Coagulation Profiles of Unexpected DCDD Donors Do Not Indicate a Role for Exogenous Fibrinolysis

Abstract

It has been suggested that vascular stasis during cardiocirculatory arrest leads to the formation of microvascular thrombi and the viability of organs arising from donation after circulatory determination of death (DCDD) donors may be improved through the application of fibrinolytic therapy. Our aim was to comprehensively study the coagulation profiles of Maastricht category II DCDD donors in order to determine the presence of coagulation abnormalities that could benefit from fibrinolytic therapy. Whole blood from potential DCDD donors suffering out-of-hospital cardiac arrest was sampled after declaration of death in the emergency department, and rotational thromboelastomeric analysis was performed. Between July 2012 and December 2013, samples from 33 potential DCDD donors were analyzed. All patients demonstrated hyperfibrinolysis (HF), as reflected by maximum clot lysis of 98-100% in all cases, indicating that there is no role for additional fibrinolytic therapy in this setting. As well, we observed correlations between thromboelastomeric lysis parameters and maximum hepatic transaminase levels measured in potential donors and renal artery flows measured during ex situ hypothermic oxygenated machine perfusion, indicating that further studies on the utility of thromboelastometry to evaluate organ injury and perhaps even viability in unexpected DCDD may be warranted.

Thrombolytic protocol minimizes ischemic‐type biliary complications in liver transplantation from donation after circulatory death donors

“…Moreover, several studies have indicated that hypoxia due to circulatory arrest (as occurs in a dying person) is associated with a pronounced stimulation of the fibrinolytic system because of the release of endogenous plasminogen activators. 2,3 In accordance with this, Vendrell et al 4 recently reported evidence of clinically relevant endogenous hyperfibrinolysis in DCD donors (Maastricht type II). These investigators, therefore, argued against the need for additional fibrinolytic therapy in DCD donors.…”

Heparin but not tissue plasminogen activator improves outcomes in donation after circulatory death liver transplantation in a porcine model

“…Several years ago, Porte and Clavien highlighted the fact that platelet activation is reduced and coagulation altered early after death, with less stable clot formation and marked activation of the fibrinolytic system . More recently, our group used ROTEM to show that potential uDCD donors universally suffer hyperfibrinolysis at the moment death is declared . Other groups have used thromboelastometry to study patients suffering CA, and it appears that the incidence of hyperfibrinolysis increases in relation to the length of arrest and warm ischemia .…”

“…(22) More recently, our group used ROTEM to show that potential uDCD donors universally suffer hyperfibrinolysis at the moment death is declared. (23) Other groups have used thromboelastometry to study patients suffering CA, and it appears that the incidence of hyperfibrinolysis increases in relation to the length of arrest and warm ischemia. (24) When organs and tissues suffer progressive ischemia, thrombomodulin, an integral membrane protein expressed on the surface of endothelial cells, is induced.…”

Can we prevent ischemic‐type biliary lesions in donation after circulatory determination of death liver transplantation?

“…Coagulation studies performed in DCD donors help explain why a microvascular clot does not form even in the presence of a cardiac standstill. Using rotational thromboelastometry, our group has shown that potential uDCD donors universally suffer hyperfibrinolysis at the moment death is declared, obviating the need for fibrinolytic therapy . Other groups have used thromboelastometry to study patients suffering cardiac arrest, and it appears that the incidence of hyperfibrinolysis increases in relation to the length of arrest and warm ischemia time (WIT) .…”