Disseminated intravascular coagulation at an early phase of trauma is associated with consumption coagulopathy and excessive fibrinolysis both by plasmin and neutrophil elastase

Hayakawa, Mineji; Sawamura, Atsushi; Gando, Satoshi; Kubota, Nobuhiko; Uegaki, Shinji; Shimojima, Hidekazu; Shinoda, Masahiro; Ieko, Masahiro

doi:10.1016/j.surg.2010.06.010

Cited by 93 publications

(102 citation statements)

References 29 publications

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“…Activated platelets adhere to damaged tissues and serve as catalysts for amplification of thrombin generation. These processes are reflected in the findings of observational clinical studies that show reduced clotting factor and physiological anticoagulant levels [21][22][23], high thrombin generating capacity [3,4,21,[24][25][26] and reduced platelet counts [27,28] Overall, these data indicate a consumptive coagulopathy. The most depleted coagulation factors are fibrinogen and factor V [22,28], which are likely consumed in part by activated Protein C or free plasmin [29,30], although the relative importance of these proteases in reducing factor levels remains unknown.…”

Section: Pathophysiologymentioning

confidence: 98%

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The pathogenesis of traumatic coagulopathy

2014

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SummaryOver the last 10 years, the management of major haemorrhage in trauma patients has changed radically. This is mainly due to the recognition that many patients who are bleeding when they come in to the emergency department have an established coagulopathy before the haemodilution effects of fluid resuscitation. This has led to the use of new terminology: acute traumatic coagulopathy, acute coagulopathy of trauma shock or trauma‐induced coagulopathy. The recognition of acute traumatic coagulopathy is important, because we now understand that its presence is a prognostic indicator, as it is associated with poor clinical outcome. This has driven a change in clinical management, so that the previous approach of maintaining an adequate circulating volume and oxygen carrying capacity before, as a secondary event, dealing with coagulopathy, has changed to haemostatic resuscitation as early as possible. While there is as yet no universally accepted assay or definition, many experts use prolongation of the prothrombin time to indicate that there is, indeed, a coagulopathy. Hypoxia, acidosis and hypothermia and hormonal, immunological and cytokine production, alongside consumption and blood loss, and the dilutional effects of resuscitation may occur to varying extents depending on the type of tissue damaged, the type and extent of injury, predisposing to, or amplifying, activation of coagulation, platelets, fibrinolysis. These are discussed in detail within the article.

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Section: Pathophysiologymentioning

confidence: 98%

“…Stimulation of t-PA release from the endothelium by other factors such as hypoxia, epinephrine and vasopressin, is known as primary fibrinolysis. High t-PA levels have been reported in coagulopathic trauma patients [4,26]. In addition, when bound to the endothelial receptor, thrombomodulin, thrombin activates Protein C.…”

Section: Pathophysiologymentioning

confidence: 99%

The pathogenesis of traumatic coagulopathy

2014

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“…These data suggests manifestation of fibrinolysis in DIC that occurs at an early phase of trauma more intensive in patients from non-survival group. The measurements of coagulation markers and fibrinolysis have demonstrated that DIC at an early phase of trauma (24-48 hours) progresses dependently at a late phase until 5 or 6 days after the trauma [22]. The lowest p-value on 5-6-th day of posttraumatic period supports recent experimental evidences that DIC is the predominant and initiative pathogenesis of TIC and that the acute coagulopathy of traumatic shock and coagulopathy of trauma equal DIC with a fibrinolytic phenotype at an early phase of polytrauma [22].…”

Section: Controlmentioning

confidence: 99%

“…Six primary mechanisms involved in the development of TIC: tissue injury, traumatic shock, hypothermia, acidemia, hemodilution and inflammation [22]. Shock is the main etiologic factor of early coagulopathy, but requires initiator -tissue injury [23].…”

Section: Introductionmentioning

confidence: 99%

Evidence of Posttraumatic Coagulopathy in Case of the Severe Combined Thoracic Trauma

Stupnytskyi¹,

Жуков²

2016

AMS

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“…Brohi et al, postulated that acute traumatic coagulopathy is initiated by hypoperfusion and leads to systemic anticoagulation and hyper fibrinolysis via the activated protein C pathway [5,7]. Gando [7] and others [8] have suggested that the pathology develops more from a consumptive coagulopathy consistent with the hemorrhagic DIC phenotype. A recent and possibly unifying theory by Johansson et al, [9,10] proposes that with increasing severity of trauma, there is an increase in sympathoadrenal activation.…”

Section: Introductionmentioning

confidence: 99%

Untitled

2015

ETS

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Introduction: Trauma patients presenting with coagulopathy are four times more likely to die. After observing patients presenting with isolated severe Pulmonary Contusion (PC) on admission Chest X-ray (CXR) who were also coagulopathic, we hypothesized that patients with PC on admission CXR were more likely to be coagulopathic than other trauma patients. Methods:This was an IRB approved, single-center, retrospective cohort study of patients admitted over an 18 month period. Data were obtained from the trauma registry and medical records including demographics, laboratory values, injury severity scores, coagulation parameters and PC diagnostic modality. Patients on anticoagulants were excluded. The PC group consisted of patients diagnosed with PC by admission CXR. The control group were those patients without a PC or those diagnosed only by CT. Coagulopathy was defined as INR>1.4 or PTT>35 seconds. The PC group was further stratified into mild, moderate or severe PC. Data were analyzed with univariate analyses followed by development of a logistic regression model. Significance was set at p<0.05. Results:The PC group contained 189 subjects and controls 333. As expected ISS was higher in the PC group (25 vs 21) as was AIS chest (3 vs 1); both p<0.001. The prevalence of coagulopathy was also greater in PC (31% vs. 17%, p<0.001). After adjusting for ISS, PC patients were more likely to be coagulopathic (OR=1.76, 95% CI: 1.12-2.75) and had higher 24 hour (7% vs 3%, p=0.04) and overall mortality rates (15% vs 7%, p=0.006). The prevalence of coagulopathy increased with severity of pulmonary contusion in PC patients (Mild

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Disseminated intravascular coagulation at an early phase of trauma is associated with consumption coagulopathy and excessive fibrinolysis both by plasmin and neutrophil elastase

Cited by 93 publications

References 29 publications

The pathogenesis of traumatic coagulopathy

The pathogenesis of traumatic coagulopathy

Evidence of Posttraumatic Coagulopathy in Case of the Severe Combined Thoracic Trauma

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