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MANAGEMENT OF SPONTANEOUS PYOGENIC SPONDYLODISCITIS: A
DESCRIPTIVE COHORT STUDY
Sattorov Bekhruz Kobilovich
Assistant of Bukhara state medical institute named after Abu ali Ibn Sino
Email: sattorovbehruz804@gmail.com
https://doi.org/10.5281/zenodo.13923605
Background
Spondylodiscitis (SD) refers to an infection affecting the intervertebral discs, vertebral
endplates, and vertebral bodies, sometimes spreading to the spinal canal. The annual incidence
of infectious SD in Western countries ranges from 0.4 to 2.4 per 100,000 people, with numbers
increasing due to the aging population, a rise in immune-compromised patients, and a growing
number of spinal surgeries.
In cases of spontaneous SD, the infection typically spreads hematogenously, most often
originating from the genitourinary tract, skin, soft tissues, respiratory tract, gastrointestinal
tract, or oral cavity. Alternatively, infection can be directly introduced into the disc space during
invasive spinal procedures, complicating 0.1–4% of cases with septic discitis, which accounts
for 20–30% of all SD cases. Globally, tuberculosis is a leading cause of spontaneous SD, while
the most common non-tuberculous pathogen is Staphylococcus aureus, responsible for nearly
half of the cases, followed by Gram-negative bacilli (e.g., Escherichia coli), and
streptococci/enterococci.
Several risk factors are associated with an increased risk of infectious SD, including
advanced age, diabetes, immunosuppressive therapy, renal failure, intravenous drug use, and
liver cirrhosis.
Pain is the most common symptom of SD, occurring in 90% of patients. Fever is present
in about 60%, and other constitutional symptoms, such as weight loss and anorexia, may also
occur. Neurological deficits vary between 10% and 50% of patients, often due to delayed
diagnosis, which can lead to neural compromise. Erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP) are elevated in most cases, whereas total leukocyte count (TLC) is raised
in only about half of cases and is less useful for monitoring than ESR and CRP.
Magnetic resonance imaging (MRI) is the most sensitive imaging method for early
detection of SD, allowing for the evaluation of neural structures and paraspinal infection
pockets. Computed tomography (CT) is useful for assessing bone destruction and guiding disc
biopsies. The lumbar spine is the most commonly affected region in non-tuberculous SD,
followed by the thoracic and cervical spine.
Identifying the causative organism is crucial, though it is not always possible. Blood
cultures are positive in about 50% of cases, while CT-guided biopsy can reveal an organism in
up to 70% of cases. However, prior antibiotic use significantly reduces the yield of both blood
cultures and biopsy results. Infection may lead to structural collapse and kyphosis, potentially
causing neural compromise, and epidural abscesses can also contribute to this. Chronic
illnesses, such as diabetes, increase the risk of epidural extension, and the extent of neurological
damage suggests vascular compromise in addition to mechanical compression.
The cornerstone of SD management is antimicrobial therapy, with antibiotic selection based on
culture results. In cases where no pathogen is identified, empirical antibiotics are used.
Treatment duration varies, but a minimum of 8–12 weeks is generally recommended to reduce
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the risk of relapse. ESR and CRP levels, along with clinical improvement, are used to monitor
treatment response. A reduction in CRP by 50% or more, combined with decreased pain and
the absence of neurological deficits, is a good indicator for switching to oral antibiotics.
Surgery is typically indicated for patients with neurological compromise, progressive
deformity, persistent severe pain, or epidural abscesses. Surgical intervention allows for neural
decompression, spinal stabilization, and the opportunity for an open biopsy, which offers better
bacterial yield and may facilitate earlier patient mobilization.
Methods
This study is a retrospective review of a prospective registry of patients with spine
infections treated at Republican Scientific-Practical Center of Neurosurgery between 2019 and
2023. We included patients aged 18 years and older, from both sexes, who were diagnosed with
spontaneous spondylodiscitis based on clinical, radiological, and laboratory data. Spontaneous
SD refers to SD occurring in patients without any prior spinal surgery or percutaneous
procedures. The diagnosis was made in patients with significant axial back or neck pain,
accompanied by MRI findings of abnormal hyperintense fluid signals in at least one disc space,
along with irregular adjacent endplates and subchondral edema. Any presence of epidural
abscesses, collections, or deformities was also recorded. Inflammatory markers such as ESR,
CRP, and TLC were documented, with an elevated CRP being required for diagnosis. Patients
with tuberculous SD were excluded due to their distinct disease course and extended treatment
requirements.
Patient demographics, comorbidities, clinical, radiological, and surgical data were
reviewed at the start of therapy and at intervals over a minimum follow-up period of one year.
Disease resolution was defined by symptomatic improvement, normalization of ESR and CRP
levels, and at least one follow-up MRI demonstrating resolution of radiological signs of disease.
Pain intensity was measured using the Visual Analogue Scale (VAS) on a scale from 1 to
10, where 1 represents minimal pain and 10 represents the most severe pain imaginable. VAS
was used during hospital admission and subsequent clinic visits to assess pain. Additionally,
the Oswestry Disability Index (ODI) questionnaire was used to evaluate the level of disability
at the start of treatment and one year post-treatment. The version of the ODI used was from the
American Academy of Orthopaedic Surgeons (AAOS) website, which was administered in
Arabic by a resident or surgeon who recorded the responses. The questionnaire consists of 10
items, each with six possible answers, scored from 0 to 5. The total score was interpreted into
a disability level based on the sum of the 10 items.
Similarly, the Neck Disability Index (NDI), a modified version of the ODI designed for neck
and upper back pain, was used for patients with cervical and upper dorsal spine disease. The
NDI follows the same scoring system as the ODI. Patients with missing primary data (ODI/NDI)
were excluded from the study.
Results
A total of 38 patients were included in the study, comprising 14 males and 24 females,
with a mean age of 49 years (range: 22–70). The demographic, clinical, and radiological data
prior to treatment are summarized in Table 2. Twenty-three patients underwent surgical
treatment from the outset, while 15 patients were initially treated with medical management,
including bed rest and antibiotics. The decision to begin with conservative medical treatment
or surgery was made by the treating surgeon. Factors such as motor deficits, epidural abscesses,
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and kyphosis at presentation were significantly associated with the decision to assign patients
to the surgical group rather than medical treatment alone (p = 0.002, 0.0001, and 0.01,
respectively). In fact, all patients who received surgery at the outset had at least one of these
conditions: epidural abscess, significant spinal deformity, or neurological deficit.
The mean baseline CRP level in the medical group was 53 mg/L, compared to 72 mg/L in
the surgical group, although this difference was not statistically significant (p = 0.1). The
baseline Oswestry Disability Index (ODI) or Neck Disability Index (NDI) was significantly higher
in the surgical group compared to the medical group (p = 0.0002). Likewise, the mean baseline
Visual Analogue Scale (VAS) score was significantly higher in the surgical group than in the
medical group (p = 0.0001).
Of the 23 patients who underwent surgery initially, 8 out of the 15 patients in the medical
group (53%) experienced deterioration between weeks 2 and 4. The deterioration included
increased pain, with a VAS score of 10 in one patient, the development of new motor deficits in
four patients, and worsening kyphosis, with or without increased pain on serial imaging, in
three patients.
Discussion
Despite advancements in diagnostic methods, antibiotic therapies, and surgical
techniques, infectious spondylodiscitis remains a complex condition to manage. First, diagnosis
can be delayed because the pain is often initially misinterpreted as degenerative spine disease
or masked by symptoms of the primary infection source. Second, even when clinical and
radiological diagnoses are made, microbiological confirmation is not always possible. Tissue
biopsies and blood cultures often fail to identify a causative pathogen, resulting in the
prolonged use of broad-spectrum antibiotics. In our series, the causative organism was
identified in approximately 55% of cases, allowing for a targeted antibiotic approach. The
distribution of microorganisms in our study was consistent with previous reports, with
Staphylococcus aureus being the most common, followed by Escherichia coli, while other
pathogens were much less frequent. The relatively high rate of undetermined bacterial
identification (37%) is primarily due to prior antibiotic treatment prescribed by referring
physicians in an attempt to slow bacterial progression. We believe that identifying the bacterial
pathogen is crucial, even if it means delaying the start of antibiotic therapy.
Non-specific laboratory tests, such as C-reactive protein (CRP) and erythrocyte
sedimentation rate (ESR), have proven to be essential initial steps for diagnosing an
inflammatory condition. Both CRP and ESR are elevated in nearly all cases of acute
spondylodiscitis. In our study, CRP was a reliable, though non-specific, marker of infection,
being highly elevated in all cases and correlating well with treatment response. At eight weeks
of treatment, CRP levels had significantly decreased compared to pre-treatment levels. Notably,
the baseline CRP level in the group that started with medical management but later required
surgical intervention (mean baseline CRP = 73) was significantly higher than in the group that
successfully continued conservative treatment (mean baseline CRP = 30) (p = 0.036). White
blood cell counts, on the other hand, were high-normal to slightly elevated (mean 10,950
cells/µL). Although the total leukocyte count (TLC) at eight weeks showed a statistically
significant reduction (mean 8660 cells/µL) compared to pre-treatment levels, the change was
not clinically significant, making TLC less useful than CRP for monitoring treatment response.
Conclusions
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Infectious spondylodiscitis continues to pose significant diagnostic and therapeutic
challenges. In uncomplicated cases, treatment typically begins with systemic antibiotics and
rest, but close follow-up is essential to identify any treatment failures or disease progression.
Investigating larger case series could provide insights into potential predictors of medical
treatment failure, such as baseline CRP levels, the specific spinal levels affected, and existing
comorbidities. Conversely, patients presenting with initial spinal instability, progressive
deformity, or neurological deficits resulting from active neural compression are suitable
candidates for surgical debridement and decompression, which may include instrumented
fusion. In both our series and many others, the use of instrumentation did not appear to
increase the risk of persistent infection. However, the optimal duration of antibiotic therapy
and the best surgical approach remain unclear. Randomized controlled trials are necessary to
better define these aspects of treatment.
References:
1.
Hadjipavlou AG, Mader JT, Necessary JT, Muffoletto AJ. Hematogenous pyogenic spinal
infections and their surgical management. Spine (Phila Pa 1976). 2000;25(13):1668–79.
2.
Cottle L, Riordan T. Infectious spondylodiscitis. J Infect. 2008;56(6):401–12.
3.
Lam KS, Webb JK. Discitis. Hosp Med. 2004;65(5):280–6.
4.
Silber JS, Anderson DG, Vaccaro AR, Anderson PA, McCormick P. Management of
postprocedural discitis. Spine J. 2002;2(4):279–87.
5.
Gasbarrini AL, Bertoldi E, Mazzetti M, Fini L, Terzi S, Gonella F, et al. Clinical features,
diagnostic and therapeutic approaches to haematogenous vertebral osteomyelitis. Eur Rev Med
Pharmacol Sci. 2005;9(1):53–66.
6.
Friedman JA, Maher CO, Quast LM, McClelland RL, Ebersold MJ. Spontaneous disc space
infections in adults. Surg Neurol. 2002;57(2):81–6.
7.
Lee JH, Kim J, Kim TH. Clinical outcomes in older patients aged over 75 years who
underwent early surgical treatment for pyogenic vertebral osteomyelitis. J Clin Med.
2021;10(22):5451.
8.
Govender S. Spinal infections. J Bone Joint Surg Br. 2005;87-B(11):1454–8.
9.
Colmenero JD, Jimenez-Mejias ME, Sanchez-Lora FJ, Reguera JM, Palomino-Nicas J, Martos
F, et al. Pyogenic, tuberculous, and brucellar vertebral osteomyelitis: a descriptive and
comparative study of 219 cases. Ann Rheum Dis. 1997;56(12):709–15.
10.
Dhodapkar MM, Patel T, Rubio DR. Imaging in spinal infections: current status and future
directions. N Am Spine Soc J. 2023;16: 100275.