Neurology · PANCE / PANRE

Epidural Hematoma (EDH)

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.

🔒 Free preview limit reached

Keep reading — start your free trial

You've read your 2 free diagnosis previews. Create your free account to unlock the full Epidural Hematoma (EDH) outline — plus all 514 diagnoses, 3,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.

Free to start · No credit card · Cancel anytime

Risk factors

  • 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)
  • Contralateral hemiparesis (corticospinal tract compression)
  • Cushing triad (hypertension, bradycardia, irregular respirations) — late sign of elevated ICP
  • Battle sign (mastoid bruising), CSF otorrhea/rhinorrhea if basilar fracture

Classic findings

Lucid interval after temporal trauma + ipsilateral blown pupil + contralateral hemiparesis = uncal herniation from expanding EDH.

Differential diagnosis

  • Acute subdural hematoma — Crescent-shaped, crosses sutures, venous source, often more diffuse underlying brain injury
  • Subarachnoid hemorrhage (traumatic) — Blood in sulci/cisterns rather than extra-axial collection
  • Cerebral contusion — Coup-contrecoup injuries; intra-axial hyperdensities
  • 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 (PCC, vitamin K, FFP, idarucizumab, andexanet alfa)
  • 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)

Practice Neurology questions on FirstPassPA

Turn this outline into retention. 3,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.

Start studying free → Browse all 514 diagnoses

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants.