A spinal epidural abscess threatens the spinal cord or cauda equina by compression and also by vascular compromise (see images below). If untreated, an expanding suppurative infection in the spinal epidural space impinges on the spinal cord, producing sensory symptoms and signs, motor dysfunction, and, ultimately, paralysis and death. Intervention early in the course of the disease undoubtedly improves the outcome. Frequently, diagnosis is understandably delayed because the initial presentation may be only nonspecific back pain. One half of cases are estimated to be misdiagnosed or have a delayed diagnosis.[1] At times, radicular symptoms may lead to a chief complaint of chest pain or abdominal pain[2] , mimicking a myocardial infarction or an acute abdomen.[3]
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Cervical epidural abscess with spinal cord compression and spinal cord edema.
The spinal epidural space is not a uniform space. Posteriorly, the epidural space contains fat, small arteries, and the venous plexus. Infections in this space may spread over several vertebral levels. Anteriorly, the epidural space is a potential space with the dura tightly adherent to the vertebral bodies and ligaments. Abscesses occur more frequently in the larger posterior epidural space. Most spinal epidural abscesses occur in the thoracic area, which is anatomically the longest of the spinal regions.
Some series suggest that dorsal spinal epidural abscesses are much more likely to present with weakness and severe neurologic deficit than ventral spinal epidural abscesses.[4]
Hematogenous spread with seeding of the epidural space is the suspected source of infection in most children and is thought to occur in many adults as well. Reported sources of infection are numerous and include bacterial endocarditis, infected indwelling catheters, urinary tract infection, peritoneal and retroperitoneal infections, and others.
Direct extension of infection from vertebral osteomyelitis occurs in adults and rarely in children.
Epidural catheters and injections may lead to direct inoculation of the epidural space. The source of infection is not identified in many patients. There was a recent outbreak of fungal infections including epidural abscesses associated with injection of methylprednisolone that was contaminated with environmental molds.[5]
The more clinically significant effects of the epidural abscess may be from involvement of the vascular supply to the spinal cord and subsequent infarction rather than direct compression. Staphylococcus aureus is the most commonly reported pathogen[6] , though many other bacteria have been implicated, including Staphylococcus and Pseudomonas species, Escherichia coli, Brucella, and Mycobacterium tuberculosis. Methicillin-resistant Staphylococcus aureus (MRSA) is increasingly reported particularly in patients with a history of MRSA abscesses, spinal surgery, or implanted devices. Immunosuppressed patients may have infections from unusual bacterial or fungal organisms. Fungal infections may also occur. Environmental mold Exserohilum rostratum was the unusual pathogen associated with the outbreak of contaminated methylprednisolone.
The frequency in large tertiary care centers is estimated to be about 2.8 cases per 10,000 admissions. The incidence is suspected to be increasing in relation to intravenous (IV) drug abuse.[7]
International
Because these abscesses occur rarely, the frequency is unknown. It probably parallels the US experience of rarity, although limited diagnostic capabilities in medically underserved countries might increase its importance as a health risk.
Mortality/Morbidity
If untreated, spinal epidural abscess causes progressive paraplegia and death.
Sex
Older studies found an equal sex ratio; more recent data indicate a male predominance, likely reflecting the pattern of IV drug use.
Age
The average age is older than 50 years, but spinal epidural abscess can occur at any age.
Clinical presentation may be quite variable. The clinical triad of fever, back pain, and neurologic deficit is not present in most patients.[6, 8] Early presentations may be subtle, and atypical presentations are not unusual. A 4-phase sequential evolution has been described, with (1) localized spinal pain, (2) radicular pain and paresthesias, (3) muscular weakness, sensory loss, and sphincter dysfunction, and finally (4) paralysis.[1]
The virulence of the infecting organism and the mode of infection contribute to the tempo of this progression. Abscesses from hematogenous spread tend to progress rapidly, while abscesses from osteomyelitis or discitis may evolve over weeks or months with slow progression of symptoms.
Frequently the patient gives a history of back strain or mild injury.
An evident source of infection in skin or soft tissue may be found.
IV drug users are a high-risk group. Occurrences have been cited even in patients with a remote history of IV drug abuse.[7]
Cases are frequently reported in patients with diabetes mellitus, which is a risk factor in 50% of reported patients; alcoholism; and conditions involving chronic immunosuppression.
Hematogenous seeding of the epidural space with abscess formation may stem from intravenous lines, urinary catheters, or implantable devices. Direct inoculation of the epidural space may follow spinal surgery, epidural catheter placement, or epidural injections.
Symptoms may include the following:
Fever, present in only about one third of patients
Localized back pain in most patients, often the first symptom
Radiculopathy with radiating or lancinating pain, including chest or abdominal pain (At times this may simulate myocardial infarction or other causes of chest or abdominal pain.)
Spinal cord syndromes, typically involving paraparesis with prospective progression to paraplegia (Epidural abscesses at the level of the cauda equina cause symptoms consistent with cauda equina syndrome rather than a spinal cord syndrome.)
Central cord syndrome from epidural abscess has also been reported.[9]
Sphincter dysfunction, including incontinence or increased residual urine volumes
Headache and neck pain may be present, especially with cervical epidural abscesses. (Of course, these symptoms might also suggest meningitis.)
Physical findings vary with the degree of spinal cord compression or dysfunction.
In the most advanced cases, a transverse cord syndrome is seen with motor and sensory levels found with neurologic examination.
Localized tenderness to percussion or palpation at the site of the abscess may be noted. Paraspinal muscle spasm may be present.
Signs of spinal cord dysfunction may be observed.
Complete transverse spinal cord syndrome with paraplegia and sphincter dysfunction
Incomplete spinal cord syndromes
Unilateral motor or sensory deficits[10]
Gait ataxia[10]
Reflexes may vary from absent to hyperreflexia with clonus and extensor plantar (Babinski) responses. Areflexia may indicate spinal shock with transient inhibition of spinal reflexes.
Nuchal stiffness or rigidity may be present, notably with cervical epidural abscesses.
Errors in diagnosis of spinal epidural abscessesare common and involve inadequate history, physical examination, and test ordering. According to one study of retrospective chart reviews of 250 randomly selected patients, 119 had a new diagnosis of spinal epidural abscess, 66 (55.5%) of which experienced diagnostic error. Red flags that were frequently not evaluated in error cases included unexplained fever, focal neurological deficits with progressive or disabling symptoms, and active infection.[12]
CBC count, blood cultures, and preoperative lab studies. Leukocytosis is present in about two thirds of patients.[1]
Elevated erythrocyte sedimentation rate (ESR): In one report, the mean ESR was 51 mm/h.[13] ESR may be highly elevated.
Leukocytosis and ESR elevation are nonspecific laboratory findings and are not invariably present. Neither the presence of these findings nor the degree of laboratory abnormality is specific for spinal epidural abscess.[1]
A treatment guideline incorporating ESR, C-reactive protein, and other risk factors has been proposed based on a small patient series.[14]
Immediate imaging of the spine and spinal cord is imperative when the diagnosis is clinically suspected.
If available, spinal MRI is the procedure of choice. Recall that symptoms are often defined by spinal cord level, while MRI is ordered by regional or vertebral levels. Because abscesses frequently extend for several levels, be certain to order the anatomically correct region.
If MRI is unavailable, CT myelography or conventional myelography can reveal an intraspinal extramedullary mass—a "surgical" lesion.
Lumbar puncture (LP) is relatively contraindicated if spinal epidural abscess is suspected. However, LP may be essential to exclude meningitis from the differential diagnosis. Lumbar puncture runs the risk of introducing purulent material into the subarachnoid space. Some advocate slowly advancing the needle with gentle syringe aspiration if spinal epidural abscess is suspected; if purulent material is encountered, it should be aspirated gently to obtain laboratory specimens, and the needle should not be advanced further.
Cerebrospinal fluid (CSF) may show inflammatory cells, often a mixture of polymorphonuclear and mononuclear cells. Cell counts usually are increased, ranging from 10-1000 leukocytes/µL.
CSF protein usually is elevated above 100 mg/dL but may be higher, particularly if spinal block is present.
CSF glucose is usually normal; depression may indicate coexisting meningitis.
Treatment most often consists of both medical[15] and surgical therapy.
Empiric antibiotic coverage should include antistaphylococcal antibiotics. With the increasing incidence of methicillin-resistant staphylococcal infections, coverage that includes antibiotics effective against MRSA is recommended. If the infection follows a neurosurgical procedure, an antistaphylococcal penicillin, a third-generation cephalosporin, and an aminoglycoside are prescribed in combination. Culture results guide definitive therapy.
If the patient remains neurologically stable and has a mechanically stable spine, some recommend that antibiotic treatment be delayed until material is obtained for a culture.[16]
Antibiotic treatment with CT-guided aspiration of the epidural space is increasingly used in patients without neurologic deficits.
Resolution of the abscess with antibiotics alone has been reported in patients who are not candidates for surgery because of spine instability or coexisting medical problems.
Deterioration of clinical and functional status while undergoing antibiotic therapy alone has been observed and may dictate emergency surgical decompression.
Because of the rarity of the disorder, no randomized trial results are available to guide the clinician.
For the rare case associated with the recent outbreak of fungal-contaminated methylprednisolone injections, the recommended drug is voriconazole at a dose of 6 mg/kg of body weight twice daily.[5]
No specific guidelines exist for children, but a recent case series showed benefit with medical therapy of most patients in that case series.[17]
Emergency surgical decompression of the spinal cord with drainage of the abscess is the usual surgical treatment.[18, 19]
Successful treatment with a combination of abscess aspiration and antibiotic treatment has been reported and seems to be used increasingly.
Increasing neurologic deficit, persistent severe pain, or persistent fever and leukocytosis are all indications for decompressive surgery.
Patients with spinal epidural abscess may be clinically unstable because of concomitant systemic infection, shock, complications of diabetes mellitus, or other complications. As a result, an increased surgical risk often must be weighed in the decision process.
Antibiotic treatment should be initiated as soon as the diagnosis is reasonably considered, and is most often used in conjunction with abscess aspiration or surgical therapy. The usual duration of antibiotic therapy is 3-4 weeks, but may be lengthened in the presence of osteomyelitis.
As mentioned above, in select stable patients, antibiotic therapy may be briefly delayed until material is obtained for culture.
Clinical Context:
Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. By binding to penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth.
Clinical Context:
Treats infections caused by penicillinase-producing staphylococci. Used to initiate therapy in any patient in whom penicillin G-resistant staphylococcal infection suspected. Should not be used for treatment of penicillin G-susceptible staphylococci.
Parenteral therapy used initially in severe infections. Very severe infections may require very high doses. As condition improves, parenteral therapy should be changed to oral therapy.
Because of occasional occurrence of thrombophlebitis associated with parenteral route, particularly in the elderly, parenteral route should be used only for short term (24-48 h) and changed to oral route, if clinically possible.
Clinical Context:
First-generation semisynthetic cephalosporin, which by binding to penicillin-binding proteins arrests bacterial cell wall synthesis and inhibits bacterial growth. Active primarily against skin flora, including S aureus. Total daily dosage is same for both IV and IM routes.
Clinical Context:
Used in combination with other antibiotics in epidural abscess following neurosurgical procedures. Active against various anaerobic bacteria and protozoa. Appears to be absorbed into cells, and intermediate-metabolized compounds formed bind DNA and inhibit protein synthesis, causing cell death.
Clinical Context:
Used in combination with other antibiotics for epidural abscess following neurosurgical procedures. Aminoglycoside antibiotic used for gram-negative bacterial coverage. Commonly used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution. May be administered IV or IM.
Clinical Context:
Often used when MRSA or other resistant organisms are suspected. Potent antibiotic directed against gram-positive organisms and active against enterococci species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or whose conditions have failed to respond to penicillins and cephalosporins, or those who have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.
To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to adjust dose in patients with renal impairment.
Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures.
Because S aureus is a common pathogen, anti-staphylococcal drugs should be included in the treatment regimen. An anti-staphylococcal penicillin, a cephalosporin, or vancomycin may be used. Again, with the increasing incidence of methicillin-resistant staphylococcal infections, coverage that includes an antibiotic that is effective against MRSA is recommended, which can be narrowed once cultures and sensitivities have resulted. If the patient has undergone a neurosurgical procedure recently, the penicillin should be combined with a third-generation cephalosporin and an aminoglycoside. Gram-stain and culture results are used to guide therapy.
What is spinal epidural abscess?What is the pathophysiology of spinal epidural abscess?What is the prevalence of spinal epidural abscess in the US?What is the global prevalence of spinal epidural abscess?How does spinal epidural abscess progress if untreated?What are the sexual predilections of spinal epidural abscess?Which age groups have the highest prevalence of spinal epidural abscess?Which clinical history findings are characteristic of spinal epidural abscess?Which physical findings are characteristic of spinal epidural abscess?What causes spinal epidural abscess?Which conditions should be included in the differential diagnoses of spinal epidural abscess?What are the differential diagnoses for Spinal Epidural Abscess?What causes errors in the diagnosis of spinal epidural abscess?What is the role of lab studies in the diagnosis of spinal epidural abscess?What is the role of imaging studies in the diagnosis of spinal epidural abscess?What is the role of CSF analysis in the diagnosis of spinal epidural abscess?How are spinal epidural abscesses treated?What is the role of surgery in the treatment of spinal epidural abscess?Which specialist consultations are beneficial to patients with spinal epidural abscess?What is the role of antibiotics in the treatment of spinal epidural abscess?Which medications in the drug class Antibiotics are used in the treatment of Spinal Epidural Abscess?What is included in outpatient care for the treatment for spinal epidural abscess?What is included in inpatient care for the treatment for spinal epidural abscess?When is patient transfer indicated for the management of spinal epidural abscess?What are the possible complications of spinal epidural abscess?What is the prognosis of spinal epidural abscess?
J Stephen Huff, MD, FACEP, Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Florian P Thomas, MD, PhD, MA, MS, Chair, Neuroscience Institute and Department of Neurology, Director, National MS Society Multiple Sclerosis Center and Hereditary Neuropathy Foundation Center of Excellence, Hackensack University Medical Center; Founding Chair and Professor, Department of Neurology, Hackensack Meridian School of Medicine at Seton Hall University; Professor Emeritus, Department of Neurology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine
Disclosure: Nothing to disclose.
Chief Editor
Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM, Adjunct Associate Professor of Neurology, University of Missouri-Columbia School of Medicine; Medical Director of St Mary's Stroke Program, SSM Neurosciences Institute, SSM Health
Disclosure: Nothing to disclose.
Additional Contributors
Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
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