The impact of obesity on compensatory mechanisms in response to progressive sagittal malalignment

Background context: Obesity's impact on standing sagittal alignment remains poorly understood, especially with respect to the role of the lower limbs. Given energetic expenditure in standing, a complete understanding of compensation in obese patients with sagittal malalignment remains relevant.

Purpose: This study compares obese and non-obese patients with progressive sagittal malalignment for differences in recruitment of pelvic and lower-limb mechanisms.

Study design/setting: Single-center retrospective review.

Patient sample: A total of 554 patients (277 obese, 277 non-obese) were identified for analysis.

Outcome measures: Upper body alignment parameters: sagittal vertical axis (SVA) and T1 spinopelvic inclination (T1SPi). Compensatory lower-limb mechanisms: pelvic translation (pelvic shift [PS]), knee (KA) and ankle (AA) flexion, hip extension (sacrofemoral angle [SFA]), and global sagittal angle (GSA).

Methods: Inclusion criteria were patients ≥18 years who underwent full-body stereographic x-rays. Included patients were categorized as non-obese (N-Ob: body mass index [BMI]<30 kg/m²) or obese (Ob: BMI≥30 kg/m²). To control for potential confounders, groups were propensity score matched by age, gender, and baseline pelvic incidence (PI), and subsequently categorized by increasing spinopelvic (pelvic incidence minus lumbar lordosis [PI-LL]) mismatch: <10°, 10°-20°, >20°. Independent t tests and linear regression models compared sagittal (SVA, T1SPi) and lower limb (PS, KA, AA, SFA, GSA) parameters between obesity cohorts.

Results: A total of 554 patients (277 Ob, 277 N-Ob) were included for analysis and were stratified to the following mismatch categories: <10°: n=367; 10°-20°: n=91; >20°: n=96. Obese patients had higher SVA, KA, PS, and GSA than N-Ob patients (p<.001 all). Low PI-LL mismatch Ob patients had greater SVA with lower SFA (142.22° vs. 156.66°, p=.032), higher KA (5.22° vs. 2.93°, p=.004), and higher PS (4.91 vs. -5.20 mm, p<.001) than N-Ob patients. With moderate PI-LL mismatch, Ob patients similarly demonstrated greater SVA, KA, and PS, combined with significantly lower PT (23.69° vs. 27.14°, p=.012). Obese patients of highest (>20°) PI-LL mismatch showed greatest forward malalignment (SVA, T1SPi) with significantly greater PS, and a concomitantly high GSA (12.86° vs. 9.67°, p=.005). Regression analysis for lower-limb compensation revealed that increasing BMI and PI-LL predicted KA (r²=0.234) and GSA (r²=0.563).

Conclusions: With progressive sagittal malalignment, obese patients differentially recruit lower extremity compensatory mechanisms, whereas non-obese patients preferentially recruit pelvic mechanisms. The ability to compensate for progressive sagittal malalignment with the pelvic retroversion is limited by obesity.