Complications, Length of Hospital Stay, and Cost of Care after Surgery for Pyogenic Spondylodiscitis.

BACKGROUND: Infectious Spondylodiscitis is a heterogeneous disease usually affecting a fragile patient population with multiple comorbidities. Therefore, surgical and medical complications are important considerations before initiating treatment. METHODS: This retrospective analysis included data of 218 patients who underwent surgical treatment for pyogenic Spondylodiscitis between 2008 and 2016. Groups were divided into length of hospital stay (LOS) (group I ≤21 days and group II>21 days). Analysis included patient age, gender, Charlson comorbidity index, smoking, obesity, osteoporosis, colonization with multidrug-resistant bacteria, preoperative neurologic deficit, pre- and postoperative inflammation markers (CRP and WBC), duration of surgery, number of operated segments, vertebrectomy, and postoperative medical and surgical complications. The case value for each patient expressed in Euro was retrieved from hospital records and included in the analysis. RESULTS: Duration of stay after surgical treatment of Spondylodiscitis was ≤21 days (range: 4-21 days; mean: 16 days) in 41% of patients and >21 days (range: 22-162 days; mean: 41 days) in 59% of the patients. Multivariate analysis showed that both medical complications (odds ratio [OR]: 2.62; 95% confidence interval [CI]: 1.24-5.56; p=0.012) and surgical site infection (OR: 6.04; 95% CI: 2.35-15.51; p<0.001) were independently associated with a long hospital stay. Case values averaged at €21,667±1,579 (minimum: €2,888; maximum: €203,802) and correlated significantly with the length of hospital stay (Pearson's correlation coefficient: 0.681; p<0.05). The occurrence of a postoperative complication increased the cost of care significantly from €17,790 to 24,527 on average (p=0.025). CONCLUSIONS: This study provides benchmark data for patients treated surgically for Spondylodiscitis. Surgical site infection and medical complications are the main drivers of prolonged hospital stays and cost of care.

The Role of Diskectomy in Reducing Infectious Complications after Surgery for Lumbar Spondylodiscitis.

BACKGROUND: Surgery for pyogenic Spondylodiscitis as an adjunct to antibiotic therapy is an established treatment. However, the technique and extent of surgical debridement remains a matter of debate. Some propagate diskectomy in all cases. Others maintain that stand-alone instrumentation is sufficient. METHODS: We reviewed charts of patients who underwent instrumentation for pyogenic Spondylodiscitis with a minimum follow-up of 1 year. Patients were stratified according to whether they underwent diskectomy plus instrumentation or posterior instrumentation alone. Outcome measures included the need for surgical revision due to recurrent epidural intraspinal infection, wound revision, and construct failure. RESULTS: In all, 257 patients who underwent surgery for pyogenic Spondylodiscitis were identified. Diskectomy and interbody procedure (group A) was performed in 102 patients, while 155 patients underwent instrumentation surgery for Spondylodiscitis without intradiskal debridement (group B). The mean age was 67 ± 12 years, and 102 patients (39.7%) were females. No significant differences were found in the need for epidural abscess recurrence therapy (group A [2.0%] and 5 cases in group B [3%; p = 0.83]) and construct failure (p = 0.575). The need for wound revisions showed a tendency toward higher rates in the posterior instrumentation-only group, which failed to reach significance (p = 0.078). CONCLUSIONS: Overall, intraspinal relapse of surgically treated pyogenic diskitis was low in our retrospective series. The choice of surgical technique was not associated with a significant difference. However, a somewhat higher rate of wound infections requiring revision in the group where no diskectomy was performed has to be weighed against a longer duration of surgery in an already ill patient population.

Postoperative Quality of Life in Patients with Pyogenic Spondylodiscitis.

BACKGROUND: Pyogenic spondylodiskitis affects a fragile patient population frequently fraught with severe comorbidities. Data on long-term outcomes, especially for patients undergoing surgery, are scarce. The aim of this study was to assess the long-term quality of life after surgical instrumentation. METHODS: Data of 218 patients who were treated for spondylodiskitis at our institution between January 2008 and July 2017 were reviewed. In-hospital death and mortality rates at 1 year and follow-up were assessed. A survey was conducted using the following questionnaires: Oswestry Disability Index (ODI), Short Form Work Ability Index (SF-WAI), 36-Item Short Form Health Survey (SF-36), and Short Form McGill Pain Questionnaire (SF-MPQ). We investigated the correlation between the assessed variables and clinical data including patient age, comorbidity score at admission, number of operated levels, corpectomy, and length of hospital stay. RESULTS: In-hospital mortality rate was 1.8% and 1-year mortality rate was 5.5%. At the final follow-up (mean 7 ± 6 years), the mortality rate was 45.4%. Seventy-four patients were lost to follow-up or refused to participate in the study. Forty-four patients responded to the survey and had a mean age of 73 years and mean follow-up of 7 ± 2 years. In the ODI questionnaire, disability grades were classified as minimal (23%), moderate (21%), severe (19%), complete (33%), and bed bound (4%). We found a significant correlation between inability to return to work and severe disability on ODI (p < 0.001), as well as a low score on any component of the SF-36 (p < 0.05). CONCLUSION: Despite low in-hospital and 1-year mortality rates, patients with surgically treated pyogenic spondylodiskitis are prone to long-term limitation in all domains of quality of life, especially in physical health and work ability.

Do we underdiagnose osteoporosis in patients with pyogenic spondylodiscitis?

OBJECTIVE: Pyogenic spondylodiscitis affects a fragile patient population. Surgical treatment in cases of instability entails instrumentation, and loosening of this instrumentation is a frequent occurrence in pyogenic spondylodiscitis. The authors therefore attempted to investigate whether low bone mineral density (BMD)-which is compatible with the diagnosis of osteoporosis-is underdiagnosed in patients with pyogenic spondylodiscitis. How osteoporosis was treated and how it affected implant stability were further analyzed. METHODS: Charts of patients who underwent operations for pyogenic spondylodiscitis were retrospectively reviewed for clinical data, prior medical history of osteoporosis, and preoperative CT scans of the thoracolumbar spine. In accordance with a previously validated high-fidelity opportunistic CT assessment, average Hounsfield units (HUs) in vertebral bodies of L1 and L4 were measured. Based on the validation study, the authors opted for a conservative cutoff value for low BMD, being compatible with osteoporosis ≤ 110 HUs. Baseline and outcome variables, including implant failure and osteoporosis interventions, were entered into a multivariate logistic model for statistical analysis. RESULTS: Of 200 consecutive patients who underwent fusion surgery for pyogenic spondylodiscitis, 64% (n = 127) were male and 66% (n = 132) were older than 65 years. Seven percent (n = 14) had previously been diagnosed with osteoporosis. The attenuation analysis revealed HU values compatible with osteoporosis in 48% (95/200). The need for subsequent revision surgery due to implant failure showed a trend toward an association with estimated low BMD (OR 2.11, 95% CI 0.95-4.68, p = 0.067). Estimated low BMD was associated with subsequent implant loosening (p < 0.001). Only 5% of the patients with estimated low BMD received a diagnosis and pharmacological treatment of osteoporosis within 1 year after spinal instrumentation. CONCLUSIONS: Relying on past medical history of osteoporosis is insufficient in the management of patients with pyogenic spondylodiscitis. This is the first study to identify a substantially missed opportunity to detect osteoporosis and to start pharmacological treatment after surgery for prevention of implant failure. The authors advocate for routine opportunistic CT evaluation for a better estimation of bone quality to initiate diagnosis and treatment for osteoporosis in these patients.

CCR6 (CC Chemokine Receptor 6) Is Essential for the Migration of Detrimental Natural Interleukin-17-Producing γδ T Cells in Stroke.

BACKGROUND AND PURPOSE: Immune-mediated tissue damage after stroke evolves within the first days, and lymphocytes contribute to the secondary injury. Our goal was to identify T-cell subpopulations, which trigger the immune response. METHODS: In a model of experimental stroke, we analyzed the immune phenotype of interleukin-17 (IL-17)-producing γδ T cells and explored the therapeutic potential of neutralizing anti-IL-17 antibodies in combination with mild therapeutic hypothermia. RESULTS: We show that brain-infiltrating IL-17-positive γδ T cells expressed the Vγ6 segment of the γδ T cells receptor and were largely positive for the chemokine receptor CCR6 (CC chemokine receptor 6), which is a characteristic for natural IL-17-producing γδ T cells. These innate lymphocytes are established as major initial IL-17 producers in acute infections. Genetic deficiency in Ccr6 was associated with diminished infiltration of natural IL-17-producing γδ T cells and a significantly improved neurological outcome. In the ischemic brain, IL-17 together with tumor necrosis factor-α triggered the expression of CXC chemokines and neutrophil infiltration. Therapeutic targeting of synergistic IL-17 and tumor necrosis factor-α pathways by IL-17 neutralization and therapeutic hypothermia resulted in additional protective effects in comparison to an anti-IL-17 antibody treatment or therapeutic hypothermia alone. CONCLUSIONS: Brain-infiltrating IL-17-producing γδ T cells belong to the subset of natural IL-17-producing γδ T cells. In stroke, these previously unrecognized innate lymphocytes trigger a highly conserved immune reaction, which is known from host responses toward pathogens. We demonstrate that therapeutic approaches targeting synergistic IL-17 and tumor necrosis factor-α pathways in parallel offer additional neuroprotection in stroke.