Hyperfibrinolysis is common in out-of-hospital cardiac arrest

Schöchl, Herbert; Cadamuro, Janne; Seidl, S.; Franz, Alexander; Solomon, Cristina; Schlimp, Christoph J.; Ziegler, Bernd

doi:10.1016/j.resuscitation.2012.08.318

Cited by 71 publications

(45 citation statements)

References 32 publications

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“…Recently, it has been appreciated that trauma patients presenting to the hospital with hyperfibrinolysis detected by TEG have elevated tPA levels (20). These investigators found a correlation to low systolic blood pressure and hyperfibrinolysis and elevated tPA, which is consistent with existing literature that hypoperfusion promotes fibrinolysis in trauma patients (10) and in patients without injury (9). Our model supports that hemorrhagic shock, but not tissue injury, promotes fibrinolysis through a tPA mediated mechanism.…”

Section: Discussionsupporting

confidence: 89%

“…Principal component analyses suggest that hyperfibrinolysis does not correlate with impaired clot formation (7, 8). In a human study, patients with non-traumatic cardiac arrest had a high prevalence of hyperfibrinolysis (9). Although significant hypotension in injured patients is associated with hyperfibrinolysis, there is no correlation with injury severity (ISS) (10).…”

Section: Introductionmentioning

confidence: 99%

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Fibrinolysis shutdown phenotype masks changes in rodent coagulation in tissue injury versus hemorrhagic shock

Moore

Lawson

et al. 2015

Surgery

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Introduction Systemic hyperfibrinolysis (accelerated clot degradation) and fibrinolysis shutdown (impaired clot degradation) are associated with increased mortality compared to physiologic fibrinolysis following trauma. Animal models have not reproduced these changes. We hypothesize rodents have a shutdown phenotype that require an exogenous profibrinolytic to differentiate mechanisms that promote or inhibit fibrinolysis. Methods Fibrinolysis resistance was assessed by thrombelastography (TEG) using exogenous tissue plasminogen activator (tPA) titrations in whole blood. There were three experimental groups: 1)tissue injury (laparotomy/bowel crush), 2)shock (hemorrhage to mean arterial pressure 20 mmHg), and 3)control (arterial cannulation and tracheostomy). Baseline and 30-minute post-intervention blood samples were collected, and assayed with TEG challenged with taurocholic acid (TUCA). Results Rats were resistant to exogenous tPA; CL30 (Percent clot remaining 30 minutes after maximum amplitude) at 150ng/ml (p=0.511) and 300ng/ml (p=0.931) was similar to baseline, while 600ng/ml (p=0.046) provoked fibrinolysis. Using the TUCA challenge, the percent change in CL30 from baseline was increased in tissue injury compared to control (p=0.048.), whereas CL30 decreased in shock versus control (p=0.048). TPA increased in the shock group compared to tissue injury (p=0.009) and control (p=0.012). Conclusion Rats have an innate fibrinolysis shutdown phenotype. The TEG TUCA challenge is capable of differentiating changes in clot stability with rats undergoing different procedures. Tissue injury inhibits fibrinolysis while shock promotes tPA-mediated fibrinolysis.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Fibrinolysis shutdown phenotype masks changes in rodent coagulation in tissue injury versus hemorrhagic shock

Moore

Lawson

et al. 2015

Surgery

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“…Profound shock is the most consistent clinical predictor of hyperfibrinolysis in retrospective trauma studies (6–8). This is further supported by non-trauma literature in which hyperfibrinolysis is prevalent in patients with prehospital cardiac arrest (9). The observation that inadequate perfusion promotes fibrinolysis is not new.…”

Section: Introductionsupporting

confidence: 58%

Shock-induced systemic hyperfibrinolysis is attenuated by plasma-first resuscitation

Moore

Morton

et al. 2015

Journal of Trauma and Acute Care Surgery

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Background We developed a hemorrhagic shock animal model to replicate an urban prehospital setting where resuscitation fluids are limited to assess the effect of saline versus plasma in coagulopathic patients. An in vitro model of whole blood dilution with saline exacerbated tPA mediated fibrinolysis, while plasma dilution did not change fibrinolysis. We hypothesize that shock induced hyperfibrinolysis can be attenuated by resuscitation with plasma while exacerbated by saline. Methods Sprague Dawley rats were hemorrhaged to a mean arterial pressure (MAP) of 25 mmHg and maintained in shock for 30 minutes. Animals were resuscitated with either normal saline (NS) or platelet free plasma (PFP) with a 10% total blood volume bolus, followed by an additional 5 minutes of resuscitation with NS to increase blood pressure to a MAP of 30 mmHg. Animals were observed for 15 minutes for assessment of hemodynamic response and survival. Blood samples were analyzed with thrombelastography (TEG) paired with protein analysis. Results The median percent of total blood volume shed per group were similar (NS 52.5% vs PFP 55.7 p=0.065). Survival was 50% in NS compared to 100% in PFP. The change in LY30 and tPA levels from baseline to shock was similar between groups (LY30 PFP10 IQR 4.3 to 11.2, NS 4.5 IQR 4.1 to 14.2 p=1.00; tPA PFP 16.6 ng/ml IQR 13.7–27.8, NS 22.4 IQR 20.1 to 25.5 p=0.240). After resuscitation, the median change in LY30 was greater in the NS group (13.5 IQR 3.5 to 19.9) compared to PFP (−4.9 % IQR −9.22 to 0.25 p=0.004) but tPA levels did not significantly change (NS 1.4 IQR-6.2 to 7.1 vs PFP 1.7 IQR-5.2 to 6.8 p=0.699). Conclusions Systemic hyperfibrinolysis is driven by hypoperfusion and associated with increased levels of tPA. Plasma is a superior resuscitation fluid to normal saline in a prehospital model of severe hemorrhagic shock as it attenuates hyperfibrinolysis and improves systemic perfusion.

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“…23 Hyperfibrinolysis is reportedly common in OHCA patients and has been associated with markers of hypoperfusion in these patients. 24,25 If not improved, DIC with the fibrinolytic phenotype during the early stage of OHCA proceeds to the thrombotic phenotype at the later stage of OHCA. 20 Both types of DIC affect the patient outcomes.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2017

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Objective: This study aimed to test the hypothesis that coagulation, fibrinolytic markers and disseminated intravascular coagulation (DIC) score (International Society on Thrombosis and Haemostasis) at hospital admission of out-of-hospital cardiac arrest (OHCA) patients can predict neurological outcomes 1 month after cardiac arrest. Results: We analyzed data for 315 patients. Except for fibrinogen level, all coagulation variables, fibrinolytic variables, and DIC score were associated with favorable neurological outcomes. In the receiver operating characteristic curve analysis, FDP level had the largest area under the curve (AUC; 0.795). In addition, the AUC of FDP level was larger than that of 4 lactate level. The AUC value of FDP level might indicate that FDP is an independent predictor of favorable neurological outcomes. Conclusions:All of the coagulation and fibrinolytic markers, except for fibrinogen level, and DIC score at hospital admission, were associated with favorable neurological outcomes. Of all of the variables, FDP level was most closely associated with favorable neurological outcomes in OHCA patients who successfully achieved ROSC. 5

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Hyperfibrinolysis is common in out-of-hospital cardiac arrest

Cited by 71 publications

References 32 publications

Fibrinolysis shutdown phenotype masks changes in rodent coagulation in tissue injury versus hemorrhagic shock

Fibrinolysis shutdown phenotype masks changes in rodent coagulation in tissue injury versus hemorrhagic shock

Shock-induced systemic hyperfibrinolysis is attenuated by plasma-first resuscitation

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

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