Posterior Decompression and Fusion: Whole-Spine Functional and Clinical Outcomes

The mobility of the spine and the change in the angle of the curvatures are directly related to spinal pain and spinal stenosis. The aim of the study was the evaluation of morphology and mobility of the spine in patients who were subjected to decompression and posterior fusion with pedicle screws. The treatment group consisted of 20 patients who underwent posterior fixation of lumbar spine (one and two level fusion). The control group consisted of 39 healthy subjects. Mobility and curvatures of the spine were measured with a non-invasive device, the Spinal Mouse. Pain was evaluated with the Visual Analogue Scale (VAS). The Oswestry Disability Index (ODI) and the SF-36 were used to evaluate the degree of the functional disability and the quality of life, respectively. The measurements were recorded preoperatively and at 3, 6 and 12 months postoperatively. The mobility of the lumbar spine in the sagittal plane increased (p = 0.009) at 12 months compared to the measurements at 3 months. The mobility of the thoracic spine in the frontal plane increased (p = 0.009) at 12 months compared to the preoperative evaluation. The results of VAS, ODI and SF-36 PCS improved significantly (p<0.001). The levels of fusion exhibited a strong linear correlation (r = 0.651, p = 0.002) with the total trunk inclination in the upright position. Although pain, quality of life and spinal mobility in the sagittal and frontal planes significantly improved in the treatment group, these patients still had limited mobility and decreased curves/angles values compared to control group

The Effects of Amicar and TXA on Lumbar Spine Fusion in an Animal Model

Study Design. Animal model. Objective. To determine whether aminocaproic acid (Amicar) and tranexamic acid (TXA) inhibit spine fusion volume. Summary of Background Data. Amicar and TXA are antifibrinolytics used to reduce perioperative bleeding. Prior in vitro data showed that antifibrinolytics reduce osteoblast bone mineralization. This study tested whether antifibrinolytics Amicar and TXA inhibit spine fusion. Methods. Posterolateral L4-L6 fusion was performed in 50 mice, randomized into groups of 10, which received the following treatment before and after surgery: (1) saline; (2) TXA 100 mg/kg; (3) TXA 1000 mg/kg; (4) Amicar 100 mg/kg; and (5) Amicar 1000 mg/kg. High-resolution plane radiography was performed after 5 weeks and micro-CT (computed tomography) was performed at the end of the 12-week study. Radiographs were graded using the Lenke scale. Micro-CT was used to quantify fusion mass bone volume. One-way analysis of variance by ranks with Kruskal-Wallis testing was used to compare the radiographical scores. One-way analysis of variance with least significant difference post hoc testing was used to compare the micro-CT bone volume. Results. The average +/- standard deviation bone volume/total volume (%) measured in the saline, TXA 100 mg/kg, TXA 1000 mg/kg, Amicar 100 mg/kg, and Amicar 1000 mg/kg groups were 10.8 +/- 2.3%, 9.7 +/- 2.2%, 13.4 +/- 3.2%, 15.5 +/- 5.2%, and 17.9 +/- 3.5%, respectively. There was a significant difference in the Amicar 100 mg/kg (P < 0.05) and Amicar 1000 mg/kg (P < 0.001) groups compared with the saline group. There was greater bone volume in the Amicar groups compared with the TXA group (P < 0.001). There was more bone volume in the TXA 1000 mg/kg group compared with TXA 100 mg/kg (P < 0.05) but the bone volume in neither of the TXA groups was different to saline (P = 0.49). There were no between-group differences observed using plane radiographical scoring. Conclusion. Amicar significantly "enhanced" the fusion bone mass in a dose-dependent manner, whereas TXA did not have a significant effect on fusion compared with saline control. These data are in contrast to prior in vitro data that antifibrinolytics inhibit osteoblast bone mineralization

The effects of Amicar and TXA on lumbar spine fusion in an animal model

Objective. To determine whether aminocaproic acid (Amicar) and tranexamic acid (TXA) inhibit spine fusion volume. Summary of Background Data. Amicar and TXA are antifibrinolytics used to reduce perioperative bleeding. Prior in vitro data showed that antifibrinolytics reduce osteoblast bone mineralization. This study tested whether antifibrinolytics Amicar and TXA inhibit spine fusion. Methods. Posterolateral L4–L6 fusion was performed in 50 mice, randomized into groups of 10, which received the following treatment before and after surgery: (1) saline; (2) TXA 100 mg/kg; (3) TXA 1000 mg/kg; (4) Amicar 100 mg/kg; and (5) Amicar 1000 mg/kg. High-resolution plane radiography was performed after 5 weeks and micro-CT (computed tomography) was performed at the end of the 12-week study. Radiographs were graded using the Lenke scale. Micro-CT was used to quantify fusion mass bone volume. One-way analysis of variance by ranks with Kruskal-Wallis testing was used to compare the radiographical scores. One-way analysis of variance with least significant difference post hoc testing was used to compare the micro-CT bone volume. Results. The average ± standard deviation bone volume/total volume (%) measured in the saline, TXA 100 mg/kg, TXA 1000 mg/kg, Amicar 100 mg/kg, and Amicar 1000 mg/kg groups were 10.8 ± 2.3%, 9.7 ± 2.2%, 13.4 ± 3.2%, 15.5 ± 5.2%, and 17.9 ± 3.5%, respectively. There was a significant difference in the Amicar 100 mg/kg (P < 0.05) and Amicar 1000 mg/kg (P < 0.001) groups compared with the saline group. There was greater bone volume in the Amicar groups compared with the TXA group (P < 0.001). There was more bone volume in the TXA 1000 mg/kg group compared with TXA 100 mg/kg (P < 0.05) but the bone volume in neither of the TXA groups was different to saline (P = 0.49). There were no between-group differences observed using plane radiographical scoring. Conclusion. Amicar significantly “enhanced” the fusion bone mass in a dose-dependent manner, whereas TXA did not have a significant effect on fusion compared with saline control. These data are in contrast to prior in vitro data that antifibrinolytics inhibit osteoblast bone mineralization