Adjacent Level Tuberculous Spondylodiscitis Leading to Proximal Junctional Kyphosis: Rare and Unusual Presentation.

Background: Vertebral osteomyelitis manifesting as a compression fracture misdiagnosed in the setting of steroid-induced or senile osteoporosis is very rare, although such patients are prone to infection or reactivation, as their immune system is exhausted. Spondylodiscitis occurring at adjacent levels following instrumented spinal fusion leading to pathologic fracture and proximal junctional failure, especially caused by tuberculosis, to our knowledge, has not been discussed in the literature.
Methods: In case 1, a 61-year-old woman with osteoporotic T12 collapse was treated with corpectomy, anterior reconstruction, and posterior fixation from T9-L2. Initial biopsy and culture were normal. She presented 4 months later with compression fracture of T8; T8 corpectomy with anterior reconstruction and proximal extension of the construct was performed. In case 2, a 65-year-old woman with multiple comorbidities and osteoporotic L1 compression fracture was treated with L1 corpectomy, anterior reconstruction, and posterior instrumentation from T11-L3. She presented 4 months later with T10 vertebral body acute collapse; 2-stage anterior corpectomy and reconstruction was performed. In both cases, probing the affected vertebral body yielded pus. Pus and bone tissue samples sent for culture and histopathologic examination were positive for tuberculosis suggesting tuberculous spondylitis in both cases.
Results: In both patients, tuberculous spondylodiscitis at the proximal adjacent level was diagnosed <1 year after the initial spinal surgery. Neither patient had a previous history of pulmonary or extrapulmonary tuberculosis. They were successfully treated with antituberculous therapy and proximal extension of the construct with anterior reconstruction.
Conclusions: Adjacent segment spondylodiscitis should be suspected and intraoperative biopsy must be considered for histopathologic and microbiologic examination to rule out subclinical infection in immunosuppressed patients with multiple comorbidities. Management should be individualized, considering the context of infection, causative organism, extent of bone destruction, and neurologic involvement.
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