Abstract

Background: Presently, a number of specific observations have been performed on microcirculatory function in a coronavirus disease-19 (COVID-19) setting. We hypothesized that, in the critically ill, endothelial dysfunction secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the subsequent inflammation and coagulopathy may lead to microcirculatory alterations, further exacerbated by the hypoxemic state. A dysfunctional microcirculation may represent the hidden motor underlying the development of COVID-19’s clinical manifestations. Methods: A single center, prospective, observational study. We analyzed bedside sublingual microcirculation in twenty-four consecutive COVID-19-associated acute respiratory distress syndrome (ARDS) patients mechanically ventilated in an Intensive Care Unit (ICU), together with macro-hemodynamics, clinical parameters, echocardiography, and laboratory data at a single time-point after ICU admission. All participants were recruited between March and May 2020. Results: The microcirculatory pattern was characterized by increased values of total vessel density and perfused vessel density, a reduced value of proportion of perfused vessels and microvascular flow index, and high values of heterogeneity index. The duration of mechanical ventilation before microcirculation assessment was inversely associated with the proportion of perfused vessels (p = 0.023). Within the macro-hemodynamic parameters, the right ventricle end-diastolic diameter was inversely associated with proportion of perfused vessels and microvascular flow index (p = 0.039 and 0.014, respectively) and directly associated with the heterogeneity index (p = 0.033). Conclusions: In COVID-19-associated ARDS patients, the microcirculation showed impaired quality of flow parameters coupled with a high vessel density.

Highlights

  • IntroductionMacroscopic clinical features of the SARS-CoV-2 infection, such as the different phenotypes of acute respiratory distress syndrome (ARDS) or the COVID-19-associated coagulopathy, are relatively well recognized entities, but there is still poor evidence about the micro-level aspects of the disease

  • The pathophysiology of COVID-19 is still under investigation

  • Twenty-four patients were included in the study

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Summary

Introduction

Macroscopic clinical features of the SARS-CoV-2 infection, such as the different phenotypes of ARDS or the COVID-19-associated coagulopathy, are relatively well recognized entities, but there is still poor evidence about the micro-level aspects of the disease. States of severe inflammation or cardiovascular disease can induce microcirculatory alterations in terms of perfusion patterns, through the damage of cellular sensing mechanisms needed to modulate blood flow [2–6]. The main events underlying microvascular perfusion impairment are inflammation and endothelial activation/dysfunction. Glycocalyx breakdown disrupts the natural anti-inflammatory and anti-coagulant properties of the endothelium, and may create a prothrombotic condition triggered by platelet adhesion and aggregation, causing altered local perfusion, functional shunting, and consequent tissue dysoxia [7–10]. (SARS-CoV-2) infection and the subsequent inflammation and coagulopathy may lead to microcirculatory alterations, further exacerbated by the hypoxemic state. A dysfunctional microcirculation may represent the hidden motor underlying the development of COVID-19’s clinical manifestations

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