Readmission Rates After Passage of the Hospital Readmissions Reduction Program: A Pre-Post Analysis.

BACKGROUND: Whether hospitals with the highest risk-standardized readmission rates (RSRRs) subsequently experienced the greatest improvement after passage of the Medicare Hospital Readmissions Reduction Program (HRRP) is unknown. OBJECTIVE: To evaluate whether passage of the HRRP was followed by acceleration in improvement in 30-day RSRRs after hospitalizations for acute myocardial infarction (AMI), congestive heart failure (CHF), or pneumonia and whether the lowest-performing hospitals had faster acceleration in improvement after passage of the law than hospitals that were already performing well. DESIGN: Pre-post analysis stratified by hospital performance groups. SETTING: U.S. acute care hospitals. PATIENTS: 15 170 008 Medicare patients discharged alive from 2000 to 2013. INTERVENTION: Passage of the HRRP. MEASUREMENTS: 30-day readmission rates after hospitalization for AMI, CHF, or pneumonia for hospitals in the highest-performance (0% penalty), average-performance (>0% and <0.50% penalty), low-performance (≥0.50% and <0.99% penalty), and lowest-performance (≥0.99% penalty) groups. RESULTS: Of 2868 hospitals serving 1 109 530 Medicare discharges annually, 30.1% were highest performers, 44.0% were average performers, 16.8% were low performers, and 9.0% were lowest performers. After controlling for prelaw trends, an additional 67.6 (95% CI, 66.6 to 68.4), 74.8 (CI, 74.0 to 75.4), 85.4 (CI, 84.0 to 86.8), and 95.1 (CI, 92.6 to 97.5) readmissions per 10 000 discharges were found to have been averted per year in the highest-, average-, low-, and lowest-performance groups, respectively, after passage of the law. LIMITATION: Inability to distinguish between improvement caused by the magnitude of the penalty or by different levels of health improvement in different patient populations. CONCLUSION: After passage of the HRRP, 30-day RSRRs for myocardial infarction, heart failure, and pneumonia decreased more rapidly than before the law's passage. Improvement was most marked for hospitals with the lowest prelaw performance. PRIMARY FUNDING SOURCE: National Institutes of Health.

Causal Inference Methods for Estimating Long-Term Health Effects of Air Quality Regulations.

INTRODUCTION: The regulatory and policy environment surrounding air quality management warrants new types of epidemiological evidence. Whereas air pollution epidemiology has typically informed previous policies with estimates of exposure-response relationships between pollution and health outcomes, new types of evidence can inform current debates about the actual health impacts of air quality regulations. Directly evaluating specific regulatory strategies is distinct from and complements estimating exposure-response relationships; increased emphasis on assessing the effectiveness of well-defined regulatory interventions will enhance the evidence supporting policy decisions. The goal of this report is to provide new analytic perspectives and statistical methods for what we refer to as "direct"-accountability assessment of the effectiveness of specific air quality regulatory interventions. Toward this end, we sharpened many of the distinctions surrounding accountability assessment initially raised by the HEI Accountability Working Group (2003) through discussion, development, and deployment of statistical methods for drawing causal inferences from observational data. The methods and analyses presented here are unified in their focus on anchoring accountability assessment to the estimation of the causal consequences of well-defined actions or interventions. These analytic perspectives are discussed in the context of two direct-accountability case studies pertaining to four different links in the so-called chain of accountability, the related series of events leading from the intervention to the expected outcomes (see Preface; HEI Accountability Working Group 2003). METHODS: The statistical methods described in this report consist of both established methods for drawing causal inferences from observational data and newly developed methods for assessing causal accountability. We have sharpened the analytic distinctions between studies that directly evaluated the effectiveness of specific policies and those that estimated exposure-response relationships between pollution and health. We emphasized how a potential-outcomes paradigm for causal inference can elevate policy debates by means of more direct evidence of the extent to which complex regulatory interventions affect pollution and health outcomes. We also outlined the potential-outcomes perspective and promoted its use as a means to frame observational studies as approximate randomized experiments. Our newly developed methods for assessing causal accountability draw on propensity scores, principal stratification, causal mediation analysis, spatial hierarchical models, and Bayesian estimation. The first case study made use of health outcomes among approximately four million Medicare beneficiaries living in the Western United States to estimate the causal health impacts of areas designated as being in nonattainment for particulate matter ≤10 µm in aerodynamic diameter (PM10*) according to the 1987 National Ambient Air Quality Standards (NAAQS). The second case study focused on developing and testing our new, advanced methodology for multipollutant accountability assessment by examining the extent to which sulfur dioxide (SO2) scrubbers on coal-fired power plants causally affect emissions of SO2, nitrogen oxides (NO(x)), and carbon dioxide (CO2) as well as the extent to which emissions reductions mediate the causal effect of a scrubber on ambient concentrations of PM2.5. Both case studies were anchored in our compilation of national, linked data on ambient air quality monitoring, weather, population demographics, Medicare hospitalization and mortality outcomes, continuous-emissions monitoring for electricity-generating units (EGUs) in power plants, and a variety of regulatory control interventions. The resulting database has unprecedented accuracy and granularity for conducting the types of accountability assessments presented in this report. A key component of our work was the creation of tools to help distribute our linked database and to facilitate reproducible research. RESULTS: In the first case study, we focused on illustrating the most fundamental features of a causal-inference perspective on direct-accountability assessment. The results indicated that all-cause Medicare mortality and respiratory-related hospitalization rates were causally reduced in areas designated as nonattainment for PM10 during 1990 to 1995 compared with the rates that would have occurred without the designation. In the second case study, which examined power-plant emissions and illustrated our newly developed statistical methods, the results indicated that the presence of an SO2 scrubber causally reduced ambient PM2.5 and that this reduction was mediated almost entirely through causal reductions in SO2 emissions. The results were interpreted in light of the well-documented relationships between scrubbers, power-plant emissions, and PM2.5. CONCLUSION: By grounding accountability research in a potential-outcomes framework and applying our new methods to our collection of national data sets, we were able to provide additional sound evidence of the health effects of long-term, large-scale air quality regulations. This additional, rigorous evidence of the causal effects of well-defined actions augments the existing body of research and ensures that the highest-level epidemiological evidence will continue to support regulatory policies. Ultimately, our research contributed to the evidence available to support to the U.S. Environmental Protection Agency (U.S. EPA) and other stakeholders for incorporating health outcomes research into policy development.

Accounting for uncertainty in confounder and effect modifier selection when estimating average causal effects in generalized linear models.

Confounder selection and adjustment are essential elements of assessing the causal effect of an exposure or treatment in observational studies. Building upon work by Wang et al. (2012, Biometrics 68, 661-671) and Lefebvre et al. (2014, Statistics in Medicine 33, 2797-2813), we propose and evaluate a Bayesian method to estimate average causal effects in studies with a large number of potential confounders, relatively few observations, likely interactions between confounders and the exposure of interest, and uncertainty on which confounders and interaction terms should be included. Our method is applicable across all exposures and outcomes that can be handled through generalized linear models. In this general setting, estimation of the average causal effect is different from estimation of the exposure coefficient in the outcome model due to noncollapsibility. We implement a Bayesian bootstrap procedure to integrate over the distribution of potential confounders and to estimate the causal effect. Our method permits estimation of both the overall population causal effect and effects in specified subpopulations, providing clear characterization of heterogeneous exposure effects that may vary considerably across different covariate profiles. Simulation studies demonstrate that the proposed method performs well in small sample size situations with 100-150 observations and 50 covariates. The method is applied to data on 15,060 US Medicare beneficiaries diagnosed with a malignant brain tumor between 2000 and 2009 to evaluate whether surgery reduces hospital readmissions within 30 days of diagnosis.

Point: clarifying policy evidence with potential-outcomes thinking--beyond exposure-response estimation in air pollution epidemiology.

The regulatory environment surrounding policies to control air pollution warrants a new type of epidemiologic evidence. Whereas air pollution epidemiology has typically informed policies with estimates of exposure-response relationships between pollution and health outcomes, these estimates alone cannot support current debates surrounding the actual health effects of air quality regulations. We argue that directly evaluating specific control strategies is distinct from estimating exposure-response relationships and that increased emphasis on estimating effects of well-defined regulatory interventions would enhance the evidence that supports policy decisions. Appealing to similar calls for accountability assessment of whether regulatory actions impact health outcomes, we aim to sharpen the analytic distinctions between studies that directly evaluate policies and those that estimate exposure-response relationships, with particular focus on perspectives for causal inference. Our goal is not to review specific methodologies or studies, nor is it to extoll the advantages of "causal" versus "associational" evidence. Rather, we argue that potential-outcomes perspectives can elevate current policy debates with more direct evidence of the extent to which complex regulatory interventions affect health. Augmenting the existing body of exposure-response estimates with rigorous evidence of the causal effects of well-defined actions will ensure that the highest-level epidemiologic evidence continues to support regulatory policies.

The Central Role of Bayes' Theorem for Joint Estimation of Causal Effects and Propensity Scores.

Although propensity scores have been central to the estimation of causal effects for over 30 years, only recently has the statistical literature begun to consider in detail methods for Bayesian estimation of propensity scores and causal effects. Underlying this recent body of literature on Bayesian propensity score estimation is an implicit discordance between the goal of the propensity score and the use of Bayes theorem. The propensity score condenses multivariate covariate information into a scalar to allow estimation of causal effects without specifying a model for how each covariate relates to the outcome. Avoiding specification of a detailed model for the outcome response surface is valuable for robust estimation of causal effects, but this strategy is at odds with the use of Bayes theorem, which presupposes a full probability model for the observed data that adheres to the likelihood principle. The goal of this paper is to explicate this fundamental feature of Bayesian estimation of causal effects with propensity scores in order to provide context for the existing literature and for future work on this important topic.

Uncertainty in Propensity Score Estimation: Bayesian Methods for Variable Selection and Model Averaged Causal Effects.

Causal inference with observational data frequently relies on the notion of the propensity score (PS) to adjust treatment comparisons for observed confounding factors. As decisions in the era of "big data" are increasingly reliant on large and complex collections of digital data, researchers are frequently confronted with decisions regarding which of a high-dimensional covariate set to include in the PS model in order to satisfy the assumptions necessary for estimating average causal effects. Typically, simple or ad-hoc methods are employed to arrive at a single PS model, without acknowledging the uncertainty associated with the model selection. We propose three Bayesian methods for PS variable selection and model averaging that 1) select relevant variables from a set of candidate variables to include in the PS model and 2) estimate causal treatment effects as weighted averages of estimates under different PS models. The associated weight for each PS model reflects the data-driven support for that model's ability to adjust for the necessary variables. We illustrate features of our proposed approaches with a simulation study, and ultimately use our methods to compare the effectiveness of surgical vs. nonsurgical treatment for brain tumors among 2,606 Medicare beneficiaries. Supplementary materials are available online.