Mitigating Microaggressions in Medical Education Through the TRAUMA Framework.

ABSTRACT: Microaggressions are defined as brief communications directed at members of a stigmatized group that are received as derogatory but are unrecognized by the offender. Studies show that microaggressions are detrimental to those of all identities who endure them. Given that microaggressions can result in specific emotional, psychological, and physical challenges for underrepresented medical students from minoritized backgrounds, it is imperative that the medical education community focus efforts on reducing them and their impact through appropriate responses. The TRAUMA framework was developed by the authors and can be used to organize a thorough response to the threat that microaggressions create for all students. The framework includes improved student support, guidelines for faculty and institutional responses to microaggressions, improved faculty development for addressing microaggressions, recommendations to improve classroom environments, and interventions both to create and measure culture change in medical education.

Disparities Associated with Discharge Patterns in Firearm-Associated Ocular Trauma.

Importance: Firearm injuries are associated with devastating visual outcomes. Several studies have demonstrated disparities in trauma care and discharge to rehabilitation and other advanced care facilities (ACFs) due to race and ethnicity and insurance status. The identification of possible disparities in disposition of patients admitted with firearms-associated ocular injuries (FAOIs) is a crucial step in moving toward health equity. Objective: To describe disposition patterns following admission for FAOI trauma. Design, Setting, and Participants: This retrospective analysis of National Trauma Data Bank (NTDB) from 2008 through 2014 used hospitalized trauma cases from over 900 US facilities detailed in the NTDB. Participants included patients admitted with ocular injuries. Statistical analysis was conducted between April 16, 2017, and December 15, 2021. Exposure: Firearm injuries. Main Outcomes and Measures: Patients admitted with FAOIs were identified using International Classification of Diseases, Ninth Revision, Clinical Modification diagnostic codes and E-codes. Demographic data, location, injury type and severity, and insurance status were documented. The primary outcome was the odds of discharge to ACFs. Results: A total of 8715 of 235 254 firearms injuries involved the eye (3.7%). Of the 8715 included patients, 7469 were male (85.7%), 3050 were African American (35.0%), and 4065 White (46.6%), with a mean (SD) age of 33.8 (16.9) years. Common payments were government insurance (31.5%), self-paid insurance (29.4%), and commercial insurance plans (22.8%). Frequent dispositions were home (48.8%) and ACF (20.5%). Multivariate analysis demonstrated that the following factors were associated with the highest odds of discharge to an ACF: hospital stays 6 days or longer (odds ratio [OR], 3.05; 95% CI, 2.56-3.63; P < .001), age 65 years or older (OR, 2.94; 95% CI, 1.94-4.48; P < .001), associated traumatic brain injury (OR, 2.32; 95% CI, 1.94-2.78; P < .001), severe traumatic brain injury (OR, 2.10; 95% CI, 1.79-2.46; P < .001), and very severe Injury Severity Score (OR, 2.22; 95% CI, 1.88-2.62; P < .001). White race (OR, 2.00; 95% CI, 1.71-2.33; P < .001) was associated with higher odds than Medicare insurance (OR, 1.64; 95% CI, 1.16-2.31; P = .01). Conclusions and Relevance: These findings suggest that older, more severely injured, Medicare-insured, or White patients have higher odds of ACF placement than younger, less severely injured, otherwise insured, and Black and Hispanic patients. This study is limited by its retrospective nature and the study team was unable to explore the basis for these disposition differences. Nevertheless, this work highlights that disparities may exist in disposition after FAOIs that may limit the rehabilitation potential of specific populations.

A Novel, Low-Cost Glaucoma Calculator to Identify Glaucoma Patients and Stratify Management.

Glaucoma is a leading cause of preventable blindness globally. Nearly, half of the patients who have glaucoma in the United States are unaware of their diagnosis, and this number is far greater in resource poor areas. The risk of progressive and irreversible loss of vision is decreased with an early diagnosis, and better access to treatment is vital to improve the visual outcome for patients. We therefore postulated that a minimally invasive, low-cost calculator used to predict the risk of glaucoma and inform the course of follow-up care will improve patient prognosis. We retrospectively examined data from 104 eyes of patients who underwent a complete ocular examination, visual field, and corneal pachymetry at Advanced Eye Care of New York (54 with glaucoma and 50 controls). Receiver operating curves (ROC) were utilized to determine the correct glaucoma classification rates of the Laroche glaucoma calculator (Range -3 to 18), a novel tool that combines age, intraocular pressure (IOP), and central corneal thickness (CCT) into a composite metric. Additionally, we compared the discriminatory power of this calculator to age, intraocular pressure (IOP), and central corneal thickness (CCT) separately. A score of greater than or equal to 6 on the Laroche glaucoma calculator (sensitivity 90.74%, specificity 64.00%, correct classification 77.88%) optimizes the accuracy of this tool. Compared to IOP (Area Under the Curve (AUC) = 0.72, chi2 = 4.21, p=0.04) and CCT (AUC = 0.53), chi2 24.72 p < 0.001), the Laroche glaucoma calculator (AUC = 0.81) was significantly better at discriminating against glaucoma patients vs. controls. These results demonstrate that the Laroche calculator is a novel, effective tool for identifying glaucoma, and it may provide a low-cost risk stratification tool, particularly in areas with limited resources.

Preserving Vision in the COVID-19 Pandemic: Focus on Health Equity.

The coronavirus 19 (COVID-19) pandemic has overwhelmed our healthcare systems and caused the deaths of tens of thousands of Americans. Black and Hispanic individuals comprise a disproportionate number of those deaths, primarily because of pre-existing health conditions such as hypertension, obesity, and asthma. Health inequities that underlie these disparities also exist within ophthalmology around the world, and more ophthalmologists should advocate for healthcare reform that advances health equity. Immediate actions to reduce health disparities in ophthalmology during the pandemic include taking time to ensure all ophthalmology leadership and industry is diversified with people reflecting the fabric of their countries, embracing telemedicine to increase access to medical care, and advocating for legislation that will increase health insurance coverage during this unprecedented time. Longitudinal actions include recognizing structural racism as a root cause of health inequity and actively rejecting it through addressing modifiable risk factors, increasing cultural competency training, promoting diversity in the workforce, and global leadership.

A Novel Microglia-Specific Transcriptional Signature Correlates With Behavioral Deficits in Neuropsychiatric Lupus.

Neuropsychiatric symptoms of systemic lupus erythematosus (NP-SLE) affect over one-half of SLE patients, yet underlying mechanisms remain largely unknown. We demonstrate that SLE-prone mice (CReCOM) develop NP-SLE, including behavioral deficits prior to systemic autoimmunity, reduced brain volumes, decreased vascular integrity, and brain-infiltrating leukocytes. NP-SLE microglia exhibit numerical expansion, increased synaptic uptake, and a more metabolically active phenotype. Microglia from multiple SLE-prone models express a "NP-SLE signature" unrelated to type I interferon. Rather, the signature is associated with lipid metabolism, scavenger receptor activity and downregulation of inflammatory and chemotaxis processes, suggesting a more regulatory, anti-inflammatory profile. NP-SLE microglia also express genes associated with disease-associated microglia (DAM), a subset of microglia thought to be instrumental in neurodegenerative diseases. Further, expression of "NP-SLE" and "DAM" signatures correlate with the severity of behavioral deficits in young SLE-prone mice prior to overt systemic disease. Our data are the first to demonstrate the predictive value of our newly identified microglia-specific "NP-SLE" and "DAM" signatures as a surrogate for NP-SLE clinical outcomes and suggests that microglia-intrinsic defects precede contributions from systemic SLE for neuropsychiatric manifestations.

Lipocalin-2 is a pathogenic determinant and biomarker of neuropsychiatric lupus.

Neuropsychiatric manifestations in lupus (NPSLE) affect ∼20-40% of patients. In the central nervous system, lipocalin-2 (LCN2) can promote injury through mechanisms directly linked to NPSLE, including brain barrier disruption, neurotoxicity, and glial activation. Since LCN2 is elevated in lupus and has been implicated in neuroinflammation, we investigated whether LCN2 is required for the pathogenesis of NPSLE. Here, we investigated the effects of LCN2 deficiency on the development of neurobehavioral deficits in the B6.Sle1.Sle3 (Sle1,3) mouse lupus model. Sle1,3 mice exhibited depression-like behavior and impaired spatial and recognition memory, and these deficits were attenuated in Sle1,3-LCN2KO mice. Whole-brain flow cytometry showed a significant increase in brain infiltrating leukocytes in Sle1,3 mice that was not reduced by LCN2 deficiency. RNA sequencing on sorted microglia revealed that several genes differentially expressed between B6 and Sle1,3 mice were regulated by LCN2, and that these genes are key mediators of the neuroinflammatory cascade. Importantly, LCN2 is upregulated in the cerebrospinal fluid of NPSLE patients across 2 different ethnicities. Our findings establish the Sle1,3 strain as an NPSLE model, demonstrate that LCN2 is a major regulator of the detrimental neuroimmune response in NPSLE, and identify CSF LCN2 as a novel biomarker for NPSLE.

Neuropsychiatric Systemic Lupus Erythematosus Is Dependent on Sphingosine-1-Phosphate Signaling.

About 40% of patients with systemic lupus erythematosus experience diffuse neuropsychiatric manifestations, including impaired cognition and depression. Although the pathogenesis of diffuse neuropsychiatric SLE (NPSLE) is not fully understood, loss of brain barrier integrity, autoreactive antibodies, and pro-inflammatory cytokines are major contributors to disease development. Fingolimod, a sphingosine-1-phosphate (S1P) receptor modulator, prevents lymphocyte egress from lymphoid organs through functional antagonism of S1P receptors. In addition to reducing the circulation of autoreactive lymphocytes, fingolimod has direct neuroprotective effects such as preserving brain barrier integrity and decreasing pro-inflammatory cytokine secretion by astrocytes and microglia. Given these effects, we hypothesized that fingolimod would attenuate neurobehavioral deficits in MRL-lpr/lpr (MRL/lpr) mice, a validated neuropsychiatric lupus model. Fingolimod treatment was initiated after the onset of disease, and mice were assessed for alterations in cognitive function and emotionality. We found that fingolimod significantly attenuated spatial memory deficits and depression-like behavior in MRL/lpr mice. Immunofluorescent staining demonstrated a dramatic lessening of brain T cell and macrophage infiltration, and a significant reduction in cortical leakage of serum albumin, in fingolimod treated mice. Astrocytes and endothelial cells from treated mice exhibited reduced expression of inflammatory genes, while microglia showed differential regulation of key immune pathways. Notably, cytokine levels within the cortex and hippocampus were not appreciably decreased with fingolimod despite the improved neurobehavioral profile. Furthermore, despite a reduction in splenomegaly, lymphadenopathy, and circulating autoantibody titers, IgG deposition within the brain was unaffected by treatment. These findings suggest that fingolimod mediates attenuation of NPSLE through a mechanism that is not dependent on reduction of autoantibodies or cytokines, and highlight modulation of the S1P signaling pathway as a novel therapeutic target in lupus involving the central nervous system.