Thromboelastography Defines Late Hypercoagulability After TBI: A Pilot Study

Massaro, Allie; Doerfler, Sean; Nawalinski, Kelsey; Michel, Bernard; Driscoll, Nicolette; Ju, Connie; Patel, Hiren; Quattrone, Francis; Frangos, Suzanne; Maloney-Wilensky, Eileen; Grady, M. Sean; Stein, Sherman C.; Kasner, Scott E.; Kumar, Monisha A.

doi:10.1007/s12028-014-0051-3

Cited by 31 publications

(17 citation statements)

References 42 publications

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“…Two studies also found that platelets became hyperactive following their initial dysfunction [29,37]. This was supported by a TEG study that noted increasing maximum amplitude (MA) levels 7 days after TBI [57] (MA represents clot strength that is mainly dependent on platelet function). Platelet hyperactivity could explain the increased risk of thrombosis seen in TBI patients [10][11][12][13][14][15][16][17][18]58], but future studies are warranted to assess its clinical significance.…”

Section: Primary Hemostasismentioning

confidence: 82%

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

et al. 2020

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Almost two-thirds of patients with severe traumatic brain injury (TBI) develop some form of hemostatic disturbance, which contributes to poor outcome. While the initial head injury often leads to impaired clot formation, TBI is also associated with an increased risk of thrombosis. Most likely there is a progression from early bleeding to a later prothrombotic state. In this paper, we systematically review the literature on the time course of hemostatic disruptions following TBI. A MEDLINE search was performed for TBI studies reporting the trajectory of hemostatic assays over time. The search yielded 5,049 articles, of which 4,910 were excluded following duplicate removal as well as title and abstract review. Full-text assessment of the remaining articles yielded 33 studies that were included in the final review. We found that the first hours after TBI are characterized by coagulation cascade dysfunction and hyperfibrinolysis, both of which likely contribute to lesion progression. This is then followed by platelet dysfunction and decreased platelet count, the clinical implication of which remains unclear. Later, a poorly defined prothrombotic state emerges, partly due to fibrinolysis shutdown and hyperactive platelets. In the clinical setting, early administration of the antifibrinolytic agent tranexamic acid has proved effective in reducing head-injury-related mortality in a subgroup of TBI patients. Further studies evaluating the time course of hemostatic disruptions after TBI are warranted in order to identify windows of opportunity for potential treatment options.

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Section: Primary Hemostasismentioning

confidence: 82%

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

et al. 2020

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“…2 We similarly found no difference in our results after excluding all patients with dissections. Hypercoagulability occurs during post-TBI hospitalization and leads to a 3-to 4-fold increase in VTE regardless of the presence or timing of anticoagulation 31,32 ; nonetheless, the duration of the hypercoagulability and relationship to arterial clot and ischemic stroke remain unknown. As with ischemic stroke, we found no significant relationship between tSAH and VTE.…”

Section: Discussionmentioning

confidence: 99%

Subarachnoid Hemorrhage and Long-Term Stroke Risk After Traumatic Brain Injury

Morris

Cool

Merkler

et al. 2016

The Neurohospitalist

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“…Previous studies have used TEG to identify an early hypo-coagulable state after TBI [18,19]. Massaro et al, identified and reported high MA values compared to control at 24 h after TBI (GCS \ 12) [20]. TEG has also been suggested as a screening and monitoring device for deep venous thrombosis and pulmonary embolism following brain injury [21].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Thromboelastography (TEG) in Predicting Acute Trauma-Induced Coagulopathy (ATIC) in Isolated Severe Traumatic Brain Injury (iSTBI)

Albert¹,

Subramanian²,

Pati

et al. 2018

Indian J Hematol Blood Transfus

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To evaluate the efficacy of point-of-care thromboelastography (TEG) to predict acute trauma-induced coagulopathy (ATIC) in isolated severe TBI (iSTBI). We conducted an observational diagnostic cohort. Patients for whom TEG was performed before blood transfusion were stratified by conventional coagulation tests (CCTs) on admission and classified as ''ATIC'' (prothrombin time C 16.70 s; international normalized ratio C 1.27; activated partial thromboplastin time C 28.80 s) (n = 24) or ''no ATIC'' (n = 34). Univariate analysis to compare groups, receiver operating characteristic analysis to establish cut-off and diagnostic validation was done. Fifty-eight patients were included [32(25-45) years; 97% male; GCS 6.3 ± 1.5]. 41% developed ATIC. Compared to no-ATIC, ATIC group had significantly prolonged j-time (4.6 vs. 2.5 min; p = 0.01) and shortened a-angle (40.2°vs. 56.3°; p = 0.03). A cut-off for j-time C 3.7 (AUC 0.68 95% CI 0.54-0.82, specificity 70%, sensitivity 63%) and a angle B 48.0 (AUC 0.66, 95% CI 0.51-0.81, specificity 67%, sensitivity 67%) was established. The diagnostic accuracy of this cut-off for identifying ATIC, was 55.6% with sensitivity (81.8%) and specificity (14.3%). TEG may be a clinically sensitive test for identifying the underlying coagulopathy following TBI. However confirmation with CCTs is recommended.

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Thromboelastography Defines Late Hypercoagulability After TBI: A Pilot Study

Abstract: The data suggest a progressive and delayed hypercoagulable state observed days after initial TBI. The hypercoagulable state may reflect excess platelet activity.

Cited by 31 publications

References 42 publications

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

Time Course of Hemostatic Disruptions After Traumatic Brain Injury: A Systematic Review of the Literature

Subarachnoid Hemorrhage and Long-Term Stroke Risk After Traumatic Brain Injury

Efficacy of Thromboelastography (TEG) in Predicting Acute Trauma-Induced Coagulopathy (ATIC) in Isolated Severe Traumatic Brain Injury (iSTBI)

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