Background: Thoracic spinal tuberculosis (TB) causes destruction of the spine and compression of the adjacent spinal cord. This study aimed to identify the risk factors for neurological deterioration in patients with thoracic spinal TB to guide decision-making regarding immediate surgery before the onset of weakness.Methods: Demographic, clinical, laboratory, and radiologic (x-ray and magnetic resonance imaging) data of 115 patients with active thoracic spinal TB were retrospectively analyzed. Patients with neurological status categorized as Frankel grades A, B, or C (n = 71) were classified as the neurological deficit group, while those with neurological status categorized as Frankel grades D and E (n = 44) constituted the control group. Univariate and multivariate logistic regression analyses were used to predict the risk factors for neurological deficits.Results: The mean patient age was 57.2 years. The most common lesion location was the distal thoracic region (T9-L1; 62.6%). Paradiscal involvement was the most common form of involvement (73%). In the univariate analysis, the significant risk factors associated with neurological worsening were overweight (body mass index [BMI] >25), C-reactive protein level > 20 mg/L, panvertebral involvement, loss of cerebrospinal fluid posterior to the cord, cord signal changes, and canal compromise. The multivariate analysis revealed that only BMI >25 (adjusted OR = 16.18; 95% CI 1.60-163.64; P = 0.018), cord signal changes (adjusted OR = 7.42; 95% CI 1.85-29.74; P = 0.005), and canal encroachment >50% ( adjusted OR = 51.86; 95% CI 5.53-486.24; P = 0.001) were independent risk factors for predicting the risk of neurological deficits.Conclusions: Overweight (BMI >25), cord signal changes, and canal compromise >50% significantly predicted neurological deficits in patients with thoracic spinal TB. Prompt spinal surgery should be considered before progressive worsening of the neurological condition in patients with all of these risk factors.Clinical Relevance: Predictive factors for neurological deficits in thoracic spinal TB were determined. Overweight, cord signal changes, and canal compromise >50% showed predictive value. These factors can help identify patients who require early surgical intervention.
Purpose: We aimed to present a case of spondylodiscitis with extensive spinal epidural abscess (SEA) that was successfully treated using a minimally invasive technique supplemented with fluoroscopically guided catheter drainage and systemic antibiotic therapy. Methods: A 58-year-old man presented with severe back pain and high-grade fever. He had progressive radiating pain in the lower extremities, followed by sensory deficits in both the lower limbs. Laboratory investigations revealed leukocytosis and high C-reactive protein levels. Magnetic resonance imaging of the thoracic and lumbar regions revealed an extremely large posterior SEA that extends from T6 to S1. As the patient did not respond to intravenous antibiotics alone, he underwent skipped laminectomies with fluoroscopically guided catheter drainage and irrigation. Results: Escherichia coli were detected in purulent material from the abscess. His clinical symptoms were dramatically and immediately relieved after the procedure. The patient achieved complete neurological recovery after six weeks of antibiotic therapy. Conclusions: We suggest a limited approach to the spine with the use of small radio-opaque catheters, representing an interesting option to effectively drain extensive SEAs with less morbidity than the conventional open extensive surgical drainage.
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