Peri-operative CDK4/6 inhibitors in DIEP flap breast reconstruction: Early safety data and proposed management strategy.

Sharp, O; Yousif, Y; Battisti, N M L; Ramsey, K W D; Khan, A A · J Plast Reconstr Aesthet Surg · 2026

case_series · Level IV

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Abstract

The introduction of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors has significantly altered the treatment paradigm for hormone receptor-positive, HER2-negative breast cancer. Increasingly, surgeons encounter patients receiving these agents at the time of breast reconstruction, yet there is no published evidence on the safety of free tissue transfer in this context. We present the first series examining post-operative outcomes in patients exposed to CDK4/6 inhibitors undergoing deep inferior epigastric perforator (DIEP) flap breast reconstruction and outline a pragmatic management approach. We report a retrospective, consecutive cohort series of all unilateral DIEP breast reconstructions undertaken between January 2024 and January 2026 at our institution. We include 232 patients, 9 of whom (4%) underwent peri-operative CDK4/6 inhibition. The median age was 51 years. Overall, 18% of patients were obese (BMI ≥ 30), 7% had a smoking history, and 2% had diabetes. CDK4/6 inhibitors administered were Abemaciclib (n=6), Ribociclib (n=2) and Palbociclib (n=1), and patients were recommended a median of 2 weeks off treatment pre-operatively. Pre-operative haemoglobin, white cell, neutrophil and lymphocyte counts were all significantly lower in the CDK4/6 inhibitor group (p<0.05). No minor complications occurred in CDK4/6 patients compared with 11% in non-exposed patients (p=0.6). Major complications were rare, occurring in 0% of CDK4/6 inhibitor patients and 2.2% of non-exposed patients (p=1.0). In this early series, CDK4/6 inhibition did not adversely affect surgical outcomes. We advocate for close coordination with oncology regarding temporary treatment interruption. Larger, multi-centre studies are needed to fully assess the risk profile of peri-operative CDK4/6 inhibitors in autologous reconstruction.