eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Epidural Abscess

Author: Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
Coauthor(s): Aadia Rana, MD, Research Fellow, Department of Medicine, Division of Infectious Diseases, The Miriam Hospital, Brown University School of Medicine; Gopala K Yadavalli, MD, Associate Program Director of Internal Medicine, Assistant Professor of Medicine, Division of Infectious Diseases, Case Western Reserve University School of Medicine and Louis Stokes Cleveland Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Apr 20, 2009

Introduction

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 two types of epidural abscess, and the difference is based on where they develop within the CNS and some variations in risk factors (see Pathophysiology) and symptoms (see History).

A loose association between the dura and vertebral bodies enables extension of spinal epidural abscess to numerous levels, frequently resulting in extensive neurological findings and often necessitating multiple laminectomies. The lumbar and thoracic spine are more commonly affected than the cervical spine.

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

Early recognition of these diseases and timely consultation with a neurosurgeon and infectious disease specialist is vital to optimizing the neurological outcome.

Pathophysiology

Spinal epidural abscess

Causes of spinal epidural abscess1,2,3

  • Ten to thirty percent of spinal epidural abscesses result from direct extension of local infection, usually vertebral osteomyelitis, psoas abscess, or contiguous soft-tissue infection.
  • About half are due to hematogenous seeding. The most likely source is a soft-tissue process, but anything capable of causing bacteremia can result in spinal epidural abscess (endocarditis, urinary tract infection, respiratory tract infections, intravenous drug use, vascular access devices). Hematogenous seeding of the spinal epidural abscess can result in multilevel noncontiguous spinal epidural abscess.
  • Fifteen to twenty-two percent of spinal epidural abscesses are due to invasive procedures or instrumentation. Spinal surgery, epidural anesthesia, steroid and pain-relieving injections, and placement of pain pumps are all associated with spinal epidural abscess. Short-term epidural anesthesia is obviously much less risky than a catheter left in place for days or permanently implanted.
  • In some cases (up to 30% in some series), the source of the spinal epidural abscess is not identified.

Risk factors for spinal epidural abscess4,5,1,2  

  • The most common risk factor for spinal epidural abscess is diabetes mellitus, followed by spinal trauma (may be remote) or surgery, intravenous drug abuse, alcoholism, renal insufficiency, immunosuppression (including HIV infection and malignancy), and spinal/epidural injections.
  • Intravenous drug use seems to represent an increasing risk factor in many series.

Anatomy of spinal epidural abscess2,1

  • Most abscesses occur posteriorly. An anterior location is often associated with vertebral osteomyelitis.
  • The thoracic and lumbar areas are the most likely sites of involvement, with the cervical spine accounting for approximately 20% of cases.5
  • Spread to multiple vertebral levels is common and occurs as the abscess extends up and down the spinal dural sheath. In some cases, this process involves most or all of the spine.

Mechanism of injury1

  • Direct compression of the cord is clearly a major factor.
  • Vascular occlusion due septic thrombophlebitis and/or vasculitis is also a factor
  • The exact mechanism of injury remains controversial.

Intracranial epidural abscess

  • Because intracranial epidural abscess can cross the cranial dura along emissary veins, an accompanying subdural empyema is often present.6
  • Risk factors for intracranial epidural abscess include prior craniotomy, head injury, sinusitis, otitis media, and mastoiditis.7,6

Frequency

United States

The annual incidence of spinal epidural abscess has risen in the past 2-3 decades from 0.2-1 cases per 10,000 hospital admissions to 2.5-3 per 10,000 admissions.1 The rising incidence of spinal epidural abscess has been attributed to the increasing prevalence of injection drug use, as well as to an increased performance of invasive spinal procedures.

The annual incidence of intracranial epidural abscess is difficult to determine but is recognized to be much less common than spinal epidural abscess.

International

Few data on epidural abscesses are available outside the United States, but the frequency appears to be similar to that in the United States.

Mortality/Morbidity

  • Spinal epidural abscess: At the beginning of the 20th century, almost all individuals with spinal epidural abscess died. However, associated mortality rates have dropped significantly over the past 50 years, likely because of better diagnostic modalities. Nonetheless, despite advances in imaging and surgical care, the current mortality rate ranges from 2%-20%.2,1,5 Not surprisingly, the mortality risk is greater in those with severe underlying comorbidities or uncontrolled sepsis. Differences in etiology (ie, iatrogenic vs noniatrogenic) do not affect the prognosis. The essential problem of spinal epidural abscess lies in the necessity of early diagnosis, as permanent neurological deficits and possible mortality can be avoided or reduced only with timely treatment.
  • Intracranial epidural abscess: With antibiotic and surgical management, intracranial epidural abscess carries a good prognosis, with an attributable mortality rate of less than 10%.
  • The neurological status of the patient at the time of diagnosis is the best predictor of neurological outcome, and morbidity is increased in both conditions when indicated surgery is delayed.7,1,2

Sex

Most studies report that epidural abscess is more common in males than in females.

Age

  • Spinal epidural abscess can occur at any age. The median age of onset of spinal epidural abscess is approximately 50-60 years.
  • Intracranial epidural abscess is most common in the second and third decades of life.

Clinical

History

  • Spinal epidural abscess5,1
    • Most symptoms of a spinal epidural abscess are due to enlargement of the abscess and surrounding inflammation, which can lead to tissue compression and spinal cord ischemia. 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.1
    • Back or neck pain is the most common symptom in individuals with spinal epidural abscess, occurring in 70%-100% of cases.
    • The classic diagnostic triad of fever, spinal pain, and neurological deficits is present in only 10-15% of cases at first physician contact and must not be relied on for diagnosis.
    • If left untreated, the progression of symptoms is usually sequential and forms the basis for the staging of spinal epidural abscess (see Staging): (1) back pain; (2) radicular irritation; (3) motor weakness, sphincter dysfunction, sensory changes; and, finally, (4) paralysis. Note that this progression may occur very rapidly, and some symptoms may be skipped.
    • The patient's neurological status at the time of diagnosis is the most accurate predictor of outcome and prognosis.
  • Intracranial epidural abscess7,6
    • The symptoms of intracranial epidural abscess are generally more acute but may be difficult to discern from the inciting process (eg, sinusitis, postoperative infection). When intracranial epidural abscess is combined with a subdural empyema, as is often the case, the course is compressed.
    • Signs and symptoms are due to both infection and the slowly expanding intracranial mass. Fever, headache, malaise, lethargy, nausea, and vomiting may be present. Intracranial epidural abscesses due to sinus infections can cause purulent drainage from the nose or ear.
    • Patients without a history of recent cranial manipulation who develop intracranial epidural abscess 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 more than 90% showing evidence of wound infection.

Physical

  • Findings associated with spinal epidural abscess from multiple studies include the following:1
    • Fever (range, 13%-95%; median, 32%) (However, note that many patients with spinal epidural abscess are afebrile.)
    • Spinal tenderness (range, 17%-98%; median, 58%)
    • Weakness of the extremities (range, 26%-87%; median, 40%)
    • Sensory abnormalities (range, 13%-45%; median, 36%)
    • Paralysis (range, 5%-39%; median, 27%)
    • Reflex abnormalities (up to 40% of cases) (Early hyperreflexia may give way to diminished or absent reflexes.)
    • Respiratory compromise (with cervical lesions)
  • Findings associated with intracranial epidural abscess include the following:7,6
    • Fever (However, fewer than half of patients are febrile, so this symptom is unreliable.)
    • 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

The microbiologic causes of spinal epidural abscess and intracranial epidural abscess are considered separately.

  • Staphylococcus aureus infection causes most cases of spinal epidural abscess. This is followed in frequency by streptococcal and Enterobacteriaceae infections. Coagulase-negative staphylococcal infections are observed almost exclusively in the context of recent spinal instrumentation or other medical procedures. The most common organisms that cause spinal epidural abscess include the following:5,1
  • In intracranial epidural abscess, upper-respiratory bacterial pathogens predominate in sinus-associated disease, whereas nosocomial pathogens are of concern in cases that develop after craniotomy. The most common causative organisms include the following:
    • Staphylococci, both coagulase-positive and coagulase-negative
    • Streptococci, including anaerobic and microaerophilic species
    • Aerobic gram-negative bacilli
    • Propionibacterium acnes
    • Other anaerobes
    • Can be polymicrobial

More on Epidural Abscess

Overview: Epidural Abscess
Differential Diagnoses & Workup: Epidural Abscess
Treatment & Medication: Epidural Abscess
Follow-up: Epidural Abscess
References

References

  1. Sendi P, Bregenzer T, Zimmerli W. Spinal epidural abscess in clinical practice. QJM. Jan 2008;101(1):1-12. [Medline].

  2. Darouiche RO. Spinal epidural abscess. N Engl J Med. Nov 9 2006;355(19):2012-20. [Medline].

  3. Tsiodras S, Falagas ME. Clinical assessment and medical treatment of spine infections. Clin Orthop Relat Res. Mar 2006;444:38-50. [Medline].

  4. Tang HJ, Lin HJ, Liu YC, Li CM. Spinal epidural abscess--experience with 46 patients and evaluation of prognostic factors. J Infect. Aug 2002;45(2):76-81. [Medline].

  5. 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].

  6. 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.

  7. 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].

  8. Chen WC, Wang JL, Wang JT, Chen YC, Chang SC. Spinal epidural abscess due to Staphylococcus aureus: clinical manifestations and outcomes. J Microbiol Immunol Infect. Jun 2008;41(3):215-21. [Medline].

  9. Lury K, Smith JK, Castillo M. Imaging of spinal infections. Semin Roentgenol. Oct 2006;41(4):363-79. [Medline].

  10. An HS, Seldomridge JA. Spinal infections: diagnostic tests and imaging studies. Clin Orthop Relat Res. Mar 2006;444:27-33. [Medline].

  11. 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].

  12. Sørensen P. Spinal epidural abscesses: conservative treatment for selected subgroups of patients. Br J Neurosurg. Dec 2003;17(6):513-8. [Medline].

  13. 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].

  14. Pereira CE, Lynch JC. Spinal epidural abscess: an analysis of 24 cases. Surg Neurol. 2005;63 Suppl 1:S26-9. [Medline].

  15. Savage K, Holtom PD, Zalavras CG. Spinal epidural abscess: early clinical outcome in patients treated medically. Clin Orthop Relat Res. Oct 2005;439:56-60. [Medline].

  16. Löhr M, Reithmeier T, Ernestus RI, Ebel H, Klug N. Spinal epidural abscess: prognostic factors and comparison of different surgical treatment strategies. Acta Neurochir (Wien). Feb 2005;147(2):159-66; discussion 166. [Medline].

  17. Kowalski TJ, Layton KF, Berbari EF, Steckelberg JM, Huddleston PM, Wald JT. Follow-up MR imaging in patients with pyogenic spine infections: lack of correlation with clinical features. AJNR Am J Neuroradiol. Apr 2007;28(4):693-9. [Medline].

  18. 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].

Further Reading

Keywords

epidural abscess, spinal epidural abscess, SEA, intracranial epidural abscess, IEA, increased intracranial pressure, ICP, diabetes mellitus, subdural empyema

Contributor Information and Disclosures

Author

Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
Mark Raymond Wallace, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Aadia Rana, MD, Research Fellow, Department of Medicine, Division of Infectious Diseases, The Miriam Hospital, Brown University School of Medicine
Disclosure: Nothing to disclose.

Gopala K Yadavalli, MD, Associate Program Director of Internal Medicine, Assistant Professor of Medicine, Division of Infectious Diseases, Case Western Reserve University School of Medicine and Louis Stokes Cleveland Veterans Affairs Medical Center
Gopala K Yadavalli, MD is a member of the following medical societies: American Society for Microbiology, American Society of Transplantation, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Fred A Lopez, MD, Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine
Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist  Speaking and teaching

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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