key: cord-1041841-jxigsdzh
authors: Gattinoni, Luciano; Camporota, Luigi; Marini, John J.
title: COVID-19 phenotypes: leading or misleading?
date: 2020-07-02
journal: Eur Respir J
DOI: 10.1183/13993003.02195-2020
sha: 80e93f52da681c2fc7043202db7db821b8d73949
doc_id: 1041841
cord_uid: jxigsdzh

Comment to an Editorial where we invite the authors to express with clarity the risks they are referring to and how their argument is furthering the cause of patients and clinicians.

We read the editorial by Bos et al [1] with a mixture of interest, irritation and serious concern.

Our interest derives from a simple fact: the debate on terms like 'typical ARDS' or 'atypical ARDS' is not just question of semantics, but these terms represent concepts linked to specific clinical, mechanical and radiological criteria, and not merely based on the severity of gas exchange. It should not be a surprise to the authors that different radiological patterns and mechanical characteristics should suggest different ventilatory strategies, each with possible benefits and harm. The management of individual patients needs to take into consideration various factors, and not just the gas exchange that currently defines ARDS. This is precisely the point of bringing attention to the novel 'L & H' phenotypes of COVID-19 that bracket the extremes of the clinical encounter [2] .

Usually, there is overlap, depending in large part on disease duration. The 'L & H' were not intended to be tightly prescriptive nor mutually exclusive 'bins' into which each patient falls, as we clearly stated [3] . Rather, the object was to alert clinicians in order to avert potential harm from assuming usual ARDS associations between hypoxemia and mechanics at all stages. In so doing, we hoped to help prevent use of high PEEP when there is no benefit, and equally important, to avoid maintaining low pressures when higher pressures can be beneficial.

The Irritation derives from the fact the authors seem to have deliberately decided to ignore the pathophysiological 'evidence' readily available and ventured into a philosophical and semantic discourse against 'premature phenotyping', and in so doing committing the greater sin of 'premature adjudication'. After reading sentences such as "…by needlessly clouding the clinical picture, false phenotypes … upon inspection of patient data, simply do not exist" , It is not clear to us -and without a doubt to most readers -what sort of clear, and self-evident truth we (and other authors) have been trying to cloud. The fact that COVID-19 patients with similar oxygenation efficiency may have markedly different compliance (and VILI risk) is apparent to any clinician who has ever looked after a number of these patients. The reasoning put forward by the editorialists seems purely argumentative and inflammatory, as it seems to imply that what we propose is based on non-existent data, i.e., a perception that we invented.

Our concern derives from noting that the observations of Bos and colleagues are expressed with a tone which goes beyond healthy and reasonable scientific debate. We note also with concern the conclusions of the editorial: "by prematurely phenotyping patients with COVID-19, we expose ourselves and our patients to considerable and preventable risk" and we invite the authors to express with clarity the risks they are referring to and how their argument is furthering the cause of patients and clinicians. Time and emerging literature will undoubtedly demonstrate where "Truth" lies.

The perils of premature phenotyping in COVID: a call for caution

COVID-19 pneumonia: different respiratory treatments for different phenotypes?

Management of COVID-19 Respiratory Distress