Public Interest in Breast Augmentation: Analysis and Implications of Google Trends Data.

INTRODUCTION: Breast augmentation is the most common aesthetic surgery performed in the United States (US) annually. Analysis of Google Trends (GT) data may give plastic surgeons useful information regarding worldwide, national, and regional interest for breast augmentation and other commonly performed aesthetic surgeries. METHODS: Data were collected using GT for breast augmentation and associated search terms from January 2004 to May 2017. Case volume was obtained from the American Society of Plastic Surgeons (ASPS) annual reports for the calendar year 2005-2016. RESULTS: Trend analysis showed that total search term volume for breast augmentation and breast implants gradually decreased worldwide and in the US over the study period while the search term boob job slowly increased. Univariate linear regression demonstrated a statistically significant positive correlation between average annual Google search volume of "breast augmentation" and the annual volume of breast augmentations performed in the US according to ASPS data (R 2 = 0.44, p = 0.018). There was no significant correlation between national volume of breast augmentations performed and search volume using the terms "breast implants" or "boob job" over time (p = 0.84 and p = 0.07, respectively). In addition, there appears to be country specific variation in interest based on time of year and peaks in interest following specific policies. CONCLUSIONS: To our knowledge, this is the first and only analysis of GT data in the plastic surgery literature to date. To that end, this study highlights this large and potentially powerful data set for plastic surgeons both in the US and around the world. LEVEL OF EVIDENCE V: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Lower Eyelid Blepharoplasty: Does the Literature Support the Longevity of this Procedure?

BACKGROUND: Lower eyelid blepharoplasty has continued to evolve with ongoing debate regarding optimal techniques. Despite large case series publishing excellent results and minimal complications, the true longevity of these procedures remains unclear. OBJECTIVES: The aim of this study was to determine how thoroughly the aesthetic surgery literature assesses the longevity of lower blepharoplasty. METHODS: A 20-year comprehensive literature review from 1997 to 2017 was conducted. The titles and abstracts of 180 articles were reviewed, yielding 86 potential publications; 49 studies met inclusion criteria and were analyzed. RESULTS: A total of 10,698 patients were included for analysis. Reported follow-up ranged between 1 week and 192 months. Mean follow-up was 14.8 months for the 29 studies (59.2%) that reported these data. Pooled analysis of complication rates demonstrated 0.77% (n = 82) reoperation, 0.37% (n = 39) scleral show, 0.25% (n = 27) lid malposition, and 0.24% (n = 25) ectropion rates, among others. Forty-four studies (89.8%) published postoperative photographs with a total of 141 unique postoperative time points that were supported with photographic evidence (mean: 15.3 months; range: 1 week-192 months). In this series, for only 10 patients (0.094%) were postoperative photographs available at time points beyond 24 months. CONCLUSIONS: Lower eyelid blepharoplasty is a powerful procedure with seemingly minimal morbidity despite its technical demands. The longevity of this procedure is poorly supported with photographic evidence in the literature. Studies do not adequately report or represent their follow-up to capture long-lasting results. Standardized reporting of results is needed to ensure that anyone seeking this treatment can be adequately counseled.

Substrate reduction therapy for Krabbe's disease.

Krabbe's disease (KD) is a lysosomal storage disorder in which galactosylceramide, a major glycosphingolipid of myelin, and psychosine (galactose-sphingosine) cannot be adequately metabolized because of a deficiency in galactosylceramidase. Substrate reduction therapy (SRT) has been tested in preclinical studies. The premise of SRT is to reduce the synthesis of substrates that are not adequately digested so that the substrate burden is lowered, resulting in less accumulation of unmetabolized material. SRT is used for Gaucher's disease, in which inhibitors of the terminal biosynthetic step are used. Unfortunately, an inhibitor for the final step of galactosylceramide biosynthesis, i.e., UDP glycosyltransferase 8 (a.k.a. UDP-galactose ceramide galactosyltransferase), has not been found. Approaches that inhibit an earlier biosynthetic step or that lessen the substrate burden by other means, such as genetic manipulations, have been tested in the twitcher mouse model of KD. Either as a stand-alone therapy or in combination with other approaches, SRT slowed the disease course, indicating that this approach has potential therapeutic value. For instance, in individuals with adult-onset disease, SRT theoretically could lessen the production of substrates so that residual enzymatic activity could adequately manage the lower substrate burden. In more severe forms of disease, SRT theoretically could be part of a combination therapy. However, SRT has the potential to impair normal function by reducing the synthesis of galactosylceramide to levels that impede myelin function, or SRT could have other deleterious effects. Thus, multiple issues need to be resolved before this approach is ready for testing in humans. © 2016 Wiley Periodicals, Inc.

Albumin and multiple sclerosis.

Leakage of the blood-brain barrier (BBB) is a common pathological feature in multiple sclerosis (MS). Following a breach of the BBB, albumin, the most abundant protein in plasma, gains access to CNS tissue where it is exposed to an inflammatory milieu and tissue damage, e.g., demyelination. Once in the CNS, albumin can participate in protective mechanisms. For example, due to its high concentration and molecular properties, albumin becomes a target for oxidation and nitration reactions. Furthermore, albumin binds metals and heme thereby limiting their ability to produce reactive oxygen and reactive nitrogen species. Albumin also has the potential to worsen disease. Similar to pathogenic processes that occur during epilepsy, extravasated albumin could induce the expression of proinflammatory cytokines and affect the ability of astrocytes to maintain potassium homeostasis thereby possibly making neurons more vulnerable to glutamate exicitotoxicity, which is thought to be a pathogenic mechanism in MS. The albumin quotient, albumin in cerebrospinal fluid (CSF)/albumin in serum, is used as a measure of blood-CSF barrier dysfunction in MS, but it may be inaccurate since albumin levels in the CSF can be influenced by multiple factors including: 1) albumin becomes proteolytically cleaved during disease, 2) extravasated albumin is taken up by macrophages, microglia, and astrocytes, and 3) the location of BBB damage affects the entry of extravasated albumin into ventricular CSF. A discussion of the roles that albumin performs during MS is put forth.

Plastic Surgery Mortality: An 11-Year, Single-Institution Experience.

BACKGROUND: Systematic reporting of mortality data is lacking in many surgical fields including plastic surgery. Current plastic surgery literature is largely limited to adverse events associated with specific procedures. Without mortality data, it is unclear how the recent growth of patient safety initiatives can rationally impact outcomes. METHODS: We evaluated 11 years of patient outcome data collected prospectively and updated monthly by our department. Paper records were entered into a Health Insurance Portability and Accountability Act-compliant digital database capable of prospectively maintaining future data. Data were reviewed for 5 surgical services in 4 different hospitals that comprise our department's activity. RESULTS: Between 2000 and 2011, a total of 60,834 cases were performed. In this time, a total of 829 (1.4%) negative outcome reports were identified. Of these, a total of 25 (0.04%) cases had an outcome of death (24) or brain death (1). Deaths were either directly or indirectly associated with cardiopulmonary causes, multisystem organ failure, sepsis, massive bleeding, CVA, saddle embolism, or unknown causes. CONCLUSIONS: This study is the largest reported series of cases performed by a single academic plastic surgery service to report overall mortality data.

Aspirin and multiple sclerosis.

Aspirin is widely used to lessen the risks of cardiovascular events. Some studies suggest that patients with multiple sclerosis have an increased risk for some cardiovascular events, for example, venous thromboembolism and perhaps ischemic strokes, raising the possibility that aspirin could lessen these increased risks in this population or subgroups (patients with limited mobility and/or antiphospholipid antibodies). However, aspirin causes a small increased risk of hemorrhagic stroke, which is a concern as it could potentially worsen a compromised blood-brain barrier. Aspirin has the potential to ameliorate the disease process in multiple sclerosis (for example, by limiting some components of inflammation), but aspirin also has the potential to inhibit mitochondrial complex I activity, which is already reduced in multiple sclerosis. In an experimental setting of a cerebral ischemic lesion, aspirin promoted the proliferation and/or differentiation of oligodendrocyte precursors, raising the possibility that aspirin could facilitate remyelination efforts in multiple sclerosis. Other actions by aspirin may lead to small improvements of some symptoms (for example, lessening fatigue). Here we consider potential benefits and risks of aspirin usage by patients with multiple sclerosis.

Exploring Potential Mechanisms Accounting for Iron Accumulation in the Central Nervous System of Patients with Alzheimer's Disease.

Elevated levels of iron occur in both cortical and subcortical regions of the CNS in patients with Alzheimer's disease. This accumulation is present early in the disease process as well as in more advanced stages. The factors potentially accounting for this increase are numerous, including: (1) Cells increase their uptake of iron and reduce their export of iron, as iron becomes sequestered (trapped within the lysosome, bound to amyloid ß or tau, etc.); (2) metabolic disturbances, such as insulin resistance and mitochondrial dysfunction, disrupt cellular iron homeostasis; (3) inflammation, glutamate excitotoxicity, or other pathological disturbances (loss of neuronal interconnections, soluble amyloid ß, etc.) trigger cells to acquire iron; and (4) following neurodegeneration, iron becomes trapped within microglia. Some of these mechanisms are also present in other neurological disorders and can also begin early in the disease course, indicating that iron accumulation is a relatively common event in neurological conditions. In response to pathogenic processes, the directed cellular efforts that contribute to iron buildup reflect the importance of correcting a functional iron deficiency to support essential biochemical processes. In other words, cells prioritize correcting an insufficiency of available iron while tolerating deposited iron. An analysis of the mechanisms accounting for iron accumulation in Alzheimer's disease, and in other relevant neurological conditions, is put forward.

Current thoughts for the prevention and treatment of pressure ulcers: using the evidence to determine fact or fiction.

OBJECTIVE: To use an evidenced-based approach to better understand the management and treatment of pressure ulcers. BACKGROUND: Pressure sores are a cause of significant morbidity in the medical community. Although there are a multitude of preventative and treatment options, there remains some degree of uncertainty in the literature in defining the best way to treat and manage pressure sores. METHODS: An exhaustive literature search was performed using several electronic databases. The search revealed several identified modalities for treatment and/or prevention of pressure ulcers. We then assessed each modality individually for the level of evidence that exists in the most current literature, with preference given to more recent studies (2005 to present). RESULTS: We reviewed the most relevant, high-level evidence that exists for the following modalities for understanding, preventing, and treating pressure ulcers: wound cleansers, repositioning, negative pressure therapy, debridement, enteral and parenteral feeding, vitamin and mineral supplementation, specialized mattresses, ultrasound therapy, honey, cellular therapy, musculocutaneous and fasciocutaneous flap closure, and other miscellaneous therapies. CONCLUSIONS: Although many of these modalities are used, we encourage clinicians and health care providers to consider the evidence-based data when deciding how to most appropriately manage their patients' pressure sores.

Allelic variation on murine chromosome 11 modifies host inflammatory responses and resistance to Bacillus anthracis.

Anthrax is a potentially fatal disease resulting from infection with Bacillus anthracis. The outcome of infection is influenced by pathogen-encoded virulence factors such as lethal toxin (LT), as well as by genetic variation within the host. To identify host genes controlling susceptibility to anthrax, a library of congenic mice consisting of strains with homozygous chromosomal segments from the LT-responsive CAST/Ei strain introgressed on a LT-resistant C57BL/6 (B6) background was screened for response to LT. Three congenic strains containing CAST/Ei regions of chromosome 11 were identified that displayed a rapid inflammatory response to LT similar to, but more severe than that driven by a LT-responsive allele of the inflammasome constituent NRLP1B. Importantly, increased response to LT in congenic mice correlated with greater resistance to infection by the Sterne strain of B. anthracis. The genomic region controlling the inflammatory response to LT was mapped to 66.36-74.67 Mb on chromosome 11, a region that encodes the LT-responsive CAST/Ei allele of Nlrp1b. However, known downstream effects of NLRP1B activation, including macrophage pyroptosis, cytokine release, and leukocyte infiltration could not fully explain the response to LT or the resistance to B. anthracis Sterne in congenic mice. Further, the exacerbated response in congenic mice is inherited in a recessive manner while the Nlrp1b-mediated response to LT is dominant. Finally, congenic mice displayed increased responsiveness in a model of sepsis compared with B6 mice. In total, these data suggest that allelic variation of one or more chromosome 11 genes in addition to Nlrp1b controls the severity of host response to multiple inflammatory stimuli and contributes to resistance to B. anthracis Sterne. Expression quantitative trait locus analysis revealed 25 genes within this region as high priority candidates for contributing to the host response to LT.

A novel approach to frontal sinus surgery: treatment algorithm revisited.

BACKGROUND: Access to the frontal sinus remains a challenging problem for the craniofacial surgeon. A wide array of techniques including minimally invasive endoscopic approaches have been described. Here we present our technique using medical modeling to gain fast and safe access for multiple indications. METHODS: Computer-aided surgery involves several distinct phases: planning, modeling, surgery, and evaluation. Computer-aided, precise cutting guides are designed preoperatively and allowed to perfectly outline and then cut the anterior table of the frontal sinus at its junction to the surrounding frontal bone. The outcomes are evaluated by postoperative three-dimensional computed tomography scan. RESULTS: Eight patients sustaining frontal sinus fractures were treated with the aid of medical modeling. Three patients (37.5%) had isolated anterior table fractures, and 4 (50%) had combined anterior and posterior table fractures, whereas 1 patient (12.5%) sustained isolated posterior table fractures. Operative times were significantly shorter using the cutting guides, and fracture reduction was more precise. There was no statistically significant difference in complication rates or overall patient satisfaction. CONCLUSIONS: The surgical approach to the frontal sinus can be made more efficient, safe, and precise when using computer-aided medical modeling to create customized cutting guides.

Chairs and chiefs of plastic surgery: is it an insider job?

PURPOSE: There is no more important decision an academic Plastic Surgery Department or Division can make than naming a chair or chief. Externally recruited leadership brings fresh perspectives and connections. Critics, however, argue that they lack the in-depth knowledge of the institution's culture and history that may be needed to succeed. The ability and skill of an internal candidate is already known and can increase the odds of that person's success in the leadership position. Finally, external recruitment can be a more costly process. Ultimately, the decision is really a litmus test for a Plastic Surgery program. The authors aim to evaluate factors influencing ascent in Plastic Surgery leadership, including training history, internal promotion, and external recruiting. METHODS: All Plastic Surgery residency programs accredited by the Accreditation Council for Graduate Medical Education were noted (n = 71). Academic departmental chairs or divisional chiefs of these residency programs were identified at the time of study design (October 1, 2011). For each chair or chief, gender, training history, and faculty appointment immediately prior to the current leadership position was recorded. RESULTS: There were 71 academic chairs or chiefs of Plastic Surgery residency programs at the time of data collection. The majority (62%) had done fellowship training following Plastic Surgery residency. Fellowships included hand (43%), craniofacial (29%), microsurgery (18%), and other types (10%). The majority (73%) of leaders were internal hires (P < 0.01), having faculty appointments at their institutions prior to promotion. However, only a fraction (22%) of these internal hires had done Plastic Surgery residency or fellowship training at that institution (P < 0.01). External recruits consisted of 27% of all 71 academic hires (P < 0.01). CONCLUSIONS: Many factors influence the decision to recruit leadership from internally or to hire an external candidate. These include the time to fill the position, program culture, candidate experience, and cost. These results support that the insider/outsider hire decision is ultimately one of duality. That dichotomy is achieved with an emphasis on internal promotion, but always with an eye towards the advantages of bringing in external talent as a valuable contribution to increase organizational success.

Ten-year evolution utilizing computer-assisted reconstruction for giant ameloblastoma.

BACKGROUND: The authors describe our current practice of computer-aided virtual planned and pre-executed surgeries using microvascular free tissue transfer with immediate placement of implants and dental prosthetics. METHODS: All patients with ameloblastomas treated at New York University (NYU) Medical Center during a 10-year period from September 2001 to December 2011 were identified. Of the 38 (36 mandible/2 maxilla) patients that were treated in this time period, 20 were identified with advanced disease (giant ameloblastoma) requiring aggressive resection. Reconstruction of the resultant defects utilized microvascular free tissue transfer with an osseocutaneous fibular flap in all 20 of these patients. RESULTS: Of the patients reconstructed with free vascularized tissue transfer, 35% (7/20) developed complications. There were two complete flap failures with consequent contralateral fibula flap placement. Sixteen patients to date have undergone placement of endosteal implants for complete dental rehabilitation, nine of which received immediate placement of the implants at the time of the free flap reconstruction. The three most recent patients received immediate placement of dental implants at the time of microvascular free tissue transfer as well as concurrent placement of dental prosthesis. CONCLUSIONS: To our knowledge, this patient cohort represents the largest series of comprehensive computer aided free-flap reconstruction with dental restoration for giant type ameloblastoma.

The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.

Chlorosis in azaleas is characterized by an interveinal yellowing of leaves that is typically caused by a deficiency of iron. This condition is usually due to the inability of cells to properly acquire iron as a consequence of unfavorable conditions, such as an elevated pH, rather than insufficient iron levels. The causes and effects of chlorosis were found to have similarities with those pertaining to a recently presented hypothesis that describes a pathogenic process in Alzheimer disease. This hypothesis states that iron becomes sequestered (e.g., by amyloid ß and tau), causing a functional deficiency of iron that disrupts biochemical processes leading to neurodegeneration. Additional mechanisms that contribute to iron becoming unavailable include iron-containing structures not undergoing proper recycling (e.g., disrupted mitophagy and altered ferritinophagy) and failure to successfully translocate iron from one compartment to another (e.g., due to impaired lysosomal acidification). Other contributors to a functional deficiency of iron in patients with Alzheimer disease include altered metabolism of heme or altered production of iron-containing proteins and their partners (e.g., subunits, upstream proteins). A review of the evidence supporting this hypothesis is presented. Also, parallels between the mechanisms underlying a functional iron-deficient state in Alzheimer disease and those occurring for chlorosis in plants are discussed. Finally, a model describing the generation of a functional iron deficiency in Alzheimer disease is put forward.

Examining the Role of a Functional Deficiency of Iron in Lysosomal Storage Disorders with Translational Relevance to Alzheimer's Disease.

The recently presented Azalea Hypothesis for Alzheimer's disease asserts that iron becomes sequestered, leading to a functional iron deficiency that contributes to neurodegeneration. Iron sequestration can occur by iron being bound to protein aggregates, such as amyloid ß and tau, iron-rich structures not undergoing recycling (e.g., due to disrupted ferritinophagy and impaired mitophagy), and diminished delivery of iron from the lysosome to the cytosol. Reduced iron availability for biochemical reactions causes cells to respond to acquire additional iron, resulting in an elevation in the total iron level within affected brain regions. As the amount of unavailable iron increases, the level of available iron decreases until eventually it is unable to meet cellular demands, which leads to a functional iron deficiency. Normally, the lysosome plays an integral role in cellular iron homeostasis by facilitating both the delivery of iron to the cytosol (e.g., after endocytosis of the iron-transferrin-transferrin receptor complex) and the cellular recycling of iron. During a lysosomal storage disorder, an enzyme deficiency causes undigested substrates to accumulate, causing a sequelae of pathogenic events that may include cellular iron dyshomeostasis. Thus, a functional deficiency of iron may be a pathogenic mechanism occurring within several lysosomal storage diseases and Alzheimer's disease.

Exploring Whether Iron Sequestration within the CNS of Patients with Alzheimer's Disease Causes a Functional Iron Deficiency That Advances Neurodegeneration.

The involvement of iron in the pathogenesis of Alzheimer's disease (AD) may be multifaceted. Besides potentially inducing oxidative damage, the bioavailability of iron may be limited within the central nervous system, creating a functionally iron-deficient state. By comparing staining results from baseline and modified iron histochemical protocols, iron was found to be more tightly bound within cortical sections from patients with high levels of AD pathology compared to subjects with a diagnosis of something other than AD. To begin examining whether the bound iron could cause a functional iron deficiency, a protein-coding gene expression dataset of initial, middle, and advanced stages of AD from olfactory bulb tissue was analyzed for iron-related processes with an emphasis on anemia-related changes in initial AD to capture early pathogenic events. Indeed, anemia-related processes had statistically significant alterations, and the significance of these changes exceeded those for AD-related processes. Other changes in patients with initial AD included the expressions of transcripts with iron-responsive elements and for genes encoding proteins for iron transport and mitochondrial-related processes. In the latter category, there was a decreased expression for the gene encoding pitrilysin metallopeptidase 1 (PITRM1). Other studies have shown that PITRM1 has an altered activity in patients with AD and is associated with pathological changes in this disease. Analysis of a gene expression dataset from PITRM1-deficient or sufficient organoids also revealed statistically significant changes in anemia-like processes. These findings, together with supporting evidence from the literature, raise the possibility that a pathogenic mechanism of AD could be a functional deficiency of iron contributing to neurodegeneration.

Pathogenic implications of iron accumulation in multiple sclerosis.

Iron, an essential element used for a multitude of biochemical reactions, abnormally accumulates in the CNS of patients with multiple sclerosis (MS). The mechanisms of abnormal iron deposition in MS are not fully understood, nor do we know whether these deposits have adverse consequences, that is, contribute to pathogenesis. With some exceptions, excess levels of iron are represented concomitantly in multiple deep gray matter structures often with bilateral representation, whereas in white matter, pathological iron deposits are usually located at sites of inflammation that are associated with veins. These distinct spatial patterns suggest disparate mechanisms of iron accumulation between these regions. Iron has been postulated to promote disease activity in MS by various means: (i) iron can amplify the activated state of microglia resulting in the increased production of proinflammatory mediators; (ii) excess intracellular iron deposits could promote mitochondria dysfunction; and (iii) improperly managed iron could catalyze the production of damaging reactive oxygen species (ROS). The pathological consequences of abnormal iron deposits may be dependent on the affected brain region and/or accumulation process. Here, we review putative mechanisms of enhanced iron uptake in MS and address the likely roles of iron in the pathogenesis of this disease.

Potential immunological consequences of pharmacological suppression of gastric acid production in patients with multiple sclerosis.

Corticosteroids are standard treatment for patients with multiple sclerosis experiencing acute relapse. Because dyspeptic pain is a common side effect of this intervention, patients can be given a histamine receptor-2 antagonist, proton pump inhibitor or antacid to prevent or ameliorate this disturbance. Additionally, patients with multiple sclerosis may be taking these medications independent of corticosteroid treatment. Interventions for gastric disturbances can influence the activation state of the immune system, a principal mediator of pathology in multiple sclerosis. Although histamine release promotes inflammation, activation of the histamine receptor-2 can suppress a proinflammatory immune response, and blocking histamine receptor-2 with an antagonist could shift the balance more towards immune stimulation. Studies utilizing an animal model of multiple sclerosis indicate that histamine receptor-2 antagonists potentially augment disease activity in patients with multiple sclerosis. In contrast, proton pump inhibitors appear to favor immune suppression, but have not been studied in models of multiple sclerosis. Antacids, histamine receptor-2 antagonists and proton pump inhibitors also could alter the intestinal microflora, which may indirectly lead to immune stimulation. Additionally, elevated gastric pH can promote the vitamin B12 deficiency that patients with multiple sclerosis are at risk of developing. Here, we review possible roles of gastric acid inhibitors on immunopathogenic mechanisms associated with multiple sclerosis.

Cutting edge: resistance to Bacillus anthracis infection mediated by a lethal toxin sensitive allele of Nalp1b/Nlrp1b.

Pathogenesis of Bacillus anthracis is associated with the production of lethal toxin (LT), which activates the murine Nalp1b/Nlrp1b inflammasome and induces caspase-1-dependent pyroptotic death in macrophages and dendritic cells. In this study, we investigated the effect of allelic variation of Nlrp1b on the outcome of LT challenge and infection by B. anthracis spores. Nlrp1b allelic variation did not alter the kinetics or pathology of end-stage disease induced by purified LT, suggesting that, in contrast to previous reports, macrophage lysis does not contribute directly to LT-mediated pathology. However, animals expressing a LT-sensitive allele of Nlrp1b showed an early inflammatory response to LT and increased resistance to infection by B. anthracis. Data presented here support a model whereby LT-mediated activation of Nlrp1b and subsequent lysis of macrophages is not a mechanism used by B. anthracis to promote virulence, but rather a protective host-mediated innate immune response.

Hemangioma update: pearls from 30 years of treatment.

This manuscript is a compilation of clinical lessons learned from 30 years of treating hemangiomas. We review relevant clinical anatomy, the role of lasers and medications, timing of surgery, and operative judgment, as it pertains to the treatment of hemangiomas.

Outcomes of delayed abdominal-based autologous reconstruction versus latissimus dorsi flap plus implant reconstruction in previously irradiated patients.

BACKGROUND: Local recurrence after breast conservation therapy is usually managed with salvage mastectomy. Multiple methods of reconstruction are possible, although delayed autologous reconstruction provides the most reliable results. METHODS: We compared complications in delayed abdominal-based [transverse rectus abdominis muscle (TRAM)/deep inferior epigastric perforator (DIEP)] reconstruction with delayed latissimus dorsi plus implant-based reconstruction in previously irradiated breasts. The authors reviewed 133 consecutive cases of delayed breast reconstructions performed in patients who had postmastectomy radiation therapy and reconstruction with abdominal-based methods (single-pedicle TRAM, supercharged pedicle TRAM, muscle-sparing TRAM free flap, DIEP flap, and superficial inferior epigastric artery flap) or a pedicled latissimus dorsi flap plus implant. Complications for donor and recipient sites were recorded including infection, seroma, hematoma, and partial flap loss. RESULTS: Seventy-five patients were reconstructed with abdominal-based flaps (37 muscle-sparing TRAMs, 19 pedicled TRAMs, 12 DIEPs, 6 supercharged pedicled TRAMs, and 1 superficial inferior epigastric artery). Their median age was 50 years and mean follow-up was 22.7 months. Three (4.0%) patients required reoperation during the same hospital visit for vascular compromise that resulted in 2 (2.7%) flap failures. Three (4.0%) patients had partial flap loss that ultimately required debridement and primary closure. Seventeen (22.7%) patients had minor complications including seroma, small hematoma, cellulitis, and abdominal bulge. Fifty-six patients were reconstructed with latissimus dorsi flaps plus implants. Their median age was 47 years and mean follow-up was 32 months. Three (5.4%) patients developed infections resulting in implant loss. Four (7.1%) patients had partial flap loss that required debridement and primary closure. Thirteen (23.2%) patients had minor complications including seroma (12 patients) and hematoma (1 patient) that required drainage. Fisher exact test was used to determine statistical significance of complication and failure rates between the 2 types of reconstruction. In patients who had postmastectomy radiation therapy, those with abdominal-based reconstructions had fewer complications compared with latissimus dorsi flap plus implant reconstructions (28.0% vs 30.4%, P=0.846). Also, fewer reconstructions failed in patients with abdominal-based reconstruction (2.7% vs 5.4%, P=0.650). CONCLUSIONS: Abdominal-based autologous reconstruction had fewer complications and fewer reconstruction failures than latissimus dorsi flap plus implant reconstructions in patients with postmastectomy radiation therapy in our series; however, these rates were not statistically significant.