Thromboelastography as a Better Indicator of Hypercoagulable State After Injury Than Prothrombin Time or Activated Partial Thromboplastin Time

Park, Myung S.; Martini, Wenjun Z.; Dubick, Michael A.; Salinas, José; Butenas, Saulius; Kheirabadi, Bijan S.; Pusateri, Anthony E.; Vos, Jeffrey A.; Guymon, Charles H; Wolf, Steven E.; Mann, Kenneth G.; Holcomb, John B.

doi:10.1097/ta.0b013e3181ae6f1c

Cited by 274 publications

(249 citation statements)

References 57 publications

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“…TEG analysis has also been shown to be a better indicator of hemostasis than PT (20,23). Recently, Zaar et al (37) demonstrated a reduction in time to fibrin formation after LBNP to presyncope demonstrated by shortened R-time.…”

Section: Discussionmentioning

confidence: 99%

Coagulation changes during lower body negative pressure and blood loss in humans

Helmond

Johnson

Curry

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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van Helmond N, Johnson BD, Curry TB, Cap AP, Convertino VA, Joyner MJ. Coagulation changes during lower body negative pressure and blood loss in humans. Am J Physiol Heart Circ Physiol 309: H1591-H1597, 2015. First published September 9, 2015; doi:10.1152/ajpheart.00435.2015.-We tested the hypothesis that markers of coagulation activation are greater during lower body negative pressure (LBNP) than those obtained during blood loss (BL). We assessed coagulation using both standard clinical tests and thrombelastography (TEG) in 12 men who performed a LBNP and BL protocol in a randomized order. LBNP consisted of 5-min stages at 0, Ϫ15, Ϫ30, and Ϫ45 mmHg of suction. BL included 5 min at baseline and following three stages of 333 ml of blood removal (up to 1,000 ml total). Arterial blood draws were performed at baseline and after the last stage of each protocol. We found that LBNP to Ϫ45 mmHg is a greater central hypovolemic stimulus versus BL; therefore, the coagulation markers were plotted against central venous pressure (CVP) to obtain stimulus-response relationships using the linear regression line slopes for both protocols. Paired t-tests were used to determine whether the slopes of these regression lines fell on similar trajectories for each protocol. Mean regression line slopes for coagulation markers versus CVP fell on similar trajectories during both protocols, except for TEG ␣°angle (Ϫ0.42 Ϯ 0.96 during LBNP vs. Ϫ2.41 Ϯ 1.13°/mmHg during BL; P Ͻ 0.05). During both LBNP and BL, coagulation was accelerated as evidenced by shortened R-times (LBNP, 9.9 Ϯ 2.4 to 6.2 Ϯ 1.1; BL, 8.7 Ϯ 1.3 to 6.4 Ϯ 0.4 min; both P Ͻ 0.05). Our results indicate that LBNP models the general changes in coagulation markers observed during BL. blood coagulation; hemorrhage; lower body negative pressure; blood coagulation tests; humans; central hypovolemia NEW & NOTEWORTHYOur study provides noteworthy data that directly compare blood coagulation activation induced by lower body negative pressure to those observed during blood loss in conscious humans.HEMORRHAGE IS ONE OF THE LEADING causes of accidental death (1) and is the leading cause of death on the battlefield (8, 9). Activation of the coagulation system is vital following a hemorrhagic injury to reduce the risk of exsanguination. Consequently, studying the activation of the coagulation system during blood loss (BL) is of upmost importance so new therapies and treatment algorithms, such as fluid resuscitation, can be developed. However, using invasive methods to experimentally induce BL is challenging to perform in humans.Lower body negative pressure (LBNP) is a technique that is used as a noninvasive surrogate to study many of the physiological responses to BL (4, 15, 18). LBNP sequesters circulating blood in the lower body, thereby reducing central blood volume and mimicking hemodynamic responses generated during BL (4,15,18). However, it is unclear if markers of coagulation system activation respond similarly during these protocols. Reductions in central blood volume by LBNP (38) ...

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Section: Discussionmentioning

confidence: 99%

Coagulation changes during lower body negative pressure and blood loss in humans

Helmond

Johnson

Curry

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…In burn patients, Park et al (24) reported that only thrombelastography analysis of whole blood revealed that patients were in a hypercoagulable state. Like in our experiment, hypercoagulability was not detectable by plasma-based clotting assays (PT and aPTT).…”

Section: Discussionmentioning

confidence: 99%

Thromboelastometry (TEM®) Findings in Disseminated Intravascular Coagulation in a Pig Model of Endotoxinemia

Schöchl

Solomon²,

Schulz

et al. 2010

Mol Med

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Standard coagulation tests have a low specificity and sensitivity for diagnosing disseminated intravascular coagulation. The aim of this study was to determine whether whole blood thromboelastometry (TEM) detects lipopolysaccharide (LPS)-induced changes in coagulation. Blood samples from 10 pigs were drawn at baseline, before and at the end of LPS infusion and 2, 3, 4 and 5 h after the start of endotoxinemia. Simultaneous to TEM, standard coagulation tests and extended coagulation analysis including tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) were performed. Endotoxinemia resulted in a significant acceleration of the nonactivated TEM (NATEM) clotting time 2 h after the end of LPS infusion; in contrast, the changes in international normalized ratio and activated partial thromboplastin time suggested delayed initiation of coagulation. NATEM maximum clot firmness (MCF) and fibrin-based thromboelastometry test (FIBTEM ® )-MCF decreased significantly from baseline until the last time point (from 64.6 ± 7.8 and 35.1 ± 12.8 mm to 52.8 ± 4.6 and 21.4 ± 11.8 mm, respectively; P = 0.01 for both parameters). A sharp, transient increase of t-PA had no effect on maximum lysis in the NATEM test. PAI-1 increased significantly 3 h after the start of LPS infusion, paralleled by a decrease in maximum lysis. In conclusion, TEM was superior to standard coagulation tests in reflecting initial activation of coagulation during endotoxinemia. TEM further suggested consumption of coagulation substrate; at the same time, inhibition of plasminogen activation was accompanied by improved clot stability. Further investigations are necessary to establish the clinical relevance of these findings.

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“…[19] However, with increasing tissue trauma, the progressively increasing catecholamine level further enhances thrombin generation, which exceeds the released level of tPA and PC; the net hemostatic effect is hypercoagulability. [19,20] This pathway may underlie the changes in coagulation function in group 3. In group 4, both R time and K time were signifi cantly prolonged compared with those of the other groups, and MA significantly decreased.…”

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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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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Thromboelastography as a Better Indicator of Hypercoagulable State After Injury Than Prothrombin Time or Activated Partial Thromboplastin Time

Cited by 274 publications

References 57 publications

Coagulation changes during lower body negative pressure and blood loss in humans

Coagulation changes during lower body negative pressure and blood loss in humans

Thromboelastometry (TEM®) Findings in Disseminated Intravascular Coagulation in a Pig Model of Endotoxinemia

Diverse coagulopathies in a rabbit model with different abdominal injuries

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