An Evaluation of the Impact of Apheresis Platelets Used in the Setting of Massively Transfused Trauma Patients

Perkins, Jeremy G.; Andrew, Cap P.; Spinella, Philip C.; Blackbourne, Lorne H.; Grathwohl, Kurt W.; Repine, Thomas B.; Ketchum, Lloyd H.; Waterman, Paige; Lee, Ruth E.; Beekley, Alec C.; Sebesta, James A.; Shorr, Andrew F.; Wade, Charles E.; Holcomb, John B.

doi:10.1097/ta.0b013e31819d8936

Cited by 139 publications

(136 citation statements)

References 17 publications

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“…Platelets are relatively unresponsive to collagen, ADP and arachidonic acid after trauma [54,55]. The pathophysiology underlying this dysfunction, which remains obscure, probably explains improved outcomes associated with platelet transfusion despite adequate platelet counts [56,57]. Lower platelet counts on hospital admission predict trauma mortality, even when within the normal range [58,59].…”

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confidence: 99%

The pathogenesis of traumatic coagulopathy

2014

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SummaryOver the last 10 years, the management of major haemorrhage in trauma patients has changed radically. This is mainly due to the recognition that many patients who are bleeding when they come in to the emergency department have an established coagulopathy before the haemodilution effects of fluid resuscitation. This has led to the use of new terminology: acute traumatic coagulopathy, acute coagulopathy of trauma shock or trauma‐induced coagulopathy. The recognition of acute traumatic coagulopathy is important, because we now understand that its presence is a prognostic indicator, as it is associated with poor clinical outcome. This has driven a change in clinical management, so that the previous approach of maintaining an adequate circulating volume and oxygen carrying capacity before, as a secondary event, dealing with coagulopathy, has changed to haemostatic resuscitation as early as possible. While there is as yet no universally accepted assay or definition, many experts use prolongation of the prothrombin time to indicate that there is, indeed, a coagulopathy. Hypoxia, acidosis and hypothermia and hormonal, immunological and cytokine production, alongside consumption and blood loss, and the dilutional effects of resuscitation may occur to varying extents depending on the type of tissue damaged, the type and extent of injury, predisposing to, or amplifying, activation of coagulation, platelets, fibrinolysis. These are discussed in detail within the article.

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confidence: 99%

The pathogenesis of traumatic coagulopathy

2014

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“…Recientemente se han publicado varios estudios [38][39][40][41][42][43][44][45][46][47] que han reportado que un aporte precoz y generoso de todos los hemoderivados, con una relación entre ellos cercana a 1:1, puede asociarse a menor mortalidad y disminución de las transfusiones totales en pacientes con trauma con riesgo de transfusión masiva (TM.) La TM traduce sangrado masivo, es decir, la pérdida de más de una volemia (70 ml/kg de peso) en 24 h. El sangrado masivo implica mayor morbilidad y mortalidad 10 .…”

Section: Aporte De Transfusiones En Pacientes Con Traumaunclassified

Reanimación con fluidos y hemoderivados en trauma

Ruíz

2014

Rev. méd. Chile

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“…Two studies addressed the effect of high vs. low PLT transfusion rates in 641 massively bleeding trauma patients, of whom 333 received high PLT/RBC ratio [40,41]. According to these two studies, patients receiving PLT/RBC in a high ratio had a significantly lower mortality (odds ratio 0.45, 95% confidence interval 0.37-0.55).…”

Section: Ratio Of the Platelet Transfusionmentioning

confidence: 99%

Trauma-induced coagulopathy and critical bleeding: the role of plasma and platelet transfusion

Ishikura

Kitamura

2017

j intensive care

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Hemorrhage is responsible for 30 to 40% of all trauma-related mortality. Among adult trauma patients, 94% of hemorrhage-related deaths occur within 24 h and approximately 60% of these deaths within 3 h of hospital admission. Therefore, appropriate initial fluid resuscitation for bleeding is crucial to avoid preventable traumarelated death. In particular, the resuscitation strategy must be designed to complement prompt correction of anemia, coagulopathies, and thrombocytopenia. Conventional damage control resuscitation (DCR) of patients with severe trauma and massive hemorrhage is usually begun with rapid infusion of 1000 to 2000 mL of crystalloid fluids with subsequent transfusion of type O or uncross-matched red blood cells (RBCs) without plasma such as fresh frozen plasma (FFP) or platelets (PLTs). However, this DCR technique often leads to several adverse events such as abdominal compartment syndrome, acute respiratory distress syndrome, multiple organ failure, and dilutional coagulopathy. Simultaneous transfusion of FFP and PLTs along with the first units of RBCs while minimizing crystalloid infusion was recently recommended as a renewed DCR strategy. This aggressive RBC transfusion with FFP and PLTs is not only essential for the correction of coagulopathies and thrombocytopenia but also has the potential to ensure a good outcome in trauma patients. Additionally, it is important to maintain the resuscitation ratios of FFP/RBC and PLT/RBC. Most recently, DCR has been advocated for rapid hemorrhage control through early administration of a mixture of FFP, PLTs, and RBCs in a balanced ratio of 1:1:1.

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An Evaluation of the Impact of Apheresis Platelets Used in the Setting of Massively Transfused Trauma Patients

Cited by 139 publications

References 17 publications

The pathogenesis of traumatic coagulopathy

The pathogenesis of traumatic coagulopathy

Reanimación con fluidos y hemoderivados en trauma

Trauma-induced coagulopathy and critical bleeding: the role of plasma and platelet transfusion

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