The aim of this study was to report the restoration of normal vertebral morphology and the absence of curve progression after the removal of instrumentation in AIS patients that underwent posterior correction of the deformity by a common all-screws construct without fusion. A series of 36 AIS immature patients (Risser 3 or less) were included in the study. Instrumentation was removed once the maturity stage was complete (Risser 5). The curve correction was assessed pre- and postoperatively, before instrumentation removal, directly post-removal, and more than two years after instrumentation was removed. Epiphyseal vertebral growth modulation was assessed by the coronal wedging ratio (WR) at the apical level of the main curve (MC). The mean preoperative coronal Cobb was corrected from 53.7° ± 7.5 to 5.5° ± 7.5° (89.7%) at the immediate postop. After implant removal (31.0 ± 5.8 months), the MC was 13.1°. T5–T12 kyphosis showed significant improvement from 19.0° before curve correction to 27.1° after implant removal (p < 0.05). Before surgery, the WR was 0.71 ± 0.06, and after removal, 0.98 ± 0.08 (p < 0.001). At the end of the follow-up, the mean sagittal range of motion (ROM) of the T12-S1 segment was 51.2 ± 21.0°. The SRS-22 scores improved from 3.31 ± 0.25 preoperatively to 3.68 ± 0.25 at the final assessment (p < 0.001). In conclusion, a fusionless posterior approach using common all-pedicle screws correctly constructed satisfactory scoliotic main curves and permitted the removal of instrumentation once bone maturity was reached. The final correction was highly satisfactory, and an acceptable ROM of the previously lower instrumented segments was observed.
In healthy subjects, respiratory maximal volumes are highly dependent on the sagittal range of motion of the T7–T10 segment. In AIS, the abolition of T7–T10 dynamics related to the stiffness induced by the apex region in Lenke IA curves could harm ventilation during maximal breathing. The aim of this study was to analyze the dynamics of the thoracic spine during deep breathing in AIS patients and in healthy matched controls. This is a cross-sectional, case–control study. 20 AIS patients (18 girls, Cobb angle, 54.7 ± 7.9°; Risser 1.35 ± 1.2) and 15 healthy volunteers (11 girls) matched in age (12.5 versus 15.8 years mean age) were included. In AIS curves, the apex was located at T8 (14) and T9 (6). Conventional sagittal radiographs of the whole spine were performed at maximal inspiration and exhalation. The ROM of each spinal thoracic functional segment (T1–T7, T7–T10, T10–T12) and the global T1–T12 ROM were measured. In healthy subjects, the mean T1–T12 ROM during forced breathing was 16.7 ± 3.8. AIS patients showed a T1–T12 ROM of 1.1 ± 1.5 (p < 0.05), indicating a sagittal stiffness of the thoracic spine. A wide T7–T10 ROM (15.3 ± 3.0) was found in healthy controls (91.6% of the T1–T12 ROM). AIS patients showed only 0.4 ± 1.4 ROM at T7–T10 (36.4% of the T1–T12 ROM) (p < 0.001). There was a linear relationship between the magnitude of T7–T10 kyphosis in maximal exhalation and both FVC (% of predicted FVC) and FEV1. In conclusion, Lenke 1A AIS patients show a restriction of the thoracic spine motion with an almost complete abolition of T7–T10 ROM, a crucial segment for deep breathing. T7–T10 stiffness could explain the ventilatory limitations found in AIS patients.
To analyze the dynamics of the thoracic spine during deep breathing in AIS patients and in healthy matched controls.Case-control cross-sectional study. 20 AIS patients (18 girls, Cobb angle, 54.7±7.9°; Risser 1.35±1.2) and 15 healthy volunteers (11 girls) matched in age (12.5 versus 15.8 yr. mean age) were included. In AIS curves, the apex was located in T8 (14) and T9 (6). Conventional sagittal radiographs of the whole spine were performed at maximal inspiration and expiration. The ROM of each spinal thoracic functional segment (T1-T7, T7-T10, T10-T12), the global T1–T12 ROM were measured. Respiratory function was assess by forced vital capacity (FVC), expiratory volume (FEV1), FEV1/FVC, inspiratory vital capacity (IVC) and peak expiratory flow (PEF).In healthy subjects, the mean T1–T12 ROM during forced breathing was 16.7±3.8. AIS patients showed a T1-T12 ROM of 1.1±1.5 (p<0.05) indicating a sagittal stiffness of thoracic spine. A wide T7–T10 ROM (15.3±3.0) was found in healthy controls (91.6% of the T1–T12 ROM). AIS patients showed only 0.4±1.4 ROM at T7-T10 (36.4% of the T1–T12 ROM) (p<0.001). There was a significant correlation between T7-T10 ROM and IVC.Lenke 1A AIS patients show a restriction of the thoracic spine motion with an almost complete abolition of T7-T10 ROM, a crucial segment participating in the deep breathing. T7-T10 stiffness could explain the ventilatory limitations found in AIS patients.
The aim of this study was to analyze the impact of surgical correction of the thoracic deformity on the cardiorespiratory function of patients with moderate-severe Scheuermann’s hyperkyphosis (SK). A series of 23 adolescents with SK who underwent surgery through an only posterior approach using all pedicle screw constructs were included in the study. Cardiorespiratory parameters were measured during a maximal exercise tolerance test before and 2 years after surgery. Heart rate, oxygen saturation (SatO2), maximum oxygen uptake (VO2 max), ventilatory capacity at maximal exercise (VEmax), and energy costs were recorded. There were statistically significant differences in the forced vital capacity (FVC) (P < 0.05), total VO2max (ml/min) (P < 0.01), maximum expired volume (VEmax) per minute (P < 0.01) and cardiovascular efficiency (HR/VO2 ratio) (P < 0.05). None of these changes were clinically relevant. There were no changes in the VO2max per kg of body mass. The magnitude of the kyphosis correction did not correlate with the change in normalized VO2max or VEmax. In conclusion, patients with moderate-severe SK improve their baseline respiratory limitations and the tolerance to maximum exercise 2 years after surgery. However, the slight cardiorespiratory functional improvements should not necessarily be attributed to the surgery, and could also be caused solely by the residual growth of the lungs and thorax. Furthermore, respiratory functional changes are under thresholds considered as clinically relevant.
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