The Use of Higher Platelet

Hallet, Julie; Lauzier, François; Mailloux, Olivier; Trottier, Vincent; Archambault, Patrick; Zarychanski, Ryan; Turgeon, Alexis F.

doi:10.1097/ccm.0b013e31829a6ecb

Cited by 62 publications

(13 citation statements)

References 60 publications

(96 reference statements)

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“…However, the results of these studies may have been affected by survival bias [100-103]. Other published studies have not shown any improvement in survival utilizing this approach [104-106]. In contrast, two recent studies have still shown a benefit of using a high FFP-blood ratio after adjusting for survival bias [107, 108].…”

Section: Transfusion Of Blood and Plasmamentioning

confidence: 99%

Coagulopathy After Severe Pediatric Trauma

Christiaans¹,

Duhachek-Stapelman

Russell

et al. 2014

Shock

102

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Trauma remains the leading cause of morbidity and mortality in the United States among children from the age 1 year to 21 years old. The most common cause of lethality in pediatric trauma is traumatic brain injury (TBI). Early coagulopathy has been commonly observed after severe trauma and is usually associated with severe hemorrhage and/or traumatic brain injury. In contrast to adult patients, massive bleeding is less common after pediatric trauma. The classical drivers of trauma-induced coagulopathy (TIC) include hypothermia, acidosis, hemodilution and consumption of coagulation factors secondary to local activation of the coagulation system following severe traumatic injury. Furthermore, there is also recent evidence for a distinct mechanism of TIC that involves the activation of the anticoagulant protein C pathway. Whether this new mechanism of posttraumatic coagulopathy plays a role in children is still unknown. The goal of this review is to summarize the current knowledge on the incidence and potential mechanisms of coagulopathy after pediatric trauma and the role of rapid diagnostic tests for early identification of coagulopathy. Finally, we discuss different options for treating coagulopathy after severe pediatric trauma.

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Section: Transfusion Of Blood and Plasmamentioning

confidence: 99%

Coagulopathy After Severe Pediatric Trauma

Christiaans¹,

Duhachek-Stapelman

Russell

et al. 2014

Shock

102

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“…These surrogates are considered “validated” by their strong associations with injury mortality, and have become standard covariates for stratification or adjustment by injury severity. Because of time-honored conventions, trusted validation, lack of reliable alternatives, and the subtlety of collider bias, the widespread research use of these surrogate biomarkers of injury severity is likely to persist and frustrate systematic reviews 40,41 due to the unpredictable occurrence and variable impact of collider bias (e.g., conflicting findings) on trauma resuscitation research.…”

Section: Discussionmentioning

confidence: 99%

Collider bias in trauma comparative effectiveness research: The stratification blues for systematic reviews

Junco¹,

Bulger²,

Fox³

et al. 2015

Injury

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Background Collider bias, or stratifying data by a covariate consequence rather than cause (confounder) of treatment and outcome, plagues randomized and observational trauma research. Of the seven trials of prehospital hypertonic saline in dextran (HSD) that have been evaluated in systematic reviews, none found an overall between-group difference in survival, but four reported significant subgroup effects. We hypothesized that an avoidable type of collider bias often introduced inadvertently into trauma comparative effectiveness research could explain the incongruous findings. Methods The two most recent trials, a single-site pilot and a multi-site pivotal study, provided data for a secondary analysis to more closely examine the potential for collider bias. The two trials had followed the a priori statistical analysis plan to subgroup patients by a post-randomization covariate and well-established surrogate for bleeding severity, massive transfusion (MT), ≥10 units of red blood cells within 24 hours of admission. Despite favorable HSD effects in the MT subgroup, opposite effects in the non-transfused subgroup halted the pivotal trial early. In addition to analyzing the data from the two trials, we constructed causal diagrams and performed a meta-analysis of the results from all seven trials to assess the extent to which collider bias could explain null overall effects with subgroup heterogeneity. Results As in previous trials, HSD induced significantly greater increases in systolic blood pressure (SBP) from prehospital to admission than control crystalloid (p=0.003). Proportionately more HSD than control decedents accrued in the non-transfused subgroup, but with paradoxically longer survival. Despite different study populations and a span of over 20 years across the seven trials, the reported mortality effects were consistently null, summary RR=0.99 (p=0.864, homogeneity p=0.709). Conclusions HSD delayed blood transfusion by modifying standard triggers like SBP with no detectable effect on survival. The reported heterogeneous HSD effects in subgroups can be explained by collider bias that trauma researchers can avoid by improved covariate selection and data capture strategies.

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“…In December 2013, Hallet et al [50] systematically reviewed randomized control and observational studies to determine if benefit existed for high ratio Platelet: RBC transfusion (another term for 1:1:1 therapy). Their review suggested that insufficient evidence existed to support high ratio therapy in all bleeding patients, though early survival benefit did exist in massively transfused patients.…”

Section: Hemostatic Resuscitationmentioning

confidence: 99%

Trauma-Induced Coagulopathy

Simmons

Pittet

Pierce

2014

Curr Anesthesiol Rep

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Trauma is the leading cause of death among people under the age of 44. Hemorrhage is a major contributor to deaths related to trauma in the first 48 h. Accordingly, the management of these patients is a time-sensitive and critical affair that anesthesiologists responsible for surgical resuscitation will face. Coagulopathy associated with trauma exists in one-third of all severely injured patients upon presentation to the hospital. Trauma patients presenting with coagulopathy have significantly higher mortality. This trauma-induced coagulopathy (TIC) must be managed adroitly in the resuscitation of these patients. Recent advancements in our understanding of TIC have led to new protocols and therapy guidelines. Anesthesiologists must be aware of these to effectively manage this form of shock. TIC driven by a combination of endogenous biological processes, as well as iatrogenic causes, can ultimately lead to the lethal triad of hypothermia, acidemia, and coagulopathy. Providers should understand how to promptly diagnose TIC and be aware of the early indicators of massive transfusion. The use of common laboratory studies and patient vital signs serve as our current guide, but the importance of each is still under debate. Thromboelastography is a tool used often in the diagnosis of TIC and can be used to guide blood product transfusion. Certain pharmaceutical strategies and non-transfusion strategies also exist, which aid in the management of hemorrhagic shock. Damage control surgery, rewarming, tranexamic acid, and 1:1:1 transfusion protocols are promising methods used to treat the critically wounded. Though protocols have been developed, controversies still exist on the optimal resuscitation strategy.

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The Use of Higher Platelet

Abstract: There is insufficient evidence to strongly support the use of a precise platelet:RBC ratio for trauma resuscitation, especially in nonmassively bleeding patients. Randomized controlled trials evaluating both the safety and efficacy of liberal platelet transfusions are warranted.

Cited by 62 publications

References 60 publications

Coagulopathy After Severe Pediatric Trauma

Coagulopathy After Severe Pediatric Trauma

Collider bias in trauma comparative effectiveness research: The stratification blues for systematic reviews

Trauma-Induced Coagulopathy

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