Transient Phagocytic Dysfunction Mimicking Chronic Granulomatous Disease: A Rare Complication in Delayed Transverse Rectus Abdominis Myocutaneous Flap Breast Reconstruction

Summary:

Autologous breast reconstruction depends on intact wound healing. Chronic granulomatous disease (CGD) results from nicotinamide adenine dinucleotide phosphate oxidase dysfunction and predisposes patients to opportunistic infections; acquired forms can transiently mimic the congenital disorder. We report a case of transient phagocytic dysfunction that complicated delayed transverse rectus abdominis myocutaneous flap reconstruction. A 43-year-old woman with Stage IIB breast cancer underwent delayed reconstruction 18 months after cytotoxic chemotherapy. A delay procedure (inferior epigastric vessel ligation) was performed 14 days before flap elevation to reduce ischemic risk. When atypical wound failure developed postoperatively, deep tissue biopsies grew opportunistic pathogens ( Pseudomonas putida , Staphylococcus epidermidis , and Candida tropicalis ) and immune workup was initiated. Neutrophil oxidative function was assessed by dihydrorhodamine (DHR) 123 flow cytometry. Initial DHR testing showed absent oxidative burst (oxidation index <1.0; reference >5.0), indicating severe phagocytic dysfunction. Targeted antimicrobials (levofloxacin, fluconazole) and negative pressure wound therapy were started. Repeat DHR at 6 weeks was fully normal (oxidation index 58.80), excluding genetic CGD. The patient healed completely by secondary intention without further surgery. Phagocytic dysfunction can emerge as a late sequela of cytotoxic therapy and complicate autologous reconstruction, mimicking genetic CGD. When flap failure is unexplained and opportunistic organisms are recovered despite intact perfusion, DHR testing should be part of the workup. Serial assays distinguish transient acquired dysfunction from a permanent genetic defect and determine how aggressively to intervene.