Coagulopathy in Traumatic Brain Injury and Its Correlation with Progressive Hemorrhagic Injury: A Systematic Review and Meta-Analysis

Yuan, Qiang; Sun, Yirui; Wu, Xing; Yu, Jian; Li, Zhiqi; Du, Zhuoying; Wu, Xuehai; Zhou, Lei; Hu, Jin

doi:10.1089/neu.2015.4205

Cited by 80 publications

(64 citation statements)

References 34 publications

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“…5,6,9 However, very little is known about the clinical implications of DCR for patients with TBI and HS, especially considering the coagulopathy that often accompanies TBI. 1,10–15 Additionally, there is virtually no data on how DCR affects neurologic status and outcomes with concomitant TBI.…”

Section: Introductionmentioning

confidence: 99%

Outcomes after concomitant traumatic brain injury and hemorrhagic shock

Galvagno

Fox

Appana

et al. 2017

Journal of Trauma and Acute Care Surgery

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Background Often the clinician is faced with a diagnostic and therapeutic dilemma in patients with concomitant traumatic brain injury (TBI) and hemorrhagic shock (HS), as rapid deterioration from either can be fatal. Knowledge about outcomes following concomitant TBI and HS may help prioritize the emergent management of these patients. We hypothesized that patients with concomitant TBI and HS (TBI+HS) had worse outcomes and required more intensive care compared to patients with only one of these injuries. Methods This is a post-hoc analysis of the Pragmatic, Randomized Optimal Platelets and Plasma Ratios (PROPPR) trial. TBI was defined by a head abbreviated injury scale >2. HS was defined as a base excess ≤ −4 and/or shock index ≥ 0.9. The primary outcome for this analysis was mortality at 30 days. Logistic regression, using generalized estimating equations (GEE), was used to model categorical outcomes. Results 670 patients were included. Patients with TBI+HS had significantly higher lactate (median 6.3; IQR 4.7,9.2) compared to the TBI group (median 3.3; IQR 2.3,4). TBI+HS patients had higher activated prothrombin times and lower platelet counts. Unadjusted mortality was higher in the TBI+HS (51.6%) and TBI (50%) groups compared to the HS (17.5%) and neither group (7.7%). Adjusted odds of death in the TBI and TBI+HS groups were 8.2 (95% CI, 3.4–19.5) and 10.6 (95% CI, 4.8–23.2) times higher, respectively. Ventilator, ICU- and hospital-free days were lower in the TBI and TBI+HS groups compared to the other groups. Patients with TBI+HS or TBI had significantly greater odds of developing a respiratory complication compared to the neither group. Conclusions The addition of TBI to HS is associated with worse coagulopathy prior to resuscitation, and increased mortality. When controlling for multiple known confounders, the diagnosis of TBI alone or TBI+HS was associated with significantly greater odds of developing respiratory complications.

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Section: Introductionmentioning

confidence: 99%

Outcomes after concomitant traumatic brain injury and hemorrhagic shock

Galvagno

Fox

Appana

et al. 2017

Journal of Trauma and Acute Care Surgery

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“…6 Additionally, post-TBI coagulation disorders are associated with progressive hemorrhagic injury (PHI) and ICH, particularly in older patients with intraparenchymal contusions. 15,18,19 Laboratory manifestations of fibrinolysis are associated with PHI, poorer outcomes, and the need for neurosurgical intervention. Furthermore, patients who displayed evidence of abnormal clot formation dynamics in their clots were approximately five times more likely to die from PHI versus patients with clot dynamics values within reference ranges.…”

Section: Coagulopathy As Prognostic Indicatormentioning

confidence: 99%

“…Most data underlying the initiation and progression of coagulopathy are speculative and not linked to causative data. The heterogeneity with respect to defining both TBI and coagulopathy presents additional challenges when attempting to study this complicated disease state 18 (►Table 1). One key factor in our understanding of this disease process may be the recognition that coagulopathy alone does not result in parenchymal bleeding without the presence of micro or macrovascular injury.…”

Section: Hemorrhagic Expansion and Mechanism Of Hemostatic Derangemenmentioning

confidence: 99%

“…A recent meta-analysis described inconsistencies between CCA results (particularly with aPTT and PT) and post-TBI hemocoagulative alterations. 18 "Global" clotting assays such as the viscoelastic tests (VETs) (e.g., rotational thromboelastometry [ROTEM; TEM International] and thromboelastography [TEG; Haemonetics]) and thrombin generation tests may provide more detailed, useful data concerning the body's overall ability to achieve hemostasis (i.e., kinetics of thrombin generation and clot strength during clot formation). 32 ►Fig.…”

Section: New Diagnostic Tools For the Coagulopathy Of Tbimentioning

confidence: 99%

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Changes in Coagulation following Brain Injury

Maegele

Aversa

Marsee

et al. 2020

Semin Thromb Hemost

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Traumatic brain injury (TBI) is a worldwide public health concern due to increasing mortality, affecting around 10 million patients per year. A wide variety of clinical presentations are a function of the magnitude of injury and the anatomical perturbation of the brain parenchyma, supporting structures, and cerebral vasculature, with subsequent alteration of the blood–brain barrier. These disturbances correspond with the evolution of intracerebral hemorrhage and clinical outcomes. The associated hemostatic alterations associated with TBI are caused by the disruption of the delicate balance between bleeding and thrombosis formation, which can exacerbate initial injury. TBI-associated coagulopathy is a function of a cross-talk between coagulation and inflammation, with varying influences on the immunomodulation and regulation of coagulation that occur on platelets and the endothelium of injured TBI patients. In addition to the severity of initial injury, the following factors modulate the hemocoagulative response to TBI: time from the onset of injury to treatment, age, gender, catecholamine secretion, platelet dysfunction, endotheliopathy, premorbid anticoagulation, fibrinolysis, tissue factor, and activated protein C contribution. All these entities are intertwined and influence the pathologic evolution of TBI. These factors have implications for therapeutic options such as the choice of blood components for transfusion and hemostatic agents such as tranexamic acid. Monitoring hemostatic changes of TBI patients requires an understanding of these interactions between immunology and coagulation, which can be discerned by point-of-care viscoelastic testing with specific limitations. This review considers the implications of these interrelated influences on the evaluation of coagulopathy in TBI.

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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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Coagulopathy in Traumatic Brain Injury and Its Correlation with Progressive Hemorrhagic Injury: A Systematic Review and Meta-Analysis

Cited by 80 publications

References 34 publications

Outcomes after concomitant traumatic brain injury and hemorrhagic shock

Outcomes after concomitant traumatic brain injury and hemorrhagic shock

Changes in Coagulation following Brain Injury

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

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