Spinal Epidural Abscess: Current Diagnostic and Management Protocols
Author: Kenneth H. Butler, DO, FACEP, Associate Director, Emergency Medicine Residency Program, Division of Emergency Medicine, Department of Surgery, University of Maryland Medical Center, Baltimore, MD.
Peer Reviewer: Andrew D. Perron, MD, Assistant Professor of Emergency Medicine, Department of Emergency Medicine, University of Virginia, Charlottesville, VA.
Back pain is one of the most common complaints among individuals who come to emergency departments. As for most emergency department presentations, the physician will initially consider life-threatening conditions (e.g., ruptured abdominal aortic aneurysm) as well as nonurgent conditions (e.g., musculoskeletal strain); unfortunately, spinal epidural abscess (SEA) is rarely included in the differential. Many patients in whom SEA should be considered have a history of narcotic abuse and are written off as coming to the emergency department to refill their narcotic prescriptions. Others are "bounce-back" patients, who were seen recently in an emergency department or an outpatient clinic for assessment of back pain and discharged with analgesics but who continued to have pain and thus have returned for medical help.
The clinician must have a high index of suspicion for SEA to make an early and accurate diagnosis and to prevent the development of permanent neurologic dysfunction. Depending on the level of spinal involvement, root pain may mimic a variety of other conditions, including classic sciatica, and therefore, the patient might be discharged home inappropriately. About half of patients with SEA are febrile during the course of the disease; in addition, patients may exhibit mild leukocytosis as well as an elevation in the erythrocyte sedimentation rate (ESR). The classic clinical presentation of SEA consists of four sequential phases: 1) spinal pain; 2) radicular pain; 3) muscular weakness, sensory loss, and sphincter dysfunction; and, finally, 4) complete paralysis. The point at which neurologic dysfunction begins is critical because, once initiated, the time from onset of weakness to complete paralysis is often less than 24 hours and may be as short as 30 minutes. This feature of SEA emphasizes the need for rapid diagnosis and emergency surgical intervention.
The cornerstone of the diagnosis of SEA lies in contemporary neuroimaging studies. Magnetic resonance imaging (MRI) with gadolinium is currently the diagnostic procedure of choice. Prompt neurosurgical consultation should be initiated as early as possible. Traditionally, the management of SEA has consisted of immediate surgery followed by antibiotic therapy. Surgical management has advantages, most importantly the ability to decompress compromised neural tissues, thereby preventing further neurologic deterioration. In certain patients who are neurologically intact and for whom the surgical morbidity rate is unacceptably high, conservative medical management may be appropriate. An acute epidural abscess should be suspected in any patients with back pain and fever, particularly in those who have abused drugs intravenously.
— The Editor
Introduction
Epidural abscess of the spinal column is a rare but potentially devastating disease. When it is recognized early and treated appropriately, the outcome can be excellent. However, because this disease process and its associated illnesses frequently advance rapidly, the mortality rate is as high as 20%, even in modern series.1-3 MRI aids greatly in the diagnostic process and should be obtained, if available, as soon as epidural abscess is suspected. Surgical therapy is preferable in the majority of cases, and as newer surgical techniques and approaches are developed, the indications for medical therapy have become narrower.4-9
Abscesses in the spinal subdural space or in the spinal cord proper are even more unusual but can also lead to complete and irreversible loss of neurologic function if not diagnosed and treated rapidly.
An acute epidural abscess should be suspected in patients with back pain and fever, particularly in those with underlying risk factors.8,10
Epidemiology
A bacterial infection in the epidural space can lead to the formation of a pyogenic SEA, resulting in the accumulation of purulent fluid or infected granulation tissue. Although now well recognized as a distinct clinical entity of growing neurosurgical significance, not so long ago SEA was regarded as a relatively rare condition. The incidence of SEA has been estimated at 0.2 to 1.2 cases per 10,000 hospital admissions per year, but more recent series have documented an increasing incidence during the past 10 years.9,11-13 A number of reasons for this increase can be cited, including an aging population, increased intravenous drug abuse, and an increase in the use of spinal instrumentation and epidural anesthesia. Finally, one cannot exclude the possibility that contemporary imaging procedures have enhanced our ability to detect this disorder.
Blunt trauma contributes to the formation of SEA in 17-30% of cases. The thoracic spine is reportedly involved in 31-63% of cases, the lumbar spine in 21-44%, and the cervical spine in 14-26%. Older studies found that the male-to-female ratio for this disease was about 1; more recent data indicate that men are more likely to be affected.11,13,14
Pathophysiology
The mechanism by which neurologic deficit occurs in patients with SEA has been attributed to a variety of factors, including mechanical compression of the neural elements; thrombosis of major arteries and/or veins supplying and draining the cord, respectively; impairment of the intrinsic microcirculation of the cord; and infectious vasculitis. Since SEA is a space-occupying lesion, mechanical compression usually contributes to the observed deficit.
The spinal epidural space is the area surrounding the thecal sac and separating the dura from its bony encasement. (See Figure 1.) It is not a uniform space.12 Instead, it is a metameric segmented structure in which some areas contain loose, areolar tissue, fat, and numerous veins (see Figure 2) and, in others, the dura is in direct contact with bone or ligament (thus creating only a "potential space"). In addition, individual metamers are separated, preventing free communication between the anterior and posterior epidural space. This anatomic arrangement may explain why the majority of epidural abscesses are caused by hematogenous spread and are located posteriorly. In general, the infection does not involve the anterior epidural space or circumferentially surround the thecal sac. In contrast, cases associated with discitis or vertebral osteomyelitis typically involve the anterior epidural space and, possibly because these cases commonly occur after surgery, the abscess may be circumferential because of the disruption of the normal anatomic septations. The metameric segmentation of the epidural space may also limit the longitudinal spread of the pyogenic process. In most cases, the extent of the abscess is usually limited to an average of three to four vertebral segments.2,6,9
The spinal epidural space is limited to the dorsal aspect of the spinal canal; ventrally, the dura is tightly adherent to the posterior aspect of the vertebral bodies and their ligaments from the first cervical through the second sacral vertebra. It is only caudal to S2 that the epidural space becomes circumferential, surrounding the dura on all sides.
An important anatomic feature that affects the distribution of SEA is the regional variation in the size of the epidural space. In the cervical spine, the epidural space is more a potential than an actual space. The epidural compartment becomes more apparent at the cervicothoracic junction and becomes wider in a rostral-to-caudal direction. The space then tapers between approximately T11 and L2, caudal to which the epidural space attains its greatest depth. These factors account for the rostral-caudal distribution of SEA, as well as its preference for the dorsal epidural space.15 (See Figure 3.)
The precise pathophysiologic cause of the neurologic impairment is not known. Many patients suffer rapid and irreversible deterioration, which has prompted several authors to postulate an ischemic mechanism from either arterial occlusion or venous stasis.15,16 Other studies using an experimental rabbit model of SEA demonstrated that the progressive neurologic deficits were secondary to compression.17-20 It seems likely that the cause of the neurologic deficit is multifactorial, with compression being the major component, and ischemia induced by this compression adding to spinal cord damage.
Risk Factors and Underlying Disease
Various risk factors and underlining illnesses are often identified in patients with SEA. (See Table 1.) Studies have identified factors associated with altered immune status in more than 50% of these patients, notably those with diabetes mellitus, chronic alcoholism, chronic renal failure, and underlying malignancy.9,21,22 Intravenous drug abuse, HIV infection, and acquired immunodeficiency syndrome (AIDS) have become increasingly important factors that predispose individuals to the development of SEA.3,11,23,24
| Table 1. Risk Factors for Spinal Epidural Abscess |
| • Altered immune status |
| • Diabetes mellitus |
| • Alcoholism |
| • Chronic renal failure |
| • Malignancy |
| • AIDS |
| • Intravenous drug abuse |
| • Skin or soft tissue infection |
| • Steroid dependency |
| • Antecedent trauma |
| • Acupuncture |
| • Tattooing |
Suppurative processes within the epidural space can develop in three ways: 1) by direct extension from a contiguous site of infection, such as in vertebral osteomyelitis; 2) by hematogenous seeding from a remote source of infection (intravenous drug abuse, skin infections, urinary tract infections, respiratory infections, pharyngeal or dental abscess, subacute bacterial endocarditis, long bone osteomyelitis, pulmonary abscesses); or 3) by direct contamination during invasive procedures, such as spinal surgery, administration of an epidural anesthetic, CT-guided biopsy, or lumbar puncture.2,6,25
If carefully sought, a definitive etiology for SEA can be found in more than 50% of patients. SEA most often results from hematogenous seeding of the epidural space from a metastatic source of infection, most commonly skin or soft tissue.2,9,26,27 Other relatively common sources of infection include urinary or respiratory tract infections, intra-abdominal abscesses, subacute bacterial endocarditis, and septic arthritis. SEA frequently occurs as a complication of vertebral body osteomyelitis.28 In some cases where an infectious source cannot be found, patients may have only a history of minor spinal trauma.28-30
Clinical Presentation
Back pain and fever are the most common symptoms and signs of spinal epidural abscesses. SEA has been described as a "painful, febrile, spinal syndrome," which remains the best summation of the clinical presentation of this disease.10
A high index of suspicion remains necessary to diagnose SEA and to prevent the development of permanent neurologic dysfunction. In patients with chronic back pain or narcotic-seeking behavior, this is most difficult.30 Caution is warranted when evaluating a patient who previously visited an emergency department or an outpatient clinic complaining of back pain and was discharged on analgesics, only to return with persistent or worsening symptoms (the "bounce-back" patient).8
One of the most important aspects of SEA is the variable clinical presentation. Early findings can be subtle, and underlying illness may dominate the clinical picture. The variability in the clinical presentation of SEA is related to a number of factors, including the region of the spine involved, whether the infection is due to hematogenous seeding or to extension of a local process, the immune status of the patient, and the virulence of the infectious agent. From a diagnostic perspective, the triad of pain, fever, and progressive neurological deficits is seen in a minority of patients; consequently, the diagnosis may be delayed in a large percentage of patients. Finally, about 10% of patients with SEA present with encephalopathy.
The classic presentation of SEA consists of four phases that evolve in the following sequence: 1) spinal pain; 2) radicular pain; 3) muscular weakness, sensory loss, and sphincter dysfunction; and finally, 4) complete paralysis.26,31 (See Table 2.) The rapidity of progression from one stage to another depends on the factors outlined above. With spontaneous abscess resulting from hematogenous seeding, progression from spinal to radicular pain and neurologic dysfunction tends to occur more rapidly, and systemic manifestations are often a prominent part of the clinical picture. In cases of SEA that result from local extension of adjacent vertebral osteomyelitis, the evolution tends to be slower, at times progressing over weeks or even months until the infection becomes clinically apparent.
| Table 2. Signs and Symptoms of Spinal Epidural Abscess |
| Stage I |
| • Fever |
| • Back pain |
| • Malaise |
| Stage II |
| • Radiculopathy |
| • Paresthesias |
| Stage III |
| • Motor deficits |
| • Sensory deficits |
| • Bladder dysfunction |
| • Bowel dysfunction |
| Stage IV |
| • Paralysis |
Spinal pain is almost universally present with SEA and in most patients is associated with localized spinal tenderness to palpation or percussion. Once spinal pain occurs, it becomes progressively more severe and intractable.6,8 Most patients also develop radicular pain, which usually follows the onset of spinal pain.32 Depending on the level of spinal involvement, root pain may mimic a variety of other conditions, including classic sciatica, an acute abdominal process, or herpes zoster.9 Two-thirds to three-fourths of patients will be febrile, with temperature in excess of 38°C at some point during the course of the illness. Headache and nucal rigidity may occur, reflecting a parameningeal reaction or, in some cases, frank meningitis.33-35
Unfortunately, SEA is all too frequently diagnosed after the onset of neurologic dysfunction, which occurs in as many as 90% of patients.2,3 Most patients with SEA have some degree of motor weakness, which may be unilateral or bilateral or involve a single extremity. Sensory loss is usually incomplete and may occur in a radicular pattern or present at a discrete sensory level. The point at which neurologic dysfunction begins is especially critical because, once initiated, the time from onset of weakness to complete paralysis is often less than 24 hours and can occur in as little as 30 minutes. This deterioration is a feature of SEA that emphasizes the need for rapid diagnosis and emergency surgical intervention.36 Continued and timely neurologic examinations should performed in the emergency department and the results documented, because the neurologic status of these patients can change quickly.
Pediatric Considerations
The characteristic features of SEA may not be prominent in children. The clinical picture may be dominated by nonspecific findings such as fever, malaise, irritability, headache, and vomiting. Reluctance of the child to lie prone, irritability with movement, and rigidity of the spine may be the only clues to the diagnosis prior to the onset of neurologic deficit. The classic four-stage sequence described in Table 2 may not occur. Back pain may be absent.26
Differential Diagnosis
The differential diagnosis in a patient with suspected SEA includes common conditions that share the clinical features of epidural infection. Acute transverse myelitis, which is more common than SEA, should be part of the differential diagnosis in patients with back pain, fever, and progressive neurologic deficit. The two can be differentiated on myelography, which is often normal in transverse myelitis but classically shows a subtotal to complete block in SEA. The routine use of MRI may obviate the need for invasive studies. Metastatic neoplasms of the spine (lymphoma in particular), as well as spontaneous intraspinal hematomas, may mimic the presentation of SEA.23,37-43
Diagnostic Studies
Laboratory Findings. Routine laboratory studies in patients with SEA are nonspecific; in fact, no one laboratory study is pathognomonic of this condition. Most patients have a mild leukocytosis (10,000 to 13,000/mm3) and an elevated ESR, usually in excess of 30 mm/hr.44 Blood cultures may isolate an organism in more than half of patients and should be obtained routinely.8 Lumbar puncture is generally discouraged in patients with SEA, especially those with dorsal lumbar abscesses, because of the risk of introducing infection into the cerebrospinal fluid (CSF). Moreover, unless there are clinical features suggesting concomitant meningitis, CSF analysis yields little information. If a lumbar puncture is performed, the CSF usually shows evidence of a parameningeal process manifested by pleocytosis, elevated protein levels, and normal glucose concentration. The CSF can also be entirely normal or reveal frank pus, consistent with accompanying bacterial meningitis.
Plain Films. Bony changes on plain film may be evident in only 33-65% of all patients.21,22 Up to 70% of patients with chronic epidural abscess may be expected to show such changes, but only about 10% of acute cases have positive findings on plain films. It takes time for bone erosion, sclerosis, vertebral collapse, disc space changes, and paravertebral infection to become radiologically evident.8
The findings are usually nonspecific, showing degenerative changes or signs of discitis or osteomyelitis, such as disc-space narrowing or vertebral end-plate destruction. (See Figure 4.) If osteomyelitis is not yet apparent on plain film, nuclear bone scans may confirm the diagnosis.
Myelography. Myelography is a highly reliable method for diagnosing SEA. Myelography can diagnose or confirm infection in virtually all cases, but unless contrast is injected above the collection, the rostral extent of involvement may not be delineated. In performing myelography for suspected SEA, one should enter the epidural space with great caution to avoid introducing bacteria into the subarachnoid space.
Myelography was the diagnostic study of choice before MRI, but now, with the almost universal availability of MRI and the inherent risk of inserting a needle in the thecal sac in the face of infection, myelography is rarely indicated.45,46 Myelography should be performed if SEA is suspected but not found by newer imaging techniques.
Computer-Assisted Tomography. Computed tomography (CT) alone has about an even chance of diagnosing SEA. If it is combined with intravenous contrast, the rate of successful diagnosis approaches 100%. CT reveals an extra-axial mass compressing adjacent structures. It may better define destructive bony changes and may be more sensitive in detecting subtle osseous changes not apparent on plain film.47
Magnetic Resonance Imaging. Recently, MRI has become an increasingly important modality in the evaluation of patients with suspected SEA. In many emergency departments, it has supplemented myelography as the procedure of choice.45,48,49 MRI has a sensitivity equivalent to that of CT-myelography. Additionally, MRI can exclude many entities included in the differential diagnosis, such as herniated disc, neoplasm, spinal hematoma, and transverse myelitis.50 MRI also provides greater anatomic detail in demonstrating the rostral-caudal extent of the lesion, spinal cord compression, and the status of the spinal cord. The degree of thecal sac compression seen on MRI examination tends to correlate well with the severity of neurologic deficit detected on physical examination. (See Figure 5.) Patients who use drugs intravenously tend to have abscesses in locations that correlate with their sites of injection.
MRI may not allow diagnosis of SEA in the presence of meningitis or encephalopathy if excessive motion artifact is present.50
Bacteriology
Staphylococcus aureus is the most common organism isolated from patients harboring SEA and may account for more than 90% of cases.2,6,9 S. aureus is implicated, in most cases, secondary to skin and soft tissue infections, in cases related to intravenous drug abuse, and in patients with infections following spinal surgery. It is also the most common organism encountered in children. Other gram-positive cocci such as Staphylococcus epidermidis, Streptococcus pneumoniae, and Streptococcus viridans account for an additional 10% of cases. In recent years, gram-negative aerobes (Escherichia coli, Pseudomonas aeruginosa, Citrobacter, and Klebsiella pneumoniae) have been responsible for a larger percentage of cases. Mycobacterium tuberculosis continues to play an important role in this disease, particularly in economically depressed countries and large urban areas, where tuberculosis accounts for nearly one-fourth of cases.51 Fungal infections caused by Echinococcus, Cryptococcus, Brucella, Blastomyces, and Aspergillus organisms also have been reported.
Management
Once the diagnosis of SEA is made, management depends on the condition of the patient. Surgical decompression with specific antibiotic therapy remains the mainstay of treatment. Patients who present in good clinical condition with no neurological compromise or findings, as well as those who are too ill for surgical intervention, may be considered candidates for medical therapy alone. This decision should be made in consultation with a spinal surgeon.
Emergency Department Management. Patients who present with a high clinical probability of SEA require emergent neurosurgical consultation and should not be subjected to any unnecessary delays in the emergency department before surgery. Intravenous fluid resuscitation, if required, should be performed. Patients should be made NPO and have appropriate OR laboratory tests (complete blood count, electrolytes, and coagulation factors), electrocardiogram, and chest film. Specimens for blood cultures should be drawn prior to administration of any intravenous antibiotic. Cultures should be done for aerobic, anaerobic, and fungal organisms and tuberculosis.
Antibiotics should be initiated in the emergency department in patients who appear septic or show neurologic deterioration. If presurgical antibiotic administration is deemed prudent, broad-spectrum antibiotics, including those for methicillin-resistant organisms, should be used. Antibiotic agents chosen must be active against Staphylococcus aureus because this is the most common organism isolated. If surgery is scheduled within a few hours and the patient with suspected SEA has not been started on antibiotics, is not septic, and has good neurologic status, many neurosurgeons prefer not to start antibiotics until cultures have been taken at surgery. This approach maximizes the probability of obtaining organism growth so the most specific antimicrobial therapy can be given. Steroids may adversely affect outcome and are not indicated.
Surgery
Decompressive laminectomy and drainage of purulent material or debridement of granulation tissue is the best method of preventing neurologic deficits and, if performed quickly after the onset of deficits, may allow full recovery. This is followed by antibiotic therapy of variable duration, usually a four-week course of intravenous antibiotics, which may be extended to eight weeks if vertebral osteomyelitis is present.
Pyogenic epidural abscesses should be considered a neurosurgical emergency because patients, even those receiving appropriate antibiotics, may deteriorate neurologically, rapidly, and unpredictably. The effects of cord compression, especially in the cervical region, can be devastating. If the infection is in the cervical or thoracic area, decompression should be undertaken expeditiously. If the epidural infection involves the lumbar region adjacent to the cauda equina, the surgeon has a little more leeway regarding surgical timing.
Medical Management
Although SEA has traditionally been considered a surgical disease, some authors have advocated conservative treatment, particularly in patients who are neurologically intact and in selected patients in whom the surgical morbidity is unacceptably high.47,52-54 (See Table 3.) This approach is predicated on early identification of the organism so that specific antibiotic therapy can be initiated. In selected patients who are neurologically intact, this has been a reasonable approach, particularly applicable in patients with abscesses in the lumbar region, where the epidural space is relatively large and the spinal cord terminates. However, these patients require vigilant monitoring, as neurologic deterioration is not uncommon despite appropriate antibiotic therapy.
| Table 3. Proposed Criteria for Exclusive Medical Treatment in Spinal Epidural Abscess |
| • Poor surgical candidates because of severe, concomitant medical problems |
| • Patients in which the abscess involves a considerable length of the spinal canal and who have an epiduritis from the cervical to the lumbar level |
| • Patients not suffering from severe loss of spinal cord or cauda equina function |
| • Patients with complete paralysis for more than three days |
| Reproduced with permission from: Leys D, Lesion F, Viaud C, et al. Decreased morbidity from acute bacterial spinal epidural abscesses using computed tomography and nonsurgical treatment in selected patients. Ann Neurol 1985;17:350-355. |
Morbidity and Mortality
The functional outcome of the SEA depends greatly on timely diagnosis and rapid institution of therapy. It is therefore imperative that the diagnosis is confirmed quickly and that appropriate consultations be obtained by the emergency physician.
The ability to diagnose SEA in a timely fashion, coupled with improvements in antibiotics and surgical technique, has resulted in a steady decline in mortality rates. Despite these advances, the mortality rate among patients with SEA remains unacceptably high. Additionally, 20-30% of patients who survive will be left with significant neurologic impairment resulting in long-term disability.55 The outcome in patients who survive primarily depends on the degree and duration of neurologic impairment at the time of diagnosis. Not surprisingly, patients with severe neurologic deficit have a much poorer prognosis than do patients who are neurologically intact. The single most important factor in reducing morbidity is early diagnosis and institution of treatment prior to the onset or progression of neurologic deficit.
Summary
Once thought of as a rare disease entity, and usually a postoperative or surgical complication, epidural abscesses have been increasing in occurrence during the past decade. This increase is related to several factors: widespread intravenous drug abuse (even among adolescents); routine use of epidural anesthesia; and the use of the emergency department as the primary care provider by uninsured, debilitated, alcoholic, and/or immunosuppressed individuals, particularly those with HIV infection or AIDS. Routine use and increasing availability of MRI has also brought this neurosurgical emergency to light. Infections may reach the spinal epidural space by direct extension from an inflammatory process in adjacent tissues, by metastasis, or by perforating wounds. Skin and soft tissue infections (e.g., "skin-popping ulcers" from substance abuse or abscesses), urinary tract infections, dental infections, chronic pulmonary disease, decubitus ulcers, acupuncture, and tattooing have all been associated with SEA.56,57 The usual focus is an adjacent vertebral osteomyelitis with direct extension into the epidural space. Surgical wounds, retroperitoneal abscesses, and lumbar punctures represent other potential causes. As these risk factors echo so many of our emergency department patients, a high index of suspicion for SEA must be maintained when treating patients with back pain and fever.
Staphylococcus aureus remains the most common etiologic agent in adults as well as children and is usually related to an underlying skin or soft tissue infection. Fungal organisms as well as Mycobacterium tuberculosis are common in urban areas.
The differential diagnosis of back pain presents a clinical challenge and may be difficult and exhausting in a patient with drug-seeking behavior. The emergency physician should be weary of "red flags" in the patient’s history as well as in the physical examination, such as repeated visits for the same complaint, risky social behaviors and associated risk factors, underlying fever in the course of their disease, or a change in neurologic examination results from previous encounters. Since we so often associate a delay in time as a critical factor for an organ system’s salvageability in a surgical emergency (e.g., testicular torsion), patients with SEA must be thought of in the same context. The time between emergence of neurologic dysfunction and complete paralysis may be less than one hour.
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Physician CME Questions
65. Spinal epidural abscess is usually diagnosed:
A. early in its clinical course.
B. after the onset of neurologic deficit.
C. on routine MRI.
D. in children with back pain.
66. Which of the following statements is true regarding laboratory studies for spinal epidural abscess?
A. Lumbar puncture is recommended for all patients.
B. Blood cultures are rarely positive.
C. No one laboratory study is pathognomonic for spinal epidural abscess.
D. Neutropenia is usually present.
67. The epidural space:
A. contains numerous veins, loose areolar tissue, and fat.
B. is in free communication between the anterior and posterior epidural space.
C. remains constant in size throughout the length of the spinal column.
D. is structured so that most abscesses involve only one vertebral segment.
68. Plain films of the spine:
A. are usually positive in acute cases of spinal epidural abscess.
B. reveal specific degenerative changes caused by spinal epidural abscess.
C. show rapid bone erosion, sclerosis, and vertebral collapse in patients with spinal epidural abscess.
D. may not indicate osteomyelitis; in this case, a nuclear bone scan is suggested.
69. The most common isolated organism in children with spinal epidural abscess is:
A. Staphylococcus aureus.
B. Staphylococcus epidermidis.
C. Klebsiella pneumoniae.
D. Echinococcus.
70. In the emergency department management of spinal epidural abscess:
A. high-dose steroids should be infused rapidly.
B. intravenous antibiotics should be given to all patients with suspected spinal epidural abscess.
C. blood cultures for aerobic, anaerobic, tuberculosis, and fungal organisms should be drawn.
D. Multiple neurologic examinations over time should be performed prior to consulting neurosurgery.
71. In spinal imaging for epidural abscess:
A. myelography is the noninvasive study of choice.
B. computer-assisted tomography poorly defines subtle osseous changes.
C. MRI may exclude the diagnosis of transverse myelitis.
D. the level of thecal sac compression on MRI correlates poorly with the neurologic deficit on physical examination.
72. Spinal epidural abscess:
A. rarely produces the findings of classic sciatica on physical examination.
B. may occur in individuals with a history of only minor spinal trauma.
C. is never associated with penetrating trauma.
D. is not related to lumbar puncture or epidural anesthesia.
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