Epidural Hematoma

EPIDEMIOLOGY ........................................................................................................................................ 1 ETIOPATHOPHYSIOLOGY ......................................................................................................................... 1 Locations .......................................................................................................................................... 2 CLINICAL FEATURES ............................................................................................................................... 2 DIAGNOSIS................................................................................................................................................ 3 TREATMENT ............................................................................................................................................. 5 Surgical treatment ............................................................................................................................ 5 Conservative treatment ..................................................................................................................... 5 Embolization .................................................................................................................................... 5 PROGNOSIS ............................................................................................................................................... 5

epidural hematoma can extend across midline in frontal region anterior to coronal suture because it is not limited by dural reflections within anterior interhemispheric fissure  body has no mechanism for absorption of extradural hemorrhage -clotted blood remains in epidural space as tumor (until it is removed); if hematoma is chronic, collection may liquefy, but this is rare.
Underlying brain usually is minimally injured (vs. subdural hematomas) → excellent prognosis if treated aggressively!
N.B. posterior fossa EDH may compress venous sinuses and imitate venous sinus thrombosis on imagingerroneous heparin administration may cause more harm (e.g. EDH expansion).
Percentage distribution of site of epidural hematoma: Top of skull is removed to reveal middle meningeal artery which has emerged from foramen spinosum to branch over surface of dura:

CLINICAL FEATURES
1. Following injury, patient may or may not lose consciousness.  external evidence of head injury is present.
2. ≈ 47% (10-50%) demonstrate classic LUCID INTERVAL (for several hours); but often no return to completely normal mental status occurs.  other patients: a) ≈ 33% -initial concussion is insufficient to cause any loss of consciousness. b) ≈ 33% -brain damage at time of injury is so severe that immediate coma lasts long enough to merge with that resulting from brain compression.
*course is protracted if bleeding source is venous **75 ml is critical EDH volume -any volume above → loss of consciousness  small EDH may remain asymptomatic, but this is rare.
N.B. posterior fossa EDH may have dramatic rapid delayed deterioration -patient can be conscious and talking and minute later apneic, comatose, and minutes from death.

DIAGNOSIS
For other DIAGNOSTIC EVALUATION → see p. TrH1 >> LP is absolutely contraindicated!!! CSF pressure > 200 mmH2O, CSF clear (bloody if there was contusion or laceration of brain) Skull X-ray may show associated skull fracture (e.g. crossing shadow of middle meningeal artery branches).
Unenhanced CT -classic lens-shaped (biconvex) density: 1) homogenous; unclotted blood (active bleeding or coagulopathy) may give focal isodense / hypodense zones within EDH. chronic EDH may be heterogeneous (neovascularization and granulationperipheral contrast enhancement). 2) situated between brain and skull 3) smoothly marginated 4) does not follow sulcal margins 5) may cross midline (external to falx). 6) mass effect (underlying brain is displaced, but often appears intrinsically normal).  causes of hematoma density↓: severe anemia, hyperacute hematoma (no clots at all).  air in acute EDH suggests fracture of sinuses or mastoid air cells.  coronal CT may be required to correctly evaluate vertex EDH.  EDHs in posterior fossa may cross midline and extend above tentorium.  if patient's condition is rapidly deteriorating → take patient directly to operating room for diagnostic and therapeutic BURR HOLES (practically, with modern availability of CT, such scenario is unlikely).  if EDH becomes chronicall features remain, but attenuation values are reduced and margin shows marked enhancement. CT bone window -two adjacent fractures (arrows); anterior fracture is at site of groove for middle meningeal artery: Midline shift is apparent; ill-defined area of blood density in right occipital region -small contusion; increased density in left temporal region -contrecoup contusion; small round density deep within right frontal cortex -shear injury: Large posterior fossa EDH; size of lesion at this high level suggests that it probably crosses into supratentorial compartment: Left frontal acute EDH (black arrow) with midline shift (white arrow); left posterior falx subdural hematoma and left frontoparietal cortical contusion: Right frontal EDH -deep aspect of hematoma is homogeneous, whereas peripheral (outer part) is more isoattenuating relative to braindue to presence of unclotted blood (dark) within hematoma: EDH + coma (GCS score < 9) + anisocoria → surgical evacuation ASAP* *delays of more than 2 h (between clinical deterioration and evacuation) are unacceptable (Mendelow et al. 1979)  EDH < 30 mL and < 15 mm thickness and < 5-mm midline shift and GCS score > 8 and no focal deficit -can be managed nonoperatively with serial CT* and close neurological observation in a neurosurgical ICU. *first routine repeat CT within 6 hrs after TBI  craniotomy provides a more complete evacuation of the hematoma than other surgical approaches. see p. Op320 >>

CONSERVATIVE TREATMENT
 very close serial neurologic examinations (clinical deterioration → repeat CT). N.B. EDHs tend to expand more rapidly than subdural hematomas!  general management of head injury (incl. ICP treatment, seizure prophylaxis) → see p. TrH1 >>  bedrest during initial phase → progressive increase in activity (avoid strenuous activity).