Bilateral DIEP Flap Breast Reconstruction to a Single Set of Internal Mammary Vessels: Technique, Safety, and Outcomes after 250 Flaps

BACKGROUND: The deep inferior epigastric artery perforator (DIEP) flap is considered the gold standard in autologous breast reconstruction. In bilateral cases, both flaps are often anastomosed to the internal mammary vessels on either side of the sternum. The authors propose a method in which both flaps are anastomosed to only the right side internal mammary artery and vein. METHODS: Between November of 2009 and March of 2018, 125 patients underwent bilateral DIEP flap breast reconstruction with this technique. One flap is perfused by the anterograde proximal internal mammary artery and the second one by the retrograde distal internal mammary artery after presternal tunneling. Patient demographics and operative details were reviewed retrospectively. RESULTS: Two hundred fifty flaps were performed. One hundred fifty-two flaps were prophylactic or primary reconstructions (60.8 percent), 70 were secondary reconstructions (28 percent), and 28 were tertiary reconstructions (11.2 percent). Mean patient age was 46 years, and the mean body mass index was 25 kg/m. Sixty patients underwent radiation therapy or chemotherapy (48 percent). The authors encountered one significant partial failure (0.4 percent) and nine complete flap failures (3.6 percent). The authors did not see a statistically significant predisposition for failure comparing the retrograde with the anterograde flow flaps, nor when comparing the tunneled with the nontunneled flaps. CONCLUSIONS: The authors' results show that anastomosing both DIEP flaps to a single set of mammary vessels is safe and reliable. The authors conclude that the retrograde flow through the distal internal mammary artery is sufficient for free flap perfusion and that subcutaneous tunneling of a free flap pedicle does not predispose to flap failure. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV

Intratissular expansion–mediated, serial fat grafting: A step-by-step working algorithm to achieve 3D biological harmony in autologous breast reconstruction

Background Breast reconstruction involves the use of autologous tissues or implants. Occasionally, microsurgical reconstruction is not an option because of insufficient donor tissues. Fat grafting has become increasingly popular in breast surgery. The challenge with this technique is how to reconstruct a stable and living “scaffold” that resembles a breast. Methods Breast reconstruction (n = 7) was performed using intratissular expansion with serial deflation–lipofilling sessions. Mean age of the patients was 41 years (22–53). The expander generated a vascularized capsule at 8 weeks, which demarcated a recipient site between the skin and the capsule itself, and functioned as a vascular source for angiogenesis. Serial sessions of deflation and lipofilling were initiated at 8 weeks with removal of the expander at the completion of the treatment. An average of 644 ml (range, 415 ml–950 ml) of lipoaspirate material was injected to reconstruct the breast mound. An average of 4 (range, 3 to 5) fat-grafting sessions with a 3-month interval was needed to achieve symmetry with the contralateral breast. The average follow-up was 14 months (range, 9–29 months). MRI examination was performed at 8 months to analyze tissue survival and the residual volume. Results MRI examination retained tissue survival and the mean reconstructed breast volume was 386 ml (range, 231 ml–557 ml). An aesthetically pleasant breast mound was created, with a high satisfaction rate. Conclusion We could reconstruct an aesthetically pleasant and stable breast mound in a selected group of patients by using intratissular expansion and fat grafting

Optimising the cell source and biomaterials for the generation of vascularized adipose tissue in vivo

We initially described a rat chamber model with an inserted arteriovenous pedicle which spontaneously generates 3-dimensional vascularized connective tissue (Tanaka Y et al., Br J Plast Surg 2000; 53: 51-7). More recently we have developed a murine chamber model containing reconstituted basement membrane (Matrigel®) and FGF-2 that generates vascularized adipose tissue in vivo (Cronin K et al., Plast Reconstr Surg 2004; in press). We have extended this work to assess the cellular and matrix requirements for the Matrigel®- induced neo-adipogenesis. We found that chambers sealed to host fat were unable to grow new adipose tissue. In these chambers the Matrigel® became vascularized with maximal outgrowth of vessels extending to the periphery at 6 weeks. A small amount of adipose tissue was found adjacent to the vessels, most likely arising from periadventitial adipose tissue. In contrast, chambers open to interaction with endogenous adipose tissue showed abundant new fat, and partial exposure to adjacent adipose tissue clearly showed neo-adipogenesis only in this area. Addition of small amounts of free fat to the closed chamber containing Matrigel® was able to induce neo-adipogenesis. Addition of small pieces of human fat also caused neo-adipogenesis in immunocompromised (SCID) mice. Also, we found Matrigel® to induce adipogenesis of Lac-Z-tagged (Rosa-26) murine bone marrow-derived mesenchymal stem cells, and cells similar to these have been isolated from human adipose tissue. Given that Matrigel® is a mouse product and cannot be used in humans, we have started investigating alternative matrix scaffolds for adipogenesis such as the PDA-approved PLGA, collagen and purified components derived from Matrigel®, such as laminin-1. The optimal conditions for adipogenesis with these matrices are still being elucidated. In conclusion, we have demonstrated that a precursor cell source inside the chamber is essential for the generation of vascularized adipose tissue in vivo. This technique offers unique potential for the reconstruction of soft tissue defects and may enable the generation of site-specific tissue using the correct microenvironment

Dynamic changes in high and low mammographic density human breast tissues maintained in murine tissue engineering chambers during various murine peripartum states and over time

Mammographic density (MD) is a strong heritable risk factor for breast cancer, and may decrease with increasing parity. However, the biomolecular basis for MD-associated breast cancer remains unclear, and systemic hormonal effects on MD-associated risk is poorly understood. This study assessed the effect of murine peripartum states on high and low MD tissue maintained in a xenograft model of human MD. Method High and low MD human breast tissues were precisely sampled under radiographic guidance from prophylactic mastectomy specimens of women. The high and low MD tissues were maintained in separate vascularised biochambers in nulliparous or pregnant SCID mice for 4 weeks, or mice undergoing postpartum involution or lactation for three additional weeks. High and low MD biochamber material was harvested for histologic and radiographic comparisons during various murine peripartum states. High and low MD biochamber tissues in nulliparous mice were harvested at different timepoints for histologic and radiographic comparisons. Results High MD biochamber tissues had decreased stromal (p = 0.0027), increased adipose (p = 0.0003) and a trend to increased glandular tissue areas (p = 0.076) after murine postpartum involution. Stromal areas decreased (p = 0.042), while glandular (p = 0.001) and adipose areas (p = 0.009) increased in high MD biochamber tissues during lactation. A difference in radiographic density was observed in high (p = 0.0021) or low MD biochamber tissues (p = 0.004) between nulliparous, pregnant and involution groups. No differences in tissue composition were observed in high or low MD biochamber tissues maintained for different durations, although radiographic density increased over time. Conclusion High MD biochamber tissues had measurable histologic changes after postpartum involution or lactation. Alterations in radiographic density occurred in biochamber tissues between different peripartum states and over time. These findings demonstrate the dynamic nature of the human MD xenograft model, providing a platform for studying the biomolecular basis of MD-associated cancer risk. © 2013 Springer Science+Business Media New York