COVID-19 and Pulmonary Embolism: A Comprehensive Review of Epidemiology, Pathophysiology, and Management

Global public health has suffered greatly as a result of the coronavirus illness 2019 (Covid-19) pandemic; yet when vaccinations against Covid-19 are available, they have contributed to the containment of the spread of SARS Coronavirus 2 (SARS-CoV-2) infection. However, there have been isolated reports of vaccine-induced cerebral venous sinus thrombosis (CVST) and vaccine-induced immune thrombotic thrombocytopenia (VITT) following viral vector vaccinations (Ad26.COV2 vaccine, AdOx1 nCoV-19 vaccine).One of the most effective ways to address the global health issue as the new SARS-CoV-2 virus spreads around the world is immunization against COVID-19.This condition manifests as thrombocytopenia, the formation of an autoantibody against platelet-factor 4,and widespread thrombosis in unusual places, mainly in the cerebral venous. (PF4). The human Freia receptor on platelets can be bound by the PF4 autoantibody, which can then cause the platelets to aggregate. This is an uncommon side effect that closely mimics the clinical presentation of the traditional immune-mediated HIT illness that develops after heparin exposure. We will talk about the recently reported side effect known as vaccine-induced immune thrombotic thrombocytopenia (VITT),which can happen after receiving specific COVID-19 vaccinations, in this Spotlight. Since the vaccinations have been employed, questions have been raised about their safety. Following the COVID-19 vaccine, the most frequent side effects include local reactions at the injection site and general systemic symptoms like fever, headache, weariness, and myalgia. These side effects could appear shortly after immunization and go away quickly. Nonetheless, a few uncommon cases of vaccine-induced immune thrombotic thrombocytopenia (VITT) have been documented, mostly in relation to vaccinations utilizing viral vectors. Platelet expression of spike protein and subsequent immune response, platelet expression of other adenoviral proteins and subsequent reactions, the role of antibodies against platelet factor 4 (PF4), the direct interaction between adenoviral vector and platelets, the cross-reactivity of antibodies against SARS-CoV-2 spike protein with PF4, the cross-reactivity of anti-adenovirus antibodies and PF4 interaction between spike protein and platelets. Because severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can activate platelets, thrombocytopenia while rare in the first presentation may also be an indicator of the severity of the disease. The spike protein-angiotensin converting enzyme 2 (ACE2) connection causes this directly, and the activation of coagulation and inflammation causes it indirectly. In COVID-19, dysregulation of the innate and adaptive immune systems is a significant contributing factor to thrombosis and thrombocytopenia.