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Many injured patients are transported directly to trauma centers, found to be minimally injured, and discharged directly home from the emergency department (ED). Our objectives were to characterize the short-term outcomes in this discharged patient population and to identify patient factors predictive of ED return visits.We conducted a retrospective population-based cohort study using linked administrative data sets involving patients assessed at trauma centers in Ontario, Canada between April 1, 2009, and March 31, 2020. Patients who were assessed by a trauma team and discharged directly home from ED were included. The primary outcome was the percentage of patients with an ED return visit within 14 days. We used multivariate logistic regression analyses to identify patient characteristics predictive of at least one ED return visit.There were 5,550 patients included in the study. A total of 1,004 (18.1%) of patients had at least one ED return visit, but only 100 patients (1.8%) were admitted to hospital following initial discharge. Common reasons for ED return visits included wound care concerns (17.2%), head injury complaints (15.6%), and substance misuse (6.8%). Rural residence (odds ratio [OR], 1.83; 95% CI, 1.45-2.29), history of anxiety disorder (OR, 2.05; 95% CI, 1.54-2.73), high baseline ED usage (OR, 2.58; 95% CI, 2.03-3.28), penetrating injury (OR, 1.42; 95% CI, 1.20-1.68), and extremity fracture (OR, 1.52; 95% CI, 1.24-1.88) predicted return visits.Patients discharged directly have high rates of ED return visits but low rates of hospital admission or delayed surgical intervention. Trauma services should expand quality assurance initiatives to capture return visits, understand any gaps in clinical service provision, and aim to minimize unnecessary ED return visits.Prognostic/Epidemiological; Level IV.

Introduction Children with Apert syndrome have hypertelorism and midfacial hypoplasia, which can be treated with facial bipartition (FB), often aided by rigid external distraction. The technique involves a midline osteotomy that lateralizes the maxillary segments, resulting in posterior cross-bites and midline diastema. Varying degrees of spontaneous realignment of the dental arches occurs postoperatively. This study aims to quantify these movements and assess whether they occur as part of a wider skeletal relapse or as dental compensation. Methods Patients who underwent FB and had high quality computed tomography scans at the preoperative stage, immediately postsurgery, and later postoperatively were reviewed. DICOM files were converted to three-dimensional bone meshes and anatomical point-to-point displacements were quantified using nonrigid iterative closest point registration. Displacements were visualized using arrow maps, thereby providing an overview of the movements of the facial skeleton and dentition. Results Five patients with Apert syndrome were included. In all cases, the arrow maps demonstrated initial significant anterior movement of the frontofacial segment coupled with medial rotation of the orbits and transverse divergence of the maxillary arches. The bony position following initial surgery was shown to be largely stable, with primary dentoalveolar relapse correcting the dental alignment. Conclusions This study showed that spontaneous dental compensation occurs following FB without compromising the surgical result. It may be appropriate to delay active orthodontic for 6-months postoperatively until completion of this early compensatory phase.

Kidneys donated after circulatory death (DCD) are increasingly being used for transplantation in adults to alleviate organ shortage. Pediatric data on survival benefits of DCD transplantation compared with remaining on the waitlist for a kidney donated after brain death (DBD) offer are lacking.We used Scientific Registry of Transplant Recipients to identify 285 pediatric (18 y) DCD kidney transplants performed between 1987 and 2017. Propensity score matching was used to create a comparison group of 1132 DBD transplants. We used sequential Cox analysis to evaluate survival benefit of DCD transplantation versus remaining on the waitlist and Cox regression to evaluate patient and graft survival.DCD transplantation was associated with a higher incidence of delayed graft function (adjusted odds ratio: 3.0; P 0.001). The risks of graft failure (adjusted hazard ratio [aHR], 0.89; P = 0.46) and death (aHR, 1.2; P = 0.67) were similar between DCD and DBD recipients. We found a significant survival benefit of DCD transplantation compared with remaining on the waitlist awaiting a DBD kidney (aHR, 0.44; P = 0.03).Despite a higher incidence of delayed graft function, long-term patient and graft survival are similar between pediatric DCD and DBD kidney transplant recipients. DCD transplantation in children is associated with a survival benefit, despite pediatric priority for organ allocation, compared with remaining on the waitlist.

BACKGROUND Preoperative thrombocytopenia is associated with inferior outcomes in surgical patients, though concurrent anemia may obfuscate these relationships. This investigation assesses the prevalence and clinical significance of preoperative thrombocytopenia with thorough consideration of preoperative anemia status. METHODS This is an observational cohort study of adults undergoing elective surgery with planned postoperative hospitalization from January 1, 2009 to May 3, 2018. Patients were designated into 4 groups: normal platelet and hemoglobin concentrations, isolated thrombocytopenia (ie, platelet count

Background Microtia is an inherited condition that results in varying degrees of external ear deformities; the most extreme form is anotia. Effective surgical reconstruction techniques have been developed. However, these usually require multistage procedures and have other inherent disadvantages. Tissue engineering technologies offer new approaches in the field of external ear reconstruction. In this setting, chondrocytes are cultured in the laboratory with the aim of creating bioengineered cartilage matrices. However, cartilage engineering has many challenges, including difficulty in culturing sufficient chondrocytes. To overcome these hurdles, the authors propose a novel model of cartilage engineering that involves co-culturing chondrocytes and adipose-derived stem cells on an allograft adipose-derived extracellular matrix scaffold. Methods Auricular chondrocytes from porcine ear were characterized. Adipose-derived stem cells were isolated and expanded from human lipoaspirate. Then, the auricular chondrocytes were cultured on the allograft adipose matrix either alone or with the adipose-derived stem cells at different ratios and examined histologically. Results Cartilage induction was most prominent when the cells were co-cultured on the allograft adipose matrix at a ratio of 1:9 (auricular chondrocyte-to-adipose-derived stem cell ratio). Furthermore, because of the xenogeneic nature of the experiment, the authors were able to determine that the adipose-derived stem cells contributed to chondrogenesis by means of a paracrine stimulation of the chondrocytes. Conclusions In this situation, adipose-derived stem cells provide sufficient support to induce the formation of cartilage when the number of auricular chondrocytes available is limited. This novel model of cartilage engineering provides a setting for using the patient's own chondrocytes and adipose tissue to create a customized ear framework that could be further used for surgical reconstruction.

Objective: LIPA (lysosomal acid lipase) mediates cholesteryl ester hydrolysis, and patients with rare loss-of-function mutations develop hypercholesterolemia and severe disease. Genome-wide association studies of coronary artery disease have identified several tightly linked, common intronic risk variants in LIPA which unexpectedly associate with increased mRNA expression. However, an exonic variant (rs1051338 resulting in T16P) in linkage with intronic variants lies in the signal peptide region and putatively disrupts trafficking. We sought to functionally investigate the net impact of this locus on LIPA and whether rs1051338 could disrupt LIPA processing and function to explain coronary artery disease risk. Approach and Results: In monocytes isolated from a large cohort of healthy individuals, we demonstrate both exonic and intronic risk variants are associated with increased LIPA enzyme activity coincident with the increased transcript levels. To functionally isolate the impact of rs1051338, we studied several in vitro overexpression systems and consistently observed no differences in LIPA expression, processing, activity, or secretion. Further, we characterized a second common exonic coding variant (rs1051339), which is predicted to alter LIPA signal peptide cleavage similarly to rs1051338, yet is not linked to intronic variants. rs1051339 also does not impact LIPA function in vitro and confers no coronary artery disease risk. Conclusions: Our findings show that common LIPA exonic variants in the signal peptide are of minimal functional significance and suggest coronary artery disease risk is instead associated with increased LIPA function linked to intronic variants. Understanding the mechanisms and cell-specific contexts of LIPA function in the plaque is necessary to understand its association with cardiovascular risk.

In FGFR2 craniosynostosis, midfacial hypoplasia features oculo-orbital disproportion and symptomatic exorbitism. Clinical consequences may mandate surgery at a young age to prevent globe subluxation, corneal ulceration, and potential loss of vision. Monobloc osteotomy and distraction osteogenesis (monobloc distraction) seek to correct exorbitism. A report of the age-related impact of monobloc osteotomy and distraction osteogenesis on orbital volume, globe volume, and globe protrusion is presented.Computed tomographic scan data from 28 Crouzon-Pfeiffer patients were assessed at preoperative, early postoperative, and 1-year follow-up time points. Orbital volumes, globe volumes, and globe protrusions were measured by manual and semiautomatic segmentation techniques, and these were compared to 40 age-matched controls.Crouzon-Pfeiffer syndrome orbital volumes are significantly small, and are significantly overexpanded by distraction to endpoints correcting symptomatic exorbitism. Globe volumes are significantly larger than controls under 5 years, do not independently correlate with globe protrusion, and are unaffected by surgery. Correlation between orbital volume expansion and reduction of globe protrusion is not significant. Age-related variations of postoperative growth potential occur to 1 year postoperatively. The Crouzon-Pfeiffer syndrome FGFR2 orbit exhibits early growth acceleration followed by premature growth arrest at 10 to 14 years.Orbital volume expansion by monobloc osteotomy and distraction osteogenesis is not the sole determinant of reduced globe protrusion. Mean volume relapse of the orbit at 1 year is insignificant across the series. Derived Crouzon-Pfeiffer growth curves suggest that "early functional monobloc" in infants occurs on a background of dynamic orbital growth, which remains programmed to a Crouzon-Pfeiffer FGFR2 phenotype and aligns with the incidence of delayed clinical regression and later secondary surgery.Therapeutic, IV.

This article describes the formation of the International Confederation of Plastic Surgery Societies (ICOPLAST) as a novel, transparent, dynamic, and proactive confederation of national plastic surgery societies. ICOPLAST aspires to provide a voice for the entire international community of plastic surgeons. ICOPLAST has been designed to benefit the patient, plastic surgery as a profession, and each individual plastic surgeon. Its principal objective is to enhance international communication, education, and advocacy processes to ultimately improve patient outcomes for plastic surgery patients globally. The new ICOPLAST's focus is to add true value for patients. ICOPLAST's evolution, philosophy, governance, and bylaws are explained and all societies worldwide are encouraged and cordially invited to join. An open and warm invitation is provided. Additional information is found at www.ICOPLAST.org.

BACKGROUND Although recent estimates predict a large impending shortage of plastic surgeons, graduate medical education funding through the Centers for Medicare and Medicaid Services remains capped by the 1997 Balanced Budget Act. The authors' aim was to develop a plan to stimulate legislative action. METHODS The authors reviewed responses of the American Society of Plastic Surgeons, American College of Surgeons, and American Medical Association from January of 2015 to a House Energy & Commerce Committee request for input on graduate medical education funding. In addition, all program directors in plastic surgery were surveyed through the American Council of Academic Plastic Surgeons to determine their graduate medical education funding sources. RESULTS All three organizations agree that current graduate medical education funding is inadequate to meet workforce needs, and this has a significant impact on specialty selection and distribution for residency training. All agreed that funding should be tied to the resident rather than to the institution, but disagreed on whether funds should be divided between direct (allocated to residency training) and indirect (allocated to patient care) pools, as is currently practiced. Program directors' survey responses indicated that only 38 percent of graduate medical education funds comes from the Centers for Medicare and Medicaid Services. CONCLUSIONS Organized medicine is at risk of losing critically needed graduate medical education funding. Specific legislation to support additional graduate medical education positions and funding (House Resolutions 1180 and 4282) has been proposed but has not been universally endorsed, in part because of a lack of collaboration in organized medicine. Collaboration among major organizations can reinvigorate these measures and implement real change in funding.

Background: Autophagy, lipid metabolism, and inflammation are interrelated cellular processes that implicate lysosomes in human disease. After ischemia reperfusion (IR) injury, inflammasome activation and interleukin 1-beta (IL1-beta) secretion promote heart failure progression. Whether macrophage autophagy and lysosomal biogenesis can attenuate post-IR remodeling and inflammation is unknown. We hypothesized that macrophages exhibit lysosome dysfunction and autophagic impairment after IR injury, and that augmentation of macrophage lysosomal biogenesis via macrophage-specific overexpression of transcription factor EB (Mf-TFEB), a master regulator of autophagy and lysosomal biogenesis, would attenuate myocardial remodeling and inflammation in ischemic cardiomyopathy. Methods and Results: In mice subject to IR injury and humans with ischemic cardiomyopathy, we observed evidence of lysosomal and autophagic impairment. To ameliorate post-IR macrophage lysosomal injury, we expressed Mf-TFEB in a closed-chest IR murine model using a tamoxifen-inducible CX3CR1erCre and TFEB overexpression cassette bearing a Cre-excisable STOP codon. Compared to Cre-only controls, Mf-TFEB mice had significantly increased left ventricular (LV) ejection fraction 28-days post-IR (40% relative increase, p=0.002, n=15-17 per group), decreased abundance of pro-inflammatory macrophages, and reduced levels of IL1-beta in myocardial tissue. Surprisingly, neither inflammasome suppression nor TFEB-mediated attenuation of post-IR remodeling required intact macro-autophagy as evidenced by Mf-TFEB-mediated rescue of post-IR LV dysfunction in mice with concomitant inducible ATG5 ablation. RNA sequencing of flow-sorted macrophages from post-IR mice identified lysosomal acid lipase amongst other lipases regulated by TFEB. Mechanistically, pharmacologic inhibition of lysosomal acid lipase specifically abrogated the in vivo effects of TFEB on post-IR remodeling. Conclusions: Our findings suggest that macrophage TFEB regulates lysosomal lipolysis to attenuate inflammasome activity and protect against post-IR LV dysfunction, suggesting an alternative paradigm for how lysosome function may impact acute inflammation in vivo.

BackgroundTamoxifen is an important adjunct therapy in breast cancer treatment; however, it has been implicated in increasing microvascular flap complications. Current recommendations on stopping tamoxifen are conflicting and do not address tamoxifen therapy that is continued perioperatively. The pu

The ability of macrophage lysosomes to degrade both exogenous and internally derived cargo is paramount to handling the overabundance of lipid and cytotoxic material present in the atherosclerotic plaque. We will discuss recent insights in both classical and novel functions of the lysosomal apparatus, as it pertains to the pathophysiology of atherosclerosis.Lipid-mediated dysfunction in macrophage lysosomes appears to be a critical event in plaque progression. Consequences include enhanced inflammatory signalling [particularly the inflammasome/interleukin-1β axis] and an inability to interface with autophagy leading to a proatherogenic accumulation of dysfunctional organelles and protein aggregates. Aside from degradation, several novel functions have recently been ascribed to lysosomes, including involvement in macrophage polarization, generation of lipid signalling intermediates and serving as a nutrient depot for mechanistic target of rapamycin activation, each of which can have profound implications in atherosclerosis. Finally, the discovery of the transcription factor transcription factor EB as a mechanism of inducing lysosomal biogenesis can have therapeutic value by reversing lysosomal dysfunction in macrophages.Lysosomes are a central organelle in the processing of exogenous and intracellular biomolecules. Together with recent data that implicate the degradation products of lysosomes in modulation of signalling pathways, these organelles truly do lay at a nexus in nutrient sensing and processing. Dissecting the full repertoire of lysosome function and ensuing dysfunction in plaque macrophages is pivotal to our understanding of atherogenesis.

Background Anticipating poor recovery due to impaired self-management and appointment-keeping, clinicians may consider serious mental illness (SMI) a significant concern in organ transplantation. However, little empirical evidence exists regarding posttransplantation outcomes for patients with SMI. Methods This study analyzed health services data to evaluate posttransplantation 3-year survival by SMI status in a nationwide cohort of patients in the Veterans Health Administration (VHA). Results A total of 960 recipients of solid organ or bone marrow transplants were identified from Veterans Health Administration administrative data extracts for fiscal years 2006 to 2009. Of these, 164 (17%) had an SMI diagnosis before transplantation (schizophrenia, posttraumatic stress, major depressive, and bipolar disorders); 301 (31%) had some other mental illness diagnosis (such as anxiety, adjustment reactions, or substance abuse); and 495 (52%) had no mental health diagnosis. Twenty-two patients (2%) required retransplantation and 208 patients (22%) died during follow-up. Data on whether these were primary or repeat transplantations were unavailable. Rates of attendance at postoperative outpatient visits and number of months for which immunosuppressive drugs fills were recorded were similar among mental illness groups, as were rates of diagnosed immunological rejection. Three-year mortality was equivalent among mental health groups: no mental health (19%) versus other mental illness (23%) versus SMI (27%; χ(2) = 5.11; df = 2; P = .08). In adjusted survival models, no effect of mental health status was observed. Conclusions Serious mental illness diagnosis does not appear to be associated with adverse transplantation outcomes over the first 3 years; however, a potentially diverging survival curve may portend higher mortality at 5 years.

The authors present a review of biomaterials, substances traditionally derived from human or animal tissue or, more recently, biodegradable synthetics modeled after naturally occurring resources. These constructs differ from purely synthetic materials in that they are degraded or incorporated into a host's tissue. These biomaterials include a diverse array of medical products, such as acellular dermal matrix, bone substitutes, and injectables. In this review, the authors examine various clinical applications, including burn reconstruction and wound healing, breast surgery, complex abdominal wall reconstruction, craniofacial repair, and cosmetic surgery. Biomaterials such as acellular dermal matrix have proven beneficial in difficult-to-treat applications; however, more prospective data are needed to determine their true efficacy and cost-effectiveness.

BACKGROUND There are limited data regarding blood transfusion following abdominoplasty, especially in post-bariatric surgery patients. The purpose of this study was to evaluate (1) the frequency and outcomes of blood transfusion in post-bariatric surgery patients undergoing abdominoplasty and (2) the predictive risk factors of blood transfusion in this patient population. METHODS Using the Nationwide Inpatient Sample database, the authors examined the clinical data of patients with a history of bariatric surgery who underwent abdominoplasty from 2007 to 2011 in the United States. RESULTS A total of 20,130 post-bariatric surgery patients underwent abdominoplasty during this period. Overall, 1871 patients (9.3 percent) received blood transfusion. Chronic anemia patients had the highest rate of blood transfusion (25.6 percent). Post-bariatric surgery patients who received blood transfusion experienced a significantly higher complication rate (10.1 percent versus 4.8 percent; p < 0.01), longer mean hospital stay (4.0 days versus 2.4 days; p < 0.01), and higher mean total hospital charges ($49,116 versus $33,927; p < 0.01). Multivariate regression analysis showed that deficiency anemia (adjusted OR, 3.8), congestive heart failure (adjusted OR, 2.4), concurrent breast reduction (adjusted OR, 1.5), diabetes mellitus (adjusted OR, 1.4), coronary artery disease (adjusted OR, 1.4), African American race (adjusted OR, 1.4), Hispanic race (adjusted OR, 1.4), and female sex (adjusted OR, 1.3) were all independent risk factors for blood transfusion. CONCLUSIONS The blood transfusion rate in post-bariatric surgery abdominoplasty patients is not insignificant. Chronic anemia and congestive heart failure are the two major predictors of transfusion. Modifying risk factors such as anemia before abdominoplasty might significantly decrease the possibility of blood transfusion. CLINICAL QUESTION/LEVEL OF EVIDENCE Risk, III.

Although lipotransfer, or fat grafting, is a commonly used procedure in aesthetic and reconstructive surgery, there is still variability in graft survival and neoadipogenesis from one procedure to the next. A better understanding of the sequential molecular events occurring with grafting would allow us to strategize methods to improve the regenerative potency of the grafted tissue. These steps begin with an autophagic process, followed by the inclusion of stromal vascular fraction and matrix components. By tailoring and modifying each of these steps for a particular type of aesthetic or reconstructive procedure, strategic sequencing represents a dynamic approach to lipotransfer with the aim of maximizing adipocyte viability and growth. In the implementation of the strategic sequence, it remains important to consider the clinical viability of each step and its compliance with the US Food and Drug Administration regulations. This review highlights the basic science behind clinically translatable approaches to supplementing various fat grafting procedures.

The autophagy-lysosome system is a catabolic cellular mechanism that degrades dysfunctional proteins and organelles. In atherosclerosis, there is mounting evidence that this process is rendered dysfunctional particularly in plaque macrophages and is an important trigger for plaque progression. In an effort to characterize practical inducers of macrophage degradative capacity, we now describe the unique vascular benefits of a natural sugar called trehalose, a recognized autophagy inducer with a currently unknown mechanism of action. Trehalose-treated macrophages display enhanced autophagy via a process that involves lysosomal stress and resultant activation of TFEB, the master transcriptional regulator of autophagy-lysosomal biogenesis. We find an important downstream effect of trehalose to be the induction of p62-dependent selective autophagy of cytotoxic polyubiquitinated protein aggregates and dampening of IL-1β/inflammasome function. We confirm the relevance of these in vitro observations in several pro-atherogenic (ApoE-/-) mouse models. Administration of trehalose during eight weeks of Western diet feeding potently induces autophagy and TFEB in plaque macrophages with concomitant reductions in polyubiquitinated protein aggregate burden along with significantly reduced plaque size and complexity. Importantly, these findings are completely abrogated in mice deficient in macrophage autophagy (ATG5-/-) or the selective autophagy chaperone (p62-/-). Further detailed pharmacokinetic evaluation of trehalose shows that physiologically relevant concentrations are indeed achievable in mice. Taken together, our data support the serious consideration of this safe and natural sugar as a potent inducer of macrophage degradative capacity in the treatment of atherosclerotic vascular disease.

Low carbohydrate high protein (LCHP) diets are commonly used in weight loss programs. However, the overall health benefits of such regimens are controversial with recent studies even suggesting an increased cardiovascular risk in certain populations. A few reports in animal models corroborate these concerns demonstrating increased LCHP-induced atherosclerosis. Interestingly, the downstream sequelae of such diets on tissues and cellular signaling are largely inferred with relevant mechanisms undefined. We first confirmed in the ApoE-null mouse model that LCHP diets are indeed atherogenic with the development of complex lesions. Using mass spectrometry, we find high protein feeding not only increases serum amino acid levels but increases amino acid load to tissues including the spleen and aorta with resultant activation of the mTORC1 signaling pathway particularly in macrophages. The involvement of mTORC1 is clearly causal as the atherogenic effect of LCHP-feeding is abrogated in macrophage-specific Raptor-null mice. Further mechanistic evaluation of the effects of amino acids on macrophages reveals dichotomous roles on a predominant mTORC1 target, autophagy. Certain amino acids such as Leucine potently activate mTORC1 via recruitment to lysosome and in turn suppress autophagy via ULK1 phosphorylation, whereas others such as glutamine act indirectly by downregulating the transcription of autophagy chaperones including p62/SQSTM1. This combined suppressive effect on autophagy leads to macrophage inflammasome activation and IL-1β release, accumulation of deleterious protein aggregates, and increased cell death. The in vivo relevance of this LCHP-amino acid-mTORC1-autophagy axis is supported by 1) the absence of increased atherosclerosis in macrophage autophagy-deficient (ATG5-/-) mice fed a LCHP diet, and 2) the absence of reduced atherosclerosis in mice dually deficient in macrophage mTORC1 and autophagy (Raptor/ATG5-/-). Our data provide the first mechanistic details of the deleterious effects of high protein diets on macrophages and the development of atherosclerosis. Incorporation of these concepts in clinical studies will be important to define the vascular effects of dietary protein.

Two tightly linked common intronic variants at the LIPA locus (which encodes for Lysosomal Acid Lipase - LAL) are present in nearly one-third of the population and are known to increase the risk of coronary artery disease (CAD) by 13-17% in large-scale genome-wide association studies. LAL mediates the hydrolysis of cholesteryl esters and patients with rare loss-of-function mutations develop hypercholesterolemia and CAD. However, these common LIPA variants are non-coding, not associated with lipid abnormalities, and result in increased LIPA transcripts in monocytes, a constellation of findings that has hindered further mechanistic understanding. We have discovered a previously unrecognized coding variant in tight linkage with the intronic variants that is equally associated with CAD risk. This coding variant involves a shift from a nonpolar to polar amino acid (T16P) in the predicted signal peptide region of LAL, providing a highly biologically plausible link to altered enzyme trafficking and function. We hypothesized that the coding variant is the causative SNP by altering LAL subcellular distribution and enzyme activity with functional consequences in lipid handling. In monocytes isolated from a large cohort of human patients, we show the coding variant leads to both increased LIPA mRNA expression and LAL enzyme activity in whole-cell lysates. To more precisely implicate the coding variant’s effects on LAL function, we studied several in vitro overexpression models assessing the coding variant in the absence of the intronic variants. We show the T16P alteration is sufficient to alter LAL trafficking away from the lysosome with a portion favoring the secretory pathway. These findings have important implications for macrophage lipid handling in the atherosclerotic plaque and provide a novel mechanism for one of the most common genomic variants in cardiovascular disease.

BACKGROUND The aims of this study were (1) to evaluate the frequency of various reconstructive techniques for autologous breast reconstruction and (2) to compare perioperative outcomes of autologous breast reconstruction in teaching versus nonteaching hospitals. MATERIALS The authors analyzed clinical data of patients who underwent autologous breast reconstructive surgery from 2009 to 2010 using the Nationwide Inpatient Sample database. Autologous breast reconstruction operations included latissimus dorsi myocutaneous, pedicled transverse rectus abdominis myocutaneous (TRAM), free TRAM, free deep inferior epigastric artery perforator (DIEP), free superficial inferior epigastric artery, and free gluteal artery perforator flaps. RESULTS A total of 35,883 patients underwent autologous breast reconstructive surgery in that period. Most reconstructions were performed in teaching hospitals (74 percent). The two most common breast reconstruction types in teaching hospitals were latissimus dorsi myocutaneous (26 percent) and DIEP flaps (26 percent), compared with latissimus dorsi myocutaneous (39 percent) and pedicled TRAM flaps (22 percent) in nonteaching hospitals. In addition, the rate of free flap breast reconstruction was significantly higher in teaching hospitals (46 percent) compared with nonteaching hospitals (31 percent) (p < 0.01). There was no statistically significant difference for total in-hospital complication rate (teaching, 6.9 percent; nonteaching, 7.1 percent; p = 0.54) or total in-hospital mortality rate (teaching, 0.04 percent; nonteaching, 0.05 percent; p = 0.56). CONCLUSIONS Three-fourths of autologous breast reconstructions performed from 2009 to 2010 were performed in teaching hospitals, with free flaps also more likely to be performed in teaching hospitals. Despite more complex free flap breast reconstructions being performed in teaching hospitals, there was no statistically significant difference in perioperative outcomes (morbidity and mortality) between teaching and nonteaching hospitals. CLINICAL QUESTION/LEVEL OF EVIDENCE Therapeutic, III.

The development of autologous fat grafting to augment or reconstruct tissue defects has become an increasingly popular modality among plastic surgeons. Despite its popularity, a standardized fat grafting protocol has yet to be developed. Great variations exist with regard to almost all the technical features, yielding a reported fat graft survivability that ranges from 40% to 80%. Recent bench approaches have been proposed to improve the long-term viability of fat grafts: although promising results have been shown, empirical evidence has yet to prove the superiority of one particular method. Nevertheless, currently available literature still provides some evidence for optimal results in differing clinical scenarios, in the wait of validating and ultimate studies.The issues of enriched fat grafting techniques and variations in harvesting and delivery in the background of US regulatory constraints demand alterations and variations in techniques. These only complicate the process of validation of any single technique. However, recent studies have brought us closer to making informed decisions on technical choices in lipotransfer. These are elaborated on in this review.

BACKGROUND Venous thromboembolism (VTE) can be a significant cause of morbidity and mortality in autologous breast reconstruction surgery. The aim of this study was to evaluate the effect of patient characteristics, comorbidities, payer type, reconstruction type, reconstruction timing, radiation, chemotherapy, and teaching status of hospital on VTE (deep venous thrombosis and/or pulmonary embolism) in autologous breast reconstructive surgery. METHODS Using the Nationwide Inpatient Sample (NIS) database, we examined the clinical data of patients who underwent autologous breast reconstructive surgery in 2009 to 2010 in the United States. Univariate and multivariate regression analyses were performed to identify factors predictive of in-hospital VTE. RESULTS A total of 35,883 patients underwent autologous breast reconstructive surgery during this period. Overall rate of VTE was 0.13%. The highest rate of VTE (0.26%) was observed in pedicled transverse rectus abdominis myocutaneous flap. Patients who experienced VTE had significantly longer mean hospital stay (11.6 vs 3.9 days; P < 0.001) and higher mean total hospital charges ($146,432 vs $61,794; P < 0.001) compared with non-VTE patients; however, there was no significant difference observed in mortality rate (VTE, 0.0% vs non-VTE, 0.04%; P = 0.886). Using multivariate regression analysis, immediate reconstruction after mastectomy (adjusted odds ratio [AOR], 5.4), older than 65 years (AOR, 4.2), obesity (AOR, 3.7), history of chemotherapy (AOR, 3.5), and chronic lung disease (AOR, 2.5) were associated with higher risk of VTE. There was no association between race, payer type, diabetes, hypertension, liver disease, congestive heart failure, peripheral vascular disease, chronic kidney disease, smoking, reconstruction type, radiation, or teaching status of hospital on VTE. CONCLUSIONS In patients undergoing autologous breast reconstruction surgery, immediate reconstruction, older than 65 years, obesity, history of chemotherapy, and chronic lung disease are all independent predictors of higher VTE. Surgeons should consider these factors and use appropriate prophylaxis to minimize the risk of VTE development.

After studying this article, the participant should be able to: 1. Describe the anatomy of the zygoma and the common signs and symptoms of fracture. 2. Describe the different operative approaches for zygomatic fractures and understand the essentials of proper reduction and fixation. 3. Avoid and manage common complications associated with zygomatic fracture repair.Methods for the evaluation and management of patients with zygomatic fractures continue to evolve. It is the purpose of this Maintenance of Certification article to provide updated recommendations for preoperative assessment, surgical care, and postoperative management of patients with zygomatic fractures.

Background The purpose of this study was to determine the evidenced-based value of prophylactic drainage of subcutaneous wounds in surgery. Methods An electronic search was performed. Articles comparing subcutaneous prophylactic drainage with no drainage were identified and classified by level of evidence. If sufficient randomized controlled trials were included, a meta-analysis was performed using the random-effects model. Fifty-two randomized controlled trials were included in the meta-analysis, and subgroups were determined by specific surgical procedures or characteristics (cesarean delivery, abdominal wound, breast reduction, breast biopsy, femoral wound, axillary lymph node dissection, hip and knee arthroplasty, obesity, and clean-contaminated wound). Studies were compared for the following endpoints: hematoma, wound healing issues, seroma, abscess, and infection. Results Fifty-two studies with a total of 6930 operations were identified as suitable for this analysis. There were 3495 operations in the drain group and 3435 in the no-drain group. Prophylactic subcutaneous drainage offered a statistically significant advantage only for (1) prevention of hematomas in breast biopsy procedures and (2) prevention of seromas in axillary node dissections. In all other procedures studied, drainage did not offer an advantage. Conclusions Many surgical operations can be performed safely without prophylactic drainage. Surgeons can consider omitting drains after cesarean section, breast reduction, abdominal wounds, femoral wounds, and hip and knee joint replacement. Furthermore, surgeons should consider not placing drains prophylactically in obese patients. However, drain placement following a surgical procedure is the surgeon's choice and can be based on multiple factors beyond the type of procedure being performed or the patient's body habitus. Clinical question/level of evidence Therapeutic, II.

BACKGROUND: Bipartition distraction is a novel procedure combining frontofacial bipartition and monobloc distraction. Apert syndrome and other syndromic craniofacial dysostoses are often characterized by hypertelorism, with a negative canthal axis and counterrotated orbits. Central midface hypoplasia can result in a biconcave face in both midsagittal and axial planes. Bipartition distraction can correct these facial abnormalities. METHODS: Twenty patients (19 Apert syndrome patients and one Pfeiffer syndrome patient, aged 1.6 to 21 years) underwent bipartition distraction. Severity of appearance was graded preoperatively and postoperatively as mild, moderate, or severe. Functional problems were documented by a multidisciplinary team. Central and lateral midface skeletal advancement were measured. Follow-up ranged from 15 months to 7 years. RESULTS: Bipartition distraction consistently produced more central than lateral facial advancement. Mean central advancement was 13.2 ± 5.9 mm at sella-nasion and 11.7 ± 5.4 mm at sella-A point. Lateral advancement was 4.7 ± 2.8 mm. Unbending the face improved aesthetic appearance. Airway function, eye exposure, and elevated intracranial pressure were improved. Complications included six temporary cerebrospinal fluid leaks (four needing a lumbar drain), five patients with postoperative seizures, five patients requiring Rigid External Distraction frame repositioning, one palatal fistula, one velopharyngeal incompetence, five pin-site infections, one abscess under frontal bone, three cases of sepsis, nine patients with worsened strabismus, two patients with enophthalmos, one patient with partial visual field loss, and three patients who required reintubation because of aspiration. CONCLUSIONS: : Bipartition distraction is an effective procedure with which to differentially advance the central face in Apert syndrome. It improves both function and aesthetics. CLINICAL QUESTION/LEVEL OF EVIDENCE: : Therapeutic, IV.

The autophagy-lysosome system is a catabolic cellular mechanism that degrades dysfunctional proteins and organelles. The pro-atherogenic phenotype of mice with macrophage-specific autophagy deficiency (ATG5-/-) confirm the importance of this degradation system in the pathogenesis of atherosclerosis. The mechanistic basis appears to involve a two-step process in macrophages: the development of lysosomal dysfunction/membrane integrity by atherogenic lipids followed by an inability of lysosomes to handle and degrade cargo supplied by autophagy. A prominent sequelae of such blockage is the accumulation of cytoplasmic inclusions composed of polyubiquitinated protein aggregates and organelles which are normally targeted for selective autophagy by the protein chaperone p62. In order to stimulate the degradative capacity of macrophages, we developed mice with macrophage-specific overexpression of TFEB, a master transcriptional activator of both autophagy and lysosomal biogenesis. Macrophage TFEB ameliorated several deleterious effects of atherogenic lipids, namely the blunting of inflammasome activation, enhancing cholesterol efflux, accelerating the degradation of protein aggregates, and decreasing apoptosis. In vivo, macrophage TFEB overexpression reduced both plaque burden and plaque complexity in pro-atherogenic ApoE-/- mice fed a Western diet. Interestingly, TFEB’s atheroprotective effects were not only abrogated in the background of macrophage autophagy deficiency (ATG5-/-) but also in the background of p62-deficiency (p62-/-) suggesting the critical importance of selective autophagy and degradation of p62-enriched protein aggregates. Taken together, these data support the induction of a holistic pro-degradative response in macrophages (i.e. selective autophagy followed by lysosomal degradation) as a viable therapeutic strategy in atherosclerosis.

Autophagy is a highly conserved cellular process designed to degrade long-lived and dysfunctional protein aggregates and organelles. Recent work has established an important role for macrophage autophagy in the control of inflammatory signaling, maintenance of efficient cholesterol homeostasis, and degradation of deleterious protein aggregates. The absence of macrophage autophagy renders many of these processes dysfunctional and leads to significant increases in atherosclerotic plaque formation. Thus, there has been intense interest in the cardiovascular community to devise strategies to induce autophagy as an atheroprotective measure. We approached this by pharmacologically manipulating a critical upstream activator of autophagy, Beclin-1, a protein involved in the formation of the autophagy initiation complex and biogenesis of the autophagosome. A cell-permeable Beclin-1 peptide (known to induce autophagy both in vitro and in vivo) was administered to pro-atherogenic ApoE-null mice fed a Western diet for a period of 8 weeks. Despite its autophagy-inducing properties in vivo, Beclin-1 peptide failed to reduce the development of atherosclerosis. Moreover, the peptide’s autophagy-inducing properties in vitro were also insufficient to blunt atherogenic lipid-induced hyperactivation of the inflammasome/IL-1β or stimulate the clearance of cytotoxic protein aggregates. These data lead us to conclude that the induction of autophagy is not sufficient to curb atherosclerotic progression. It is increasingly appreciated that macrophages of the atherosclerotic plaque also progressively develop a profound lysosomal dysfunction which likely precedes and exacerbates autophagy dysfunction. This raises that notion that combined stimulation of both autophagy and lysosomes would be necessary to ameliorate atherosclerosis and that efforts to stimulate autophagy in isolation are unlikely to be successful.

Adipose tissue inflammation is a fundamental feature of obesity and is strongly implicated in progression to overt cardiometabolic disease. In situ, this response is defined by a notable increase in number of adipose tissue macrophages (ATM’s) surrounding dying adipocytes and a phenotypic switch towards pro-inflammatory “M1” polarization. However, recent data suggest an equally notable upregulation of lysosomal catabolic pathways in these cells, and that inflammatory phenotypes may regulated by these processes. We and others speculate ATM lysosomal biogenesis is an adaptive response that can be harnessed for therapeutic benefit in treating cardiometabolic disease. To this end, we examined the effects of macrophage-specific overexpression of TFEB (mϕ-TFEB), a transcription factor master regulator of lysosomal biogenesis, in a murine model of diet induced obesity. We show broad physiological metabolic benefits including attenuated weight gain, improved body composition, and increased metabolic rate. Further, mϕ-TFEB mice demonstrate increased insulin sensitivity and glucose tolerance (Insulin and Glucose Tolerance Tests). These phenotypes are linked to profound changes in cellular, tissue, and systemic inflammation. mϕ-TFEB overexpression greatly reduces circulating interleukin 1β, and polarizes adipose tissue macrophages isolated from epididymal fat to an anti-inflammatory “M2” state in a manner that is dependent on lysosomal lipolysis. In cultured primary macrophages, TFEB overexpression attenuates LPS-induced proinflammatory M1 activation, and predisposes to IL-4 induced M2 polarization. Thus, harnessing the lysosomal biogenesis response in macrophages abrogates diet induced metabolic pathophysiology, potentially through regulation of inflammatory phenotypes. We postulate that ATM lysosomal biogenesis is a crucial, adaptive cellular response to obesity that can be preemptively induced to slow progression of cardiometabolic disease.

BACKGROUND There are many approaches to the medial orbital wall. However, most of them have problems with limitation of exposure, scarring, and postoperative inflammatory symptoms related to the eye. The authors used an upper eyelid crease approach to overcome these problems and investigate the usefulness of this approach. METHODS Between 2009 and 2011, the authors used this approach in 22 patients with medial orbital wall fractures. Incisions were performed on the medial one-third of the crease and a 2- to 3-mm superomedial extension along a relaxed skin tension line. RESULTS Postoperative computed tomographic scans demonstrated complete reduction and accurate reconstitution of the bony defect in all cases. The initial two cases had revision to correct the implant position. Follow-up ranged from 8 to 28 months, with an average of 12 months. Complications related to the operation were not observed. Diplopia and limitation of eye movement resolved in most cases. Two patients had persistent diplopia for more than 6 months that decreased with time. Enophthalmos of more than 2 mm was not observed in any orbit. The operative scar was inconspicuous. CONCLUSIONS This approach provides several advantages, including ease of exposure, and is more familiar to the plastic surgeon than the transconjunctival approach. There is little need to retract the globe laterally, thus minimizing postoperative inflammatory symptoms related to the eye. Therefore, the authors suggest that this method should be considered as a natural and useful surgical approach to medial orbital blowout fractures.

Introduction: Our recent experiments demonstrate that demyelination enhances peripheral nerve regeneration after contusion injury in the adult rat sciatic nerve. The role of demyelination in peripheral nerve regeneration in a sciatic nerve transection model has yet to be elucidated. We hypothesize that (1) axon regeneration within a region of injury increases after experimental, immunologic demyelination, and (2) regenerated axons are partially derived from the proximal motor axons. Methods: Sciatic nerves of adult female Sprague-Dawley rats (n = 20) were injected with a demyelinating agent immediately after transection injury. The sciatic nerves were harvested 1 month (n = 5) and 2 months (n = 5) after surgery. In the control groups, the cut nerves were reapproximated without demyelination therapy. The lesion containing length of nerve was cut into 1-mm transverse blocks and processed to preserve orientation. Specimens were evaluated using structural and immunohistochemical analyses. Results: A single epineural injection of complement proteins plus antibodies to galactocerebroside resulted in demyelination followed by Schwann cell remyelination. At 1 month, remyelination was clearly shown throughout the injured sciatic nerve segment. At 2 months, there was a statistically significant increase in peripheral nerve regeneration following demyelination therapy as evidenced by total axon count, axon density, and fiber diameter. Conclusion: This study demonstrates enhanced histomorphologic nerve regeneration in the rat sciatic nerve after local delivery of experimental, immunologic demyelination following transection injury. It highlights the utility of demyelination in peripheral nerve regeneration. This therapy may be applicable for tissue-engineered constructs, cell-based systems, and nerve transfers to improve outcomes in peripheral nervous system injuries.

The knowledge of patient preference is crucial for plastic surgeons to determine optimal marketing strategies. Conjoint analysis is a statistical technique whereby research participants make a series of trade-offs. Analysis of these trade-offs reveals the relative importance of component attributes. This study will evaluate the relative importance of attributes that influence the selection and decision-making process when choosing a plastic surgeon. A questionnaire consisting of 18 plastic surgeon profiles was rated by 111 patients. Attributes analyzed were as follows: travel distance, number of years in practice, board certification status, method of referral, office decor, and procedure cost. A traditional full-profile conjoint analysis was performed. Subjects consisted of 10 men and 101 women (n = 111). Median age was 51 years (range, 19―72). The "mean importance" of the attributes are as follows: board certification status, 39.7%; method of referral, 23.5%; distance from home to office, 13.2%; office decor, 9.0%; number of years in practice, 7.5%; and cost of procedure, 7.2%. Internal validity checks showed a high correlation (Pearson p = 0.995; P < 0.001). This pilot study demonstrates that conjoint analysis is a very powerful tool for market research in the health care system. The level of importance for each attribute reliably helps plastic surgeons to understand the preferences of their patients, thus being able to improve marketing strategies for private practices and institutions. The present study indicates that the most important attributes were board certification and method of referral.

Author(s): Yafi, Amr; Vetter, Thomas S; Scholz, Thomas; Patel, Sarin; Saager, Rolf B; Cuccia, David J; Evans, Gregory R; Durkin, Anthony J | Abstract: BackgroundThe purpose of this study was to investigate the capabilities of a novel optical wide-field imaging technology known as spatial frequency domain imaging to quantitatively assess reconstructive tissue status.MethodsTwenty-two cutaneous pedicle flaps were created on 11 rats based on the inferior epigastric vessels. After baseline measurement, all flaps underwent vascular ischemia, induced by clamping the supporting vessels for 2 hours (either arteriovenous or selective venous occlusions); normal saline was injected into the control flap and hypertonic-hyperoncotic saline solution was injected into the experimental flap. Flaps were monitored for 2 hours after reperfusion. The spatial frequency domain imaging system was used for quantitative assessment of flap status over the duration of the experiment.ResultsAll flaps demonstrated a significant decline in oxyhemoglobin and tissue oxygen saturation in response to occlusion. Total hemoglobin and deoxyhemoglobin were increased markedly in the selective venous occlusion group. After reperfusion and the administration of solutions, oxyhemoglobin and tissue oxygen saturation in those flaps that survived gradually returned to baseline levels. However, flaps for which oxyhemoglobin and tissue oxygen saturation did not show any signs of recovery appeared to be compromised and eventually became necrotic within 24 to 48 hours in both occlusion groups.ConclusionsSpatial frequency domain imaging technology provides a quantitative, objective method of assessing tissue status. This study demonstrates the potential of this optical technology to assess tissue perfusion in a very precise and quantitative way, enabling wide-field visualization of physiologic parameters. The results of this study suggest that spatial frequency domain imaging may provide a means for prospectively identifying dysfunctional flaps well in advance of failure.

Background HEK-293 cells can be genetically modified to release and regulate nerve growth factor (NGF) in vitro. The aim of this study was to evaluate the impact of this NGF delivery system on peripheral nerve regeneration in vivo. Methods HEK-293 cells were transfected with an ecdysone receptor, NGF cDNA, and herpes simplex virus-thymidine kinase suicide vector. NGF production is induced by ponasterone A and stopped by ganciclovir. A 13-mm sciatic nerve gap was bridged with Silastic conduits in 120 nude rats, and transfected HEK-293 cells were added, induced, and boostered to secrete bioactive NGF. Results The induction of the cell line and additional booster with ponasterone A demonstrated significantly higher levels of bioactive NGF, enhanced macroscopic nerve growth, improved functional recovery, and histologic regeneration when compared with control groups after 7, 14, and 21 days, and 2 and 4 months. The treatment with ganciclovir resulted in suppression of the NGF production and decreased functional and histologic outcomes. Conclusions Transfected HEK-293 cells can be regulated to inducibly produce bioactive NGF in vivo over prolonged periods. This tissue-engineered nerve construct including the NGF delivery system is able to improve peripheral nerve regeneration and functional recovery and appears to be superior to nerve isografts.

Background: in April of this past year, Transatlantic Innovations brought a variety of organizations and industry together for an international exchange of ideas, new technology, and current trends in plastic surgery. Methods: The meeting was highly interactive and included audience response devices. The focus was on 10 major areas: (1) new surgical techniques; (2) composite allografts versus conventional techniques, facing the future; (3) interspecialty collaboration versus competition; (4) the business of plastic surgery, best practices; (5) the image of the plastic surgeon, branding yourself; (6) medical tourism; (7) publicity; (8) the regulation of innovation, U.S. Food and Drug Administration and European Medicines Agency perspective; (9) the future of plastic surgery, cutting edge technologies; and (10) applications and controversies in fat grafting. The meeting concluded with the 8th International Committee for Quality Assurance, Medical Technologies and Devices in Plastic Surgery Consensus Conference with the development of a consensus statement. Results: Through an interactive audience response system, additional questions and attitudes were asked of the audience and, in real time, international differences were identified, which led to further discussions from panelists. Responses were identified in three major groups: European Union, North America, and the Rest of the World. Responses and data are included in this article. Conclusions: The meeting brought participants, industry, regulators, and educators from both sides of the Atlantic. The interaction of these groups in these outlined topics brought a unique perspective to the meeting and, in the end, volumes of data. We have more in common than we believe. It is our anticipation that as we as plastic surgeons move forward, we can use these interactions to help our own practices but more specifically the specialty as a whole. (Plast. Reconstr. Surg. 126: 316, 2010.)

The aim of the study was to provide information about the feasibility of peripheral nerve studies in a large animal model for future research. Seven Yorkshire pigs (25-30 kg) were used in a cadaver study. The accessibility, surgical approach, maximum length of possible nerve defect, diameter, and histologic characteristics of the sural, ulnar, laryngeal, and facial nerve were evaluated. All nerves are easily accessible and demonstrate desirable histologic qualities. The differences in nerve length and diameter vary among the nerves studied and a maximum nerve gap of up to 9.62 +/- 0.93 cm for the right sural nerve is recommended considering the interposition of a nerve graft or tissue engineered nerve construct. The facial nerve demonstrates the largest diameter and the highest number of axons. The sural and laryngeal nerve display significantly less myelination compared with the facial and ulnar nerve. The porcine model for the studies of peripheral nerve regeneration is an attractive alternative to other large animal models.

The study investigates adipose tissue-derived stem cells (ADSCs) to differentiate into insulin-secreting cells in vitro. ADSCs were exposed to differentiation medium or control medium. Culture medium was harvested for quantification of insulin and cells were classified into stages of differentiation ranging from normal appearance to islet-like clusters. Morphologic analysis demonstrated marked phenotypic changes towards the islet cell lineage. Thirty-six percent of cells exposed to differentiation medium had progressed to morphologic end-stage after 15 days. Chemiluminescence of the culture medium determined that insulin secretion by differentiated cells progressively increased, reaching a maximum at day 7. Insulin secretion by control cells was significantly less at all time points. A high correlation of secreted insulin and the presence of stage 3 cells were observed throughout the entire experiment. ADSCs can be differentiated into insulin-secreting cells in response to defined culture conditions. The secreted insulin significantly correlates with phenotypic changes throughout the differentiation process.

Background: Immunological demyelination is a proposed strategy to improve nerve regeneration in the peripheral nervous system. To investigate the remyelinating potential of Schwann cells in vivo in the peripheral nervous system, the authors have reproduced and expanded upon a novel model of immunological demyelination in the adult rat sciatic nerve. The authors demonstrate (1) the peripheral nervous system's quantitative, regenerative response to immunolog- ical demyelination and (2) whether Schwann cells within a region of demyelination are induced to divide in the presence of demyelinated axons. Methods: The sciatic nerves of female Sprague-Dawley rats were exposed and injected with demyelinating agent bilaterally. At 3 days (n = 3), 7 days (n = 3), and 14 days (n = 3), the animals were euthanized for histological evaluation. A second group of animals (n = 3) was similarly injected with demyelinating agent and then exposed to bromodeoxyuridine between 48 and 72 hours after the onset of demyelination. These animals were euthanized soon after the last injection of bromodeoxyuridine. The tissue was analyzed for Schwann cells (labeled with antibodies to S100) and bromodeoxyuridine assay. Results: A single epineural injection of complement proteins plus antibodies to galactocerebroside resulted in demyelination followed by Schwann cell remyelination. At 3 days after injection, peripheral nerve demyelination and Schwann cell proliferation were evident. Maximum demyelination was seen at 7 days; however, Schwann cell proliferation and remyelination peaked at 14 days after injection. Conclusions: These studies demonstrate an immunological model of demyelination and remyelination in the peripheral nervous system and quantitatively measure regenerative potential. This model will be used to isolate nerve segments and to measure their regenerative potential when given demyelinating agent after acute contusion and transection injuries.

Frontofacial advancement by distraction osteogenesis using the rigid external distraction device has become an accepted treatment for the deformity associated with craniofacial dysostoses (e.g., Crouzon, Apert, and Pfeiffer syndromes). The technical and physiological principles of osteogenesis distraction are well understood. This study documents the pattern of calcification at the osteotomy sites after distraction by analysis of serial three-dimensional computed tomography (CT) scans. The CT scans of 25 patients (11 with Crouzon, 6 with Apert, and 8 with Pfeiffer syndrome) were analyzed. Eleven individual areas along the osteotomy lines were assessed for evidence of bone formation. Scores were assigned within 4 categories ranging from no bone, calcification without bridge formation, a bony bridge, to complete bony infill (995%). The scans were reviewed on 2 separate occasions by 2 independent assessors. There was high concordance both for intraobserver and interobserver scores. Rigid external distraction frame removal was undertaken after a 6-week consolidation period. All CT scan timings were calculated from this date. Of the 25 patients studied, 16 patients had CT scans available at 3 to 6 months, 12 at 9 to 12 months, and 7 at or more than 18 months. The scans were available in standard coronal slices with three-dimensional reconstructions. Bone formation is most consistently seen in the pterygoid region with calcification consistently occurring earlier and more completely in this area. Bone formation was often delayed in the orbital region and severely delayed or absent in the frontal region and zygomatic arches. There was no significant difference in the order or quality of bony union for the 3 underlying craniofacial dysostoses. This preliminary study confirms the clinical impression that bone formation after distraction is greatest in the pterygoid regions. The clinical implications of these findings are discussed.