Epidural and subdural infections are similar in that both are suppurative infections that may cause clinical problems by extrinsic compression of CNS structures. They differ in almost all other ways. Both are unusual and are often discovered in the course of investigation for other more common clinical entities.
Approximately 90% of epidural infections are located along the spinal neuraxis and cause symptoms referable to the spinal cord. In contrast, 95% of subdural infections are located intracranially with a predilection for frontal lobe involvement. The unusual intracranial epidural infection is often associated with an intracranial subdural infection.[1]
For purposes of this discussion, epidural infection is considered synonymous with spinal epidural abscess, and subdural infection is considered synonymous with intracranial subdural empyema, unless otherwise noted.
Epidural infection, by definition, involves the epidural space between bone and dura. This is a true space in the spinal canal that is filled posteriorly with epidural fat, small arteries, and a venous plexus. Infections tend to spread over several vertebral levels. Anteriorly, the spinal epidural space is a potential space because the dura adheres tightly to the vertebral body. Abscesses are more frequent in the larger posterior epidural space.
Hematogenous spread with seeding of the epidural space is the suspected source of infection in most children and is thought to occur in many adult cases as well. Reported sources of seeding are numerous and include endocarditis, infected indwelling catheters, urinary tract infections, abdominal infections, and others. Direct extension of infection from vertebral osteomyelitis occurs in adults but rarely in children. A source of infection is not identified in many patients. Spinal epidural abscess following epidural steroid injection and epidural catheter placement has been reported.[2] A recent outbreak of fungal infections associated with epidural injections of contaminated methylprednisolone also included epidural abscesses.[3]
Spinal epidural abscesses in the thoracic spine may progress more quickly and have more severe consequences. This is believed to result from the relatively small size of the spinal canal compared to other spine levels.[4]
See the image below.
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Spinal epidural abscess with cord edema and compression. Abscess extends into paravertebral tissues.
The effects of epidural abscess are often from involvement of the vascular supply to the spinal cord and subsequent infarction rather than from direct compression.[5]
Subdural infections (eg, subdural empyema) occur beneath the dura. Infection spreads over the brain and may penetrate into the parenchyma of the brain or may cause diffuse cerebral edema. These infections frequently result from direct extension from paranasal sinusitis (most common), otitis media, or mastoiditis; from complications of neurosurgical procedures including craniotomies; or, less commonly, from posttraumatic extra-axial hematomas.
The incidence of spinal epidural abscesses has nearly doubled over the last 50 years, possibly because of increased intravenous drug abuse, increased spinal operative procedures, an aging population, and increased sensitivity of detection using MRI.[6] Reported incidence ranges from 0.2-1.2 cases per 10,000 hospital admissions up to 12.5 cases per 10,000 admissions at a tertiary care center.[7] A recent population study of spontaneous epidural abscess in Olmsted County, Minnesota, found the incidence to be 0.88 cases per 100,000 person-years.[8]
No clear estimate of frequency for subdural empyema exists, but it is uncommon. Subdural empyema is said to account for 15-25% of pyogenic intracranial infections. Extrapolating from frequency figures for brain abscess yields roughly 1-2 cases per 10,000 admissions to a tertiary care center.
Mortality/Morbidity
Spinal epidural abscesses are, in themselves, not fatal. However, with complications and associated conditions, mortality rates of 5-23% are reported.[1]
Most case series of subdural empyema report mortality in the 30% range. A declining mortality rate in recent years has been reported.[9] This disorder was uniformly fatal in the pre-antibiotic era.
Sex
No predilection exists with epidural abscess.
In subdural empyema, men are 3-4 times more commonly affected than women.
Age
Spinal epidural abscess may be found in all age groups; on average, patients are older than 50 years. Intravenous drug users with spinal epidural abscesses are, on average, aged 35 years.
Subdural empyema may occur at any age but is most frequent in the second and third decades of life.
Recent pediatric case series and reviews confirms that these entities do occur in children.[10, 11]
Fewer than half of individuals who survive spinal epidural abscesses fully recover.[12] Paraplegia or quadriplegia is a frequent sequela. Disability seems related to severity and duration of symptoms prior to institution of therapy. A spinal rehabilitation program may be necessary to minimize long-term problems.
Acute subdural empyema fatality rate is about 40%. About 40% of survivors develop a seizure disorder, either in the acute phase or during convalescence.
Early presentations may be subtle, and diagnosis may be difficult, if not impossible, at early stages.
History of fever is often but not invariably present.
Localized back pain may be present.
If present, neurologic deficit is consistent with a spinal cord syndrome.
History may suggest a source or cause of infection (eg, soft tissue infection, intravenous drug abuse, indwelling catheters, recent epidural injections, neurosurgical procedures or other instrumentation).
Duration of symptoms is typically a few days but may extend over weeks. Symptom onset may also be abrupt.
Radicular pain consistent with nerve root irritation may confound evaluation, particularly if the pain occurs in the abdomen or the chest.
Progressive sensory disturbances in the extremities, weakness, and incontinence suggest progression to spinal cord involvement.
An immunosuppressive condition, such as diabetes, alcoholism, HIV infection, or chronic liver or kidney disease, is often present.
Subdural empyema
Headaches may be initially unilateral but then become generalized.
Fever and vomiting may be present.
Focal or generalized seizures may be present.
Tempo of clinical course usually is fulminant with rapid deterioration.
Unusual indolent courses may follow neurosurgical procedures.
A history of recent sinusitis or otitis media may be present.
Both spinal epidural abscess and subdural empyema may manifest generalized signs and symptoms of infection such as fever, sepsis, or septic shock.
Spinal epidural abscess
The classic triad of spinal epidural abscess includes spinal pain, fever, and neurological deficits, but this is seen in only 10%-15% of cases.[6]
Localized tenderness to percussion or palpation over the involved region may or may not be present.
Signs of spinal cord dysfunction, such as loss of sphincter tone, sensory loss, or localized motor weakness are late findings.
Reflexes may vary from hypoactive or absent to brisk and spastic.
An abnormal postvoiding residual volume may be a sign of spinal cord disfunction.
Subdural empyema
The classic presentation of subdural empyema is an acute febrile illness accompanied by progressive neurological deterioration. Focal neurologic deficit, such as hemiparesis or aphasia, or focal seizures may be present, in addition to signs of meningeal irritation.
Altered mental status is present in most patients.
Papilledema is absent in most patients, reflecting a short duration of increased intracranial pressure.
Spinal epidural abscess may impair spinal cord function through compression, although current thinking is that thrombosis of vertebral vessels with secondary infarction of the cord may be the mechanism of injury.
Subdural empyema may precipitate cerebral venous thrombosis or cause increased intracranial pressure, resulting in decreased cerebral perfusion and diffuse cerebral edema. Seizures are common.
Sedimentation rate is often elevated and, in cases with low pretest probability for spinal epidural abscess, may be useful as a screening laboratory test.[14]
Liberal use of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) evaluation following historical risk factor assessment for spinal epidural abscess have been incorporated into a clinical decision guideline based on experience at one institution.[15]
CBC may reveal a high WBC count (but normal WBC counts reported as well).
Other tests may include blood cultures, electrolyte levels, and preoperative laboratory studies (as needed by neurosurgery, eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], ECG, chest radiograph [CXR]).
Postsurgical tissue/fluid cultures of infected space may be indicated.
Immediate imaging of the spinal cord is needed upon suspicion for spinal epidural abscess. Techniques that are immediately available vary at different institutions.
MRI with gadolinium contrast is the procedure of choice because of the noninvasive nature of the test. It also delineates the extent of the abscess, which frequently extends over several levels.
For patients with signs or symptoms suggestive of spinal cord compression, it is prudent to image the lumbar and thoracic spine because of the bony spine and spinal cord anatomy. Thoracic spine lesions may cause lower extremity neurologic symptoms, and imaging confined to the lumbar vertebrae may not demonstrate the level of spinal cord compression.
"Skip lesions," which are concurrent noncontiguous spinal epidural abscess lesions, may be present, and imaging should be considered to detect these, especially in patients with delayed presentations, concurrent infection outside the spine, or a very high sedimentation rate.[16]
CT scan myelography or conventional myelography may be used if MRI is unavailable.
Lumbar puncture (LP) is relatively contraindicated in both conditions because of the risk of precipitating shifts of CNS content in the presence of a mass lesion. However, LP often is performed in the course of patient evaluation, particularly since meningitis is in the differential diagnosis. A typical cerebrospinal fluid (CSF) profile for these parameningeal infections would reveal only a few inflammatory cells with elevated protein level and decreased glucose level.
Stabilization procedures may be needed. Most efforts are directed at examination and appropriate imaging for definitive diagnosis. Do not delay antibiotic therapy for imaging procedures or other workup in toxic patients or in those patients with a high likelihood of these disorders or when meningitis remains a possibility in the differential diagnosis. For nontoxic and stable patients, antibiotic therapy is ideally guided by results of abscess aspiration or drainage.
Spinal epidural abscess
Treatment is medical and surgical, with surgery frequently necessary if signs of spinal cord compression are present.
Empiric antibiotic coverage should include an antistaphylococcal penicillin or a cephalosporin.
Empirical antibiotic therapy in most cases should provide coverage against MRSA with vancomycin.[5]
Subdural empyema
Immediate surgical evacuation of the empyema is necessary.
Some controversy exists as to whether a craniotomy flap or multiple burr holes are the superior therapy.
Antibiotic therapy against S aureus, the most common pathogen, is necessary.
If a neurosurgical procedure has recently occurred, combination therapy, as described above, is recommended.
Seizure treatment or prophylaxis may be indicated, depending on the clinical situation.
To decrease the likelihood of spinal epidural abscesses, high-risk neurosurgical procedures must be performed using strict sterile surgical techniques. Efforts to reduce injection drug use will also decrease spinal epidural abscesses from hematogenous spread.
Appropriate and early treatment of sinus and otic infections, prior to invasion into bone, will reduce the occurrence of subdural empyema.
Spinal epidural abscess: Once diagnosed, further inpatient and outpatient care will be under the direction of the neurosurgeon and/or infectious disease consultant. Generally, if signs of spinal cord compression are present, the treatment includes prompt surgical drainage with antibiotic treatment. If spinal cord compression is not present, some advocate CT-guided abscess aspiration and a prolonged antibiotic course or antibiotic medication alone. Patients must be carefully monitored, and immediate surgical decompression is recommended should neurologic dysfunction develop.
Up to 30%-41% of spinal epidural abscesses fail medical management.[17] Several factors may contribute to failure of medical management, including delayed diagnosis, anatomical location of the abscess, timing and type of antibiotic used, virulence of the causative organism, and patient age and health status, including the presence of diabetes. Factors such as age (>65 years), neurological impairment, MRSA infections, a white blood cell count of more than 12,000/µL, C-reactive protein level more than 115 mg/L, and positive blood culture results have been shown to correlate with failure of medical management.[17]
Subdural empyema: Immediate surgical evacuation is recommended as discussed above. Initiate antibiotic therapy as early as possible and continue through the postoperative period. Antibiotics and duration are at the discretion of the admitting physician.
Transfer to a facility with appropriate resources (neurosurgical and neuroimaging), if necessary. If these infections are suspected, antibiotic therapy should be initiated prior to transfer. Physician-to-physician contact is necessary to coordinate care.
Clinical Context:
A third-generation cephalosporin that has a broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms.
By binding to one or more penicillin-binding proteins, it 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 whom a penicillin G-resistant staphylococcal infection is suspected. Do not use for treatment of penicillin G-susceptible Staphylococcus.
Use parenteral therapy initially in severe infections. Very severe infections may require very high doses. Change to PO as condition improves.
Because of occasional occurrence of thrombophlebitis associated with the parenteral route, particularly in elderly patients, administer parenterally only for a short term (24-48 h) and change to PO if clinically possible.
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, binds DNA, and inhibits protein synthesis, causing cell death.
Clinical Context:
Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who can not receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora, anaerobes, or both.
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.
S aureus is a common pathogen in these conditions, although subdural empyema is often polymicrobial with streptococcal species. Methicillin-resistant S aureus (MRSA) should be suspected pending definitive results.
Recent clinical practice guidelines for treatment of MRSA have been published.[18]
Antistaphylococcal therapy should also be included in any regimen. For spinal epidural abscess, vancomycin can be used pending culture results. For subdural empyema, recommendations vary, but reasonable empiric therapy would include vancomycin, a third-generation cephalosporin, and metronidazole pending bacterial identification with drug sensitivities. Linezolid has been reported as effective in a few cases of recurrent streptococcal subdural empyema that failed to respond to conventional antibiotic therapy.[19]
Hina Z Ghory, MD, Associate Physician, Department of Emergency Medicine, Robert Wood Johnson University Hospital at Hamilton
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.
Barry J Sheridan, DO, Chief Warrior in Transition Services, Brooke Army Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Jeter (Jay) Pritchard Taylor, III, MD, Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Employed contractor - Chief Editor for Medscape.
Additional Contributors
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.
Mark S Slabinski, MD, FACEP, FAAEM, Vice President, USACS Central
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the medical review of this article by Joseph U Becker, MD.
References
Tunkel AR. Subdural empyema, epidural abscess, and suppurative intracranial thrombophlebitis. Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Disease. Elsevier Churchill Livingstone Inc; 2010. Vol 1: 1279-1287.
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