16 Epidural and Soft-Tissue Infections Abstract Infections of the spinal column are uncommon. These infections have variable clinical presentation and represent a diagnostic and therapeutic challenge. Spinal column infections often originate in the disc space and are often labeled vertebral osteomyelitis, spondylitis, discitis, and spondylodiscitis. Infections can extend to adjacent paravertebral soft tissues to form epidural or other soft-tissue abscesses. Epidural abscess may be present with or without associated disc space infection. Spinal epidural abscess (SEA) and disc space infection are often the result of hematogenous seeding of a distant focus of infection or a transient bacteremia. Uncommonly, direct and iatrogenic inoculation of the fragile epidural space may also cause an SEA. Abscesses, secondary to vertebral osteomyelitis, are usually anterior to the spine. SEA is more common in the thoracic spine than in the lumbar and cervical regions. Diabetes mellitus and intravenous drug abuse are the two most common risk factors for SEAs. Common presenting symptoms include back pain, fever, or spinal tenderness. Magnetic resonance imaging can establish a radiological diagnosis. Surgical intervention may be needed in selected patients to decompress the neural elements and to establish a microbiological diagnosis. Keywords: spine infection, epidural abscess, spine surgery, soft-tissue infection, thoracic spine, vertebral osteomyelitis, spondylodiscitis, spondylitis Clinical Pearls • Spinal epidural abscess (SEA) is a challenging pathology with an incidence of 0.2 to 2 cases per 10,000 hospital admissions. • SEA may involve a hematogenous pathogenesis, that is, spread through blood vessels from other sites in the body, a nonhematogenous pathogenesis via a contaminated needle or a contiguous site including the disc space, or an iatrogenic pathogenesis, for instance from contamination during spinal surgery. • The most important risk factors for an SEA include intravenous drug abuse and diabetes. • The most common region affected is the thoracic region. On presentation, there is severe tenderness on palpation and percussion of the affected spinal segment, while gibbus deformity, neurological findings of dermatomal sensory and/or motor loss, as well as bowel and bladder dysfunction are indicative of a spinal cord injury and are seen in advanced cases with extensive bony erosion. • Magnetic resonance imaging is considered as the gold standard for establishing the diagnosis. For microbiology, depending on the situation, a biopsy may be required for culture in the absence of bloodstream infection. • Empiric antibiotic therapy should be considered once an SEA is suspected. Prolonged antibiotic therapy is the mainstay of treatment while surgical intervention may be needed in selected patients to decompress the neural elements and to establish a microbiological diagnosis. • Owing to modern therapeutic mechanisms, the mortality rate associated with SEA has reduced to 5 to 20%, but neurological sequelae still remain a challenge. Infections of the spinal column encompass a wide spectrum of pathologies including infection of the vertebral body, discitis, and epidural abscess where the epidural space, paraspinal soft tissue, or the spinal canal become infected and form a walled-off purulent mass.1,2 Recent advances in the diagnostic imaging, including magnetic resonance imaging (MRI), has prompted a departure from the use of anatomically specific nomenclature. MRI studies have shown that most infections of the spinal column involve more than one, of the tissue planes in this area.3 This chapter will primarily focus on spinal epidural abscesses (SEAs) while later chapters will discuss the pathogenesis and microbiological details of osteomyelitis. Evidence of spinal infections dates back to prehistoric era circa 3400 BC as per the discovery of tuberculous spondylitis (or Pott’s disease) in Egyptian mummies.4 Recent technological advances in imaging techniques have made the diagnosis easier and timely. Modern proliferation and complexity of spine instrumentation along with increased life expectancy have led to an increase in incidence of SEA. Spine infections account for 2 to 7% of all musculoskeletal infections.2,5,6 Reported incidence rates of vertebral osteomyelitis vary by study and have ranged between 0.2 and 6 cases per 100,000.7,8,9 The incidence is higher in older patients and patients that are younger than 20 years of age.10,11,12 SEA incidence rates are reported to be between 0.2 and 2 cases per 10,000 hospital admissions.13,14,15 The increased incidence in one study of 2.7 per 10,000 admissions has been attributed to intravenous (IV) drug abuse and AIDS.16,17 SEA predominantly affects patients aged between 30 and 70 years of age.18 There is also a reported male preponderance with male to female ratios ranging from 2:1 to 5:1.10,19 Other risk factors include indwelling intravascular devices, end-stage renal disease, immunosuppressive state, transplant recipients, chemotherapy, chronic indwelling catheters, splenectomy, genitourinary instrumentation, and liver cirrhosis.20 The details of causative organisms in osteomyelitis will be discussed in a later chapter. The origin of infection is typically classified as (1) hematogenous or (2) nonhematogenous. Nonhematogenous infection can be the result of surgery or direct inoculation. Hematogenous seeding is considered the most common mechanism by which the disc or epidural space often becomes infected. Pathogenic microorganisms often seed the spine via the arterial route or less commonly the vertebral venous plexus.21 The nidus of infection forms in the metaphyseal artery, a branch of the periosteal artery. This infected thrombus leads to avascular necrosis of a portion of the metaphysis. Subsequently, the infection travels through the anastomotic arteries to reach the opposite ends of the vertebra causing vertebral body infection. The ischemia also causes aseptic necrosis of the disc space causing gradual loss of disc height and pus formation. This purulence leads to a septic thrombosis of draining veins, which serve as a conduit for infection that reach the epidural venous plexus resulting in epidural abscess.1,2,3 In addition to the arterial route, seeding of disc space may travel in a transvenous fashion, often involving the valveless veins of Batson’s plexus.22 This explains why infections involving the left kidney parenchyma increase the risk of spine infection given that the left kidney communicates directly with the plexus. Spine infection can also originate from other pelvic organs such as the bladder, bowel, and female genital tract.1,2 Pathogenic microorganisms may also travel via epidural veins directly resulting in epidural abscess involving multiple segments without involvement of the bony vertebral body or disc space.1,3 Nonhematogenous inoculation of disc or epidural space may result from the use of contaminated needles or other surgical instruments during interventional or diagnostic procedures such as discography, chemonucleolysis,23,24 epidural anesthesia, or surgery.3 In contrast to hematogenous spread, the infection originating in the disc space following direct inoculation spreads into the adjacent vertebral body marrow through the endplates.2,22 Up to one-third of spinal infection cases are considered iatrogenic, resulting from contamination during spine surgery.25,26 In spite of modern advances in surgical prophylaxis, postoperative surgical site infections have continued to jeopardize selected patient outcomes after spinal surgery.27 The risk of postoperative spine infection is increased with extensive instrumentation.3 Recent reports on the rate of surgical site infection after spine surgery have ranged from 0.7 to 16%.28,29,30,31,32,33 Risk factors for postoperative infections are either nonmodifiable or modifiable. Nonmodifiable factors include patient age (> 70), the American Society of Anesthesiologists (ASA) score, diabetes mellitus (DM), cardiovascular disease, obesity, smoking, malignancy, steroid use, previous lumbar surgery, malnutrition, chronic obstructive pulmonary disease, and immunological competency.34,35,36,37 Modifiable factors include Staphylococcus aureus nasal screen and decolonization, duration of surgery, blood loss, transfusions, use of instrumentation, multiple staged interventions, amount of levels fused, and prolonged hospital stay.35,36,37,38,39,40 In addition to risk factors discussed above for spondylitis, certain factors may predispose patients to develop SEA. A meta-analysis of 915 patients found that DM and IV drug abuse are among the most common risk factors and found in 15 and 8.5%, respectively.18 Patients with DM have reduced chemotaxis, phagocytosis, and bactericidal activity of neutrophilic granulocytes which accentuate the progression to abscess. IV drug abuse is associated with an increased risk of transient bacteremia that may lead to the development of SEA as well as compromised cellular and humoral immunity.41 Akin to vertebral osteomyelitis, the most mechanism of seeding of the epidural space occurs via hematogenous spread. Carbuncles, furuncles, and skin abscesses are often found to be the primary source of SEA. Cutaneous infections were found to be present in 33 to 44% cases of SEA.18,42,43,44 Other sites include the respiratory tract (otitis media, sinusitis, or pneumonia45), the genitourinary tract, visceral organs, oral cavity,46 and endocarditis.14 Direct extension or lymphatic spread to the epidural space from a contiguous infection, osteomyelitis, or spondylodiscitis may also occur. In one series, osteomyelitis was present in up to two-thirds of patients with SEA.14 Inoculation of epidural space may also occur with a psoas or retropharyngeal abscess, decubitus ulcer, pharyngeal infections, mediastinitis, pyelonephritis with perinephric abscess, and dermal sinus. Traumatic injuries and spinal hematoma associated with such injuries form another important group of risk factors with frequencies of such cases ranging from 10 to 34.7%.26,47,48 SEA can also be caused by iatrogenic inoculation during an invasive procedure of the spine or the surrounding vasculature.46 Patients with evidence of any perioperative infections are at a greater risk of developing a subsequent SEA.14 Among open procedures, lumbar discectomy has the highest risk of SEA (0.67%).49 Interventional, diagnostic, and therapeutic closed procedures may also be associated with an increased risk of SEA. Epidural catheterization, often employed for pain control or local anesthesia, may provide a portal of entry of skin flora such as Staphylococcus epidermidis or S. aureus in at-risk patients. The duration of catheterization is the most important risk factor. For a duration of less than 2 days, the incidence rate is 0.2 per 1,000 catheter-days3,50,51 with longer duration of use, the rate increases to 0.77 per 1,000 catheter-days.15,52,53,54 Overall, only 3.9% of all SEA is associated with anesthetic interventions occurring at a rate of 1 in 100,000 for epidural interventions.18 The clinical presentation is dependent on the extent, site, and level of the SEA. A history of recent infection should be delineated. Heusner in 1948 described stages of SEA.55 Earliest symptoms are back pain and fever often accompanied by local tenderness. The next stage is signs of spinal irritation which may be elucidated by straight leg raise (SLR) test, Kernig’s (painful extension of the knee subsequent to knee and hip flexion) and Lhermitte’s signs (burst of shock-like pain extending caudally from the neck), Brudzinski’s reflex neck stiffness, and even extremity symptoms such as radiating pain depending on the craniocaudal level of abscess. During the third stage, patients will exhibit neurological dysfunction such as fecal or urinary incontinence, muscle weakness, and/or sensory deficits. The fourth and final stage is complete paralysis secondary to severe muscle weakness. The classic triad of back pain, fever, and neurological deficit is present in 13% of cases.56,57,58 Atypical symptoms such as abdominal pain, headache, bowel dysfunction, and sudden paralysis have also been reported.56,59,60 SEA leading to neurological disability is more common in cervical and thoracic spine than in the lumbar region.3 In one meta-analysis of 915 number of SEAs found that the thoracic region affected (50%), followed by lumbar (34%) and cervical (19%).18 Most SEAs are located posterior to the spinal cord (80 vs. 20%).61 However, it’s worth noting that SEA originating from an adjacent osteomyelitis is often confined to the anterior portion of the spinal cord.62 Circumferential extension of the abscess around the thecal sac is uncommon ( On physical examination, patient exhibits severe tenderness on palpation and percussion of the affected spinal segment. Gibbus deformity is seen in advanced cases with extensive bony erosion. Neurological findings of dermatomal sensory and/or motor loss as well as bowel and bladder dysfunction are indicative of a spinal cord injury. Though rare, prolonged infection may cause chronic compression of the spinal cord, manifesting as long tract signs and symptoms.3 Neurological signs associated with SEA are due to mechanical compression or microvascular damage.63,64,65,66,67 In one animal model of SEA, investigators found no evidence of gross compression or histopathological thrombosis of blood vessels suggesting that mechanical compression of nerve roots is the main cause of neurological symptoms.63 However, it is widely believed that the neurological compromise is often the result of both.14 The most important step in establishing a diagnosis of SEA is having a high level of clinical suspicion based on clinical or laboratory studies.68 It’s imperative to consider SEA in the differential of back pain and irritative neurological symptoms. A combination of back pain, neurological symptoms, and elevated systemic inflammatory markers should raise the clinical suspicion of SEA. This should promptly lead providers to proceed with confirmatory radiological or microbiological testing. Any delay in establishing the diagnosis of SEA may lead to irreversible neurological sequelae including paralysis.18 Spine MRI with and without gadolinium is considered the radiological test of choice for establishing the diagnosis of SEA. Elevation of systemic inflammation markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) is present in a majority of the patients with SEA. Patients with recalcitrant back, signs of systemic infection, or progressive neurological symptoms should have ESR and CRP testing as part of their work-up.69 Leukocytosis is uncommon in patients with SEA. Radiological investigations often follow clinical suspicion based on clinical presentation and laboratory testing. Spine roentgenograms are often obtained and may be able to rule out fracture, bone loss, and provide gross assessment of spinal stability.62,70,71,72,73,74,75,76 Specific findings on radiographs in protracted SEA cases may show loss of disc height, trabecular erosion of bone, prevertebral and paravertebral soft-tissue volume, endplate destruction, vertebral collapse with loss of lordosis, and the development of gibbus or kyphotic deformity at the level of lesion.3 Computerized tomography (CT) of the spine offers a better sensitivity compared to radiographs and provides better visualization and extent of prevertebral and paravertebral soft-tissue inflammation as stranding and loss of normal tissue planes.3 Distinguishing spinal cord from epidural space can sometimes be challenging on CT.76 CT is often performed when MRI is contraindicated such as presence of implantable cardiac devices, ferromagnetic aneurysm clips, or shrapnels.69 The advantage of CT over MRI in the evaluation of SEA is that it will be able to better delineate concomitant spondylodiscitis, with sclerotic endplate changes. CT is also performed prior to a planned spinal instrumentation in order to evaluate the quality of existing boney structures as well as the extent of bone loss ( Myelography used to be the investigation of choice until the late 1990s.18 It delineates the extent of epidural abscess accurately as the contrast medium can be visualized surrounding and outlining the abscess above and below it.62,71,72,76,77,78 Myelography combined with CT may help better visualize the paraspinal space.14,72,76 Some older publications believed the combination to be the only definitive source of diagnosis.79 MRI is considered the gold standard for the diagnosis of epidural abscess with greater than 90% sensitivity and specificity.69,80 Imaging should be obtained both with and without contrast (
16.1 Introduction
16.2 Epidemiology
16.3 Pathogenesis
16.3.1 Hematogenous Spread
16.3.2 Nonhematogenous Spread/Extension from an Infected Contiguous Infection
16.3.3 Iatrogenic Inoculations
16.4 Spinal Epidural Abscess
16.4.1 Risk Factors
16.4.2 Source Site of Infection
Hematogenous Spread
Direct Extension from a Contiguous Site
Iatrogenic Inoculation
16.4.3 Clinical Presentation
Fig. 16.1a, b).
16.4.4 Pathogenesis of Neurological Dysfunction
16.4.5 Diagnosis
16.4.6 Laboratory Investigation
16.4.7 Radiological Investigation
Fig. 16.2b).
Fig. 16.3a–c). T1 image is helpful in detecting a hypointense signal in the vertebral body, specifically at the endplates signifying the loss of normal hyperintense fat signal. The disc height can be visualized to be markedly reduced on T1. T2 helps delineate soft-tissue edema in disc space as well as bone and paravertebral soft tissue3 (
Fig. 16.4a, b). Contrast-enhanced T1 provides the best visualization of vertebral endplates, vertebral body, prevertebral and paravertebral soft tissue, and epidural space. There can also be ring-like enhancement or linear dural enhancement which is considered indications for surgery by some authors.81,82 Some authors have recommended scanning the whole spine to exclude noncontiguous SEA when symptoms suggestive of abscess have persisted for at least a week, when there is presence of coexisting infection outside the spinal region, and when ESR is greater than 95 mm/h.83
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