Venous Thromboembolism in Trauma: A Local Manifestation of Systemic Hypercoagulability?

Meissner, Mark H.; Chandler, Wayne L.; Elliott, Jennifer S.

doi:10.1097/01.ta.0000046253.33495.70

Cited by 133 publications

(91 citation statements)

References 37 publications

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“…It remains to be further established whether additional indirect effects of RNA may contribute to its procoagulant function. Despite the rapid degradation of RNA, the apparent procoagulant sensitization of plasma or whole blood could contribute to the as yet poorly understood hypercoagulable state observed in patients under thrombotic risk (36). Under conditions of tissue injury in association with sepsis, bacterial or viral infections, the expected increase of extracellular RNA may very well be related to the prothrombotic state in the affected patients.…”

Section: Discussionmentioning

confidence: 99%

Extracellular RNA constitutes a natural procoagulant cofactor in blood coagulation

Kannemeier

Shibamiya²,

Nakazawa

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

492

463

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Upon vascular injury, locally controlled haemostasis prevents lifethreatening blood loss and ensures wound healing. Intracellular material derived from damaged cells at these sites will become exposed to blood components and could contribute to blood coagulation and pathological thrombus formation. So far, the functional and mechanistic consequences of this concept are not understood. Here, we present in vivo and in vitro evidence that different forms of eukaryotic and prokaryotic RNA serve as promoters of blood coagulation. Extracellular RNA was found to augment (auto-)activation of proteases of the contact phase pathway of blood coagulation such as factors XII and XI, both exhibiting strong RNA binding. Moreover, administration of exogenous RNA provoked a significant procoagulant response in rabbits. In mice that underwent an arterial thrombosis model, extracellular RNA was found associated with fibrin-rich thrombi, and pretreatment with RNase (but not DNase) significantly delayed occlusive thrombus formation. Thus, extracellular RNA derived from damaged or necrotic cells particularly under pathological conditions or severe tissue damage represents the long sought natural ''foreign surface'' and provides a procoagulant cofactor template for the factors XII/XI-induced contact activation/amplification of blood coagulation. Extracellular RNA thereby reveals a yet unrecognized target for antithrombotic intervention, using RNase or related therapeutic strategies.contact phase activation ͉ thrombosis ͉ RNase ͉ vascular injury ͉ wound healing

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Section: Discussionmentioning

confidence: 99%

Extracellular RNA constitutes a natural procoagulant cofactor in blood coagulation

Kannemeier

Shibamiya²,

Nakazawa

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

492

463

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“…Meissner et al [24] analysed markers of the clotting system in 101 trauma patients, and found significantly elevated F1 þ 2 levels on admission. The levels remained elevated throughout the first month of follow-up, indicating an activation of the clotting system.…”

Section: Discussionmentioning

confidence: 99%

“…A plethora of studies have demonstrated a pronounced imbalance between proand anticoagulatory factors in the setting of trauma, e.g. upregulation of tissue factor (TF) and markers of thrombin generation [19,[24][25][26] and simultaneous reduction of natural anticoagulants/fibrinolytic factors such as antithrombin (AT), protein C (PC), and protein S (PS) [25,26]. However, to which extent the posttraumatic hypofibrinolytic state contributes to this hypercoagulability with all its deleterious clinical consequences remains unclear [18,27].…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

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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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“…1,2,4,5 Limited data suggest that patients with penetrating injuries have a lower risk of thrombosis than those who sustain blunt trauma.…”

Section: Major Traumamentioning

confidence: 99%

Prevention of Venous Thromboembolism in High-Risk Patients

Geerts

2006

Hematology

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The prevention of venous thromboembolism (VTE) in patients recovering from major trauma, spinal cord injury (SCI), or other critical illness is often challenging. These patient groups share a high risk for VTE, they often have at least a temporary high bleeding risk, and there are relatively few thromboprophylaxis trials specific to these populations. A systematic literature review has been conducted to summarize the risks and prevention of VTE in these three groups. It is concluded that routine thromboprophylaxis should be provided to major trauma, SCI and critical care patients based on an individual assessment of their thrombosis and bleeding risks. For patients at high risk for VTE, including those recovering from major trauma and SCI, prophylaxis with a low molecular weight heparin (LMWH) should commence as soon as hemostasis has been demonstrated. For critical care patients at lower thrombosis risk, either LMWH or lowdose heparin is recommended. For those with a very high risk of bleeding, mechanical prophylaxis should be instituted as early as possible and continued until pharmacologic prophylaxis can be initiated. The use of prophylactic inferior vena caval filters is strongly discouraged because their potential benefit has not been shown to outweigh the risks or substantial costs. Implementation of thromboprophylaxis in these patients requires a local commitment to this important patient safety priority as well as a highly functional delivery system, based on the use of pre-printed orders, computer prompts, regular audit and feedback, and ongoing quality improvement efforts.Across the spectrum of hospitalized patients, the rates of venous thromboembolism (VTE) vary substantially.1 Although a large number of patient-specific thrombosis risk factors have been shown to contribute to this variability, the principal factor that determines VTE risk is the patient's primary reason for hospitalization, whether this is a surgical procedure or an acute medical illness. This paper will discuss the risks of VTE in three populations: major trauma, spinal cord injury (SCI) and critical care patients. The reasons for selecting these patient groups are as follows: each is associated with a high risk of VTE; there is often also a temporary high risk of bleeding; and there have been relatively few studies of prophylaxis in each of these groups. Despite the challenges involved in preventing VTE in these patients, recent evidence allows clinicians to provide effective and safe prophylaxis (see Figure 1).

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Venous Thromboembolism in Trauma: A Local Manifestation of Systemic Hypercoagulability?

Cited by 133 publications

References 37 publications

Extracellular RNA constitutes a natural procoagulant cofactor in blood coagulation

Extracellular RNA constitutes a natural procoagulant cofactor in blood coagulation

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

Prevention of Venous Thromboembolism in High-Risk Patients

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