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

Epidural Abscess

Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
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

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 abscess^1,2,3

• 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 abscess^4,5,1,2  

• 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 abscess^2,1

• 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 abscess^5,1
  • 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 abscess^7,6
  • 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
  • S aureus (60%; increasingly often methicillin-resistant S aureus [MRSA])
  • Enteric gram-negative bacilli, especially Escherichia coli (10%)
  • Coagulase-negative staphylococci (3-5%), primarily involving spinal instrumentation or epidural anesthesia/injections
  • Bacteroides species and other anaerobes (2%)
  • Pseudomonas species (2%)
  • Streptococci, including Streptococcus viridans, group B streptococci, and pneumococcus (10%)
  • Mycobacteria, usually Mycobacterium tuberculosis (<1% in Western countries but more common in developing countries)
  • Less-common organisms -Acinetobacter , enterococci, Actinomyces species, Nocardia species, Brucella species, and fungi, including Candida, Coccidioides, Aspergillus, Blastomyces, and Sporothrix species
  • Polymicrobial (possibly 5%-10%)
  • Unknown (6%-10%)
• 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

Differential Diagnoses

Other Problems to Be Considered

Myofascial pain syndrome^8,5
Herniated disc
Transverse myelitis
Guillain-Barré syndrome
Stroke
Mycotic aneurysm
Brain tumor
Herpes zoster virus infection prior to dermatologic manifestation
Vasculitis
Malignancy
Vertebral compression fracture

Workup

Laboratory Studies

• Routine tests^4,1,2
  • The CBC count may reveal leukocytosis, left shift, thrombocytopenia, and anemia. Only about two thirds of patients who present with spinal epidural abscess have leukocytosis at the time of initial evaluation.
  • The erythrocyte sedimentation rate (ESR) is almost invariably elevated; this is a nonspecific finding.
  • Always obtain blood cultures, as they are positive in 60% of cases.
• Abscess fluid/operative material
  • Perform Gram staining and routine aerobic and anaerobic cultures on aspirated or surgically obtained abscess fluid.
  • Special stains and cultures for mycobacteria and fungi are indicated.

Imaging Studies

• MRI is the cornerstone of diagnosis in both intracranial epidural abscess and spinal epidural abscess. MRI has the greatest diagnostic accuracy and is the method of first choice in the diagnostic process.^9,10,1
  • The sensitivity of MRI is 90%-95%, and its specificity also exceeds 90%. In some cases, MRI findings are indeterminate, necessitating a repeat of the study.
  • Gadolinium enhancement increases sensitivity for detecting spinal epidural abscess, even in the absence of contiguous bony infection, and enables better differentiation between abscess and surrounding neurological structures.
• 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 spinal epidural abscess, but it carries considerable risk, including introduction of infection, bleeding, nerve injury, and spinal shock. Myelography may underestimate the length of a spinal epidural abscess and carries a risk of paralysis.
• Plain radiographs may demonstrate osteomyelitis or vertebral collapse. While these should be performed in all cases, they are never enough to establish the diagnosis.

Procedures

• Make every effort to establish a microbiological diagnosis. Blood cultures are positive in 60% of patients with spinal epidural abscess and are essential.²
• CT-guided needle aspiration may be used to obtain material for analysis.
• Surgical specimens must be stained and cultured appropriately (see Causes).
• Lumbar puncture is generally not indicated in spinal epidural abscess and carries the risk of spreading the bacteria into the subarachnoid space, with consequent meningitis. It is contraindicated in intracranial epidural abscess because of the high risk of cerebellar tonsillar herniation due to increased intracranial pressure. When obtained in spinal epidural abscess, lumbar puncture usually reveals a nonspecific parameningeal infection picture, 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, but almost all of these patients have positive blood cultures.²

Staging

A staging system for the progression of spinal epidural abscess exists and may be of some diagnostic value, but it must be stressed that not all patients move sequentially through the stages, and that deterioration may be rapid.¹

1. Back pain, tenderness, and fever
2. Radicular pain, reflex abnormalities
3. Sensory abnormalities, motor weakness, bowel and bladder problems
4. Paralysis, which rapidly becomes permanent without surgical intervention

Treatment

Medical Care

Spinal epidural abscess

A combined medical-surgical approach, with emergent surgical decompression and drainage of purulent material, has been the traditional approach to spinal epidural abscess. Antibiotic-based therapy, sometimes combined with CT-directed needle aspiration, has traditionally been used only in patients who are determined to be at prohibitively high risk of surgery or who have a fixed paralysis that lasts more than 72 hours and that is presumed to be irreversible.

Wider use of the antibiotic-based therapy for spinal epidural abscess has been advocated,^11,12 condemned,^13,14 and cautiously discussed.^8,15 The current literature on the subject consists largely of small case series and is inadequate to resolve the controversy.^1,2

If medical therapy is to be used as initial therapy for spinal epidural abscess and surgery held in reserve, a number of caveats apply, as follows:

• The patient should have no neurological deficits.
• A culture-proven microbiological diagnosis should be available (from blood culture or aspiration).
• Stringent follow-up by both the primary team and neurosurgeons must be available and emergent surgery available, if needed.  
• The physicians caring for the patient must be aware that rapid deterioration may occur at any time (the first 72 hours being most risky) and that even prompt rescue surgery may leave the patient with a neurological deficit that might have been avoided with surgery at first diagnosis.  
• A follow-up MRI is necessary within 2-4 weeks to evaluate for improvement with medical therapy.

Empirical antibiotic therapy should include coverage of gram-positive cocci, particularly staphylococci (including MRSA), and gram-negative bacilli. Vancomycin has been the standard agent for gram-positive infections, although linezolid, daptomycin, or tigecycline could be considered. The third- and fourth-generation cephalosporins and meropenem offer excellent gram-positive (except MRSA) and gram-negative coverage in addition to CNS penetration. Additional coverage may be needed if some of the less-common etiologic agents (see Causes) are suspected. Always tailor coverage once culture data are available; for example, nafcillin is a much better drug for MSSA infections than vancomycin.

Intracranial epidural abscess

A combined medical-surgical approach is used for intracranial epidural abscess. A craniotomy is usually performed. Empiric antibiotic therapy is similar to that described for spinal epidural abscess; since many of these infections result from prior interventions, the possibility of more-resistant nosocomial organisms must be considered. Vancomycin plus cefepime or meropenem would be good starting choices, with metronidazole added to the cefepime if anaerobes are a major concern.

Surgical Care

• Prompt decompression is used to manage intracranial epidural abscess, as it is uniformly considered a neurosurgical emergency.
• As discussed in detail above, most patients with spinal epidural abscess require urgent decompressive laminectomy; other surgical techniques may be preferred in certain situations.¹⁶ In some patients without neurologic deficits, medical therapy might be cautiously attempted, recognizing that disastrous outcomes may ensue from this conservative approach (see Medical Therapy). CT-guided drainage might be helpful in some cases of posterior spinal epidural abscess, but the literature on this is scant.

Consultations

Emergent consultation with a neurosurgeon is mandatory for surgical decompression and drainage of purulent material in patients with intracranial epidural abscess. Emergent surgical intervention is needed in most patients with spinal epidural abscess, and prompt consultation and tight follow-up are mandatory in those in whom surgery is deferred (see Treatment). Consultation with an infectious disease specialist is strongly recommended for both diagnostic and therapeutic assistance.

Medication

The course of medication therapy is not well defined, but 4-12 weeks is generally considered adequate. Concomitant osteomyelitis requires a 6- to 12-week course. A transition to highly bioavailable oral agents might be appropriate in some cases. Rely on an infectious disease specialist consultant for guidance. (See Medical Treatment for empiric selections.)

Antibiotics

Empiric antimicrobial therapy must be comprehensive and cover all likely pathogens. Antibiotic combinations, usually vancomycin or another MRSA agent plus a broad gram-negative agent, are recommended in both intracranial epidural abscess and spinal epidural abscess while awaiting culture data. This approach ensures coverage for a broad range of organisms and polymicrobial infections. Once organisms and sensitivities are known, antibiotic monotherapy is recommended.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with fair gram-negative and gram-positive activity. Superior CNS penetration. Arrests bacterial growth by binding to one or more penicillin-binding proteins. Does not cover MRSA, Pseudomonas species, or resistant nosocomial enterics.

Dosing

Adult

2 g IV q12-24h

Pediatric

100 mg/kg/d given IM/IV divided q12-24h (infants and children-not neonates)

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

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 breastfeeding women and patients with allergy to penicillin; excreted in bile and may cause sludging in gall bladder or biliary tree. Pseudomembranous colitis may occur, requiring discontinuation of medication; superinfection is possible with long courses of therapy; adjust dose in severe renal impairment

Ceftazidime (Ceptaz, Fortaz)

Third-generation cephalosporin with broad-spectrum, gram-negative activity (including Pseudomonas species). Poor efficacy against gram-positive organisms and some resistant gram-negative organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.

Dosing

Adult

2 g IV q8h

Pediatric

50 mg/kg IV q8h (1 month-12 years old)

Interactions

Nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase 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

Pseudomembranous colitis may occur, requiring discontinuation of medication; superinfection is possible with long courses of therapy; adjust dose in renal impairment

Meropenem (Merrem IV)

Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria, with excellent CNS penetration. Has slightly increased activity against gram-negative bacteria and slightly decreased activity against staphylococci and streptococci compared with imipenem, but much less likely than imipenem to cause seizures.

Dosing

Adult

1-2 g IV q8h

Pediatric

<3 months: Not established
>3 months: 40 mg/kg IV q8h

Interactions

Probenecid may inhibit renal excretion, increasing 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

Pseudomembranous colitis may occur, requiring discontinuation of medication; superinfection is possible with long courses of therapy; adjust dose in renal impairment

Metronidazole (Flagyl, Protostat)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Not active against any aerobes. Must be used in combination for most bacterial infections.

Dosing

Adult

500 mg PO/IV q8h or 1 g IV q12-24h

Pediatric

30 mg/kg/d PO/IV usually divided q6h

Interactions

Cimetidine may increase toxicity; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

May be contraindicated during first trimester of pregnancy; adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy; metallic taste and nausea may occur

Vancomycin (Lyphocin, Vancocin)

Potent antibiotic directed against most gram-positive organisms and active against most Enterococcus species. Indicated in patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with MRSA or another susceptible gram-positive organism.

Dosing

Adult

1 g IV q12h traditional, but many patients will require higher doses to achieve optimal AUC/MIC ratios; consult ID or pharmacy for dosing assistance

Pediatric

10-15 mg/kg IV q6-8h for ages 1 month-12 years

Interactions

Erythema, histaminelike flushing, and anaphylactic reactions may occur ; when taken concurrently with aminoglycosides, risk of nephrotoxicity increases above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered 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 renal failure and neutropenia; red man syndrome is caused by too rapid IV infusion (dose administered over a few min) but rarely happens when dose is administered over 2 h or as PO or IP administration; red man syndrome is an anaphylactoid reaction caused by histamine release

Nafcillin (Nafcil, Unipen)

A penicillin used almost exclusively for MSSA. Is not effective against MRSA infections. Do not use empirically when MRSA infection is possible.

Dosing

Adult

2 g IV q4h

Pediatric

>1 month: 25 mg/kg/d IV q6h

Interactions

Associated with warfarin resistance when administered concurrently; effects may decrease with bacteriostatic action of tetracycline derivatives; probenecid can increase effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Only use for MSSA. May cause interstitial nephritis, cytopenias.

Follow-up

Further Inpatient Care

• Frequent neurological examination is warranted during the postsurgical recovery period and is especially critical in patients undergoing medical treatment for spinal epidural abscess.
• Fever, leukocytosis, or new neurological deficit necessitates repeated imaging, and further (or initial) surgical exploration may be required.¹⁶
• Follow-up MRIs to evaluate spinal epidural abscess in patients who are doing well may not be helpful, as the findings may not correlate well with clinical course.¹⁷
• Physical therapy may be necessary for individuals with a residual neurological deficit.

Further Outpatient Care

• Follow-up MRI should be obtained if any clinical deterioration is noted in patients with an intracranial epidural abscess or spinal epidural abscess. Follow-up MRI at 2-4 weeks should be performed in patients with spinal epidural abscess undergoing medical treatment to ensure the abscess has improved. It is unclear whether surgically treated patients with spinal epidural abscess who are doing well require follow-up MRI, as the MRI findings do seem not to correlate with the clinical course.¹⁷
• Follow-up with the neurosurgeon is needed.
• Follow-up with an infectious diseases specialist is advised to monitor intravenous antibiotics.

Inpatient & Outpatient Medications

See Treatment and Medication.

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.

Complications

Death or permanent neurologic sequelae occur in a substantial proportion of patients with epidural abscess, especially those who present with major neurological deficits or sepsis.

Prognosis

• The degree of neurologic recovery after surgery correlates with the duration and initial severity of the neurologic defect.
• Spinal epidural abscess carries a mortality rate of 2%-20%; intracranial epidural abscess, about 10% (see Mortality).
• A worse outcome has been observed in patients with the following:¹
  • Multiple medical problems
  • Prior spinal surgery
  • Prior cervical or thoracic abscess location
  • Thrombocytopenia
  • Leukocytosis (>14,000 WBCs/µL)
  • Persistently elevated inflammatory markers
  • Infection with methicillin-resistant staphylococci
  • Significant degree of thecal sac compression
  • Sepsis

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

Medicolegal Pitfalls

• Diagnostic delays are common in both spinal epidural abscess and intracranial epidural abscess and can lead to poor outcomes and legal action.¹⁸ Although these are rare infections, all clinicians who might encounter these patients must be aware of their presentation and be ready to obtain an MRI. Waiting for the classic triad of spinal epidural abscess (see History) or for a possible intracranial epidural abscess to progress is fraught with hazard.
• Delay in surgical drainage and decompression has repeatedly been associated with high morbidity and mortality rates.

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].

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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