Coagulopathy in COVID-19 from Pathogenesis until Treatment: A systemic Review

Abstract

Background: Nowadays, the new coronavirus-induced severe acute respiratory syndrome (COVID-19) outbreak was primarily stated in December 2019. Three months later, the Director-General of the World Health Organization, avowed the COVID-19 a global pandemic. Gathered evidence discloses that coagulation syndrome is repeatedly seen in COVID-19, and the incidence is higher in severe cases. The worsening lung functions and coagulopathy are some of the most significant poor prognostic criteria in the outcome of COVID-19. The pragmatic coagulopathy in patients hospitalized with COVID-19 (COVID-19 associated coagulopathy) is categorized by the increased level of D-dimer and fibrinogen/fibrin degradation products. They are interrelated with the severity of COVID-19. This elevation will aid the arrangement of the patients consistent with the disease severity and management. These coagulation parameters elevation can point to a poor prognosis. Coagulopathy in COVID-19 mainly affects immobilized patients, those in critical care units, and those who have extra risk factors that predispose to coagulopathy, for instance, acute inflammatory conditions and hypoxia. The exact pathogenesis of hypercoagulability in COVID-19 is unwell understood. The signs suggest that the COVID-19 coagulopathy is an evolving phenomenon in which endothelial damage, platelet aggregation, augmented innate immune response, and other measures as systemic inflammation favoring coagulation would divide up the severity of this disease. Understanding the pathophysiology of COVID-19 related coagulopathy is crucial for suitable treatment and monitoring of these patients. Encouraging interest in the potential uses of anticoagulation in COVID-19 particularly is the use of heparin that has a potential benefit over other anticoagulants due to its anticoagulant role, anti-inflammatory, and potentially anti-viral properties. The incidence of thrombotic phenomena associated with COVID-19. Importantly, laboratory and imaging studies found an increased risk of thrombotic complications in patients with SARS-CoV-2 infection. Klok et al assessed the incidence of thrombotic complications in COVID-19 patients admitted to the ICU. They found that 31% of these patients had thrombotic complications, even in patients who were already getting standard doses of prophylactic

Assessment of COVID -19 associated coagulopathy and multiple hemostatic markers: a single center study in Egypt

“…Its form and severity could determine the path of the patient in the hospital and his outcome [ 1 , 2 ]. While d -dimer is proven to reflect the severity and the prognosis of COVID-19 patients, prothrombin time (PT), international normalized ratio (INR), partial thromboplastin time (APTT) and fibrinogen role is not well-defined [ 2 , 3 ].…”

“…As the endothelial cell injury is a constant feature in the pathogenesis of COVID-19 [ 2 , 3 ], Von Willebrand factor (VWF) and factor VIII (FVIII) excess, release and degree of elevation could be a good diagnostic and prognostic marker of the disease [ 6 – 9 ]. Lupus anticoagulant is reported to associate with the COVID-19 infection but still its frequency, significance, the relation of its existence to other inhibitor like CRP [ 10 – 16 ] are debatable.…”

Hemostatic system and COVID-19 crosstalk: A review of the available evidence

“…Much International and National guidance regarding VTE thromboprophylaxis has been published; however, more extensive studies are required to investigate the potential therapeutic approach. Most of the international guidelines and recommendations (ISTH-IG, ACF, CDC, and ASH) adopt stopping anticoagulation in patients who developed bleeding or severely thrombocytopenic; furthermore, they also do not recommend a particular platelet count threshold[ 123 ]. Furthermore, the expert panel reports by CHEST/AIPPD/AABIP stated that empiric use of therapeutic anticoagulation regimens in ICU patients with COVID-19 is not beneficial and may be harmful, while its use in hospitalized, noncritically ill patients with COVID-19 remains uncertain[ 123 ].…”