Semin Thromb Hemost 2012; 38(03): 268-273
DOI: 10.1055/s-0032-1309287
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Fibrinogen as a Hemostatic Agent

Benny Sørensen
1   Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Guy's and St Thomas's NHS Foundation Trust, London, United Kingdom
2   King's College London School of Medicine, London, United Kingdom
3   Department of Clinical Biochemistry, Centre for Haemophilia and Thrombosis, Aarhus University Hospital, Skejby, Denmark
,
Ole Halfdan Larsen
1   Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Guy's and St Thomas's NHS Foundation Trust, London, United Kingdom
3   Department of Clinical Biochemistry, Centre for Haemophilia and Thrombosis, Aarhus University Hospital, Skejby, Denmark
,
Catherine J. Rea
1   Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Guy's and St Thomas's NHS Foundation Trust, London, United Kingdom
2   King's College London School of Medicine, London, United Kingdom
,
Mariann Tang
1   Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Guy's and St Thomas's NHS Foundation Trust, London, United Kingdom
3   Department of Clinical Biochemistry, Centre for Haemophilia and Thrombosis, Aarhus University Hospital, Skejby, Denmark
4   Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Skejby, Denmark
,
Jonathan H. Foley
1   Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Guy's and St Thomas's NHS Foundation Trust, London, United Kingdom
2   King's College London School of Medicine, London, United Kingdom
,
Christian Fenger-Eriksen
1   Haemostasis Research Unit, Centre for Haemostasis and Thrombosis, Guy's and St Thomas's NHS Foundation Trust, London, United Kingdom
3   Department of Clinical Biochemistry, Centre for Haemophilia and Thrombosis, Aarhus University Hospital, Skejby, Denmark
5   Department of Anaesthesiology, Aarhus University Hospital, Skejby, Denmark
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Publikationsdatum:
29. März 2012 (online)

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Abstract

Coagulation factor I (fibrinogen) plays an essential role in the hemostatic system by bridging activated platelets and being the key substrate for thrombin in establishing a consolidating fibrin network. Fibrinogen is synthesized in the liver and the plasma concentration is 1 to 5–4.0 g/L. During recent 10 years, fibrinogen has been recognized to play an important role in controlling hemorrhage. Dilutional coagulopathy induced by colloid plasma expanders is characterized by fibrinogen deficiency and dysfunctional fibrin polymerization. Trauma and use of extracorporeal circulation is also known to reduce levels of fibrinogen. A series of laboratory experiments and experimental animal studies have suggested fibrinogen as a potent hemostatic agent. These data are supported by retrospective surveys as well as a series of prospective proof of principal clinical trials. This article provides a description of the biochemistry and mechanisms of fibrinogen as well as the etiology for developing fibrinogen deficiency. Furthermore, it summarizes laboratory and experimental data on the role of fibrinogen in dilutional coagulopathy and addresses laboratory monitoring issues. Finally, it lists retrospective and prospective studies, which have been designed to assess the clinical efficacy and safety of hemostatic intervention with fibrinogen concentrate.