We assessed the effects of initiation of continuous glucose monitoring (CGM) on emergency department (ED) visits among individuals covered by a large commercial health insurer in the southeastern U.S. (1).
Our sample includes beneficiaries with diabetes who were using insulin between 1 December 2017 and 31 December 2020. To be included, member–index date combinations had to 1) have four or more adjudicated claims for insulin and one or more medical claims with a diabetes diagnostic code in the 365 days before index, 2) be eligible for ≥10 months throughout the preperiod, 3) not turn 65 years old before the end of the postperiod, and 4) have one or more health care charges in the pre- or postperiod.
We implemented a pre-post nonequivalent groups design via differences-in-differences (DiD) with administrative claims data, and we used generalized estimating equations with a negative binomial distribution, log link, and exchangeable correlation structure to model all-cause ED visits per 1,000 members.
The intervention date (among the treated individuals) was the first date of a filled prescription for any personal-use CGM (real time or intermittently scanned) after 1 December 2018, the policy implementation date. The index date for the control group was the day of a health care encounter that included both a diabetes-related diagnostic code and an evaluation and management code. The DiD timeline included 180 days of observation before and after the index date.
To reduce confounding, we used a two-phase, one-to-one matching approach across the treatment and control groups. We first exact-matched control individuals to each treatment individual on endocrinology office visits, claim-identifiable hypoglycemic events, insulin type, source of insurance, diabetes type, professional CGM use in the preindex period, and year and season of index. Subsequently, we used a propensity score model among this set that further accounted for age at index, chronic conditions (2), residential rurality, and sex. Data on race and ethnicity were not available for our analytic data set. Our final set of matched individuals was selected using the control individual who had the minimum absolute distance of propensity score from the treated individual.
Data from 6,180 individuals (3,090 in each group) were analyzed. Standardized absolute mean differences across all variables were <0.1 after matching. Roughly half saw an endocrinologist in the prior year, 17% used long-acting insulin only, 18% used rapid-acting insulin only, and 65% used both. Approximately one-fourth lived in a rural zip code, and slightly more than half had type 2 diabetes (versus type 1). The DiD estimate was an incidence rate ratio (IRR) of 0.86 (95% CI 0.74, 1.00), representing a 14% lower incidence rate of ED visits for CGM initiators compared with those who did not initiate CGM (rates are depicted in Fig. 1). When stratified, the effect estimate was an IRR of 0.83 for those with type 1 diabetes and 0.88 for those with type 2 diabetes, although the subgroup estimates were less precise and not statistically significant.
Pre-post rates of ED visits per 1,000 analytic cohort members (individuals). Shown are differences in ED visits among intervention (personal CGM initiators) and control patients matched on diabetes type, source of insurance, 6-month time period, endocrinology visits in the past year, claim-identifiable hypoglycemic event in the past year, insulin type, professional CGM use in the preperiod, sex, age, residence in a rural zip code, and chronic conditions defined by hierarchical condition categories.
Pre-post rates of ED visits per 1,000 analytic cohort members (individuals). Shown are differences in ED visits among intervention (personal CGM initiators) and control patients matched on diabetes type, source of insurance, 6-month time period, endocrinology visits in the past year, claim-identifiable hypoglycemic event in the past year, insulin type, professional CGM use in the preperiod, sex, age, residence in a rural zip code, and chronic conditions defined by hierarchical condition categories.
Our analysis, based on data from beneficiaries of a large private health insurer in the southeastern U.S., underscores the potential for CGM to reduce emergency health service use among people with diabetes who also use insulin. Limitations include that the data do not capture individuals using cash to pay for CGM, although this would conservatively bias results toward the null by reducing the pre-post change difference between groups. We were also unable to evaluate CGM initiation and outcomes across different racial and ethnic subgroups. Our inclusion criteria for person-time combinations make parallel trend testing infeasible, so the estimated treatment effect may be attributable to differing trends in ED use between the groups prior to CGM initiation (3). Our matching approach led us to estimate the treatment effect in the treated individuals; thus, findings are not generalizable to adults with diabetes who are not on CGM.
Statistically significant associations between CGM initiation and several emergency health service use measures, including ED visits for hypoglycemia, although all-cause ED visits were not statistically significant in this association (4). Our estimates are similar in magnitude and have greater precision. However, we could not replicate the outcomes evaluated in the aforementioned study due to the limited number of ED visits; more work is needed to evaluate the broad spectrum of CGM-derived health outcomes across diverse cohorts.
Growing empirical support for a link between CGM use and reduced emergency health services use is nontrivial in the context of the economic, clinical, and patient-oriented burden of diabetes and may provide evidence for health insurers that aim to minimize the frequency of ED visits. Additionally, based on previous research that showed notably more hypoglycemia episodes occur at home and do not result in an ED visit, CGM may affect hypoglycemia that is not captured in claims data (5).
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Funding and Duality of Interest. This project was supported by funds from Dexcom, Inc., a company that develops, manufactures, and distributes CGM systems for diabetes management. The database infrastructure used for this project was funded by the University of North Carolina (UNC) Cecil G. Sheps Center for Health Services Research, the Department of Health Policy and Management, UNC Gillings School of Global Public Health, the Comparative Effectiveness Research Strategic Initiative of UNC’s Clinical and Translational Science Award (UM1TR004406), and the UNC School of Medicine. At the time of this work, B.U. was an employee of the University of North Carolina. He is currently a Principal Health Outcomes Researcher with Prime Therapeutics. T.S. receives investigator-initiated research funding and support as Principal Investigator (R01AG056479) from the National Institute on Aging (NIA), and as Co-Investigator (R01CA174453, R01HL118255, R01MD011680), National Institutes of Health (NIH). He also receives salary support as Director of Comparative Effectiveness Research (CER), NC TraCS Institute, UNC Clinical and Translational Science Award (UM1TR004406), the Center for Pharmacoepidemiology (current members: GlaxoSmithKline, UCB BioSciences, Takeda, AbbVie, Boehringer Ingelheim), from pharmaceutical companies (Novo Nordisk), and from a generous contribution from Dr. Nancy A. Dreyer to the Department of Epidemiology, University of North Carolina at Chapel Hill. T.S. does not accept personal compensation of any kind from any pharmaceutical company. He owns stock in Novartis, Roche, and Novo Nordisk.
A.R.K. is supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through UNC Clinical and Translational Science Award (UM1TR004406). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. A.R.K. also reports receiving research grants from the Diabetes Research Connection and the American Diabetes Association, and a prize from the National Academy of Medicine, outside the submitted work.
J.B.B. is supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through grant UM1TR004406. Contracted consulting fees and travel support for contracted activities for his efforts from Novo Nordisk are paid to the University of North Carolina. J.B.B. has grant support from Dexcom, NovaTarg, Novo Nordisk, Sanofi, Tolerion and vTv Therapeutics. J.B.B. is a consultant to Alkahest, Altimmune, Anji, AstraZeneca, Bayer, Biomea Fusion Inc, Boehringer-Ingelheim, CeQur, Cirius Therapeutics Inc, Corcept Therapeutics, Eli Lilly, GentiBio, Glycadia, Glyscend, Janssen, MannKind, Mellitus Health, Moderna, Pendulum Therapeutics, Praetego, Sanofi, Stability Health, Terns Inc, Valo, and Zealand Pharma. J.B.B. has stock/options in Glyscend, Mellitus Health, Pendulum Therapeutics, PhaseBio, Praetego, and Stability Health. J.M.W. reports work as a research consultant on a project sponsored by Dexcom unrelated to this work.
Dexcom, Inc., was not involved in the collection, analysis, or interpretation of the data, writing of the manuscript, or the decision to submit the manuscript for publication. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Author Contributions. B.U. and S.P. conducted the data analysis. B.U., S.P., J.A., T.S., and J.B.B. conceived the study design. J.M.W. and A.R.K. prepared the manuscript, and all authors contributed feedback on writing. B.U. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.