Intracranial Epidural Abscess 

  • Author: Tarakad S Ramachandran, MBBS, FRCP(C), FACP; Chief Editor: Karen L Roos, MD   more...
 
Updated: Feb 6, 2012
 

Background

Intracranial epidural abscess was first described in 1760 by Sir Percival Pott. Pott also documented the associated scalp swelling, the so-called Pott puffy tumor. Cranial epidural abscess (CEA) is the third most common localized intracranial infection, after brain abscess and subdural empyema.

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Pathophysiology

Cranial epidural abscess is defined as a suppurative infection of the epidural space, which is the space between the dura mater and the inner table of the skull (see the image below). With the advent of antibiotics, it most often occurs as a complication of neurosurgery. As many as 2% of craniotomies result in cranial epidural abscess. In approximately 10% of cases, epidural abscess is associated with subdural abscess. At autopsy, 81% of patients with cranial epidural abscess are found to have infections extending into the subdural space. Autopsy evidence of meningitis is present in 35% of patients with cranial epidural abscess, and evidence of brain abscess is present in 17%. The dura adheres tightly to the skull, resulting in sharp demarcation and slow progression of the empyema, often accompanied by osteomyelitis of the overlying bone.[1]

CT scan showing lenticular-shaped intracranial epiCT scan showing lenticular-shaped intracranial epidural abscess.

Intracranial epidural abscess can result from spread of infection to the epidural space from the paranasal sinuses, middle ear, orbit, or mastoids. Routes of spread include direct contamination from penetrating trauma or contamination at the time of surgery, direct spread from osteomyelitis, septic thrombus entering emissary veins, and hematogenous spread. Cranial epidural empyema may rarely occur as a result of metastatic hematogenous seeding.[2]

The usual causative organisms are streptococci associated with sinusitis and anaerobes and staphylococci when accompanied by trauma. Dural attachments, especially at sutures, and the sagittal sinus contain the infection. When this fails because of trauma, surgery, or previous surgery, further spread of the infection results in complications, including cranial osteomyelitis, dural sinus thrombosis, subdural empyema, purulent leptomeningitis, and brain abscess. Virulence of the organism and the resistance of the host influence the outcome of this condition significantly.

Once the organism enters the epidural space, hyperemia and fibrin deposition occur, followed by collection of purulent material and development of chronic granulation and fibrous tissue.

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Epidemiology

Frequency

United States

Overall incidence of intracranial epidural abscess is unknown. Epidural abscess is a relatively rare cause of focal intracranial infection; in fact, 90% of epidural abscesses occur in the spine. Because of early and adequate treatment of bacterial middle ear and sinus infections, occurrence of epidural abscess is uncommon. It accounts for only 2-5% of cases of cranial suppuration. Surgical site infections (SSIs) after neurosurgical procedures are decreasing gradually, and the recent rate of SSIs in clean neurosurgical operations with prophylactic antibiotics was between 1.0% and 6.2%.[3, 4] Consequently, epidural abscesses after craniotomy have been relatively uncommon recently.

Mortality/Morbidity

  • Mortality from intracranial epidural abscess was 100% in the preantibiotic period. With advanced imaging techniques, better antibiotics, and surgical techniques, the mortality rate has declined to 6-20%.
  • The outcome of this infection is often influenced by the virulence of the infecting organism, resistance of the host, presence of altered mental status on presentation, age of the patient, comorbid conditions, neurologic deterioration, and any delay in instituting appropriate treatment. Harris et al reported 31 cases of localized central nervous system infection over a 7-year period in their community hospital.[5] Cranial subdural empyema (CSE) was the cause in 6 cases (20%) and cranial epidural abscess was the cause in 2 cases (6%). Although all patients with cranial subdural empyema and cranial epidural abscess survived, half had severe residual neurologic deficits. With the advent of new antibiotics, improved surgical techniques and aggressive surgical approach prognosis is much improved.
  • Germiller et al report a consecutive sample of 25 children and adolescents treated for 35 intracranial complications associated with intracranial complications of sinusitis.[6] Epidural abscess was most common (13 complications), followed by subdural empyema (n = 9), meningitis (n = 6), encephalitis (n = 2), intracerebral abscess (n = 2), and dural sinus thrombophlebitis (n = 2). Only 1 death occurred from sepsis secondary to meningitis (mortality 4%) and only 2 patients had permanent neurologic sequelae. Overall, neurologic outcome was excellent because of aggressive medical and surgical management.

Sex

Cranial epidural abscess occurs with greater frequency in men.

Age

Intracranial epidural abscess can occur in people of any age, but it has been reported more commonly in people in the sixth decade of life. It is most common in older children and adults and is rare in children younger than 12 years. Woods et al report that epidural abscess is rare and occurs almost exclusively in older children and adults.[7]

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Contributor Information and Disclosures
Author

Tarakad S Ramachandran, MBBS, FRCP(C), FACP  Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine

Disclosure: Abbott Labs None None; Teva Marion None None; Boeringer-Ingelheim Honoraria Speaking and teaching

Coauthor(s)

Arun Ramachandran  State University of New York Upstate Medical University

Arun Ramachandran is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Ramon Diaz-Arrastia, MD, PhD  Professor, Department of Neurology, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director, North Texas TBI Research Center, Comprehensive Epilepsy Center, Parkland Memorial Hospital

Ramon Diaz-Arrastia, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, New York Academy of Sciences, and Phi Beta Kappa

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

Florian P Thomas, MD, MA, PhD, Drmed  Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

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

Karen L Roos, MD  John and Nancy Nelson Professor of Neurology, Professor of Neurological Surgery, Department of Neurology, Indiana University School of Medicine

Karen L Roos, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association

Disclosure: Nothing to disclose.

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CT scan showing lenticular-shaped intracranial epidural abscess.
Intracranial epidural abscess. Enhanced MRI of the brain, axial section, revealing a left temporal epidural abscess with an abscess cavity and a thickened enhancing capsule. Adjacent thickened dura enhances as well. In addition, mass effect is evident.
Intracranial epidural abscess. A coronal section of the MRI revealing a left temporal epidural abscess with an abscess cavity and a thickened enhancing capsule. Adjacent thickened dura enhances as well. In addition, mass effect is evident.
Intracranial epidural abscess. MRI of the brain, unenhanced. A T1-weighted image (axial view) showing a left temporal epidural abscess with an abscess cavity, surrounding capsule, and the thickened dura underneath. Mass effect is evident.
 
 
 
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