Sciatic nerve atrophy as a predictor of impaired wound healing in patients with chronic limb-threatening ischemia following endovascular therapy: A prospective pilot study

Background: A prior retrospective single-center study involving patients with chronic limb-threatening ischemia (CLTI) demonstrated that sciatic nerve atrophy (SNA) is associated with impaired wound healing (IWH) and reduced amputation-free survival (AFS). We conducted a prospective single-center pilot study to validate the prognostic implications of SNA in predicting wound healing and AFS. Methods: Patients diagnosed with CLTI and associated tissue loss were recruited for participation in this prospective, noninterventional study. The cross-sectional area (CSA) of the sciatic nerve at the mid-to-lower femoral quarter was quantified utilizing computed tomography imaging. SNA was identified based on the predefined CSA threshold. Patient outcomes were evaluated through outpatient clinic visits and telephone follow-ups. Outcomes assessed included wound healing rate, adverse wound outcomes (AWO), and AFS. Results: In the cohort of 52 limbs with CLTI from 52 patients, 19 individuals were categorized into the SNA group. The 6-month wound healing rate was significantly lower in the SNA group (15.8%) compared to the normal group (87.9%) ( p < 0.001). The sensitivity and specificity of SNA for predicting AWO at 6 months were 80.0% and 90.6%, respectively. Patients in the SNA group had significantly lower AFS at 1 year (68.4% vs 93.9%, p = 0.011). Multivariable analysis further established that SNA was an independent prognostic factor for both AWO (hazard ratio [HR]: 0.113; 95% CI: 0.034–0.381; p < 0.001) and AFS (HR: 6.135; 95% CI: 1.236–30.303; p = 0.026) following endovascular therapy (EVT). Conclusions: SNA was identified as a predictor for AWO and AFS in patients with CLTI after EVT. Future research should involve rigorous basic and large-scale clinical studies to elucidate the association between SNA and prognosis in patients with peripheral artery disease (PAD)/CLTI and explore the underlying pathophysiological mechanisms.