Trauma Blood Management: Avoiding the Collateral Damage of Trauma Resuscitation Protocols

Hematology ◽  
2010 ◽  
Vol 2010 (1) ◽  
pp. 463-464 ◽  
Author(s):  
Timothy Hannon

Abstract The use of high ratios of red blood cells to platelets and plasma in trauma resuscitation protocols is quickly gaining favor in civilian trauma centers. The use of higher ratios of coagulation factors to red blood cells has been shown to improve outcomes in both military and civilian centers, but does the evidence support the use of a 1:1:1 ratio, as has been suggested? There is growing evidence that the use of such high ratios may be excessive and potentially harmful, and there has not been enough emphasis on the other components of evidence-based “damage control” resuscitation.

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 2552-2552
Author(s):  
Majd T Ghanim ◽  
Jennifer H Voeks ◽  
Julie Kanter

Abstract Introduction/Background: There are no evidence-based guidelines for optimal transfusion practices for patients undergoing chemotherapy and stem cell transplant. There are minimal low-quality studies regarding transfusion thresholds as well as the efficacy of pre-transfusion medications (to reduce febrile non-hemolytic transfusion reactions) for these patients. To pursue a prospective quality improvement study, it is important to know the current transfusion standards used by practitioners regarding: 1) transfusion thresholds for platelets and red blood cells and 2) routine use of pre medications prior to transfusions. Additional research questions included differences in the above standards by region or by pediatrics vs. adult providers. Study Design and Methods: Expedited IRB approval was obtained. We conducted a REDCap survey from 3/1/18-4/12/18 targeting hematology oncology providers of both pediatric and adult providers. The survey was emailed through multiple databases with members form several countries that included both adult and pediatric hematology/oncology practitioners. Results: One hundred and nineteen hematology/oncology practitioners completed the survey: 94 attending physicians, 19 fellows and 6 nurse practitioners. Most respondents practiced in United States (90 %, 107/119), the rest practiced in Canada, India, Italy and Iran. The majority of participants were pediatric hematology/oncology providers (84 %, 100/119). Of the remaining providers 10 treated only adults and 9 treated both adults and children. The vast majority (97%, 115/119) of participants did not utilize a standard policy for premedication prior to red blood cell transfusions. Similarly, 95 % (111/117) or participants made individual decisions on premedication with platelet transfusions rather than using an institutional policy. When asked about the threshold to transfuse blood products, 71% (75/105) of those who treated patients undergoing chemotherapy said they would transfuse red blood cells when patients had a hemoglobin of</= 7 g/dL, and 79% (82/104) would transfuse platelets when patients had a platelet count <10 K/mL. Practitioners treating bone marrow transplant (BMT) patients had more variability and used higher transfusion thresholds. Fifty-two percent (33/64) of them would transfuse red blood cells for patients undergoing BMT with a higher threshold of hemoglobin of 8 g/dL while only 36% used the lower threshold of 7 g/dL. Similarly, for platelet transfusions for patients undergoing BMT, 47% (31/66) would use a 20K/mL threshold, and 45% would transfuse platelets at a threshold of 10 K/mL. Conclusion: There is currently no routine practice of utilizing pre-medications prior to transfusions of red blood cells or platelets. Instead, practitioners surveyed indicated a preference for individualizing the use of pre-medications only if patients had a previous transfusion reaction. As the use of these medications is not evidence-based, additional studies are needed to determine their efficacy. Transfusion thresholds are relatively consistent among providers with the majority aiming for more liberal thresholds in patients undergoing chemotherapy and more conservative for those undergoing BMT. More studies are needed to evaluate the risks and benefits of using different transfusion thresholds. Disclosures Kanter: Sancilio: Research Funding; ASH: Membership on an entity's Board of Directors or advisory committees; NHLBI: Membership on an entity's Board of Directors or advisory committees, Research Funding; bluebird bio: Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding; Global Blood Therapeutics: Research Funding; Apopharma: Research Funding; AstraZeneca: Membership on an entity's Board of Directors or advisory committees; Pfizer: Research Funding.


Blood ◽  
1992 ◽  
Vol 79 (2) ◽  
pp. 380-388 ◽  
Author(s):  
EM Bevers ◽  
T Wiedmer ◽  
P Comfurius ◽  
SJ Shattil ◽  
HJ Weiss ◽  
...  

The erythrocytes from a patient with Scott syndrome, a bleeding disorder characterized by an isolated defect in expression of platelet procoagulant activity, have been studied. When incubated with the calcium ionophore A23187, Scott syndrome red blood cells (RBCs) expressed less than 10% of the prothrombinase (enzyme complex of coagulation factors Va and Xa) activity of A23187-treated RBCs obtained from normal controls. Consistent with the results from enzyme assay, the ionophore-treated Scott syndrome erythrocytes exhibited diminished membrane vesiculation and decreased exposure of membrane binding sites for factor Va compared with identically treated controls. When examined by scanning electron microscopy, untreated Scott syndrome RBCs were indistinguishable from normal cells. After incubation with A23187, however, the morphology of Scott syndrome RBCs contrasted markedly from normal erythrocytes. Whereas the Ca2+ ionophore induced marked echinocytosis and spiculation of normal RBCs, Scott syndrome RBCs remained mostly discoid under these conditions, with only an occasional echinocyte-like cell observed. These aberrant responses to intracellular Ca2+ were also observed for resealed ghosts prepared from Scott syndrome erythrocytes, indicating that they are related to a defect in the membrane or membrane-associated cytoskeleton. The finding that the erythrocytes of this patient share many of the membrane abnormalities reported previously for Scott syndrome platelets suggests that this defect is common to both cell lines and involves a membrane component required for vesicle formation and for expression of prothrombinase sites.


Blood ◽  
1992 ◽  
Vol 79 (2) ◽  
pp. 380-388 ◽  
Author(s):  
EM Bevers ◽  
T Wiedmer ◽  
P Comfurius ◽  
SJ Shattil ◽  
HJ Weiss ◽  
...  

Abstract The erythrocytes from a patient with Scott syndrome, a bleeding disorder characterized by an isolated defect in expression of platelet procoagulant activity, have been studied. When incubated with the calcium ionophore A23187, Scott syndrome red blood cells (RBCs) expressed less than 10% of the prothrombinase (enzyme complex of coagulation factors Va and Xa) activity of A23187-treated RBCs obtained from normal controls. Consistent with the results from enzyme assay, the ionophore-treated Scott syndrome erythrocytes exhibited diminished membrane vesiculation and decreased exposure of membrane binding sites for factor Va compared with identically treated controls. When examined by scanning electron microscopy, untreated Scott syndrome RBCs were indistinguishable from normal cells. After incubation with A23187, however, the morphology of Scott syndrome RBCs contrasted markedly from normal erythrocytes. Whereas the Ca2+ ionophore induced marked echinocytosis and spiculation of normal RBCs, Scott syndrome RBCs remained mostly discoid under these conditions, with only an occasional echinocyte-like cell observed. These aberrant responses to intracellular Ca2+ were also observed for resealed ghosts prepared from Scott syndrome erythrocytes, indicating that they are related to a defect in the membrane or membrane-associated cytoskeleton. The finding that the erythrocytes of this patient share many of the membrane abnormalities reported previously for Scott syndrome platelets suggests that this defect is common to both cell lines and involves a membrane component required for vesicle formation and for expression of prothrombinase sites.


2009 ◽  
Vol 23 (4) ◽  
pp. 255-265 ◽  
Author(s):  
Lynn G. Stansbury ◽  
Richard P. Dutton ◽  
Deborah M. Stein ◽  
Grant V. Bochicchio ◽  
Thomas M. Scalea ◽  
...  

2018 ◽  
Vol 118 (10) ◽  
pp. 1765-1775 ◽  
Author(s):  
Keunyoung Kim ◽  
Youn-Kyeong Chang ◽  
Yiying Bian ◽  
Ok-Nam Bae ◽  
Kyung-Min Lim ◽  
...  

Background Paclitaxel is one of the most widely used anti-cancer drugs, but numerous case reports of thrombotic events in the cancer patients using paclitaxel raise concern over its pro-thrombotic risk. Materials and Methods We investigated whether paclitaxel can elicit pro-thrombotic properties in red blood cells (RBCs) through phosphatidylserine (PS) exposure and microvesicle (MV) release. Results In freshly isolated human RBCs, paclitaxel induced thrombin generation through PS exposure and MV release, whereas either coagulation factors or platelets were unaffected. Paclitaxel-induced PS exposure in RBC was mediated by scramblase activation which was induced by calcium-independent protein kinase C (PKC)ζ activation. Paclitaxel also increased RBC-endothelial cell adhesion and RBC aggregate formation which can also contribute to thrombosis. Indeed, intravenous administration of paclitaxel to rats induced PS exposure and PKCζ activation in RBCs in vivo which ultimately promoted venous thrombus formation. Conclusion These results demonstrated that paclitaxel may elicit pro-thrombotic properties in RBCs through PS exposure and MV release, which can ultimately promote thrombus formation.


Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1309
Author(s):  
Efthimia G. Pavlou ◽  
Hara T. Georgatzakou ◽  
Sotirios P. Fortis ◽  
Konstantina A. Tsante ◽  
Andreas G. Tsantes ◽  
...  

Coagulation abnormalities in renal pathology are associated with a high thrombotic and hemorrhagic risk. This study aims to investigate the hemostatic abnormalities that are related to the interaction between soluble coagulation factors and blood cells, and the effects of hemodialysis (HD) on it, in end stage renal disease (ESRD) patients. Thirty-two ESRD patients under HD treatment and fifteen healthy controls were included in the study. Whole blood samples from the healthy and ESRD subjects were collected before and after the HD session. Evaluation of coagulation included primary and secondary hemostasis screening tests, proteins of coagulation, fibrinolytic and inhibitory system, and ADAMTS-13 activity. Phosphatidylserine (PS) exposure and intracellular reactive oxygen species (iROS) levels were also examined in red blood cells and platelets, in addition to the platelet activation marker CD62P. Platelet function analysis showed pathological values in ESRD patients despite the increased levels of activation markers (PS, CD62P, iROS). Activities of most coagulation, fibrinolytic, and inhibitory system proteins were within the normal range, but HD triggered an increase in half of them. Additionally, the increased baseline levels of ADAMTS-13 inhibitor were further augmented by the dialysis session. Finally, pathological levels of PS and iROS were measured in red blood cells in close correlation with variations in several coagulation factors and platelet characteristics. This study provides evidence for a complex coagulation phenotype in ESRD. Signs of increased bleeding risk coexisted with prothrombotic features of soluble factors and blood cells in a general hyperfibrinolytic state. Hemodialysis seems to augment the prothrombotic potential, while the persisted platelet dysfunction might counteract the increased predisposition to thrombotic events post-dialysis. The interaction of red blood cells with platelets, the thrombus, the endothelium, the soluble components of the coagulation pathways, and the contribution of extracellular vesicles on hemostasis as well as the identification of the unknown origin ADAMTS-13 inhibitor deserve further investigation in uremia.


2018 ◽  
Vol 28 (6) ◽  
pp. 457-457
Author(s):  
M. L. Tonglet ◽  
F. Swerts ◽  
P. Y. Mathonet ◽  
D. Moens ◽  
V. D'Orio ◽  
...  

2014 ◽  
Vol 111 (03) ◽  
pp. 447-457 ◽  
Author(s):  
Marisa Ninivaggi ◽  
Gerhardus Kuiper ◽  
Marco Marcus ◽  
Hugo ten Cate ◽  
Marcus Lancé ◽  
...  

SummaryBlood dilution after transfusion fluids leads to diminished coagulant activity monitored by rotational thromboelastometry, assessing elastic fibrin clot formation, or by thrombin generation testing. We aimed to determine the contributions of blood cells (platelets, red blood cells) and plasma factors (fibrinogen, prothrombin complex concentrate) to fibrin clot formation under conditions of haemodilution in vitro or in vivo. Whole blood or plasma diluted in vitro was supplemented with platelets, red cells, fibrinogen or prothrombin complex concentrate (PCC). Thromboelastometry was measured in whole blood as well as plasma; thrombin generation was determined in parallel. Similar tests were performed with blood from 48 patients, obtained before and after massive fluid infusion during cardiothoracic surgery. Addition of platelets or fibrinogen, in additive and independent ways, reversed the impaired fibrin clot formation (thromboelastometry) in diluted whole blood. In contrast, supplementation of red blood cells or prothrombin complex concentrate was ineffective. Platelets and fibrinogen independently restored clot formation in diluted plasma, resulting in thromboelastometry curves approaching those in whole blood. In whole blood from patients undergoing dilution during surgery, elastic clot formation was determined by both the platelet count and the fibrinogen level. Thrombin generation in diluted (patient) plasma was not changed by fibrinogen, but improved markedly by prothrombin complex concentrate. In conclusion, in dilutional coagulopathy, platelets and fibrinogen, but not red blood cells or vitamin K-dependent coagulation factors, independently determine thromboelastometry parameters measured in whole blood and plasma. Clinical decisions for transfusion based on thromboelastometry should take into account the platelet concentration.


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