Compensatory mechanisms recruited against proximal junctional kyphosis by patients instrumented from the thoracolumbar junction to the iliac.

Abstract

The compensatory mechanisms recruited by un-instrumented patients against sagittal imbalance are well documented. However, there is a lack of information regarding instrumented patients. We performed aretrospective analysis of data collected prospectively in a multicenter adult spinal deformity database. We included patients suffering PJK/PJF after (T8-L2) to iliac instrumentation with minimum two-year follow-up. We measured quantitative sagittal spinopelvic and qualitative sagittal distribution parameters in the immediate postoperative period (6w) and at the time of PJK/PJF appearance. We analyzed how these parameters changed comparing these two time points with univariate and multivariate logistic regression analyses. A total of 69 patients were included. Two different patterns at PJK/PJF were found: 36 patients activated compensation (defined as an increase in pelvic retroversion (ΔRPV > 5º), and 33 did not (ΔRPV < 5º). The difference in behavior relied mostly on the amount of not surgically restored pelvic rotation at 6w (OR: 0.6; CI95%: 0.4-9.2; P = 0.017). Non-compensators had less rotation reserve (PTx100/PI = 33.9% vs 47.8%;P < 0.001) associated with worse 6w relative pelvic version and lower lumbar arc restoration, worse 6w relative sagittal alignment and GAP-score, compared with compensators (P < 0.001). Compensators' response was based on pelvic retroversion, causing lower lumbar arc decrease, lumbar apex caudal migration, and upper lumbar arc posterior inclination. Despite compensation, a thoracic kyphosis increase in both upper and lower arches gradually evolved into a PJK/PJF. Non-compensators did not react to PJK/PJF, which forced them into kyphosis from the lumbar apex and extending cranially, mainly throughout the upper thoracic arc. In patients fused from the TL junction to the iliac, those having greater postoperative pelvic rotation reserve showed greater capacity to recruit compensatory mechanisms against PJK/PJF.