According to the China there are four severity levels of COVID-19 based on the clinical manifestations. The criteria used for classification are respiratory factors such as respiratory rate, oxygen saturation, and lesion progression in pulmonary imaging. 
In clinical practice thrombotic complications have been reported, including microvasular thrombosis, ischemic limbs, strokes, venous and arterial thromboembolism, and acute arterial thrombosis.  The observed pulmonary vessels occlusions that have been described in reports on COVID-19 patients are exclusively caused by pulmonary embolism.  However, in the experience of Cattaneo M et al  and in some reports [3, 4] filling defects of pulmonary vessels that are detected by computed tomography angiography (CTA) scans are in many instances more reminiscent of pulmonary thrombi rather than emboli, because they are not fully occlusive. This observation is compatible with postmortem description of presence of manifestations of thrombotic microangiopathy, enlarged pulmonary blood vessels containing microthrombi, presence of fibrin thrombin within distended small vessels and capillaries and extensive extracellular fibrin deposition. [3, 6] Diffuse thrombotic material is observed also in other organs, compatibly with the development of clinical signs of multiorgan failure.  Therefore, local thrombi, rather than emboli from peripheral veins, appear to be the hallmark, which are responsible for the severe ischemic clinical manifestations.  Pulmonary thrombi in COVID-19 probably develop as a consequence of vascular damage associated with viral infection and severe inflammation, with the pathogenic contribution of platelets interacting with the vascular wall and leukocytes, factor XIIa with other components of the contact phase of coagulation, von Willebrand factor, complement, and other players in thromboinflammation, some of which have been shown to be implicated in the pathogenesis of acute respiratory distress syndrome already many years ago. 
Soluble markers of thrombosis including D-dimer, von Willebrand antigen levels and soluble platelet-derived factors including platelet factor 4 (PF4) levels were significantly elevated in COVID-19 patients leading to the COVID-19 hyercoagulability and thrombosis that are observed clinically.  Importantly, D-dimer positively correlates with PF4 and monocyte tissue factor (TF) expression.  Increased D-dimer, a early predictor of outcome in severe, is associated with high mortality. [8–10]
TF is normally present in the circulation at very low levels.  An increase in TF expression caused by inflammation tends to shift the haemostatic balance in favor coagulation/thrombosis, generating thrombin.  Thrombin has a variety of activities on cells that result in augmentation of the inflammatory response. Its ability to augment leukocyte adhesion and activation likely contributes to amplification of the inflammatory response. Thrombin activation of the endothelium results in high levels of platelet-activating factor formation, which works as a potent neutrophil agonist, especially when neutrophils are tethered to selectins. [13, 14] In addition, thrombin activation of platelets releases CD40 ligand which in turn can induce TF formation [15, 16] and increase inflammatory cytokines, including inteleukin-6 (IL-6) and IL-8. [17, 18] Increased levels of IL-6 have been shown in vivo to increase platelet reactivity increasing their thrombogenic potential, thus further linking inflammation and thrombosis.  Inflammation also elevates fibrinogen synthesis.  Fibrinogen levels rise under these conditions unless a consumptive coagulopathy occurs. The natural anticoagulant and anti-inflammatory properties of endothelial cells are critically important to limit microvascular thrombosis, inflammation and organ injury.  TFPI is a endogenous serine protease inhibitor producted by the endothelium that directly inhibits FXa and the FVIIa/TF complex and a significant percentage of this seems to be stored in endothelial cell granules that can be released by thrombin treatment. [21, 22] Preclinical trials have demonstrated that recombinant TFPI (rTFPI) attenuates cytokine responses (tumor-necrosis factor-α and IL-8) in a pig peritonitis-induced bacteriemia model without improving survival.  However, rTFPI reduced bacterial sepsis.  and it was associated with lower levels of inflammatory and coagulation biomarkers (IL-6 and TAT, respectively).  rTFPI has been tested and demonstrated to be safe in healthy humans following bolus IV injection of endotoxin. rTFPI attenuated endotoxin-induced α-thrombin generation with complete blockade of coagulation by high-dose rTFPI. Interestingly, rTFPI did not affect endotoxin-induced changes.  rTFPI has also been trialed in phase 2 studies on patients with severe sepsis and it appeared to be safe and effective, with reduction in TAT and IL-6 levels  and reduced mortality. However, results from trail failed to demonstrated an effect of rTFPI (tifacogin). 
Here, we investigated the coagulopathy in severe and mild COVID-19. We confirm that severe COVID-19 patients exhibit increased inflammation including IL-6 and TNF-α, endotheliopathy including TF and von Willebrand factor, and coagulopathy including D-dimer, TAT, and Fibrinogen. As PF4 has a rapid removal from plasma,  we also measured β-TG levels which exceeded the PF4 and increased platelet adhesion was observed as well as shortened CT and CFT, high MCF and low LY at 30 minutes. It is reported that TFPI is a natural anticoagulant that lowes inflammation and coagulation. Therefore, we measured TFPI levels which exceeded without shutdown documenting the clinical severity.