Disseminated intravascular coagulation in cardiac arrest and resuscitation

Abstract

The aims of this review are to demonstrate that the changes in coagulation and fibrinolysis observed in cardiac arrest and resuscitation can be recognized as disseminated intravascular coagulation (DIC), and to discuss the probability of DIC being a therapeutic target. The appearance of triggers of DIC, such as damage-associated molecular patterns, inflammatory cytokines, and adrenaline, is associated with platelet activation, marked thrombin generation and fibrin formation, insufficient anticoagulation pathways, and increased fibrinolysis by tissue-type plasminogen activator, followed by the suppression of fibrinolysis by plasminogen activator inhibitor-1, in patients with cardiac arrest and resuscitation. Simultaneous neutrophil activation and endothelial injury associated with glycocalyx perturbation have been observed in these patients. The degree of these changes is more severe in patients with prolonged precardiac arrest hypoxia and long no-flow and low-flow times, patients without return of spontaneous circulation, and non-survivors. Animal and clinical studies have confirmed decreased cerebral blood flow and microvascular fibrin thrombosis in vital organs, including the brain. The clinical diagnosis of DIC in patients with cardiac arrest and resuscitation is associated with multiple organ dysfunction, as assessed with the sequential organ failure assessment score, and increased mortality. This review confirms that the coagulofibrinolytic changes in cardiac arrest and resuscitation meet the definition of DIC proposed by the ISTH, and that DIC is associated with organ dysfunction and poor patient outcomes. This evidence implies that established DIC should be considered to be one of the main therapeutic targets in post-cardiac arrest syndrome. K E Y W O R D Scardiac arrest, disseminated intravascular coagulation, fibrinolysis, inflammation, resuscitation

Thrombotic Microangiopathy Score as a New Predictor for Neurologic Outcome in Patients Undergoing Targeted Temperature Management After Out-of-hospital Cardiac Arrest

“…Accordingly, the unfavorable neurologic outcome is attributed to the cerebral microvascular occlusion that causes the no-re ow phenomenon [31]. Many animal and clinical studies demonstrated a more severe degree of microvascular changes is associated with poor outcomes including severe hypoxic brain injury, immediate death without ROSC, and high mortality [32].…”

“…In patients who achieve ROSC after CA, PCAS mimics the immunologic and coagulation disorders in severe sepsis [8]. the development of disseminated intravascular coagulation (DIC) as a serious disease results in an increased tendency of bleeding, microvascular thrombosis, thrombocytopenia, and multiple organ dysfunction, consequently affecting the clinically unfavorable outcomes of patients with PCAS [32]. DIC and TMA show similar laboratory ndings and presenting symptoms [32].…”

“…the development of disseminated intravascular coagulation (DIC) as a serious disease results in an increased tendency of bleeding, microvascular thrombosis, thrombocytopenia, and multiple organ dysfunction, consequently affecting the clinically unfavorable outcomes of patients with PCAS [32]. DIC and TMA show similar laboratory ndings and presenting symptoms [32]. Although microvascular thrombosis is mainly caused by platelet activation in both DIC and TMA, DIC is signi cantly associated with all coagulation and brinolysis systems, while TMA is signi cantly associated with vascular endothelial cells [33].…”

Hyperfibrinolyse nach Reanimation bei akuter Lungenarterienembolie

“…Deswegen imponiert die DIC regelhaft (manche Autoren konstatieren "immer" [7] als thrombotische Koagulopathie.…”

“…Unter physiologischen Bedingungen verhindert u. a. das Enzym Plasminogen-Aktivator-Inhibitor-1 (PAI-1) durch Bindung von tPA dessen unkontrollierte Wirkung auf Plasminogen. Einen durch Ischämie/Reperfusion ausgelösten schnellen Anstieg der tPA-Konzentration kann jedoch PAI-1 nicht zeitnah kompensieren, weil dessen Synthese und Freisetzung mehrere Stunden (4-6 h) in Anspruch nimmt [7]. Zweiphasiger Verlauf der Fibrinolysestörung Die Störung des fibrinolytischen Systems bei DIC kann demnach zweizeitig verlaufen.…”