eMedicine Specialties > Neurology > Neurological Infections

Intracranial Epidural Abscess

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
Arun Ramachandran, State University of New York Upstate Medical University

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.

Differential Diagnoses

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

Laboratory 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

• Neuroimaging narrows the potential diagnoses and enables prompt empirical therapy until a specific microbiological diagnosis is made.
• 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.
  
  

  

  CT scan showing lenticular-shaped intracranial epidural abscess.

  
  
• 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 cranial epidural abscess.
• 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 cranial epidural abscess. 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 cranial 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 (see Image 2).

  
  
  
  

  

  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.

  
  
• 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.¹⁰ 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

Medical Care

Early diagnosis and treatment of epidural abscess cannot be overemphasized as neurologic outcome mainly depends on the patient’s neurologic status immediately prior to surgery.

• 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 cranial epidural abscess, 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 cranial epidural abscess 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

Surgical intervention is an integral part of treatment for epidural abscesses in patients with neurologic symptoms or who have not responded to medical management.

• 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 cranial epidural abscess.
• The type of emergency surgery for cranial epidural abscess 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.
• Noggle et al report that frontal, supraorbital epidural abscesses of the anterior and middle cranial fossa can be adequately and safely debrided via a minimally invasive supraciliary craniotomy. This approach has a cosmetic benefit and may decrease approach-related morbidity.¹¹
• Eviator et al recommend that in cases of epidural abscess secondary to sinusitis that are located in the anterior base of the skull, draining the abscess endoscopically via nasal space may be considered by an experienced surgeon. This is minimally invasive, particularly so when osteomyelitis and other anatomical abnormalities of the skull exist.¹²

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

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.

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.

Penicillin G (Pfizerpen)

Along with chloramphenicol, constitutes first-line regimen for empiric treatment of intracranial epidural abscess in the ED. Provides coverage for anaerobes and streptococci.

Dosing

Adult

6 million U IV q6h

Pediatric

<14 kg (30 lb): 600,000 U IV q6h
14-27 kg (30-60 lb): 900,000-1,200,000 U IV q6h

Interactions

Probenecid can increase penicillin effectiveness by decreasing its clearance; concurrent administration of tetracycline can decrease effects of penicillin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with impaired renal function

Chloramphenicol (Chloromycetin)

Constitutes the other half of classic first-line empiric regimen. Enhances anaerobic coverage to include Bacteroides fragilis, Enterobacteriaceae, and Haemophilus species infections.

Dosing

Adult

4-6 g/d IV

Pediatric

Not established

Interactions

When taken concurrently with barbiturates, chloramphenicol serum levels may decrease while barbiturate levels may increase, resulting in increased toxicity; clinical manifestations of hypoglycemia may occur when taken concurrently with sulfonylureas; concomitant administration with rifampin may reduce serum chloramphenicol levels, presumably through hepatic enzyme induction; concurrent administration of anticoagulants may increase effects of anticoagulants; serum hydantoin levels may be increased, possibly resulting in toxicity; in addition, chloramphenicol levels may be increased or decreased

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Must not be used to treat trivial infections other than those indicated or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and periodic blood studies approximately q2d during therapy; discontinue if reticulocytopenia, leukopenia, thrombocytopenia, anemia, or any other findings attributable to chloramphenicol appear; recommended dose in patients with impaired liver or kidney function may result in toxic drug levels; exercise caution during pregnancy at term or during labor because of potential toxic effects to fetus (Gray syndrome)

Cefotaxime (Claforan)

In combination with metronidazole, can replace penicillin G and chloramphenicol. In this regimen, cefotaxime covers streptococci, staphylococci, Haemophilus species, and Enterobacteriaceae. Third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.

Dosing

Adult

12 g/d IV

Pediatric

Neonates > 1 week: 50 mg/kg IV q12h
Neonates 1-4 weeks: 50 mg/kg IV q18h
Infants and children: 50-100 mg/kg IV/IM q6h or q8h

Interactions

Probenecid may decrease cefotaxime clearance, causing increase in cefotaxime levels; furosemide and aminoglycosides may increase nephrotoxicity when used concurrently with cefotaxime

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients diagnosed with severe renal impairment; has been associated with severe colitis

Metronidazole (Metro IV Injection)

Second half of alternative regimen to penicillin/chloramphenicol. Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Has proved especially effective in otogenic intracranial epidural abscesses.

Dosing

Adult

400-600 mg IV q6h

Pediatric

Not established

Interactions

Potentiates anticoagulant effect of warfarin; agents that alter hepatic P450 system also affect its clearance; phenytoin and phenobarbital may decrease half-life of metronidazole; cimetidine may reduce metronidazole clearance and increase its toxicity; metronidazole may increase effect of anticoagulants and may decrease lithium and phenytoin clearance, increasing their toxicity; disulfiramlike reaction may occur when used concurrently with PO ingested ethanol; although risk for most patients may be slight, caution is advised

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients with severe hepatic disease because they may metabolize metronidazole slowly; monitor patients for seizures and peripheral neuropathy

Nafcillin (Unipen)

Should be added to either regimen mentioned above if S aureus is strongly suspected. Treats infections caused by penicillinase-producing staphylococci. Used to initiate therapy when patients are suspected of having penicillin G resistant staphylococcal infection. Do not use for treatment of penicillin G susceptible staphylococci. Use parenteral therapy initially in severe infections. Very severe infections may require very high doses. Change to PO therapy as condition improves. Because of occasional occurrence of thrombophlebitis associated with parenteral route (particularly in elderly individuals), administer parenterally only for a short period (24-48 h) and change to PO route if clinically possible.

Dosing

Adult

12-18 g/d IV

Pediatric

Not established

Interactions

Has been associated with warfarin resistance when administered concurrently; bacteriostatic action of tetracycline derivatives may impair bactericidal effects of penicillin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Perform bacteriologic studies to determine causative organisms and their susceptibility so that appropriate therapy is administered; therapy duration must be sufficient to eliminate organism (minimum 10 d), otherwise sequelae (eg, endocarditis, rheumatic fever) may ensue; take cultures after treatment to confirm that streptococci are eradicated

Vancomycin (Vancocin, Lyphocin)

Replaces nafcillin in patients who are allergic to penicillin and in patients who are suspected to have MRSA as an etiologic agent. Potent antibiotic directed against gram-positive organisms and active against enterococci species. Also useful in treating septicemia and skin structure infections.

Dosing

Adult

15 mg/kg IV q8-12h

Pediatric

Not established

Interactions

Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; when taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that associated with aminoglycoside alone; effects on neuromuscular blockade may be enhanced when used concurrently with nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with renal failure or neutropenia; adjust dose as needed in patients diagnosed with renal impairment; red man syndrome is caused by a too-rapid IV infusion (dose administered over a few min) but rarely happens when dose is administered as 2-h administration or as PO or intraperitoneal administration; red man syndrome is not an allergic reaction; monitor for ototoxicity

Ceftazidime (Fortaz, Ceptaz)

Should be added to empiric regimens if pseudomonads are suspected. Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.

Dosing

Adult

6 g/d IV

Pediatric

Not established

Interactions

Aminoglycosides, furosemide, and ethacrynic acid increase nephrotoxic potential; probenecid may decrease ceftazidime clearance, causing increase in ceftazidime levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in patients diagnosed with renal impairment

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.

Dexamethasone (Decadron, Dexasone)

Corticosteroid of choice for reducing ICP. Used in treatment of inflammatory diseases. May decrease inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Dosing

Adult

10-12 mg IV loading dose, followed by 4 mg IV q6h

Pediatric

Loading dose: 1-2 mg/kg/dose IV once
Follow-up maintenance dose: 1-1.5 mg/kg/d IV; not to exceed 16 mg/d divided q4-6h for 5 d; taper dose for 5 d and discontinue use

Interactions

May decrease antibiotic penetration in abscesses; use of barbiturates, phenytoin, and rifampin can decrease dexamethasone effects; decreases effects of salicylates and vaccines used for immunization

Contraindications

Documented hypersensitivity; untreated active infection; fungal infection

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for adrenal insufficiency when tapering drug; patients receiving glucocorticoids are at risk of multiple complications including severe infections; abrupt discontinuation may cause an adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use

Follow-up

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 neurologic deficit on initial presentation
  • Absence of neurologic 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.
• Pradilla et al report that prognosis for both spinal epidural abscesses and intracranial epidural abscesses is typically poor because of delayed diagnosis and intervention and that prognosis largely depends on the neurologic status at the time of diagnosis. Increased clinical awareness can help achieve an earlier diagnosis, thereby greatly improving outcomes.¹³

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

Medicolegal Pitfalls

A high index of suspicion is often needed to diagnose a cranial epidural abscess. Onset of symptoms is often insidious, and a variety of inflammatory and neoplastic disorders might mimic cranial epidural abscess. 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 neurologic residuals, often resulting in litigation.

Multimedia

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

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.

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).

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.

References

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3. Erman T, Demirhindi H, Göçer AI, Tuna M, Ildan F, Boyar B. Risk factors for surgical site infections in neurosurgery patients with antibiotic prophylaxis. Surg Neurol. Feb 2005;63(2):107-12; discussion 112-3. [Medline].

4. Korinek AM, Golmard JL, Elcheick A, Bismuth R, van Effenterre R, Coriat P. Risk factors for neurosurgical site infections after craniotomy: a critical reappraisal of antibiotic prophylaxis on 4,578 patients. Br J Neurosurg. Apr 2005;19(2):155-62. [Medline].

5. Harris LF, Haws FP, Triplett JN Jr, Maccubbin DA. Subdural empyema and epidural abscess: recent experience in a community hospital. South Med J. Oct 1987;80(10):1254-8. [Medline].

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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

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

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
Disclosure: Nothing to disclose.

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