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The evolving science of translating research evidence into clinical practice
  1. Ian Scott, FRACP, MHA, MBBS
  1. Princess Alexandra Hospital
 Brisbane, Queensland, Australia

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    Practising clinicians have to swim in an ocean of clinical research evidence that varies in rigour, consistency, and applicability to the care of individual patients. They are expected to stay up to date, be authoritative, and practice to a high standard. They work in an environment that obliges them to reconcile patient preferences and societal/professional expectations with the need for cost restraint and accountability for quality and safety of care.

    Numerous reports of variations in practice patterns1 and substandard care2 have placed increased pressure on clinicians, healthcare institutions, and professional organisations to improve their ability to provide optimal care. This is essential for the continuation of public trust and funding from public and private payers. While standards of care may not be definable in the absence of definitive evidence, the fact that clinical practice in many instances appears to be at odds with even clear-cut research evidence has become of increasing concern. What have we learned, and what can we apply, in lessening the pressure drops in the pipeline from generation of research evidence to its consistent application in clinical decision making? This article looks at 6 models of evidence dissemination that have evolved over the past few decades.


    In the beginning, many implicitly believed in the “passive diffusion” model of putting evidence into practice.3 In this naive model, evidence published in journals and publicised at medical conferences would rain down and change clinical practice via an osmotic pressure gradient driven by strength of evidence and magnitude of treatment effect. Where the gradient was strongest, as in the case of large, definitive trials showing commonly used therapies to be, in fact, harmful, change was often dramatic, as exemplified by marked reduction in use of antiarrhythmic agents to prevent sudden cardiac death following myocardial infarction4 and hormonal …

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