eMedicine Specialties > Neurology > Critical Care Neurology

Epidural Hematoma

Author: David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
Contributor Information and Disclosures

Updated: Mar 10, 2009

Introduction

Background

Epidural hematoma (ie, accumulation of blood in the potential space between dura and bone) may be intracranial (EDH) or spinal (SEDH). Intracranial epidural hematoma occurs in approximately 2% of patients with head injuries and 5-15% of patients with fatal head injuries. Intracranial epidural hematoma is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention. Intracranial epidural hematoma may be acute (58%), subacute (31%), or chronic (11%). Spinal epidural hematoma may also be traumatic, though it may occur spontaneously.

This MRI demonstrates spinal epidural hematoma.

This MRI demonstrates spinal epidural hematoma.

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This MRI demonstrates spinal epidural hematoma.

This MRI demonstrates spinal epidural hematoma.


Pathophysiology

Epidural hematoma usually results from a brief linear contact force to the calvaria that causes separation of the periosteal dura from bone and disruption of interposed vessels due to shearing stress. Skull fractures occur in 85-95% of adult cases, but they are much less common in children because of the plasticity of the immature calvaria. Arterial or venous structures may be compromised, causing rapid expansion of the hematoma; however, chronic or delayed manifestations may occur when venous sources are involved. Extension of the hematoma usually is limited by suture lines owing to the tight attachment of the dura at these locations. Recent analyses have revealed that epidural hematomas may actually traverse suture lines in a minority of cases.1

The temporoparietal region and the middle meningeal artery are involved most commonly (66%), although the anterior ethmoidal artery may be involved in frontal injuries, the transverse or sigmoid sinus in occipital injuries, and the superior sagittal sinus in trauma to the vertex. Bilateral epidural hematomas account for 2-10% of all acute epidural hematomas in adults but are exceedingly rare in children. Posterior fossa epidural hematomas represent 5% of all cases of epidural hematomas.

Spinal epidural hematoma may be spontaneous or may follow minor trauma, such as lumbar puncture or epidural anesthesia. Spontaneous spinal epidural hematoma may be associated with anticoagulation, thrombolysis, blood dyscrasias, coagulopathies, thrombocytopenia, neoplasms, or vascular malformations. The peridural venous plexus usually is involved, though arterial sources of hemorrhage also occur. The dorsal aspect of the thoracic or lumbar region is involved most commonly, with expansion limited to a few vertebral levels.

Frequency

United States

Epidural hematoma complicates 2% of cases of head trauma (approximately 40,000 cases per year). Spinal epidural hematoma affects 1 per 1,000,000 people annually. Alcohol and other forms of intoxication have been associated with a higher incidence of epidural hematoma.

International

International frequency is unknown, though it is likely to parallel the frequency in the United States.

Mortality/Morbidity

Mortality rate associated with epidural hematoma has been estimated to be 5-50%.

  • The level of consciousness prior to surgery has been correlated with mortality rate: 0% for awake patients, 9% for obtunded patients, and 20% for comatose patients.
  • Bilateral intracranial epidural hematoma has a mortality rate of 15-20%.
  • Posterior fossa epidural hematoma has a mortality rate of 26%.

Race

No racial predilection has been reported.

Sex

Intracranial and spinal epidural hematomas are more frequent in men, with a male-to-female ratio of 4:1.

Age

  • Intracranial epidural hematoma is rare in individuals younger than 2 years.
  • Intracranial epidural hematoma is also rare in individuals older than 60 years because the dura is tightly adherent to the calvaria.
  • Spinal epidural hematoma has a bimodal distribution with peaks during childhood and during the fifth and sixth decades of life. Increasing age has been noted as a risk factor for postoperative spinal epidural hematoma.

Clinical

History

Epidural hematoma should be suspected in any individual who sustains head trauma. Although classically associated with a lucid interval between the initial loss of consciousness at the time of impact and a delayed decline in mental status (10-33% of cases), alterations in the level of consciousness may have a variable presentation. Posterior fossa epidural hematoma may exhibit a rapid and delayed progression from minimal symptoms to even death within minutes.

  • Symptoms of epidural hematoma include the following:
    • Headache
    • Nausea/vomiting
    • Seizures
    • Focal neurologic deficits (eg, visual field cuts, aphasia, weakness, numbness)
  • Spinal epidural hematoma typically causes severe localized back pain with delayed radicular radiation that may mimic disk herniation. Associated symptoms may include the following:
    • Weakness
    • Numbness
    • Urinary incontinence
    • Fecal incontinence

Physical

  • The physical examination should include a thorough evaluation for evidence of traumatic sequelae and associated neurological deficits, including the following:
    • Bradycardia and/or hypertension indicative of elevated intracranial pressure
    • Skull fractures, hematomas, or lacerations
    • Cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with disruption of the dura
    • Hemotympanum
    • Instability of the vertebral column
    • Alteration in level of consciousness (ie, Glasgow Coma Scale score)
    • Anisocoria (eg, ipsilateral dilation of the pupil due to uncal herniation with compression of the oculomotor nerve)
    • Facial nerve injury
    • Weakness (eg, contralateral hemiparesis due to compression of the cerebral peduncle)
    • Other focal neurological deficits (eg, aphasia, visual field defects, numbness, ataxia)
  • Spinal epidural hematoma may have variable findings on physical examination, determined by the level of the lesion. The findings include the following:
    • Weakness (unilateral or bilateral)
    • Sensory deficits with radicular paresthesias (unilateral or bilateral)
    • Various alterations in reflexes
    • Alterations of bladder or anal sphincter tone

Causes

  • Trauma
  • Anticoagulation
  • Thrombolysis
  • Lumbar puncture
  • Epidural anesthesia
  • Coagulopathy or bleeding diathesis
  • Hepatic disease with portal hypertension
  • Cancer
  • Vascular malformation
  • Disk herniation
  • Paget disease of bone
  • Valsalva maneuver
  • Hypertension
  • Chiropractic manipulation2

More on Epidural Hematoma

Overview: Epidural Hematoma
Differential Diagnoses & Workup: Epidural Hematoma
Treatment & Medication: Epidural Hematoma
Follow-up: Epidural Hematoma
Multimedia: Epidural Hematoma
References
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References

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Further Reading

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Keywords

epidural hemorrhage, extradural hematoma, extradural hemorrhage, cerebral epidural hematoma, spinal epidural hematoma, EDH, SEDH, head injury, intracranial epidural hematoma

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Contributor Information and Disclosures

Author

David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
David S Liebeskind, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
Edward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Neurological Association, American Society for Biochemistry and Molecular Biology, Phi Beta Kappa, Sigma Xi, Society for Neuroscience, and Southern Clinical Neurological Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health and Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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