BACKGROUND: Entrustable Professional Activities (EPAs) allow for the assessment of specific, observable, essential tasks in medical education. Since being developed in non-surgical fields, EPA assessments have been implemented in surgery to explore intraoperative entrustment. However, assessment burden is a significant problem for faculty, and it is unknown whether EPA assessments enable formative technical feedback. EPAs formative utility could inform how surgical programs facilitate technical feedback for trainees. We aimed to assess the extent to which narrative comments provided through the Fellowship Council (FC) EPA assessments contained technical feedback. METHODS: The FC previously collected EPA assessments for subspecialty surgical fellows from September 2020 to October 2022. Two raters reviewed assessments narrative comments for inclusion of each skill area that makes up part of the Objective Structured Assessment of Technical Skills (OSATS). A third rater reconciled discrepant ratings. RESULTS: During the study period, there were 3302 completed EPA assessments, including 1191 fellow self-assessments, 1124 faculty assessments, and 987 assessments without an identified assessor role. We found that assessments narrative comments related to a median of two of the seven OSATS areas (IQR:1-2). There were no comments relevant to any of the seven OSATS areas in 16.0 % of all assessments. CONCLUSIONS: In this review of narrative comments for EPA assessments from the FC, we found that limited technical feedback of the kind included in the OSATS was provided in many assessments. These results suggest benefit to adjusting the EPA form, enhancing faculty development, or continuing additional types of targeted technical assessment intraoperatively. KEY MESSAGE: This analysis of narrative comments from fellowship EPA assessments showed that many assessments included limited technical feedback. To allow for continued technical feedback for fellows, these results highlight the need for further refinements of the EPA assessment form, additional faculty development, or ongoing use of other types of technical assessment.

ABSTRACT

Despite a robust literature associating IL-31 with pruritic inflammatory skin diseases, its influence on cutaneous inflammation and on the interplay between inflammatory and neurosensory pathways remain unmapped. Here, we examined the effects of IL-31 and its receptor IL31RA on both inflammation and pruritus in mouse models of dermatitis, including chronic topical house dust mite (HDM) exposure. Unexpectedly, Il31 deficiency increased cutaneous adaptive type 2 cytokine-producing cells and serum IgE. In addition, M2-like macrophages capable of fueling feedforward pro-inflammatory loops were selectively enriched in Il31ra -deficient skin. Thus, IL-31 is not strictly a pro-inflammatory cytokine, but rather an immunoregulatory factor that limits the magnitude of allergic skin inflammation. In contrast, Il31 -deficient mice displayed a deficit in HDM-induced scratching. Itch reduction occurred despite intact – and in some cases increased – responsiveness of sensory neurons to other pruritogens released during HDM challenge, highlighting the non-redundant contribution of IL-31-receptive sensory afferents to pruritus in environmental allergen-induced dermatitis. When present, therefore, IL-31 uncouples circuits driven by sensory neurons and immune cells that converge in inflamed skin.

Despite robust literature associating IL-31 with pruritic inflammatory skin diseases, its influence on cutaneous inflammation and the interplay between inflammatory and neurosensory pathways remain unmapped. Here, we examined the consequences of disrupting Il31 and its receptor Il31ra in a mouse model of house dust mite (HDM)-induced allergic dermatitis. Il31-deficient mice displayed a deficit in HDM dermatitis-associated scratching, consistent with its well-established role as a pruritogen. In contrast, Il31 deficiency increased the number and proportion of cutaneous type 2 cytokine-producing CD4+ T cells and serum IgE in response to HDM. Furthermore, Il4ra+ monocytes and macrophages capable of fueling a feedforward type 2 inflammatory loop were selectively enriched in Il31ra-deficient HDM dermatitis skin. Thus, IL-31 is not strictly a proinflammatory cytokine but rather an immunoregulatory factor that limits the magnitude of type 2 inflammatory responses in skin. Our data support a model wherein IL-31 activation of IL31RA+ pruritoceptors triggers release of calcitonin gene-related protein (CGRP), which can mediate neurogenic inflammation, inhibit CD4+ T cell proliferation, and reduce T cell production of the type 2 cytokine IL-13. Together, these results illustrate a previously unrecognized neuroimmune pathway that constrains type 2 tissue inflammation in the setting of chronic cutaneous allergen exposure and may explain paradoxical dermatitis flares in atopic patients treated with anti-IL31RA therapy.