Trans-carotid endovascular repair of ascending aortic pseudoaneurysms.

We present an endovascular technique to repair an ascending aortic pseudoaneurysm in a patient with multiple previous sternotomies using access via the right common carotid artery.

Persistent injury-associated anemia: the role of the bone marrow microenvironment.

BACKGROUND: The regulation of erythropoiesis involves hematopoietic progenitor cells, bone marrow stroma, and the microenvironment. Following severe injury, a hypercatecholamine state develops that is associated with increased mobilization of hematopoietic progenitor cells to peripheral blood and decreased growth of bone marrow erythroid progenitor cells that manifests clinically as a persistent injury-associated anemia. Changes within the bone marrow microenvironment influence the development of erythroid progenitor cells. Therefore, we sought to determine the effects of lung contusion, hemorrhagic shock, and chronic stress on the hematopoietic cytokine response. MATERIALS AND METHODS: Bone marrow was obtained from male Sprague-Dawley rats (n = 6/group) killed 7 d after lung contusion followed by hemorrhagic shock (LCHS) or LCHS followed by daily chronic restraint stress (LCHS/CS). End point polymerase chain reaction was performed for interleukin-1ß, interleukin-10, stem cell factor, transforming growth factor-ß, high-mobility group box-1 (HMGB-1), and B-cell lymphoma-extra large. RESULTS: Seven days following LCHS and LCHS/CS, bone marrow expression of prohematopoietic cytokines (interleukin-1ß, interleukin-10, stem cell factor, and transforming growth factor-ß) was significantly decreased, and bone marrow expression of HMGB-1 was significantly increased. B-cell lymphoma-extra large bone marrow expression was not affected by LCHS or LCHS/CS (naïve: 44 ± 12, LCHS: 44 ± 12, LCHS/CS: 37 ± 1, all P > 0.05). CONCLUSIONS: The bone marrow microenvironment was significantly altered following severe trauma in a rodent model. Prohematopoietic cytokines were downregulated, and the proinflammatory cytokine HMGB-1 had increased bone marrow expression. Modulation of the bone marrow microenvironment may represent a therapeutic strategy following severe trauma to alleviate persistent injury-associated anemia.

Faculty perception of resident promotion and prevention associated behaviors in the operating room to facilitate intra-operative learning.

BACKGROUND: Previous work has demonstrated that residents are able to accurately perceive the intraoperative motivational style of faculty. Additionally, alignment of motivational style between residents and faculty has been demonstrated to enhance resident intraoperative autonomy. This study evaluated if faculty perception of resident behaviors aligned with resident self-perception in order to identify ways of enhancing intraoperative learning. METHODS: General surgery residents were asked to complete a self-assessment evaluating their own intraoperative behaviors. Conversely, faculty rated how strongly the residents exhibited these behaviors in the operating room. RESULTS: Of the 10 intraoperative behaviors that were evaluated, eight demonstrated no correlation between resident self-perception and faculty perception of resident behavior. Similarly, inconsistent correlations emerged when behaviors were assessed according to the self-reported gender and race of the resident. CONCLUSION: Faculty are not able to accurately perceive the motivational style of residents. Strategies to improve faculty perception of resident motivational style may enhance intraoperative learning.

Endothelial to mesenchymal transition in the interleukin-1 pathway during aortic aneurysm formation.

OBJECTIVE: Endothelial to mesenchymal transition may represent a key link between inflammatory stress and endothelial dysfunction seen in aortic aneurysm disease. Endothelial to mesenchymal transition is regulated by interleukin-1ß, and previous work has demonstrated an essential role of interleukin-1 signaling in experimental aortic aneurysm models. We hypothesize that endothelial to mesenchymal transition is present in murine aortic aneurysms, and loss of interleukin-1 signaling attenuates this process. METHODS: Murine aortic aneurysms were created in novel CDH5-Cre lineage tracking mice by treating the intact aorta with peri-adventitial elastase. Endothelial to mesenchymal transition transcription factors as well as endothelial and mesenchymal cell markers were analyzed via immunohistochemistry and immunofluorescence (n = 10/group). To determine the role of interleukin-1 signaling, endothelial-specific interleukin-1 receptor 1 knockout and wild-type mice (n = 10/group) were treated with elastase. Additionally, C57/BL6 mice were treated with the interleukin-1 receptor 1 antagonist Anakinra (n = 7) or vehicle (n = 8). RESULTS: Elastase treatment yielded greater aortic dilation compared with controls (elastase 97.0% ± 34.0%; control 5.3% ± 4.8%; P < .001). Genetic deletion of interleukin-1 receptor 1 attenuated aortic dilation (control 126.7% ± 38.7%; interleukin-1 receptor 1 knockout 35.2% ± 14.7%; P < .001), as did pharmacologic inhibition of interleukin-1 receptor 1 with Anakinra (vehicle 146.3% ± 30.1%; Anakinra 63.5% ± 23.3%; P < .001). Elastase treatment resulted in upregulation of endothelial to mesenchymal transition transcription factors (Snail, Slug, Twist, ZNF) and mesenchymal cell markers (S100, alpha smooth muscle actin) and loss of endothelial cell markers (vascular endothelial cadherin, endothelial nitric oxide synthase, von Willebrand factor). These changes were attenuated by interleukin-1 receptor 1 knockout and Anakinra treatment. CONCLUSIONS: Endothelial to mesenchymal transition occurs in aortic aneurysm disease and is attenuated by loss of interleukin-1 signaling. Endothelial dysfunction through endothelial to mesenchymal transition represents a new and novel pathway in understanding aortic aneurysm disease and may be a potential target for future treatment.

Faculty Entrustment and Resident Entrustability.

Importance: As the surgical education paradigm transitions to entrustable professional activities, a better understanding of the factors associated with resident entrustability are needed. Previous work has demonstrated intraoperative faculty entrustment to be associated with resident entrustability. However, larger studies are needed to understand if this association is present across various surgical training programs. Objective: To assess intraoperative faculty-resident behaviors and determine if faculty entrustment is associated with resident entrustability across 4 university-based surgical training programs. Design, Setting, and Participants: This cross-sectional study was conducted at 4 university-based surgical training programs from October 2018 to May 2022. OpTrust, a validated tool designed to assess both intraoperative faculty entrustment and resident entrustability behaviors independently, was used to assess faculty-resident interactions. A total of 94 faculty and 129 residents were observed. Purposeful sampling was used to create variation in type of operation performed, case difficulty, faculty-resident pairings, faculty experience, and resident training level. Main Outcomes and Measures: Observed resident entrustability scores (scale 1-4, with 4 indicating full entrustability) were compared with reported measures (faculty level, case difficulty, resident postgraduate year [PGY], resident gender, observation month) and observed faculty entrustment scores (scale 1-4, with 4 indicating full entrustment). Path analysis was used to explore direct and indirect effects of the predictors. Associations between resident entrustability and faculty entrustment scores were assessed by pairwise Pearson correlation coefficients. Results: A total of 338 cases were observed. Cases observed were evenly distributed by faculty experience (1-5 years' experience: 67 [20.9%]; 6-14 years' experience: 186 [58%]; ≥15 years' experience: 67 [20.9%]), resident PGY (PGY 1: 28 [8%]; PGY 2: 74 [22%]; PGY 3: 64 [19%]; PGY 4: 40 [12%]; PGY 5: 97 [29%]; ≥PGY 6: 36 [11%]), and resident gender (female: 183 [54%]; male: 154 [46%]). At the univariate level, PGY (mean [SD] resident entrustability score range, 1.44 [0.46] for PGY 1 to 3.24 [0.65] for PGY 6; F = 38.92; P < .001) and faculty entrustment (2.55 [0.86]; R2 = 0.94; P < .001) were significantly associated with resident entrustablity. Path analysis demonstrated that faculty entrustment was associated with resident entrustability and that the association of PGY with resident entrustability was mediated by faculty entrustment at all 4 institutions. Conclusions and Relevance: Faculty entrustment remained associated with resident entrustability across various surgical training programs. These findings suggest that efforts to develop faculty entrustment behaviors may enhance intraoperative teaching and resident progression by promoting resident entrustability.

A 42-Year-Old Man With Shortness of Breath, Fever, and Pleural Effusions.

CASE PRESENTATION: A 42-year-old man with a history of progressive multiple myeloma and chronic kidney disease presented with worsening shortness of breath and fever. He was scheduled for a planned admission for chemotherapy on the day of presentation and had developed these symptoms the night before. He had also developed worsening fatigue but denied any new cough, sputum production, or abdominal pain. The patient had been previously admitted 3 weeks prior for neutropenic fever and colitis during his first cycle of chemotherapy.

The effects of propranolol and clonidine on bone marrow expression of hematopoietic cytokines following trauma and chronic stress.

BACKGROUND: Attenuating post-injury neuroendocrine stress abrogates persistent injury-associated anemia. Our objective was to examine the mechanisms by which propranolol and clonidine modulate this process. We hypothesized that propranolol and clonidine would decrease bone marrow expression of high-mobility group box-1 (HMGB1) and increase expression of stem cell factor (SCF) and B-cell lymphoma-extra large (Bcl-xL). METHODS: Male Sprague-Dawley rats were allocated to naïve control, lung contusion followed by hemorrhagic shock (LCHS), or LCHS plus daily chronic restraint stress (LCHS/CS) ±propranolol, ±clonidine. Day seven bone marrow expression of HMGB1, SCF, and Bcl-xL was assessed by polymerase chain reaction. RESULTS: Following LCHS, HMGB1 was decreased by propranolol (49% decrease, p = 0.012) and clonidine (54% decrease, p < 0.010). SCF was decreased following LCHS/CS, and was increased by propranolol (629% increase, p < 0.001) and clonidine (468% increase, p < 0.001). Bcl-xL was decreased following LCHS/CS, and was increased by propranolol (59% increase, p = 0.006) and clonidine (77% increase, p < 0.001). CONCLUSIONS: Following severe trauma, propranolol and clonidine abrogate persistent injury-associated anemia by modulating bone marrow cytokines, favoring effective erythropoiesis.

Clonidine restores vascular endothelial growth factor expression and improves tissue repair following severe trauma.

BACKGROUND: We hypothesized that clonidine and propranolol would increase VEGF and VEGF-receptor expression and promote lung healing following severe trauma and chronic stress. METHODS: Sprague-Dawley rats were subjected to lung contusion (LC), lung contusion/hemorrhagic shock (LCHS), or lung contusion/hemorrhagic shock/daily restraint stress (LCHS/CS). Clonidine and propranolol were administered daily. On day seven, lung VEGF, VEGFR-1, VEGFR-2, and HMGB1 were assessed by PCR. Lung injury was assessed by light microscopy (*p < 0.05). RESULTS: Clonidine increased VEGF expression following LCHS (43%*) and LCHS/CS (46%*). Clonidine increased VEGFR-1 and R-2 expression following LCHS/CS (203%* and 47%*, respectively). Clonidine decreased HMGB1 and TNF-alpha expression following LCHS/CS (22%* and 58%*, respectively.) Clonidine decreased inflammatory cell infiltration and total Lung Injury Score following LCHS/CS. Propranolol minimally affected VEGF and did not improve lung healing. CONCLUSIONS: Clonidine increased VEGF and VEGF-receptor expression, decreased HMGB1 expression, decreased lung inflammation, and improved lung tissue repair.