Optimizing Breast Pocket Irrigation: The Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL) Era.

BACKGROUND: Specific antimicrobial breast pocket irrigations have been proven over the past 20 years to reduce the incidence of capsular contracture by a factor of 10, and the emergence of breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) and its link to bacteria/technique has created renewed interest in different antimicrobial breast pocket preparation agents. Our previous studies have identified that both Betadine-containing and non-Betadine-containing antimicrobial irrigations provide excellent broad-spectrum bacterial coverage. The current science of BIA-ALCL has implicated the Gram-negative microbiome as a key in pathogenesis. OBJECTIVES: The aim of this study was to revisit the antimicrobial effectiveness of clinically utilized Betadine and non-Betadine solutions, along with other antimicrobial agents that have not yet been tested, against multiple organisms, including additional common Gram-negative bacteria associated with chronic breast implant infections/inflammation. METHODS: Current and new antimicrobial breast irrigations were tested via standard techniques for bactericidal activity against multiple Gram-positive and Gram-negative strains. Test results are detailed and clinical recommendations for current antimicrobial irrigations are provided. RESULTS: Betadine-containing irrigations were found to be superior according to the testing performed. CONCLUSIONS: There are quite few misconceptions with regard to antimicrobial breast pocket irrigation. These are discussed and final evidence-based recommendations for practice are given.

Effects of Topical Mandelic Acid Treatment on Facial Skin Viscoelasticity.

Mandelic acid is an α-hydroxy acid with reported benefit in treating acne and hyperpigmentation. The authors have developed a topical mandelic acid formulation that subjectively improves the quality of aged skin. Although the gold standard for assessing outcomes, photographic documentation is limited by subjective interpretation. Tools for measuring physical skin properties allow for an objective assessment of changes in skin quality. The authors sought to objectively study the viscoelastic changes to the skin following treatment with topical mandelic acid, using the Cutometer MPA 580. Twenty-four patients, twenty females and four males, aged 42 to 68 years, were studied over a four-week period. Mandelic acid was applied topically to the face twice a day for four weeks. The lower eyelid skin viscoelastic properties were assessed weekly using the Cutometer. After four weeks of topical mandelic acid treatment, the elasticity of lower eyelid skin increased 25.4% (P = .003). Skin firmness increased 23.8% (P = .029). Improvement in photographic appearance correlated with these findings. Mandelic acid is another topical treatment option for improving skin quality, and is well tolerated by patients. The authors feel that the Cutometer or similar device should be used routinely in facial plastic surgery to objectively assess outcomes of various treatment modalities.

Macrotextured Breast Implants with Defined Steps to Minimize Bacterial Contamination around the Device: Experience in 42,000 Implants.

BACKGROUND: Bacteria/biofilm on breast implant surfaces has been implicated in capsular contracture and breast implant-associated anaplastic large-cell lymphoma (ALCL). Macrotextured breast implants have been shown to harbor more bacteria than smooth or microtextured implants. Recent reports also suggest that macrotextured implants are associated with a significantly higher incidence of breast implant-associated ALCL. Using techniques to reduce the number of bacteria around implants, specifically, the 14-point plan, has successfully minimized the occurrence of capsular contracture. The authors hypothesize that a similar effect may be seen in reducing the risk of breast implant-associated ALCL. METHODS: Pooled data from eight plastic surgeons assessed the use of macrotextured breast implants (Biocell and polyurethane) and known cases of breast implant-associated ALCL. Surgeon adherence to the 14-point plan was also analyzed. RESULTS: A total of 42,035 Biocell implants were placed in 21,650 patients; mean follow-up was 11.7 years (range, 1 to 14 years). A total of 704 polyurethane implants were used, with a mean follow-up of 8.0 years (range, 1 to 20 years). The overall capsular contracture rate was 2.2 percent. There were no cases of implant-associated ALCL. All surgeons routinely performed all 13 perioperative components of the 14-point plan; two surgeons do not routinely prescribe prophylaxis for subsequent unrelated procedures. CONCLUSIONS: Mounting evidence implicates the role of a sustained T-cell response to implant bacteria/biofilm in the development of breast implant-associated ALCL. Using the principles of the 14-point plan to minimize bacterial load at the time of surgery, the development and subsequent sequelae of capsular contracture and breast implant-associated ALCL may be reduced, especially with higher-risk macrotextured implants. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.

Early laparotomy wound failure as the mechanism for incisional hernia formation.

BACKGROUND: Incisional hernia is the most common complication of abdominal surgery leading to reoperation. In the United States, 200,000 incisional hernia repairs are performed annually, often with significant morbidity. Obesity is increasing the risk of laparotomy wound failure. METHODS: We used a validated animal model of incisional hernia formation. We intentionally induced laparotomy wound failure in otherwise normal adult, male Sprague-Dawley rats. Radio-opaque, metal surgical clips served as markers for the use of x-ray images to follow the progress of laparotomy wound failure. We confirmed radiographic findings of the time course for mechanical laparotomy wound failure by necropsy. RESULTS: Noninvasive radiographic imaging predicts early laparotomy wound failure and incisional hernia formation. We confirmed both transverse and craniocaudad migration of radio-opaque markers at necropsy after 28 d that was uniformly associated with the clinical development of incisional hernias. CONCLUSIONS: Early laparotomy wound failure is a primary mechanism for incisional hernia formation. A noninvasive radiographic method for studying laparotomy wound healing may help design clinical trials to prevent and treat this common general surgical complication.

Reversibility of abdominal wall atrophy and fibrosis after primary or mesh herniorrhaphy.

OBJECTIVE: To determine whether primary or mesh herniorrhaphy reverses abdominal wall atrophy and fibrosis associated with hernia formation. BACKGROUND: We previously demonstrated that hernia formation is associated with abdominal wall atrophy and fibrosis after 5 weeks in an animal model. METHODS: A rat model of chronic incisional hernia was used. Groups consisted of uninjured control (UC, n = 8), sham repair (SR, n = 8), unrepaired hernia (UR, n = 8), and 2 repair groups: primary repair (PR, n = 8) or tension-free polypropylene mesh repair (MR, n = 8) hernia repair on postoperative day (POD) 35. All rats were killed on POD 70. Intact abdominal wall strips were cut perpendicular to the wound for tensiometric analysis. Internal oblique muscles were harvested for fiber type and size determination. RESULTS: No hernia recurrences occurred after PR or MR. Unrepaired abdominal walls significantly demonstrated greater stiffness, increased breaking and tensile strengths, yield load and yield energy, a shift to increased type IIa muscle fibers than SR (15.9% vs 9.13%; P < 0.001), and smaller fiber cross-sectional area (CSA, 1792 vs 2669 µm(2); P < 0.001). PR failed to reverse any mechanical changes but partially restored type IIa fiber (12.9% vs 9.13% SR; P < 0.001 vs 15.9% UR; P < 0.01) and CSA (2354 vs 2669 µm(2) SR; P < 0.001 vs 1792 µm(2) UR; P < 0.001). Mesh-repaired abdominal walls demonstrated a trend toward an intermediate mechanical phenotype but fully restored type IIa muscle fiber (9.19% vs 9.13% SR; P > 0.05 vs 15.9% UR; P < 0.001) and nearly restored CSA (2530 vs 2669 µm(2) SR; P < 0.05 vs 1792 µm(2) UR; P < 0.001). CONCLUSIONS: Mesh herniorrhaphy more completely reverses atrophic abdominal wall changes than primary herniorrhaphy, despite failing to restore normal anatomic muscle position. Techniques for hernia repair and mesh design should take into account abdominal wall muscle length and tension relationships and total abdominal wall compliance.

Loss of mechanical strain impairs abdominal wall fibroblast proliferation, orientation, and collagen contraction function.

BACKGROUND: Laparotomy wound load forces are reduced when dehiscence and incisional hernia formation occur. The purpose of this study was to determine the effects of strain loss on abdominal fascial fibroblast proliferation, orientation, and collagen compaction function. METHODS: Cultured rat linea alba fibroblasts were subjected to continuous cyclic strain (CS), CS interrupted at 24 or 48 hours followed by culture at rest (IS-24 and IS-48) or were cultured without mechanical strain (NS). Cell number was measured and images analyzed for cell orientation. Fibroblasts from these groups were seeded onto the surface of (FPCL-S) or mixed into (FPCL-M) a collagen gel matrix and gel area was measured over time. RESULTS: Continuous strain stimulated proliferation when compared with the nonstrained cells. The loss of strain (IS) delayed proliferation compared with CS throughout (P < .05). CS fibroblasts aligned perpendicular to the direction of strain within 12 hours. Within 12 hours of strain loss, IS-48 fibroblasts became significantly less aligned (P < .0001), and seemed similar to the randomly organized NS fibroblasts 48 hours after strain removal. The CS and IS-24 groups demonstrated faster and greater overall FPCL-M compaction than both the IS-48 and NS groups (P < .0002). The CS group contracted the gel faster than the NS group in FPCL-S (P = .029). CONCLUSION: Mechanical strain rapidly induces a proliferative, morphologic, and functional response in abdominal wall fibroblasts that is dependent on the continued presence of the strain signal and quickly lost when the load force is removed. The loss of wound edge tension that occurs during laparotomy wound separation and hernia formation may contribute to impaired wound healing through loss of a key stimulatory mechanical signal with important implications for abdominal wall reconstruction.

Impaired laparotomy wound healing in obese rats.

BACKGROUND: Obesity increases the risk of laparotomy dehiscence and incisional hernia. The aim of this study was to measure the biological effect of obesity on laparotomy wound healing and the formation of incisional hernias. METHODS: Normal-weight Sprague-Dawley (SD) and obese Zucker rats were used in an established laparotomy wound healing and incisional ventral hernia model. Mechanical testing was performed on abdominal wall strips collected from laparotomy wounds. Hernia size was measured by digital imaging. Picrosirius staining for collagen isoforms was observed with polarized microscopy. Abdominal wall fibroblasts were cultured to measure collagen matrix remodeling and proliferation. RESULTS: Laparotomy wound healing was significantly impaired in obese rats. Mechanical strength was lower than in normal-weight rats. Yield load was reduced in the obese group at all time points. Picrosirius red staining showed increased immature type III collagen content and disorganized type I collagen fibers within laparotomy wounds of obese rats. Wound size was significantly larger in the obese group. Collagen matrix remodeling was impaired with fibroblasts from obese rats, but there was no difference in fibroblast proliferation between the obese and normal-weight groups. CONCLUSIONS: We observed for the first time that laparotomy wound healing is impaired in obese rats. The recovery of laparotomy wound strength is delayed due to abnormal collagen maturation and remodeling, possibly due to a defect in fibroblast function. Strategies to improve outcomes for laparotomy wound healing in obese patients should include correcting the wound healing defect, possibly with growth factor or cell therapy.