Acute respiratory distress syndrome: a life threatening associated complication of SARS-CoV-2 infection inducing COVID-19

Abstract

Acute Respiratory Distress Syndrome (ARDS) is a form of respiratory failure in human. The number of deaths caused by SARS-CoV-2 infection inducing this severe pneumonia (ARDS) is relatively high. In fact, COVID-19 might get worsen in ARDS and provoke respiratory failure. A better understood of ARDS key features and the pathophysiological injuries of the pulmonary parenchyma are linked to lessons learned from previous severe diseases associated previous coronaviruses outbreaks (especially SARS-CoV and MERS-CoV) and more the ongoing SARS-CoV-2. The ARDS mechanism includes a diffuse alveolar damage associated disruption of alveolar capillary membrane, pulmonary edema, damaged endothelium and increased permeability. A diffuse inflammation, with acute onset, on the lung tissue accompanied by release of biochemical signal and inflammatory mediators (TNFα, IL-1 and IL-6) leading to hypoxemia, low PaO₂/FiO₂ ratio and the chest radiological expression of bilateral infiltrates in ARDS. The ongoing outbreak could lead to a better understood of ARDS pathophysiology and prognostic. An overview is also highlighted about the seven coronaviruses proved to infect human especially those having ability to cause severe disease SARS-CoV, MERS-CoV and SARS-CoV-2. In this review, we focused on the major pathological mechanisms leading to the ARDS development as a result of viral infection, severe COVID-19 worsening.

Communicated by Ramaswamy H. Sarma

Keywords:

• SARS-CoV-2
• ARDS
• COVID-19
• coronavirus
• pathophysiology
• ACE2

Acknowledgements

The authors have no acknowledgments to declare.

Disclosure statement

The authors declare no competing financial interest.

Author contributions

RB drafted of the manuscript. Additional content has been provided by MMA, FB an MVE then the critical revision of the final manuscript has been done by all the authors. All authors red and approved the version of manuscript to be submitted.

Ethical approval

The Ethical approval: This article does not contain any studies with human participants or animals performed by any of the authors.

Additional information

Funding

Authors (RB, FB and MMA) received grants from the Scientific Research Deanship at University of Ha’il - Saudi Arabia through project number COVID-1942 and focuses mainly on polymorphism of ACE2 and its susceptibility to the severity of COVID-19.