Sir: Important work has been published recently in further establishing the cause of capsular contracture as being secondary to subclinical biofilm formation.1 As this issue of biofilms and contracture has now been investigated in multiple well-designed studies from separate institutions, the cause of capsular fibrosis has been demonstrated beyond much reasonable doubt. We must now more vigorously transition from the question, “what causes this?” to “how can we prevent this?” In prior elegant studies by Adams et al., it has been established that antibiotic irrigation is efficacious in reducing rates of capsular contracture.2 Despite a significant reduction in contracture by means of intraoperative irrigation and meticulous sterile technique, the literature and anecdotal experience suggest that contracture remains a common complication following augmentation mammaplasty. Despite the most stringent precautions, there is likely some level of unavoidable exposure to Staphylococcus epidermidis when introducing the implant into the breast pocket. In addition, the implant is always at risk of inherent exposure to the natural flora of the breast, particularly when using a periareolar incision. Thus, relying strictly on intraoperative precaution is fraught with limitations. It remains to be determined whether any further preventative measures can be taken beyond the aforementioned intraoperative precautions. Unlike intraoperative antibiotic irrigation, postoperative antibiotic prophylaxis has been met with much less conclusive laboratory or prospective clinical data. At the 2010 meeting of the American Society for Aesthetic Plastic Surgery, we presented data examining the efficacy of postoperative prophylactic antibiotics in 249 patients undergoing primary and secondary cosmetic breast augmentation (Table 1).3 We were unable to demonstrate a reduction in capsular contracture with postoperative antibiotics. However, it would be shortsighted to definitively declare that postoperative antibiotics have no effect regarding the reduction of capsular contracture. As this was a retrospective cohort study, we were unable to determine patient compliance. Furthermore, we effectively examined only one duration of postoperative prophylaxis (3 days) and only one class of antibiotics (nearly all patients received cephalosporins). In fact, in a recent experimental trial, various classes of antibiotics, such as aminoglycosides and fluoroquinolones, were demonstrated to be more effective against Staphylococcus biofilms.4Table 1: Comparison of Complications between Patients Who Received Postoperative Antibiotics and Those Who Did NotUsing Tamboto's experimental model, we suggest that a study should be conducted examining postoperative antibiotics. Assuming that the pharmacokinetics are at all comparable in a porcine model, confounding variables that plague the study of postoperative prophylaxis in clinical trials would be all but eliminated. Perhaps a particular duration of postoperative prophylaxis or class of antibiotics will be found to reduce biofilms. In contrast, if it can be proven that postoperative antibiotics of any reasonable class or duration are ineffective against these often resistant biofilms, the need for postoperative prophylaxis can be further put to rest.5 Perhaps no reduction will be seen with postoperative prophylaxis and our clinical observation will be upheld. In summary, our retrospective clinical information yielded no signs that administration of postoperative antibiotics for 3 days was effective in reducing capsular contracture (i.e., biofilms). However, we are recommending further study of postoperative prophylaxis and biofilms. DISCLOSURE The authors have no disclosures or sources of funding to acknowledge. Michael N. Mirzabeigi, M.S. Hani Sbitany, M.D. Shareef Jandali, M.D. Joseph M. Serletti, M.D. Division of Plastic Surgery University of Pennsylvania Health System Philadelphia, Pa.
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Jan 1, 2012
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