Emergency Department Physician Attitudes, Practices, and Needs Assessment for the Management of Patients with Chest Pain Secondary to Anxiety and Panic

poster abstractBackground Chest pain is a common medical complaint, accounting for 7 million annual visits to US Emergency Departments (EDs) [1]. Most research and clinical resources are focused on the management of the life-threatening acute coronary syndrome (ACS); however, about 80% of all patients presenting to EDs with chest pain do not have a cardiopulmonary emergency [2-4]. Non-ACS chest pain can be caused by anxiety or a panic disorder, and such etiologies remain undiagnosed in almost 90% of cases, and frequently have worse outcomes [5-9]. Objective and Methods The study objective was to assess ED physician’s attitudes, practices, and needs in managing chest pain related to anxiety and panic. A REDCap survey of 15 Likert-style questions was constructed using expert consensus to ensure content validity then administered to all faculty and resident physicians in the IU Department of Emergency Medicine (113 individuals, 65.5% response-rate). Results ED providers believe a significant proportion (31.5%) of patients with chest pain at low risk for ACS are due to panic/anxiety. Providers give such patients instructions on how to manage their panic/anxiety only 34.8% of the time, while even fewer (19.0%) make a diagnosis of anxiety or panic disorder in their documentation. Most providers (77.0%) would welcome a narrative to aid in discussing anxiety/panic as a cause of chest pain and nearly all (85.1%) would find it helpful to have specific clinic information available to aid in follow-up. Conclusions A significant number of ED patients with chest pain are likely due to anxiety, and a majority of physicians report not having the resources necessary to manage these patients. Further work to develop relevant resources would aim to improve provider confidence in treating these patients, and would hope to improve management of anxiety or panic as a cause of chest pain in the ED

Emergency Department Cardiopulmonary Evaluation of Low-Risk Chest Pain Patients with Self-Reported Stress and Anxiety

Background Chest pain is a high-risk emergency department (ED) chief complaint; the majority of clinical resources are directed toward detecting and treating cardiopulmonary emergencies. However, at follow-up, 80%–95% of these patients have only a symptom-based diagnosis; a large number have undiagnosed anxiety disorders. Objective Our aim was to measure the frequency of self-identified stress or anxiety among chest pain patients, and compare their pretest probabilities, care processes, and outcomes. Methods Patients were divided into two groups: explicitly self-reported anxiety and stress or not at 90-day follow-up, then compared on several variables: ultralow (<2.5%) pretest probability, outcome rates for acute coronary syndrome (ACS) and pulmonary embolism (PE), radiation exposure, total costs at 30 days, and 90-day recidivism. Results Eight hundred and forty-five patients were studied. Sixty-seven (8%) explicitly attributed their chest pain to “stress” or “anxiety”; their mean ACS pretest probability was 4% (95% confidence interval 2.9%–5.7%) and 49% (33/67) had ultralow pretest probability (0/33 with ACS or PE). None (0/67) were diagnosed with anxiety. Seven hundred and seventy-eight did not report stress or anxiety and, of these, 52% (403/778) had ultralow ACS pretest probability. Only one patient (0.2%; 1/403) was diagnosed with ACS and one patient (0.4%; 1/268) was diagnosed with PE. Patients with self-reported anxiety had similar radiation exposure, associated costs, and nearly identical (25.4% vs. 25.7%) ED recidivism to patients without reported anxiety. Conclusions Without prompting, 8% of patients self-identified “stress” or “anxiety” as the etiology for their chest pain. Most had low pretest probability, were over-investigated for ACS and PE, and not investigated for anxiety syndromes

Anxiety Associated With Increased Risk for Emergency Department Recidivism in Patients With Low-Risk Chest Pain

Anxiety contributes to the chest pain symptom complex in 30% to 40% of patients with low-risk chest pain seen in the emergency department (ED). The validated Hospital Anxiety Depression Scale-Anxiety subscale (HADS-A) has been used as an anxiety screening tool in this population. The objective was to determine the prevalence of abnormal HADS-A scores in a cohort of low-risk chest pain patients and test the association of HADS-A score with subsequent healthcare utilization and symptom recurrence. In a single-center, prospective, observational cohort study of adult ED subjects with low-risk chest pain, the HADS-A was used to stratify participants into 2 groups: low anxiety (score <8) and high anxiety (score ≥8). At 45-day follow-up, chest pain recurrence was assessed by patient report, whereas ED utilization was assessed through chart review. Of the 167 subjects enrolled, 78 (47%) were stratified to high anxiety. The relative risk for high anxiety being associated with at least one 30-day ED return visit was 2.6 (95% confidence interval 1.4 to 4.7) and this relative risk increased to 9.1 (95% confidence interval 2.18 to 38.6) for 2 or more ED return visits. Occasional chest pain recurrence was reported by more subjects in the high anxiety group, 68% vs 47% (p = 0.029). In conclusion, 47% of low-risk chest pain cohort had abnormal levels of anxiety. These patients were more likely to have occasional recurrence of their chest pain and had an increased risk multiple ED return visits

Characteristics of COVID-19 Patients with Bacterial Co-infection Admitted to the Hospital from the Emergency Department in a Large Regional Healthcare System

Introduction The rate of bacterial coinfection with SARS‐CoV‐2 is poorly defined. The decision to administer antibiotics early in the course of SARS‐CoV‐2 infection depends on the likelihood of bacterial coinfection. Methods We performed a retrospective chart review of all patients admitted through the emergency department with confirmed SARS‐CoV‐2 infection over a 6‐week period in a large healthcare system in the United States. Blood and respiratory culture results were abstracted and adjudicated by multiple authors. The primary outcome was the rate of bacteremia. We secondarily looked to define clinical or laboratory features associated with bacteremia. Results There were 542 patients admitted with confirmed SARS‐CoV‐2 infection, with an average age of 62.8 years. Of these, 395 had blood cultures performed upon admission, with six true positive results (1.1% of the total population). An additional 14 patients had positive respiratory cultures treated as true pathogens in the first 72 h. Low blood pressure and elevated white blood cell count, neutrophil count, blood urea nitrogen, and lactate were statistically significantly associated with bacteremia. Clinical outcomes were not statistically significantly different between patients with and without bacteremia. Conclusions We found a low rate of bacteremia in patients admitted with confirmed SARS‐CoV‐2 infection. In hemodynamically stable patients, routine antibiotics may not be warranted in this population

Cellular Immune Responses and Viral Diversity in Individuals Treated during Acute and Early HIV-1 Infection

Immune responses induced during the early stages of chronic viral infections are thought to influence disease outcome. Using HIV as a model, we examined virus-specific cytotoxic T lymphocytes (CTLs), T helper cells, and viral genetic diversity in relation to duration of infection and subsequent response to antiviral therapy. Individuals with acute HIV-1 infection treated before seroconversion had weaker CTL responses directed at fewer epitopes than persons who were treated after seroconversion. However, treatment-induced control of viremia was associated with the development of strong T helper cell responses in both groups. After 1 yr of antiviral treatment initiated in acute or early infection, all epitope-specific CTL responses persisted despite undetectable viral loads. The breadth and magnitude of CTL responses remained significantly less in treated acute infection than in treated chronic infection, but viral diversity was also significantly less with immediate therapy. We conclude that early treatment of acute HIV infection leads to a more narrowly directed CTL response, stronger T helper cell responses, and a less diverse virus population. Given the need for T helper cells to maintain effective CTL responses and the ability of virus diversification to accommodate immune escape, we hypothesize that early therapy of primary infection may be beneficial despite induction of less robust CTL responses. These data also provide rationale for therapeutic immunization aimed at broadening CTL responses in treated primary HIV infection

Gender Differences in Acute and Chronic Pain in the Emergency Department: Results of the 2014 Academic Emergency Medicine Consensus Conference Pain Section

Pain is a leading public health problem in the United States, with an annual economic burden of more than $630 billion, and is one of the most common reasons that individuals seek emergency department (ED) care. There is a paucity of data regarding sex differences in the assessment and treatment of acute and chronic pain conditions in the ED. The Academic Emergency Medicine consensus conference convened in Dallas, Texas in May of 2014 to develop a research agenda to address this issue among others related to sex differences in the ED. Prior to the conference, experts and stakeholders from emergency medicine and the pain research field reviewed the current literature and identified eight candidate priority areas. At the conference, these eight areas were reviewed and all eight were ratified using a nominal group technique to build consensus. These priority areas were: 1) gender differences in the pharmacologic and non-pharmacologic interventions for pain, including differences in opioid tolerance, side effects, or misuse; 2) gender differences in pain severity perceptions, clinically meaningful differences in acute pain, and pain treatment preferences; 3) gender differences in pain outcomes of ED patients across the lifespan; 4) gender differences in the relationship between acute pain and acute psychological responses; 5) the influence of physician-patient gender differences and characteristics on the assessment and treatment of pain; 6) gender differences in the influence of acute stress and chronic stress on acute pain responses; 7) gender differences in biologic mechanisms and molecular pathways mediating acute pain in ED populations; and 8) gender differences in biologic mechanisms and molecular pathways mediating chronic pain development after trauma, stress, or acute illness exposure. These areas represent priority areas for future scientific inquiry, and gaining understanding in these will be essential to improving our understanding of sex and gender differences in the assessment and treatment of pain conditions in emergency care settings

Prior Sexual Trauma Exposure Impacts Posttraumatic Dysfunction and Neural Circuitry Following a Recent Traumatic Event in the AURORA Study

Background: Prior sexual trauma (ST) is associated with greater risk for posttraumatic stress disorder after a subsequent traumatic event; however, the underlying neurobiological mechanisms remain opaque. We investigated longitudinal posttraumatic dysfunction and amygdala functional dynamics following admission to an emergency department for new primarily nonsexual trauma in participants with and without previous ST. Methods: Participants (N = 2178) were recruited following acute trauma exposure (primarily motor vehicle collision). A subset (n = 242) completed magnetic resonance imaging that included a fearful faces task and a resting-state scan 2 weeks after the trauma. We investigated associations between prior ST and several dimensions of posttraumatic symptoms over 6 months. We further assessed amygdala activation and connectivity differences between groups with or without prior ST. Results: Prior ST was associated with greater posttraumatic depression (F1,1120 = 28.35, p = 1.22 × 10−7, ηp2 = 0.06), anxiety (F1,1113 = 17.43, p = 3.21 × 10−5, ηp2 = 0.05), and posttraumatic stress disorder (F1,1027 = 11.34, p = 7.85 × 10−4, ηp2 = 0.04) severity and more maladaptive beliefs about pain (F1,1113 = 8.51, p = .004, ηp2 = 0.02) but was not related to amygdala reactivity to fearful versus neutral faces (all ps \u3e .05). A secondary analysis revealed an interaction between ST and lifetime trauma load on the left amygdala to visual cortex connectivity (peak Z value: −4.41, corrected p \u3c .02). Conclusions: Findings suggest that prior ST is associated with heightened posttraumatic dysfunction following a new trauma exposure but not increased amygdala activity. In addition, ST may interact with lifetime trauma load to alter neural circuitry in visual processing regions following acute trauma exposure. Further research should probe the relationship between trauma type and visual circuitry in the acute aftermath of trauma

Structural covariance of the ventral visual stream predicts posttraumatic intrusion and nightmare symptoms: a multivariate data fusion analysis

Visual components of trauma memories are often vividly re-experienced by survivors with deleterious consequences for normal function. Neuroimaging research on trauma has primarily focused on threat-processing circuitry as core to trauma-related dysfunction. Conversely, limited attention has been given to visual circuitry which may be particularly relevant to posttraumatic stress disorder (PTSD). Prior work suggests that the ventral visual stream is directly related to the cognitive and affective disturbances observed in PTSD and may be predictive of later symptom expression. The present study used multimodal magnetic resonance imaging data (n = 278) collected two weeks after trauma exposure from the AURORA study, a longitudinal, multisite investigation of adverse posttraumatic neuropsychiatric sequelae. Indices of gray and white matter were combined using data fusion to identify a structural covariance network (SCN) of the ventral visual stream 2 weeks after trauma. Participant\u27s loadings on the SCN were positively associated with both intrusion symptoms and intensity of nightmares. Further, SCN loadings moderated connectivity between a previously observed amygdala-hippocampal functional covariance network and the inferior temporal gyrus. Follow-up MRI data at 6 months showed an inverse relationship between SCN loadings and negative alterations in cognition in mood. Further, individuals who showed decreased strength of the SCN between 2 weeks and 6 months had generally higher PTSD symptom severity over time. The present findings highlight a role for structural integrity of the ventral visual stream in the development of PTSD. The ventral visual stream may be particularly important for the consolidation or retrieval of trauma memories and may contribute to efficient reactivation of visual components of the trauma memory, thereby exacerbating PTSD symptoms. Potentially chronic engagement of the network may lead to reduced structural integrity which becomes a risk factor for lasting PTSD symptoms

Neighborhood Disadvantage and Neural Correlates of Threat and Reward Processing in Survivors of Recent Trauma

IMPORTANCE: Differences in neighborhood socioeconomic characteristics are important considerations in understanding differences in risk vs resilience in mental health. Neighborhood disadvantage is associated with alterations in the function and structure of threat neurocircuitry. OBJECTIVE: To investigate associations of neighborhood disadvantage with white and gray matter and neural reactivity to positive and negative stimuli in the context of trauma exposure. DESIGN, SETTING, AND PARTICIPANTS: In this cross-sectional study, survivors of trauma who completed sociodemographic and posttraumatic symptom assessments and neuroimaging were recruited as part of the Advancing Understanding of Recovery After Trauma (AURORA) study between September 2017 and June 2021. Data analysis was performed from October 25, 2022, to February 15, 2023. EXPOSURE: Neighborhood disadvantage was measured with the Area Deprivation Index (ADI) for each participant home address. MAIN OUTCOMES AND MEASURES: Participants completed separate threat and reward tasks during functional magnetic resonance imaging. Diffusion-weighted and high-resolution structural images were also collected. Linear models assessed the association of ADI with reactivity, microstructure, and macrostructure of a priori regions of interest after adjusting for income, lifetime trauma, sex at birth, and age. A moderated-mediation model tested whether ADI was associated with neural activity via microstructural changes and if this was modulated by PTSD symptoms. RESULTS: A total of 280 participants (183 females [65.4%]; mean [SD] age, 35.39 [13.29] years) completed the threat task and 244 participants (156 females [63.9%]; mean [SD] age, 35.10 [13.26] years) completed the reward task. Higher ADI (per 1-unit increase) was associated with greater insula (t274 = 3.20; β = 0.20; corrected P = .008) and anterior cingulate cortex (ACC; t274 = 2.56; β = 0.16; corrected P = .04) threat-related activity after considering covariates, but ADI was not associated with reward reactivity. Greater disadvantage was also associated with altered microstructure of the cingulum bundle (t274 = 3.48; β = 0.21; corrected P = .001) and gray matter morphology of the ACC (cortical thickness: t273 = -2.29; β = -0.13; corrected P = .02; surface area: t273 = 2.53; β = 0.13; corrected P = .02). The moderated-mediation model revealed that ADI was associated with ACC threat reactivity via cingulum microstructural changes (index of moderated mediation = -0.02). However, this mediation was only present in individuals with greater PTSD symptom severity (at the mean: β = -0.17; standard error = 0.06, t= -2.28; P = .007; at 1 SD above the mean: β = -0.28; standard error = 0.08; t = -3.35; P \u3c .001). CONCLUSIONS AND RELEVANCE: In this study, neighborhood disadvantage was associated with neurobiology that supports threat processing, revealing associations of neighborhood disadvantage with neural susceptibility for PTSD and suggesting how altered structure-function associations may complicate symptoms. Future work should investigate specific components of neighborhood disadvantage that may be associated with these outcomes