Practical coagulation for the blood banker

Hoffman, Maureane; Cichon, Lisa

doi:10.1111/trf.12201

Cited by 23 publications

(11 citation statements)

References 49 publications

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“…17 Hemostasis occurs, according to the cell-based model, in 3 phases: initiation, amplification, and propagation, with the magnitude of the thrombin generation, the "thrombin burst," ultimately determining the hemostatic capacity of the formed clot. 18 Therefore, tests that reflect this new understanding of hemostasis such as the viscoelastical hemostatic assays (VHAs) thrombelastography (TEG) and rotational thrombelastometry (ROTEM) appear appropriate to accurately monitor hemostasis.…”

Section: The Hemostatic System and Its Monitoringmentioning

confidence: 99%

How I treat patients with massive hemorrhage

Johansson

Stensballe

Oliveri

et al. 2014

Blood

181

127

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Massive hemorrhage is associated with coagulopathy and high mortality. The transfusion guidelines up to 2006 recommended that resuscitation of massive hemorrhage should occur in successive steps using crystalloids, colloids, and red blood cells (RBCs) in the early phase and plasma and platelets in the late phase. With the introduction of the cell-based model of hemostasis in the mid-1990s, our understanding of the hemostatic process and of coagulopathy has improved. This has contributed to a change in resuscitation strategy and transfusion therapy of massive hemorrhage along with an acceptance of the adequacy of whole blood hemostatic tests to monitor these patients. Thus, in 2005, a strategy aiming at avoiding coagulopathy by proactive resuscitation with blood products in a balanced ratio of RBC:plasma:platelets was introduced, and this has been reported to be associated with reduced mortality in observational studies. Concurrently, whole blood viscoelastic hemostatic assays have gained acceptance by allowing a rapid and timely identification of coagulopathy along with enabling an individualized, goal-directed transfusion therapy. These strategies joined together seem beneficial for patient outcome, although final evidence on outcome from randomized controlled trials are lacking. We present how we in Copenhagen and Houston, today, manage patients with massive hemorrhage.

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Section: The Hemostatic System and Its Monitoringmentioning

confidence: 99%

How I treat patients with massive hemorrhage

Johansson

Stensballe

Oliveri

et al. 2014

Blood

181

127

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“…This is most likely related to standardized levels of coagulation factors in the OctaplasLG, ensuring that adequate thrombin generation, pivotal for intact hemostasis. 38 Standard FFP has large variations in coagulation factor levels between units depending on the individual blood donor 39 and low levels of just 1 coagulation factor involved in thrombin generation will result in impaired clot strength and reduced hemostatic competence. 34 …”

Section: Discussionmentioning

confidence: 99%

Resuscitation of Endotheliopathy and Bleeding in Thoracic Aortic Dissections: The VIPER-OCTA Randomized Clinical Pilot Trial

Stensballe

Ulrich²,

Nilssøn³

et al. 2018

Anesthesia &Amp; Analgesia

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BACKGROUND:Thoracic aorta dissection is an acute critical condition associated with shock-induced endotheliopathy, coagulopathy, massive bleeding, and significant morbidity and mortality. Our aim was to compare the effect of coagulation support with solvent/detergent-treated pooled plasma (OctaplasLG) versus standard fresh frozen plasma (FFP) on glycocalyx and endothelial injury, bleeding, and transfusion requirements.METHODS:Investigator-initiated, single-center, blinded, randomized clinical pilot trial of adult patients undergoing emergency surgery for thoracic aorta dissection. Patients were randomized to receive OctaplasLG or standard FFP as coagulation factor replacement related to bleeding. The primary outcome was glycocalyx and endothelial injury. Other outcomes included bleeding, transfusions and prohemostatics at 24 hours, organ failure, length of stay in the intensive care unit and in the hospital, safety, and mortality at 30 and 90 days.RESULTS:Fifty-seven patients were included to obtain 44 evaluable on the primary outcome. The OctaplasLG group displayed significantly reduced damage to the endothelial glycocalyx (syndecan-1) and reduced endothelial tight junction injury (sVE-cadherin) compared to standard FFP. In the OctaplasLG group compared to the standard FFP, days on ventilator (1 day [interquartile range, 0–1] vs 2 days [1–3]; P = .013), bleeding during surgery (2150 [1600–3087] vs 2750 [2130–6875]; P = .046), 24-hour total transfusion and platelet transfusion volume (3975 mL [2640–6828 mL] vs 6220 mL [4210–10,245 mL]; P = .040, and 1400 mL [1050–2625 mL] vs 2450 mL [1400–3500 mL]; P = .027), and goal-directed use of prohemostatics (7/23 [30.4%] vs 13/21 [61.9%]; P = .036) were all significantly lower. Among the 57 patients randomized, 30-day mortality was 20.7% (6/29) in the OctaplasLG group and 25% (7/28) in the standard FFP group (P = .760). No safety concern was raised.CONCLUSIONS:In this randomized, clinical pilot trial of patients undergoing emergency surgery for thoracic aorta dissections, we found that OctaplasLG reduced glycocalyx and endothelial injury, reduced bleeding, transfusions, use of prohemostatics, and time on ventilator after surgery compared to standard FFP. An adequately powered multicenter trial is warranted to confirm the clinical importance of the findings.

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“…Hemorrhage and shock continue, and both adaptive and maladaptive changes begin to occur in the blood. The coagulation cascade and platelets are activated to form a hemostatic plug in the hemorrhage source [28]. Probably to prevent the development of microvascular thrombosis, fibrinolytic activity increases away from hemorrhage site [29].…”

Section: Physiopathology and Metabolic Alterationsmentioning

confidence: 99%

Hemorrhagic Shock

Türker¹

2020

Clinical Management of Shock - The Science and Art of Physiological Restoration

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Hemorrhagic shock is a type of hypovolemic shock, where intravascular blood loss and consequent alterations in the cell due to the hypoxia result in tissue and organ dysfunction, leading to death, once a certain threshold level is exceeded. Inadequate oxygen delivery results with Na/K ATPase pump dysfunction and cell death by this way, but erythrocytes do not use oxygen for their survival. A depolarizing protein can be a reason under in vivo conditions. In severe injury, rapid loss of 25% and more blood volume cause irreversible shock. For blood restoration, crystalloid solutions temporarily provide a practical approach, but they cannot replace the lost erythrocyte mass occurred due to bleeding, and they have no therapeutic value. Excessive use causes several problems, especially coagulopathy and increases the mortality risk. The prompt transfer of patient to an ultimate center for treatment, use of blood and blood products in the treatment, and a swift restoration of hemorrhage source are essential. Tourniquet use in the extremities and balloon occlusion of the aorta can be lifesaving.

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Practical coagulation for the blood banker

Cited by 23 publications

References 49 publications

How I treat patients with massive hemorrhage

How I treat patients with massive hemorrhage

Resuscitation of Endotheliopathy and Bleeding in Thoracic Aortic Dissections: The VIPER-OCTA Randomized Clinical Pilot Trial

Hemorrhagic Shock

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