The contemporary timing of trauma deaths

Bardes, James M.; Inaba, Kenji; Schellenberg, Morgan; Grabo, Daniel; Strumwasser, Aaron; Matsushima, Kazuhide; Clark, Damon; Brown, Niquelle; Δημητριάδης, Δημήτριος

doi:10.1097/ta.0000000000001882

Cited by 71 publications

(50 citation statements)

References 17 publications

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“…The deficiencies seen at the time of ED arrival were mostly resolved by the next time point 8 h later (ADP and collagen aggregation, TEG MA, and PCF). This dysfunction occurs in the critical early hours after injury, during which most mortality attributable to hemorrhage after trauma takes place . The recovery time is not due to the loss of data from non‐survivors in later time points, as all patients who did not survive the full 72 h were excluded from this analysis.…”

Section: Discussionmentioning

confidence: 99%

Platelets retain inducible alpha granule secretion by P‐selectin expression but exhibit mechanical dysfunction during trauma‐induced coagulopathy

John

Newton

Martin

et al. 2019

Journal of Thrombosis and Haemostasis

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Platelets in trauma‐induced coagulopathy (TIC) are impaired, but the mechanism is not known. We performed comprehensive longitudinal platelet function testing in trauma patient samples. Platelets in TIC are widely impaired early after injury, but platelet activatability is intact. This suggests a mechanism of transient platelet cytoskeletal/integrin dysfunction during TIC. Summary BackgroundTrauma‐induced coagulopathy (TIC) is a common and deadly bleeding disorder. Platelet dysfunction is present during TIC, but its mechanisms remain unclear. Platelets are currently thought to become “exhausted,” a state in which they have released their granule contents and can no longer aggregate or contract. MethodsThis prospective observational cohort study tested the hypothesis that platelet exhaustion is present during TIC and characterized the early time course of platelet dysfunction. Blood was collected from 95 adult trauma patients at a Level I trauma center at time of Emergency Department arrival and several time points over 72 h. Platelet activation state and function were characterized using CD62P (P‐selectin) and PAC‐1 surface membrane staining, platelet function analyzer (PFA‐100), aggregometry, viscoelastic platelet mapping, and, to test for exhaustion, their ability to express CD62P after ex vivo adenosine diphosphate (ADP) agonism. Platelet function was compared between patients with and without TIC, defined by prothrombin time ≥18 s. ResultsPlatelets in TIC showed no initial increase in their level of surface activation markers or impairment of their capacity to express CD62P in response to ADP stimulation. However, TIC platelets were impaired in nearly all functional assays, spanning adhesion, aggregation, and contraction. These effects largely remained after controlling for platelet count and fibrinogen concentration and resolved after 8 h. ConclusionThe TIC platelets exhibit early impairment of adhesion, aggregation, and contraction with retained alpha granule secretion ability, suggesting a specific mechanism of cytoskeletal or integrin dysfunction that is not a result of more general platelet exhaustion.

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Section: Discussionmentioning

confidence: 99%

Platelets retain inducible alpha granule secretion by P‐selectin expression but exhibit mechanical dysfunction during trauma‐induced coagulopathy

John

Newton

Martin

et al. 2019

Journal of Thrombosis and Haemostasis

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“…17,18 Most fatalities in major trauma occur during the first 24 hours of injury with massive hemorrhage and traumatic brain injury. [19][20][21][22][23] The clinical course in those who survive is one of sepsis, multiorgan failure, or recovery. Several fibrinolytic phenotypes are recognized at presentation in trauma patients based on viscoelastographic findings.…”

Section: Historical Aspects: Discovery Of Fibrinolysis In Traumamentioning

confidence: 99%

The Central Role of Fibrinolytic Response in Trauma-Induced Coagulopathy: A Hematologist's Perspective

Kwaan

2019

Semin Thromb Hemost

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Severe trauma is the leading cause of death globally. Though improved resuscitation, particularly early initiation, has reduced the 24-hour mortality rate, the overall morbidity and 30-day mortality remain high mostly due to massive hemorrhage and head injury in the early stages and sepsis and multiorgan failure later on. With recent clinical trials of antifibrinolytic treatment with tranexamic acid, and with the observations that fibrinolytic activity varies widely among the injured patients, the role of the fibrinolytic system in trauma has become a major focus of investigations in trauma-induced coagulopathy. Most of the body's response to trauma involves the endothelium, tissue factor release, and platelet activation. In addition, there are inflammatory and immune responses. All these events directly or indirectly affect the fibrinolytic system. A full understanding of these mechanisms has translational implications on the management of these patients. In this article, the multifaceted responses of fibrinolysis following injury are reviewed.

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“…Despite major advances in the treatment of trauma-haemorrhage, it is important to recognise the limitations in contemporary resuscitation practices. Haemorrhage remains the dominant cause of preventable death from injury, and massive haemorrhage carries a mortality of around 50% (Stanworth et al, 2016, Bardes et al, 2018. Outcomes in patients requiring damage control surgery for intra-abdominal haemorrhage have not improved significantly in the last decade (Harvin et al, 2017.…”

Section: Future Directionsmentioning

confidence: 99%

“…An estimated 1 billion injuries requiring healthcare occur each year, accounting for around 5 million deaths and 10% of the total global burden of disease (Global Burden of Disease Collaborators, 2017). Uncontrolled haemorrhage is the leading cause of preventable death from injury, the majority of which occur within the first three hours of hospital admission (Bardes et al, 2018). Modern trauma systems and resuscitation practices have therefore evolved to prioritise early definitive haemorrhage control whilst supporting haemostasis during active bleeding.…”

Section: Manuscript Text Introductionmentioning

confidence: 99%

What's new for trauma haemorrhage management?

2019

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Uncontrolled haemorrhage is the leading cause of preventable death from injury and is a major contributor to the global burden of disease. The majority of deaths resulting from bleeding occur within the first 3 hours of hospital admission, and the window for meaningful intervention is therefore extremely small. Resuscitative efforts during active bleeding should focus on maintaining haemostatic function with blood product transfusion and early administration of tranexamic acid. Achieving control of haemorrhage is the overarching treatment priority and may require temporising measures before definitive surgical or radiological intervention. This review summarizes the contemporary approaches to resuscitation of bleeding trauma patients, options for achieving haemorrhage control, and current areas of active research including organ protective resuscitation and suspended animation.

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The contemporary timing of trauma deaths

Abstract: Epidemiologic, level IV.

Cited by 71 publications

References 17 publications

Platelets retain inducible alpha granule secretion by P‐selectin expression but exhibit mechanical dysfunction during trauma‐induced coagulopathy

Platelets retain inducible alpha granule secretion by P‐selectin expression but exhibit mechanical dysfunction during trauma‐induced coagulopathy

The Central Role of Fibrinolytic Response in Trauma-Induced Coagulopathy: A Hematologist's Perspective

What's new for trauma haemorrhage management?

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