AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

Section 2 of 11  

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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

CEA 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 CEA. In approximately 10% of cases, epidural abscess is associated with subdural abscess. At autopsy, 81% of patients with CEA are found to have infections extending into the subdural space. Autopsy evidence of meningitis is present in 35% of patients with CEA, 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 (CEA) was the cause in 2 cases (6%). Although all patients with CSE and CEA 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 (ICS).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

CEA 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

Section 3 of 11  

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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.

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 CEA.

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.

DIFFERENTIALS

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Other Problems to be Considered

Central retinal artery occlusion
Delirium tremens
Encephalitis
Meningitis
Headache, cluster
Headache, migraine
Headache, tension
Neoplasms, brain
Tuberculoma of brain
Subdural empyema
Septic dural venous thrombosis
Brain abscess

WORKUP

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Lab Studies

• Findings from routine laboratory tests are not diagnostic but are essential in the preparation of the patient for operation. These tests may reveal polymorphonuclear (PMN) leukocytosis and an elevated erythrocyte sedimentation rate (ESR).
• Results of blood cultures may be positive.
• Hyponatremia has been reported in approximately 30% of cases.

Imaging Studies

• Radiography of the skull may demonstrate the responsible sinusitis, mastoiditis, or osteomyelitis.
• Before the advent of CT scanning, cerebral angiography was often required. Cerebral angiography demonstrated an avascular mass that displaced the dural sinuses away from the inner table of the skull.
• CT scanning of the brain without enhancement is often used as a screening tool in the assessment. Abscess appears as a poorly defined lentiform area of low or intermediate density (see Media file 1). CT scanning can also show bony destruction and fragmentation in patients with underlying mastoiditis. When contrast is administered, the convex inner side of the low-density lesion becomes enhanced and appears as rim enhancement caused by the inflamed dura.
• Because MRI is free from bony artifacts and easily demonstrates fluid collections outside the brain, it is the diagnostic procedure of choice to delineate a CEA. Epidural fluid is observed as higher signal intensity than the ventricular cerebral spinal fluid (CSF) on both T1- and T2-weighted MRI. Use of gadolinium can significantly enhance the dura on T1-weighted MRI. MRI is also useful for visualizing small fluid collections that can be missed by CT scanning and in differentiating postoperative abscesses from hematomas or sterile effusions. MRI is particularly useful in differentiating subdural empyema from CEA. The characteristic MRI abnormality includes a crescentic or lentiform fluid collection overlying the hemisphere or in the interhemispheric fissure, which is mildly hyperintense relative to the CSF on T1-weighted images and isointense to CSF on T2-weighted images. A hypointense medial rim, representing the displaced dura is very characteristic of CEA.
• The vein of Labbe may masquerade as an epidural abscess. Recognition of the vein of Labbe on CT scan is therefore essential for the appropriate management of otological and neurotological disease.
  
  Kraus et al present a 12-month-old male with acute coalescent mastoiditis and a subperiosteal abscess.⁸ An epidural abscess was suspected on preoperative CT scan. No abscess was found on surgery. Based on the surgical finding, they determined that this misdiagnosis was due to a vascular variant, the occipitotemporal vein (OTV, vein of Labbe) that masqueraded as an abscess on the CT scan. The OTV runs in an anterior-to-posterior direction along the lateral surface of the left temporal lobe and drains into the transverse sinus near its junction with the sigmoid sinus. It can be recognized on unenhanced MRIs as a prominent flow void apposed to the lateral aspect of the temporal lobe, and is readily demonstrated on MR and computed tomographic (CT) venographic images and on cerebral arteriograms obtained during the venous phase of enhancement.

Other Tests

• Lumbar puncture carries the risk of precipitating herniation in the setting of increased ICP. Risks and benefits should be carefully weighed before a decision is made to proceed with a spinal tap. Findings on CSF studies can often be unremarkable, with reference range glucose and protein levels. CSF pressure may be increased. Spinal fluid may contain excess cells that are usually polymorphonuclear cells. The cell count is usually less than 200 cells, but it can be as high as 7000/mm³. Protein may be elevated as much as 100 mg/dL and the glucose level is often within the reference range unless associated meningitis is present, in which case it may be decreased.

TREATMENT

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Medical Care

• Prehospital management
• • Rapid transport and early stabilization are highly essential in the prehospital setting.
  • Endotracheal intubation and hyperventilation may be required in some patients who are critically ill.
• Initial management (depends upon the type of clinical presentation)
• • The presence of seizures and focal neurological deficits requires emergent intubation, anticonvulsant therapy, hyperventilation, and hemodynamic stabilization before proceeding with diagnostic tests.
  • Patients who are not critically ill or who have a subtle presentation may undergo CT scanning after initial clinical evaluation. Neurologic status should be monitored closely.
• Antibiotic therapy
  • Until the culture and sensitivity report of the infectious agent becomes available, the choice of empiric antibiotic therapy should be based on the underlying etiology. For example, when an intracranial abscess is thought to be due to extension of infection from paranasal sinuses involving staphylococcal, aerobic, and anaerobic bacteria, more than one antibiotic is necessary. Likewise, an antistaphylococcal agent would be an appropriate choice for infection occurring after a neurosurgical procedure.
  • For patients presenting in the emergency department (ED) with CEA, empirical antibiotics are the first-line pharmacologic therapy. These antibiotics must cover a broad spectrum of both aerobic and anaerobic bacterial organisms.
  • Usually, length of therapy is determined by the patient's response to treatment and by resolution of the epidural abscess on follow-up MRI and/or CT scanning. As a general rule, antibiotic therapy should be continued for a minimum of 8 weeks if surgery is not undertaken and for at least 4 weeks if the abscess is drained. Antibiotics have been administered from 6 weeks to 6 months. In general, follow-up CT scanning or MRI should be obtained 10-14 days after antibiotic therapy has been discontinued.
• Seizure therapy
• • Prophylactic seizure therapy is not generally recommended. If CEA is not associated with subdural empyema, seizures are unlikely to ensue. In the event of the administration of anticonvulsant therapy, consider weaning patients off anticonvulsant therapy if patients remain seizure free for more than 2 years and the EEG findings do not show any evidence of seizure disorder.
  • Discontinuing anticonvulsant therapy suddenly can be risky because it can lead to recurrent seizures, which may be prolonged. This is true even if the medication was not successfully controlling the seizures. Weaning patients off the drug gradually after fully understanding the potential possibility of recurrent seizure(s) and related consequences, including losing a driving license and the possible impact on employment, is strongly advised. If seizures do recur, resuming the previous medication immediately usually results in the same level of seizure control as before. However, in rare instances, the original antiepileptic medication may not be as effective, even if previously successful; alternative therapy should be considered.

Surgical Care

• Optimal management of an intracranial epidural abscess should include neurosurgical drainage; Gram stain, India ink, and acid-fast bacilli (AFB) staining of the purulent material; and administration of appropriate intravenous antibiotic(s). In case of small abscesses, adequate appropriate antibiotic therapy alone might suffice, without the need for surgical intervention.
• The goal of therapy is to eradicate the infection and prevent further complications. Surgical exploration, decompression, and debridement, along with antibiotic therapy, are the mainstays of surgical treatment in CEA.
• The type of emergency surgery for CEA depends on the extent of the lesion and involvement of the overlying skull bone.
• • When burr holes cannot provide sufficient drainage or when debridement with drainage is indicated, craniotomy is undertaken.
  • When the dura is affected by infection, a dural graft may be required. During anesthesia, anesthetics that can cause intracranial vasodilation should be avoided because this might result in further increase in intracranial pressure, heralding herniation.

Consultations

• Immediate neurosurgical consultation is highly warranted.
• A multidisciplinary approach involving an otolaryngologist may be necessary if the patient presents with concurrent paranasal sinusitis.

MEDICATION

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Until the culture and sensitivity report of the infectious agent becomes available, choice of empiric antibiotic therapy should be based on the underlying etiology. For example, when an intracranial abscess is believed to be due to extension of infection from paranasal sinuses involving staphylococcal, aerobic, and anaerobic bacteria, more than one antibiotic is necessary. Similarly, an antistaphylococcal agent is an appropriate choice for infection occurring after a neurosurgical procedure.

Drug Category: Antibiotics

For patients presenting in the ED with intracranial epidural abscess, empiric antibiotics are the first-line pharmacologic therapy. These antibiotics must cover a broad spectrum of both aerobic and anaerobic bacterial organisms.

Drug Category: Corticosteroids

Anti-inflammatory effects of steroid therapy can decrease associated cerebral edema, reducing ICP. These benefits are offset somewhat by the fact that steroid use decreases antibiotic penetration into the abscess and may slow encapsulation of the abscess site.

FOLLOW-UP

Section 8 of 11  

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Complications

• Seizures
• Uncal or tonsillar herniation due to increased ICP
• Hemorrhage into the abscess
• Spread of infection: The infection may spread into the bones of the skull, resulting in osteomyelitis. It may also spread deeper because of spread of infection along the emissary veins, causing subdural empyema, meningitis, and intraparenchymal brain abscess or even a spinal cord abscess.
• Septic shock

Prognosis

• Because of the insidious onset of symptoms, neuroimaging by CT scanning and MRI, as well as the availability of strong antibiotics have resulted in decreased morbidity and mortality from this condition in recent years.
• Signs associated with an excellent prognosis include the following:
• • Young age
  • No altered mental status
  • Absence of severe neurological deficit on initial presentation
  • Absence of neurological deterioration during initial management
  • No comorbid factors
• Poorer prognosis is often associated with the following:
• • Signs of herniation present on initial presentation, when the mortality rate exceeds 50%
  • Failure to obtain a brain CT scan in patients with altered mental status, headache, or new neurologic deficit
  • Failure to address family concerns about unusual patient behavior, especially when other symptoms indicative of intracranial epidural abscess are present
• Early and accurate diagnosis of this potentially invalidating but treatable disease is of paramount importance.

Patient Education

For excellent patient education resources, visit eMedicine's Infections Center and Brain and Nervous System Center. Also, see eMedicine's patient education articles Brain Infection, Antibiotics, and Spinal Tap.

MISCELLANEOUS

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Medical/Legal Pitfalls

A high index of suspicion is often needed to diagnose a CEA. Onset of symptoms is often insidious, and a variety of inflammatory and neoplastic disorders might mimic CEA. A careful clinical history and a thorough search for physical and laboratory evidence of disease often help in making the correct diagnosis. Prognosis is good in surgically treated cases, but delays in diagnosis often lead to permanent dense neurological residuals, often resulting in litigation.

MULTIMEDIA

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Media file 1:  CT scan showing lenticular-shaped intracranial epidural abscess.
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Media type:  CT

Media file 2:  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.
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Media type:  MRI

Media file 3:  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 (see Image 2).
	View Full Size Image
Media type:  MRI

Media file 4:  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.
	View Full Size Image
Media type:  MRI

REFERENCES

Section 11 of 11

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Article Last Updated: Nov 30, 2007