eMedicine Specialties > Neurology > Neurological Infections

Intracranial Epidural Abscess

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
Coauthor(s): Arun Ramachandran, State University of New York Upstate Medical University
Contributor Information and Disclosures

Updated: Sep 9, 2009

Introduction

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.

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. 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

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.

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

Clinical

History

An intracranial epidural abscess often has an insidious onset, with symptoms developing over several weeks to months. Symptoms of the initiating infection might dominate the picture. Signs and symptoms are as follows:

  • Usually, the patient presents with headache that is either diffuse or localized to one side with scalp tenderness. Headache may be the only presenting symptom. The patient may have persistent fever that develops during or after treatment for sinus or middle ear infection. Purulent discharge from the ears or sinuses, periorbital swelling, and brawny edema of the scalp might accompany.
  • Because the epidural abscess usually enlarges slowly, the following signs do not develop until the infection has reached the subdural space, resulting in subdural empyema, at which time the patient might present with neck stiffness, nausea, vomiting, lethargy, and hemiparesis. Seizures might very well be the first presenting symptom in some cases.
  • Symptoms and signs of increased intracranial pressure (ICP) include nausea, vomiting, and papilledema. Rarely, when the epidural abscess develops near the petrous bone and involves the fifth and sixth cranial nerves, the patient may present with ipsilateral facial pain and weakness of the lateral rectus muscle (ie, the so-called Gradenigo syndrome). Many times, scalp cellulitis, sinusitis, or skull fracture may draw the attention of the physician to such an extent that the diagnosis of epidural abscess may be missed.
  • One should consider the diagnosis of intracranial epidural abscess when a patient presents with unresolving frontal sinus symptoms. Also consider this diagnosis in patients with new neurologic symptoms after trauma or cranial surgery, even if months or years have elapsed since operation or trauma.
  • Onset can be acute, especially in patients without any history of previous cranial neurosurgery. They often present with acute symptoms of encephalopathy and focal neurological deficits.
  • Mittal et al present the case of an 11-year-old girl who presented with typical features of meningitis, suggesting that sinusitis can rarely be latent and present directly with intracranial complications. She underwent neuroimaging because of slow improvement and concern for a brain abscess. Although no history or examination findings were suggestive of sinusitis, the patient was found to have pansinusitis with intracranial extension causing meningitis and epidural abscess.8

Causes

Because the intracranial epidural space is only a potential space and the dura is essentially adherent to the inner table of the skull, infection in the epidural space can result from the following:

Sinusitis (mastoid, ethmoid, sphenoid, and frontal sinusitis); trauma associated with skull fracture; and following craniotomy, orbital cellulitis, cranial osteomyelitis, sagittal sinus phlebitis, fetal monitoring, and mucormycosis.

The risk of infection is increased when multiple neurosurgical operations are performed or if the operation also involves implantation of foreign material. Even though hematogenous spread to the epidural space from a remote site of infection is a common cause of spinal epidural abscess, it is a rare cause of cranial epidural abscess.

Mallur et al reported on 11 children with acute mastoiditis. Complications in these children were as follows: 4 cases of cranial epidural abscess, 4 cases of sigmoid sinus thrombosis, 2 cases of perisigmoid abscess or bony erosion, and 1 case of tegmen mastoideum dehiscence). The authors claim that, although uncommon, intracranial complications of acute mastoiditis may present without clinical signs or symptoms. Computed tomography of the temporal bone with contrast is essential for identifying asymptomatic complications.9


Bacteriology

Epidural abscess usually occurs as a result of infection caused by Staphylococcus aureus, Staphylococcus epidermidis, enteric gram-negative bacilli (especially Escherichia coli), Pseudomonas species, Bacteroides species, and other anaerobes. Aerobic and microaerophilic streptococci are usually responsible for infection that has spread from the paranasal sinuses. Rarely, Salmonella species, Eikenella corrodens, and Mucor species have been isolated. Haemophilus influenzae may also be the responsible organism, in addition to Mycobacterium tuberculosis, Proteus penneri, Actinomyces species, Blastomyces species, Aspergillus fumigatus, and Cladosporium species.

More on Intracranial Epidural Abscess

Overview: Intracranial Epidural Abscess
Differential Diagnoses & Workup: Intracranial Epidural Abscess
Treatment & Medication: Intracranial Epidural Abscess
Follow-up: Intracranial Epidural Abscess
Multimedia: Intracranial Epidural Abscess
References
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Further Reading

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Keywords

epidural abscess, cranial epidural abscess, CEA, epidural empyema, patchy meningitis externa, increased intracranial pressure, ICP, intracranial infection, infection of the epidural space, epidural space infection

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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  Honoraria Consulting; Teva Marion Honoraria Consulting; 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.

Medical Editor

Ramon Diaz-Arrastia, MD, PhD, Assistant Professor, Department of Neurology, Comprehensive Epilepsy Center, University of Texas Southwestern
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.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

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

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
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