Integrating the evidence: confronting the COVID-19 elephant
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EDITORIAL
Integrating the evidence: confronting the COVID‑19 elephant John J. Marini1* , R. Phillip Dellinger2 and Daniel Brodie3 © 2020 Springer-Verlag GmbH Germany, part of Springer Nature
Coronavirus disease 2019 (COVID-19) is an unfamiliar illness with potentially devastating consequences. The pandemic is unfolding at different rates with wide geographic separation and seemingly erratic expression. There is well-justified urgency to describe the inconsistently expressed features of this new viral disease and implement strategies to avoid and treat it [1–4]. Because COVID-19-related illness is caused by a single virus, it seems reasonable to assume a degree of uniformity across populations. Yet, some observations are universal while others apparently conflict. In this urgent situation, we feel impelled to skip steps in the traditional methodology of first making careful observations and then conducting evidence-building research to inform rational management. We have been down this road before of needing to act while not fully understanding a new pathogen variant. But this SARS-CoV-2/COVID-19 seems different. This time around, the disease may infect anyone and most organ systems and is readily and rapidly transmitted. We have a right to be frightened of this novel virus. Mastering the entirety of medicine is impossible; practicing doctors are trained to diagnose (label) by interpreting observations using their prior education and experience, and then manage on that basis. We have a natural tendency to ‘force-fit’ newly encountered fragments of unfamiliar information into our existing constructs and understandings. (In psychology, this is known as the Barnum effect [5].) Although usually a functional approach to decision-making when dealing with too little information, we may unintentionally make errors *Correspondence: [email protected] 1 Departments of Pulmonary and Critical Care Medicine, Regions Hospital and University of Minnesota, Minneapolis/St. Paul, MN, USA Full author information is available at the end of the article
when the disease seems as alien and multifaceted as COVID-19. The acute respiratory distress syndrome (ARDS) that figures so prominently in severe cases of COVID infection may seem familiar but has historically predisposed to such logical missteps [6]. ARDS itself was originally perceived as a high permeability edema and low lung compliance condition that disrupted function of all alveolar units and resulted primarily from surfactant deficiency [7]. Cause and histologic manifestations went hand-inhand. This simple perception provided for adult patients a convenient explanation that paralleled that of the infant respiratory distress syndrome, a condition for which the root cause mechanism had already been confirmed [8]. Indeed, for some years after its initial description, the designation of ‘Adult Respiratory Distress’ reflected this flawed theory of cause and effect. More recently, considerations of lung compliance and underlying pathology have yielded to a broader definition of ARDS b
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