JULY 2022 | The Surgical Technologist | 307 for assessing the risk of postoperative complications. Hypercoagulability markers are often associated with postoperative complications in non-COVID-19 perioperative settings (e.g., PAI-1, TAFI, increased fibrinogen and platelet counts) (7, 95–97). Research on these and other biomarkers in assessing postoperative morbidity and mortality in convalescent COVID-19 patients undergoing elective surgery, however, is lacking. Future studies are required in order to determine the most prognostic biomarkers for evaluating this patient population (88). Treatment and Thromboprophylaxis for the Postoperative COVID-19 Patient COVID-19 and the subsequent damage to endothelial cells result in a progression from hemostasis to a relatively prothrombotic/ antifibrinolytic state (31, 38, 43–45). Clinical data demonstrate significant thrombophilia with fibrinolysis shutdown being a primary component, regulated by higher circulating levels of antifibrinolytic factors, namely PAI-1 and TAFI. Yet, coagulation is a rigorously regulated process: fibrinolytic and thrombotic pathways are continuously competing against each other such that neither hemorrhage nor thrombosis is favored under normal physiological conditions (98). Therapeutic strategies for COVID-19 patients that utilize these findings, including the use of fibrinolytics, have been under examination and show potential for improving patient outcomes. For patients being treated with COVID-19, therapeutic anticoagulation is the standard regimen for patients with macrothrombosis. Furthermore, the use of anticoagulant heparinoids is advised for all COVID-19 patients (99). The use of tPa has been suggested for patients with severe ARDS caused by COVID-19 (100). In these studies, the use has been late in the disease course. Theoretically, if tPa is used earlier FIGURE 3 | The “rollercoaster” phenomenon of COVID-19-associated coagulopathy. The three stages of COVID-19-associated coagulopathy and their relationship to the immuno-thrombotic derangement caused by the cytokine storm are represented above by viscoelastic hemostatic assays (e.g., thromboelastography [TEG]). (A) represents the acute fibrinolytic shutdown phenotype (short R, steep α, thick MA, no lysis). (B) represents the eventual evolution to a normal physiologic fibrinolytic phenotype (normal R, α, MA, and LY30). (C) represents the TEG in evolution without anticoagulation and the subacute recovery stage where the patient is less hypercoagulable (parameters intermediate between acute and remote). (D) represents the patient with or without anticoagulant with a hypocoagulopathic phenotype due to hypofibrinogenemia and/or a thrombocytopenia in spite of persistent fibrinolytic shutdown (long R, flat α, narrow MA, no lysis) (17, 20, 77, 79–81). Created using Adobe Illustrator. Bunch et al. COVID-19 Immuno-Thrombosis and Surgery Frontiers in Surgery | www.frontiersin.org 7 2022 | Volume 9 | Article 889999
RkJQdWJsaXNoZXIy MTExMDc1