Following nipple-sparing mastectomy (NSM), patients commonly experience significant impairment or total loss of nipple sensitivity, which negatively impacts the patients’ quality of life, whereas patients who retain nipple sensation postoperatively experience enhanced physical, psychosocial, and sexual well-being. Reinnervation techniques such as nerve allografting have been utilized to retain sensation. Despite the benefits of nerve allografts, such as lack of donor site morbidity, ease of use, and potentially shorter surgery time, there are shortcomings, such as the cost of commercially available acellular nerve allografts, and, most importantly, decreased sensory and motor function recovery for acellular nerve allografts with a diameter greater than 3 mm or a length greater than 50 mm. We present a technique where we performed immediate implant-based breast reconstruction combined with nipple–areola complex reinnervation using an autologous nerve graft. Following the procedure, the patient had improved sensory outcomes in the reconstructed breast and good quality-of-life indices. This report highlights the potential for sural nerve autografts in restoring breast sensation following mastectomy.
Background and Objectives: Sural nerve grafts are increasingly used to restore sensation after reconstructive surgery, including nipple–areola complex (NAC) reinnervation following nipple-sparing mastectomy, but donor-site morbidity has not been characterized using combined objective and patient-reported measures. We quantified this morbidity prospectively. Materials and Methods: Ten women who had undergone mastectomy with direct-to-implant reconstruction and NAC reinnervation using a sural nerve graft were assessed by photographic mapping of the donor-site deficit, the FootQ symptom and scar-satisfaction questionnaire (preoperatively, 6 months, 1 year), sural nerve conduction studies (NCS) at 12 months (at 10 months in one patient), and bedside Semmes–Weinstein monofilament and two-point discrimination (2PD) testing. Spearman correlation, Wilcoxon signed-rank, and Friedman tests were used. Results: Harvest length and deficit area were not significantly associated (ρ = −0.588, p = 0.074; bootstrap 95% CI −0.90 to +0.08); with ten patients, the analysis was underpowered and neither establishes nor excludes an association. Deficit area was strikingly variable (coefficient of variation 56%) and did not differ by neurotoxic chemotherapy exposure (five per subgroup). At 1 year, seven of nine patients (78%) had an unrecordable sural sensory action potential, yet monofilament thresholds were normal in every evaluable patient, and 2PD did not differ between limbs. FootQ symptoms increased from the preoperative assessment to 6 months (composite 1.34 to 2.19; p = 0.047), then remained mild and unchanged to 1 year (all p ≥ 0.50); scar satisfaction remained high. Conclusions: Sural graft harvest produces a highly variable and often electrophysiologically persistent donor-site sensory deficit that bedside testing and patient-reported outcomes did not detect at 1 year; because those tests used fixed anatomical sites, the discordance may reflect the territory assessed as much as test sensitivity or peripheral compensation. This small cohort neither establishes nor excludes an association between harvest length and the residual deficit, and the donor site remained clinically well tolerated.