ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Vertebral osteomyelitis and discitis in adults

Vertebral osteomyelitis and discitis in adults
Literature review current through: Jan 2024.
This topic last updated: Aug 16, 2022.

INTRODUCTION — Vertebral osteomyelitis most often occurs as a result of hematogenous seeding of one or more vertebral bodies from a distant focus [1]. Infection may also involve the adjacent intervertebral disc space, which has no direct blood supply in adults. Infection can also arise following surgery or injection of the disc space or via contiguous spread from adjacent soft tissue infection.

Vertebral osteomyelitis and discitis may occur together or independently. The term pyogenic spondylitis refers to either vertebral osteomyelitis or discitis. The diagnosis and management of these two entities are similar in most patients.

Issues related to vertebral osteomyelitis will be reviewed here. Issues related to other forms of hematogenous osteomyelitis in adults are discussed separately. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Hematogenous osteomyelitis'.)

Issues related to spinal epidural abscess and tuberculous spinal infections are discussed separately. (See "Spinal epidural abscess" and "Bone and joint tuberculosis".)

EPIDEMIOLOGY — Vertebral osteomyelitis is primarily a disease of adults; most cases occur in patients >50 years old [2]. The incidence increases with age. Men are affected approximately twice as often as women in most case series; the reason for this is not fully understood. Risk factors for vertebral osteomyelitis include injection drug use, infective endocarditis, degenerative spine disease, prior spinal surgery, diabetes mellitus, corticosteroid therapy, or other immunocompromised state. (See 'Pathogenesis' below.)

The annual incidence of hospitalization for vertebral osteomyelitis in the United States between 1998 and 2013 rose from 2.9 to 5.4 per 100,000, with lengthy hospital stays and substantial long-term burden for patients and the health system [3]. Similar increases have been reported elsewhere, including in France where nationwide discharge data revealed an increase from 6.1 to 11.3 per 100,000 from 2010 to 2019 [4].Reasons for the increase in incidence include [1]:

Increasing rates of bacteremia due to intravascular devices and other forms of instrumentation. An increasing proportion of vertebral osteomyelitis is health care related and/or post-procedural (up to one-third of new cases) [5,6].

Increasing age of the population

Increasing number of patients on renal replacement therapy

Increasing number of patients on immunosuppressive medications

PATHOGENESIS

Mechanisms of infection — Bacteria can reach the bones of the spine by three basic routes (see "Pathogenesis of osteomyelitis"):

Hematogenous spread from a distant site or focus of infection

Direct inoculation from trauma, invasive spinal diagnostic procedures, or spinal surgery (image 1)

Contiguous spread from adjacent soft tissue infection

Potential sources of hematogenous or contiguous spread of infection include the genitourinary tract, skin and soft tissue (eg, injection drug use), respiratory tract, infected intravascular devices, postoperative wound infection, infective endocarditis, and dental infection. In many cases, the primary site of infection cannot be identified [7]. Less common causes include infected native or prosthetic heart valve infections, direct spread from a ruptured esophagus, diverticular or renal abscesses, and infected aortic lesions (image 2) [8].

Vertebral osteomyelitis has been reported as a complication of lumbar puncture, myelography, translumbar aortography, chemonucleolysis, discography, facet joint corticosteroid injection [9], epidural catheter placement, and epidural corticosteroid injection [10].

Hematogenous spread — Hematogenous spread is by far the most common cause of vertebral osteomyelitis. Adult vertebral bone has abundant, highly vascular marrow with a sluggish but high-volume blood flow via nutrient vessels of the posterior spinal artery. With aging, these vessels progressively develop a characteristic "corkscrew" anatomy that may predispose to bacterial hematogenous seeding.

Bloodborne organisms that transit the vertebral marrow cavity can produce a spontaneous local suppurative infection. Initiation of infection may be facilitated by recent or prior bone trauma with disruption of normal architecture.

Segmental arteries supplying the vertebrae usually bifurcate to supply two adjacent end plates of the vertebrae. Thus, hematogenous vertebral osteomyelitis often causes bone destruction in two adjacent vertebral bodies and usually destroys their intervertebral disc. The lumbar vertebral bodies are most often involved, followed by thoracic and, less commonly, cervical vertebrae. Hematogenous sacral osteomyelitis is rare.

Skip lesions with more than one level of spinal infection occur in less than 5 percent of reported cases. Noncontiguous epidural abscesses appear to be more common (10 percent) [11].

It was previously postulated that spread of infection might occur via vertebral veins known as Batson plexus [12,13]; this theory has been discounted.

Contiguous spread — Contiguous spread of infection may occur from tissues adjacent to the spine, such as the aorta, esophagus, or bowel. In such cases, extension of infection is facilitated by absence of a circumferential cartilage plate or a layer of subchondral compact bone [14].

Sacral osteomyelitis most commonly occurs as a complication of a sacral pressure ulcer, although it can follow pelvic infection, trauma, and/or surgery. Typically, it is polymicrobial and restricted to cortical bone [15,16]. (See "Infectious complications of pressure-induced skin and soft tissue injury", section on 'Osteomyelitis'.)

Extension of infection — Extension of infection posteriorly can lead to epidural abscess, subdural abscess, or meningitis (image 1). Extension of infection anteriorly or laterally can lead to paravertebral, retropharyngeal, mediastinal, subphrenic, retroperitoneal, or psoas abscess (image 3 and table 1). Development of epidural or paravertebral abscess is more common in the setting of gram-positive infection than gram-negative infection [17]. In addition, thoracic vertebral infections can extend into the pleural space to produce an empyema [18].

Infection can occur in spinal elements other than the vertebral bodies, including the posterior spinous processes, the facet joints, the pedicles, and, rarely, the odontoid process [19].

MICROBIOLOGY — Most patients have monomicrobial infection. The most common cause of vertebral osteomyelitis is Staphylococcus aureus, accounting for more than 50 percent of cases in most series from developed countries. The relative importance of methicillin-resistant S. aureus as a cause of vertebral osteomyelitis has increased as the community and hospital proportion of S. aureus strains that are methicillin resistant have increased.

Other causes of vertebral osteomyelitis include [20,21]:

Enteric gram-negative bacilli, particularly following urinary tract instrumentation

Nonpyogenic streptococci, including viridans group, milleri group, Streptococcus bovis, and enterococci [22,23]

Pyogenic streptococci, including groups B and C/G, especially in patients with diabetes mellitus (see "Group C and group G streptococcal infection" and "Group B streptococcal infections in nonpregnant adults", section on 'Microbiology')

Pseudomonas aeruginosa, coagulase-negative staphylococci, and Candida spp, especially in association with intravascular access, sepsis, or injection drug use [21,24] (see "Candida osteoarticular infections")

Tuberculous infection (see "Bone and joint tuberculosis")

Brucellosis, especially Brucella melitensis in North Africa, the Mediterranean rim, and the Middle East [25] (see "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis")

Geography also influences the organisms associated with vertebral osteomyelitis. Burkholderia pseudomallei (melioidosis) is a potential pathogen in patients from peri-equatorial regions, and Salmonella and Entamoeba histolytica are occasional causes in sub-Saharan Africa or South America.

CLINICAL FEATURES

Symptoms and signs — The major clinical manifestation of vertebral osteomyelitis is pain; pain is typically localized to the infected disc space area and is exacerbated by physical activity or percussion to the affected area. Pain may radiate to the abdomen, leg, scrotum, groin, or perineum.

Spinal pain usually begins insidiously and progressively worsens over several weeks to months. In one series of 64 patients with hematogenous vertebral osteomyelitis, the mean duration of symptoms was 48±40 days [21]. The pain is often worse at night; initially, it may be relieved by bed rest. Pain may be absent in patients with paraplegia.

Patients whose infections extend posteriorly into the epidural space may present with clinical features of an epidural abscess; this often consists of focal and severe back pain, followed by radiculopathy, then motor weakness and sensory changes (including loss of bowel and bladder control and loss of perineal sensation), and eventual paralysis. The risk of severe neurologic deficit is increased in the presence of epidural abscess, especially with thoracic or cervical spinal involvement [26]. (See "Spinal epidural abscess".)

Fever is an inconsistent finding. One review noted a frequency of 52 percent [2]; lower rates have been noted in other studies [27].

Local tenderness to gentle spinal percussion is the most useful clinical sign but is not specific. Back pain is often accompanied by reduced mobility and/or spasm of nearby muscles. Rarely, a mass or spinal deformity may be visible.

The physical examination should include palpation for a distended bladder (may reflect spinal cord compression), evaluation for signs of psoas abscess (eg, flank pain and pain with hip extension), and a careful neurologic assessment of the lower limbs. (See "Psoas abscess".)

A careful general examination is essential to evaluate for potential sources of hematogenous spread; these include injection sites and recent skin or soft tissue infection.

Laboratory findings — The leukocyte count may be elevated or normal. Elevations in the erythrocyte sedimentation rate (ESR), which can exceed 100 mm/h, and C-reactive protein (CRP) are observed in more than 80 percent of patients [28-30].

If elevated, the ESR and CRP are useful for following the efficacy of therapy. (See 'Clinical and laboratory monitoring' below.)

DIAGNOSIS — Vertebral osteomyelitis should be suspected in the setting of new or worsening back or neck pain, especially with fever, and/or presence of bloodstream infection or infective endocarditis (IE) [1]. It should also be suspected in patients with fever and new peripheral neurologic symptoms (with or without back pain) and in patients with new back or neck pain following a recent episode of bacteremia (especially with S. aureus) or fungemia.

The diagnosis of vertebral osteomyelitis or discitis is established based on positive culture obtained from image guided biopsy (via computed tomography [CT] or fluoroscopic guidance) of the involved vertebra(e) and/or disc space [31-33]. The diagnosis may be inferred in the setting of clinical and radiographic findings typical of vertebral osteomyelitis and positive blood cultures with a likely pathogen such as S. aureus. Similarly, the diagnosis may be inferred in the setting of histopathologic findings consistent with infection in the absence of positive culture data, particularly in the setting of recent antibiotic administration. For circumstances in which there are no positive microbiologic cultures or Gram stains and a biopsy cannot be performed, the diagnosis may be inferred in the setting of suggestive clinical and typical radiographic findings and persistently elevated inflammatory markers.

Back pain due to vertebral osteomyelitis may respond initially to bed rest and conservative measures, leading to the erroneous conclusion of minor trauma, muscle strain, or other noninfectious cause. In addition, a history of degenerative spinal disease or recent trauma sometimes obscures or delays the true diagnosis. In such cases a sedimentation rate (or serial sedimentation rates) can be useful; a normal result is reassuring.

Suggested clinical approach — Initial evaluation of patients with suspected vertebral osteomyelitis begins with careful history and physical examination; patients should have a thorough neurologic exam and should be questioned about predisposing factors including presence of indwelling devices, recent instrumentation, and injection drug use. Initial diagnostic tests include inflammatory markers (erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]) and cultures (blood and urine), followed by spinal imaging (magnetic resonance imaging [MRI] preferred if available) (algorithm 1). (See 'Radiographic imaging' below.)

Evaluation for surgery is warranted for patients with neurologic deficits, radiographic evidence of epidural or paravertebral abscess, and/or cord compression (threatened or actual). Ongoing monitoring for emergence or progression of neurologic signs is essential. In one case-control study including 97 patients with vertebral osteomyelitis and severe neurologic deficit, risk factors for neurologic deficit included epidural abscess and thoracic vertebral involvement [26]. (See 'Surgery' below.)

In the absence of the above conditions warranting surgical intervention, patients with radiographic evidence of vertebral osteomyelitis should undergo a CT-guided needle biopsy of the affected bone and disc space as well as aspiration of abscess if present [20,33]. The specimens should be sent for bacterial (aerobic and anaerobic), fungal, and mycobacterial culture as well as histologic examination.

If possible, antimicrobial therapy should be withheld until a microbiologic diagnosis is confirmed. Clinical exceptions include neurologic compromise and sepsis; in these circumstances, empiric antibiotic therapy is warranted [1]. (See 'Antimicrobial therapy' below.)

A needle biopsy may not be necessary in patients with clinical and radiographic findings typical of vertebral osteomyelitis and positive blood cultures with a likely pathogen (such as S. aureus, Staphylococcus lugdunensis) or in patients with positive serology for Brucella (which is warranted for patients with relevant risk factors) [1]. Similarly, a positive blood culture due to a gram-negative enteric rod, P. aeruginosa, or other invasive pathogen is usually good evidence that the same pathogen is also the cause of the spinal infection. However, blood culture isolates do not always correlate with culture results from needle biopsy; therefore, needle biopsy is warranted for cases in which an alternate source for the bacteremia is present or strongly suspected [24]. (See "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

If cultures of blood and the needle aspirate are negative and the clinical suspicion for vertebral osteomyelitis remains high (on the basis of clinical and radiographic findings), we advocate performing a second biopsy. In one retrospective study including 136 patients with vertebral osteomyelitis in the absence of bacteremia, first biopsy was positive in 43 percent of cases and a second biopsy in 40 percent of cases; when combined with blood culture results, this approach led to microbiological diagnosis in nearly 75 percent of cases [34]. Performing blood cultures immediately following biopsy does not appear to add any benefit.

If repeat biopsy specimens and initial blood cultures are nondiagnostic, we usually initiate empiric therapy as discussed below. If such therapy does not result in objective clinical improvement in three to four weeks, a third percutaneous needle biopsy or an open surgical biopsy should be performed. Some suggest that, if the first set of cultures is negative, open biopsy be pursued before starting antibiotic therapy [20]. (See 'Antimicrobial therapy' below.)

The individual clinical approach must include consideration of the location of the infection, the underlying health of the patient, and the experience of the local surgeons.

Diagnostic tools — Diagnostic tools for vertebral osteomyelitis include cultures (blood and urine), imaging studies, and biopsy.

Microbiology cultures — Blood and urine cultures should be obtained in all patients with suspected vertebral osteomyelitis; they are positive in up to 50 of cases [21,24]. (See 'Suggested clinical approach' above.)

In the setting of positive blood cultures for gram-positive organisms, evaluation for concurrent IE is warranted in patients with underlying valvular disease and/or new-onset heart failure. (See 'Evaluation for endocarditis' below.)

Radiographic imaging — MRI is the most sensitive radiographic technique for diagnosis of vertebral osteomyelitis and epidural abscess [35]. CT is a reasonable alternative imaging modality when MRI is not available. If neither CT nor MRI is available, plain films should be pursued; however, plain films typically demonstrate radiographic findings only after the disease has become advanced. If a plain film demonstrates vertebral osteomyelitis, additional imaging is still warranted to assess the extent of disease and presence of complications (epidural or paraspinal abscess). Radionuclide scanning may be useful if MRI is contraindicated because of claustrophobia or presence of an implantable cardiac or cochlear device [1].

Magnetic resonance imaging – MRI is the most sensitive radiographic technique for diagnosis vertebral osteomyelitis [35]. Typical MRI findings in vertebral osteomyelitis include (image 4) [36,37]:

Decreased signal intensity in the vertebral bodies and disc and loss of endplate definition (T1-weighted images) (image 5).

Increased disc signal intensity; less often, increased vertebral body signal intensity (T2-weighted images) (image 1).

Contrast enhancement of the vertebral body and disc (image 6). Ring enhancement of paraspinal and epidural processes correlates with abscess formation, whereas homogeneous enhancement correlates with phlegmon formation.

Vertebral osteomyelitis rarely occurs without characteristic involvement of the intervertebral disc. For cases in which the disc is spared, an erroneous diagnosis of malignancy or compression fracture may be made [38].

MRI abnormalities consistent with osteomyelitis can be observed long before plain films become abnormal. In a review of 103 patients, MRI demonstrated changes suggestive of osteomyelitis in 91 percent of patients with symptoms of less than two weeks duration and in 96 percent of those with symptoms of more than two weeks duration [39].

False-negative MRI findings have been reported in patients with vertebral osteomyelitis and epidural abscess, especially in those with concurrent meningitis or with long, linear abscesses lacking discrete margins [40]. False-positive results can occur with bone infarction or fracture.

Radiographic findings in the setting of tuberculous vertebral osteomyelitis overlap with those seen in the setting of bacterial osteomyelitis. Extension into surrounding soft tissue tends to be more prominent in tuberculosis (TB) of the spine, and some patients with spinal TB have vertebral body abnormalities in the absence of disc space involvement. These issues are discussed further separately. (See "Bone and joint tuberculosis", section on 'Radiography'.)

The role of follow-up MRI is discussed below. (See 'Role of imaging' below.)

Computed tomography – CT demonstrates findings of vertebral osteomyelitis before changes are apparent on plain films (image 7). CT is also useful for detecting bony sequestra or involucra, adjacent soft tissue abscesses (image 8), and in localizing the optimal approach for a biopsy (image 9) [35].

Subtle abnormalities detected by CT, such as end plate irregularities, may not be specific for osteomyelitis, and early destructive changes may be missed. CT has a high false-negative rate for epidural abscess [35].

Plain radiography – Plain radiographs are often normal in the early phases of infection. Typical findings in vertebral osteomyelitis consist of destructive changes of two contiguous vertebral bodies with collapse of the intervening disc space.

Bone destruction may not be apparent for three weeks or more after the onset of symptoms (image 10) [20,41]. Rarely, infection is confined to a single vertebra and produces collapse of the vertebral body, mimicking vertebral compression fracture [42,43].

Chest radiography is warranted in the setting of clinical suspicion for TB, but a normal chest film does not reduce clinical suspicion of spinal TB. (See "Diagnosis of pulmonary tuberculosis in adults" and "Bone and joint tuberculosis".)

Radionuclide scanning – Radioisotope studies may be useful adjuncts to diagnosis when radiographic changes on plain films or CT scans are absent or equivocal and the suspicion for osteomyelitis is high. They are relatively sensitive but their specificity for infection is low. Radionuclide scanning may be useful when MRI is contraindicated [44].

Labeled-leukocyte scans are rarely useful for the diagnosis of vertebral osteomyelitis because abnormalities typically manifest as a nonspecific photopenic defect with a reduced uptake of isotope [45].

Three-phase bone scintigraphy using labeled technetium is a relatively sensitive and specific test, but it may produce false-positive results in patients with noninfectious disorders such as fracture. False-negative results also can occur early in infection or in cases in which bone infarction accompanies bone infection.

Gallium imaging is a sensitive and specific radionuclide scanning technique for vertebral osteomyelitis. A typical positive test reveals intense uptake in two adjacent vertebrae with loss of the intervening disc space. In a series of 41 patients with suspected vertebral osteomyelitis, increased gallium uptake was detected in all of the 39 patients with biopsy-proven osteomyelitis; subsequent biopsy showed only degenerative changes in two patients with negative gallium scans [46].

Positron emission tomography (PET) scanning using 18-fluorodeoxyglucose (FDG), especially when combined with CT (PET-CT), is highly sensitive, with a negative predictive value for vertebral osteomyelitis of close to 100 percent. The specificity is good but may be compromised by the presence of tumor, degenerative spinal disease, and/or spinal implants [47]. In one prospective study including 32 patients with suspected vertebral osteomyelitis who underwent both MRI and fluorine-18-fluorodeoxyglucose-PET/CT (18F-FDG-PET/CT), MRI was more useful for detection of epidural/spinal abscess and 18F-FDG-PET/CT was more useful for detection of metastatic infection [48].

Biopsy — In general, biopsy is warranted to confirm clinical and/or radiographic suspicion of vertebral osteomyelitis and to establish a microbiologic and histologic diagnosis.

Biopsy material is obtained via an open procedure or needle biopsy by CT or fluoroscopic guidance (image 9) [31-33]. The diagnostic accuracy of CT-guided versus fluoroscopic-guided biopsy is similar [32]. In one study of 92 patients with vertebral osteomyelitis who had a biopsy, open biopsies had a higher microbiologic yield than needle biopsies (91 versus 53 percent) [49]. In a subsequent study including 129 patients with vertebral osteomyelitis, open biopsy had a higher diagnostic yield (70 percent) than fine needle aspirate (41 percent) or core biopsy (30 percent) [23].

Biopsies from infected disc spaces may have higher microbiologic yield than bone biopsies. In one study of 173 individuals with vertebral osteomyelitis and/or discitis, 6 of 43 (14 percent) bone biopsies and 66 of 152 (43 percent) disc specimens were culture positive [33]. Forty-seven (56 percent) of 84 histopathology (bone or disc) specimens were positive for osteomyelitis or discitis. In an earlier study of 102 patients, comparison of the yield of cultures from the vertebral endplate disk, disk space, and adjacent paravertebral soft tissues revealed a trend favoring disk space or paravertebral soft tissue versus endplate disk cultures [50]. Prior antibiotic therapy confounded the results of both studies, and the overall yield of positive cultures was less than 50 percent.

Clinicians should not be deterred from obtaining a biopsy if the patient has received antibiotics recently [49,51]. Prior antibiotic exposure is likely to reduce the yield but not critically [33,52].

Samples should be sent for aerobic, anaerobic, mycobacterial, and fungal cultures and histopathology [20]. The sensitivity (measured by yield of positive cultures or Gram stain of aspirated material) varies between studies from a low of 50 percent [53] to a high of 73 to 100 percent [27,54].

Rarely, nucleic acid amplification testing may be useful if initial aerobic and anaerobic cultures are negative [1]. In one study including 19 patients with discitis, amplification-based DNA analysis of aspirated disc material correlated well with traditional culture methods [55]. A subsequent study demonstrated the potential value of 16S rRNA gene polymerase chain reaction (PCR) assay of biopsy material/aspirates as an adjunct to culture, although there were some false-positive results [56]. Contamination with skin flora is a potential problem with DNA-based diagnostic methods.

Recent studies have also highlighted the potential role of metagenomic next-generation sequencing in diagnosis of spinal infection. In one study with 30 cases of spinal infection, the application of metagenomic next-generation sequencing demonstrated improved sensitivity and preserved specificity when compared to traditional culture-based approaches [57]. However, costs and access to this approach limits clinical utility.

Additional tests — Additional diagnostic tests may be warranted based on epidemiologic factors; these include:

Brucellosis serology – Brucellosis serologic testing is warranted in the setting of unexplained fever, fatigue, and arthralgia in an individual with a possible source of exposure (eg, contact with animal tissues, ingestion of unpasteurized milk or cheese). Major endemic areas include countries of the Mediterranean basin, Persian Gulf, the Indian subcontinent, and parts of Mexico and Central and South America. (See "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Tuberculosis – Diagnostic evaluation for TB is warranted in the setting of relevant risk factors; these include a family history of TB, birth or long-term residence in a highly endemic region, HIV/AIDS, chest radiograph suggestive of latent TB infection, and/or diabetes. (See "Diagnosis of pulmonary tuberculosis in adults".)

Evaluation for endocarditis — Evaluation for concurrent IE is warranted in patients with underlying valvular disease and/or new-onset heart failure in the setting of positive blood cultures for gram-positive organisms [22,58,59]. This is warranted even though the duration of therapy for vertebral osteomyelitis (at least six weeks) is an adequate duration for treatment of IE in most cases. Patients with IE require additional follow-up evaluation for valvular disease as well as prophylactic antibiotics for prevention of subsequent IE. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis" and "Prevention of endocarditis: Antibiotic prophylaxis and other measures".)

A retrospective review including 91 cases of vertebral osteomyelitis (excluding TB, brucellosis, and culture-negative and postsurgical cases) identified 28 patients (31 percent) with IE [58]. When patients with and without IE were compared, the following risk factors were significantly associated with coincident IE:

Age >75 years [22]

Predisposing heart condition

Heart failure

Positive blood cultures

Infection due to gram-positive organisms, especially nonpyogenic streptococci or staphylococci

IE was less likely in patients with a urinary tract–presumed source of infection and with infection due to gram-negative organisms.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of vertebral osteomyelitis includes the following conditions; they are all distinguished radiographically.

Spinal epidural abscess – Clinical manifestations of spinal epidural abscess include fever, back pain, and neurologic deficits. (See "Spinal epidural abscess".)

Psoas abscess – Clinical manifestations of psoas abscess include back or flank pain, fever, and pain with hip extension. (See "Psoas abscess".)

Degenerative spine disease – Degenerative spine disease is common with aging, is associated with back pain, but does not usually result in radiculopathy. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)

Herniated disc – Clinical manifestations of disc herniation include back pain and radiculopathy. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)

Metastatic tumor – Metastatic spinal tumor is typically associated with back pain in the setting of known malignancy; the most common primary cancers associated with skeletal metastasis include breast, prostate, thyroid, lung, and renal cancer. (See "Evaluation of low back pain in adults", section on 'Serious etiologies' and "Epidemiology, clinical presentation, and diagnosis of bone metastasis in adults".)

Vertebral compression fracture – Clinical manifestations of vertebral compression fracture consist of acute onset of localized back pain in the setting of risk factors for osteoporosis. (See "Evaluation of low back pain in adults", section on 'Less serious etiologies'.)

TREATMENT — Management of vertebral osteomyelitis consists of antimicrobial therapy and percutaneous drainage of paravertebral abscess(es) if present. Timely surgical intervention is usually warranted for patients with neurologic deficits, radiographic evidence of epidural or paravertebral abscess, and/or cord compression (threatened or actual).

During the course of treatment for vertebral osteomyelitis, the pace of progression can change suddenly, with potential for catastrophic complications. Therefore, close observation (especially in the first two weeks after diagnosis) is essential. New neurologic manifestation(s), persistent back pain, and/or features of sepsis require immediate investigation.

Antimicrobial therapy

Clinical approach — Selection of antimicrobial therapy should be tailored to results of biopsy or blood culture.

If possible, antimicrobial therapy should be withheld until a microbiologic diagnosis is confirmed. Clinical exceptions include neurologic compromise and sepsis; in these circumstances, empiric antibiotic therapy is warranted [1].

If blood and biopsy cultures are negative and the clinical suspicion for vertebral osteomyelitis is high based on clinical and radiographic findings, initiation of empiric therapy is warranted. (See 'Empiric therapy' below.)

Pathogen-directed therapy — No randomized controlled studies have compared antibiotic regimens for vertebral osteomyelitis. Choice of antibiotic therapy should be guided by biopsy or blood culture results:

Staphylococcal spp – If the organism is found to be methicillin-susceptible Staphylococcus, we recommend treatment with an anti-staphylococcal penicillin such as nafcillin or oxacillin (2 g intravenously [IV] every 4 hours) or cefazolin (2 g IV every 8 hours); flucloxacillin is also an acceptable agent (not available in the United States).

If the Staphylococcus is methicillin resistant or if the patient is allergic to beta-lactam antibiotics, we favor beta-lactam desensitization or treatment with vancomycin (table 2). We do not use ceftriaxone as an alternative to cefazolin or antistaphylococcal penicillin in the absence of special circumstances (such as inability to give multiple daily intravenous doses). For patients who are unable to tolerate vancomycin due to allergy, daptomycin (6 mg/kg IV once daily) is an acceptable alternative.

Streptococcal spp – If the streptococci is fully sensitive to penicillin (minimum inhibitory concentration [MIC] <0.12 mcg/mL), we recommend treatment with either ceftriaxone (2 g IV every 24 hours) or penicillin G (12 to 18 million units/day by continuous infusion or in six divided daily doses).

If the Streptococcus has intermediate susceptibility to penicillin (MIC between 0.12 and 0.5 mcg/mL), we typically treat with ceftriaxone (2 g IV every 24 hours). Alternatively, penicillin (24 million units/day per continuous infusion or in six divided daily doses) may be used. Patients with intermediate or fully resistant streptococci should be treated in collaboration with an infectious disease specialist. Specialized in vitro testing may be needed to select an appropriate antibiotic regimen for infections caused by fully resistant streptococci.

Gram-negative bacilli – Choice of a specific agent for empiric therapy of gram-negative bacilli should be based on knowledge of the prevailing pathogens (and susceptibility patterns) within the health care setting. Initial treatment with one of the following is appropriate:

Third-generation cephalosporin (ceftriaxone 2 g IV daily or ceftazidime 2 g IV every 8 hours or cefotaxime 2 g IV every 6 hours).

Fourth-generation cephalosporin (cefepime 2 g IV every 8 to 12 hours). Dosing every 12 hours is sufficient in most cases; dosing every 8 hours is reasonable in patients with febrile neutropenia (particularly in the setting of known or suspected osteomyelitis due to Pseudomonas spp).

Fluoroquinolone (ciprofloxacin 400 mg IV every 12 hours or 500 to 750 mg orally every 12 hours).

Cutibacterium (formerly Propionibacterium) acnes – For treatment of infection due to C. acnes, we favor penicillin (20 million units IV daily by continuous infusion or in six divided doses) or ceftriaxone (2 g IV every 24 hours). Patients allergic to beta-lactams may be treated with vancomycin (table 2).

Fungal infection – Treatment of fungal vertebral osteomyelitis is discussed separately. (See "Candida osteoarticular infections".)

Empiric therapy — Patients with negative Gram stain and culture results should be treated with an antimicrobial regimen with activity against the common causes of vertebral osteomyelitis, including staphylococci, streptococci, and gram-negative bacilli.

An appropriate empiric regimen consists of vancomycin (table 2) plus one of the following: cefotaxime (2 g IV every 6 hours), ceftazidime (1 to 2 g IV every 8 to 12 hours), ceftriaxone (2 g IV daily), cefepime (2 g IV every 12 hours), or ciprofloxacin (400 mg IV every 12 hours or 500 to 750 mg orally twice daily).

Anaerobes are uncommon pathogens in patients with vertebral osteomyelitis, and we do not routinely add anaerobic coverage to initial empiric therapy. Such coverage is warranted if clinical features suggest that the infection may be due to anaerobic organisms (such as in the setting of a concomitant intra-abdominal abscess) or if the Gram stain is positive but aerobic cultures are negative. In such cases, metronidazole (500 mg IV every six hours) may be added to the above regimen.

If empiric therapy does not result in objective clinical improvement (decreasing inflammatory markers, resolving fever and back discomfort) in three to four weeks, a repeat percutaneous needle biopsy or open surgical biopsy is required (algorithm 1).

Duration of therapy and follow-up — We routinely treat for a minimum of six weeks, with careful review to determine if further treatment is required [1,60]. Longer duration of therapy (eight weeks in some cases) is warranted for patients with undrained paravertebral abscess(es) and/or infection due to drug-resistant organisms (including methicillin-resistant S. aureus [MRSA]) [61]. In some cases, up to 12 weeks of therapy may be necessary, particularly in the setting of extensive bone destruction; the duration of therapy should be tailored to individual circumstances during the course of clinical follow-up. (See 'Clinical and laboratory monitoring' below.)

The above approach to duration of therapy is supported by the following studies:

A randomized trial including 351 patients with vertebral osteomyelitis demonstrated that six weeks of antibiotic treatment was not inferior to 12 weeks of antibiotic therapy with respect to the proportion of patients cured at one year [60]. The number of patients with abscesses in the trial was low (19 percent), and computed tomography (CT)-guided drainage was needed in only 4 percent of cases. In addition, a short duration of intravenous therapy was administered (median 14 days); the most common oral antibiotic regimen was a fluoroquinolone with rifampin. The trial did not include patients with culture-negative infections. The most commonly isolated pathogen was S. aureus; fluoroquinolones are not regarded as ideal drugs for treatment of staphylococcal infections.

A retrospective review including 314 patients with vertebral osteomyelitis noted that independent risk factors conferring an increased likelihood of relapse in patients treated <8 weeks included presence of undrained paravertebral abscess(es) and MRSA infection; in the absence of these findings, the likelihood of relapse in patients treated <8 weeks was much lower [61].

Following at least two weeks of parenteral therapy, completion of treatment with oral therapy may be reasonable in the following circumstances [1,62,63]:

The infection is uncomplicated and the patient has no significant comorbidities.

A favorable clinical response to initial parenteral therapy is observed.

A suitable drug is available, with proven susceptibility to the causative organism and excellent bioavailability.

There is a high chance of reliable absorption of oral medication. Clinicians should check for concomitant medication that may hinder absorption.

Compliance with oral therapy can be assured or carefully monitored.

Oral antibiotic regimens for completing treatment of vertebral osteomyelitis are summarized in the table (table 3).

Patients with laboratory and radiographic evidence of treatment failure warrant repeat tissue biopsy (via image-guided aspiration or surgery) for microbiologic and histologic examination.

Clinical and laboratory monitoring — During antimicrobial therapy, patients should be followed carefully for clinical signs of soft tissue extension, paraspinal abscess, and cord compression.

Patients should also be followed with weekly monitoring of inflammatory markers (erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]) [1]. In one retrospective study including 44 patients with vertebral osteomyelitis, those without a significant decline in the ESR during the first month of therapy were more likely to fail medical therapy (9 of 18 cases compared with 3 of 26 cases with a >50 percent fall in ESR) [29]. However, a rapid decline was not common: the ESR either rose or failed to decline during the first two weeks of treatment in 19 of 32 patients who were ultimately cured with medical therapy. Similar findings have been reported by others [64]. CRP normalizes more rapidly than the ESR after successful treatment of spinal infections and after uncomplicated spinal fusion surgery [35].

Role of imaging — Routine follow-up imaging studies are not necessary. Regular imaging during treatment and in the presence of clinical improvement will not benefit the outcome. Magnetic resonance imaging (MRI), CT, and plain films may appear to worsen for several weeks after the initiation of antibiotic therapy that will be ultimately successful [39].

Follow-up imaging studies are warranted in patients whose clinical status has not improved at the planned time for discontinuation of antibiotics in order to evaluate for the presence of an abscess in need of drainage or to detect spinal instability amenable to surgical intervention [1].

The utility of obtaining imaging studies four to eight weeks after completion of treatment of vertebral osteomyelitis was examined in a retrospective study including 79 patients [65]; none of 27 patients who demonstrated improvement in follow-up MRI studies had evidence of treatment failure after one year of follow-up. In contrast, 5 of 38 patients (13 percent) and 4 of 14 patients (29 percent) whose initial follow-up images demonstrated equivocal changes or evidence of radiographic worsening subsequently failed medical treatment during long-term follow-up.

Associated hardware — Development of vertebral osteomyelitis in the presence of spinal hardware typically reflects a complication of the hardware placement. Most patients have an associated wound infection, although rarely hematogenous seeding of hardware can occur. In such cases, treatment should be based on culture data obtained from wound drainage and/or operative debridement. Typically such infections are treated with intravenous antimicrobial therapy tailored to culture results until bone fusion has been achieved (at least six weeks). If removal of the hardware following union is feasible, repeat cultures should be obtained at the time of hardware removal to guide subsequent therapy, which typically includes at least another six weeks of antimicrobial therapy. If hardware removal is not feasible, antimicrobial suppression (tailored to culture and susceptibility data) may be required either after or in lieu of a long course of parenteral therapy. Rarely oral therapy can be used as primary therapy if the causative organism is susceptible to an oral agent such as fluoroquinolone.

Issues related to treatment of infections associated with hardware are discussed further separately. (See "Nonvertebral osteomyelitis in adults: Treatment", section on 'Presence of orthopedic hardware'.)

Surgery — Indications for surgery include [1,20]:

Presence of neurologic deficits

Presence of epidural or paravertebral abscesses in need of drainage (see "Spinal epidural abscess")

Threatened or actual cord compression due to vertebral collapse and/or spinal instability

Progression, persistence, or recurrence of disease (as documented by persistently positive blood cultures or worsening pain) despite appropriate antimicrobial therapy

There are no randomized trials evaluating surgical management of vertebral osteomyelitis [1]. Placing hardware in the setting of spinal infection has raised concern regarding recurrent or chronic infection due to adherence of bacteria to foreign material. It is common practice to administer an additional six-week 'tail' of oral antibiotics, although there is little evidence to guide management. One retrospective study has indicated that, when spinal stabilization is required, timely instrumentation may be safe in the setting of appropriate selection and duration of antimicrobial therapy [66]. Another study reported outcomes for 100 patients with vertebral osteomyelitis who underwent a variety of surgical procedures, which were highly variable; approximately one-quarter of patients had residual pain and a similar proportion required repeat surgery [67].

In contrast to the preceding study, a report of 42 patients with vertebral osteomyelitis who required surgery, 40 had complete resolution of their deficits with no recurrences following a two-stage procedure that included anterior debridement and strut grafting followed by delayed instrumented posterior fusions [68]. Patients received an average of 14.4 days of intravenous antibiotics after the anterior debridement and six weeks of intravenous therapy following the posterior instrumentation (see 'Prognosis' below). In a systematic review of nine observational studies with 299 patients, reinfection rates were similar for patients undergoing acute versus delayed instrumentation (15.7 versus 15.9 percent), although the analysis was limited by lack of clarity regarding the type of surgery performed in included studies [69].

In general, paravertebral abscess can be managed by CT-guided catheter drainage. Epidural abscess in the setting of neurologic deficit should be managed with surgical intervention; this may include open drainage, bone debridement, and interbody fusion (with or without bone grafting and posterior instrumentation). (See "Spinal epidural abscess".)

Adjunctive measures — Bed rest and analgesics are generally helpful in managing pain after the diagnosis is established. A fitted back brace often provides substantial back relief and enhances mobility for patients with severe pain. Clinicians should have a low threshold for referral to a specialist pain service.

Early bed rest may be particularly important, especially in lumbar osteomyelitis. When the patient is upright, the whole weight of the upper body is transmitted to the point of active infection. It is our practice to put patients with severe pain to bed for at least 10 days and use intensive in-bed, nonweight-bearing physical therapy and long-acting oral analgesics. In such circumstances, prophylactic measures for prevention of deep venous thrombosis are warranted. (See "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults".)

PROGNOSIS — The most serious complication of vertebral osteomyelitis is neurologic impairment secondary to either abscess formation or bony collapse. Most patients have gradual improvement in back pain after therapy is begun, and the pain typically disappears after bone fusion occurs. However, back pain can persist. The best way to reduce the morbidity and mortality associated with vertebral osteomyelitis is to minimize the time between the onset of symptoms and the initiation of appropriate therapy.

The long-term outcome in vertebral osteomyelitis was evaluated in a retrospective study of 253 patients with vertebral osteomyelitis with median duration of follow-up 6.5 years (range 2 days to 38 years) [70]. Relapse occurred in 14 percent and residual symptoms occurred in 31 percent; 11 percent died (all-cause mortality). Surgery was performed in 43 percent of patients and was successful in 79 percent of cases. Independent risk factors for death or residual symptoms included neurologic compromise at the time of diagnosis (eg, motor weakness, spinal instability, paralysis), nosocomial acquisition of infection, and delay in diagnosis. The results of this study need to be interpreted with caution since cases were collected over a long time period (1950 to 1994), which means that some cases occurred prior to the development of modern imaging and diagnostic techniques.

In another study including 260 patients with vertebral osteomyelitis, three-quarters of treatment failures occurred within 4.7 months of diagnosis [5]. Multivariate analysis indicated that infection with S. aureus was associated with increased risk of relapse. Longer-term outcomes included neurological deficit (16 percent) and persistent back pain (32 percent).

Major depression is a well-recognized complication of chronic back pain (about a third of patients) and is an important potential long-term consequence [71,72].

Overall morbidity and mortality tends to increase with age [73]; this may be related to delayed diagnosis (especially when people have background degenerative spinal disease or have communication difficulties), multiple comorbidities, and age-related frailty [74]. Older patients are also more likely to have concomitant infective endocarditis (IE); in one study including 351 patients with vertebral osteomyelitis (85 of whom were ≥75 years of age), IE was diagnosed in 37 percent of patients ≥75 years compared with 14 percent of patients <75 years [75].

Mortality — Prior to the discovery of antibiotics, vertebral osteomyelitis was fatal in approximately 25 percent of cases [14]. Mortality due to vertebral osteomyelitis in the antibiotic era is less than 5 percent, and the rate of residual neurologic deficits among survivors is less than 7 percent. Delays in diagnosis can lead to disabling complications [1].

In a large retrospective study including more than 7000 patients with vertebral osteomyelitis, in-hospital mortality (6 percent) was largely determined by comorbidities including diabetes, end-stage kidney disease, cirrhosis, and malignancy [76].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Osteomyelitis and prosthetic joint infection in adults" and "Society guideline links: Outpatient parenteral antimicrobial therapy".)

SUMMARY AND RECOMMENDATIONS

Pathogenesis – Vertebral osteomyelitis occurs by three basic routes: hematogenous spread from a distant site or focus of infection (this is the most common mechanism), direct inoculation from trauma or spinal surgery, and contiguous spread from adjacent soft tissue infection. (See 'Mechanisms of infection' above.)

Microbiology – The most important infecting organism in vertebral osteomyelitis is Staphylococcus aureus, accounting for more than 50 percent of cases. Other pathogens include nonpyogenic streptococci, pyogenic streptococci including groups B and C/G, enteric gram-negative bacilli, Candida spp, Pseudomonas aeruginosa, Brucella spp, and Mycobacterium tuberculosis. (See 'Microbiology' above.)

Clinical features – The major clinical manifestation of vertebral osteomyelitis is back or neck pain, with or without fever. The most common clinical finding is local tenderness to percussion over the involved posterior spinous processes. The most common laboratory abnormalities are elevated erythrocyte sedimentation rate and C-reactive protein. (See 'Clinical features' above.)

Diagnosis – Vertebral osteomyelitis should be suspected on the basis of clinical features and radiographic studies (magnetic resonance imaging is the most sensitive radiographic technique) and confirmed by biopsy of the infected intervertebral disc space or vertebral bone. Blood cultures are positive in up to 50 to 70 percent of patients; a biopsy may not be necessary in patients with clinical and radiographic findings typical of vertebral osteomyelitis and positive blood cultures with a likely pathogen. (See 'Diagnosis' above.)

Diagnostic evaluation – Every effort should be made to identify the pathogen(s) before starting antimicrobial treatment. In patients with suspected vertebral osteomyelitis, we favor the clinical approach described above and summarized in the algorithm (algorithm 1). Evaluation for concurrent infectious endocarditis may be warranted in select patients. (See 'Suggested clinical approach' above.)

Role of surgery – Most cases of vertebral osteomyelitis respond to antimicrobial therapy. Surgery is necessary in a minority of patients with vertebral osteomyelitis; prompt surgery is warranted for patients with focal neurologic deficits, epidural or paravertebral abscess, and/or cord compression. (See 'Treatment' above and 'Surgery' above.)

Antibiotic therapy – If possible, antimicrobial therapy should be withheld until a microbiologic diagnosis is confirmed. Clinical exceptions include neurologic compromise and sepsis; in these circumstances, empiric antibiotic therapy is warranted. Choice of antibiotic therapy should be guided by biopsy or blood culture results if available. For patients with negative culture results, empiric treatment is warranted based on the most likely organisms to cause infection. (See 'Clinical approach' above.)

Duration of antibiotic therapy – We routinely treat for a minimum duration of six weeks. Longer duration of therapy (at least eight weeks) is warranted for patients with undrained paravertebral abscess(es) and/or infection due to drug-resistant organisms (including methicillin-resistant S. aureus). The duration of therapy should be tailored to individual circumstances during the course of clinical follow-up. (See 'Duration of therapy and follow-up' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Malcolm McDonald, MD, who contributed to an earlier version of this topic review.

  1. Berbari EF, Kanj SS, Kowalski TJ, et al. 2015 Infectious Diseases Society of America (IDSA) Clinical Practice Guidelines for the Diagnosis and Treatment of Native Vertebral Osteomyelitis in Adults. Clin Infect Dis 2015; 61:e26.
  2. Sapico FL, Montgomerie JZ. Pyogenic vertebral osteomyelitis: report of nine cases and review of the literature. Rev Infect Dis 1979; 1:754.
  3. Issa K, Diebo BG, Faloon M, et al. The Epidemiology of Vertebral Osteomyelitis in the United States From 1998 to 2013. Clin Spine Surg 2018; 31:E102.
  4. Conan Y, Laurent E, Belin Y, et al. Large increase of vertebral osteomyelitis in France: a 2010-2019 cross-sectional study. Epidemiol Infect 2021; 149:e227.
  5. Gupta A, Kowalski TJ, Osmon DR, et al. Long-term outcome of pyogenic vertebral osteomyelitis: a cohort study of 260 patients. Open Forum Infect Dis 2014; 1:ofu107.
  6. Pigrau C, Rodríguez-Pardo D, Fernández-Hidalgo N, et al. Health care associated hematogenous pyogenic vertebral osteomyelitis: a severe and potentially preventable infectious disease. Medicine (Baltimore) 2015; 94:e365.
  7. Cahill DW, Love LC, Rechtine GR. Pyogenic osteomyelitis of the spine in the elderly. J Neurosurg 1991; 74:878.
  8. McHenry MC, Rehm SJ, Krajewski LP, et al. Vertebral osteomyelitis and aortic lesions: case report and review. Rev Infect Dis 1991; 13:1184.
  9. Falagas ME, Bliziotis IA, Mavrogenis AF, Papagelopoulos PJ. Spondylodiscitis after facet joint steroid injection: a case report and review of the literature. Scand J Infect Dis 2006; 38:295.
  10. Hooten WM, Mizerak A, Carns PE, Huntoon MA. Discitis after lumbar epidural corticosteroid injection: a case report and analysis of the case report literature. Pain Med 2006; 7:46.
  11. Ju KL, Kim SD, Melikian R, et al. Predicting patients with concurrent noncontiguous spinal epidural abscess lesions. Spine J 2015; 15:95.
  12. Batson OV. THE FUNCTION OF THE VERTEBRAL VEINS AND THEIR ROLE IN THE SPREAD OF METASTASES. Ann Surg 1940; 112:138.
  13. HENRIQUES CQ. Osteomyelitis as a complication in urology; with special reference to the paravertebral venous plexus. Br J Surg 1958; 46:19.
  14. Kulowski J. Pyogenic vertebral osteomyelitis of the spine: An analysis and discussion of 102 cases. J Bone Joint Surg 1936; 1:343.
  15. Larson DL, Hudak KA, Waring WP, et al. Protocol management of late-stage pressure ulcers: a 5-year retrospective study of 101 consecutive patients with 179 ulcers. Plast Reconstr Surg 2012; 129:897.
  16. Türk EE, Tsokos M, Delling G. Autopsy-based assessment of extent and type of osteomyelitis in advanced-grade sacral decubitus ulcers: a histopathologic study. Arch Pathol Lab Med 2003; 127:1599.
  17. Park KH, Cho OH, Jung M, et al. Clinical characteristics and outcomes of hematogenous vertebral osteomyelitis caused by gram-negative bacteria. J Infect 2014; 69:42.
  18. Bass SN, Ailani RK, Shekar R, Gerblich AA. Pyogenic vertebral osteomyelitis presenting as exudative pleural effusion: a series of five cases. Chest 1998; 114:642.
  19. Michel-Batôt C, Dintinger H, Blum A, et al. A particular form of septic arthritis: septic arthritis of facet joint. Joint Bone Spine 2008; 75:78.
  20. Lew DP, Waldvogel FA. Osteomyelitis. Lancet 2004; 364:369.
  21. Nolla JM, Ariza J, Gómez-Vaquero C, et al. Spontaneous pyogenic vertebral osteomyelitis in nondrug users. Semin Arthritis Rheum 2002; 31:271.
  22. Murillo O, Grau I, Gomez-Junyent J, et al. Endocarditis associated with vertebral osteomyelitis and septic arthritis of the axial skeleton. Infection 2018; 46:245.
  23. Chong BSW, Brereton CJ, Gordon A, Davis JS. Epidemiology, Microbiological Diagnosis, and Clinical Outcomes in Pyogenic Vertebral Osteomyelitis: A 10-year Retrospective Cohort Study. Open Forum Infect Dis 2018; 5:ofy037.
  24. Patzakis MJ, Rao S, Wilkins J, et al. Analysis of 61 cases of vertebral osteomyelitis. Clin Orthop Relat Res 1991; :178.
  25. Koubaa M, Maaloul I, Marrakchi C, et al. Spinal brucellosis in South of Tunisia: review of 32 cases. Spine J 2014; 14:1538.
  26. Lemaignen A, Ghout I, Dinh A, et al. Characteristics of and risk factors for severe neurological deficit in patients with pyogenic vertebral osteomyelitis: A case-control study. Medicine (Baltimore) 2017; 96:e6387.
  27. Torda AJ, Gottlieb T, Bradbury R. Pyogenic vertebral osteomyelitis: analysis of 20 cases and review. Clin Infect Dis 1995; 20:320.
  28. Beronius M, Bergman B, Andersson R. Vertebral osteomyelitis in Göteborg, Sweden: a retrospective study of patients during 1990-95. Scand J Infect Dis 2001; 33:527.
  29. Carragee EJ, Kim D, van der Vlugt T, Vittum D. The clinical use of erythrocyte sedimentation rate in pyogenic vertebral osteomyelitis. Spine (Phila Pa 1976) 1997; 22:2089.
  30. Unkila-Kallio L, Kallio MJ, Eskola J, Peltola H. Serum C-reactive protein, erythrocyte sedimentation rate, and white blood cell count in acute hematogenous osteomyelitis of children. Pediatrics 1994; 93:59.
  31. Diffre C, Jousset C, Roux AL, et al. Predictive factors for positive disco-vertebral biopsy culture in pyogenic vertebral osteomyelitis, and impact of fluoroscopic versus scanographic guidance. BMC Infect Dis 2020; 20:512.
  32. Lee SA, Chiu CK, Chan CYW, et al. The clinical utility of fluoroscopic versus CT guided percutaneous transpedicular core needle biopsy for spinal infections and tumours: a randomized trial. Spine J 2020; 20:1114.
  33. Weihe R, Taghlabi K, Lowrance M, et al. Culture Yield in the Diagnosis of Native Vertebral Osteomyelitis: A Single Tertiary Center Retrospective Case Series With Literature Review. Open Forum Infect Dis 2022; 9:ofac026.
  34. Gras G, Buzele R, Parienti JJ, et al. Microbiological diagnosis of vertebral osteomyelitis: relevance of second percutaneous biopsy following initial negative biopsy and limited yield of post-biopsy blood cultures. Eur J Clin Microbiol Infect Dis 2014; 33:371.
  35. An HS, Seldomridge JA. Spinal infections: diagnostic tests and imaging studies. Clin Orthop Relat Res 2006; 444:27.
  36. Dagirmanjian A, Schils J, McHenry M, Modic MT. MR imaging of vertebral osteomyelitis revisited. AJR Am J Roentgenol 1996; 167:1539.
  37. Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR imaging findings in spinal infections: rules or myths? Radiology 2003; 228:506.
  38. Kayani I, Syed I, Saifuddin A, et al. Vertebral osteomyelitis without disc involvement. Clin Radiol 2004; 59:881.
  39. Carragee EJ. The clinical use of magnetic resonance imaging in pyogenic vertebral osteomyelitis. Spine (Phila Pa 1976) 1997; 22:780.
  40. Post MJ, Quencer RM, Montalvo BM, et al. Spinal infection: evaluation with MR imaging and intraoperative US. Radiology 1988; 169:765.
  41. Gold RH, Hawkins RA, Katz RD. Bacterial osteomyelitis: findings on plain radiography, CT, MR, and scintigraphy. AJR Am J Roentgenol 1991; 157:365.
  42. Abe E, Yan K, Okada K. Pyogenic vertebral osteomyelitis presenting as single spinal compression fracture: a case report and review of the literature. Spinal Cord 2000; 38:639.
  43. Markus HS. Haematogenous osteomyelitis in the adult: a clinical and epidemiological study. Q J Med 1989; 71:521.
  44. Censullo A, Vijayan T. Using Nuclear Medicine Imaging Wisely in Diagnosing Infectious Diseases. Open Forum Infect Dis 2017; 4:ofx011.
  45. Palestro CJ, Torres MA. Radionuclide imaging in orthopedic infections. Semin Nucl Med 1997; 27:334.
  46. Hadjipavlou AG, Cesani-Vazquez F, Villaneuva-Meyer J, et al. The effectiveness of gallium citrate Ga 67 radionuclide imaging in vertebral osteomyelitis revisited. Am J Orthop (Belle Mead NJ) 1998; 27:179.
  47. Palestro CJ. Radionuclide imaging of osteomyelitis. Semin Nucl Med 2015; 45:32.
  48. Kouijzer IJE, Scheper H, de Rooy JWJ, et al. The diagnostic value of 18F-FDG-PET/CT and MRI in suspected vertebral osteomyelitis - a prospective study. Eur J Nucl Med Mol Imaging 2018; 45:798.
  49. Marschall J, Bhavan KP, Olsen MA, et al. The impact of prebiopsy antibiotics on pathogen recovery in hematogenous vertebral osteomyelitis. Clin Infect Dis 2011; 52:867.
  50. Chang CY, Simeone FJ, Nelson SB, et al. Is Biopsying the Paravertebral Soft Tissue as Effective as Biopsying the Disk or Vertebral Endplate? 10-Year Retrospective Review of CT-Guided Biopsy of Diskitis-Osteomyelitis. AJR Am J Roentgenol 2015; 205:123.
  51. Saravolatz LD 2nd, Labalo V, Fishbain J, et al. Lack of effect of antibiotics on biopsy culture results in vertebral osteomyelitis. Diagn Microbiol Infect Dis 2018; 91:273.
  52. Kim CJ, Song KH, Park WB, et al. Microbiologically and clinically diagnosed vertebral osteomyelitis: impact of prior antibiotic exposure. Antimicrob Agents Chemother 2012; 56:2122.
  53. Rawlings CE 3rd, Wilkins RH, Gallis HA, et al. Postoperative intervertebral disc space infection. Neurosurgery 1983; 13:371.
  54. McGahan JP, Dublin AB. Evaluation of spinal infections by plain radiographs, computed tomography, intrathecal metrizamide, and CT-guided biopsy. Diagn Imaging Clin Med 1985; 54:11.
  55. Lecouvet F, Irenge L, Vandercam B, et al. The etiologic diagnosis of infectious discitis is improved by amplification-based DNA analysis. Arthritis Rheum 2004; 50:2985.
  56. Choi SH, Sung H, Kim SH, et al. Usefulness of a direct 16S rRNA gene PCR assay of percutaneous biopsies or aspirates for etiological diagnosis of vertebral osteomyelitis. Diagn Microbiol Infect Dis 2014; 78:75.
  57. Ma C, Wu H, Chen G, et al. The potential of metagenomic next-generation sequencing in diagnosis of spinal infection: a retrospective study. Eur Spine J 2022; 31:442.
  58. Pigrau C, Almirante B, Flores X, et al. Spontaneous pyogenic vertebral osteomyelitis and endocarditis: incidence, risk factors, and outcome. Am J Med 2005; 118:1287.
  59. Koslow M, Kuperstein R, Eshed I, et al. The unique clinical features and outcome of infectious endocarditis and vertebral osteomyelitis co-infection. Am J Med 2014; 127:669.e9.
  60. Bernard L, Dinh A, Ghout I, et al. Antibiotic treatment for 6 weeks versus 12 weeks in patients with pyogenic vertebral osteomyelitis: an open-label, non-inferiority, randomised, controlled trial. Lancet 2015; 385:875.
  61. Park KH, Cho OH, Lee JH, et al. Optimal Duration of Antibiotic Therapy in Patients With Hematogenous Vertebral Osteomyelitis at Low Risk and High Risk of Recurrence. Clin Infect Dis 2016; 62:1262.
  62. Babouee Flury B, Elzi L, Kolbe M, et al. Is switching to an oral antibiotic regimen safe after 2 weeks of intravenous treatment for primary bacterial vertebral osteomyelitis? BMC Infect Dis 2014; 14:226.
  63. Li HK, Rombach I, Zambellas R, et al. Oral versus Intravenous Antibiotics for Bone and Joint Infection. N Engl J Med 2019; 380:425.
  64. Khan MH, Smith PN, Rao N, Donaldson WF. Serum C-reactive protein levels correlate with clinical response in patients treated with antibiotics for wound infections after spinal surgery. Spine J 2006; 6:311.
  65. Kowalski TJ, Berbari EF, Huddleston PM, et al. Do follow-up imaging examinations provide useful prognostic information in patients with spine infection? Clin Infect Dis 2006; 43:172.
  66. Park KH, Cho OH, Lee YM, et al. Therapeutic outcomes of hematogenous vertebral osteomyelitis with instrumented surgery. Clin Infect Dis 2015; 60:1330.
  67. Valancius K, Hansen ES, Høy K, et al. Failure modes in conservative and surgical management of infectious spondylodiscitis. Eur Spine J 2013; 22:1837.
  68. Dimar JR, Carreon LY, Glassman SD, et al. Treatment of pyogenic vertebral osteomyelitis with anterior debridement and fusion followed by delayed posterior spinal fusion. Spine (Phila Pa 1976) 2004; 29:326.
  69. Sanda M, Singleton A, Yim J, et al. The effect of instrumentation staging on patient outcomes in pyogenic vertebral osteomyelitis: A systematic review. N Am Spine Soc J 2021; 8:100083.
  70. McHenry MC, Easley KA, Locker GA. Vertebral osteomyelitis: long-term outcome for 253 patients from 7 Cleveland-area hospitals. Clin Infect Dis 2002; 34:1342.
  71. Von Korff M, Crane P, Lane M, et al. Chronic spinal pain and physical-mental comorbidity in the United States: results from the national comorbidity survey replication. Pain 2005; 113:331.
  72. Demyttenaere K, Bruffaerts R, Lee S, et al. Mental disorders among persons with chronic back or neck pain: results from the World Mental Health Surveys. Pain 2007; 129:332.
  73. Zarrouk V, Gras J, Dubée V, et al. Increased mortality in patients aged 75 years or over with pyogenic vertebral osteomyelitis. Infect Dis (Lond) 2018; 50:783.
  74. Amadoru S, Lim K, Tacey M, Aboltins C. Spinal infections in older people: an analysis of demographics, presenting features, microbiology and outcomes. Intern Med J 2017; 47:182.
  75. Courjon J, Lemaignen A, Ghout I, et al. Pyogenic vertebral osteomyelitis of the elderly: Characteristics and outcomes. PLoS One 2017; 12:e0188470.
  76. Akiyama T, Chikuda H, Yasunaga H, et al. Incidence and risk factors for mortality of vertebral osteomyelitis: a retrospective analysis using the Japanese diagnosis procedure combination database. BMJ Open 2013; 3.
Topic 7663 Version 49.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟