The pathophysiology of the haematological manifestations of COVID-19: a review

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and the coronavirus disease 2019 (COVID-19) it causes, are associated with several haematological abnormalities which manifest as some of the clinical syndromes seen in COVID-19. The main organ affected by COVID-19 is the lung, where an intense inflammatory response occurs in the alveoli and the lung vasculature. This may result in severely compromised gaseous exchange consistent with acute respiratory disease syndrome (ARDS). Multiple organ failure and death may ensue. The extent to which SARS-CoV-2 directly affects erythroid, granulocytic and monocytic progenitors is unknown, however related Coronaviridae have previously been shown to infect megakaryocytes and their progenitors. Furthermore, SARS-CoV-2 may directly infect lymphocytes or monocytes causing the production of cytokines and chemokines, which then cause lymphocyte death and lymphopenia. The quantitative changes seen in monocytes and granulocytes are at least partly due to the marked increase in various cytokines also called the “cytokine storm” and the downstream effects of these cytokines. A COVID-19-associated coagulopathy (CAC) may occur, which ranges from a mild derangement of laboratory haemostatic tests, through to sepsis-induced coagulopathy (SIC), and later, frank disseminated intravascular coagulation (DIC). The most common and devastating haemostatic abnormality is widespread thrombosis, which is associated with severe lung inflammation, hypoxia and death. COVID-19 is associated with immune perturbation states namely, immune thrombocytopenia (ITP), Guillain-Barré syndrome, the anti-phospholipid syndrome and a Kawasaki-like syndrome in children. The pathophysiology of the haematological abnormalities seen in COVID-19 is briefly reviewed in this article.