Epidural Hematoma 

  • Author: David S Liebeskind, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Jun 18, 2010
 

Background

Epidural hematoma (ie, accumulation of blood in the potential space between dura and bone) may be intracranial (EDH) or spinal (SEDH) (see the image below). 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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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.

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Epidemiology

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.
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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, Los Angeles, David Geffen School of Medicine; 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.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

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: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Helmi L Lutsep, MD  Professor, Department of Neurology, Oregon Health and Science University School of Medicine; 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; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

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CT scanning performed before and after surgical evacuation of an intracranial epidural hematoma.
This MRI demonstrates spinal epidural hematoma.
 
 
 
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