AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

An epidural abscess is a rare but potentially life-threatening disease that requires early detection and prompt management. It is defined as an inflammation that involves a collection of pus between the dura (the outer membrane that covers the brain) and spinal cord and the bones of the skull or spine. Spinal epidural abscess (SEA) and intracranial epidural abscess (IEA) are the 2 types of epidural abscess. The difference is based on the different anatomical locations within the CNS and some differences in risk factors (see Pathophysiology) and symptoms (see History).

A loose association between the dura and vertebral bodies enables extension of SEA to numerous levels, frequently resulting in extensive neurological findings and often necessitating multiple laminectomies. The lumbar spine is most commonly affected, followed by the cervical spine.

Tight adherence of the dura to the skull limits expansion of IEA, often resulting in dangerously increased intracranial pressure, which is a neurosurgical emergency.

Early recognition of these diseases and timely consultation with neurosurgical and infectious disease specialists is of paramount importance in optimizing neurological outcome.

Pathophysiology

SEA can be caused by direct extension from a contiguous focus or by hematogenous spread. However, in up to one third of patients, no source of infection is identified. Skin abscesses and furuncles are the most common source of infection; infective endocarditis and vertebral osteomyelitis are also common sources. The most common risk factor of SEA is diabetes mellitus, followed by trauma, intravenous drug abuse, and alcoholism.

Because IEA can cross the cranial dura along emissary veins, an accompanying subdural empyema is often present. The epidemiology of these entities is essentially the same. Risk factors of IEA include chronic ear infections, mastoiditis, chronic sinusitis, head injury, and recent neurosurgery.

Frequency

United States

The annual incidence of SEA is 0.2-2 cases per 10,000 hospital admissions. The rising incidence of SEA in the past 20 years has been attributed to the increasing prevalence of injection drug use, as well as increased performance of invasive spinal procedures.

The annual incidence of IEA is difficult to determine but is recognized to be much less than SEA (SEA is 9 times more common than IEA.)

International

Few data are available outside the United States, but the frequency appears to be similar.

Mortality/Morbidity

• SEA: At the beginning of the twentieth century, almost all patients with SEA died. However, associated mortality rates have dropped significantly over the past 50 years, likely due to better diagnostic modalities. Nonetheless, despite advances in imaging and surgical care, mortality rates range from 4.6-31% in a recent series. Differences in etiology (ie, iatrogenic vs noniatrogenic) do not affect prognosis. The essential problem of SEA lies in the necessity of early diagnosis, as permanent neurological deficits can be avoided or reduced only with timely treatment.
• IEA: With antibiotic and surgical management, the prognosis of IEA is good, with an attributable mortality rate of below 10%.
• The neurological status of the patient at the time of diagnosis is the best predictor of neurological outcome, and morbidity is increased when surgery is delayed.

Sex

Most studies report a male predominance.

Age

SEA can occur at any age. The median age of onset of SEA is approximately 50 years, with most patients aged 30-60 years.

IEA is most common in the second and third decades of life.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Spinal epidural abscess
• • Most symptoms of a spinal epidural abscess (SEA) are due to enlargement of the abscess and surrounding inflammation, which can lead to tissue compression in the brain and spinal cord. Onset of symptoms usually occurs within hours to days but may be more chronic in nature, presenting with weeks to months of symptoms. The microbiology often dictates the pace of progression.
  • Back pain is the most common symptom in individuals with SEA, occurring in 70-100% of cases.
  • The classical diagnostic triad consists of fever, spinal pain, and neurological deficits but is not very sensitive. The rate of this progression is highly variable. Once paralysis develops, irreversibility is a risk, emphasizing the importance of early diagnosis.
  • If left untreated, the progression of symptoms is usually sequential: back pain (70-100%), radicular irritation (50%), motor weakness/sphincter incontinence (30-40%) and sensory changes (12%), and then paralysis (6-48%).
  • The patient's neurological status at the time of diagnosis is the most accurate predictor of outcome and prognosis.
• Intracranial abscess
• • The symptoms of intracranial epidural abscess (IEA) are generally more acute.
  • Signs and symptoms are due to both infection and the slowly expanding intracranial mass. Fever, headache, malaise, lethargy, nausea, and vomiting may be present. IEAs due to sinus infections can cause purulent drainage from the nose or ear.
  • Patients without a history of recent cranial manipulation present with encephalopathy and focal neurological deficits. Most patients who have undergone craniotomy (67%) tend to be afebrile at presentation, and their neurological deficits are often less severe and less acute, with 90% showing evidence of wound infection.
  • This patient population is usually given prophylactic anticonvulsants.

Physical

• Findings associated with SEA include the following:
• • Fever (45-75%)
  • Spinal tenderness (70-100%)
  • Weakness of the extremities (35-40%)
  • Sensory level (12%)
  • Paralysis (6-48%)
  • Hyperreflexia, although a rapidly developing lesion may cause diminished or absent reflexes (reflex abnormalities observed in as many as 40% of cases)
  • Respiratory compromise (with cervical lesions)
• Findings associated with IEA include the following:
• • Fever (45-55%)
  • Headache (50-73%)
  • Altered mental status (44-50%)
  • Sinus tenderness (32-90%)
  • Focal neurological deficits
  • Evidence of wound infection (>90% of patients who have undergone craniotomy)
  • Seizure (4-63%)

Causes

Microbiology in SEA and IEA is considered separately.

• Staphylococcus aureus infection causes most cases of SEA. This is followed in frequency by streptococci and Enterobacteriaceae infections. Coagulase-negative staphylococci infections are observed only in the context of recent spinal instrumentation. The most common organisms include the following:
• • S aureus (57-63%), often methicillin-resistant S aureus (MRSA; both hospital-acquired and community-acquired strains described in case reports)
  • Enteric gram-negative bacilli, especially Escherichia coli (16%)
  • Coagulase-negative staphylococci (3-5%), primarily involving spinal instrumentation
  • Bacteroides species and other anaerobes (2%)
  • Pseudomonas species
  • Streptococci
  • Less common organisms - Actinomyces species; Nocardia species; Brucella species; mycobacteria (especially Mycobacterium tuberculosis); and fungi, including Candida, Aspergillus, Blastomyces, and Sporothrix species.
  • Unknown (6-10%)
• In IEA, upper respiratory bacterial pathogens predominate in sinus-associated disease, whereas nosocomial pathogens are of concern in cases that develop after craniotomy. The most common organisms include the following:
• • Staphylococci, both coagulase-positive and coagulase-negative
  • Streptococci, including anaerobic and microaerophilic species
  • Aerobic gram-negative bacilli
  • Other anaerobes

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Vertebral osteomyelitis
Herniated disc
Transverse myelitis
Guillain-Barré syndrome
Stroke
Mycotic aneurysm
Brain tumor
Herpes zoster virus infection prior to dermatologic manifestation
Vasculitis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Routine tests
• • The CBC count may reveal leukocytosis, left shift, and anemia. In one retrospective analysis, only 60% of patients in whom spinal epidural abscess (SEA) was diagnosed had leukocytosis at the time of initial evaluation.
  • The erythrocyte sedimentation rate (ESR) is very commonly elevated; this is a nonspecific finding.
  • Obtain blood cultures.
• Abscess fluid
• • Perform Gram staining and cultures of aspirated abscess fluid.
  • Obtain special stains and cultures for mycobacteria and fungi.

Imaging Studies

• Magnetic resonance imaging (MRI) is the cornerstone of diagnosis. MRI has the greatest diagnostic accuracy and is the method of first choice in the diagnostic process.
• • When vertebral osteomyelitis is present, the sensitivity of MRI is 95%, and its specificity is 92%.
  • Gadolinium enhancement increases sensitivity for detecting SEA, even in the absence of contiguous bony infection, and enables better differentiation between abscess and surrounding neurological structures. Use MRI in intracranial epidural abscess (IEA) diagnosis, as well.
• Computed tomography (CT) scanning with intravenous contrast may demonstrate fluid collections in the epidural space. CT scanning is the procedure of choice when MRI cannot be performed.
• When combined with myelography, CT scanning is a fairly sensitive tool to diagnose SEA, but it carries considerable risk, including introduction of infection, bleeding, nerve injury, and spinal shock. Myelography may underestimate the length of an SEA and also carries a risk of paralysis.
• Plain radiographs occasionally demonstrate osteomyelitis but are of almost no utility.

Procedures

• Make every effort to establish a microbiological diagnosis.
• CT-guided needle aspiration may be used to obtain material for analysis.
• Lumbar puncture is generally not indicated in SEA and entails the risk of spreading the bacteria into the subarachnoid space with consequent meningitis. It is contraindicated in IEA because of the high risk of cerebellar tonsillar herniation due to increased intracranial pressure. When obtained, lumbar puncture usually reveals parameningeal infection, with elevated protein levels, normal or slightly depressed glucose levels, and modest pleocytosis. Results may also be normal or indicative of frank bacterial meningitis. Culture results may be positive in up to 25% of cases.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Surgical decompression and drainage of purulent material is essential.
• Empirical antibiotic therapy should include coverage of gram-positive cocci, particularly staphylococci, and gram-negative bacilli. Third-generation cephalosporins offer excellent gram-positive and gram-negative coverage and CNS penetration. Narrow coverage once culture data are available.
• Given the increasing incidence of community-acquired MRSA in patients who present with soft-tissue infections, the inclusion of vancomycin in initial empiric therapy should be carefully considered.
• Few case reports describe successful treatment of spinal epidural abscess (SEA) with antibiotics alone. Rarely, persons with SEA whose neurological status has not progressed beyond radicular pain may be considered for nonsurgical management.
• In patients at high risk for operative mortality, consider treatment with antibiotics alone.

Surgical Care

• Delay in surgical drainage and decompression has repeatedly been associated with high morbidity and mortality.
• Given the life-threatening nature of subdural empyema, decompression of intracranial epidural abscess (IEA) is uniformly considered a neurosurgical emergency.
• Persistent fever and neurological deterioration warrant surgical exploration.

Consultations

Emergent neurosurgical consultation is mandatory for surgical decompression and drainage of purulent material.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The course of therapy generally is 4-6 weeks or until MRI reveals resolution of the abscess. The presence of osteomyelitis may extend treatment to 8 weeks or longer. Antistaphylococcal penicillins (eg, nafcillin) are the agents of choice for susceptible staphylococci. Use vancomycin when methicillin resistance is of concern. If anaerobes are suspected clinically, metronidazole offers superior coverage and easily penetrates the blood-brain barrier. Good antipseudomonal agents include ceftazidime, cefepime, imipenem and cilastatin, and meropenem, which are used for nosocomially acquired disease.

Drug Category: Antibiotics

Empirical antimicrobial therapy must be comprehensive and should cover all likely pathogens in the clinical setting. Antibiotic combinations are usually recommended for serious gram-negative bacillary infections. This approach ensures coverage for a broad range of organisms and polymicrobial infections. In addition, it prevents resistance from bacterial subpopulations and provides additive or synergistic effects. Once organisms and sensitivities are known, antibiotic monotherapy is recommended.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Frequent neurological examination is warranted during the recovery period. Fever, leukocytosis, or new neurological deficit necessitates repeated imaging, and further surgical exploration may be required.
• Physical therapy may be necessary for individuals with residual neurological deficit.

Further Outpatient Care

• The first follow-up MRI is obtained at about 4 weeks if the patient is improving or at any time if clinical deterioration occurs.
• Follow-up with a neurosurgeon is needed for monitoring repeat imaging.
• Follow-up with an infectious diseases specialist is advised to monitor intravenous antibiotics.

Transfer

• In the United States, by law, any unstable patient must be stabilized to the extent possible, including consultation and surgery, if indicated, before transfer.

Prognosis

• The degree of neurologic recovery after surgery is related to the duration of the neurologic defect.
• A worse outcome has been observed in patients with the following:
• • Multiple medical problems
  • Prior spinal surgery
  • Prior cervical or thoracic abscess location
  • Thrombocytopenia
  • Leukocytosis (WBC count >14,000 10³/µL)
  • Significantly elevated levels of inflammatory markers
  • Infection with methicillin-resistant staphylococci
  • Significant degree of thecal sac compression

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 and Antibiotics.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Delay in surgical drainage and decompression has repeatedly been associated with high morbidity and mortality.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Chen HC, Tzaan WC, Lui TN. Spinal epidural abscesses: a retrospective analysis of clinical manifestations, sources of infection, and outcomes. Chang Gung Med J. May 2004;27(5):351-8.
• Curry WT, Hoh BL, Amin-Hanjani S. Spinal epidural abscess: clinical presentation, management, and outcome. Surg Neurol. Apr 2005;63(4):364-71; discussion 371. [Medline].
• Davis DP, Wold RM, Patel RJ. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med. Apr 2004;26(3):285-91. [Medline].
• Hlavin ML, Kaminski HJ, Fenstermaker RA. Intracranial suppuration: a modern decade of postoperative subdural empyema and epidural abscess. Neurosurgery. Jun 1994;34(6):974-80; discussion 980-1. [Medline].
• Hlavin ML, Kaminski HJ, Ross JS. Spinal epidural abscess: a ten-year perspective. Neurosurgery. Aug 1990;27(2):177-84. [Medline].
• Lohr M, Reithmeier T, Ernestus RI. Spinal epidural abscess: prognostic factors and comparison of different surgical treatment strategies. Acta Neurochir (Wien). Feb 2005;147(2):159-66; discussion 166.
• Nussbaum ES, Rigamonti D, Standiford H. Spinal epidural abscess: a report of 40 cases and review. Surg Neurol. Sep 1992;38(3):225-31. [Medline].
• Pereira CE, Lynch JC. Spinal epidural abscess: an analysis of 24 cases. Surg Neurol. 2005;63 Suppl 1:S26-9. [Medline].
• Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-analysis of 915 patients. Neurosurg Rev. Dec 2000;23(4):175-204; discussion 205. [Medline].
• Rigamonti D, Liem L, Sampath P. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol. Aug 1999;52(2):189-96; discussion 197. [Medline].
• Siddiq F, Chowfin A, Tight R. Medical vs surgical management of spinal epidural abscess. Arch Intern Med. Dec 13-27 2004;164(22):2409-12. [Medline].
• Sorensen P. Spinal epidural abscesses: conservative treatment for selected subgroups of patients. Br J Neurosurg. Dec 2003;17(6):513-8.
• Tang HJ, Lin HJ, Liu YC. Spinal epidural abscess--experience with 46 patients and evaluation of prognostic factors. J Infect. Aug 2002;45(2):76-81.
• Tunkell, AR. Subdural empyema, epidural abscess, and suppurative intracranial thrombophlebitis. In: Mandell GL, Bennet JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practices of Infectious Diseases. 2005;1165-8.

Article Last Updated: Feb 12, 2007