Effect of fibrinogen on reversal of dilutional coagulopathy: a porcine model

Fries, Dietmar; Krismer, Anette C.; Klingler, Antón; Streif, Werner; Klima, G.; Wenzel, Volker; Haas, Thorsten; Innerhofer, Petra

doi:10.1093/bja/aei160

Cited by 181 publications

(145 citation statements)

References 18 publications

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“…[15][16][17][18] Substitution of fibrinogen in our dilutional model up to 2 g/l significantly improved the coagulation status of the blood samples. Fibrinogen is the substrate to form a clot thereby explaining its key role in coagulation.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 Fibrinogen is a key coagulation factor (substrate to form a clot) and isolated fibrinogen substitution in severe 5 models of dilutional coagulopathy resulted in a significantly improved clot strength and reduced blood loss. [15][16][17][18] The aim of this in vitro study was to determine the efficacy of rFVIIa in a model of severe dilutional coagulopathy by two different viscoelastic point of care (POC) coagulation analyzers (ROTEM system, Pentapharm GmbH, Munich, Germany and the Sonoclot Analyzer, Sienco Inc. Arvada, CO, USA). Our hypothesis was that rFVIIa may only reverse severe dilutional coagulopathy in presence of sufficient fibrinogen levels.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Monitoring Recombinant Factor VIIa Treatment: Efficacy Depends on High Levels of Fibrinogen in a Model of Severe Dilutional Coagulopathy

Ganter

Schmuck

Hamiel

et al. 2008

Journal of Cardiothoracic and Vascular Anesthesia

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Monitoring Recombinant Factor VIIa Treatment: Efficacy Depends on High Levels of Fibrinogen in a Model of Severe Dilutional Coagulopathy

Ganter

Schmuck

Hamiel

et al. 2008

Journal of Cardiothoracic and Vascular Anesthesia

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“…Terms such as acidosis, hypothermia, dilution, consumption, hyperfibrinolysis, multiple transfusions and dysfunctional fibrinogen resulting from resuscitation with colloid plasma expanders [1,2] add to the complexity and reflect elements of the pathogenesis in the development of coagulopathy in trauma. The potential benefit of thrombelastography as a point-of-care tool in evaluation of dynamics of whole blood formation has been reported in a number of studies [3,4].…”

Section: Introductionmentioning

confidence: 99%

Citrate artificially masks the haemostatic effect of recombinant factor VIIa in dilutional coagulopathy

Fenger-Eriksen

Ingerslev²,

Tønnesen³

et al. 2008

Ann Hematol

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International audienceMost often, thrombelastographic analyses are carried out using citrated blood and re-calcification. However, calcium chelation may affect dynamics of tissue-factor-initiated thrombin generation. The present study investigates the effect of sample anticoagulant on the response of a colloid induced dilutional coagulopathy model to recombinant activated factor VII (rFVIIa) as measured by thrombelastography. Thrombelastographic evaluation of whole blood coagulation activated with minute amounts of tissue factor in a model of in vitro haemodilution with hydroxyethyl starch (HES) 130/0.4 in a prospective laboratory study. Whole blood coagulation was evaluated before and after 30% dilution with HES 130/0.4, and following in vitro addition of rFVIIa to whole blood collected into tubes containing citrate, corn trypsin inhibitor (CTI), and no stabilizers. Haemodilution with HES 130/0.4 induces a coagulopathy characterised by a reduced maximum rate of clot formation and a pronounced reduction in the final clot firmness. With all test mediums investigated, rFVIIa significantly shortened clot initiation phase. In cases of native whole blood and CTI-stabilised whole blood, rFVIIa shortens the clotting time but also demonstrated an acceleration of the maximum velocity of clot formation. When citrate is used as anticoagulants in thrombelastographic clotting assays, these may artificially mask the haemostatic effect of rFVIIa in colloid haemodilution. The effect in vitro of rFVIIa in citrated blood samples may underestimate the haemostatic potential of rFVIIa

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“…71 Furthermore, fibrinogen has been suggested as a key coagulation factor needed to ensure sufficient and stable hemostasis during severe hemorrhage. [72][73][74] Transfusion of packed red blood cells (pRBCs) also result in dilution of clotting factors and reduction in clotting ability. 15,22,75 PRBCs contain no functional platelets and only little plasma.…”

Section: Dilutionmentioning

confidence: 99%

New insights into acute coagulopathy in trauma patients

Ganter

Pittet

2010

Best Practice & Research Clinical Anaesthesiology

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Abnormal coagulation parameters can be found in 25% of trauma patients with major injuries. Furthermore, trauma patients presenting with coagulopathy on admission have worse clinical outcome. Tissue trauma and systemic hypoperfusion appear to be the primary factors responsible for the development of acute traumatic coagulopathy immediately after injury. As a result of overt activation of the protein C pathway, the acute traumatic coagulopathy is characterised by coagulopathy in conjunction with hyperfibrinolysis. This coagulopathy can then be exacerbated by subsequent physiologic and physical derangements such as consumption of coagulation factors, haemodilution, hypothermia, acidemia and inflammation, all factors being associated with ongoing haemorrhage and inadequate resuscitation or transfusion therapies. Knowledge of the different mechanisms involved in the pathogenesis of acute traumatic coagulopathy is essential for successful management of bleeding trauma patients. Therefore, early evidence suggests that treatment directed at aggressive and targeted haemostatic resuscitation can lead to reductions in mortality of severely injured patients. ABSTRACTAbnormal coagulation parameters can be found in 25% of trauma patients with major injuries. Furthermore, trauma patients presenting with coagulopathy on admission have worse clinical outcome. Tissue trauma and systemic hypoperfusion appear to be the primary factors responsible for the development of acute traumatic coagulopathy immediately after injury. As a result of overt activation of the protein C pathway, the acute traumatic coagulopathy is characterized by coagulopathy in conjunction with hyperfibrinolysis. This coagulopathy can then be exacerbated by subsequent physiologic and physical derangements like consumption of coagulation factors, hemodilution, hypothermia, acidemia, and inflammation; all factors being associated with ongoing hemorrhage and inadequate resuscitation or transfusion therapies. Knowledge of the different mechanisms involved in the pathogenesis of acute traumatic coagulopathy is essential for successful management of bleeding trauma patients. Therefore, early evidence suggests that treatment directed at aggressive and targeted hemostatic resuscitation can lead to reductions in mortality of severely injured patients.

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Effect of fibrinogen on reversal of dilutional coagulopathy: a porcine model

Abstract: Replacing 65% of the estimated blood volume with gelatin in swine resulted in dilutional coagulopathy; subsequent fibrinogen administration improved clot formation and reduced blood loss significantly.

Cited by 181 publications

References 18 publications

Monitoring Recombinant Factor VIIa Treatment: Efficacy Depends on High Levels of Fibrinogen in a Model of Severe Dilutional Coagulopathy

Monitoring Recombinant Factor VIIa Treatment: Efficacy Depends on High Levels of Fibrinogen in a Model of Severe Dilutional Coagulopathy

Citrate artificially masks the haemostatic effect of recombinant factor VIIa in dilutional coagulopathy

New insights into acute coagulopathy in trauma patients

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