key: cord-0050262-pgmu5wx1
authors: Thachil, Jecko
title: Usefulness of Combining D-Dimers with Thromboelastography
date: 2020-09-18
journal: J Am Coll Surg
DOI: 10.1016/j.jamcollsurg.2020.07.004
sha: 002b48e6f0350e5ce48a1cf54e62b876f286a800
doc_id: 50262
cord_uid: pgmu5wx1

nan

Jecko Thachil, MD, FRCPath Manchester, UK Wright and colleagues 1 have elegantly shown that fibrinolytic shutdown is hugely contributory to the hypercoagulability in COVID-19. In addition, they demonstrate a very important clinical point that combining D-dimers with thromboelastography can predict the need for dialysis in patients with COVID-19. Several other important considerations can be derived from this study. First, it is well-known that D-dimers are an inflammatory marker and can elevate several inflammatory diseases, including COVID-19, even in the absence of thrombosis. 2 The report by Wright and colleagues would suggest the addition of thromboelastography to D-dimer would help in understanding how much of the D-dimers are from clot breakdown and how much are nonthrombotic D-dimers. Second, because D-dimers are markers of clot breakdown, their elevation in conjunction with fibrinolysis shutdown would mean some of these D-dimers are not created from plasmin action on crosslinked fibrin. It is possible that these D-dimers are created in the lungs from bronchoalveolarspecific clot breakdown, which might not be detected by thromboelastography on peripheral blood. 3 It is also possible that a proportion of D-dimers are not generated by clot breakdown at all, but by the action of plasmin on the extravascular fibrin. Lung exudates seen in acute lung injury could constitute large amounts of fibrinogen and thrombin leaked from the intravascular space along with other plasma proteins. 4 Plasmin breakdown of fibrin formed from these large amounts of fibrinogen could be another cause of these nonthrombotic D-dimers. In the case of extravascular D-dimers, these fibrinolytic markers would signify the intense intrapulmonary inflammatory reaction and could be considered a marker of ongoing or increasing inflammation. Recognizing the roles of this intense inflammation in combination with microvascular thrombi for renal impairment is crucial. Anticoagulation could only prevent the thrombotic component of this contribution and anti-inflammatory strategies might also be required to minimize the renal damage. 5 Of course, the dual anticoagulant and anti-inflammatory properties of heparin might be helpful in this scenario, but possibly only in the early stages before marked inflammation sets in. Future studies would complement this current article by examining the timing of marked D-dimer elevation and fibrinolysis shutdown by viscoelastic testing to better understand the thromboinflammatory concept.

Fibrinolysis shutdown correlates to thromboembolic events in severe COVID-19 infection

D-dimer: preanalytical, analytical, postanalytical variables, and clinical applications

Bronchoalveolar coagulation and fibrinolysis in endotoxemia and pneumonia

Extravascular fibrin, plasminogen activator, plasminogen activator inhibitors, and airway hyperresponsiveness

Recent advances in the pathogenetic mechanisms of sepsis-associated acute kidney injury