Coagulation and fibrinolysis after injury.

Flute, P.T.

doi:10.1136/jcp.s3-4.1.102

Cited by 19 publications

(18 citation statements)

References 55 publications

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“…It has been demonstrated that both the intrinsic and extrinsic coagulation systems are enhanced after injury (11). Dis turbed microcirculation a few hours after the infliction o f a crush fracture, such as used in our experiments, has been described by other authors in several animal species (3,13,47).…”

Section: Discussionmentioning

confidence: 64%

Trauma and Acetylsalicylic Acid-Induced Changes in Hemostasis during Liver Resection in the Rat

Bengmark¹,

Göransson²,

Zoucas³

1980

Eur Surg Res

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The effect of acetylsalicylic acid and bilateral femoral crush fractures on hemostasis after liver resection was studied in the rat. Serum salicylate levels were dose-dependent and similar in traumatized and non-traumatized animals. Bleeding time was significantly shortened and blood loss significantly decreased after bilateral femoral crush fractures. Both these values were significantly increased in salicylate pretreated animals compared to controls. Combination of bilateral femoral crush fractures and administration of 0.7 mg/100 g b.w. acetylsalicylic acid brought blood loss to normal values, while administration of 4.3 mg/l00 g b.w. acetylsalicylic acid after bilateral femoral crush fractures increased blood loss significantly. Normal APT times indicated that the intrinsic coagulation system was not affected. ADP- and collagen-induced platelet aggregation was diminished in all animals as compared to controls.

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Section: Discussionmentioning

confidence: 64%

Trauma and Acetylsalicylic Acid-Induced Changes in Hemostasis during Liver Resection in the Rat

Bengmark¹,

Göransson²,

Zoucas³

1980

Eur Surg Res

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“…87 Since the late 1960s, there have been ample instances of DIC after traumatic shock. 88 Direct tissue damage to the cellular elements of the blood, shock and hemorrhage, ischemia, and hypoxia provide ample reasons to expect exposure of the blood to foreign surfaces and the entry of tissue factor into the circulation. 88 …”

Section: Traumatic Shock Associated With Hemorrhage and Injurymentioning

confidence: 99%

Trauma, Shock, and Disseminated Intravascular Coagulation

Gando

Sawamura²,

Hayakawa³

2011

Annals of Surgery

173

231

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A trauma patient's survival depends on the ability to control 2 opposing conditions, bleeding at the early phase and thrombosis at a late phase of trauma. The mixed existence of physiological responses for hemostasis and wound healing and pathological hemostatic responses makes it difficult to understand the mechanisms of the 2 stages of coagulopathy after trauma. Traumatic coagulopathy is multifactorial but disseminated intravascular coagulation (DIC) with the fibrinolytic phenotype is the predominant and initiative pathogenesis of coagulopathy at the early stage of trauma. High levels of inflammatory cytokines and severe tissue injuries activate the tissue-factor-dependent coagulation pathway followed by massive thrombin generation and its activation. Low levels of protein C and antithrombin induce insufficient coagulation control and the inhibition of the anticoagulation pathway. Primary and secondary fibrin(ogen)olysis is highly activated by the shock-induced tissue hypoxia and disseminated fibrin formation, respectively. Consumption coagulopathy and severe bleeding are subsequently observed in trauma patients. Persistently high levels of plasminogen activator inhibitor-1 expressed in the platelets and endothelium then change the DIC with the fibrinolytic phenotype into the thrombotic phenotype at approximately 24 to 48 hours after the onset of trauma. All of these changes coincide with the definition of DIC, which can be clearly distinguished from normal responses for hemostasis and wound healing by using sensitive molecular markers and DIC diagnostic criteria such as those outlined by the Japanese Association for Acute Medicine and the International Society on Thrombosis and Haemostasis. Treatments of DIC with the fibrinolytic phenotype involve the surgical repair of the trauma, improvement of shock, and the rapid and sufficient replacement of platelet concentrate, fresh frozen plasma, and depleted coagulation factors. The administration of an antifibrinolytic agent (tranexamic acid) may reduce the risk of death in bleeding trauma patients associated with this type of DIC.

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“…Let us therefore consider the diverse problems of fibrinolysis (Flute, 1970;McNicol, 1973)-The remainder of this paper will be divided into a summary of the following topics; fibrinolysis, its assessment, its function, healing and ulcers, vasculitis and therapy thereof and hyperfibrinolytic states. There is circulating in the blood an inactive betaglobulin plasminogen which is synthesized in the liver and under the appropriate stimulus, such as a damaged endothelium or thrombus formation, the vasculo-endothelium releases the activator enzyme of plasminogen, the so-called plasminogen activator (Fig.…”

mentioning

confidence: 99%

Dowling oration 1975. FIBRINOLYSIS AND VASCULITIS

Cunliffe

1976

Clin Exp Dermatol

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Coagulation and fibrinolysis after injury.

Cited by 19 publications

References 55 publications

Trauma and Acetylsalicylic Acid-Induced Changes in Hemostasis during Liver Resection in the Rat

Trauma and Acetylsalicylic Acid-Induced Changes in Hemostasis during Liver Resection in the Rat

Trauma, Shock, and Disseminated Intravascular Coagulation

Dowling oration 1975. FIBRINOLYSIS AND VASCULITIS

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