Epidemiology

Etiology

Inciting event

• Traumatic EDH
  • Head injury (most common; e.g., due to motor vehicle accidents, falls, assault)

Source of hemorrhage

• Arterial EDH
  • Source: middle meningeal artery rupture or tear (a branch of the maxillary artery and the most common source of hemorrhage in EDH)
  • Sites of rupture
    • 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

Pathophysiology

• Venous shunting of blood out from the epidural space and initial asymptomatic compression of the anterior temporal lobe → lucid interval
• Continued expansion of EDH → increased intracranial pressure → transtentorial uncal herniation (Monro-Kellie principle) which leads to:
  • 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

Clinical features

• Classic presentation of EDH
  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)
  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)
     • Pupillary abnormalities (sign of uncal herniation)
       • Anisocoria with ipsilateral mydriasis (most common)
       • Unilateral or bilateral fixed dilated pupils
       • Potentially contralateral or bilateral mydriasis
     • Signs of cerebral herniation syndromes

Diagnostics

Differential diagnostics

See Intracranial hemorrhage

Treatment