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Objective:To investigate the risk factors and interventions for surgical failure of spinal tuberculosis (STB).Methods:A total of 317 STB patients aged from 11 to 86 years with an average age of 53.5±16.7 years, who received debridement and fusion with bone grafting from January 2013 to December 2019, were retrospectively analyzed, including 206 males and 111 females. The follow-up duration was at least 1 year. During the follow-up, any one of the following 1)-3) was defined as surgical failure, namely 1) the same tubercular lesion treated by surgery more than 2 times, 2) the number of unplanned readmissions related to tubercular lesion≥1, 3) drug-resistant STB or delayed healing, recurrent lesion with cold abscess/sinus tract, combined with other bacterial infection, or loosening of internal fixation. The other cases were regarded as "curative" cases. Patients' symptoms, medication history, auxiliary examination and surgical plan were collected for univariate analysis. Further, the potential risk factors for surgical failure were analyzed by binary Logistic regression. Failed cases were treated with etiological intervention, such as puncture pumping pus or debridement or revision. The necrosis or granulation tissue was collected and further detected by tuberculosis culture, metagenomic next-generation sequencing (mNGS) and real-time fluorescent quantitative PCR (RT-qPCR).Results:There were 27 cases with surgical failure. Abscess or sinus tract formation was developed in 17 cases, which accounted for 63% (17/27). Among these patients, there were 3 cases of resistance to isoniazid or rifampicin and 2 cases of resistance to isoniazid and rifampicin (multidrug resistance, MDR). Seventeen cases were treated by anti-tuberculosis treatment, while 14 cases by puncture drainage (or puncture catheter irrigation) and 3 cases by debridement and suturing. Seven cases with wound infection or poor healing accounted for 26% (7/27). Among them, 5 kinds of pathogens were detected, none of which showed tuberculosis drug resistance. All of them were treated by anti-infection and debridement suturing, while 2 of them were treated with internal fixation removal. Three cases (11%, 3/27) with internal fixation loosening were treated by revision surgery. There was statistically significant difference between the failed group and the cured group in involved multi-/jumping segment, history of type 2 diabetes, a history of more than three basic diseases, CRP at one week after surgery, WBC at one week after surgery, time of first dose, operation duration and intraoperative blood loss ( P<0.10). Binary Logistic regression analysis showed that multi-/jumping segment ( OR= 3.513, P=0.047), CRP at one week after surgery ( OR=1.021, P=0.005), first dose time ≥20 weeks ( OR=2.895, P=0.039), blood loss ≥800 ml ( OR=5.950, P=0.001) and more than three basic diseases involved ( OR=3.671, P=0.027) were independent risk factors for surgical failure. Conclusion:Early diagnosis, especially the diagnosis of drug-resistant STB and standardized anti-tubercular treatment, should be carried out effectively. Puncture and drainage of abscess is an effective therapy to treat the cases with abscess/sinus tract formation. Some cases involved multi-/jumping segments could be with higher risk of failure after internal fixation. Thus, they should be treated individually with emphasis on the segmental stability reconstruction.
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Objective: To study the local vascular remodeling, inflammatory response, and their correlations following acute spinal cord injury (SCI) with different grades, and to assess the histological changes in SCI rats. Methods: One hundred and sixteen adult female Sprague Dawley rats were randomly divided into 4 groups ( n=29). The rats in sham group were received laminectomy only. A standard MASCIS spinal cord compactor was applied with drop height of 12.5, 25.0, or 50.0 mm to establish the mild, moderate, or severe SCI model, respectively. Quantitative rat endothelial cell antigen 1 (RECA1) and CD68 positive areas and the correlations were studied by double immunofluorescent (DIF) staining at 12 hours, 24 hours, 3 days, 7 days, and 28 days following SCI. Moreover, qualitative neurofilament-H (NF-H) and glial fibrillary acidic protein (GFAP) positive glial cells were studied by DIF staining at 28 days. ELISA was used to detect the levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 in spinal cord homogenates at 12 hours, 24 hours, and 3 days, and the correlations between TNF-α, IL-1β, or IL-6 levels and microvascular density (RECA1) were accordingly studied. Moreover, the neural tissue integrity and neuron damage were assessed by HE staining at 12 hours, 24 hours, 3 days, 7 days, and 28 days, and Nissl's staining at 28 days following SCI, respectively. Results: DIF staining revealed that the ratio of RECA1 positive area was the highest in moderate group, higher in mild and severe groups, and the lowest in sham group with significant differences between groups ( P0.05). There was no significant correlation between the RECA1 and CD68 expressions in sham group at different time points ( P>0.05). At 12 and 24 hours after SCI, the RECA1 and CD68 expressions in mild and moderate groups showed significant positive correlations ( P0.05). No significant correlations between the RECA1 and CD68 expressions was shown in all SCI groups at 3 days and in severe group at 7 days ( P>0.05), while the negative correlations were shown in mild and moderate groups at 7 days, and in all SCI groups at 28 days ( P0.05). The differences in TNF-α, IL-1β, and IL-6 levels between SCI groups at different time points were sinificant ( P0.05). Three inflammatory factors were all significantly correlated with the microvascular density grades ( P<0.05). Histological analysis indicated that the damage to spinal cord tissue structure correlated with the extent of SCI. In severe group, local hemorrhage, edema, and infiltration of inflammatory cells were found the most drastic, the grey/white matter boundary was disappeared concurrently with the formation of cavity and shortage of normal neurons. Conclusion: In the acute stage following mild or moderate SCI, progressively aggravated injury result in higher microvessel density and increased inflammation. However, at the SCI region, the relation between microvessel density and inflammation inverse with time in the different grades of SCI. Accordingly, the destruction of neural structures positively relate to the grades of SCI and severity of inflammation.