Venous thromboembolic events in critically ill traumatic brain injury patients

Skrifvars, Markus B.; Bailey, Michael; Presneill, Jeffrey; French, Craig; Nichol, Alistair; Little, Lorraine; Duranteau, Jacques; Huet, Olivier; Haddad, Samir H.; Arabi, Yaseen M.; McArthur, Colin; Cooper, Jamie; Bellomo, Rinaldo

doi:10.1007/s00134-016-4655-2

Cited by 94 publications

(89 citation statements)

References 33 publications

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“…Our study revealed that almost half of the VTE events were located in neck and upper extremity veins, and only 2 cases were lower extremity DVTs. This might be an important new finding since many previous studies only examined the lower extremities when screening for DVTs in the ICU . This may also be clinically relevant, since one study of ICU patients revealed that DVTs remote from the legs was associated with increased risk for PE and prolonged ICU LOS …”

Section: Discussionmentioning

confidence: 80%

Venous thromboembolism in the critically ill: A prospective observational study of occurrence, risk factors and outcome

Beitland

Wimmer

Lorentsen

et al. 2019

Acta Anaesthesiol Scand

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Background:The aim of the study was to explore occurrence, risk factors and outcome of venous thromboembolism (VTE) in intensive care unit (ICU) patients. Methods: Prospective observational study of ICU patients receiving thromboprophylaxis at Oslo University Hospital in Norway. Adult medical and surgical patients with ICU length of stay (LOS) longer than 48 hours were included. For detection of VTE, Doppler ultrasound screening of neck, upper and lower extremity veins was used, and computed tomography angiography when clinically indicated for any medical reason.Results: Among 70 included patients, 79% were males and mean age was 62 (±12.1) years. All received thromboprophylaxis with dalteparin, and 44 (63%) used graduated compression stockings. VTE was found in 19 (27%) patients; deep vein thrombosis in 15 (21%) and pulmonary embolism in 4 (6%). Among the VTEs, 11 (58%) presented within the first 48 hours after admission, two (11%) were located in the lower limbs and five (26%) were symptomatic. Risk factors for VTE in multivariable analyses were malignancy, abdominal surgery and SAPS II score <41 with an AuROC (95% CI) of 0.72 (0.58-0.85, P = 0.01). Patients with and without VTE had comparable ICU LOS (13 vs 11 days, P = 0.27) and mortality (16% vs 20%, P = 0.72). Conclusion:Venous thromboembolism was observed in 27% of ICU patients receiving thromboprophylaxis. Factors associated with increased risk of VTE were malignancy, abdominal surgery and SAPS II score <41. Presence of VTE did not impact on patient outcome.

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Section: Discussionmentioning

confidence: 80%

Venous thromboembolism in the critically ill: A prospective observational study of occurrence, risk factors and outcome

Beitland

Wimmer

Lorentsen

et al. 2019

Acta Anaesthesiol Scand

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“…Moreover, in a study examining the potential antithrombotic benefit of HCQ in patients with anti‐phospholipid syndrome, patients treated with HCQ in addition to standard oral anticoagulant therapy had no increased bleeding events . The trauma literature demonstrates persistently elevated VTE rates despite the use of gold standard therapy via low‐molecular‐weight heparins, suggesting that perhaps targeting the coagulation cascade alone is insufficient in this high‐risk patient population . The addition of platelet inhibition for DVT prophylaxis in trauma has been advocated by some but remains controversial .…”

Section: Discussionmentioning

confidence: 99%

“…56,57 The trauma literature demonstrates persistently elevated VTE rates despite the use of gold standard therapy via low-molecular-weight heparins, suggesting that perhaps targeting the coagulation cascade alone is insufficient in this high-risk patient population. 3,4,[58][59][60][61] The addition of platelet inhibition for DVT prophylaxis in trauma has been advocated by some but remains controversial. [61][62][63] Whether HCQ represents a potential VTE thromboprophylaxis strategy in addition to current standard of care warrants further clinical investigation.…”

Section: Discussionmentioning

confidence: 99%

Platelet‐derived extracellular vesicles released after trauma promote hemostasis and contribute to DVT in mice

Dyer

Alexander

Hassoune

et al. 2019

Journal of Thrombosis and Haemostasis

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Background Traumatic injury can lead to dysregulation of the normal clotting system, resulting in hemorrhagic and thrombotic complications. Platelet activation is robust following traumatic injury and one process of platelet activation is to release of extracellular vesicles (PEV) that carry heterogenous cargo loads and surface ligands. Objectives We sought to investigate and characterize the release and function of PEVs generated following traumatic injury. Methods PEV content and quantity in circulation following trauma in humans and mice was measured using flow cytometry, size exclusion chromatography, and nanoparticle tracking analysis. PEVs were isolated from circulation and the effects on thrombin generation, bleeding time, hemorrhage control, and thrombus formation were determined. Finally, the effect of hydroxychloroquine (HCQ) on PEV release and thrombosis were examined. Results Human and murine trauma results in a significant release of PEVs into circulation compared with healthy controls. These PEVs result in abundant thrombin generation, increased platelet aggregation, decreased bleeding times, and decreased hemorrhage in uncontrolled bleeding. Conversely, PEVs contributed to enhanced venous thrombus formation and were recruited to the developing thrombus site. Interestingly, HCQ treatment resulted in decreased platelet aggregation, decreased PEV release, and reduced deep vein thrombosis burden in mice. Conclusions These data demonstrate that trauma results in significant release of PEVs which are both pro‐hemostatic and pro‐thrombotic. The effects of PEVs can be mitigated by treatment with HCQ, suggesting the potential use as a form of deep vein thrombosis prophylaxis.

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“…Currently, there is controversy within the literature regarding the exact nature of hemostatic perturbations after TBI, and evidence exists for the presence of both a hypercoagulable and hypocoagulable state [2]. For example, while the initial head injury often leads to increased bleeding tendency and the exacerbation of hemorrhagic lesions [2,[46][47][48], TBI is also independently associated with an increased risk for venous thromboembolism [49][50][51][52] and ischemic stroke [53][54][55][56][57]. Autopsy studies have also revealed that micro-thrombosis is present in the majority patients who have died from head trauma [58].…”

Section: Hemostatic Disturbance In Tbimentioning

confidence: 99%

Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol

Fletcher‐Sandersjöö

Maegele

Bellander

2020

IJMS

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Despite improvements in medical triage and tertiary care, traumatic brain injury (TBI) remains associated with significant morbidity and mortality. Almost two-thirds of patients with severe TBI develop some form of hemostatic disturbance, which contributes to poor outcome. In addition, the complement system, which is abundant in the healthy brain, undergoes significant intra- and extracranial amplification following TBI. Previously considered to be structurally similar but separate systems, evidence of an interaction between the complement and coagulation systems in non-TBI cohorts has accumulated, with the activation of one system amplifying the activation of the other, independent of their established pathways. However, it is not known whether this interaction exists in TBI. In this review we summarize the available literature on complement activation following TBI, and the crosstalk between the complement and coagulation systems. We demonstrate how the complement system interacts with the coagulation cascade by activating the intrinsic coagulation pathway and by bypassing the initial cascade and directly producing thrombin as well. This crosstalk also effects platelets, where evidence points to a relationship with the complement system on multiple levels, with complement anaphylatoxins being able to induce disproportionate platelet activation and adhesion. The complement system also stimulates thrombosis by inhibiting fibrinolysis and stimulating endothelial cells to release prothrombotic microparticles. These interactions see clinical relevance in several disorders where a deficiency in complement regulation seems to result in a prothrombotic clinical presentation. Finally, based on these observations, we present the outline of an observational cohort study that is currently under preparation and aimed at assessing how complement influences coagulation in patients with isolated TBI.

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Venous thromboembolic events in critically ill traumatic brain injury patients

Abstract: Despite mechanical and pharmacological prophylaxis, VTE occurs in one out of every five patients with TBI treated in the ICU. Higher age, greater weight and greater severity of TBI increase the risk. The development of VTE was not associated with excess mortality.

Cited by 94 publications

References 33 publications

Venous thromboembolism in the critically ill: A prospective observational study of occurrence, risk factors and outcome

Venous thromboembolism in the critically ill: A prospective observational study of occurrence, risk factors and outcome

Platelet‐derived extracellular vesicles released after trauma promote hemostasis and contribute to DVT in mice

Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol

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