Background Deep inferior epigastric perforator (DIEP) reconstruction can be performed in an immediate (at time of mastectomy), delayed–immediate (immediate tissue expander followed by staged DIEP), or delayed timing following mastectomy. Avoiding flap radiation is a known benefit of the delayed–immediate approach. The purpose of this study is to evaluate patients who chose DIEP flap as the reconstructive method during initial consultation and compared characteristics of surgery in relation to their final reconstructive choice. Methods Consecutive patients having breast reconstruction from 2017 to 2019 were divided into three groups: immediate DIEP after mastectomy (Group I); delayed–immediate DIEP with tissue expander first followed by DIEP (Group II); and patients who initially chose delayed–immediate DIEP but later decided on implants for the second stage of reconstruction (Group III). Exclusion criteria were patients that had delayed DIEP (no immediate reconstruction) or had initially chose implant-based reconstruction. Results The study included 59 patients. Unilateral free flaps in Group II had shorter operative times (318 minutes) compared with Group I unilateral free flaps (488 minutes) (p = 0.024). Eleven patients (30.6%) had prophylactic mastectomies in Group I compared with none in Group II (p = 0.004). Patients who had immediate tissue expansion frequently changed their mind from DIEP to implant for second stage reconstruction frequently (52.2%). Conclusion Delayed–immediate DIEP reconstruction has several advantages over immediate DIEP flap including shorter free flap operative times. Patients commonly alter their preference for second stage reconstruction. A patient-centered advantage of delayed–immediate reconstruction is prolonging the time for patients to make their choice for the final reconstruction.

Background. Breast implants are commonly placed postbreast cancer reconstruction, cosmetic augmentation, and gender-affirming surgery. Breast implant illness (BII) is a systemic complication associated with breast implants. Patients with BII may experience autoimmune symptoms including fatigue, difficulty concentrating, hair loss, weight change, and depression. BII is poorly understood, and the etiology is unknown. The purpose of this literature review is to characterize BII autoimmune disorders and determine possible causes for its etiology. Methods. The PubMed, Google Scholar, Embase, Web of Science, and OVID databases were interrogated from 2010 to 2020 using a query strategy including search term combinations of “implants,” “breast implant illness,” “autoimmune,” and “systemic illness.” Results. BII includes a spectrum of autoimmune symptoms such as fatigue, myalgias/arthralgias, dry eyes/mouth, and rash. A review of epidemiological studies in the past ten years exhibited evidence affirming an association between breast implants and autoimmune diseases. The most commonly recognized were Sjogren’s syndrome, rheumatoid arthritis, systemic sclerosis, chronic fatigue syndrome, and Raynaud’s syndrome. Explantation resulted in alleviation of symptoms in over 50% of patients, strengthening the hypothesis linking breast implants to BII. Studies have shown that silicone is a biologically inert material and unlikely to be the cause of these symptoms. This is supported by the fact that increased risk of autoimmune disease was also reported in patients with other implantable biomaterials such as orthopedic implants. Recent studies shed light on a possible role of bacterial biofilm and subsequent host-pathogen interactions as a confounding factor to this problem. Conclusion. BII could be dependent on biofilm infection and the microenvironment around the implants. The true pathophysiology behind these complaints must be further investigated so that alternative treatment regimens other than explantation can be developed. Translational significance of these studies is not limited to breast implants but extends to other implants as well.

Over 10 million women worldwide have breast implants for breast cancer/prophylactic reconstruction or cosmetic augmentation. In recent years, a number of patients have described a constellation of symptoms that are believed to be related to their breast implants. This constellation of symptoms has been named Breast Implant Illness (BII). The symptoms described include chronic fatigue, joint pain, muscle pain and a host of other manifestations often associated with autoimmune illnesses. In this work, we report that bacterial biofilm is associated with BII. We postulate that the pathogenesis of BII is mediated via a host-pathogen interaction whereby the biofilm bacteria Staphylococcus epidermidis interacts with breast lipids to form the oxylipin 10-HOME. The oxylipin 10-HOME was found to activate CD4+ T cells to Th1 subtype. An increased abundance of CD4+Th1 was observed in the breast tissue of BII subjects. The identification of a mechanism of immune activation associated with BII via a biofilm enabled pathway provides insight into the pathogenesis for implant-associated autoimmune symptoms.

We hypothesize that soft tissue infections (SSIs) related to intravenous drug usage (IVDU) are associated with a more complicated and costly course than those not associated with IVDU. For the period 2005–2018, ICD 9/ICD 10 billing codes were used to identify patients admitted with SSIs and their causes/complications and associated costs. IVDU-related infections were then compared with non-IVDU–related infections. t test was used to compare treatment costs and length of stay. Logistic regression analysis was used to assess the likelihood/risk of specific events in the IVDU versus non-IVDU populations. Of 47,281 patients admitted with SSIs, 1323 were associated with IVDU. IVDU-related patients tended to be younger (36.2 vs 49.3 years, P = 0.001). Both cost and length of stay were significantly greater in the IVDU group ($30,471 vs $16,020, P = 0.001; 5.7days vs 3.7days, P = 0.001). In addition, IVDU admissions were more likely to be associated with chronic blood-borne infections (hepatitis B/C, HIV, P = 0.001) and a significantly greater incidence of secondary infectious complications, including endocarditis ( P = 0.001), bacteremia ( P = 0.001), and osteomyelitis ( P = 0.003). SSI admissions related to IVDU are a unique subgroup of patients. These patients not only have longer and more costly lengths of stay but are also at higher risk for secondary complications such as chronic blood-borne viral illness and secondary bacterial infectious complications, such as bacteremia, endocarditis, and osteomyelitis. Further prospective study of these findings is warranted as we continue to battle the growing problem of IVDU in the United States

Introduction  Lymphedema is a chronic condition that affects over 250 million people worldwide. It results from impaired lymphatic drainage, causing fluid and fat accumulation and eventually fibrosis of the affected limb. Lymphedema can be inherited (primary) or iatrogenic to surgery or parasitic infection (secondary). Breast cancer-related lymphedema is the most common etiology in the U.S. Current treatments have limited success and the disease mechanisms are not well understood. The purpose of this article is to review translational research into lymphedema therapies and its potential clinical impact.     Methods  A Pubmed search for novel treatment methods was performed with terms “lymphedema,” “cell therapy,” and “gene therapy.” Inclusion criteria were use of in vivo models, English language, and publication dates during the years 2000-2020.    Results  Secondary lymphedema is currently treated with compression garments and surgery; other approaches are being pursued. These include gene therapy (13 articles), stem cell transplant (16 articles), and immunosuppression (4 articles), which have all demonstrated considerable success in animal models of lymphedema. Growth factors such as VEGF-C are administered through adenoviral vectors and resolve limb swelling by inducing lymphangiogenesis. Stem cells derived from bone marrow or adipose tissue repair lymphatic damage directly by acquiring lymphatic characteristics or indirectly through paracrine signaling to surrounding cells. Immunosuppressive agents reduce inflammation and block antilymphangiogenic factors. Although these mechanisms have been studied in animals, only six human small studies were found, providing limited evidence.     Conclusion  Despite success in animal models, treatment in human subjects has been sparse. This limited translational feasibility is because of inadequate animal models, safety concerns, and lack of understanding about lymphedema pathophysiology. Although progress in lymphedema research has been made, further inquiry into its mechanism is needed in order to develop more effective and targeted therapies.