COVID-19 update: Covid-19-associated coagulopathy

Abstract

We are too much accustomed to attribute to a single cause that which is the product of several, and the majority of our controversies come from that. Marcus AureliusThe Covid-19 pandemic has introduced an array of organspecific and systemic phenotypes-some previously observed in viral infections, including severe acute respiratory syndrome (SARS) and others that appear to be unique to SARScoronavirus (CoV)-2. Rapidly emerging information from clinical observations, autopsy-based findings, extrapolations from in vitro and ex vivo studies and dynamic modeling are informing management guidelines; however, many questions remain unanswered and clinical trials that are required to provide evidence have not been completed in most areas. Among the many questions that require careful thought, reflection and investigation are the mechanism(s) underlying the development of a systemic coagulopathy and acquired thrombophilia characterized in a majority of cases by a proclivity for venous, arterial and microvascular thrombosis.The following review summarizes emerging insights into the pathobiology, mechanism(s), diagnosis, management, foundations for research and either planned or ongoing clinical trials for Covid-19-associated coagulopathy.

Anti-SARS-CoV-2 IgG from severely ill COVID-19 patients promotes macrophage hyper-inflammatory responses

“…Coronavirus disease 2019 (COVID- 19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is characterized by mild flu-like symptoms in the majority of patients(1, 2). However, approximately 20% of the cases have more severe disease outcomes, with bilateral pneumonia that may rapidly deteriorate into acute respiratory distress syndrome (ARDS) and even death by respiratory failure.…”

“…In addition to excessive lung inflammation through a cytokine storm, severe COVID-19 is characterized by pulmonary edema, following disruption of the microvascular endothelium (18), and by coagulopathy, which in many patients is characterized by pulmonary thrombosis (19). To test whether the excessive macrophage activation by anti-Spike IgG may contribute to pulmonary edema and thrombosis, we applied in vitro models for endothelial barrier integrity (20) and in situ thrombosis (21) using primary human pulmonary artery endothelial cells (HPAEC), where thrombocytes can be added under flow conditions.…”

Acute portal vein thrombosis secondary to COVID-19: a case report

“…The attachment of the viruses to the endothelial surfaces via angiotensin-converting enzyme receptor (ACE-R), leads to the lymphocytic endothilitis, interferon-1 (INF-1), and prothrombotic genes overexpression (11). Becker speculated that the attachment of COVID-19related extracellular RNA to the factor and which belongs to the contact pathway of the coagulation cascade leads to the interferon-γ (INF-γ) suppression and a hyper-in ammatory state (12) Our report of portal vein thrombosis in the setting of COVID-19 pneumonia add portal vein thrombosis to other COVID-19 associated thrombotic phenomenon and denote that clinician who is caring these patients should have a high index of suspicion to diagnose this unusual presentation in a proper clinical scenario. Figures Figure 1 Chest CT.…”

SARS-CoV-2 causes severe alveolar inflammation and barrier dysfunction

“…In autopsies of deceased COVID-19 patients, it has been observed that particularly in severe cases viral particles can disseminate throughout the body (Deinhardt-Emmer et al, 2020b;Wichmann et al, 2020). Additionally, systemic complications have been reported, such as the massive release of proinflammatory cytokines and thromboembolic events in various organs (Becker, 2020). Consequently, SARS-CoV-2 is regarded as a pneumotropic virus that infects the patient via the lung but can also cause a systemic infection that affects different organs with a high mortality rate.…”