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      Low flow rate alters haemostatic parameters in an ex-vivo extracorporeal membrane oxygenation circuit

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          Abstract

          Background

          Extracorporeal membrane oxygenation (ECMO) is a life-saving modality used to manage cardiopulmonary failure refractory to conventional medical and surgical therapies. Despite advances in ECMO equipment, bleeding and thrombosis remain significant complications. While the flow rate for ECMO support is well recognized, less is known about the minimum-rate requirements and haemostasis. We investigated the relationship between different ECMO flow rates, and their effect on haemolysis and coagulation.

          Methods

          Ten ex-vivo ECMO circuits were tested using donated, < 24-h-old human whole blood, with two flow rates: high-flow at 4 L/min (normal adult cardiac output; n = 5) and low-flow at 1.5 L/min (weaning; n = 5). Serial blood samples were taken for analysis of haemolysis, von Willebrand factor (vWF) multimers by immunoblotting, rotational thromboelastometry, platelet aggregometry, flow cytometry and routine coagulation laboratory tests.

          Results

          Low-flow rates increased haemolysis after 2 h ( p = 0.02), 4 h ( p = 0.02) and 6 h ( p = 0.02) and the loss of high-molecular-weight vWF multimers ( p = 0.01), while reducing ristocetin-induced platelet aggregation ( p = 0.0002). Additionally, clot formation times were prolonged ( p = 0.006), with a corresponding decrease in maximum clot firmness ( p = 0.006).

          Conclusions

          In an ex-vivo model of ECMO, low-flow rate (1.5 L/min) altered haemostatic parameters compared to high-flow (4 L/min). Observed differences in haemolysis, ristocetin-induced platelet aggregation, high-molecular-weight vWF multimers and clot formation time suggest an increased risk of bleeding complications. Since patients are often on ECMO for protracted periods, extended-duration studies are required to characterise long-term ECMO-induced haemostatic changes.

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          Most cited references31

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          Extracorporeal Life Support Organization Registry International Report 2016.

          Data on extracorporeal life support (ECLS) use and survival submitted to the Extracorporeal Life Support Organization's data registry from the inception of the registry in 1989 through July 1, 2016, are summarized in this report. The registry contained information on 78,397 ECLS patients with 58% survival to hospital discharge. Extracorporeal life support use and centers providing ECLS have increased worldwide. Extracorporeal life support use in the support of adults with respiratory and cardiac failure represented the largest growth in the recent time period. Extracorporeal life support indications are expanding, and it is increasingly being used to support cardiopulmonary resuscitation in children and adults. Adverse events during the course of ECLS are common and underscore the need for skilled ECLS management and appropriately trained ECLS personnel and teams.
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            The inflammatory response to extracorporeal membrane oxygenation (ECMO): a review of the pathophysiology

            Extracorporeal membrane oxygenation (ECMO) is a technology capable of providing short-term mechanical support to the heart, lungs or both. Over the last decade, the number of centres offering ECMO has grown rapidly. At the same time, the indications for its use have also been broadened. In part, this trend has been supported by advances in circuit design and in cannulation techniques. Despite the widespread adoption of extracorporeal life support techniques, the use of ECMO remains associated with significant morbidity and mortality. A complication witnessed during ECMO is the inflammatory response to extracorporeal circulation. This reaction shares similarities with the systemic inflammatory response syndrome (SIRS) and has been well-documented in relation to cardiopulmonary bypass. The exposure of a patient’s blood to the non-endothelialised surface of the ECMO circuit results in the widespread activation of the innate immune system; if unchecked this may result in inflammation and organ injury. Here, we review the pathophysiology of the inflammatory response to ECMO, highlighting the complex interactions between arms of the innate immune response, the endothelium and coagulation. An understanding of the processes involved may guide the design of therapies and strategies aimed at ameliorating inflammation during ECMO. Likewise, an appreciation of the potentially deleterious inflammatory effects of ECMO may assist those weighing the risks and benefits of therapy.
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              Activation-independent platelet adhesion and aggregation under elevated shear stress.

              Platelet aggregation, which contributes to bleeding arrest and also to thrombovascular disorders, is thought to initiate after signaling-induced activation. We found that this paradigm does not apply under blood flow conditions comparable to those existing in stenotic coronary arteries. Platelets interacting with immobilized von Willebrand factor (VWF) aggregate independently of activation when soluble VWF is present and the shear rate exceeds 10 000 s(-1) (shear stress = 400 dyn/cm(2)). Above this threshold, active A1 domains become exposed in soluble VWF multimers and can bind to glycoprotein Ibalpha, promoting additional platelet recruitment. Aggregates thus formed are unstable until the shear rate approaches 20 000 s(-1) (shear stress = 800 dyn/cm.(2)). Above this threshold, adherent platelets at the interface of surface-immobilized and membrane-bound VWF are stretched into elongated structures and become the core of aggregates that can persist on the surface for minutes. When isolated dimeric A1 domain is present instead of native VWF multimers, activation-independent platelet aggregation occurs without requiring shear stress above a threshold level, but aggregates never become firmly attached to the surface and progressively disaggregate as shear rate exceeds 6000 s(-1). Platelet and VWF modulation by hydrodynamic force is a mechanism for activation-independent aggregation that may support thrombotic arterial occlusion.
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                Author and article information

                Contributors
                k.ki@uq.edu.au
                M.Passmore@uq.edu.au
                hoihoung.chan@griffith.edu.au
                maxmalfertheiner@gmail.com
                jonathon_fanning@me.com
                m.bouquet@uq.edu.au
                j.millar@doctors.org.uk
                j.fraser@uq.edu.au
                j.suen1@uq.edu.au
                Journal
                Intensive Care Med Exp
                Intensive Care Med Exp
                Intensive Care Medicine Experimental
                Springer International Publishing (Cham )
                2197-425X
                20 August 2019
                20 August 2019
                December 2019
                : 7
                : 51
                Affiliations
                [1 ]ISNI 0000 0004 0614 0266, GRID grid.415184.d, Critical Care Research Group, The Prince Charles Hospital, ; Brisbane, Australia
                [2 ]ISNI 0000 0000 9320 7537, GRID grid.1003.2, Faculty of Medicine, University of Queensland, ; Brisbane, Australia
                [3 ]ISNI 0000 0004 0614 0266, GRID grid.415184.d, Innovative Cardiovascular Engineering and Technology Laboratory, , Critical Care Research Group, The Prince Charles Hospital, ; Brisbane, Australia
                [4 ]ISNI 0000 0004 0437 5432, GRID grid.1022.1, Department of Engineering and Built Environment, , Griffith University, ; Gold Coast, Australia
                [5 ]ISNI 0000 0000 9194 7179, GRID grid.411941.8, Department of Internal Medicine II, , University Medical Center Regensburg, ; Regensburg, Germany
                [6 ]ISNI 0000 0004 0374 7521, GRID grid.4777.3, Wellcome-Wolfson Centre for Experimental Medicine, , Queen’s University Belfast, ; Belfast, UK
                Author information
                http://orcid.org/0000-0002-0859-8882
                Article
                264
                10.1186/s40635-019-0264-z
                6702240
                31432279
                067a090a-8478-4454-90be-1391eb0b688f
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 30 April 2019
                : 12 August 2019
                Funding
                Funded by: National Health and Medical Research Council
                Award ID: 1079421
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

                coagulation,critical illness,extracorporeal membrane oxygenation,flow rate,haemolysis,platelets

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