COVID-19 Sepsis and Microcirculation Dysfunction
Antonio Colantuoni1, Romeo Martini2, Patrizia Caprari3
1Department of Clinical Medicine and Surgery, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy.
Frontiers in Physiology
|July 18, 2020
Summary
COVID-19, a pandemic caused by SARS-CoV-2, leads to severe complications like cytokine storm and endothelial dysfunction. These contribute to fatal outcomes through multi-organ failure, emphasizing microcirculatory dysfunction
Area of Science:
- * Virology and Immunology
- * Pathophysiology of Infectious Diseases
Background:
- * The global spread of Coronavirus (SARS-CoV-2) has resulted in significant mortality and morbidity worldwide.
- * While many COVID-19 patients exhibit mild symptoms, a substantial percentage develop severe complications, including Acute Respiratory Distress Syndrome (ARDS).
- * Critically ill patients often experience a rapid and fatal disease progression.
Purpose of the Study:
- * To summarize current data on COVID-19 pathogenesis.
- * To highlight the roles of cytokine storm and endothelial dysfunction in severe cases.
- * To emphasize the significance of microcirculatory dysfunction in COVID-19 progression.
Main Methods:
- * Review and synthesis of data from multiple countries.
- * Analysis of clinical presentations and outcomes in COVID-19 patients.
- * Focus on pathogenetic mechanisms in severely ill individuals.
Main Results:
- * Severe COVID-19 is characterized by cytokine storm (CS) and endothelial dysfunction.
- * Endothelial dysfunction triggers a pro-coagulant state, leading to disseminated intravascular coagulation.
- * This cascade results in organ embolization and subsequent multi-organ failure (MOF).
Conclusions:
- * Microcirculatory dysfunction is a key pathogenetic mechanism in severe COVID-19.
- * Understanding these mechanisms is crucial for managing the global health challenge posed by COVID-19.
- * The Italian Society of Clinical Hemorheology and Microcirculation aims to advance this understanding.
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