Browsing by Author "VonDerHaar, R. Jason"
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Item 65. Prophylactic Absorbable Antibiotic Beads: Effect on Tissue Expander Reconstruction Outcomes Following Mastectomy Skin Necrosis(Wolters Kluwer, 2025-04-24) Ahmed, Shahnur; Zaidi, Shozaf S.; Fisher, Carla S.; Ludwig, Kandice K.; Imeokparia, Folasade O.; VonDerHaar, R. Jason; Bamba, Ravinder; Danforth, Rachel M.; Hassanein, Aladdin H.; Lester, Mary E.; Surgery, School of MedicinePURPOSE: Mastectomy skin necrosis is problematic in tissue expander reconstruction with rates between 7 to 30%. Partial or full-thickness skin necrosis may harbor bacterial colonization promoting infection and risk of implant loss. Absorbable antibiotic-impregnated calcium-sulfate antibiotic beads have been described to reduce tissue expander (TE)/implant infection when used prophylactically for prepectoral breast reconstruction. The purpose of this study is to evaluate the effect of absorbable antibiotic beads on outcomes in patients who develop mastectomy skin necrosis after immediate postmastectomy tissue expander breast reconstruction. METHODS: A single-center retrospective review was performed for patients who underwent mastectomy, immediate prepectoral TE reconstruction on the same day (2018-2024). Patients who developed mastectomy skin necrosis were included. Patients were divided into two groups: Group 1 (absorbable antibiotic beads with TE placement) and Group 2 (no antibiotic beads with TE). Demographical information was recorded. Surgical-site infection (90-days) and implant removal were the outcome variables. RESULTS: The study included 61 patients (75 total breasts with necrosis) who underwent prepectoral TE breast reconstruction following mastectomy and developed mastectomy skin necrosis. The patients included in the study with mastectomy skin necrosis were 12 patients in Group 1 (16 breasts) and 49 patients in Group 2 (59 breasts). Baseline characteristics were not significantly difference between groups (p=1). There was no difference between nipple-sparing mastectomy or skin-sparing mastectomy between groups (p=0.1094). Acellular dermal matrix was used in 66.7% (8/12) of Group 1 compared to 83.7% (41/49) of Group 2 (p=0.2285). Operative management of mastectomy skin necrosis including debridement and reclosure was required in 50% (6/12) of Group 1 compared to 69.4% (34/49) of Group 2 patients (p=0.3093). There was one occurrence (6.3%, 1/16 TEs) of surgical-site infection in Group 1 and 35.6% (21/59 TEs) in Group 2 (p=0.0288). TE removal resulted in 6.3% (1/16 TEs) in Group 1 and 33.9% (20/59 TEs) in Group 2 (p=0.0310). The mean follow-up time was 189 days (range 146-236 days). CONCLUSIONS: Patients who develop mastectomy skin necrosis after prepectoral tissue expander reconstruction may experience lower rates of TE removal and infection when prophylactic absorbable antibiotic-impregnated beads are used. Patients who develop mastectomy skin necrosis are at high risk for infection and TE loss. Prophylactic antibiotic beads used at the time of mastectomy with prepectoral TE reconstruction decrease the risk of infection and TE loss in patients who experience mastectomy skin necrosis.Item Biofilm Derived Oxylipin Mediated Autoimmune Response in Breast Implant Subjects(medRxiv, 2020-11-20) Khan, Imran; Minto, Robert E.; Kelley-Patteson, Christine; Natta, Bruce W. Van; Neumann, Colby R.; Suh, Lily J.; Singh, Kanhaiya; Lester, Mary; VonDerHaar, R. Jason; Gordillo, Gayle M.; Hassanein, Aladdin H.; Sen, Chandan K.; Kadin, Marshall E.; Sinha, Mithun; Chemistry and Chemical Biology, School of ScienceOver 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.Item Biofilm-derived oxylipin 10-HOME–mediated immune response in women with breast implants(ASCI, 2024-02) Khan, Imran; Minto, Robert E.; Kelley-Patteson, Christine; Singh, Kanhaiya; Timsina, Lava; Suh, Lily J.; Rinne, Ethan; Van Natta, Bruce W.; Neumann, Colby R.; Mohan, Ganesh; Lester, Mary; VonDerHaar, R. Jason; German, Rana; Marino, Natascia; Hassanein, Aladdin H.; Gordillo, Gayle M.; Kaplan, Mark H.; Sen, Chandan K.; Kadin, Marshall E.; Sinha, Mithun; Chemistry and Chemical Biology, School of ScienceThis study investigates a mechanistic link of bacterial biofilm–mediated host-pathogen interaction leading to immunological complications associated with breast implant illness (BII). Over 10 million women worldwide have breast implants. In recent years, women have described a constellation of immunological symptoms believed to be related to their breast implants. We report that periprosthetic breast tissue of participants with symptoms associated with BII had increased abundance of biofilm and biofilm-derived oxylipin 10-HOME compared with participants with implants who are without symptoms (non-BII) and participants without implants. S. epidermidis biofilm was observed to be higher in the BII group compared with the non-BII group and the normal tissue group. Oxylipin 10-HOME was found to be immunogenically capable of polarizing naive CD4+ T cells with a resulting Th1 subtype in vitro and in vivo. Consistently, an abundance of CD4+Th1 subtype was observed in the periprosthetic breast tissue and blood of people in the BII group. Mice injected with 10-HOME also had increased Th1 subtype in their blood, akin to patients with BII, and demonstrated fatigue-like symptoms. The identification of an oxylipin-mediated mechanism of immune activation induced by local bacterial biofilm provides insight into the possible pathogenesis of the implant-associated immune symptoms of BII.Item Biofilm-derived oxylipin 10-HOME–mediated immune response in women with breast implants(The American Society for Clinical Investigation, 2023-11-30) Khan, Imran; Minto, Robert E.; Kelley-Patteson, Christine; Singh, Kanhaiya; Timsina, Lava; Suh, Lily J.; Rinne, Ethan; Van Natta, Bruce W.; Neumann, Colby R.; Mohan, Ganesh; Lester, Mary; VonDerHaar, R. Jason; German, Rana; Marino, Natascia; Hassanein, Aladdin H.; Gordillo, Gayle M.; Kaplan, Mark H.; Sen, Chandan K.; Kadin, Marshall E.; Sinha, Mithun; Surgery, School of MedicineThis study investigates a mechanistic link of bacterial biofilm–mediated host-pathogen interaction leading to immunological complications associated with breast implant illness (BII). Over 10 million women worldwide have breast implants. In recent years, women have described a constellation of immunological symptoms believed to be related to their breast implants. We report that periprosthetic breast tissue of participants with symptoms associated with BII had increased abundance of biofilm and biofilm-derived oxylipin 10-HOME compared with participants with implants who are without symptoms (non-BII) and participants without implants. S. epidermidis biofilm was observed to be higher in the BII group compared with the non-BII group and the normal tissue group. Oxylipin 10-HOME was found to be immunogenically capable of polarizing naive CD4+ T cells with a resulting Th1 subtype in vitro and in vivo. Consistently, an abundance of CD4+Th1 subtype was observed in the periprosthetic breast tissue and blood of people in the BII group. Mice injected with 10-HOME also had increased Th1 subtype in their blood, akin to patients with BII, and demonstrated fatigue-like symptoms. The identification of an oxylipin-mediated mechanism of immune activation induced by local bacterial biofilm provides insight into the possible pathogenesis of the implant-associated immune symptoms of BII.Item Implant-based Breast Reconstruction Salvage with Negative Pressure Wound Therapy with Instillation: An Evaluation of Outcomes(Wolters Kluwer, 2024-09-03) Ahmed, Shahnur; Hulsman, Luci; Imeokparia, Folasade; Ludwig, Kandice; Fisher, Carla; Bamba, Ravinder; Danforth, Rachel; VonDerHaar, R. Jason; Lester, Mary E.; Hassanein, Aladdin H.; Surgery, School of MedicineBackground: Implant infection is problematic in breast reconstruction. Traditionally, infected tissue expanders (TE)/implants are removed for several months before replacement, resulting in breast reconstruction delay. Salvage involving device removal, negative pressure wound therapy with instillation and dwell (NPWTi-d) placement, and early staged TE/implant replacement within a few days has been described. The purpose of this study was to compare outcomes of the NPWTi-d salvage pathway with traditional implant removal. Methods: A retrospective review was performed on patients who underwent implant-based reconstruction and developed TE/implant infection/exposure requiring removal. Patients were divided into two groups. Group 1 had TE/implant removal, NPWTi-d placement, and TE/implant replacement 1-4 days later. Group 2 (control) underwent standard TE/implant removal and no NPWTi-d. Reinfection after TE/implant salvage, TE/implant-free days, and time to final reconstruction were assessed. Results: The study included 47 patients (76 TE/implants) in group 1 (13 patients, 16 TE/implants) and group 2 (34 patients, 60 TE/implants). The success rate (no surgical-site infection within 90 days) of implant salvage was 81.3% in group 1. No group 1 patients abandoned completing reconstruction after TE/implant loss versus 38.2% (13 of 34) in group 2 (P = 0.0094). Mean implant-free days was 2.5 ± 1.2 in group 1 versus 134.6 ± 78.5 in group 2 (P = 0.0001). The interval to final implant-based reconstruction was 69.0 ± 69.7 days in group 1 versus 225.6 ± 93.6 days in group 2 (P = 0.0001). Conclusions: A breast implant salvage pathway with infected device removal, NPWTi-d placement, and early TE/implant replacement was successful in 81.3%. Patients experienced 132 less implant-free days and faster time to final reconstruction.Item QS9: Host Biofilm Interaction In Breast Implant Illness(Wolters Kluwer, 2021-07) Khan, Imran; Minto, Robert E.; Kelley-Patteson, Christine; Van Natta, Bruce; Mohan, Ganesh; Suh, Lily; Singh, Kanhaiya; Lester, Mary; VonDerHaar, R. Jason; Gordillo, Gayle M.; Hassanein, Aladdin; Sen, Chandan K.; Kadin, Marshall E.; Sinha, Mithun; Surgery, School of MedicinePurpose: Breast Implant Illness (BII) is patient-described constellation of symptoms that are believed to be related to their breast implant. The symptoms described include fibromyalgia, chronic fatigue and a host of other symptoms that are often associated with autoimmune illnesses. In this work, we report that bacterial biofilm associated with breast implant, metabolize fatty acid oleic acid present in the breast tissue milieu to oxylipins, one such oxylipin identified from this study is (10S)-hydroxy-(8E)-octadecenoic acid (10-HOME). We hypothesize that immunomodulatory effects of oxylipin 10-HOME produced by biofilm present on the implant could be correlated with BII pathogenesis. Methods: Capsulectomy and breast implants from clinically indicated procedures for patients requesting prosthetic removal were collected using clinical parameters outlined in previous studies, and questionnaire screened for the commonly reported symptoms associated with BII. Predictive variables included age, diabetes status, co-morbidities, nature and duration of implant. Scanning electron microscopy (SEM), Wheat Germ Agglutinin (WGA) and 16SrRNA sequencing were used for bacterial biofilm bacterial identification. 10-HOME was quantitated through targeted and untargeted lipidomic analyses using LC-MS-MS. Results: Sixty eight Implant, associated capsules and breast tissue specimen were collected for BII (n=46) and two control groups, group I, (non-BII, n=14) patients with breast implants, no BII symptoms. Group II (normal tissue, n = 8), patients without an implant, whose breast tissue was removed due to surgical procedures. Bacterial biofilm was detected through SEM in both BII and non BII cohorts. However, WGA analysis (quantitative analysis) indicated increased abundance of biofilm in the BII cohort (n=7, p=0.0036). 16SrRNA (genomic) sequencing identified increased abundance of Staphylococcus epidermidis (Fisher’s exact test, p<0.001) in the BII group (63.04%) compared to non-BII group (14.3%) and the normal group. The BII group was 9.8 times significantly more likely to have Staphylococcus epidermidis colonization compared to the non-BII group (p=0.003, logistic regression), compared to normal, it is 17.4 times significantly more likely to have Staphylococcus epidermidis (p=0.0021). Elevated levels of 10-HOME BII compared to non-BII samples, (p < 0.0001) were observed through mass spectrometry. Positive correlation was observed between bacterial abundance and concentration of 10-HOME in BII subjects (R2=0.88). Similar correlation was observed in BII subjects with Staphylococcus epidermidis (R2=0.77). Conclusion: This study investigated the biofilm hypothesis of breast implant illness through a host-pathogen interaction. The breast microenvironment led to formation of biofilm derived 10-HOME from host oleic acid. The study provides the first evidence of a possible correlation between bacterial biofilm and biofilm derived 10-HOME in the context of 10-HOME. In consideration of reports of biofilm association with other metal implants, the findings of this study can possibly explain autoimmune response associated with those implants.