Slipped capital femoral epiphysis: A modern treatment protocol

The treatment of a patient with slipped capital femoral epiphysis begins with an early diagnosis and accurate classification. On the basis of symptom duration, clinical findings and radiographs, slipped capital femoral epiphysis is classified as pre-slip, acute, acute-on-chronic and chronic. The long-term outcome of slipped capital femoral epiphysis is directly related to severity and the presence or absence of avascular necrosis and/or chondrolysis. Therefore, the first priority in the treatment of slipped capital femoral epiphysis is to avoid complications while securing the epiphysis from further slippage. Medical treatment of patients with acute and acute-on-chronic slipped capital femoral epiphysis, as well as those presented in pre-slip stage, is the safest, although time-consuming. Manipulations, especially forced and repeated, are not recommended due to higher avascular necrosis risk. The use of intraoperative fluoroscopy to assist in the placement of internal fixation devices has markedly increased the success of surgical treatment. Controversy remains as to whether the proximal femoral epiphysis in severe, chronic slipped capital femoral epiphysis should be realigned by extracapsular osteotomies or just fixed in situ. The management protocol for slipped capital femoral epiphysis depends on the experience of the surgeon, motivation of the patient and technical facilities

Spinal localization of Paget disease: Case report

INTRODUCTION Paget disease, localized on thoracal vertebrae, presents a significant challenge in diagnostics and treatment. Presenting with progressive neurological symptoms, it has a broad differential diagnostic spectrum and requires additional radiological, neurological and endocrinological evaluation. Besides drug therapy, an operative decompression of nerve elements is performed when indicated. CASE OUTLINE We present a case of an older male patient complaining of chronic progressive pain localized at fourth and fifth thoracal vertebrae, with slight but progressive hypertonus and hyperreflection of leg muscles, including no plantar response. Vertebral biopsy indicated parathyreoid disturbance, excluded by further endocrinological analyses. At that point a corporectomy of fourth and fifth vertebrae and titanium cage spondylodesis of adjacent levels was performed, with pathological findings suggesting Paget disease. Postoperatively, there was initial significant neurological improvement; unfortunately, 2.5 years after the operation a relapse of the disease developed with gibbus deformity. Further treatment was surgical in two stages (first by decompression, and later by broad laminectomy), resulting in partial neurological recovery. CONCLUSION Spinal localization of Paget disease as a monoostotic form must be considered in all cases of progressive neurological impairment accompanied by biochemical disturbances in blood and urine, and with radiologically evident deformity, pathological fracture or neoplastic destruction of vertebra. A combination of medicamentous and surgical treatment should significantly improve neurological condition