Systemic Inflammatory Response Syndrome Is a Major Contributor to COVID-19–Associated Coagulopathy

Management of the thrombotic risk associated with COVID-19: guidance for the hemostasis laboratory

“…However, the relevance of the utilization of D-dimers levels to tailor thromboprophylaxis in COVID-19 patients has been questioned, as plasma D-dimers levels could depend more on the lysis of extra-vascular rather than intra-vascular fibrin deposits [43,44]. This would be consistent with the observation that SFC levels, which are thought to only depend on intra-vascular fibrin deposition, remain low in most COVID-19 patients despite high D-dimer levels [30]. Additional biomarkers of in vivo enhanced thrombin generation, such as SFC, may thus provide some additional useful information for managed care of COVID-19 [56].…”

“…Individual components of the fibrinolytic system can also be measured. Although interesting evidence is emerging especially for PAI-1 in COVID-19 [30], its measurement is limited by large inter-laboratory variability, which is attributable to the different assay methodology, antigenic specificity of the antibodies, the lack of internationally certified calibrators and quality controls, as well as to the many measuring units that can be used for reporting data.…”

“…Regarding fibrinolysis, an initial and transient increase of tissue plasminogen activator (tPA) has been described in severe acute inflammatory states, rapidly followed by a sustained release of PAI-1 by the endothelium [28], the extend of the latter being associated with a worse outcome [29]. Accordingly, t-PA and PAI-1 levels were increased at ICU admission in ARDS patients in a recent study, whether COVID-19 or not [30]. Levels of thrombin activatable fibrinolysis inhibitor (TAFI) and protein C inhibitor were also found to be significantly elevated in the bronchoalveolar fluid of patients with interstitial lung disease when compared to healthy controls, which could also add to the hypofibrinolysis observed [31,32].…”

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“…[49][50][51] In addition to significant effects on the cardiopulmonary system, SARS-CoV-2 infection has also been shown to be associated with pathological effects on the brain and the kidneys. [52][53][54][55] COVID-19 has been observed to have primary effects in the brain with patients presenting with confusion, abnormal behavior, seizures, and brain swelling. 53 Not Fig.…”

“…45 As with other organ systems involved in MODS in critically ill patients, the development of microthrombi during the systemic inflammatory response is a likely culprit for the development of acute kidney injury during COVID-19. 52,[54][55][56] However, FX also may have its own role in the development and progression of kidney injury (►Fig. 2D).…”