Epidural Hemorrhage

Epidural hemorrhage (EDH) is an event characterized by bleeding into the epidural space between the dural layers of the meninges and the skull. The primary mechanism triggering bleeding is trauma (i.e., closed head injury), which causes arterial injury, most commonly middle meningeal artery injury. Epidural hemorrhage presents acutely, usually immediately (seconds to hours) following head trauma, with an altered level of consciousness that may span from a momentary loss of consciousness to coma. Diagnosis is based on clinical suspicion following head trauma and is confirmed with neuroimaging (i.e., noncontrast head CT). Management includes stabilization, stopping (possibly, the reversal) of all anticoagulants, monitoring in a neurologic ICU, and neurosurgical intervention.

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Overview

Definition

Epidural hemorrhage (epidural hematoma (EDH)) is an event characterized by bleeding into the epidural space between the dural layer of the meninges and the skull. Epidural hemorrhage usually results from trauma.

Subarachnoid hemorrhage

Meninges and meningeal spaces:
Image depicting the 3 layers (dura mater, arachnoid mater, pia mater) surrounding the brain and spinal cord. The meninges serve as mechanical protection of the CNS, support the cerebral and spinal blood vessels, and allow for the passage of CSF. Only the subarachnoid space is a true space present in physiological conditions, whereas the epidural and subdural spaces form only during pathological processes. The epidural space may open as a result of head trauma or, rarely, due to other pathologic processes.

Image by Lecturio.

Epidemiology

  • Estimated incidence: 1%–4% of traumatic head injuries
  • Accompanied by skull fracture in > 75% of cases
  • Highest incidence in young adults aged 20–30 years
  • Rare in older adults > 50 years of age

Etiology

Head trauma:

  • Most common cause of EDH
  • Causes injury to the vascular structures that course between the dural meningeal layers and the skull
  • The trauma transmits forces to the skull base, causing injury to the:
    • Middle meningeal artery (most common), as it passes through the foramen spinosum
    • Anterior meningeal artery
    • Dural sinuses
  • Examples:
    • Motor vehicle accidents
    • Falls
    • Assaults

Nontraumatic EDH:

  • Rare
  • Possible etiologies include:
    • Infection:
      • Meningitis
      • Epidural abscess
    • Coagulopathy (inherited or iatrogenic)
    • Dural vascular malformations
    • Tumors affecting the dura mater
    • Neurosurgical complications

Pathophysiology

Vascular injury

  • Approximately 90% of the cases of EDH result from arterial bleeding:
    • A branch of the middle meningeal artery
    • Anterior meningeal artery
    • Dural arteriovenous (AV) fistula at the vertex
  • Approximately 10% of the cases of EDH result from venous bleeding (dural venous sinus).
  • Location:
    • EDH occurs in the temporal region in 75% of cases.
    • EDH occurs in children with equal frequency in the following regions:
      • Temporal
      • Occipital
      • Frontal
      • Posterior fossa
  • Accompanied by fracture of the temporal bone in the majority of cases

Hematoma expansion

  • Vascular injury causes extravasation of blood into the epidural space, which is initially compensated by venous shunting of blood:
    • Compensation is responsible for the “lucid interval.”
    • Intracranial pressure (ICP) increases with hematoma expansion.
  • Hematoma expansion may be asymptomatic until the volume reaches a critical mass.
  • As ICP increases due to hematoma expansion, neurologic deterioration ensues:
    • Cerebral parenchymal injury
    • Compression/herniation of neurologic structures:
      • Obliteration of ventricles
      • Oculomotor nerve → pupillary palsy
      • Brain stem → Cushing reflex (bradycardia, hypertension, respiratory compromise)
      • Cerebral peduncle → hemiparesis
  • Progression to coma
  • Progression to death

Clinical Presentation

Head trauma is the most common etiology of EDH. A “lucid interval” followed by rapid neurologic deterioration is common.

Neurologic symptoms

  • The nature of neurologic symptoms/signs depend largely on the following characteristics of the hematoma:
    • Location
    • Size
    • Rate of growth
    • Acuity
  • Loss of consciousness:
    • May range from momentary loss of consciousness to coma
    • Typical: momentary loss of consciousness immediately after the traumatic event → spontaneous recovery for a period of time → progressive neurologic deterioration due to progressive bleeding and hematoma expansion:
      • The period of improved consciousness is called the lucid interval.
      • Observed in approximately 50% of EDH cases
      • Arterial bleeds: The lucid interval lasts for hours.
      • Venous bleeds: The lucid interval lasts for days to weeks.
  • Headache
  • Nausea/vomiting
  • Drowsiness
  • Confusion
  • Common signs:
    • Hemiparesis
    • Seizures
    • Ipsilateral pupillary dilation
    • Cushing reflex:
      • Bradycardia
      • Hypertension
      • Respiratory compromise

Diagnosis

Neuroimaging

Noncontrast head CT:

  • Imaging modality of choice for:
    • Acute head trauma
    • Acute loss of consciousness
    • Suspected EDH (and other intracranial bleeds)
  • Acute EDH appears as a high-density lens-shaped (biconvex) collection of blood along the convexity of the affected hemisphere.
    • Fresh blood appears as high intensity on CT.
    • Acute blood collection is easily distinguishable from the surrounding anatomy.
  • The “swirl sign” may also be visible:
    • Heterogenous blood collection
    • Indicates acute extravasation of blood
    • An indication for immediate neurosurgical intervention
    • Poor prognostic indicator
  • In < 10% of cases, the hematoma may not be readily apparent on initial CT:
    • CT performed before adequate blood accumulation
    • Severe anemia lessens the density of blood collection.
    • Severe hypotension (due to associated trauma, blood loss, hypovolemia) leads to slow bleeding.
    • A venous source of bleed leads to slow bleeding.

Head MRI:

  • Less widely used and not as readily available as CT
  • More sensitive in the detection of intracranial hemorrhage compared with noncontrast CT
  • Adjunct to CT in cases where the initial CT is nondiagnostic but the clinical suspicion for EDH is high
  • May reveal the presence of other intracranial bleeding and/or the extent of associated intraparenchymal injuries

Angiography:

  • Not typically indicated for the evaluation of EDH
  • May be useful for the detection of atypical sources of bleeding

Contraindicated procedures

Lumbar puncture:

  • Contraindicated in cases where EDH is suspected
  • ↑ ICP due to expanding hematoma increases the risk of herniation
Epidural hematoma

Epidural hematoma:
CT showing an epidural hematoma in front of the surgical field after tumor resection

Image: “Ipsilateral remote hemorrhage in case 2. c, d CT showed an epidural hematoma in front of the surgical field after the tumor resection” by Yu J., et al. License: CC BY 4.0, cropped by Lecturio.

Management

Acute EDH, especially if presenting with neurologic compromise or coma, is an emergent neurologic situation often requiring surgical intervention. Failure of prompt stabilization, diagnosis, evaluation, and intervention could result in hemorrhagic expansion, parenchymal brain injury, elevated ICP, brain herniation, and death.

Stabilization

  • Affected individuals should be evaluated and stabilized using advanced trauma life support (ATLS)/advanced cardiac life support (ACLS) protocols.
  • Life-threatening injuries should be addressed.
  • Efforts to achieve/maintain hemodynamic instability
  • Reversal of anticoagulation
  • Noncontrast head CT as soon as possible
  • Emergent neurosurgical consultation:
    • Surgical/clinical decision-making
    • Placement of an ICP-monitoring device

Stratification

Decision-making tools used clinically to determine operative or nonoperative management include:

  • GCS score
  • Head CT findings:
    • Clot thickness
    • Degree of midline shift
    • Presence of associated brain lesions
  • Neurologic examination
  • Presence of pupillary palsy
  • Acuity of EDH
  • Presence of comorbidities
  • Severity of associated trauma
  • Age: EDH, if present, is rare in individuals > 55 years of age and is associated with a worse prognosis.

Nonoperative management

  • May be appropriate for:
    • Clinically stable individuals (GCS score > 8)
    • Small hematomas:
      • Clot thickness < 15 mm
      • Estimated EDH volume < 30 mL
    • Absence of signs of brain herniation based on clinical and/or radiographic evaluation:
      • Absent or minimal midline shift on CT (< 5 mm)
      • Absence of direct visualization of herniation on CT
      • Absence of physical examination findings of elevated ICP (i.e., papilledema, anisocoria)
      • Absence of elevated ICP on neuromonitoring (i.e., < 30 mm Hg)
  • Should be monitored in a neurologic ICU
  • Continuous ICP monitoring is necessary.
  • Serial head CT scans should be performed every 6–8 hours for 36 hours.
  • Hematoma may resolve or undergo gradual resorption over weeks.
  • Occasionally, EDH persists and does not resolve spontaneously:
    • Calcification/ossification may occur.
    • Persistent EDH is an indication for neurosurgical evacuation.

Surgical management

  • May be appropriate for:
    • Clinically unstable individuals:
      • GCS score < 9
      • GCS score reduction by ≥ 2 from the time of injury to the time of evaluation
      • Presence of pupillary palsy
    • Large hematomas:
      • Clot thickness > 15 mm
      • Estimated EDH volume > 30 mL
    • Presence of the “swirl sign”
    • Midline shift on CT by > 5 mm, regardless of the GCS score
    • ICP > 30 mm Hg
    • Persistent EDH that does not resorb spontaneously over a course of weeks
  • Should be undertaken as soon as clinically feasible for affected individuals meeting these criteria (within 1–2 hours of the onset of neurologic deterioration)
  • Surgical techniques:
    • Craniotomy with hematoma evacuation is the most commonly performed surgical technique.
    • Burr hole trephination
    • Decompressive craniectomy
  • Identification of the culprit vessel and tamponade may be undertaken simultaneously:
    • Traditional tamponade with ligatures
    • Endovascular embolization of the middle meningeal artery

Prognosis

  • Mortality rate:
    • Approximately 5%–10% if:
      • GCS score > 8 on presentation
      • Surgical intervention is prompt (1–2 hours from the time of injury).
    • Up to 55% if surgical intervention is delayed
  • Favorable recovery at 6 months in 50%–90% of cases if:
    • GCS score > 8 on presentation
    • Surgical intervention is prompt (1–2 hours from the time of injury).
  • Poor prognostic indicators:
    • Low GCS score on initial evaluation
    • Presence of pupillary palsy
    • Older age
    • Delayed surgical intervention
    • Elevated ICP in the postoperative period
    • Large hematoma volume
    • Large midline shift
    • Presence of the “swirl sign”
    • Comorbid intracranial pathology:
      • Parenchymal injury
      • Other intracranial bleeds (e.g., subarachnoid hemorrhage (SAH), subdural hematoma (SDH))
      • Cerebral contusion
      • Cerebral edema

Differential Diagnosis

  • Ischemic stroke: an ischemic infarct of the cerebral parenchyma caused by occlusion of a cerebral artery by atherosclerotic lesions or cardioembolic emboli. Ischemic stroke presents with neurologic deficits and/or altered mental status/altered level of consciousness that depends on the size and location of the infarct. The diagnosis is clinical and confirmed by neuroimaging. Management includes initial stabilization, possible cerebrovascular intervention, addressing identifiable underlying etiologies (severe hypertension, embolus), and management of cardiovascular risk factors.
  • Other hemorrhagic cerebral conditions: Carotid/cerebral artery dissection, epidural hemorrhage, intraparenchymal hemorrhage, and subdural hemorrhage are other hemorrhagic manifestations of the cerebral vasculature that can present with neurologic deficits and/or altered mental status/altered level of consciousness. Diagnosis is clinical and confirmed by neuroimaging. Management depends on the hemorrhagic etiology and includes initial stabilization, neurosurgical/endovascular consultation, management of ICP, and monitoring in a neurologic ICU.
  • Hypertensive encephalopathy: neurologic deficits and/or altered mental status/altered level of consciousness presenting in the setting of severe hypertension. Diagnosis is based on elevated blood pressure and neurologic signs/symptoms. Neuroimaging is useful to rule out ischemic or hemorrhagic cerebrovascular accidents.

References

  1. McBride, W. (2020). Intracranial epidural hematoma in adults. Retrieved September 18, 2021, from https://www.uptodate.com/contents/intracranial-epidural-hematoma-in-adults?search=epidural%20hematoma&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  2.  Khairat, A., Waseem, M. (2021). Epidural Hematoma. In StatPearls [Internet]. StatPearls Publishing. Retrieved September 18, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK518982/
  3. Maugeri, R., Anderson, D.G., Graziano, F., et al. (2015). Conservative vs. Surgical Management of Post-Traumatic Epidural Hematoma: A Case and Review of Literature. The American journal of case reports, 16, pp. 811–817. Retrieved September 18, 2021, from https://doi.org/10.12659/ajcr.895231

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