Neuroassistant

Epidural hematoma

Hemorrhage between the dura mater and the inner table of the skull bone
Incidence of EDH is 1-4% of head trauma admissions
Overall mortality: 20-55%. With optimal diagnosis and prompt treatment: 5-12%
20% of patients have concomitant acute subdural hematomas
Male:female ratio is 4:1
>90% are caused by traumatic arterial bleeding, often from the middle meningeal artery
90-95% have an associated skull fracture
50% of patients present with initial loss of consciousness followed by a “lucid interval” which may last several hours before deteriorating
Most evolve rapidly and manifest clinically during the initial 24 hours
Delayed development of EDH, usually within 36 hours after trauma, occurs in 10-15% of cases
In pediatric patients EDH should be suspected if the hematocrit drops ≥10% after admission
Venous EDH are often smaller and develop more slowly. Most are caused by skull fracture that crosses a dural venous sinus. They mostly occur in the posterior fossa near the skull base
Clival EDH may develop after hyperflexion/hyperextension injury or skull base fractures that cross the clival venous plexus. They may present with multiple cranial neuropathies
Non-traumatic EDH are very rare and are mostly associated with anticoagulant treatment
Progressive contralateral hemiparesis, hyperreflexia, ipsilateral pupillary dilatation, seizures, obtundation, confusion, vomiting, bradycardia may result from mass effect from hematoma expansion

CT: 84% of EDH appear as a biconvex (lens-like) hyperdensity (60-90 HU) adjacent to the skull bone
Unlike SDH, EDH may cross dural folds (eg falx) but do not cross sutures (site of dural insertions to bone)
10% of EDH in children cross sutures. EDH may also cross sutures when there is an adjacent skull bone fracture
Hyperacute EDH or EDH in extremely anemic patients (Hb 8-10g/dL) may appear isodense to brain parenchyma and may be missed
Mixed-density EDH may result from rapid bleeding (“swirl sign”)
MR: EDH are typically isointense with gray matter on T1

EDH with volume >30ml should be surgically evacuated regardless of GCS.

Nonsurgical management may be attempted if the EDH has all of the following characteristics: