Embracing Allyship in Academic Surgery: How All Surgeons Can Become Effective Champions for Change.

As the surgical community continues to work towards greater diversity, equity, and inclusion, the need for buy-in from all surgeons-including those of the White majority-becomes increasingly apparent. This article invites all surgeons to aid in diversity, equity, and inclusion efforts as "allies," "upstanders," and "champions for change," and provides 2 specific frameworks for enacting allyship within the surgical field. Overt and conscious efforts to embrace allyship are imperative as we seek to fulfill our professional responsibilities to patients and will help create a workplace environment where all persons feel accepted, valued, welcomed, and respected.

TGF-ß1 mediates pathologic changes of secondary lymphedema by promoting fibrosis and inflammation.

BACKGROUND: Secondary lymphedema is a common complication of cancer treatment, and previous studies have shown that the expression of transforming growth factor-beta 1 (TGF-ß1), a pro-fibrotic and anti-lymphangiogenic growth factor, is increased in this disease. Inhibition of TGF-ß1 decreases the severity of the disease in mouse models; however, the mechanisms that regulate this improvement remain unknown. METHODS: Expression of TGF-ß1 and extracellular matrix molecules (ECM) was assessed in biopsy specimens from patients with unilateral breast cancer-related lymphedema (BCRL). The effects of TGF-ß1 inhibition using neutralizing antibodies or a topical formulation of pirfenidone (PFD) were analyzed in mouse models of lymphedema. We also assessed the direct effects of TGF-ß1 on lymphatic endothelial cells (LECs) using transgenic mice that expressed a dominant-negative TGF-ß receptor selectively on LECs (LECDN-RII ). RESULTS: The expression of TGF-ß1 and ECM molecules is significantly increased in BCRL skin biopsies. Inhibition of TGF-ß1 in mouse models of lymphedema using neutralizing antibodies or with topical PFD decreased ECM deposition, increased the formation of collateral lymphatics, and inhibited infiltration of T cells. In vitro studies showed that TGF-ß1 in lymphedematous tissues increases fibroblast, lymphatic endothelial cell (LEC), and lymphatic smooth muscle cell stiffness. Knockdown of TGF-ß1 responsiveness in LECDN-RII resulted in increased lymphangiogenesis and collateral lymphatic formation; however, ECM deposition and fibrosis persisted, and the severity of lymphedema was indistinguishable from controls. CONCLUSIONS: Our results show that TGF-ß1 is an essential regulator of ECM deposition in secondary lymphedema and that inhibition of this response is a promising means of treating lymphedema.

Predictive accuracy of elevated mitotic rate on lymph node positivity and recurrence in thin melanomas.

Background: Mitotic rate (MR) is considered an important prognostic factor for melanoma but is not currently used for staging because its nuanced effect is not yet well-delineated. We sought to determine if T category-specific MR is predictive of sentinel lymph node (SLN) positivity, recurrence, and melanoma-specific mortality (MSM). Methods: A retrospective review of patients with primary cutaneous melanoma from 1994 to 2020 at a single academic center was performed. Patient demographics and tumor characteristics were recorded. MR was considered elevated for each AJCC8-defined T category if it was ≥2 mitoses/mm2 for T1, ≥4 mitoses/mm2 for T2, ≥6 mitoses/mm2 for T3, or ≥7 mitoses/mm2 for T4. Statistical analysis was performed to assess the predictive accuracy of MR on selected outcomes while controlling for ulceration. Results: Data from 2,984 patients with complete records were analyzed. Along with Breslow thickness and ulceration, elevated MR was associated with higher risk of MSM (HR 1.816, P=0.0001). There was no difference among patients with ulcerated T1 or T2 tumors regardless of MR, but those with non-ulcerated T1 or T2 tumors and elevated MR were more likely to have positive SLNs (P<0.0001 and P=0.0043, respectively) and recurrence (P=0.0007 and P=0.0004, respectively) compared to counterparts with low MR. There were no notable differences for T3 or T4 tumors based on MR. Conclusions: Elevated MR is associated with SLN positivity and recurrence in thin melanomas, independent of ulceration. SLN biopsy should therefore be strongly considered for patients with non-ulcerated lesions <0.8 mm thick if the MR is ≥2 mitoses/mm2.

Lymphatic-specific intracellular modulation of receptor tyrosine kinase signaling improves lymphatic growth and function.

Exogenous administration of lymphangiogenic growth factors is widely used to study changes in lymphatic function in pathophysiology. However, this approach can result in off-target effects, thereby generating conflicting data. To circumvent this issue, we modulated intracellular VEGF-C signaling by conditionally knocking out the lipid phosphatase PTEN using the Vegfr3 promoter to drive the expression of Cre-lox in lymphatic endothelial cells (LECs). PTEN is an intracellular brake that inhibits the downstream effects of the activation of VEGFR3 by VEGF-C. Activation of Cre-lox recombination in adult mice resulted in an expanded functional lymphatic network due to LEC proliferation that was independent of lymphangiogenic growth factor production. Furthermore, compared with lymphangiogenesis induced by VEGF-C injection, LECPTEN animals had mature, nonleaky lymphatics with intact cell-cell junctions and reduced local tissue inflammation. Last, compared with wild-type or VEGF-C-injected mice, LECPTEN animals had an improved capacity to resolve inflammatory responses. Our findings indicate that intracellular modulation of lymphangiogenesis is effective in inducing functional lymphatic networks and has no off-target inflammatory effects.

Comparing complications in irradiated and non-irradiated free-flaps in patients with bilateral immediate breast reconstruction and unilateral post-mastectomy radiotherapy.

BACKGROUND: Numerous studies have evaluated the effect of post-mastectomy radiotherapy (PMRT) on autologous breast reconstruction, but the variability of PMRT regimens and inadequate controls have made results difficult to interpret. Therefore, in this study, irradiated free-flaps are compared to non-irradiated internal controls in patients who underwent immediate bilateral reconstruction followed by unilateral PMRT to better delineate the effect of PMRT. The role of regional nodal irradiation (RNI) is also specifically assessed. METHODS: Appropriate patients were identified through retrospective review. Complications such as fat necrosis, fibrosis, infection, delayed healing, and flap loss, as well as revision surgeries, among the irradiated free-flaps were compared to those on the contralateral non-irradiated side. Additional analyses were performed to evaluate the effect of patient demographics and treatment characteristics, such as RNI, on complications involving the irradiated free-flaps. RESULTS: Seventy-three women were included. There was no significant difference between complication rates for the irradiated and non-irradiated free-flaps (39.7% vs. 38.4%, p = .78), although irradiated free-flaps were more likely to have fibrosis (17.0% vs. 0.0%; p < .0001) and multiple complications (9.6% vs. 0.0%; p = .02). Both groups underwent a similar number of revision surgeries (42.5% vs. 41.1%; p = .29). Looking at the irradiated free-flaps, internal mammary node (IMN) irradiation was the only factor predictive of complications (IRR 3.80, CI 1.32-10.97; p = .01). CONCLUSIONS: PMRT may contribute to free-flap fibrosis, but does not appear to affect the overall risk of complications or revision surgeries. However, additional counseling is warranted if IMN irradiation is likely, as it is potentially associated with increased complications.

Concurrent High Condylectomy and Orthognathic Surgery for Treatment of Patients With Unilateral Condylar Hyperplasia.

BACKGROUND: Facial asymmetry from unilateral condylar hyperplasia (UCH) may be definitively treated in the presence of active disease (with high condylectomy and concurrent orthognathic surgery) or after waiting for disease inactivity (orthognathic surgery alone). There is currently no consensus on the standard of care. In this study, we sought to compare functional and esthetic outcomes, as well as treatment duration, between these 2 management options. METHODS: Patients who underwent treatment for UCH were identified through retrospective review. Pre- and postoperative 3-dimensional (3D) images were obtained. Short- and long-term operative outcomes of those treated during the active (group 1) were compared to those treated in the inactive phase (group 2). Total treatment time, operative time, and length of hospital stay were evaluated. Facial asymmetry was also assessed by laypersons using a Likert scale. RESULTS: Fifteen patients (mean 25.6 years, range 14-56) were included: 6 in group 1 and 9 in group 2. All surgical outcomes were statistically independent of procedure type. Treatment time was significantly longer in the group 2 (P = 0.03). Both groups demonstrated significant improvement in facial asymmetry scores postoperatively with no significant difference in pre- or postoperative asymmetry between groups (P = 0.64). CONCLUSIONS: In patients with active UCH, high condylectomy and orthognathic surgery is a procedure that restores facial symmetry and improves jaw function while halting mandibular growth. Good esthetic and functional outcomes, as well as reduced treatment time and disease burden, support the use of this treatment option for this population.

Facial Asymmetry in Unilateral Condylar Hyperplasia: Comparing Treatment for Active versus Burnt-Out Disease.

BACKGROUND: Facial asymmetry caused by unilateral condylar hyperplasia requires treatment to address facial and occlusal imbalances. There is no definitive evidence to suggest that a single intervention strategy (during either active condylar overgrowth or the burnt-out phase) results in better/more symmetric correction. This study sought to quantify preoperative and postoperative facial asymmetry in unilateral condylar hyperplasia patients comparing treatment for active versus burnt-out disease. METHODS: Preoperative and postoperative three-dimensional photographs were obtained. Images were compared to those of unaffected controls as a standard for normal facial symmetry. Facial asymmetry was assessed using root-mean-square deviation. Paired t tests were performed to compare the root-mean-square deviations of preoperative and postoperative images between the unilateral condylar hyperplasia groups and against controls. RESULTS: Forty patients were included (11 active, nine burnt-out, and 20 controls) and 60 three-dimensional images were evaluated. Preoperatively, patients in the burnt-out group had worse asymmetry than those with active unilateral condylar hyperplasia (p = 0.011). Both groups demonstrated significantly improved symmetry postoperatively (active, p = 0.0069; burnt-out, p = 1.74E-4). However, burnt-out patients remained with some residual asymmetry (p = 4.75E-4), whereas their active counterparts showed no significant difference compared to unaffected controls (p = 0.089). CONCLUSIONS: Patients with end-stage unilateral condylar hyperplasia have more severe facial asymmetry that is more difficult to normalize compared to earlier intervention during active unilateral condylar hyperplasia. These findings suggest that, if possible, corrective intervention is preferable during active unilateral condylar hyperplasia. CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, II.

Lymph node stromal CCL2 limits antibody responses.

Nonhematopoietic stromal cells in lymph nodes such as fibroblastic reticular cells (FRCs) can support the survival of plasmablasts and plasma cells [together, antibody-forming cells (AFCs)]. However, a regulatory function for the stromal compartment in AFC accumulation has not been appreciated. Here, we show that chemokine ligand 2 (CCL2)-expressing stromal cells limit AFC survival. FRCs express high levels of CCL2 in vessel-rich areas of the T cell zone and the medulla, where AFCs are located. FRC CCL2 is up-regulated during AFC accumulation, and we use lymph node transplantation to show that CCL2 deficiency in BP3+ FRCs and lymphatic endothelial cells increases AFC survival without affecting B or germinal center cell numbers. Monocytes are key expressers of the CCL2 receptor CCR2, as monocyte depletion and transfer late in AFC responses increases and decreases AFC accumulation, respectively. Monocytes express reactive oxygen species (ROS) in an NADPH oxidase 2 (NOX2)-dependent manner, and NOX2-deficient monocytes fail to reduce AFC numbers. Stromal CCL2 modulates both monocyte accumulation and ROS production, and is regulated, in part, by manipulations that modulate vascular permeability. Together, our results reveal that the lymph node stromal compartment, by influencing monocyte accumulation and functional phenotype, has a regulatory role in AFC survival. Our results further suggest a role for inflammation-induced vascular activity in tuning the lymph node microenvironment. The understanding of stromal-mediated AFC regulation in vessel-rich environments could potentially be harnessed to control antibody-mediated autoimmunity.

Tumor Lymphatic Function Regulates Tumor Inflammatory and Immunosuppressive Microenvironments.

Proliferation of aberrant, dysfunctional lymphatic vessels around solid tumors is a common histologic finding. Studies have shown that abnormalities in lymphatic function result in accumulation of inflammatory cells with an immunosuppressive profile. We tested the hypothesis that dysfunctional lymphatic vessels surrounding solid tumors regulate changes in the tumor microenvironment and tumor-specific immune responses. Using subcutaneously implanted mouse melanoma and breast cancer tumors in a lymphatic endothelial cell-specific diphtheria toxin receptor transgenic mouse, we found that local ablation of lymphatic vessels increased peritumoral edema, as compared with controls. Comparative analysis of the peritumoral fluid demonstrated increases in the number of macrophages, CD4+ inflammatory cells, F4/80+/Gr-1+ (myeloid-derived suppressor cells), CD4+/Foxp3+ (Tregs) immunosuppressive cells, and expression of inflammatory cytokines such as TNFα, IFNγ, and IL1ß following lymphatic ablation. Tumors grown in lymphatic ablated mice exhibited reduced intratumoral accumulation of cytotoxic T cells and increased tumor PD-L1 expression, causing rapid tumor growth, compared with tumors grown in nonlymphatic-ablated mice. Our study suggests that lymphatic dysfunction plays a role in regulating tumor microenvironments and may be therapeutically targeted in combination with immunotherapy to prevent tumor growth and progression.

Small Numbers of CD4+ T Cells Can Induce Development of Lymphedema.

BACKGROUND: CD4 T cells have been implicated in the pathology of lymphedema. Interestingly, however, there have been case reports of lymphedema development in patients with low levels of CD4 T cells because of immunosuppression. In this study, the authors sought to delineate the effect of relative CD4 T-cell deficiency on the development of lymphedema in a mouse model. METHODS: A mouse model of relative CD4 T-cell deficiency was created through lethal total body irradiation of wild-type mice that then underwent bone marrow transplantation with progenitors harvested from CD4 knockout mice (wild-type/CD4 knockout). Irradiated CD4 knockout mice reconstituted with wild-type mouse-derived progenitors (CD4 knockout/wild-type), and unirradiated CD4 knockout and wild-type mice were used as controls. All mice underwent tail skin and lymphatic excision to induce lymphedema, and analysis was performed 6 weeks later. RESULTS: Wild-type/CD4 knockout chimeras were not protected from developing lymphedema. Despite a global deficit in CD4 T cells, these mice had swelling, fibrosis, inflammation, and impaired lymphatic transport function indistinguishable from that in wild-type and CD4 knockout/wild-type mice. In contrast, unirradiated CD4 knockout mice had no features of lymphedema after lymphatic injury. CONCLUSIONS: Relatively small numbers of bone marrow and peripheral CD4 T cells are sufficient to induce the development of lymphedema. These findings suggest that lymphatic injury results in expansion of CD4 T-cell populations in lymphedematous tissues.

T helper 2 differentiation is necessary for development of lymphedema.

T cells infiltrating lymphedematous tissues have a mixed T helper 1 (Th1) and Th2 differentiation profile. Treatment with neutralizing antibodies targeting cytokines that promote Th2 differentiation (interleukin 4 [IL-4] and IL-13) decreases the severity of lymphedema in preclinical models, suggesting that Th2 cells play a key role in the pathology of this disease. However, these previous studies do not address the contribution of Th1 cells and it remains unknown if IL-4 and IL-3 blockade acts primarily on T cells or decreases the pathological changes of lymphedema by other mechanisms. Therefore, this study sought to analyze the effect of lymphatic injury in transgenic mice with mutations that cause defects in Th1 and Th2 cell generation (T-bet knockout or T-betKO and STAT6 knockout or STAT6KO mice, respectively). Using both the mouse tail and popliteal lymph node dissection models of lymphedema, we show that Th2-deficient (STAT6KO) mice are protected from developing lymphedema, have decreased fibrosis, increased collateral vessel formation, and preserved collecting lymphatic vessel pumping function. In contrast, mice with defective Th1 cell generation (T-betKO) develop disease with the same severity as wild-type controls. Taken together, our results suggest that Th2 differentiation is necessary for development of lymphedema following lymphatic injury and that Th1 differentiation does not significantly contribute to the pathology of the disease. Such findings are important as immunotherapy directed at Th2 cells has been found to be effective in well-studied Th2-mediated diseases such as asthma and atopic dermatitis and may therefore be similarly useful for lymphedema management.

Baseline Lymphatic Dysfunction Amplifies the Negative Effects of Lymphatic Injury.

BACKGROUND: Genetic mutations and obesity increase the risk of secondary lymphedema, suggesting that impaired lymphatic function before surgical injury may contribute to disease pathophysiology. Previous studies show that obesity not only decreases lymphatic function, but also markedly increases pathologic changes, such as swelling, fibroadipose deposition, and inflammation. However, although these reports provide circumstantial evidence supporting the hypothesis that baseline lymphatic defects amplify the effect of lymphatic injury, the mechanisms regulating this association remain unknown. METHODS: Baseline lymphatic morphology, leakiness, pumping, immune cell trafficking, and local inflammation and fibroadipose deposition were assessed in wild-type and Prox1-haploinsufficient (Prox1) mice, which have previously been shown to have abnormal vasculature without overt evidence of lymphedema. In subsequent experiments, wild-type and Prox1 mice underwent popliteal lymph node dissection to evaluate the effect of lymphatic injury. Repeated testing of all variables was conducted 4 weeks postoperatively. RESULTS: At baseline, Prox1 mice had dilated, leaky lymphatic vessels corresponding to low-grade inflammation and decreased pumping and transport function, compared with wild-type mice. Popliteal lymph node dissection resulted in evidence of lymphedema in both Prox1 and wild-type mice, but popliteal lymph node dissection-treated Prox1 mice had increased inflammation and decreased lymphatic pumping. CONCLUSIONS: Subclinical lymphatic dysfunction exacerbates the pathologic changes of lymphatic injury, an effect that is multifactorial and related to increased lymphatic leakiness, perilymphatic accumulation of inflammatory cells, and impaired pumping and transport capacity. These findings suggest that preoperative testing of lymphatic function may enable clinicians to more accurately risk-stratify patients and design targeted preventative strategies.

CD4+ T cells are activated in regional lymph nodes and migrate to skin to initiate lymphedema.

T cell-mediated responses have been implicated in the development of fibrosis, impaired lymphangiogenesis, and lymphatic dysfunction in secondary lymphedema. Here we show that CD4+ T cells are necessary for lymphedema pathogenesis by utilizing adoptive transfer techniques in CD4 knockout mice that have undergone tail skin and lymphatic excision or popliteal lymph node dissection. We also demonstrate that T cell activation following lymphatic injury occurs in regional skin-draining lymph nodes after interaction with antigen-presenting cells such as dendritic cells. CD4+ T cell activation is associated with differentiation into a mixed T helper type 1 and 2 phenotype, as well as upregulation of adhesion molecules and chemokines that promote migration to the skin. Most importantly, we find that blocking T cell release from lymph nodes using a sphingosine-1-phosphate receptor modulator prevents lymphedema, suggesting that this approach may have clinical utility.

Lymphedema: Pathogenesis and Novel Therapies.

Lymphedema affects up to 1 in 6 patients who undergo treatment for a solid tumor in the United States. Its prevalence has increased as more effective oncologic therapies have improved patient survival, but there remains no definitive cure. Recent research has elucidated new details in the pathogenesis of the disease and has demonstrated that it is fundamentally an immunologic process that ultimately results in inflammation, fibroadipose deposition, impaired lymphangiogenesis, and dysfunctional lymphatic pumping. These findings have allowed for the development of novel medical and surgical therapies that may potentially alter the standard of care for a disease that has largely been treated by compression. This review seeks to provide an overview of the emerging therapies and how they can be utilized for effective management of lymphedema.

Regulatory T Cells Mediate Local Immunosuppression in Lymphedema.

Patients who suffer from lymphedema have impaired immunity and, as a result, are at an increased risk for infections. Furthermore, previous studies have shown that lymphadenectomy impairs acquisition of adaptive immune responses and antibody production in response to foreign antigens. Although it is clear that antigen presentation in lymph nodes plays a key role in adaptive immunity, the cellular mechanisms that regulate impaired immune responses in patients with lymphedema or following lymphatic injury remain unknown. We have previously found that axillary lymph node dissection, both clinically and in a mouse model, results in a marked increase in the number of regulatory T cells in the ipsilateral limb. In this study, we focus on the role of regulatory T cells in immunosuppression and show that regulatory T-cell proliferation in tissues distal to site of lymphatic injury contributes to impaired innate and adaptive immune responses. More importantly, using Foxp3-DTR transgenic mice, we show that depletion of regulatory T cells in the setting of lymphatic injury restores these critical immune-mediated responses. These findings provide additional evidence that immune responses following lymphatic injury play a key role in mediating the pathology of lymphedema.

Inflammatory Manifestations of Lymphedema.

Lymphedema results from lymphatic insufficiency leading to a progressive inflammatory process that ultimately manifests as discomfort, recurrent infections, and, at times, secondary malignancy. Collectively, these morbidities contribute to an overall poor quality of life. Although there have been recent advances in microsurgical interventions, a conservative palliative approach remains the mainstay of treatment for this disabling disease. The absence of a cure is due to an incomplete understanding of the pathophysiological changes that result in lymphedema. A histological hallmark of lymphedema is inflammatory cell infiltration and recent studies with animal models and clinical biopsy specimens have suggested that this response plays a key role in the pathology of the disease. The purpose of this report is to provide an overview of the ongoing research in and the current understanding of the inflammatory manifestations of lymphedema.

Lymph Node Transplantation Decreases Swelling and Restores Immune Responses in a Transgenic Model of Lymphedema.

INTRODUCTION: Secondary lymphedema is a common complication of cancer treatment and recent studies have demonstrated that lymph node transplantation (LNT) can decrease swelling, as well as the incidence of infections. However, although these results are exciting, the mechanisms by which LNT improves these pathologic findings of lymphedema remain unknown. Using a transgenic mouse model of lymphedema, this study sought to analyze the effect of LNT on lymphatic regeneration and T cell-mediated immune responses. METHODS: We used a mouse model in which the expression of the human diphtheria toxin receptor is driven by the FLT4 promoter to enable the local ablation of the lymphatic system through subdermal hindlimb diphtheria toxin injections. Popliteal lymph node dissection was subsequently performed after a two-week recovery period, followed by either orthotopic LNT or sham surgery after an additional two weeks. Hindlimb swelling, lymphatic vessel regeneration, immune cell trafficking, and T cell-mediated immune responses were analyzed 10 weeks later. RESULTS: LNT resulted in a marked decrease in hindlimb swelling, fibroadipose tissue deposition, and decreased accumulation of perilymphatic inflammatory cells, as compared to controls. In addition, LNT induced a marked lymphangiogenic response in both capillary and collecting lymphatic vessels. Interestingly, the resultant regenerated lymphatics were abnormal in appearance on lymphangiography, but LNT also led to a notable increase in dendritic cell trafficking from the periphery to the inguinal lymph nodes and improved adaptive immune responses. CONCLUSIONS: LNT decreases pathological changes of lymphedema and was shown to potently induce lymphangiogenesis. Lymphatic vessels induced by LNT were abnormal in appearance, but were functional and able to transport antigen-presenting cells. Animals treated with LNT have an increased ability to mount T cell-mediated immune responses when sensitized to antigens in the affected hindlimb.

Helmet use among motorcycle and moped riders injured in Hawaii: Final medical dispositions from a linked database.

BACKGROUND: Reports regarding helmets in motorcycle crashes have been limited by the lack of data across the spectrum of injury outcomes, generally excluding low-severity injuries that do not require further medical treatment. We hypothesized that the protective effect of helmets may be underestimated in studies that focused only on patients who arrive at a trauma center and that it may differ depending on whether the crash involved a motorcycle or moped. METHODS: The emergency medical service reports of 2,553 crash patients treated from 2007 to 2009 were linked to police crash reports, hospital billing data, death certificates, and the Fatal Analysis Reporting System for a more complete description of the crashes throughout the state. RESULTS: The number of unhelmeted riders (n = 1,674) was nearly double those who were helmeted (n = 879). Multivariate logistic regression models estimated 45% greater odds of a hospital admission (vs. no hospital treatment or a discharge from the emergency department setting) among unhelmeted riders, compared with helmeted riders. Unhelmeted riders also had an adjusted odds of a fatal injury that was more than double that of helmeted riders (odds ratio, 2.71; 95% confidence interval, 1.68-4.46). Stratified analyses showed that these protective associations between helmet use and medical disposition were apparent only among motorcyclists. CONCLUSION: The magnitude of the protective associations between helmets and medical outcomes was generally greater than that reported by other studies. Motorcyclists seem to benefit from helmet use more than moped riders. This data could be used to promote helmet use through education and public policy. LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level III.

Ethnicity as a predictive factor for hepatocellular carcinoma screening among patients in Hawaii.

OBJECTIVES: Although hepatocellular carcinoma (HCC) surveillance is associated with mortality reduction, it continues to be underutilized. The failure to conduct screening tests is a significant factor in the late diagnosis of hepatocellular carcinoma when curative interventions may not be feasible. Reasons for these low surveillance rates are unclear and need to be elucidated. DESIGN, SETTING, PATIENTS: This retrospective study reviewed 616 cases of HCC from a hepatobiliary surgery office in Hawaii for age, sex, ethnicity, birthplace, residence, education, employment, insurance, and obesity to determine their influence on HCC screening. MAIN OUTCOME MEASURES: HCC screening. RESULTS: Of the 616 cases, only 132 patients (21.4%) had undergone screening. Although the majority of patients were male, those who were screened were more likely to be female (P = .0082). However, multivariate analysis found ethnicity to be the sole determinant of screening (P < .0005). Koreans were more likely than Whites to have had screening, whereas Japanese, Pacific Islanders, and Filipinos were less likely. Age > 60 years, sex, American birthplace, urban residence, high school completion, employment status, insurance, and BMI > 35 kg/m2 were not predictors of screening. CONCLUSIONS: Of the sociodemographic factors, ethnicity was important in predicting screening. Further research is needed to understand the reasons for these ethnic differences and to develop targeted interventions to improve hepatocellular carcinoma surveillance utilization rates.

Welcome to cultural competency: surgery's efforts to acknowledge diversity in residency training.

BACKGROUND: Although cultural competency is not a new concept in healthcare, it has only recently been formally embraced as important in the field of surgery. All physicians, including and especially surgeons, must acknowledge the potential influence of culture in order to provide effective and equitable care for patients of all backgrounds. The Accreditation Council for Graduate Medical Education (ACGME) recognizes cultural competency as a component of "patient care," "professionalism," and "interpersonal and communication skills." METHODS: A systematic literature search was conducted using the MEDLINE, EBSCOhost, Web of Science, and Google Scholar databases. All publications focusing on surgical residents and the assessment of patient care, professionalism, interpersonal and communication skills, or specifically cultural competency and/or were considered. This initial search resulted in 12 articles. To further refine the review, publications discussing curricula in residencies other than surgery, the assessment of technical, or clinical skills and/or without any explicit focus on cultural competency were excluded. RESULTS: Based on the specified inclusion and exclusion criteria, 5 articles were selected. These studies utilized various methods to improve surgical residents' cultural competency, including lectures, Objective Structural Clinical Examinations (OSCE), and written exercises and evaluations. CONCLUSIONS: A number of surgical residency programs have made promising strides in training culturally competent surgeons. Ultimately, in order to maximize our collective efforts to improve the quality of health care, the development of cultural competency curricula must be made a priority and such training should be a requirement for all trainees in surgical residency programs.