The prevalence of proximal junctional kyphosis (PJK) ranges between 5% and 40% and can have a substantial clinical impact, particularly after adult spinal deformity (ASD) surgery [1,2], due to the complications that PJK poses. Adults with deformities have junctional issues adjacent to spinal fusion, one of which is PJK, which can be treated without surgery in many cases. However, in those that do, the rate of revision surgery is reported to range from 1.4% to 55%, with the primary indications being pain, neurological deficits or resulting positive sagittal malalignment [2,3].

While various definitions of PJK after ASD surgery are reported in the literature, a common definition is a kyphotic angle greater than 10° between the upper-most instrumented vertebra (UIV) and upper-most instrumented vertebra +2 (UIV+2) with an increase from preoperative alignment of at least 10° in kyphosis [4,5]. A recent review showed that PJK most commonly (66%) occurs within three months of surgery, and 80% of patients will develop it within 18 months [2]. Given the high incidence of PJK and its potentially disabling impact, the prevention of PJK is of considerable interest to spine surgeons. Accordingly, in-depth studies have been carried out and have identified various risk factors for the development of PJK.

Recently, there has been an emphasis on the importance of sagittal alignment. Patients who developed PJK after ASD surgery exhibited considerable correction of the sagittal vertical axis (SVA). Thus, the risk of PJK increased with greater baseline deformity and consequently large surgical correction [6,7]. Other variables that affected PJK were high body mass index (BMI), older age, smoking and low bone density [8-10]. Whether the level of the UIV and the number of fused vertebrae increases the risk of developing PJK is currently being debated [8,11,12]. Additionally, other risk factors include implant construct rigidity and combined anterior/posterior fusion, as well as the use of iliac fixation [1].

If validated, the association between sacral extension (SE) and PJK is of significant importance (Fig. 1). Lumbosacral fusion rates after long posterior fusions for ASD have been shown to vary substantially, and isolated fusions to the sacrum without supplemental iliac fixation can be challenging due to implant failure (screw loosening) and sacral fractures [13-15]. Furthermore, sacroiliac joint overloading and degeneration due to increased strain of the fusions may be potential sources of long-term complaints after extension to S1 [16]. Consequently, many surgeons combine S1 screws with iliac screws to help protect S1 pedicle screws that favor lumbo-sacral fusion rates [17-19]. Halting at the lumbar spine during ASD surgery, without sacral or even pelvic fixation, increases the strain at the lumbo-pelvic junction, which may cause distal junctional kyphosis.

There is evidence that sacral fixation is a risk factor for PJK. Multivariable logistic regression analysis revealed sacral fixation to be independently associated with PJK [20]. Further, Bridwell et al. [8] analyzed a consecutive series of 90 adult idiopathic/degenerative scoliosis patients and reported that a PJK angle ≥20°, although uncommon in daily practice, was significantly (p=0.029) associated with fixation to the sacrum combined with iliac screws. In daily practice, we found patients without PJK following sacral fixation as well as many patients with PJK following SE (Fig. 2). We, therefore, hypothesized that SE increases the risk of PJK.

The objective of this study was to analyze the role of SE, in the development of PJK following ASD surgery, in patients with additional iliac fixation compared to lumbar fixation (LF), with the lowest instrumented vertebra (LIV) L5 or higher (Fig. 3).

This study was performed in accordance with local ethics committee guidelines. No explicit approval was needed for this study. Institutional review board approval was obtained before study initiation. Informed consent was obtained from each patient before being included into the database.

Propensity matching, summarized in Table 1, led to the enrollment of 178 patients, 89 each assigned to the SE and LF groups. No significant differences were identified between the SE and LF groups with respect to patient age, UIV, PI–LL or the change PI–LL 1Y.

Gender distribution was similar in both groups: 77% and 78% of patients were female in the SE and LF groups, respectively. The mean BMI was 27.7±6.1 kg/m² (SE) and 26.6±7.0 kg/m² (LF) and did not significantly differ between groups (p=0.306). The number of levels fused was 12.3±4.5 (SE) and 10.7±4.3 (LF), and the difference was statistically significant (p=0.013).

In this study, we found that SE during ASD surgery was not a risk factor for PJK, and therefore refuted our hypothesis that the increased rigidity of the construct with a resulting higher load for the UIV+2 would result in higher overall PJK rate following SE. Though, our results contradict previously findings, it should be noted that others including Bridwell et al. [8] focused on the PJK angle in adult scoliosis patients, rather than SE as a potential risk factor for PJK. Inoue et al. [10] showed increased PJK rates in patients with fusion down to the sacrum after ASD realigning surgery.

In contrast to Inoue et al. [10], our data suggest that PJK is not generally linked to sacral extension except in patients with an UIV of T9–T12.

Nevertheless, there is evidence that fusion from the sacrum to the upper thoracic spine is associated with higher PJK rates compared to the lower thoracic spine, although not been shown by the results of our study [27]. However, this is still under debate. O'Shaughnessy et al. [28] found a decreased risk (10% versus 18%) of PJK when fusing to the upper thoracic spine. Annis et al. [29] performed a retrospective review of 135 cases and performed univariate and multivariate regression analysis. Similar to our data, high rates of PJK were found in patients with an UIV at T10. Instrumentation down to the pelvis was identified as risk factor for PJK [29].

Moreover, because fusion rates after sacral fixation vary considerably. Iliac screws help to offload strain from sacral screws at the lumbopelvic junction after ASD surgery [17-19]. Although it is known from previous studies that iliac screws are beneficial for fusion and protect sacral screws from loosening in spinal deformity surgery, potential problems exist. Lean patients have been reported to complain of implant prominence and focal pain, resulting in the removal of implanted iliac screws in up to 22% of cases within 2 years, though this may be technique-dependent [13-15].

While the overall rate of PJK was similar for SE and LF patients in our study, analyzing the different UIV levels did show a significantly higher rate of PJK between T9 and T12 after SE compared to LF. Therefore, the risk of PJK after SE in ASD surgery might potentially be higher for low UIV levels. The reason might be that the remaining flexibility of the lower lumbar spine disc spaces, especially L5/S1, after LF protects UIV+2 from strain, causing PJK.

Our study findings contradict the commonly assumed notion of increased PJK rates after SE/pelvic fixation due to increased rigidity, especially when using iliac screws. Instead, an increased PJK rate after SE was found only for UIV levels between T9 and T12. Therefore, our results might support surgeons’ tendency to use SE, at least in constructs involving the upper thoracic spine, instead of, for example, stopping at L5 with an increased risk for postoperative adjacent disc disease at this level [17-19].

Many risk factors have been identified to be associated with the development of PJK; however, development of prediction models is still in early stages with individual precise prediction remaining difficult so far [30].

Although this study involved comprehensive propensity matching, the methodology has limitations. We included patients with 1 year postoperative follow-up following ASD surgery. Though most PJK cases should have been detected within this period, it is plausible that a few cases were overlooked. Propensity matching was based on a sample size that was restricted to two databases, one with prospective data and the other with retrospective data. Additionally, with our limited knowledge of PJK, it is currently impossible to match for all risk factors. Moreover, we do not present data on the clinical relevance of PJK in our patient cohort.

This study focused on the role of SE in ASD surgery related to the potential risk for the development of PJK. We found that in a propensity-matched set of patients, SE increased the risk for PJK only with UIV levels at T9–T12 compared to LF. However, sacral fixation in our study was not a general risk factor for PJK.