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NARRATIVE REVIEW

Vertebral Osteomyelitis and Spinal Epidural Abscess An Evidence-based Review Barrett S. Boody, MD, Tyler J. Jenkins, MD, Joseph Maslak, MD, Wellington K. Hsu, MD, and Alpesh A. Patel, MD

Abstract: Spinal infections have historically been associated with significant morbidity and mortality. Current treatment protocols have improved patient outcomes through prompt and accurate infection identification, medical treatment, and surgical interventions. Medical and surgical management, however, remains controversial because of a paucity of high-level evidence to guide decision making. Despite this, an awareness of presenting symptoms, pertinent risk factors, and common imaging findings are critical for treating spine infections. The purpose of this article is to review the recent literature and present the latest evidence-based recommendations for the most commonly encountered primary spinal infections: vertebral osteomyelitis and epidural abscess. Key Words: spinal infections, vertebral osteomyelitis, spondylodiscitis, spinal epidural abscess (J Spinal Disord Tech 2015;28:E316–E327)

VERTEBRAL OSTEOMYELITIS Vertebral osteomyelitis is one of the most common spinal infections encountered by spine surgeons. The disease is generally classified by infectious etiology: pyogenic versus granulomatous.

Pyogenic Vertebral Osteomyelitis (PVO) PVO, also known as spondylodiscitis, is caused by a bacterial infection of the vertebral bodies that can extend into the adjacent intervertebral disk spaces. The annual incidence of PVO has been estimated at 0.059 episodes per 100,000 inhabitants over the past decade, with approximately 60% male predominance and a mean age of 66 years.1 Vertebral osteomyelitis carries significant morbidity and mortality, with a median length of hospitalization of 31.5 days.2 Factors associated with an increased mortality include elevated C-reactive protein (CRP) at admission, advanced age, and a Charlson Comorbidity index of >2.2 Received for publication April 13, 2015; accepted May 16, 2015. From the Department of Orthopaedic Surgery, Northwestern Memorial Hospital, Chicago, IL. The authors declare no conflict of interest. Reprints: Barrett S. Boody, MD, Department of Orthopaedic Surgery, Northwestern Memorial Hospital, Department of Orthopaedic Surgery Academic Office, 676 N. Saint Clair, Suite 1350, Chicago, IL 60611 (e-mail: [email protected]). Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.

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The bacterial inoculation in PVO occurs through 2 main pathways: hematogenous seeding and direct inoculation. In 50% of cases, arterial or venous conduits at the intervertebral disks or endplates allow bacteria to access the vertebral column. These relative areas of slower blood flow allow the bacteria to extend from the disk to the adjacent endplate and vice versa. Direct inoculation (15%–40% of cases) is another common method for bacterial colonization of the vertebral column. This mechanism can occur after routine spine procedures such as lumbar puncture, discography, laminectomy, discectomy, or any other spinal intervention. Less commonly, bacterial inoculation occurs through local extension from adjacent areas of infection (3% of cases), including retropharyngeal abscesses or infected aortic grafts.3

Clinical Evaluation The diagnosis of PVO is frequently delayed and can take several weeks from presenting symptoms to diagnosis, averaging 30.2 days in culture-positive PVO and 72.2 days in culture-negative PVO.1,4 Prompt and accurate diagnosis is best achieved through a composite of clinical examination findings, imaging studies, and laboratory findings. Mylona et al4 systematically reviewed PVO clinical characteristics and noted that the most common complaint is back pain (86%), with 34% presenting with neurological deficits. Fevers are present in 85% of culture-positive PVO versus 32% of culture-negative PVO.1,2,4 Concomitant infections (urinary tract infection, abscesses, skin infections, pneumonia, etc.) are relatively common, and are found in 47% of culture-positive and 4% of culture-negative PVO.1 A review of past medical history including immunosuppression, diabetes mellitus, hepatic disease, malignancy, IV drug abuse, end-stage renal disease, endocarditis, and prior surgical procedures, including spine surgeries/procedures and organ transplantation, help to identify the patients at risk for PVO.5 In a study reviewing 92 PVO cases that underwent surgical treatment, a previous spinal surgery or procedure was the most commonly noted risk factor (39.1%), followed by diabetes mellitus (15.2%).6 A thorough neurologic examination compared with prior documented examinations is essential to identify new or worsening neurological deficits. Routine laboratory analysis of complete blood count, erythrocyte sedimentation rate (ESR) and CRP are helpful in the infectious workup. Blood cultures can reveal the J Spinal Disord Tech

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microbiological etiology in 58% of patients and should be obtained during febrile episodes if possible.4 Computed tomography (CT)-guided biopsy can be a useful adjunct in the diagnosis. Recent studies demonstrate a CT-guided biopsy-positive culture rate of 19%–60% in patients with suspected PVO.7–9 Antibiotics before CT biopsy can significantly affect culture yields. de Lucas et al9 identified a causative organism in 60% of patients not previously treated with antibiotics, compared with 23% of patients who had received antibiotics. Although history and physical examination are crucial to establishing a differential diagnosis, ultimately imaging with magnetic resonance imaging (MRI) and positive cultures from blood or tissue help confirm the diagnosis.5

Imaging A standard radiographic series, including weightbearing films, is obtained to evaluate for early disk space narrowing and endplate sclerosis as well as evidence of instability. Evaluation of the entire spine should be considered in PVO, as 6% of patients demonstrate continuous lesions spanning multiple levels and 3% have noncontiguous, or skip lesions.4 While x-ray abnormalities for advanced cases of PVO can be found on nearly 90% of x-rays, early findings are nonspecific and difficult to identify. Early findings (2–3 wk) commonly are unremarkable and may only reveal endplate blurring, erosion of the endplate corners, disk height loss, and paraspinal soft-tissue swelling. Vertebral body destructive changes on x-ray are seen after greater than 30% bony destruction. Late PVO can demonstrate signs of bone formation, including peripheral sclerosis, osteophytosis, and osteolytic lesions.3 Although CT scans can provide earlier identification of bony destruction, identifying bony sequestra, presence of gas within abscesses, and canal involvement, they are limited when compared with MRI in identifying the extent of abscesses or neurological compression.3 Advanced imaging, including MRI, has improved our understanding and diagnosis of PVO (Figs. 1, 2). Early MRI changes display high T2 and low T1 signal intensity in affected disks and adjacent vertebrae. High T2 signal in the paraspinal soft tissues, with inflammation and edema visualized more clearly with fat saturation or short tau inversion recovery sequences are also associated with early MRI changes. Contrast is often used to display the diffuse enhancement of the subchondral bone and disk. The early MRI findings of high T2 disk signal with disk height loss and contrast uptake within the disk are highly sensitive (70%–100%) for PVO diagnosis.4 However, Carragee10 reviewed 103 MRIs of patients eventually diagnosed with PVO, finding a missed diagnosis rate of 9.1% with MRIs obtained within 2 weeks of presenting symptoms compared with a 3.4% missed diagnosis rate for MRIs after 2 weeks. In addition, an important diagnostic consideration is ruling out neoplastic disease, with signs that suggest infectious etiology including disk space involvement with endplate erosion. Copyright

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Vertebral Osteomyelitis and Spinal Epidural Abscess

Serial imaging should be considered in suspicious patients during the early period in its presentation (Fig. 3).

Microbiology Staphylococcal infections, including Staphylococcus aureus and Staphylococcus epidermidis, are most commonly identified in PVO, with S. aureus incidence ranging from 32% to 67%. Loibl et al2 noted worse outcomes with staphylococcus infections, with increased intensive care unit admissions (58% vs. 34.7%) and higher rates of infectious complications (76.5% vs. 40.3%). Graham et al11 noted a 12.7% incidence of gram-negative PVO in their retrospective case series, with Escherichia coli, Pseudomonas aeruginosa, Haemophilus influenzae, and Klebsiella pneumonia identified on cultures. Approximately 9% of PVO cases will display a polymicrobial etiology.4 Although positive cultures are helpful for targeted antibiotic therapy, Yoon and colleagues noted similar outcomes, duration of treatment, and normalization of labs between culture-positive and culture-negative patients. Similarly, Lora-Tamayo et al1 also noted similar long-term outcomes between culture-positive and culturenegative PVO, despite a higher rate of concomitant sepsis, fevers, and elevated labs among the culture-positive study group.

Treatment Antibiotics remain the cornerstone of PVO treatment, regardless of surgical or nonoperative management. Consultation with infectious disease specialists is useful for recommendations on duration of treatment, dosing, route, and antibiotic selection. Duration of treatment is controversial and ultimately is guided by individual clinical evaluation. Bernard et al12 reviewed antibiotic treatment lengths for PVO, comparing 6- and 12-week durations of IV and/or PO antibiotics in an open-label, noninferiority randomized-control trial, finding similar cure rates (90.9% and 90.8% cure rates, respectively) and an equal percentage of adverse events (29% each). They further noted no significant difference in treatment failure between patients receiving IV antibiotics greater than or less than 7 days.12 Risk factors for failure of treatment were ESR > 55 mm/h and CRP > 2.75 after 4 weeks of antibiotic treatment with an odds ratio of 5.15.5 In patients treated nonoperatively, bracing for comfort and prevention of deformity is a reasonable treatment option, although there is no clinical evidence to support whether or not bracing affects outcome. Surgical management should be considered in patients who are refractory to antibiotic treatment or display neurological deficits, spinal instability, or progressive deformity with vertebral body destruction.13 Although no definitive threshold for surgical management of PVO based on spinal instability or kyphotic deformity exists, Dietze et al14 recommend using the following parameters to suggest spinal instability: vertebral body collapse >50%, >20 degrees of angulation, and >5 degrees of vertebral translation. An anterior approach affords a more www.jspinaldisorders.com |

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FIGURE 1. L.G.: pictured is a 65-year-old patient with L3/L4 spondylodiscitis. The sagittal T2 (A) series demonstrate increased disk signal (arrow) and sagittal T1 fast spin echo (B) series further demonstrate endplate edema (arrow) with mild endplate erosion. Axial T2 (C) series show circumferential extension of the discitis with extension into paraspinal soft tissues and spinal canal (as outlined by arrows). Sagittal short tau inversion recovery sequences (D) further delineate endplate edema with extension into the spinal canal (arrow). This patient was treated with a course of intravenous antibiotics.

complete debridement, with removal of sequestra and devitalized vertebral bone and intervertebral disk, whereas posterior debridement affords less morbidity but risks more limited access and incomplete debridement. Beyond debridement, significant controversy exists in the use of instrumentation, 1- versus 2-staged procedures, anterior versus posterior instrumentation, and the use of autograft versus allograft. Despite controversy, multiple studies suggest favorable outcomes and low recurrent infection rates using instrumentation in the surgical treatment of PVO. Comparing outcomes of PVO treatment consisting of either debridement with or without instrumentation, Bydon et al15 retrospectively reported on 118 patients, noting similar rates of recurrent infection (8.3% for debridement and 9.8% for debridement with instrumentation) and reoperation (19.4% for debridement and 17.1% for debridement with instrumentation). Carragee and Iezza evaluated 32 immunocompromised patients with PVO treated with a variety of anterior and posterior instrumentation techniques. Of 22 living patients who were alive without evidence of clinical recurrence at 10 years, only 1 patient had a demonstrated

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recurrent infection during the follow-up time period.16 They concluded that the use of instrumentation is considered reasonable even in immunocompromised hosts with PVO. Anterior stand-alone instrumentation has been reported in small retrospective case series. Dai and colleagues reported on 22 anterior debridements with interbody fusion with either bone strut autograft or titanium mesh cages and anterior instrumentation using titanium plates. At 3-year follow-up, all patients had significant back pain relief, solid fusion, and healing of infection with an average of 93% correction of kyphosis.17 Furthermore, Si and colleagues suggested similar outcomes with anterior plate fixation versus posterior transpedicular fixation following radical anterior debridement. Both groups displayed improved Oswestry Disability Index and visual analog scale (VAS) outcomes and pain relief at 2-year follow-up with no difference in radiologic fusion time, deformity correction, and cage subsidence.18 The use of cages with bone graft placed into vertebral defects after debridement is a helpful adjunct in reconstruction. Using expandable titanium cages for reconstruction of large defects from multiple contiguous corpectomies, Copyright

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Vertebral Osteomyelitis and Spinal Epidural Abscess

FIGURE 2. A.F.: an 80-year-old patient was diagnoses with L2–L5 spondylodiscitis. Notice the advanced destruction of the disks and endplates with vertebral body collapse on T1 (A) and enhancement on postcontrast T1 imaging (B) of the vertebral bodies and adjacent soft tissues (arrows). Axial T1 postcontrast images taken at the L3/L4 level (C) show extensive paraspinal edema and vertebral destruction (arrows). Sagittal T2 (D) and short tau inversion recovery (E) sequences further demonstrate the extensive vertebral and soft-tissue edema from the advanced disease (arrows). This patient was treated with intravenous antibiotics.

Robinson et al19 reported successful outcomes in 25 patients with no PVO recurrence and significant improvements in ODI and VAS scores at 36-month follow-up. Kuklo et al20 reviewed their experience with single-stage anterior titanium cages and posterior instrumentation in 21 patients, noting 2 repeat operations, an average of 12.3-degree improvement in kyphosis, and no reported deaths or neurological complications at an average follow-up of 44 months. Sundararaj et al21 similarly reported successful outcomes in 32 patients with single-stage anterior debridement with cage placement and posterior instrumentation, with neurological Copyright

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improvement in 10/13 (76.9%) and good or excellent clinical outcomes in 30/32 (93.8%). Bone grafting is commonly used in these cases to increase the rate and probability of fusion. Common autograft sources used in spinal surgery include tricortical iliac crest, rib, and fibular strut. Humeral or femoral allograft struts are other options for bone graft in the setting of an extensive anterior debridement and/or corpectomy. Although allograft avoids the morbidity of donor site harvesting, autograft is theorized to have superior rates of incorporation. While some concern exists with introducing allograft into infected

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FIGURE 3. A.A.: a 32-year-old patient was diagnosed with T11 lymphoma and treated with intrathecal chemotherapy. Notice the largely contained lesion within the vertebral body with minimal caudad/cephalad extension into the disk spaces on sagittal T1 (arrow) (A) with further enhancement of the lesion on T1 postcontrast series (B). Axial T2 series (C) show radial extension of the lymphoma beyond the confines of the vertebral body with canal compression. Sagittal T2 (D) and sagittal short tau inversion recovery (E) sequences further demonstrate T11 edema with minimal disk involvement and radial extension of disease into the spinal canal.

surgical fields, several small case series suggest similar recurrent infection rates and clinical outcomes when compared with autograft.22,23 Performing corpectomies with cage reconstructions, Lu et al23 reported recurrent infections after initial management in one of 19 allograft cases compared with 1 of 17 autograft (rib or iliac crest) cases within an average follow-up of 21 months with no implant failures reported. Despite several case series suggesting equivalency to autograft, surgeons should exercise caution with the use of allograft in surgical management of PVO. Despite some favorable retrospective case series, complications and treatment failures during PVO manage-

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ment still occur. Arnold and colleagues reviewed 94 cases of PVO requiring surgical management with instrumentation and found a 23% (22 cases) treatment failure rate secondary to uncontrolled/recurrent infection. Ninety-one percent of these treatment failures occurred within 1 year of treatment. Nineteen of these cases underwent further debridement with an average of 2.2 repeat operations and 15 patients ultimately required hardware removal.24 A controversial randomized-control trial by Albert and colleagues suggested that patients with chronic back pain and MRI findings of Modic type 1 (bone edema) vertebral changes may have insidious osteomyelitis. Copyright

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Patients were randomized to antibiotics or placebo in a double-blind fashion, noting improved outcomes with the antibiotic group on all subjective outcome measures.25 A subsequent systematic review by Urquhart et al26 suggested moderate evidence for a relationship between the presence of bacteria and both low back pain with disk herniation and Modic type 1 change with disk herniation, with a modest evidence for a cause-effect relationship (Table 1). In summary, early detection, accurate diagnosis, and appropriate antibiotic treatment of PVO is paramount in successful treatment. Most cases are treated with nonoperative care. Debridement and surgical reconstruction are required if targeted antibiotic therapy fails to rid the infectious process, and/or there is a neurological deficit, significant pain, instability, or spinal deformity as a result of the PVO.

GRANULOMATOUS VERTEBRAL OSTEOMYELITIS Granulomatous spinal infections are a serious cause of morbidity and mortality, with Mycobacterium tuberculosis being the most common etiology of vertebral granulomatous infection. Commonly arising in the metaphyseal regions of the vertebral body, the tubercular infection can spread anteriorly and track under the anterior longitudinal ligament in a cranial-caudal direction, creating skip lesions and paravertebral abscesses. While vertebral granulomatous infections, also known as Pott disease, are only found in 10%–20% of tuberculosis (TB) cases in developed nations, the number increases to 20%– 41% in undeveloped nations.31 Approximately 3%–5% of patients with pulmonary TB develop musculoskeletal lesions and this number rises to nearly 60% in patients with HIV.32 Compared with PVO, tuberculous vertebral osteomyelitis (TBVO) displays a greater proportion of thoracic spine involvement, increased rates of deformity, neurological deficits, and paravertebral and epidural abscesses. Seventy-six percent of patients complained of neurological symptoms, with neurological deficits found on examination in 62% of patients.33

Vertebral Osteomyelitis and Spinal Epidural Abscess

In addition to a standard infectious workup, a PPD and chest x-ray should be obtained in high-risk individuals, as these patients may display pulmonary or miliary TB. Compared with PVO, TBVO is less frequently associated with elevated inflammatory markers. Tissue cultures from percutaneous biopsy for TBVO display high sensitivity (91.1%), but require significant time to result causative organisms (mean, 34 d; range, 19–83 d). While polymerase chain reaction for M. tuberculosis can dramatically reduce time to diagnosis, it displays lower diagnostic sensitivity (78.6%). Although rarely needed, open surgical biopsy can be performed to reveal causative organisms when percutaneous techniques fail or are of excessive risk.34

Imaging Similar to PVO, the imaging of TBVO commonly proceeds with a standard radiographic series of involved levels along with MRI. Similar to neoplastic lesions, the intervertebral disks are commonly not involved in the infectious process. However, tuberculous spinal infections tend to involve the areas surrounding the endplate, whereas neoplastic disease tends to involve the vertebral bodies. Findings on MRI suggestive of TBVO include well-defined paraspinal abnormal signal, presence of intraspinal/paraspinal abscesses with thin and smooth walls visualized on T1 fat-suppressed contrast-enhanced sequences, and thoracic spine involvement. Subligamentous spread to adjacent vertebral bodies, involvement of multiple vertebrae, and disk space narrowing can also be identified but may be less specific for TBVO.35 In reviewing MRI findings of TBVO, Anley et al36 revealed significantly increased vertebral body collapse in HIV-positive patients (107% vs. 75.3%) and a trend toward larger anterior epidural purulent collections, but no difference in number of vertebrae affected, prevalence of cord signal, or noncontiguous lesions. Spinal cord compression by lesions on MRI, evidence of myelomalacia on imaging, and reduced space for spinal cord are each independently associated with poor outcomes.31 CT scans are often used to better characterize the amount of bone destruction and are often useful in preoperative planning.

Treatment Clinical Evaluation The patient presentation can mimic malignancy with symptoms of malaise, night sweats, and weight loss, although documented fevers >381C are less common in TBVO than PVO (17.0% vs. 48.1%). Back pain is a common complaint and occurs in TBVO at a similar rate to PVO (87.2% vs. 83.5%).34 Neurological deficits can appear throughout the disease process, with 33% presenting in the first 4 weeks, 40% between 4 weeks to 3 months, and 27% after 3 months. Neurological deficits can present as radiculopathy, myelopathy, or cauda equina syndrome.31 Paraplegia from TBVO, also known as Pott paraplegia, can result from anterior compression from vertebral retropulsion, abscesses, or meningomyelitis. Copyright

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Three to 4 weeks of nonoperative management should be initially undertaken in most patients. Medical management should be considered in patients with preserved cord space with a predominance of fluid collections in extradural spaces. Reviewing chemotherapeutics for the treatment of TBVO, Rajasekaran and Khandelwal noted that prolonged and uninterrupted chemotherapy is crucial to successful outcomes. With a historic mortality rate of 30%–50%, first-line TB drugs (isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin) have helped reduce current mortality to 50% even without neurological symptoms, signs of spinal instability, long segment (> 4 vertebrae) disease, kyphosis >60 degrees, pan-columnar involvement, large paraspinal and epidural abscesses, and severe pain.31,37 Although any neurological symptoms should prompt early surgical management, the effect of surgery on long-term neurological recovery is unclear. While Jin-Tao et al38 found complete neurological recovery in 44% of operatively treated patients versus 16.7% nonoperative patients at 6-month follow-up, neurological recovery rates converged at 28-month follow-up (91.7% vs. 94.4%, respectively). Surgical management consists of debridement with removal of caseous purulence and sequestra, only debriding viable bone if it compresses neurological structures. In addition, voids should be bridged with bone graft and cages or bone struts followed by instrumentation.31 Approaches for surgical management of thoracic disease are important to consider. While thoracotomies provide optimal anterior visualization, the pulmonary function of the TB patient must be considered preoperatively. As a result, extrapleural and transpedicular approaches can be reasonable alternatives to thoracotomies in patients with compromised pulmonary function.29 Although previously thought to be controversial, early surgical treatment (< 2 wk after beginning chemotherapy) can commence safely and effectively, with patients demonstrating consistent improvements in ESR at long-term follow-up regardless of preoperative response to chemotherapy.39 Surgical treatment has evolved over the past several decades, with a trend toward more circumferential approaches and increasing use of instrumentation. Chandra et al37 noted that these recent treatment trends have led to decreasing paraplegia, with a 32% rate before 2004 and 11% from 2004 to 2011. Similar to PVO, controversies in surgical management of TBVO include approach considerations, timing of procedure, and deformity correction procedures. In addition, the majority of available evidence consists of retrospective case series describing a variety of approaches and techniques. Wang et al29 evaluated the long-term outcomes of anterior radical debridement and reconstruction with titanium mesh cages for thoracic and thoracolumbar TBVO. At 6-year follow-up of 69 patients, they reported maintained kyphosis correction and restoration of intervertebral height with their proposed constructs, with no failures of instrumentation. Furthermore, improvement in VAS back pain scores, solid bony fusion, eradication of infection, and improvement in neurological function were achieved in all patients.29 Comparing either anterolateral or posterior transforaminal approaches for debridement and strut graft placement for TBVO followed by posterior pedicle screw and rod instrumentation, Wang et al30 noted improvement in kyphosis for thoracolumbar junction lesions with

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SingleInfection Neurological All infections resolved with solid bony 1 superficial infection, 1 chylous institution resolution bony recovery, fusion leak retrospective fusion VAS case series SingleBony fusion Operative Improvement in kyphosis in Circumferential: 2 sinus drainage, institution improvement in time, blood circumferential (16.6 vs. 5.6 2 pleural effusion, 1 superficial prospective kyphosis loss, degrees), but increased blood loss infection, 3 delayed fusion observation hospital and longer operative time and secondary to psoas abscess case series stay hospital stay Posterior: 1 refractory intercostal neuralgia SingleInfection Neurological Infection recurrence in 1/19 allograft NA institution recurrence recovery, and 1/17 autograft retrospective pain case series

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circumferential approaches (5.6 vs. 16.6 degrees of kyphosis) but also increased operative times, estimated blood loss, complications, and increased length of hospital stays. A meta-analysis comparing isolated anterior versus posterior-based approaches for debridement and instrumentation of TBVO noted superior Cobb angle correction with posterior approaches, but otherwise no difference in length of stay, time to fusion, loss of correction, or operative time. The improved Cobb angle correction with posterior approaches was hypothesized to be related to superior deformity correction with pedicle screw fixation compared with anterior plating techniques relying on vertebral body fixation.40 Adjacent multisegment disease can be difficult to surgically manage. Li and colleagues reviewed 4 approaches on 48 patients and discussed their relative indications for each. Single-stage anterior debridement, bone grafting, and anterior screw/rod fixation was successful in patients with 2 levels. Posterior debridement with costotransversectomy for thoracic lesions versus facetectomy and pediculectomy for lumbar lesions with intervertebral bone grafting and pedicle screw fixation was utilized if no extensive abscess or spinal cord compression was identified and only one vertebrae displayed significant bony destruction. The fourth approach used CT-guided percutaneous initial treatment with a delayed procedure, most commonly performed on infirm patients who could not acutely tolerate open procedures. Ultimately, they noted that all 48 patients were cured at final follow-up with graft union in 47 patients and 2 recurrences.41 Large degrees of kyphosis (> 60 degrees) is believed to be concerning for late paraplegia due to progression of kyphosis from the disease with further bowstringing of the spinal cord along the kyphotic bend.31 Correction of late, healed kyphosis commonly requires a 3-column osteotomy, such as pedicle subtraction osteotomies (PSO) and vertebral column resection (VCR). While both PSOs and VCRs can correct sagittal alignment, the VCR allows direct anterior decompression for the common sharp, kyphotic bend and is preferred for thoracic-level kyphosis.42 Suk et als’43 experience with posterior VCR on 25 patients with postinfectious kyphosis reported upwards of 58 degrees of kyphosis correction, but warned about the morbidity of the procedure with an average estimated blood loss of 2980 mL and 10 complications including 1 cord injury and 2 root level injuries.

SPINAL EPIDURAL ABSCESSES (SEAs) SEA is a relatively infrequent but potentially devastating spinal infection and an important pathology to rapidly identify. The incidence of SEA is estimated at 1.8 per 100,000 persons per year, limiting many health care practitioners exposure to this pathology.44 Mean total charges relating to the treatment of SEA average $159,782 (recorded from 2006 to 2011), with patients

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displaying 1–3 comorbidities incurring charges on average $48,784 greater than patients without comorbidities.45 Neurological symptoms commonly occur with motor deficits present in 30% of cases, including 19% of patients displaying paralysis.45 With improved diagnostic and treatment capabilities, the mortality of SEA has dramatically decreased from 34% in the period of 1954–1960 to 15% in 1991–1997 to currently approximately 5%, with death usually resulting from uncontrolled sepsis, evolution of meningitis, or other underlying comorbidities.46,47 As delays in diagnosis can lead to irreversible neurological deficits, expedient identification of those at risk for SEA is imperative. In a retrospective case-control study examining 63 SEA patients and 126 controls, the classic triad of back pain, fever, and neurological deficit was present in only a minority of patients (13% compared with 1% of controls).48 Instead, risk factor assessment including advanced age, lack of insurance, liver disease, alcoholism, HIV infection, and renal failure, offers a high sensitivity and negative predictive value.46,48 Other risk factors identified by Rigamonti et al49 include intravenous drug use (33%), diabetes mellitus (27%), and prior spinal surgery (17%). Elevation of the ESR was more sensitive and specific than white blood cell count as a screen for SEA.48,49 Regarding infectious etiologies, methicillin-resistant Staphylococci was associated with a significantly worse prognosis (P < 0.005).49 MRI is the imaging modality of choice allowing assessment of abscess extent, location, and neurological compression Figs. 4, 5). The use of gadolinium allows distinction of purulent extradural collections from cerebrospinal fluid. Ring-enhancing lesions found on imaging are pathognomonic for SEA. Vertebral spondylodiscitis is a common concomitant finding, seen on imaging in nearly 86% of SEA cases.50 Imaging should include the entirety of the spine to evaluate for noncontiguous skip lesions. Adequate treatment depends on determining the extent and location of the abscess, which can be difficult with skip lesions. Ju and colleagues reviewed risk factors for skip lesions, noting 22 skip lesions in 233 patients with SEA. Significant risk factors for skip lesions were delayed >7 days to presentation, infection remote to spine or paraspinal muscles, and ESR > 95 mm/h at presentation. Using these risk factors, they noted that the probability of skip lesions was 73% with all 3 risk factors, 13% for 2, 2% for 1, and 0% for 0.51 Tuchman et al52 proposed treatment recommendations with medical management with systemic antibiotics recommended for patients unable to undergo a procedure, complete SCI for >24 hours without ascending lesions, and neurological stability without risk factors. Risk factors for medical management failure included documented methicillin-resistant Staphylococcus aureus infection, neurological impairment, CRP > 115 mg/L, white blood count > 12,500, ring-like enhancement on advanced imaging. Even in patients not displaying risk factors, failure of medical management was reported between 8.3% and 17%.52 Decompression should be performed promptly in patients who do not meet nonoperative criteria. The rate of progression of disease is difficult to predict and these patients should be followed closely. Direct decompression of the Copyright

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FIGURE 4. M.L.: a 63-year-old patient was diagnosed with a C6/C7 spondylodiscitis with an adjacent anterior spinal epidural abscess (SEA). Notice the C6/C7 disk space with C6 body and C7 superior endplate destruction (arrows) on sagittal T1 (A) and with enhancement on postcontrast T1 (B) images. The sagittal T2 (C) and axial T2 (D) images further detail the vertebral body edema and the anterior SEA (arrows) at the C6-C7 levels. Treatment consisted of a C6/C7 anterior irrigation and debridement with anterior cervical discectomy and fusion (E and F) and intravenous antibiotics.

abscess is accomplished with laminectomy for posterior lesions versus discectomy/corpectomy with strut grafting for anterior lesions. Rigamonti and colleagues demonstrated the risk of delayed treatment, finding that poor outcomes (death, incontinence, paraplegia) occurred in 9 of 19 patients (47%) treated after 24 hours compared with only 1 of 10 patients (10%) treated promptly. Connor et al53 reviewed 77 patients treated with either surgical or medical management and noticed a significant improvement in outcomes in operatively managed patients, although selection bias may have played a role in selecting surgical management in patients with significantly reduced pretreatment functioning. The location and etiology of the SEA can have important treatment implications. Zimmerer and colleagues reported on 16 primary SEA and 20 secondary SEA (16 of which were from discectomies), 34 of which underwent surgical management. Interestingly, 100% of the primary SEA improved with a single debridement, but 100% of the secondary SEA from discectomies required multiple deCopyright

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bridements. Improvement in neurological status was reported in 11/16 primary SEA and 14/20 secondary SEA.44 In a review of 75 cases of SEA, Sampath and Rigamonti noted that cervical and thoracic SEA patients were treated more aggressively given the small subarachnoid space around the spinal cord and the potential for greater neurological deficits. In contrast, patients with lumbosacral SEA without neurological deficits could initially proceed with medical management with close observation and subsequent surgical decompression if clinical deterioration was identified.54

CONCLUSIONS Spinal infections are associated with significant morbidity and mortality and commonly present in patients with significant medical comorbidities. Health care practitioners caring for spine patients should understand pertinent risk factors, laboratory tests analysis, and imaging modalities to expeditiously diagnose and

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FIGURE 5. J.A.: a 74-year-old patient had a history of methicillin sensitive staphylococcus aureus endocarditis and was diagnosed with holospinal spinal epidural abscess (SEA). The sagittal T1 (A) and postcontrast T1 (B) series demonstrate a posterior SEA in the upper thoracic spine (arrows), whereas the sagittal T2 (C) better visualizes the diffuse posterior SEA (posterior arrows) throughout the thoracic and lumbar spines on a single image. Also seen on sagittal images is a T5/T6 spondylodiscitis (anterior arrow). Axial MEDIC (D) images show the posterior SEA with canal compression (arrow). This patient was treated with T4/T5, T8/T9, and L2/L3 decompressive laminectomies and intravenous antibiotics.

treat spinal infections and improve patient outcomes. Although higher level of evidence studies should be conducted to strengthen treatment recommendations, the relative infrequency of these infections largely prohibits these studies. As a result spine surgeons must rely on the best available evidence as well as personal experience to make treatment decisions in these complex cases. REFERENCES 1. Lora-Tamayo J, Euba G, Narvaez JA, et al. Changing trends in the epidemiology of pyogenic vertebral osteomyelitis: the impact of cases with no microbiologic diagnosis. Semin Arthritis Rheum. 2011;41:247–255. 2. Loibl M, Stoyanov L, Doenitz C, et al. Outcome-related co-factors in 105 cases of vertebral osteomyelitis in a tertiary care hospital. Infection. 2014;42:503–510.

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Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

J Spinal Disord Tech



Volume 28, Number 6, July 2015

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E327

Vertebral Osteomyelitis and Spinal Epidural Abscess: An Evidence-based Review.

Spinal infections have historically been associated with significant morbidity and mortality. Current treatment protocols have improved patient outcom...
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