A national survey of occupational musculoskeletal injuries in cardiothoracic surgeons.

OBJECTIVE: There is growing concern that surgeons are at increased risk for work-related orthopedic injuries due to poor ergonomics. We conducted a survey of North American cardiothoracic surgeons to evaluate the prevalence of occupational injury, as well as perceptions and use of ergonomic techniques. METHODS: Cardiothoracic surgeons identified through the Cardiothoracic Surgery Network were asked to complete a 33-question survey assessing their musculoskeletal health, as well as their perceptions and use of ergonomic techniques in the operating room and office. RESULTS: Among 600 cardiothoracic surgeons, the prevalence of occupational musculoskeletal injuries was 64%, with 30% of affected surgeons requiring time away from work and 20% requiring surgery or the use of narcotics. Cervical spine injury (35%, n = 216) was the most common injury due to operating, followed by lumbar spine injury (30%, n = 180). In multivariable-adjusted analysis, cardiac surgeons were more likely than thoracic surgeons to experience occupational musculoskeletal injuries (adjusted odds ratio, 1.8 [1.2-2.8], P < .01). Notably, 90% of surgeons (n = 536) reported thinking that their institution did not provide sufficient ergonomics education or support, and only 35% (n = 205) thought that the cardiothoracic surgical community is supportive of implementing ergonomics techniques in the operating room and office. CONCLUSIONS: In this survey analysis, cardiothoracic surgeons reported experiencing work-related orthopedic injuries at an alarmingly high rate, leading to significant time away from work and for many to retire from surgery over a decade early. These findings underline a critical need for institutions to prioritize ergonomics education and implement ergonomics-directed techniques in the operating room and office.

Restructuring lung cancer care to accelerate diagnosis and treatment in patients vulnerable to healthcare disparities using an innovative care model.

The diagnosis and treatment of lung cancer is challenged by complex diagnostic pathways and fragmented care that can lead to disparities for vulnerable patients. Our model involved a multi-institutional, multidisciplinary conference to address the complexity of lung cancer care in vulnerable patient populations. The conference was conducted using a process adapted from the problem-solving method entitled FastTrack, pioneered by General Electric. Conference attendees established critical social determinants of health specific to lung cancer and designed a practical care model to accelerate diagnosis and treatment in this population. The resulting care delivery model, the Lung Cancer Strategist Program (LCSP), was led by a lung cancer trained advanced practice provider (APP) to expedite diagnosis, surgical and oncologic consultation, and treatment of a suspicious lung nodule. We compared the timeliness of care, care efficiency, and oncologic outcomes in 100 LCSP patients and 100 routine referral patients at the same thoracic surgery clinic. Patient triage through our integrated care model transitioned initial referral evaluation to a lung cancer trained APP to coordinate multidisciplinary patient-centered care that was highly individualized and significantly reduced the time to diagnosis and treatment among vulnerable patients at high-risk for treatment delay due to healthcare disparities.•To develop the Lung Cancer Strategist Program care model, we used a three-step (Design, Meeting, and Culmination), team-based, problem-solving process entitled FastTrack.•An advantage of FastTrack is its ability to overcome barriers embedded within hierarchal and institutional social systems, empowering those closest to the relevant issue to propose and enact meaningful change.•Under this framework, we engaged a diverse field of experts to assess systemic barriers in lung cancer care and design an innovative care pathway to improve the timeliness and efficiency of lung cancer care in patients at risk for healthcare disparities.

Lung Cancer Strategist Program: A novel care delivery model to improve timeliness of diagnosis and treatment in high-risk patients.

INTRODUCTION: The diagnosis and treatment of lung cancer is challenged by complex diagnostic pathways and fragmented care that can lead to care disparities for vulnerable patients. METHODS: A multi-institutional, multidisciplinary conference was convened to address the complexity of lung cancer care particularly in patients at high-risk for treatment delay. The resulting care delivery model, called the Lung Cancer Strategist Program (LCSP), was led by a thoracic-trained advanced practice provider (APP) with emphasis on expedited surgery and early oncologic consultation in the assessment of a newly diagnosed suspicious lung nodule. We performed a retrospective review to evaluate care efficiency and oncologic outcomes in the first 100 LCSP patients compared to 100 concurrent patients managed via routine surgical referral. RESULTS: In the 78 LCSP and 41 routine referral patients managed via nodule surveillance, LCSP patients had a shorter time from suspicious finding to work-up (3 vs. 26 days, p < 0.001) and to surveillance decision (12.5 vs. 39 days, p < 0.001). In the 22 LCSP and 59 routine referral patients treated for intrathoracic malignancy, LCSP patients had fewer hospital visits (4 vs 6, p < 0.001), clinicians seen (1.5 vs. 2, p = 0.08), and diagnostic studies (4 vs 5, p = 0.01) with a shorter time to diagnosis (30.5 vs. 48 days, p = 0.02) and treatment (40.5 vs. 68.5 days, p = 0.02). CONCLUSIONS: Patient triage through a thoracic-trained APP in consultation with surgical, medical, and radiation oncology facilitates rapid assessment of benign versus malignant lesions with reduced time to diagnosis and treatment, even among patients at high-risk for treatment delay.

Notch signaling regulates remodeling and vessel diameter in the extraembryonic yolk sac.

BACKGROUND: The signaling cascades that direct the morphological differentiation of the vascular system during early embryogenesis are not well defined. Several signaling pathways, including Notch and VEGF signaling, are critical for the formation of the vasculature in the mouse. To further understand the role of Notch signaling during endothelial differentiation and the genes regulated by this pathway, both loss-of-function and gain-of-function approaches were analyzed in vivo. RESULTS: Conditional transgenic models were used to expand and ablate Notch signaling in the early embryonic endothelium. Embryos with activated Notch1 signaling in the vasculature displayed a variety of defects, and died soon after E10.5. Most notably, the extraembryonic vasculature of the yolk sac displayed remodeling differentiation defects, with greatly enlarged lumens. These phenotypes were distinct from endothelial loss-of-function of RBPJ, a transcriptional regulator of Notch activity. Gene expression analysis of RNA isolated from the yolk sac endothelia of transgenic embryos indicated aberrant expression in a variety of genes in these models. In particular, a variety of secreted factors, including VEGF and TGF-ß family members, displayed coordinate expression defects in the loss-of-function and gain-of-function models. CONCLUSIONS: Morphological analyses of the in vivo models confirm and expand the understanding of Notch signaling in directing endothelial development, specifically in the regulation of vessel diameter in the intra- and extraembryonic vasculature. Expression analysis of these in vivo models suggests that the vascular differentiation defects may be due to the regulation of key genes through the Notch-RBPJ signaling axis. A number of these genes regulated by Notch signaling encode secreted factors, suggesting that Notch signaling may mediate remodeling and vessel diameter in the extraembryonic yolk sac via autocrine and paracrine cell communication. We propose a role for Notch signaling in elaborating the microenvironment of the nascent arteriole, suggesting novel regulatory connections between Notch signaling and other signaling pathways during endothelial differentiation.

Early mammalian erythropoiesis requires the Dot1L methyltransferase.

Histone methylation is an important regulator of gene expression; its coordinated activity is critical in complex developmental processes such as hematopoiesis. Disruptor of telomere silencing 1-like (DOT1L) is a unique histone methyltransferase that specifically methylates histone H3 at lysine 79. We analyzed Dot1L-mutant mice to determine influence of this enzyme on embryonic hematopoiesis. Mutant mice developed more slowly than wild-type embryos and died between embryonic days 10.5 and 13.5, displaying a striking anemia, especially apparent in small vessels of the yolk sac. Further, a severe, selective defect in erythroid, but not myeloid, differentiation was observed. Erythroid progenitors failed to develop normally, showing retarded progression through the cell cycle, accumulation during G0/G1 stage, and marked increase in apoptosis in response to erythroid growth factors. GATA2, a factor essential for early erythropoiesis, was significantly reduced in Dot1L-deficient cells, whereas expression of PU.1, a transcription factor that inhibits erythropoiesis and promotes myelopoiesis, was increased. These data suggest a model whereby DOT1L-dependent lysine 79 of histone H3 methylation serves as a critical regulator of a differentiation switch during early hematopoiesis, regulating steady-state levels of GATA2 and PU.1 transcription, thus controlling numbers of circulating erythroid and myeloid cells.