Massive blood transfusion for trauma

Hess, John R.; Zimrin, Ann B.

doi:10.1097/01.moh.0000177828.85904.70

Cited by 58 publications

(38 citation statements)

References 47 publications

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“…Enhanced insight into the pathogenesis of posttraumatic SIRS has lead to less liberal blood transfusion habits. 59 It has been shown that blood transfusion itself induces a host immunoactivation with possible increase or even induction of SIRS and MOF. 60 -63 Furthermore the use of RBC transfusions is associated with a considerable risk of infections and hemolytic transfusion reactions.…”

Section: Therapeutic Consequencesmentioning

confidence: 99%

Erythropoiesis in Multiply Injured Patients

Robinson

Hostmann

Matenov

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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Posttraumatic anemia in multiply injured patients is caused by hemorrhage, reduced red blood cell survival, and impaired erythropoiesis. Trauma-induced hyperinflammation causes impaired bone-marrow function by means of blunted erythropoietin (EPO) response, reduced iron availability, suppression and egress of erythroid progenitor cells. To treat posttraumatic anemia in severely injured patients, symptomatic therapy by blood transfusion is not sufficient. Furthermore, EPO, iron, and the use of red cell substitutes should be considered. The posttraumatic systemic inflammatory response syndrome (SIRS) induces posttraumatic anemia. Thus, a worsening of SIRS by a "second-hit" through blood transfusion ought to be avoided.

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Section: Therapeutic Consequencesmentioning

confidence: 99%

Erythropoiesis in Multiply Injured Patients

Robinson

Hostmann

Matenov

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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“…In search for effective treatments, efforts have been made to evaluate outcomes from transfusion of blood products, such as fresh whole blood, fresh frozen plasma (FFP), cryoprecipitate, and red blood cells (RBC). Recent published retrospective studies suggested potential benefits of transfusion of a higher ratio of fibrinogen to red blood cell unit ratio in trauma patients [6,7,[64][65][66][67][68][69][70][71][72].…”

Section: Fibrinogen Supplementationmentioning

confidence: 99%

Fibrinogen metabolic responses to trauma

Martini

2009

Scand J Trauma Resusc Emerg Med

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Coagulation complications are significant contributors to morbidity and mortality in trauma patients. Although the lethal triad of hypothermia, acidosis and coagulopathy has been recognized for over a decade, the underlying mechanisms related to the development of coagulopathy remain unclear. Recent data suggest that decreased fibrinogen levels contribute to the development of coagulation disorders. Thus, regulation of fibrinogen availability, not fully understood at present, may play an important role in survival of trauma patients. This review summarizes the recent findings of the studies that have explored mechanisms related to changes in fibrinogen availability following trauma-related events. Trauma alters fibrinogen metabolism in a variety of ways: hemorrhage -accelerated fibrinogen breakdown; hypothermia -inhibited fibrinogen synthesis; and, acidosis -accelerated fibrinogen breakdown. However, hemorrhage, hypothermia andcidosis all result in a consistent outcome of fibrinogen availability deficit, supporting the notion of fibrinogen supplementation in trauma patients with coagulation defects. Future prospective clinical trials are needed to confirm the beneficial effects of fibrinogen supplementation in trauma patients with bleeding complications.

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“…Despite aggressive fluid replacement, the patient's hemodynamic status remained time temperatures often exceed 49ºC [120ºF]), ensuring shelf life, and coordinating resupply caused major difficulties for our blood bank in addition to the normal complications associated with maintaining stored blood. 5 Indications for the use of fresh whole blood (FWB) have been reported. Jevtic et al 6 (Figure 2).…”

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confidence: 99%