bruises the underlying cortex, but contusional bleeding sits within the brain parenchyma as an intra-axial hyperdensity, frequently at coup and contrecoup sites, rather than forming a lens-shaped collection between the skull and the dura (coup-injury trap).
Question 2NeurologyMedium
A 22-year-old man is brought to the emergency department after a blow to the right temple during a boxing match. He briefly lost consciousness at ringside, then awoke and conversed normally for about 45 minutes. He now has a severe headache, has vomited twice, and is becoming increasingly drowsy. On exam his right pupil is fixed and dilated, and he has left-sided arm and leg weakness. A non-contrast head CT shows a biconvex (lens-shaped) hyperdense collection over the right temporal region that does not cross the cranial sutures, with an adjacent skull fracture. Which of the following is the most likely diagnosis?
AAcute subarachnoid bleed
BAcute epidural hematoma
CDiffuse axonal injury
DAcute subdural hematoma
ECerebral contusion
Reveal answer & full explanation
Correct answer: B — Acute epidural hematoma
AAcute subarachnoid bleed
BAcute epidural hematoma✓
CDiffuse axonal injury
DAcute subdural hematoma
ECerebral contusion
Why Acute epidural hematoma is correct
The vignette is the classic boards triad: a temporal blow, a lucid interval (transient normal mentation after brief loss of consciousness), then rapid deterioration from an expanding arterial bleed.
A fracture across the pterion lacerates the middle meningeal artery; arterial blood dissects the dura off the inner skull. Because the dura is tightly adherent at suture lines, the collection is biconvex (lens-shaped) and does NOT cross sutures.
The ipsilateral fixed/dilated pupil (uncal herniation compressing CN III) plus contralateral hemiparesis (corticospinal tract compression) signal herniation, a time-critical surgical emergency; outcomes are excellent if craniotomy precedes herniation.
Why the others are wrong
Acute subarachnoid bleed — blood layers within the sulci and basal cisterns rather than forming a biconvex extra-axial collection bounded by sutures.
Cerebral contusion — a temporal blow can bruise the underlying cortex, but contusions are intra-axial and show patchy hyperdensity within the brain parenchyma rather than a sharply marginated collection between the skull and the dura.
Acute subdural hematoma — venous (bridging vein) bleed producing a crescent-shaped collection that CROSSES suture lines; more typical in elderly/anticoagulated patients and with diffuse underlying brain injury, not a lens shape limited by sutures.
Diffuse axonal injury — rotational acceleration from a boxing blow can shear axons, but diffuse axonal injury typically produces immediate, persistent coma without a lucid interval, and CT is often normal or shows only small petechial hemorrhages at the gray-white junction or corpus callosum rather than a biconvex extra-axial collection.
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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)
Diffuse axonal injury — Often CT-negative initially; MRI shows punctate hemorrhages at gray-white junction; coma out of proportion to CT
Skull fracture without intracranial injury — Trauma, possible scalp hematoma; head CT confirms absence of intracranial blood
Diagnostic workup
Labs
CBC, platelets, PT/INR, PTT (rule out coagulopathy)
BMP, type and screen, alcohol/toxicology if indicated
Imaging
Non-contrast head CT — biconvex (lens-shaped) hyperdense collection limited by suture lines, often with adjacent skull fracture
CT brain windows + bone windows mandatory (fracture identification)
CT angiography if vascular injury suspected (e.g., carotid dissection from skull base fracture)
Cervical spine imaging — significant head trauma mandates C-spine clearance
Diagnostic algorithm
flowchart TD
A[Head trauma<br/>temporal blow] --> B[Initial LOC<br/>then lucid interval]
B --> C[Rapid deterioration<br/>headache, vomiting, GCS drop]
C --> D[Non-contrast head CT]
D --> E{Biconvex hyperdensity<br/>± skull fracture?}
E -->|Yes| F[Epidural hematoma]
F --> G{Size >30 mL,<br/>shift >5 mm,<br/>GCS ≤8,<br/>or pupil change?}
G -->|Yes| H[Emergency<br/>craniotomy evacuation]
G -->|No| I[ICU observation<br/>serial CT + neuro exam]
H --> J[Excellent prognosis<br/>if pre-herniation]
Epidural hematoma — recognition and surgical decision pathway.
Treatment
First-line
ABCs, cervical spine immobilization
Intubation if GCS ≤8 or airway compromise
Manage ICP: head of bed 30°, normocapnia (PaCO2 35-40), hypertonic saline (3%) or mannitol 1 g/kg if herniation signs
Reverse anticoagulation if present (warfarin → 4-factor PCC + IV vitamin K, FFP if PCC unavailable; factor Xa inhibitors → 4-factor PCC; dabigatran → idarucizumab)
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 TQP 2024 — ACS Trauma Quality Programs Best Practices Guidelines: The Management of Traumatic Brain Injury (American College of Surgeons, 2024)
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