202406292335
Status:
Tags: MCS
ECMO
Bleeding
Role of unfractionated heparin in consumptive coagulopathy
low dose UFH ↓ consumptive coagulopathy w/o ↑ bleeding risk
circuits without UFH will be more susceptible to (micro)thrombotic events (due to the ongoing activation of the plastic surface induced contact activation) and increased bleeding tendency (due to clotting factor consumptive)
Heparin coating of the circuit may delay, but will not suffice to avoid these events, particularly, given the membrane oxygenator is the predominant activation surface and is uncoated
it is strongly recommended to—at least—monitor consumptive coagulation parameters (fibrinogen, platelet counts, APTT, D-dimer levels) closely during UFH-free ECMO runs in addition to the membrane lung parameters like trans-membrane pressures and gas transfer. Even better, it may be advisable to run every circuit, even in the presence of bleeding complications, at least with a low, fixed dose of UFH (e.g., 200–300 IU/hour; 4–5 IU/kg/h ideal body weight) and not completely discontinue UFH, to prevent consumptive coagulopathy induced ongoing thrombosis and (deterioration of) bleeding
FXI/FXII (contact pathway; plastic surface) or tissue factor/FVII (intrinsic pathway; endothelial cell damage) activation in the absence of UFH -anticoagulation leads to significant and growing thrombus formation by a vicious circle of clotting factor activation/amplification, fibrinogen and platelet depletion (consumptive coagulopathy), and hyperfibrinolysis ultimately leading to enhanced bleeding
Therapeutic UFH-anticoagulation leads to a strong inhibition of clotting factor activation/amplification, resulting in the reduction of thrombosis but enhanced bleeding risk
low-dose UFH (200–300 IU/hour) results in a significant inhibition of the coagulation factor amplification, hence the consumptive coagulopathy and fibrinolysis cascade, without increasing the bleeding risk