Clinical StudyThe impact of obesity on compensatory mechanisms in response to progressive sagittal malalignment
Introduction
The rising prevalence of obesity within modern industrialized society is cause for serious public health concern and has prompted deepened attention from the orthopedic surgical community. The effects of obesity on musculoskeletal systemic degeneration, including early degenerative disease and functional impairment, are well established; however, these associations are less investigated in the context of spinal deformity. Given concurrently increasing rates of obesity and adult spinal deformity (ASD) in the United States, a deeper understanding of obesity's role as a supplemental driver of sagittal deformity is of significant value [1].
Recent research involving compensatory mechanisms used in response to progressive sagittal malalignment highlights the importance of minimizing energetic expenditure to maintain an erect, upright posture [2], [3], [4]. Deviations in spinopelvic harmony from ideal and age-specific norms are believed to contribute to regional malalignment and, subsequently, the recruitment of selective compensatory mechanisms to realign the center of gravity about the feet [4], [5]. In a long-term effort to optimize operative correction, novel analyses of compensatory mechanisms involving the pelvis and lower extremities emphasize both the importance of full-body preoperative radiographic assessment and the evaluation of patient-specific factors that may impact compensation, such as age, gender, and weight [6], [7], [8], [9].
Broadly, the impact of obesity in the setting of spinal deformity has been previously described with regard to contributions to biomechanical stress, complication rates, and clinical outcomes [10], [11], [12]. Previous biomechanical studies, for example, have demonstrated that increased body mass generates elevated compressive loads on discs and shear stresses within the lumbar spine [13], [14]. Furthermore, Vismara et al. importantly identified restricted forward flexion in obese patients with chronic back pain and postural adaptation marked by anterior pelvic shift (PS) and lumbar hyperlordosis [13].
Comprehensive radiographic analyses of obese patients with spinal deformity are rare within the literature and conflicting. In a 2013 study of 200 participants with no deformity, Romero-Vargas et al. failed to identify differences in the sagittal spinopelvic parameters of normal, overweight, and obese subjects [15]. Park et al., although noting no differences in preoperative sagittal alignment among 77 morbidly obese patients with ASD undergoing minimally invasive surgery compared with non-obese controls, did observe a significant difference in postoperative pelvic incidence minus lumbar lordosis (PI−LL) mismatch and sagittal vertical axis (SVA) [16]. Additionally, body mass has been shown to influence preliminary changes in focal alignment: in a study of 30 obese patients with back pain undergoing bariatric surgery, Lidar et al. demonstrated that following significant weight loss, patients experienced a marked increase in the L4–L5 intervertebral disc height [17]. Despite some evidence that the obese spine differs from the non-obese spine, these conflicting results collectively illustrate the need for increased attention, including head-to-toe radiographic analysis of these patients.
Recent efforts to describe compensation in response to progressive sagittal malalignment using the pelvis and lower limbs have demonstrated success using full-body stereoradiographic imaging (EOS imaging). The head-to-toe evaluation provides an illustration of musculoskeletal interdependence in the weight-bearing position, and has already been used successfully to examine a variety of lower extremity compensatory parameters in adults with spinal pathology [18].
The primary goals of this study were to compare sagittal malalignment in obese and non-obese patients with spinal pathology, and to investigate weight-dependent preferential recruitment of compensatory mechanisms with progressive sagittal malalignment. This analysis is the first to use a full-body imaging system to evaluate these differences.
Section snippets
Data collection
This study was an institutional review board–approved retrospective review of patients visiting a single academic center for spine-related complaints from November 2013 to June 2015. Inclusion criteria were age >18 years, available full-body radiographs, and degenerative spinal pathologies (scoliosis, kyphosis). Demographic data including age, body mass index (BMI), and gender were collected.
Biplanar radiographic acquisition
All included patients underwent biplanar full-body stereographs (EOS Imaging, Paris, France) [19]. The
Study sample
A total of 2,391 patients meeting inclusion criteria were identified. Before propensity score matching, obese patients (N=516) in the total cohort were significantly older (60.41 vs. 49.76 years, p<.001) and contained a greater proportion of females (57.2% vs. 42.8%, p<.001) than did the non-obese group. Following propensity score matching, there were 554 total patients identified for analysis (Ob=277; N-Ob=277). The total cohort comprised 62.3% women, had a mean age of 60.29±15.38 years, and a
Discussion
Previous studies have demonstrated that several patient-specific factors influence the activation of compensatory mechanisms to restore sagittal alignment for a given deformity [6], [7], [18], [29]. Although there are many compensatory mechanisms involving the pelvis and lower extremities, the primary aim of these efforts remains to maintain Dubousset's “conus of economy,” whereby the center of gravity is centrally positioned over the feet. To achieve this end, multiple positional adaptations
Conclusion
Obese patients demonstrate a different chain of compensatory events for a given spinopelvic mismatch when compared with non-obese cases. As mismatch increases, obese patients preferentially recruit lower extremity compensatory mechanisms, including knee flexion and posterior PS, to maintain the conus of economy. In contrast, non-obese patients recruit compensatory mechanisms involving the pelvis. This study demonstrates the negative impact of obesity on the ability to compensate for sagittal
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2021, KneeCitation Excerpt :We found that the pelvic parameters SS and PI changed gradually with KFA. Some studies have demonstrated that global sagittal spinal malalignment recruits lower extremity compensatory mechanisms [23–25]. Patients in the severe PI–LL mismatch group had more flexed knees than those in the control and mild PI–LL mismatch groups [23].
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2020, Spine JournalCitation Excerpt :Finally, several studies demonstrate similar outcomes between obese and nonobese patients when utilizing minimally invasive techniques [61,66,78]. The ability to compensate for positive sagittal malalignment is different between obese and nonobese patients, with the obese population employing lower extremity compensatory mechanisms as opposed to pelvic mechanisms [79]. Different compensatory mechanisms, in addition to various comorbidities often associated with obesity, may be just some of the reasons the obese and nonobese populations have different responses to surgery, all factors the spine surgeon must be cognizant of.
Reciprocal change of sagittal profile in unfused spinal segments and lower extremities after complex adult spinal deformity surgery including spinopelvic fixation: a full-body X-ray analysis
2020, Spine JournalCitation Excerpt :The results were based on the early postoperative radiograph (<12 months), which may limit the full presentation of compensatory mechanisms that may exist with extended follow-up. Second, as the present cohort was heterogeneous, some demographic parameters, such as diagnoses, gender, BMI, and PI, may have significant influence in the compensatory mechanisms of sagittal alignment and other alignment parameters [24–26]. Ideally, PI should be matched at the phase of patients’ enrollment; however, it was not feasible due to the relatively small sample size of the subgroups.
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Author disclosures: CMJ: Nothing to disclose. BGD: Nothing to disclose. DLC: Nothing to disclose. GWP: Nothing to disclose. SV: Nothing to disclose. AJB: Nothing to disclose. RL: Nothing to disclose. SB: Royalties: Pioneer (B); Consulting: K2 Medical (B), NuVasive (none), Innovasis (none), Allosource (B); Grants: K2 Medical (D, Paid directly to institution/employer), NuVasive (D, Paid directly to institution/employer), Innovasis (F, Paid directly to institution/employer), DePuy Synthes (F, Paid directly to institution/employer), outside the submitted work. TJE: Royalties: Fastenetix (F); Consulting: K2 Medical (C); Speaking and/or Teaching Arrangements: K2 Medical (C); Trips/Travel: K2 Medical (D); Research Support (Investigator Salary, Staff/Materials): Pfizer (B, Paid directly to institution/employer); Grants: Fridolin (E, Paid directly to institution/employer), ISSGF (E, Paid directly to institution/employer); Fellowship Support: OMEGA (E, Paid directly to institution/employer), AOSpine (E, Paid directly to institution/employer), outside the submitted work. VL: Stock Ownership: Nemaris INC (none); Speaking and/or Teaching Arrangements: NuVasive (B), DePuy Spine (B), Nemaris INC (B), Medicrea (B); Board of Directors: Nemaris INC (none); Grants: SRS (D, Paid directly to institution/employer), NIH (D, Paid directly to institution/employer), DePuy Spine (H, Paid directly to institution/employer), outside the submitted work. PGP: Consulting: Medicrea (none), outside the submitted work.
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