Ex vivo thrombin generation patterns in septic patients with and without disseminated intravascular coagulation

Carlier, Laurence; Hunault, Gilles; Lerolle, Nicolas; Macchi, Laurent

doi:10.1016/j.thromres.2014.11.001

Cited by 11 publications

(12 citation statements)

References 28 publications

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“…The rate index of the propagation phase of thrombin generation and lag time for thrombin generation in their DIC patients did not differ from healthy subjects. 20 Similarly, in 2014, Cardenas et al 59 reported wide thrombin-generating variability in a trauma population, with a subgroup of patients suffering minor injuries having profound increases in thrombin-generating capacity, and another group, with more severe injuries, including shock, showing no consistent trends. While thrombin capacity and kinetic tests have clinical utility to discriminate patients with hemophilia, antithrombin III deficiency, and lupus anticoagulant, 20 they seem to be problematic in trauma patients to predict or guide treatment of acute coagulopathy.…”

Section: Historical Perspective and Possible Mechanismsmentioning

confidence: 99%

“…4,16Y18 The PT and aPTT tests are single-point indicators of clot potential, with clot formation occurring when only approximately 5% of all physiologically relevant thrombin is formed. 19,20 These tests normally take approximately 60 minutes and provide no information on whole blood clot kinetics, elongation and retraction, or platelet-fibrin contributions. 21 Whole Figure 1.…”

Section: Trauma-induced Coagulopathymentioning

confidence: 99%

“…Loss of antithrombin III also contributes to the elevated thrombin levels seen in vitro and may have direct effects on clotting kinetics and localization. 63,65 In addition, in 2015, Carlier et al 20 concluded that the thrombin generation test was too variable to be a useful diagnostic tool in their sepsis patients with or without DIC. The rate index of the propagation phase of thrombin generation and lag time for thrombin generation in their DIC patients did not differ from healthy subjects.…”

Section: Historical Perspective and Possible Mechanismsmentioning

confidence: 99%

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Mechanisms of early trauma-induced coagulopathy

Dobson

Letson

Sharma

et al. 2015

Journal of Trauma and Acute Care Surgery

113

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Traumatic-induced coagulopathy (TIC) is a hemostatic disorder that is associated with significant bleeding, transfusion requirements, morbidity and mortality. A disorder similar or analogous to TIC was reported around 70 years ago in patients with shock, hemorrhage, burns, cardiac arrest or undergoing major surgery, and the condition was referred to as a "severe bleeding tendency," "defibrination syndrome," "consumptive disorder," and later by surgeons treating US Vietnam combat casualties as a "diffuse oozing coagulopathy." In 1982, Moore's group termed it the "bloody vicious cycle," others "the lethal triad," and in 2003 Brohi and colleagues introduced "acute traumatic coagulopathy" (ATC). Since that time, early TIC has been cloaked in many names and acronyms, including a "fibrinolytic form of disseminated intravascular coagulopathy (DIC)." A global consensus on naming is urgently required to avoid confusion. In our view, TIC is a dynamic entity that evolves over time and no single hypothesis adequately explains the different manifestations of the coagulopathy. However, early TIC is not DIC because an increased thrombin-generating potential in vitro does not imply a clinically relevant thrombotic state in vivo as early TIC is characterized by excessive bleeding, not thrombosis. DIC with its diffuse anatomopathologic fibrin deposition appears to be a latter phase progression of TIC associated with unchecked inflammation and multiple organ dysfunction.

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Section: Historical Perspective and Possible Mechanismsmentioning

confidence: 99%

Section: Trauma-induced Coagulopathymentioning

confidence: 99%

Section: Historical Perspective and Possible Mechanismsmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of early trauma-induced coagulopathy

Dobson

Letson

Sharma

et al. 2015

Journal of Trauma and Acute Care Surgery

113

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“…However, some of the hemostatic changes we observed in ACLF also occur in patients with critical illness in the absence of underlying CLD. For example, patients with sepsis or disseminated intravascular coagulation (DIC) have been reported to have high circulating levels of VWF with low levels of the VWFcleaving protease ADAMTS13, [12][13][14] low levels of pro-and anticoagulant proteins with relatively preserved thrombin generating capacity, [15][16][17] and a hypofibrinolytic state. 18 Additional similarities between ACLF and septic patients without CLD exist, such as the phenomenon of immuneparesis, 19 which may also have consequences for the hemostatic system.…”

Section: Introductionmentioning

confidence: 99%

Global hemostatic status in patients with acute‐on‐chronic liver failure and septics without underlying liver disease

Lisman

Arefaine

Adelmeijer

et al. 2021

Journal of Thrombosis and Haemostasis

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Liver diseases are associated with profound hemostatic changes proportional to severity of illness. Hemostatic changes in acute‐on‐chronic liver failure (ACLF) may in part reflect critical illness. Hemostatic changes in ACLF partly overlap with those in sepsis, with rebalanced hemostasis in both. Patients with sepsis had hyperfibrinogenemia, associated with a thrombogenic clot structure. Abstract BackgroundEven the sickest patients with chronic liver disease (CLD), such as those with acute‐on‐chronic liver failure (ACLF) remain in hemostatic balance due to a concomitant decline in pro‐ and antihemostatic factors. ObjectivesWe aimed to study whether the hemostatic status in ACLF is merely an exaggeration from the status in patients with compensated and acutely decompensated cirrhosis, or whether sepsis‐associated hemostatic changes contribute. MethodsWe performed extensive hemostatic profiling in 31 adult patients with ACLF, 20 patients with sepsis without underlying CLD, and 40 healthy controls. ResultsWe found similarly elevated plasma levels of the platelet adhesive protein von Willebrand factor (VWF) and decreased levels of the VWF‐regulating protease ADAMTS13 in both groups compared to healthy controls. In vivo markers of activation of coagulation (thrombin‐antithrombin III, D‐dimer) were similarly elevated in both groups compared to controls, but ex vivo thrombin‐generating capacity was similar between patients and controls, despite a much more profound international normalized ratio elevation in ACLF. Plasma fibrinogen levels were much higher in septics, which was accompanied by a decreased ex vivo clot permeability and an increase in ex vivo resistance to clot lysis. All hemostatic parameters were remarkably stable over the first 10 days after admission. ConclusionsWe have found hemostatic changes in ACLF to partially overlap with that of patients with sepsis, and evidence of preserved hemostatic capacity in both patient groups. The notable difference was a profound hyperfibrinogenemia, associated with a thrombogenic clot structure and a marked ex vivo resistance to fibrinolysis in patients with sepsis.

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“…Altered TGA results have been described in several clinical situations, including cirrhosis, trauma, cardiopulmonary bypass surgery, stroke, sepsis, and the use of oral anticoagulants (3)(4)(5)(6)(7)(8). There is some evidence suggesting that TGA is a better indicator of overall hemostatic capability and could provide information for transfusion support in patients with cirrhosis and coagulation factor replacement in patients with hemophilia with and without inhibitors (9)(10)(11).…”

mentioning

confidence: 99%