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Relevant bibliographies by topics / Haemostasis

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Academic literature on the topic 'Haemostasis'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Haemostasis"

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Habal, Petr, Veronika Sívková, and Petr Votava. "Comparison of Efficacy and Safety of Non-Regenerated and Regenerated Oxidized Cellulose Based Fibrous Haemostats." Acta Medica (Hradec Kralove, Czech Republic) 65, no. 2 (2022): 53–58. http://dx.doi.org/10.14712/18059694.2022.18.

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Purpose: Various forms of local haemostats are increasingly used routinely in surgical procedures. Our work is the first comparison of the efficacy and safety of non-regenerated and regenerated oxidized cellulose based fibrous haemostats. Methods: The haemostatic efficacy and safety of fibrous haemostats based on ONRC and ORC were compared in a randomized multicenter study. The primary endpoint was successful haemostasis within 3 minutes of application and no need for surgical revision within 12 hours after the procedure for recurrent bleeding. Results: There was a significant difference in the rate of successful haemostasis in 3 minutes that was achieved in 82% and 55% in the ONRC and ORC groups, respectively (confidence interval 99%; p = 0.009). Mean time to haemostasis was 133.9 ± 53.95 seconds and 178.0 ± 82.33 seconds, in the ONRC, and ORC group, respectively (p = 0.002). Revision surgery for re-bleeding was necessary in 0 (0%), and 1 (2%) of patients in the ONRC, and ORC group, respectively. No adverse events were reported. Conclusion: Fibrous haemostat based on ONRC was non-inferior compared to fibrous haemostat based on ORC when used in accordance with its intended purpose, and was safe and efficient.

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Moldovan, Horațiu, Iulian Antoniac, Daniela Gheorghiță, Maria Sabina Safta, Silvia Preda, Marian Broască, Elisabeta Badilă, et al. "Biomaterials as Haemostatic Agents in Cardiovascular Surgery: Review of Current Situation and Future Trends." Polymers 14, no. 6 (March 16, 2022): 1189. http://dx.doi.org/10.3390/polym14061189.

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Intraoperative haemostasis is of paramount importance in the practice of cardiovascular surgery. Over the past 70 years, topical haemostatic methods have advanced significantly and today we deal with various haemostatic agents with different properties and different mechanisms of action. The particularity of coagulation mechanisms after extracorporeal circulation, has encouraged the introduction of new types of topic agents to achieve haemostasis, where conventional methods prove their limits. These products have an important role in cardiac, as well as in vascular, surgery, mainly in major vascular procedures, like aortic dissections and aortic aneurysms. This article presents those agents used for topical application and the mechanism of haemostasis and offers general recommendations for their use in the operating room.

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Ibrahim, Mostafa, Ahmed El-Mikkawy, Mohamed Abdel Hamid, Haitham Abdalla, Arnaud Lemmers, Ibrahim Mostafa, and Jacques Devière. "Early application of haemostatic powder added to standard management for oesophagogastric variceal bleeding: a randomised trial." Gut 68, no. 5 (May 5, 2018): 844–53. http://dx.doi.org/10.1136/gutjnl-2017-314653.

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BackgroundAcute variceal bleeding (AVB) requires early therapeutic management by experienced endoscopists that often poses logistical challenges for hospitals. We assessed a different management concept with early application of haemostatic powder—which does not require high endoscopic expertise—added to conventional management in a randomised trial.MethodsCirrhotic patients with AVB received standard medical therapy and were randomised to either immediate endoscopy with haemostatic powder application within 2 hours of admission, followed by early elective endoscopy on the next day, that is, within 12–24 hours of admission for definitive treatment (study group) or to early elective endoscopy only (control group). In both groups, failures to achieve clinical haemostasis until the time of early elective endoscopy underwent rescue endoscopy with attempted conventional haemostasis. Primary outcome was endoscopic haemostasis at the elective endoscopy.ResultsOf 86 randomised patients with AVB, 5/43 in the study group required rescue endoscopy for failure of controlling spurting bleeding (n=4) after powder application or for early bleeding recurrence in one patient who died before repeating rescue endoscopy. In the control group, 13/43 patients required rescue endoscopic haemostasis for failure of clinical haemostasis (12%vs30%, p=0.034). In the remaining patients, early elective endoscopic haemostasis was achieved in all 38 patients in the study group, while all remaining 30 patients in the control group had fresh gastric blood or (10%) spurting bleeding at early elective endoscopy with successful haemostasis in all of them. Six-week survival was significantly improved in the study group (7%vs30%, p=0.006).ConclusionThe new concept of immediate powder application improves early clinical and endoscopic haemostasis. This simplified endoscopic approach may have an impact on early and 6-week survival.Trial registration numberNCT03061604.

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Monagle, Paul, and Patricia Massicotte. "Developmental haemostasis: Secondary haemostasis." Seminars in Fetal and Neonatal Medicine 16, no. 6 (December 2011): 294–300. http://dx.doi.org/10.1016/j.siny.2011.07.007.

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Silveira, Angela, Stella Thomassen, Lars-Olof Hansson, Jan Rosing, Anders Hamsten, Katarina Bremme, and Marianne van Rooijen. "Rapid activation of haemostasis after hormonal emergency contraception." Thrombosis and Haemostasis 97, no. 01 (2007): 15–20. http://dx.doi.org/10.1160/th06-09-0540.

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SummaryHormonal emergency contraception (EC) is a well established contraceptive method, recommended to all women, although the effects on haemostais are not fully evaluated. The aim of this study was to evaluate whether exposure to EC has effects on well established cardiovascular risk factors, and also to examine whether differences exist between two EC treatments. In a prospective randomized cross over design 11 women used two different EC methods, one with estrogen and levonorgestrel (EE-EC) and one with levonorgestrel only (LNG-EC). Plasma concentrations of haemostatic factors (APC resistance, antithrombin, fibrinogen, prothrombin fragment 1+2, free protein S, factor VII and PAI-1), sex-hormone-binding globulin (SHBG), the apolipoprotein (apo)B/apoA1 ratio and C-reactive protein (CRP) were followed frequently during the following 48 h A rapid haemostatic activation was induced with both treatments, although more pronounced with EE-EC. Already two hours after EC, the plasma concentrations of haemostatic parameters and SHBG were significantly different from baseline concentrations. An ETP-based APC-resistance method showed increased APC resistance with EE-EC and decreased APC resistance with LNG-EC. The ApoB/ApoA1 ratio was affected in a favourable direction with EE-EC.CRP increased slightly regardless of treatment. Even a very short exposure to exogenous sex hormones causes prompt effects on hepatic protein synthesis and the coagulation system. This must be taken into consideration whenever exogenous steroid hormones are administered, especially to individuals with a genetic predisposition to thrombosis or transiently disturbed haemostasis.

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Jigar Panchal, Heta, Nigel J. Kent, Andrew J. S. Knox, and Leanne F. Harris. "Microfluidics in Haemostasis: A Review." Molecules 25, no. 4 (February 14, 2020): 833. http://dx.doi.org/10.3390/molecules25040833.

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Haemostatic disorders are both complex and costly in relation to both their treatment and subsequent management. As leading causes of mortality worldwide, there is an ever-increasing drive to improve the diagnosis and prevention of haemostatic disorders. The field of microfluidic and Lab on a Chip (LOC) technologies is rapidly advancing and the important role of miniaturised diagnostics is becoming more evident in the healthcare system, with particular importance in near patient testing (NPT) and point of care (POC) settings. Microfluidic technologies present innovative solutions to diagnostic and clinical challenges which have the knock-on effect of improving health care and quality of life. In this review, both advanced microfluidic devices (R&D) and commercially available devices for the diagnosis and monitoring of haemostasis-related disorders and antithrombotic therapies, respectively, are discussed. Innovative design specifications, fabrication techniques, and modes of detection in addition to the materials used in developing micro-channels are reviewed in the context of application to the field of haemostasis.

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Aird, W. C. "Endothelium and haemostasis." Hämostaseologie 35, no. 01 (2015): 11–16. http://dx.doi.org/10.5482/hamo-14-11-0075.

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SummaryThe endothelium is a widely distributed organ system that plays an important role in health and disease. The endothelium is remarkably heterogeneous in structure and function. One vital function of the endothelium is to maintain blood in its fluid state, and to provide controlled haemostasis at sites of vascular injury. In keeping with the theme of endothelial cell heterogeneity, endothelial cells from different sites of the vascular employ different strategies to mediate local haemostatic balance. These differences are sufficient to explain why systemic imbalances of haemostatic components invariably lead to local thrombotic phenotypes. An important goal for the future is to identify diagnostic markers that reflect phenotypic changes at the level of individual vascular beds, and to develop therapies that target one or another site of the vasculature.

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Austin, Steven K. "Haemostasis." Medicine 49, no. 4 (April 2021): 199–204. http://dx.doi.org/10.1016/j.mpmed.2021.01.004.

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Allford, Sarah L., and Sam Machin. "Haemostasis." Medicine 28, no. 2 (2000): 10–14. http://dx.doi.org/10.1383/medc.28.2.10.28357.

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Allford, Sarah L., and SJ Machin. "Haemostasis." Medicine 32, no. 5 (May 2004): 11–14. http://dx.doi.org/10.1383/medc.32.5.11.33956.

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Dissertations / Theses on the topic "Haemostasis"

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Auger, Martin J. "Haemostasis and cancer." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329371.

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Faughan, Marian. "Copper and haemostasis." Thesis, University of Ulster, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284849.

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Davidson, Colin John. "Molecular evolution of haemostasis." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368908.

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Faxälv, Lars. "Imaging methods for haemostasis research." Doctoral thesis, Linköpings universitet, Klinisk kemi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-19178.

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Blood is a vital part of the human physiology; a transport system that brings nutrients and oxygen to sustain living cells and simultaneously facilitates the removal of carbon dioxide and other waste products from the body. To assure the continuity of these functions, it is of uttermost importance to keep the flowing blood inside the vascular system at any cost. The principal components of the haemostatic system are the blood platelets and the plasma coagulation system, both working in concert to create a blood stopping haemostatic plug when a vessel is ruptured. In modern health care, methods for treatment and diagnostics often implicate the contact between blood and artificial materials (biomaterials). Biomaterial surfaces may activate platelets and the coagulation cascade by exposing a surface that during blood contact shares certain characteristics with surfaces found at the site of vascular injury. Therefore it is of great importance that the mechanisms behind the interactions between foreign surfaces and blood are studied in order to minimize, and if possible, prevent unnecessary reactions that may lead to thrombosis. This thesis describes two important methods to study blood – surface interactions in terms of surface induced plasma coagulation and platelet adhesion/aggregation. The method ‘Imaging of coagulation’, a coagulation assay based on time-lapse image capture of the coagulation process was developed during the course of this work. The use of images enables the method to answer questions regarding where coagulation was initiated and how fast coagulation propagates. Such questions are highly relevant in the study of blood-biomaterial interactions but also in general haemostasis research. In vivo, platelet adhesion and aggregation are events that always proceed under flow conditions. Therefore we also developed a cone-and-plate flow model to study these mechanisms under similar conditions in vitro. The cone-and-plate setup was found to be a flexible platform and was used for both blood compatibility testing of potential biomaterials as well as for general haemostasis research. With the above mentioned methods we tested the haemocompatibility of glycerol monooleate (GMO), a proposed substance for use in biomaterial applications. It was found that GMO did not activate coagulation to any great extent either in plasma or in whole blood. Surface induced coagulation and platelet adhesion was also studied on PEG-containing hydrogels and compared with hydrogels constructed from three different non-PEG-containing monomers. It was concluded that all the grafted hydrogels, in particular those produced from the monomers 2-hydroxyethyl methacrylate (HEMA) and/or PEG- methacrylate (PEGMA), demonstrated good haemocompatibility. Supported phospholipid bilayers were used to investigate the relationship between surface charge and procoagulant activity. The coagulation process was studied in a straightforward manner using the imaging of coagulation setup. We concluded that the content of negatively charged 1-palmitoyl-2-oleoyl-sn-glycero-3-[phospho-L-serine] (POPS) in the bilayer must exceed ~ 6% for the bilayer to exert procoagulant activity. The physiological role of factor XII in human haemostasis and thrombosis was investigated in the imaging of coagulation setup and the cone and plate setup by the use of surfaces with thrombogenic coatings. We found that tissue factor initiated coagulation could be greatly accelerated by the presence of contact activating agents in a platelet dependent manner. In conclusion, the method ‘Imaging of coagulation’ and platelet adhesion/aggregation in the cone-and-plate flow model are both versatile methods with many possible applications. The combination of the two methods provides a solid foundation for biomaterial and haemostasis research.

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Turkington, Philip Thomas. "The role of polymorphonuclear proteinases in haemostasis." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317075.

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Holmes, Valerie Anne. "Early markers of haemostasis in normal pregnancy." Thesis, University of Ulster, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274405.

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McLellan, David Sinclair. "Factor VIII in health and disease - the relationship of VIII procoagulant (VIII:C) to VIII procoagulant antigen (VIII:CAg) in selected states." Thesis, Brunel University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280711.

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Hardy, Elaine. "Novel approaches to inhibition of platelet behaviour in pre-eclampsia." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282831.

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Forster, Trevor Henry. "Effect of inhibitors of platelet function in haemostasis." Thesis, Queensland University of Technology, 1986. https://eprints.qut.edu.au/36709/1/36709_Forster_1986.pdf.

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Investigation of the role of platelets in the haemostatic process has been a high priority for many years. In spite of this the mechanisms by which platelets help to maintain vascular integrity in undamaged blood vessels have not been clearly defined. The concept of endothelial support suggested by the work of Wojcik, Van Horn, Webber and Johnson (6) has been controversial as it implies a direct interaction between platelets and endothelium. An alternate theory offered has been that of platelet support by attachment to sub-endothelium following damage to the endothelial cell layer. To investigate the proposition that platelets and endothelial cells were capable of direct interaction, a reaction system using cultured human umbilical vein endothelial cells was devised. As a result of experiments using this model it has been shown that a direct reaction between platelets and endothelial cells does occur in vitro. Experiments and techniques were devised to investigate both the observed interaction and to assess the effect of inhibitors of platelet function on the reaction. Evidence gained by scanning electron microscopy and transmission electron microscopy indicates that a specific interaction actively involving endothelial cells is responsible for the observed attachment of platelets to these cells. Studies using aspirin inhibited platelets indicate that a two stage process is involved first stage of which is cyclo-oxygenase pathway. The in this interaction, independent of second stage of reaction appears to involve an active contribution endothelial cells via their cyclo-oxygenase pathway.

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Mackie, Eileen Elizabeth. "Exercise and haemostasis in health and ischaemic heart disease." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433574.

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Books on the topic "Haemostasis"

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Monagle, Paul, ed. Haemostasis. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8.

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Faughnan, Marian. Copper and Haemostasis. [S.l: The Author], 1998.

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Boldt, David H. Update on haemostasis. Edinburgh: Churchill Livinstone, 1990.

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Geddis, Alison Elaine. Haemostasis in hypercholesterolemia. [S.l: The Author], 1992.

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Roberts, Harold Ross, ed. Haemophilia and Haemostasis. Oxford, UK: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470692554.

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Monagle, Paul T. Haemostasis: Methods and protocols. New York: Humana Press, 2013.

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7

Zirlik, Andreas, Christoph Bode, and Meinrad Gawaz, eds. Platelets, Haemostasis and Inflammation. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66224-4.

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Harenberg, Job, Dieter L. Heene, Gerd Stehle, and Gotthard Schettler, eds. New Trends in Haemostasis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-84318-1.

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Szpalski, Marek, Richard B. Weiskopf, Robert Gunzburg, and Max Aebi, eds. Haemostasis in Spine Surgery. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/b139006.

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Giuseppe, Remuzzi, and Rossi Ennio Claudio 1931-, eds. Haemostasis and the kidney. London: Butterworths, 1989.

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Book chapters on the topic "Haemostasis"

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Kam, Peter, Ian Power, Michael J. Cousins, and Philip J. Siddal. "Haemostasis." In Principles of Physiology for the Anaesthetist, 317–23. Fourth edition. | Boca Raton : CRC Press, Taylor & Francis Group, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429288210-53.

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Woodrow, Philip. "Haemostasis." In Intensive Care Nursing, 268–74. Fourth edition. | Abingdon, Oxon ; New York, NY : Routledge, 2018.: Routledge, 2018. http://dx.doi.org/10.4324/9781315231174-26.

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Chan, Anthony K. C., and Nethnapha Paredes. "The Coagulation System in Humans." In Haemostasis, 3–12. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_1.

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Ignjatovic, Vera. "Thrombin Clotting Time." In Haemostasis, 131–38. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_10.

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Berry, Leslie R., and Anthony K. C. Chan. "Thrombin Generation." In Haemostasis, 139–54. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_11.

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Horton, Stephen, and Simon Augustin. "Activated Clotting Time (ACT)." In Haemostasis, 155–67. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_12.

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Opat, Stephen, Jenny Butler, Erica Malan, Elizabeth Duncan, and Huyen A. M. Tran. "Factor XIII Assays." In Haemostasis, 171–80. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_13.

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Stang, Linda J., and Lesley G. Mitchell. "Fibrinogen." In Haemostasis, 181–92. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_14.

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Salignac, Sylvain, Véronique Latger-Cannard, Nicole Schlegel, and Thomas Pierre Lecompte. "Platelet Counting." In Haemostasis, 193–205. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_15.

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Latger-Cannard, Véronique, Odile Fenneteau, Sylvain Salignac, Thomas Pierre Lecompte, and Nicole Schlegel. "Platelet Morphology Analysis." In Haemostasis, 207–25. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-339-8_16.

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Conference papers on the topic "Haemostasis"

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Berqqvist, David. "THE INFLUENCE ON EXPERIMENTAL THROMBOSIS AND HAEMOSTASIS BY LOW MOLECULAR WEIGHT HEPARIN IN COMBINATION WITH DIHYDROERGOTAMINE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644853.

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The influence of low molecular weight heparin (Mw7600) in combination with dihydroergotamine (DHE) onthrombus formation and primary haemostasis was investigated in rabbit models. The jugular veins were used, thrombosis being induced by a combination of endothelial damage (ethoxysclerol) and flow reduction (standardized narrowing of the vein). Haemostatig plug formation was studied by transecting isolated microvessels in the mesentery. Conventional heparin in the dose of 60 units anti Xa activity/kg b.w. effectively prevented thrombus formation but the same dose of a low molecular weight fragment only gave a marginal decrease of the frequency of thrombosis (from79 to 57%). Doubling the dose of the heparin fragment totally abolished thrombus formation as did thecombination of 60 units with DHE.With DHE it was also possible to diminish the low molecular weight heparin dose to 30 units with a good prophylactic effect(7 ?6).There was a small but significant increaseof haemostatic plug formation time in all treatment groups except the one with low molecular weight heparinfragment 30 units anti Xa activity combined withDHE.Thus, by combining low molecular weight heparin withDHE it is possible to prevent thrombus formation without influencing primary haemostasis in rabbits.

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Rademaker, M., R. H. Meyrick Thomas, J. D. Kirby, and I. B. Kovaos. "EFFECT OF THE CALCIUM CHANNEL BLOCKER, NIFEDIPINE, ON HAEMOSTASIS, CLOTTING, AND THROMBOLYSIS EX VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643436.

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Nifedipine, as other calcium channel blockers, has been shown to inhibit platelet aggregation induced by various agonists in vitro. The therapeutic relevance of these findings are, however, questionable, as in vitro inhibition of platelet function occurs at plasma concentrations of nifedipine in excess of 50 uM, while the peak plasma concentration following a single 10 mg oral dose of nifedipine is only 0.2 uM. We have used the Haemostatometer, to assess the effect of nifedipine on haemostasis ex vivo. This instrument allows quantitative assessment of haemostasis by monitoring the pattern of haemostatic plug formation (HPF) in holes punched through polyethylene tubing through which non-anticoagulated blood flows under standard conditions (1,2). The pattern and speed of blood coagulation subsequent to HPF was measured as was the spontaneous thrombolysis time (STT) (taken as the time until expulsion of the haemostatic plug from heparinised blood). All values are for mean + SEM.Blood samples were taken from 10 healthy volunteers before and ninety minutes after a single 10 mg oral dose of nifedipine. Following nifedipine, the initial phase of the haemostatic reaction (HPF) was prolonged from 0.95 ± 0.12 min to 1.57 ± 0.14 min, (p< 0.01); clotting time was also increased from 13.1 ± 1.1 min to 20.7 ± 2.3 min, (p=0.013), and the STT fell from 48.0 ± 9.9 min to 27.5 ± 4.6 min (p=0.014).The increased bleeding time (HPF) provides evidence that a therapeutic dose of nifedipine evokes an anti-platelet effect. The prolongation of the clotting time seen in this study could be explained by,an effect of nifedipine on platelets and hence clotting. The mechanism of the enhanced spontaneous thrombolysis following nifedipine is not known.We suggest that the effect of nifedipine on haemostasis and thrombolysis may contribute to its therapeutic effect.(1) Gorog P and Kovacs I B. Haemostasis 16: 337-345, 1986.(2) Gorog P. Angiology 37: 99-105, 1986.

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Rademaker, M., D. J. Thomas, J. D. Kirby, and I. B. Kovaos. "ACCELERATED IN VITRO HAEMOSTASIS AND DECREASED SPONATEOUS THROMBOLYSIS IN DIABETICS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643106.

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Diabetics have an increased risk of developing coronary, cerebral, and peripheral vascular occlusions. The mechanism of the accelerated haemostatic/thrombotic system is not known and studies on 'hyperactive platelets' and the fibrinolytic system in diabetes are inconclusive. We have used the Haemostatometer to assess haemostasis and thrombolysis in diabetic patients. The Haemostatometer, a new instrument, allows quantitative measurement of haemostasis by monitoring the pattern of haemostatic plug formation (HPF) in holes punched through polyethylene tubing through which non-anticoagulated blood flows under standard conditions (1,2). The pattern and speed of blood coagulation subsequent to HPF was also measured as was the spontaneous thrombolysis time (STT) (taken as the time until expulsion of the haemostatic plug from heparinised blood). Blood was sampled from 20 diabetic patients (10 insulin (IDD) and 10 non-insulin dependant (NIDD)) as well as 20 age mathched controls. All values are for mean ± SEM. Both IDD and NIDD had shorter bleeding times (HPF) than did controls: 2.16 ± 0.44 min vs 3.08 ± 1.14 min (p=0.03) (the initial phase of HPF was even more significantly shorter: 0.53 ± 0.06 min vs 1.03 ± 0.14 min (p<0.0l). The STT in NIDD was significantly longer than in controls: 56.8 ± 3.1 min vs 36.9 ± 4.0 min (p=0.002) while in IDD, the STT was shorter at 22.0 ± 0.5 min (p=0.018 when compared vs controls 36.9 ± 4.0 min).The shortened bleeding time (HPF) in diabetics is most probably a manifestation of hyperactive platelets and could contribute to the increased risk of thrombosis seen. In NIDD the prolonged thrombolysis (STT) may be a contributing factor to the development of diabetic angiopathy, which is thought to be prevented by good diabetic control (ie insulin). This suggests that the diabetic vascular endothelium retains some capacity to generate plasminogen activator in response to insulin.(1). Gorog P and Kovacs IB. Haemostasis 16: 337-345, 1986.(2). Gorog P. Angiology 37: 99-105, 1986.

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Cooper, P. C., D. R. Triger, H. Kennedy, R. G. Malia, and F. E. Preston. "FIBRINOLYSIS AND HAEMOSTASIS DURING ASCITES RECIRCULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643061.

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The use of ascites recirculation in liver disease removes litres of incapacitating fluid and the patient is reinfused with the concentrated ascites, a rich source of albumin. Ascites is thought to contain plasminogen activator (PA) which may further affect deranged haemostasis in these patients. We have examined the effect that ascites recirculation has on levels of tPA, fibrinogen, FDP and platelet count on samples taken pre and approximately 4 hours into ascites recirculation. Using plasminogen rich fibrin plates we were able to demonstrate PA in unfractioned ascitic fluid (N=10, mean diameter lysis=10.2mm); this activity was quenched by addition of antibody to tPA (mean diameter lysis=0.2mm). Despite demonstrating tPA in unfractioned ascitic fluid, we were unable to demonstrate an increase in plasma tPA, mid recirculation, using a sensitive chromogenic assay (pre, geometric mean tPA = 0.061Iu/ml; mid, geometric mean tPA = 0.024Iu/ml). In addition we have also measured the effect that an intra-abdominal injection of the glucocorticoid, dexamethosone (dex), 24 hours prior to recirculation, has on PA content of the ascites, as well as the effect on coagulation screening tests. Fibrin plate lysis showed only a small, though significant reduction in mean lysis diameter in 9 of 10 patients receiving dex, (mean 11.6 to 10.2mm). Results of the coagulation tests showed marked changes during recirculation which were similar in both groups.In conclusion, we have demonstrated free tPA in unfractionated ascites fluid of patients with liver disease, and shown a small reduction in tPA level 24 hours post injection of dex in ascites. Dexamethosone did not influence the changes in coagulation profile post recirculation. We suggest that the changes in coagulation are not due to primary fibrinolysis, but may be due to either dilution effect or DIG.

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5

Siau, Keith, Waqas Fazal, Mo Thoufeeq, Brian C. McKaig, Adrian Stanley, Allan J. Morris, and Aravinth Murugananthan. "PWE-114 Upper GI haemostasis course improves delegate confidence in theoretical and practical aspects of haemostasis management." In British Society of Gastroenterology Annual Meeting, 17–20 June 2019, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-bsgabstracts.485.

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6

Borowska, A., D. Lauri, A. Maggi, E. Dejana, G. de Gaetano, and J. Pangrazzi. "IMPAIREMENT OF PRIMARY HAEMOSTASIS BY LMW-HEPARINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643172.

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Low molecular weight (LMW) heparlns have been developed with the aim of reducing anticoagulant activity thereby minimizing the bleeding complications of conventional heparin. Unexpectedly, bleeding events were reported during treatment with some LMW-heparins, in clinical and experimental studies. We studied the effect of four different LMW-heparlns on primary haemostasis In male rats (CD COBS, Charles River) after l.v. administration of 0.75 mg/kg b.w. of the drugs. LMW heparin A was devoid of any activity on an experimental model of “template” bleeding time in rats (110.6±5.9 sec versus 108.7±4.1 control values) whereas LMW-heparins B, C and D prolonged the bleeding time to a different extent (228.7±19.9, 161.5±6.4 and 161.7±8.6 respectively). Pretreatment of animals with aspirin (100 mg/kg b.w. per o.s). resulted In a significant potentiation of the “template” bleeding time. In vitro platelet aggregation Induced by collagen (20 μg/ml) or by collagen in combination with ADP (5-10 μM) was strongly inhibited by LMW-heparln B, while LMW-heparln A showed no effect. LMW-heparins C and D exerted an Intermediate level of Inhibition of platelet aggregation. The same pattern of aggregating response was found when LMW-heparins A and B were given i.v. to rats (0.75 mg/kg b.w.) and platelet aggregation was studied “ex vivo” 15 min after drug administration.These data may help explain the impairment of primary haemostasis associated with some LMW-heparin preparations.

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7

Giles, Alan R., and Peter Vendervelden. "THE ROLE OF FACTOR VII IN HAEMOSTASIS: A DETAILED MICROSCOPIC ANALYSIS OF THE MORPHOLOGY OF THE EVOLVING HAEMOSTATIC PLUG IN NORMAL AND VII DEFICIENT DOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643783.

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The role of F.VII in haemostasis remains controversial, both in terms of the functional consequences of the deficiency state and the activation pathways to which it makes its principal contribution In vivo. We have developed a cuticle bleeding time (CBT) model in dogs and used this to investigate the functional consequence of both congenital and acquired F.VII deficiency (SD) (Blood 65:1197, 1985). There was no significant difference between the CBT of these animals when compared to controls. However, the CBT prolonged at a significantly lower Heparin level than that observed in controls. F.VIIa was also infused into F.VIII deficient and normal dogs and FPA measured as an indicator of thrombin generation. Significant change in FPA level occurred in the latter but not the former, suggesting that activation of F.IX rather than F.X was favoured. We have now performed detailed morphological studies of the evolving haemostatic plug (HP) in the injured cuticle of F.VII and normal animals by light (LM) and electron microscopy (EM). Quantification of the EM changes noted were performed by morphometric analysis. The tightness of the intravascular component of the HP was assessed by random measurement of intraplatelet distance. The degree of platelet activation was measured by comparing the area of the open canalicular system (OCS) in comparison to the total platelet area. The appearance of fibrin in the plug was also noted. Qualitative LM revealed little difference between the two sets of animals. The appearance of fibrin at the periphery of HP plug was delayed in SD and was reduced in quantity. However, by morphometry although the pattern was identical in both groups, there was a significant delay in the changes noted in SD. These results suggest that the extrinsic pathway may play an important role in triggering the intrinsic pathway, either by providing for activation of the cofactors V and VIII or pulse generation of F.IXa. This may play a critical role in haemostasis when the vessel injured is larger than those in the nail cuticle of the dog (50 - 150 μm) or when other components of haemostatic mechanism are compromised

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8

Kovacs, I. B., R. A. Hutton, and P. B. A. Kernoff. "HAEMOSTASIS IN NATIVE WHOLE BLOOD: CLINICAL STUDIES WITH THE HAEMOSTATOMETER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643073.

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The haemostatometer is a new instrument which allows quantitative assessment of haemostasis by monitoring the pattern of haemostatic plug formation (HPF) which occurs in holes in polyethylene tubing through which unanticoagulated blood is flowing under standard conditions (1). The pattern and speed of blood coagulation, subsequent to HPF is also measured by the instrument. Eight healthy volunteers were tested before and 2hr, 5dy and 12dy after a single 600mg oral dose of aspirin. Maximum prolongation of HPF time occurred at 2hr (1.97 × baseline, p=<0.001) and the effect remained significant (p=<0.01) at 5dy. The pattern of the aspirin-induced effect on HPF was characteristic. The coagulation time was not affected by aspirin. In 4 patients with platelet release defects, the HPF time, but not the clotting time, was significantly prolonged (2.1 × controls, p= <0.01). In 4 patients with von Willebrand’s disease of different severities, platelet-collagen interaction was tested simultaneously with HPF by inserting a length of catgut into the tubing and measuring the time to cessation of blood flow (2).Both impaired HPF and ineffective formation of occlusive platelet thrombus on the catgut were observed. In haemophilia A patients, HPF time as well as clotting time was prolonged in some cases and in these, improvement of platelet function (shortened HPF time) occurred following factor VIII therapy. As diabetes mellitus may be associated with a prethrombotic state, 20 diabetics were tested and shown to have a shortened HPF time.(1) Gorog P, Kovacs I. Haemostasis, 16, 337-45, 1986. (2) Gorog P, Kakkar W. Amer J Clin Path, 86, 311-16, 1986.

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Walshe, K., I. Mackie, M. Gallimore, and S. J. Machin. "PERTURBATION OF THE KALLIKREIN-KININ SYSTEM IN ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644336.

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Platelet and fibrin deposition in the small blood vessels of the lung as well as activation of the contact system with consequent kinin generation have been described in ARDS. It is thought that these haemostatic changes may play a role in the pathogenesis of the disease which include dyspnoea, hypoxaemia, pulmonary oedema, and pulmonary hypertension. We have studied a complete battery of tests for the proteases and inhibitors of the kallikrein-kinin system in an ongoing study of ARDS and haemostasis. 12 patients have so far been studied, with the following factors complicating ARDS: 5 had sepsis, 3 post surgical, 1 head injury, chronic renal and airways disease, renal transplant rejection, or after smoke inhalation during a fire. Assays for: FXI, FXII, prekallikrein (PKK), kallikrein inhibitor (KKi), betaFXIIa inhibitor, (BXIIAi), alpha-2-macroglobulin (α-2-M), alpha-l-antitrypsin (α-1-AT), and antithrombin III (ATIII) were performed by microtitre amidolytic assays to allow the economic processing of large numbers of samples. FXII, PKK, ATIII and α-2-M were invariably low, returning towards normal as the patient became clinically well. The PKK level in particular reflected the clinical course of the patient and appeared to have prognostic significance. Surprisingly, the BXIIai and KKi tended to be increased when the FXII and PKK were decreased. FXI and -1-AT levels showed no change. These results suggest that clinical concentrates of haemostatic inhibitors may be of benefit in ARDS, to stop the continuous activation of the kallikrein-kinin system and generation of biologically active peptides.

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Jarvis, P. M., D. A. J. Galvin, S. D. Blair, and C. N. McCollum. "HOW DOES CALCIUM ALGINATE ACHIEVE HAEMOSTASIS IN SURGERY?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643074.

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Calcium alginate (Kaltostat, Cair Ltd) is a new absorbable material for topical haemostasis in surgery. The possible mode of action, release of calcium ions in exchange for sodium was investigated in human blood.Calcium release was measured in 15 mg samples of calcium alginate placed in 20 ml of 0.9% saline, for intervals of 1, 3 or 10 minutes. To assess the effect on platelets, 3 mg of calcium alginate or surgical gauze were added to 5 ml of Heparinised (100 units) fresh blood for 2 minutes and platelet counts then made using plain blood as a control. Finally using a thrombelastograph, the activation of whole blood coagulation was assessed after a 2 minute contact with 3 mg of calcium alginate, surgical gauze or no additive as control.When calcium alginate was placed in saline, 26% of calcium ions were released in 1 minute giving a calcium ion concentration of 4.62 t 0.02 mmol/L, with only slight further release after 10 minutes to 4.82 ± 0.004 mmol/L. There was a corresponding decrease in sodium ion concentration. Adding calcium alginate to whole blood reduced the platelet count from a control value of 248 i 16 × 109/L to 222 f 15 × 109/L (p< 0.05) compared to 241 ± 15 × 109/L for surgical gauze. Similarly calcium alginate shortened whole blood coagulation time from 17-7 i 1.0 minutes control, to 12.9 ± 1-32 mins (p< 0.001) compared to 15.0 ± 1.5 mins (p< 0.02) for surgical gauze.Calcium alginate rapidly releases calcium ions in exchange for sodium on contact with blood stimulating both platelet activation and whole blood coagulation, significantly more than simple contact activation by surgical gauze.

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Reports on the topic "Haemostasis"

1

Haemostatic agents, sealants and tissue adhesives used in urological surgery. BJUI Knowledge, May 2017. http://dx.doi.org/10.18591/bjuik.0640.

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