Understanding pathophysiology of hemostasis disorders in critically ill patients with COVID-19
Abstract
Severe acute respiratory syndrome caused by coronavirus 2 (SARS-CoV-2), now classified coronavirus disease 2019 (COVID-19), was first identified in December 2019 in Wuhan, Hubei Province, China, and has now spread to all continents [1]. About 5–10% of COVID-19 patients require intensive care unit (ICU) admission and mechanical ventilation because of progression to a severe pneumonia including parenchymal disease, massive alveolar damage and acute respiratory distress syndrome (ARDS) with radiologic patchy shadowing or ground-glass opacity [1]. Critically ill COVID-19 patients are prone to develop not only hypoxia and excessive inflammation but frequent thrombotic manifestations like pulmonary embolisms (20–30% of cases), deep vein thrombosis (DVT), catheter-related thrombosis as well as arterial thrombosis like ischemic strokes [2–5]. In addition, microvascular thrombosis, acrosyndrome and capillary leak syndrome affecting lungs, kidneys and heart, potentially complicated by multi-organ failure (MOF), are also reported [3, 5]. The aim of this short review, which guiding thread is illustrated in the figure, is to summarize the complex mechanisms supporting the hemostasis disorders observed in critically ill COVID-19 patients. How does SARS‐CoV‐2 lead to an inappropriate immune response‐induced cytokine storm and a local and systemic inflammatory response syndrome (SIRS)? SARS-CoV-2 enters host cells by binding the angiotensin-converting enzyme 2 (ACE2), highly expressed in…
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