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      Keeping the Circuit Open: Lessons from the Lab

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          Abstract

          Background: Hemofiltration circuits generally require anticoagulation to prevent the membrane from clotting. Understanding the mechanisms involved in premature clotting of the filtration circuit is useful to optimize anticoagulation and maintain filter patency. Aims: To discuss research performed at our institution which throws light on the causes of premature clotting of the hemofilter, and to highlight our approach to anticoagulation. Discussion: Premature clotting of the circuit is related to low baseline levels of antithrombin III (AT-III), heparin co-factor II and tissue factor pathway inhibitor. Clotting is preceded by a precipitous rise in thrombin-antithrombin complexes, suggesting thrombin generation. Our standard anticoagulant is unfractionated heparin, where the primary mode of action is potentiation of endogenous AT-III. However, AT-III levels are diminished in sepsis and other causes of systemic inflammation. To supplement or prevent consumption of AT-III we use fresh frozen plasma or aprotinin (as cheaper alternatives to AT-III) in situations where filter life span is limited and mechanical obstruction has been excluded. Anticoagulation can be managed in heparin-induced thrombocytopenic patients with danaparoid, prostaglandins and/or predilution.

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          Activation of the tissue factor pathway occurs during continuous venovenous hemofiltration.

          Activation of the tissue factor pathway occurs during continuous venovenous hemofiltration (CVVH). Despite adequate exogenous anticoagulation, the occlusion of CVVH circuits can occur within minutes to a few hours of use and is associated with evidence of thrombin generation. Having found no evidence of activation of the contact factor (intrinsic coagulation) pathway during CVVH, we sought to examine the effect of the first episode of CVVH on the tissue factor (extrinsic) pathway of coagulation and thrombin generation. Twelve critically ill patients were studied prior to the commencement of hemofiltration and at regular intervals thereafter until the filter clotted. Prior to hemofiltration, most patients had increased levels of plasma tissue factor, thrombin-antithrombin (TAT) complexes, and tissue factor pathway inhibitor (TFPI); during hemofiltration, further generation of TAT complexes occurred. Initially, levels of activated factor VII (FVIIa) fell and TFPI increased, but during the course of hemofiltration, the levels of TFPI fell and FVIIa increased. Levels of tissue factor increased during CVVH in some patients, but this was not related to the generation of FVIIa. These data indicate that activation of FVII occurred during CVVH, which was related to levels of TFPI, but not tissue factor, and was coincidental to thrombin generation.
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            Author and article information

            Journal
            BPU
            Blood Purif
            10.1159/issn.0253-5068
            Blood Purification
            S. Karger AG
            978-3-8055-7371-9
            978-3-318-00812-8
            0253-5068
            1421-9735
            2002
            2002
            27 February 2002
            : 20
            : 3
            : 275-281
            Affiliations
            aPharmacy Department, Middlesex Hospital, bBloomsbury Institute of Intensive Care Medicine, and cIntensive Care Unit, University College London Hospitals, London, UK
            Article
            47020 Blood Purif 2002;20:275–281
            10.1159/000047020
            11867875
            © 2002 S. Karger AG, Basel

            Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

            Page count
            Figures: 2, References: 31, Pages: 7
            Product
            Self URI (application/pdf): https://www.karger.com/Article/Pdf/47020
            Categories
            Proceedings of the 6th International Conference on CRRT

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