Coagulofibrinolytic changes in patients with disseminated intravascular coagulation associated with post-cardiac arrest syndrome― Fibrinolytic shutdown and insufficient activation of fibrinolysis lead to organ dysfunction

Fibrin/fibrinogen degradation products (FDP) at hospital admission predict neurological outcomes in out-of-hospital cardiac arrest patients

“…16,17 DIC causes thrombotic occlusion of vessels, followed by deteriorated oxygen supply to cells and tissues. 19,20 As a result, patients resuscitated after cardiac arrest can experience multiple organ dysfunction syndrome, which causes unfavorable outcomes in OHCA patients. [19][20][21][22] Basal conditions during DIC occasionally cause a simultaneous increase in fibrin(ogen)olysis resulting from tissue-type plasminogen activator (t-PA), which is referred to as DIC with the fibrinolytic phenotype, as opposed to the thrombolytic phenotype.…”

“…19,20 As a result, patients resuscitated after cardiac arrest can experience multiple organ dysfunction syndrome, which causes unfavorable outcomes in OHCA patients. [19][20][21][22] Basal conditions during DIC occasionally cause a simultaneous increase in fibrin(ogen)olysis resulting from tissue-type plasminogen activator (t-PA), which is referred to as DIC with the fibrinolytic phenotype, as opposed to the thrombolytic phenotype. 23 Hyperfibrinolysis is reportedly common in OHCA patients and has been associated with markers of hypoperfusion in these patients.…”

Differences in coagulofibrinolytic changes between post‐cardiac arrest syndrome of cardiac causes and hypoxic insults: a pilot study

“…Post‐cardiac arrest syndrome (PCAS) is often involved in coagulofibrinolytic disorder, which occurs as a result of systemic ischemia and reperfusion 1. We are under the clinical impression that PCAS patients who experience cardiac arrest due to hypoxia are inclined to suffer from severe coagulopathy and that their condition is associated with a worse prognosis in comparison to patients in whom cardiac arrest occurs in association with a cardiogenic event.…”

“…The present study is a subgroup analysis of our previous study 1. Thirteen patients with PCAS caused by cardiogenic cardiac arrest (the cardiogenic group) and 13 patients with PCAS caused by hypoxia‐related cardiac arrest (the hypoxia group) were enrolled in the present study.…”

“…Our previous study suggested that the SF levels of PCAS patients with disseminated intravascular coagulation (DIC) were significantly higher than those in patients without DIC 1. Systemic hypoxia, ischemia, and reperfusion cause endothelial damage with a consequent increase in tissue factor activity, which forms a complex with factor VII/VIIa, and the complex results in the generation of thrombin 2.…”