Factors Associated With a Discharge Against Medical Advice From an Emergency Department in Adult Patients With Appendicitis.

BACKGROUND: Delays in care can lead to worsened outcomes with acute appendicitis. To get timely treatment, patients must consent. OBJECTIVE: To determine if there are racial and socioeconomic differences in discharge against medical advice (DAMA) rates from an emergency department after the diagnosis of acute appendicitis. METHODS: Patients were identified retrospectively from the 2019 National Emergency Department Sample. The inclusion criteria were patients 18 years of age or older with acute appendicitis. Rates were compared using chi-square or Fisher's exact test. Odds ratios were determined using multiple logistic regression. A p value of 0.05 was used to determine statistical significance. RESULTS: The overall rate of DAMA was low (0.37%). Black patients had the highest rate, and White patients had the lowest (0.72% and 0.28%, respectively, p < 0.001). When controlling for covariates, Black patients also had a higher odds ratio (OR) for DAMA (OR 1.96, 95% confidence interval [CI] 1.29-2.97). Male patients had a higher unadjusted rate (0.47% vs. 0.26% in females, p < 0.001) and were at increased risk (OR 1.78, 95% CI 1.32-2.41). Patients between 30 and 65 years old had an increased risk (OR 1.48, 95% CI 1.10-2.0). Patients with government insurance or no insurance had higher rates than private insurance (0.57% and 0.56% vs. 0.23% respectively, p < 0.001). CONCLUSION: Race, insurance status, age, and male sex were all associated with increase in DAMA. Risk stratifying patients can help to determine how to best employ mitigations strategies. Reducing DAMA may be the next area for improving reducing disparities in appendicitis care.

An Electronic Medical Record-Derived Individualized Performance Metric to Measure Risk-Adjusted Adherence with Perioperative Prophylactic Bundles for Health Care Disparity Research and Implementation Science.

BACKGROUND: Health care disparity persists despite vigorous countermeasures. Clinician performance is paramount for equitable care processes and outcomes. However, precise and valid individual performance measures remain elusive. OBJECTIVES: We sought to develop a generalizable, rigorous, risk-adjusted metric for individual clinician performance (MIP) derived directly from the electronic medical record (EMR) to provide visual, personalized feedback. METHODS: We conceptualized MIP as risk responsiveness, i.e., administering an increasing number of interventions contingent on patient risk. We embedded MIP in a hierarchical statistical model, reflecting contemporary nested health care delivery. We tested MIP by investigating the adherence with prophylactic bundles to reduce the risk of postoperative nausea and vomiting (PONV), retrieving PONV risk factors and prophylactic antiemetic interventions from the EMR. We explored the impact of social determinants of health on MIP. RESULTS: We extracted data from the EMR on 25,980 elective anesthesia cases performed at Penn State Milton S. Hershey Medical Center between June 3, 2018 and March 31, 2019. Limiting the data by anesthesia Current Procedural Terminology code and to complete cases with PONV risk and antiemetic interventions, we evaluated the performance of 83 anesthesia clinicians on 2,211 anesthesia cases. Our metric demonstrated considerable variance between clinicians in the adherence to risk-adjusted utilization of antiemetic interventions. Risk seemed to drive utilization only in few clinicians. We demonstrated the impact of social determinants of health on MIP, illustrating its utility for health science and disparity research. CONCLUSION: The strength of our novel measure of individual clinician performance is its generalizability, as well as its intuitive graphical representation of risk-adjusted individual performance. However, accuracy, precision and validity, stability over time, sensitivity to system perturbations, and acceptance among clinicians remain to be evaluated.

A prospective community engagement initiative to improve clinical research participation in patients with peripheral artery disease.

OBJECTIVE: Patients diagnosed with peripheral artery disease are difficult to recruit into clinical trials. However, there is currently no high-quality, patient-centered information explaining why peripheral artery disease patients choose to participate or not participate in clinical research studies. METHODS: The current study was a prospective community engagement initiative that specifically asked patients with and without peripheral artery disease: (1) what motivates them to participate in clinical research studies, (2) their willingness to participate in different research procedures, (3) the barriers to participation, (4) preferences about study design, and (5) demographic and disease-related factors influencing participation. Data were gathered through focus groups (n = 19, participants aged 55-79 years) and mailed questionnaires (n = 438, respondents aged 18-85 years). RESULTS: More than half of the respondents stated that they would be willing to participate in a study during evening or weekend time slots. Peripheral artery disease patients (n = 45) were more willing than those without peripheral artery disease (n = 360) to participate in drug infusion studies (48% versus 18%, p < 0.001) and trials of investigational drugs (44% versus 21%, p < 0.001). Motivating factors and barriers to participation were largely consistent with previous studies. CONCLUSION: Adults in our geographic region are interested in participating in clinical research studies related to their health; they would like their doctor to tell them what studies they qualify for and they prefer to receive a one-page advertisement that has color pictures of the research procedures. Peripheral artery disease patients are more willing than those without peripheral artery disease to participate in drug infusion studies, trials of investigational drugs, microneurography, and spinal/epidural infusions.

Medicaid insurance status predicts postoperative mortality after total knee arthroplasty in state inpatient databases.

Aim: Medicaid versus private primary insurance status may predict in-hospital mortality and morbidity after total knee arthroplasty (TKA). Materials & methods: Regression models were used to test our hypothesis in patients in the State Inpatient Database (SID) from five states who underwent primary TKA from January 2007 to December 2014. Results: Medicaid patients had greater odds of in-hospital mortality (odds ratio [OR]: 1.73; 95% CI: 1.01-2.95), greater odds of any postoperative complications (OR: 1.25; 95% CI: 1.18-1.33), experience longer lengths of stay (OR: 1.09; 95% CI: 1.08-1.10) and higher total charges (OR: 1.03; 95% CI: 1.02-1.04). Conclusion: Medicaid insurance status is associated with higher in-hospital mortality and morbidity in patients after TKA compared with private insurance.

Esmolol acutely alters oxygen supply-demand balance in exercising muscles of healthy humans.

Beta-adrenoreceptor antagonists (ß blockers) reduce systemic O2 delivery and blood pressure (BP) during exercise, but the subsequent effects on O2 extraction within the active limb muscles are unknown. In this study, we examined the effects of the fast-acting, ß1 selective blocker esmolol on systemic hemodynamics and leg muscle O2 saturation (near infrared spectroscopy, NIRS) during submaximal leg ergometry. Our main hypothesis was that esmolol would augment exercise-induced reductions in leg muscle O2 saturation. Eight healthy adults (6 men, 2 women; 23-67 year) performed light and moderate intensity bouts of recumbent leg cycling before (PRE), during (ß1 -blocked), and 45 min following (POST) intravenous infusion of esmolol. Oxygen uptake, heart rate (HR), BP, and O2 saturation (SmO2 ) of the vastus lateralis (VL) and medial gastrocnemius (MG) muscles were measured continuously. Esmolol attenuated the increases in HR and systolic BP during light (-12 ± 9 bpm and -26 ± 12 mmHg vs. PRE) and moderate intensity (-20 ± 10 bpm and -40 ± 18 mmHg vs. PRE) cycling (all P < 0.01). Exercise-induced reductions in SmO2 occurred to a greater extent during the ß1 -blockade trial in both the VL (P = 0.001 vs. PRE) and MG muscles (P = 0.022 vs. PRE). HR, SBP and SmO2 were restored during POST (all P < 0.01 vs. ß1 -blocked). In conclusion, esmolol rapidly and reversibly increases O2 extraction within exercising muscles of healthy humans.

Beta-1 vs. beta-2 adrenergic control of coronary blood flow during isometric handgrip exercise in humans.

During exercise, ß-adrenergic receptors are activated throughout the body. In healthy humans, the net effect of ß-adrenergic stimulation is an increase in coronary blood flow. However, the role of vascular ß1 vs. ß2 receptors in coronary exercise hyperemia is not clear. In this study, we simultaneously measured noninvasive indexes of myocardial oxygen supply (i.e., blood velocity in the left anterior descending coronary artery; Doppler echocardiography) and demand [i.e., rate pressure product (RPP) = heart rate × systolic blood pressure) and tested the hypothesis that ß1 blockade with esmolol improves coronary exercise hyperemia compared with nonselective ß-blockade with propranolol. Eight healthy young men received intravenous infusions of esmolol, propranolol, and saline on three separate days in a single-blind, randomized, crossover design. During each infusion, subjects performed isometric handgrip exercise until fatigue. Blood pressure, heart rate, and coronary blood velocity (CBV) were measured continuously, and RPP was calculated. Changes in parameters from baseline were compared with paired t-tests. Esmolol (Δ = 3296 ± 1204) and propranolol (Δ = 2997 ± 699) caused similar reductions in peak RPP compared with saline (Δ = 5384 ± 1865). In support of our hypothesis, ΔCBV with esmolol was significantly greater than with propranolol (7.3 ± 2.4 vs. 4.5 ± 1.6 cm/s; P = 0.002). This effect was also evident when normalizing ΔCBV to ΔRPP. In summary, not only does selective ß1 blockade reduce myocardial oxygen demand during exercise, but it also unveils ß2-receptor-mediated coronary exercise hyperemia.NEW & NOTEWORTHY In this study, we evaluated the role of vascular ß1 vs. ß2 receptors in coronary exercise hyperemia in a single-blind, randomized, crossover study in healthy men. In response to isometric handgrip exercise, blood flow velocity in the left anterior descending coronary artery was significantly greater with esmolol compared with propranolol. These findings increase our understanding of the individual and combined roles of coronary ß1 and ß2 adrenergic receptors in humans.

Esmolol infusion versus propranolol infusion: effects on heart rate and blood pressure in healthy volunteers.

Despite its widespread clinical use, the ß1-adrenergic receptor antagonist esmolol hydrochloride is not commonly used in human physiology research, and the effective dose of esmolol (compared with the nonselective ß-blocker propranolol) is unclear. In four separate studies we used cycle ergometry exercise and infusions of isoproterenol and epinephrine to test the heart rate (HR)-lowering effect of esmolol compared with propranolol and saline in healthy humans. In cohort 1, both esmolol (ΔHR 57 ± 6 beats/min) and propranolol (ΔHR 56 ± 7 beats/min) attenuated exercise tachycardia compared with saline (ΔHR 88 ± 17 beats/min). In cohort 2, we found that the HR response to exercise was similar at 5 min (ΔHR 57 ± 9 beats/min) and 60 min (ΔHR 55 ± 9 beats/min) after initiation of the esmolol maintenance infusion. In cohort 3, we confirmed that the HR-lowering effect of esmolol disappeared 45 min after termination of the maintenance infusion. In cohort 4, changes in femoral blood flow and hematological parameters in response to epinephrine infusion were not different between esmolol and saline infusion, indicating that our esmolol infusion paradigm does not block ß2-receptors. Collectively, our data indicate that infusion of ~160 mg of esmolol (range 110-200 mg in the 5 min before exercise) acutely and selectively blocks ß1-receptors in healthy humans. Additionally, ß1-receptors remain blocked 60 min later if a maintenance infusion of ~0.2 mg·kg total body mass-1·min-1 continues. The current data lay the foundation for future studies to evaluate ß1- vs. ß2-receptor control of the circulation in humans.NEW & NOTEWORTHY We used cycle ergometry exercise and infusions of isoproterenol and epinephrine to test the heart rate-lowering effect of esmolol compared with propranolol and saline in healthy humans. Collectively, our data indicate that infusion of ~160 mg of esmolol (range 110-200 mg in the 5 min before exercise) acutely and selectively blocks ß1-adrenergic receptors. These infusion parameters can be used in future experiments to evaluate ß1- vs. ß2-receptor control of the circulation in humans.

Effect of adrenergic agonists on coronary blood flow: a laboratory study in healthy volunteers.

Myocardial oxygen supply and demand mismatch is fundamental to the pathophysiology of ischemia and infarction. The sympathetic nervous system, through α-adrenergic receptors and ß-adrenergic receptors, influences both myocardial oxygen supply and demand. In animal models, mechanistic studies have established that adrenergic receptors contribute to coronary vascular tone. The purpose of this laboratory study was to noninvasively quantify coronary responses to adrenergic receptor stimulation in humans. Fourteen healthy volunteers (11 men and 3 women) performed isometric handgrip exercise to fatigue followed by intravenous infusion of isoproterenol. A subset of individuals also received infusions of phenylephrine (n = 6), terbutaline (n = 10), and epinephrine (n = 4); all dosages were based on fat-free mass and were infused slowly to achieve steady-state. The left anterior descending coronary artery was visualized using Doppler echocardiography. Beat-by-beat heart rate (HR), blood pressure (BP), peak diastolic coronary velocity (CBVpeak), and coronary velocity time integral were calculated. Data are presented as M ± SD Isometric handgrip elicited significant increases in BP, HR, and CBVpeak (from 23.3 ± 5.3 to 34.5 ± 9.9 cm/sec). Isoproterenol raised HR and CBVpeak (from 22.6 ± 4.8 to 43.9 ± 12.4 cm/sec). Terbutaline and epinephrine evoked coronary hyperemia whereas phenylephrine did not significantly alter CBVpeak. Different indices of coronary hyperemia (changes in CBVpeak and velocity time integral) were significantly correlated (R = 0.803). The current data indicate that coronary hyperemia occurs in healthy humans in response to isometric handgrip exercise and low-dose, steady-state infusions of isoproterenol, terbutaline, and epinephrine. The contribution of ß1 versus ß2 receptors to coronary hyperemia remains to be determined. In this echocardiographic study, we demonstrate that coronary blood flow increases when ß-adrenergic receptors are stimulated (i.e., during exercise and different intravenous infusions). Our infusion paradigms and beat-by-beat imaging methodologies can be used in future studies to evaluate age-, sex-, and disease- differences in adrenergic control of coronary blood flow.