Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new coronavirus (CoV) responsible for the current COVID-19 pandemic. Although it is well documented that COVID-19 is primarily manifested as a respiratory tract infection, emerging data indicate that it should be regarded as a systemic disease involving multiple systems, including cardiovascular, respiratory, gastrointestinal, neurological, hematopoietic and immune system (1). Organ dysfunction due to infection has been attributed to a non-adaptive immune response and the complement system (2). The pathophysiology of severe acute respiratory syndrome related to coronavirus induced ARDS has similarities to that of severe community-acquired pneumonia caused by other viruses or bacteria. The overproduction of early response proinflammatory cytokines (tumor necrosis factor, IL-6, and IL-1β) results in what has been described as a cytokine storm, leading to an increased risk of vascular hyperpermeability, multiorgan failure, and eventually death when the high cytokine concentrations are unabated over time.(3) Many patients with severe COVID-19 present coagulation abnormalities that mimic other systemic coagulopathies associated with severe infections, such as disseminated intravascular coagulation (DIC) or thrombotic microangiopathy, but COVID-19 has distinct features.(4) The SARS-CoV-2 virus does not appear to have intrinsic procoagulant effects itself. However, the development of coagulation test abnormalities seen in SARS-CoV-2 infected patients are most likely a result of the profound inflammatory response. (5) A hypercoagulable state appears to be a cornerstone of Covid-19 infection. Excessive coagulation activation is a key phenomenon in the pathophysiology of the disease, thrombus formation and deposition in the pulmonary microvasculature can be related to the degree of hypoxemia. Deep vein thrombosis (DVT), pulmonary embolism (PE), thrombosis in extracorporeal circuits and arterial thrombosis have been demonstrated (6). Faced with a complex coagulation disorder, a correct early diagnosis seems to be crucial for the treatment of coagulopathy with a better clinical outcome. Conventional coagulation tests such as Tp (prothrombin time) and TTpa (activated partial thromboplastin time) are useful tests to monitor the anticoagulant response such as vitamin K antagonists and heparin respectively. However, these traditional tests fail to identify specific coagulation disorders as hypercoagulability(7). Thromboelastometry or ROTEM is a point-of care viscoelastic method that can assess viscoelastic properties of whole blood in contemporary time (8). The whole process of clot formation includes the initial phase of thrombin generation, maximum clot firmness and finally, clot stabilization. This viscoelastic test (VET) was thought as a diagnostic tool in bleeding scenario capable to identify specific disorder of coagulation, such as clotting factor deficiency, thrombocytopenia, hypofibrinogenemia and heparin effect; guiding hemostatic therapy by goals. Cochrane review published in 2018 showed that the use ROTEM intraoperatively and postoperatively in cardiac surgery to guide transfusion of blood products seems to reduce mortality, as well as administration of allogeneic blood components(9). Fibrinogen and platelets are both the main determinants of coagulability (8). Fibrinogen concentration can be measured by Clauss Assay and by FIBTEM test (ROTEM). Traditional conventional tests are poor predictor of bleeding, failing in guide transfusion therapy. Fibrinogen is main substrate of clot. Fibrinogen (Factor I) is a glycoprotein that is synthesized in the liver. It is activated to fibrin by thrombin, exposing several polymerization sites that are crosslinked to an insoluble fibrin clot under the involvement of activated factor XIII(10). Activation of the coagulation system and fibrin formation is essential for stopping hemorrhage. The deposition of fibrin is carefully regulated to avoid thrombotic complication by the fibrinolytic system. Plasmin interpose the procoagulant signals, leading to clot dissolution, resulting in the generation of soluble fibrin fragments, such as d-dimers (11).
VETs provide the function of fibrinogen (FIBTEM), as well as the hypercoagulable state in a few minutes at the bedside. Unfortunately, the severity of the thrombotic phenomenon in this patient led to ischemia of the lower limb in need of amputation of this member. Surgical treatment with amputation of this limb was decisive in resolving this case. In retrospectively evaluating this case, we thought about the possibility of using fibrinolytic therapy as an important therapeutic option in the presence of severe systemic acute thrombotic disease.