Effective strategies for scaling up evidence-based practices in primary care: a systematic review

Background

While an extensive array of existing evidence-based practices (EBPs) have the potential to improve patient outcomes, little is known about how to implement EBPs on a larger scale. Therefore, we sought to identify effective strategies for scaling up EBPs in primary care.

Methods

We conducted a systematic review with the following inclusion criteria: (i) study design: randomized and non-randomized controlled trials, before-and-after (with/without control), and interrupted time series; (ii) participants: primary care-related units (e.g., clinical sites, patients); (iii) intervention: any strategy used to scale up an EBP; (iv) comparator: no restrictions; and (v) outcomes: no restrictions. We searched MEDLINE, Embase, PsycINFO, Web of Science, CINAHL, and the Cochrane Library from database inception to August 2016 and consulted clinical trial registries and gray literature. Two reviewers independently selected eligible studies, then extracted and analyzed data following the Cochrane methodology. We extracted components of scaling-up strategies and classified them into five categories: infrastructure, policy/regulation, financial, human resources-related, and patient involvement. We extracted scaling-up process outcomes, such as coverage, and provider/patient outcomes. We validated data extraction with study authors.

Results

We included 14 studies. They were published since 2003 and primarily conducted in low-/middle-income countries (n?=?11). Most were funded by governmental organizations (n?=?8). The clinical area most represented was infectious diseases (HIV, tuberculosis, and malaria, n?=?8), followed by newborn/child care (n?=?4), depression (n?=?1), and preventing seniors’ falls (n?=?1). Study designs were mostly before-and-after (without control, n?=?8). The most frequently targeted unit of scaling up was the clinical site (n?=?11). The component of a scaling-up strategy most frequently mentioned was human resource-related (n?=?12). All studies reported patient/provider outcomes. Three studies reported scaling-up coverage, but no study quantitatively reported achieving a coverage of 80% in combination with a favorable impact.

Conclusions

We found few studies assessing strategies for scaling up EBPs in primary care settings. It is uncertain whether any strategies were effective as most studies focused more on patient/provider outcomes and less on scaling-up process outcomes. Minimal consensus on the metrics of scaling up are needed for assessing the scaling up of EBPs in primary care.

Trial registration

This review is registered as PROSPERO CRD42016041461.

     

Ecological restoration of a severely degraded coastal acid sulfate soil: A case study of the East Trinity wetland,Queensland

A severely degraded acid sulfate soil wetland near Cairns, Queensland, has been returned to a functional estuarine habitat using a cost‐effective, low‐technology method based on the reintroduction of tidal water. Gradual increases in tidal inundation, combined with targeted liming of the tidal stream, restored conditions that promoted chemical and microbial processes leading to the rapid recolonisation of mangrove communities and other estuarine flora and fauna. Protocols and understanding developed at East Trinity can be readily applied to other coastal acid sulfate soil sites.     

The secondary invasion of giant African land snail has little impact on litter or seedling dynamics in rainforest

In the absence of empirical evidence, invasive species are often assumed to have negative impacts because of their conspicuously high abundance. The giant African land snail Achatina (Lissachatina) fulica is one such invader where its impact in natural ecosystems remains completely untested. On Christmas Island (Indian Ocean), A. fulica has become established across large tracts of rainforest following the impacts of invasive yellow crazy ant (Anoplolepis gracilipes) in mutualism with non‐native scale insects. Yellow crazy ants facilitate the secondary invasion of A. fulica by extirpating native red land crabs (Gecarcoidea natalis) that are normally effective predators of A. fulica. We used a multifaceted approach to investigate some potential impacts of abundant A. fulica in invaded rainforest. Over the course of a wet season, diel activity transects showed that A. fulica consumed detrital material almost exclusively. However, stable isotope analysis did not confidently identify A. fulica as a predominantly detritivorous species. We found no statistically significant treatment effects of A. fulica exclusion on standing leaf litter and seedling recruitment processes during a 6‐month manipulative field study. However, litter cover and biomass did remain slightly higher where A. fulica were excluded, albeit with overlapping confidence intervals with control plots. Our study constitutes the first empirical test for impact of A. fulica in a natural ecosystem and suggests that for Christmas Island rainforest, this species is not a damaging invader. Other studies will need to assess the impacts of A. fulica in other natural areas before these findings could be considered broadly applicable.     

Disease spread in age structured populations with maternal age effects

Fundamental ecological processes, such as extrinsic mortality, determine population age structure. This influences disease spread when individuals of different ages differ in susceptibility or when maternal age determines offspring susceptibility. We show that Daphnia magna offspring born to young mothers are more susceptible than those born to older mothers, and consider this alongside previous observations that susceptibility declines with age in this system. We used a susceptible‐infected compartmental model to investigate how age‐specific susceptibility and maternal age effects on offspring susceptibility interact with demographic factors affecting disease spread. Our results show a scenario where an increase in extrinsic mortality drives an increase in transmission potential. Thus, we identify a realistic context in which age effects and maternal effects produce conditions favouring disease transmission.     

The Triangulation WIthin a STudy (TWIST) framework for causal inference within pharmacogenetic research

In this paper we review the methodological underpinnings of the general pharmacogenetic approach for uncovering genetically-driven treatment effect heterogeneity. This typically utilises only individuals who are treated and relies on fairly strong baseline assumptions to estimate what we term the ‘genetically moderated treatment effect’ (GMTE). When these assumptions are seriously violated, we show that a robust but less efficient estimate of the GMTE that incorporates information on the population of untreated individuals can instead be used. In cases of partial violation, we clarify when Mendelian randomization and a modified confounder adjustment method can also yield consistent estimates for the GMTE. A decision framework is then described to decide when a particular estimation strategy is most appropriate and how specific estimators can be combined to further improve efficiency. Triangulation of evidence from different data sources, each with their inherent biases and limitations, is becoming a well established principle for strengthening causal analysis. We call our framework ‘Triangulation WIthin a STudy’ (TWIST)’ in order to emphasise that an analysis in this spirit is also possible within a single data set, using causal estimates that are approximately uncorrelated, but reliant on different sets of assumptions. We illustrate these approaches by re-analysing primary-care-linked UK Biobank data relating to CYP2C19 genetic variants, Clopidogrel use and stroke risk, and data relating to APOE genetic variants, statin use and Coronary Artery Disease.     

High molecular weight neurofilament proteins are physiological substrates of adduction by the lipid peroxidation product hydroxynonenal.

Protein adducts of the lipid peroxidation product trans-4-hydroxy-2-nonenal (HNE) are features of oxidative damage in neuronal cell bodies in Alzheimer's disease but are also seen in axons of normal as well as diseased individuals. In this study, focusing on the axons of the mouse sciatic nerve, we found that HNE adducts characterize axons of mice from birth to senility. Immunoblots of axonal proteins showed that HNE adducts are only detected in neurofilament heavy subunit (NFH) and, to a lesser extent, neurofilament medium subunit (NFM), both lysine-rich proteins, consistent with the adducts being limited to lysine residues. In vitro, HNE treatment of permeabilized sciatic nerve showed the same specificity, i.e. NFH and NFM are the only proteins that reacted with HNE, providing they are phosphorylated. Quantitative immunoblot analysis of two strains of mice ages 1-33 months showed that the levels of HNE adducts on NFH are consistent throughout life. Additionally, mice transgenic for human superoxide dismutase-1 with G85R mutation show no difference in HNE adduction to NFH compared with controls. Taken together, these studies indicate that HNE adduction to NFH is physiological, and its constancy from birth to senility as well as its dependence on phosphorylation argues that NFH and NFM modification may play a role in protecting the membrane-rich axon from toxic aldehydes resulting from oxidative damage.     

CD44-mediated uptake and degradation of hyaluronan.

Hyaluronan turnover occurs systemically from the lymph and serum as well as locally by the same cells responsible for its synthesis. Local turnover involves receptor-mediated uptake and delivery to lysosomes. Of the many hyaluronan binding proteins/receptors known, the participation of CD44 in the internalization of hyaluronan has been best characterized. Some fraction of the hyaluronan bound to CD44 becomes internalized and delivered to lysosomes by a mechanism that is not dependent on clatherin, caveolae or pinocytosis. In cells such as chondrocytes, anabolic and catabolic cytokines can alter the activity of CD44 toward hyaluronan internalization. However, the mechanism of cellular regulation remains unclear. Regulation may involve the participation of alternatively spliced isoforms of CD44, changes in CD44 phosphorylation, changes in cytoskeletal binding proteins or, the activity or extracellular proteolytic activity.