New insights into acute coagulopathy in trauma patients

Ganter, Michael T.; Pittet, Jean–François

doi:10.1016/j.bpa.2009.09.010

Cited by 43 publications

(42 citation statements)

References 103 publications

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“…Clotting factor activity and platelet aggregation may be reduced by hypothermia (<33-34 °C). [11,23] White et al [24] found that acidosis may reduce the activity of the factor Xa/Va complex, and the activity will be persistently reduced by the increasing acidosis severity. NEUT% values were significantly increased in group 4, implying that group 4 had inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Tissue factor, the thrombin-thrombomodulin protein C pathway, endothelium, complement proteins, proinfl ammatory cytokines, and platelets play important roles in this interaction between inflammation and coagulation. [23,[25][26][27] The inflammation cytokines enhance endothelial expression/release of thrombomodulin resulting in enhanced activation of PC. [28] With increasingly severe trauma, the excessive increases in plasma catecholamine increase the release of tPA and PC, and the excessive consumption of coagulation factors and platelets, resulting in predominant hypocoagulability.…”

Section: Discussionmentioning

confidence: 99%

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Diverse coagulopathies in a rabbit model with different abdominal injuries

Peng

Zhao

2017

World Journal of Emergency Medicine

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BACKGROUND: Although coagulopathy can be very common in severe traumatic shock patients, the exact incidence and mechanism remain unclear. In this study, a traumatic shock rabbit model with special abdomen injuries was developed and evaluated by examining indicators of clotting and fi brinolysis. METHODS:Forty New Zealand white rabbits were randomly divided into four groups: group 1 (sham), group 2 (hemorrhage), group 3 (hemorrhage-liver injury), and group 4 (hemorrhage-liver injury/intestinal injury-peritonitis). Coagulation was detected by thromboelastography before trauma (T 0 ), at 1 hour (T 1 ) and 4 hours (T 2 ) after trauma. RESULTS:Rabbits that suffered from hemorrhage alone did not differ in coagulation capacity compared with the sham group. The clot initiations (R times) of group 3 at T 1 and T 2 were both shorter than those of groups 1, 2, and 4 (P<0.05). In group 4, clot strength was decreased at T 1 and T 2 compared with those in groups 1, 2, and 3 (P<0.05), whereas the R time and clot polymerization were increased at T 2 (P<0.05). The clotting angle signifi cantly decreased in group 4 compared with groups 2 and 3 at T 2 (P<0.05).CONCLUSION: This study suggests that different abdominal traumatic shock show diverse coagulopathy in the early phase. Isolated hemorrhagic shock shows no obvious effect on coagulation. In contrast, blunt hepatic injury with hemorrhage shows hypercoagulability, whereas blunt hepatic injury with hemorrhage coupled with peritonitis caused by a ruptured intestine shows a tendency toward hypocoagulability.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Diverse coagulopathies in a rabbit model with different abdominal injuries

Peng

Zhao

2017

World Journal of Emergency Medicine

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“…Patients suffering from major trauma often turn into a hypercoagulable state, which then frequently leads to pathological thrombosis [15]. Abnormal coagulation parameters can be found in 25% of trauma patients with major injuries [16]. Previous studies in trauma patients were able to highlight a significant and persistent increase in markers of thrombin generation and action, such as F1 þ 2 and TAT [17].…”

Section: Introductionmentioning

confidence: 99%

Markers of blood coagulation and fibrinolysis in patients with early and delayed microsurgical reconstructions in the lower extremities

Kloeters

Vasilic

Hupkens

et al. 2017

Journal of Plastic Surgery and Hand Surgery

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Background: In this study, markers of coagulation and fibrinolysis were assessed during early and delayed microsurgical reconstruction in patients with traumatic defects of their lower legs to analyse whether an imbalance of the hemostasis after trauma might predispose the development of vascular complications. Methods: The prospective study included 70 patients. In 35 patients, surgery was performed within 72 hours after injury. In 35 other patients, delayed free flap transfer was performed between 14-21 days after trauma. In each group, reconstruction was performed with a fasciocutaneous anterior-lateral thigh flap (ALT, n ¼ 18) or a myocutaneous flap (latissimus dorsi flap; n ¼ 17). Blood samples were collected preoperatively, intraoperatively, and 3,6,12,24,36, 48, 72, 96 and 120 hours after the operation. Analysed parameters included markers of coagulation such as prothrombin fragment 1 þ 2 (F1 þ 2), thrombin-antithrombin III-complex (TAT), and antithrombin, as well as fibrinolysis markers such as plasminogenactivator inhibitor-I (PAI-1), tissue-plasminogenactivator (t-PA), and plasminogen. Results: Preoperatively, levels of F1 þ 2, TAT, and PAI-1 were significantly higher in patients with delayed reconstruction (p < .05). Patients with later vascular complications in this group (n ¼ 5) presented a significant higher concentration of TAT, F1 þ 2, and PAI-1 (p < .05). Twelve and 24 hours after free flap surgery, patients with vascular complications presented significant elevated levels of these markers (p < .05). Conclusions: Patients with delayed free flap surgery after lower leg trauma present a hypercoagulable state in their blood due to activation of the coagulation system and hypofibrinolysis. Early reconstruction might minimise the risk of flap failure caused by hypercoagulability.

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“…Beside the discussion about the substitution of coagulation factors and blood components, there is evolving knowledge that trauma itself has time-or incident-depending effects on coagulation [14]. Initially the combination of traumatic injury and tissue hypoperfusion results in a coagulopathy associated with a reduction in protein C levels.…”

Section: Key Parameters and Assessment Of Trauma-induced Coagulopathymentioning

confidence: 99%

“…A further anticoagulant activity is exerted by the de-activation of plasminogen activator inhibitor (PAI-1), resulting in enhanced fibrinolysis [16]. In addition to its anticoagulatory effects, protein C proteolytically activates the cell surface receptor protease-activated receptor-1 (PAR-1) and thus generates several cytoprotective effects by increasing the anti-inflammatory properties, anti-apoptotic activity, and protective function of the endothelial barrier , all being required for survival in acute shock [14]. Taken together, early post-…”

Section: Key Parameters and Assessment Of Trauma-induced Coagulopathymentioning

confidence: 99%

Massive Bleeding and Massive Transfusion

Meißner¹,

Schlenke

2012

Transfus Med Hemother

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Massive bleeding in trauma patients is a serious challenge for all clinicians, and an interdisciplinary diagnostic and therapeutic approach is warranted within a limited time frame. Massive transfusion usually is defined as the transfusion of more than 10 units of packed red blood cells (RBCs) within 24 h or a corresponding blood loss of more than 1- to 1.5-fold of the body’s entire blood volume. Especially male trauma patients experience this life-threatening condition within their productive years of life. An important parameter for clinical outcome is to succeed in stopping the bleeding preferentially within the first 12 h of hospital admission. Additional coagulopathy in the initial phase is induced by trauma itself and aggravated by consumption and dilution of clotting factors. Although different aspects have to be taken into consideration when viewing at bleedings induced by trauma compared to those caused by major surgery, the basic strategy is similar. Here, we will focus on trauma-induced massive hemorrhage. Currently there are no definite, worldwide accepted algorithms for blood transfusion and strategies for optimal coagulation management. There is increasing evidence that a higher ratio of plasma and RBCs (e.g. 1:1) endorsed by platelet transfusion might result in a superior survival of patients at risk for trauma-induced coagulopathy. Several strategies have been evolved in the military environment, although not all strategies should be transferred unproven to civilian practice, e.g. the transfusion of whole blood. Several agents have been proposed to support the restoration of coagulation. Some have been used for years without any doubt on their benefit-to-risk profile, whereas great enthusiasm of other products has been discouraged by inefficacy in terms of blood transfusion requirements and mortality or significant severe side effects. This review surveys current literature on fluid resuscitation, blood transfusion, and hemostatic agents currently used during massive hemorrhage in order to optimize patients’ blood and coagulation management in emergency medical aid.

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New insights into acute coagulopathy in trauma patients

Cited by 43 publications

References 103 publications

Diverse coagulopathies in a rabbit model with different abdominal injuries

Diverse coagulopathies in a rabbit model with different abdominal injuries

Markers of blood coagulation and fibrinolysis in patients with early and delayed microsurgical reconstructions in the lower extremities

Massive Bleeding and Massive Transfusion

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