Prelims.qxd 5/14/04 12:57 PM Page i European Journal of Anaesthesiology Volume 21, Supplement 32, 2004 Abstracts and Programme Euroanaesthesia 2004 Joint Meeting of the European Society of Anaesthesiologists and European Academy of Anaesthesiology Lisbon, Portugal, 5–8 June 2004 Greenwich Medical Media Ltd Prelims.qxd 5/14/04 12:57 PM Page ii European Journal of Anaesthesiology Editor-in-Chief Editors Editor of Supplements B. J. Pollard Manchester, UK J.-P. Haberer Paris, France J. N. Cashman London, UK G. H. Sigurdsson Reykjavik, Iceland Deputy Editor-in-Chief and Editor of K. T. Olkkola Turku, Finland Statistical Adviser Commissioned Reviews H. Bürkle Münster, Germany C. J. D. Pomfrett Manchester, UK T. A. Crozier Göttingen, Germany M. Tramèr Genève, Switzerland G. Capogna Roma, Italy Associate Editors H. Tydén Uppsala, Sweden C. J. D. Pomfrett Manchester, UK M. Leuwer Liverpool, UK N. J. N. Harper Manchester, UK A. W. Gelb London, Canada I. T. HoughtonLondon, UK Editor of Book Reviews L. Bogar Pécs, Hungary D. W. Green London, UK Editorial Board Chairman A. R. Aitkenhead Nottingham, UK Members H. Adriaensen Antwerp, Belgium P. B. Hewitt London, UK J. N. Cashman London, UK H. Van Aken Münster, Germany Editor-in-Chief Deputy Editor-in-Chief *T. Pasch Zürich, Switzerland, President of the European Academy of Anaesthesiology *J.-P. Haberer Paris, France, Treasurer of the European Academy of Anaesthesiology *K. T. Olkkola Turku, Finland, Honorary Secretary of the European Academy of Anaesthesiology *H.-J. Priebe Freiburg, Germany, President of the European Society of Anaesthesiologists *P. Amorim Porto, Portugal, Treasurer of the European Society of Anaesthesiologists *G. Hall London, UK,Secretary of the European Society of Anaesthesiologists *W. P. Blunnie Dublin, Ireland, President of the Union Européenne des Médecins Spécialistes, Section of Anaesthesiology *M. Janecsko Budapest, Hungary, Representative of the Confederation of European National Societies of Anaesthesiologists *P. Scherpereel Lille, France, President of the Fondation Européenne d’Enseignement en Anesthésiologie [*Ex-officio] Production Editor Assistant Production Editor Dan Edwards (E-mail: [email protected]) Penny Martin European Journal of Anaesthesiology (EJA) is the official publication of the Despatch. European Journal of Anaesthesiology is despatched within the UK European Academy of Anaesthesiology. The EJA is also the official journal of by 2nd class post, within Europe by airmail, and to other countries by var- the following organizations: the FEEA (Fondation Européenne ious forms of air-speeded delivery. Add to the cost of regular subscription d’Enseignement en Anesthésiologie), the CENSA (Confederation of the £12.00/$18.00 for airmail delivery outside Europe. European National Societies of Anaesthesiology), the ESA (European Society of Anaesthesiologists) and of the Section Anaesthesiology of the UEMS Editorial material should be sent to the Editor, European Journal of (Union Européenne des Médecins Spécialistes), ESCTAIC (European Society Anaesthesiology, Cambridge University Press, Edinburgh Building, for Computing and Technology in Anaesthesia and Intensive Care), EACTA Shaftesbury Road, Cambridge CB2 2RU, UK. E-mail: eja@greenwich- (European Association of Cardiothoracic Anaesthesiologists), EFAAD medical.co.uk. (European Federation for the Advancement of Anaesthesia in Dentistry) and SESAM (Society in Europe for Simulation Applied to Medicine). The Business correspondence, including orders for offprints and advertising, should Journal publishes original scientific work. Preference is given to experimen- be sent to the publishers: European Journal of Anaesthesiology, Advertis- tal work or clinical observations in man, and to laboratory work of clinical ing Department, Cambridge University Press, Edinburgh Building, relevance. There will be regular commissioned reviews by an authority in a Shaftesbury Road, Cambridge CB2 2RU, UK. E-mail: eja@greenwich- field of interest to those working in anaesthesiology or intensive care. medical.co.uk. Information on this journal is available on the website: http://www.eja-online.org Subscription information. European Journal of Anaesthesiology is published monthly (one volume per annum) and the subscription prices for 2004 are Copyright and photocopying: © 2004 European Academy of Anaesthesiology. as follows. 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Prelims.qxd 5/14/04 12:57 PM Page iii Guide to Authors of Abstracts The ESA/EAA solicits the submission of abstracts for the Euroanaesthesia 2005 Meeting, Vienna, Austria, 28–31 May 2005 The ESA encourages, in particular, non-native English speakers to submit abstracts for the Annual Meeting. Please write as simply as possible and avoid language mistakes. After submission, each blinded abstract will be judged by three reviewers. Accepted abstracts will be published in the European Journal of Anaesthesiology, only if they are presented at the Meeting. Please be sure that your abstract, particularly any graphs, can be read easily, taking into consideration that the size of the original material submitted will be reduced for publication. The use of images, graphs or illustrations in colour is not allowed. Non-adherence to these submission guidelines may be cause for rejection of abstracts submitted. All abstracts must be submitted online via the ESA Website www.euroanesthesia.org The submission module will be available to submitters from 1 November to 15 December 2004 (cid:127) You will find all necessary information in the “How to write an abstract?” and “How to submit an abstract online?” sections, in the Annual Meetings (abstracts) part of the website, as well as in the Frequently Asked Questions section of the abstracts module. (cid:127) The ESA does notaccept submission of abstracts by mail, fax or e-mail. (cid:127) Status of reviewed abstracts will be advised exclusivelythrough the ESA Website. (cid:127) Schedule of presentation of accepted abstracts and nomination to the Best Abstract Competition will also be advised through the ESA Website. Submission Conditions When submitting your abstract, you will be prompted to accept the following conditions: (cid:127) The work in the abstract should not be presented at a large English-speaking meeting before the Euroanaesthesia 2005 Meeting, nor should the work appear in another form at that meeting. (cid:127) The work will not be published before the 2005 meeting, in whole or in abstract, in an indexed journal. (cid:127) If the abstract is accepted, the author commits him/herself to present his/her work at the Annual Meeting for which the abstract is submitted. Abstracts will not be published in the supplement of the European Journal of Anaesthesiologists if the presenter does not pre-register for the Annual Meeting. (cid:127) Studies involving animal or human subjects must satisfy the requirements of the institution or organization of the authors regarding the use of human subjects or animals in research. (cid:127) In consideration of the European Society of Anaesthesiologists taking action in reviewing and editing the submission, the author(s) must transfer(s), assign(s), and otherwise convey(s) all copyright to ownership in said work to the European Society of Anaesthesiologists in the event said work is published by the Society. This copyright assignment applies only to the abstract submitted and does not apply to, or prevent, subsequent publication elsewhere of a full manuscript relating to the subject matter of such abstract. Prelims.qxd 5/14/04 12:57 PM Page iv E 2004 UROANAESTHESIA Joint Meeting of the European Society of Anaesthesiologists European Academy of Anaesthesiology Lisbon, Portugal, 5–8 June 2004 PROGRAMME Abstracts Page ESA Trainee Research Prize Competition winners Sunday June 6 17:00–17:45 TPC Room 5C A.1–3 1 ESA Best Abstract Prize Competition Sunday June 6 12:15–13:45 BAPC Auditorium 3&4 A.4–9 2 Evidence-based practice and quality assurance Saturday June 5 15:15–16:45 1AP1 Room 1.06 A.10–18 3 Sunday June 6 16:30–18:00 1AP2 Room 1.06 A.19–27 6 Monday June 7 10:45–12:15 1AP3 Room 1.06 A.28–36 8 Tuesday June 8 10:30–12:00 1AP4 Room 1.06 A.37–45 10 Ambulatory anaesthesia Saturday June 5 13:15–14:45 2AP1 Room 1.06 A.46–52 12 Sunday June 6 14:30–16:00 2AP2 Room 1.06 A.53–62 14 Tuesday June 8 10:30–12:00 2AP3 Room 1.05 A.63–66 17 Monitoring: equipment and computers Saturday June 5 13:15–14:45 3AP1 Room 1.03 A.68–77 18 Saturday June 5 15:15–16:45 3AP2 Room 1.03 A.78–87 20 Sunday June 6 12:30–14:00 3AP3 Room 1.03 A.88–97 22 Sunday June 6 14:30–16:00 3AP4 Room 1.03 A.98–107 25 Sunday June 6 16:30–18:00 3AP5 Room 1.03 A.108–117 27 Monday June 7 10:45–12:15 3AP6 Room 1.03 A.118–127 29 Monday June 7 14:00–15:30 3AP7 Room 1.03 A.128–137 32 Monday June 7 16:15–17:45 3AP8 Room 1.03 A.139–146 35 Monday June 7 16:15–17:45 3AP9 Room 1.11 A.147–154 37 Tuesday June 8 10:30–12:00 3AP10 Room 1.03 A.155–164 39 Tuesday June 8 10:30–12:00 3AP11 Room 1.13 A.165–174 42 Clinical and experimental circulation Saturday June 5 13:15–14:45 4AP1 Room 1.04 A.176–183 44 Saturday June 5 15:15–16:45 4AP2 Room 1.04 A.184–193 46 Sunday June 6 12:30–14:00 4AP3 Room 1.04 A.194–202 49 Sunday June 6 14:30–16:00 4AP4 Room 1.04 A.203–209 51 Sunday June 6 16:30–18:00 4AP5 Room 1.04 A.212–221 53 Monday June 7 10:45–12:15 4AP6 Room 1.04 A.223–231 55 Monday June 7 14:00–15:30 4AP7 Room 1.04 A.233–241 58 Monday June 7 16:15–17:45 4AP8 Room 1.04 A.242–251 60 Respiration Saturday June 5 13:15–14:45 5AP1 Room 1.05 A.252–260 62 Saturday June 5 15:15–16:45 5AP2 Room 1.05 A.261–269 65 Sunday June 6 12:30–14:00 5AP3 Room 1.05 A.270–278 67 Sunday June 6 14:30–16:00 5AP4 Room 1.05 A.279–286 69 Sunday June 6 16:30–18:00 5AP5 Room 1.05 A.287–295 72 Monday June 7 10:45–12:15 5AP6 Room 1.05 A.296–303 74 Monday June 7 14:00–15:30 5AP7 Room 1.05 A.304–312 76 Monday June 7 16:15–17:45 5AP8 Room 1.05 A.314–319 79 Transfusion and haemostasis Sunday June 6 12:30–14:00 6AP1 Room 1.06 A.321–327 81 Monday June 7 14:00–15:30 6AP2 Room 1.06 A.331–337 83 Monday June 7 16:15–17:45 6AP3 Room 1.06 A.339–347 85 Prelims.qxd 5/14/04 12:57 PM Page v v Contents Neurosciences Saturday June 5 13:15–14:45 7AP1 Room 1.07 A.356 87 Saturday June 5 15:15–16:45 7AP2 Room 1.07 A.358–366 87 Sunday June 6 12:30–14:00 7AP3 Room 1.07 A.367–374 89 Sunday June 6 14:30–16:00 7AP4 Room 1.07 A.375–383 91 Sunday June 6 16:30–18:00 7AP5 Room 1.07 A.385–394 94 Monday June 7 10:45–12:15 7AP6 Room 1.07 A.396–404 96 Monday June 7 14:00–15:30 7AP7 Room 1.07 A.405–412 98 Monday June 7 16:15–17:45 7AP8 Room 1.07 A.413–420 100 Local and regional anaesthesia Saturday June 5 15:15–16:45 8AP1 Room 1.12 A.421–431 102 Sunday June 6 12:30–14:00 8AP2 Room 1.12 A.432–441 104 Sunday June 6 14:30–16:00 8AP3 Room 1.13 A.442–451 107 Sunday June 6 16:30–18:00 8AP4 Room 1.13 A.452–461 110 Monday June 7 10:45–12:15 8AP5 Room 1.13 A.462–471 112 Monday June 7 14:00–15:30 8AP6 Room 1.13 A.472–481 115 Monday June 7 16:15–17:45 8AP7 Room 1.13 A.482–491 117 Tuesday June 8 10:30–12:00 8AP8 Room 1.11 A.492–501 120 Pharmacology Saturday June 5 13:15–14:45 9AP1 Room 1.14 A.502–511 123 Saturday June 5 15:15–16:45 9AP2 Room 1.14 A.512–520 125 Sunday June 6 12:30–14:00 9AP3 Room 1.14 A.523–531 128 Sunday June 6 14:30–16:00 9AP4 Room 1.14 A.532–541 130 Sunday June 6 16:30–18:00 9AP5 Room 1.14 A.542–551 132 Monday June 7 10:45–12:15 9AP6 Room 1.14 A.552–561 135 Monday June 7 14:00–15:30 9AP7 Room 1.14 A.562–571 138 Monday June 7 16:15–17:45 9AP8 Room 1.14 A.573–579 140 Tuesday June 8 10:30–12:00 9AP9 Room 1.14 A.582–590 142 Paediatric anaesthesia and intensive care Saturday June 5 13:15–14:45 10AP1 Room 1.11 A.591–600 145 Saturday June 5 15:15–16:45 10AP2 Room 1.11 A.601–609 147 Monday June 7 10:45–12:15 10AP3 Room 1.11 A.610–617 149 Monday June 7 14:00–15:30 10AP4 Room 1.11 A.618–626 151 Obstetric anaesthesia Sunday June 6 12:30–14:00 11AP1 Room 1.13 A.627–636 153 Tuesday June 8 10:30–12:00 11AP2 Room 1.09 A.637–645 156 Intensive care medicine Saturday June 5 13:15–14:45 12AP1 Room 1.08 A.646–655 158 Saturday June 5 15:15–16:45 12AP2 Room 1.08 A.656–665 161 Sunday June 6 12:30–14:00 12AP3 Room 1.08 A.666–675 164 Sunday June 6 14:30–16:00 12AP4 Room 1.08 A.678–684 166 Sunday June 6 16:30–18:00 12AP5 Room 1.08 A.685–691 168 Monday June 7 10:45–12:15 12AP6 Room 1.08 A.692–701 170 Monday June 7 14:00–15:30 12AP7 Room 1.08 A.702–709 172 Monday June 7 16:15–17:45 12AP8 Room 1.08 A.710–716 175 Tuesday June 8 10:30–12:00 12AP9 Room 1.04 A.718–724 176 Tuesday June 8 10:30–12:00 12AP10 Room 1.08 A.725–734 178 Resuscitation and emergency medicine Saturday June 5 13:15–14:45 13AP1 Room 1.13 A.735–743 181 Saturday June 5 15:15–16:45 13AP2 Room 1.13 A.744–751 183 Acute and chronic pain management Saturday June 5 13:15–14:45 14AP1 Room 1.09 A.752–761 185 Saturday June 5 15:15–16:45 14AP2 Room 1.09 A.762–771 187 Sunday June 6 12:30–14:00 14AP3 Room 1.09 A.773–780 190 Sunday June 6 14:30–16:00 14AP4 Room 1.09 A.781–788 192 Sunday June 6 16:30–18:00 14AP5 Room 1.09 A.790–795 194 Monday June 7 10:45–12:15 14AP6 Room 1.09 A.796–804 196 Monday June 7 14:00–15:30 14AP7 Room 1.09 A.805–814 198 Monday June 7 16:15–17:45 14AP8 Room 1.09 A.816–823 200 Tuesday June 8 10:30–12:00 14AP9 Room 1.07 A.824–833 203 Prelims.qxd 5/14/04 12:57 PM Page vi vi Contents Education, research and presentation Sunday June 6 12:30–14:00 15AP1 Room 1.11 A.834–840 205 Patient safety Sunday June 6 14:30–16:00 17AP1 Room 1.11 A.841–846 207 Sunday June 6 16:30–18:00 17AP2 Room 1.11 A.847–853 208 The abstracts published in this Supplement have been typeset from electronic submissions and camera-ready copies prepared by the authors. Every effort has been made to reproduce faithfully the abstracts as submitted. These abstracts have been prepared in accordance with the requirements of the European Society of Anaesthesiologists and have not been subjected to review nor editing by the European Journal of Anaesthesiology.However, no responsibility is assumed by the organizers or publisher for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of methods, products, instructions or ideas contained in the material herein. Because of the rapid advances in medical sciences, we recommend that independent verification of diagnoses and drug doses should be made. Abstracts 1-153....qxd 5/13/04 3:11 PM Page 1 ESA Trainee Research Prize Competition Winners A-1 We hypothesized that recombinant human activated protein C (APC), which has reduced mortality from severe sepsis with 6.1% (1) could antagonize Acute hyperinsulinemia restrains endotoxin induced LPS-induced ALI. Our goal was to assess the effect of APC on pulmonary systemic inflammatory response – an experimental hemodynamics, extravascular lung water content, and markers of coagula- study in a porcine model tion and inflammation in endotoxemic sheep. V. Brix-Christensen1,2, S.K. Andersen1,2, R. Andersen1,2, A. Mengel2, Materials and Methods: Sheep were instrumented (2) and randomized to T. Dyhr4, N.T. Andersen5, A. Larsson4, O. Schmitz3, H. Ørskov2, three groups: An APC group (n(cid:1)4) had an infusion of APC 24(cid:2)g/kg/hr E. Tønnesen1,2 (Xigris®, Eli Lilly & CO, USA) from 4 to 24h; a LPS group (n(cid:1)9) received Escherichia coliLPS 15ng/kg/min intravenously from 0 to 24h; a LPS(cid:5)APC 1Dept. of Anesthesiology and Intensive Care, Aarhus University Hospital; group (n(cid:1)9) received LPS and was treated with APC from 4 to 24h. All 2Institute of Experimental Clinical Research, Aarhus University Hospital; sheep received isotonic saline 3mL/kg/h intravenously. 3Dept. of Pharmacology, Aarhus University Hospital; 4Gentofte County Results: Continuously infused APC alone caused no changes. During Hospital; 5Institute of Biostatistics, Aarhus University, Denmark endotoxemia, APC reduced the increments in pulmonary microwedge pres- The work was performed at the Institute of Experimental Clinical Research sure and extravascular lung water index (EVLWI) by 60% and 75%, respec- (IECR), Aarhus University Hospital, Denmark. tively, paralleled by improved gas exchange. As compared to LPS alone, Background and Goal of Study: Intensive insulin therapy in critically ill APC treatment lowered the plasma level of TNF-(cid:4)by 83% and reversed the patients appears to reduce morbidity and mortality (Van den Berghe). The decrease in protein C and fibrinogen by 25%. Moreover, APC blocked the present study elucidate whether acute hyperinsulinemia per secould atten- LPS-induced translocation of (cid:4)- and (cid:6)-isoforms of protein kinase C in uate the systemic cytokine response and improve neutrophil function during the lungs. endotoxin (lipopolysaccharide (LPS)) induced sepsis in a porcine model. Conclusions: In conscious sheep, continuously infused APC alleviate LPS- Materials and Methods: Pigs were anesthetized, mechanically ventilated induced ALI, as characterized by reduced lung microvascular pressure and and randomised into 4 groups and followed for 570 minutes: Group 1 (anes- EVLWI, improved gas exchange and attenuation of the coagulation and the thesia solely, n(cid:1)10), Group 2 (hyperinsulinemic-euglycemic-clamp (HEC, inflammation dysfunctions. n(cid:1)9)), Group 3 (LPS, n(cid:1)10) and Group 4 (LPS-HEC, n(cid:1)9). Groups 3 and References: 4 were given a 180min infusion of LPS (total 10(cid:2)g/kg). Groups 2 and 4 were 1 Bernard GR et al. N Engl J Med 2001; 344: 699–709 clamped (p-glucose: 5mM/l, insulin infusion rate 0.6mUkg(cid:3)1min(cid:3)1) through- 2 Kirov MY et al. Am J Respir Crit Care Med 2002; 166(11): 1436–42. out the study period. Changes in pulmonary and hemodynamic function, cir- culating cytokines, free fatty acids (FFA), glucagon, and neutrophil chemotaxis were monitored. Results and Discussion: TNF-(cid:4)and IL-6 were significantly reduced in the A-3 LPS-HEC group compared to the LPS group (both p(cid:1)0.04). LPS induced a significant increase in glucagon (p(cid:1)0.01), and this response was signifi- Vasopressin, but not fluid resuscitation, enhances survival cantly reduced in the LPS-HEC group (p(cid:1)0.01). FFA levels were decreased in a liver trauma model with uncontrolled and otherwise in animals exposed to the HEC and LPS-HEC. Animals receiving LPS lethal hemorrhagic shock in pigs showed an increase in pulmonary pressure (p(cid:1)0.00), but otherwise there K.H. Stadlbauer*, H.G. Wagner-Berger*, C. Raedler*, W.G. Voelckel*, were no major changes in pulmonary or hemodynamic function. Neutrophil V. Wenzel*, A.C. Krismer*, G. Klima†, K. Rheinberger*, W. Nussbaumer‡, function was impaired during LPS-sepsis. D. Pressmar*, K.H. Lindner*, A. Königsrainer§ In this experimental study we demonstrated that short-term hyperinsuline- mia together with normoglycemia vastly reduced the systemic inflammatory *Department of Anesthesiology and Critical Care Medicine, †Department of and metabolic responses to LPS-induced sepsis in a porcine model. It was Histology, ‡Department of Transfusion Medicine, §Department of Surgery, clearly demonstrated that maintenance of hyperinsulinemia reduced plasma Leopold-Franzens-University, Innsbruck, Austria levels of glucagon and TNF-(cid:4), the latter supporting the hypothesis that Background: We compared the effects of vasopressin vs. fluid resuscita- insulin has antiinflammatory effects (Das). As expected the neutrophil func- tion on survival in a liver trauma model with uncontrolled and otherwise tion was impaired during LPS-sepsis. In contrast to most clinical courses of lethal hemorrhagic shock in pigs. severe sepsis, the septic insult was well defined with respect to time and LPS Methods: A midline laparotomy was performed on twenty-three domestic dose and controlled in this set up. The clinical response is highly reproducible pigs, followed by an incision, and subsequent finger fraction across the in the pigs, and analogue to the human septic response. right medial liver lobe. During hemorrhagic shock, animals were randomly Conclusion(s): Hyperinsulinemia concomitant with normoglycemia reduces assigned to receive either 0.4U/kg vasopressin (n(cid:1)9), or fluid resuscita- plasma levels of TNF-(cid:4)and the catabolic hormone glucagon in LPS-induced tion (n(cid:1)7), or saline placebo (n(cid:1)7), respectively. A continuous infusion of sepsis in a porcine model. The exogenous insulin acutely modulates the 0.08U/kg/min vasopressin in the vasopressin group, or normal saline was innate immune system by decreasing an inappropriate proinflammatory subsequently administered in the fluid resuscitation and saline placebo response, restoring normal glucose-levels and decreasing FFA and glucagons – group, respectively. After 30min of experimental therapy, bleeding was con- playing an antiinflammatory action. Longer term effects of hyperinsulinemia trolled by surgical intervention, and blood transfusion as well as rapid fluid on the proinflammatory cytokine response remains to be determined. infusion was subsequently performed. References: Results: Maximum mean arterial blood pressure during experimental 1 Van den Berghe G, Wouters R, Weekers F et al. N Engl J Med2001; 345: 1359–67. therapy in the vasopressin-treated animals was significantly higher than in 2 Das UN. Nutrition2001; 17: 409–13. the fluid resuscitation and saline placebo groups (mean(cid:7)SD, 72(cid:7)26 vs. Acknowledgements: The Danish Research Council and the Aarhus 38(cid:7)16 vs. 11(cid:7)7mmHg, respectively; P(cid:8)0.05). Subsequently, mean University Research Foundation. arterial blood pressure remained at (cid:1)40mmHg in all vasopressin-treated animals, whereas mean arterial blood pressure in all fluid resuscitation and saline placebo pigs was close to aortic hydrostatic pressure ((cid:1)15mmHg) A-2 within (cid:1)20min of experimental therapy initiation. Total blood loss was sig- Activated protein C ameliorates endotoxin-induced lung nificantly higher in the fluid resuscitation pigs compared with vasopressin or injury in sheep saline placebo after 10min of experimental therapy (65(cid:7)6 vs. 42(cid:7)4 vs. 43(cid:7)6mL/kg, respectively; P(cid:8)0.05). Seven of seven fluid resuscitation, K. Waerhaug, V.N. Kuklin, M.Y. Kirov, M.A. Sovershaev, B. Langbakk, and seven of seven saline placebo pigs died within (cid:1)20min of experimental O.C. Ingebretsen, K. Ytrehus, L.J. Bjertnaes therapy, while 8 of 9 vasopressin animals survived over a period of seven Departments of Anesthesiology, Physiology and Clinical Chemistry, University days (P(cid:8)0.05). of Tromsø and University Hospital of North Norway, Tromsø, Norway Conclusions: Vasopressin, but not fluid resuscitation or saline placebo, Background and Goal of Study: Acute lung injury (ALI) often develops after ensured survival with full recovery in this liver trauma model with uncon- sepsis due to release of endotoxin (lipopolysaccharide – LPS) to the blood. trolled and otherwise lethal hemorrhagic shock in pigs. Abstracts 1-153....qxd 5/13/04 3:11 PM Page 2 2 ESA Best Abstract Prize Competition ESA Best Abstract Prize Competition A-4 Myocardial infarction 0 Airway infection 1 Patient satisfaction with anaesthesia care: when to Myocardial ischemia 0 Wound infection 39 Deep phlebothrombosis 5 Wound rupture 5 ask the patient? Pulmonary emboli 2 Arthritis 5 D. Saal*, M. Nuebling**, Y. Husemann***, T. Heidegger* Haematoma 7 Cerebro-vascular 0 Airway bleeding 4 Other 5 *Cantonal Hospital, St. Gallen, Switzerland; **Empirische Beratung, Freiburg, Germany; ***Picker Institut, Zug, Switzerland Conclusions: Day surgery in Denmark is a safe practice and readmission to Background and Goal of Study: There is still a lack of information about hospital compares well to international centres (1,3). the effect of time in the judgment of the quality of care by the patient. References: Sociological studies describe different results: response rate decreasing, 1 Twersky R, Fishman D, Homel P. Anesth Analg1997; 84: 319–324. problem score constant or U-shaped with time in a period of up to 12 weeks 2 Mezei G, Chung F. Ann Surg1999; 230: 721–727. (1,2). The goal of this study was to compare the patient’s judgement of 3 Coley KC, Williams BA, DaPos SV, et al. J Clin Anesth2002; 14: 349–353. anaesthesia care after 3 different periods of time since discharge from hospital. A-6 Materials and Methods: After ethics approval 3 groups of patients were Heart rate variability predicts severe hypotension after spinal randomly assigned to receive a standardized, validated psychometric ques- tionnaire (3) either 1, 5 or 9 weeks after their discharge. If after 2 weeks no anaesthesia for elective cesarean section reply was received an identical reminder questionnaire was sent once to R. Hanss, B. Bein, A. Paris, E. Cavus, M. Lehmkuhl, P.H. Tonner, J. Scholz enhance response rate. We measured response rate and the total mean Department of Anaesthesiology and Intensive Care Medicine, University problem score of the underlying 6 dimensions. Data are presented as means Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany in % (95% confidence interval). *p(cid:8)0.05 for the comparison of the means Backgrounds: Routine administration of spinal anaesthesia (SPA) for elective was considered significant. cesarean section is save, nevertheless hypotension due to sympatholysis is a Results and Discussions: The randomization was successful. In group potential harm (1). Heart rate variability (HRV) can determine autonomic con- one, two and three 748, 743 and 723 questionnaires respectively were sent trol and might be feasible to detect patients with high sympathetic tone and out. Response rate including the reminder was 67%, 65% and 59%* therefore at risk for hypotension after SPA. respectively. Total mean problem score for group one, two and three was Materials and Methods: After IRB approval 5 HRV analysis were performed 17(1)%, 17(1)% and 15(1)%* respectively which was explained mainly by in 41 patients (G1:13, G2:11, G3:17). I: before volume preload (VP), II: after VP, significant changes in the dimension continuity of care by the anaesthetist. III: after SPA, IV: 5 minutes after SPA, V: 10 minutes after SPA. Relative low The other dimensions information/participation, respect/confidence, delays, frequency (LF), indicating sympathetic drive, relative high frequency (HF), care in the recovery area and pain management only showed inconsistent indicating parasympathetic drive, and LF/HF ratio, reflecting autonomic con- changes. trol (2,3) were analysed. Depending on the severity of hypotension patients Conclusion(s): The response rate and description of problems decrease were assigned into three groups (G). G1 remained stable, G2 showed moder- when asking patients 9 weeks after discharge compared to 1 and 5 weeks. ate, and G3 severe hypotension. Statistics: Two Way Anova for analysis of Questionnaires asking patients about the quality of anaesthesia care should matched pairs, Mann-Whitney-U test and Wilcoxon-Rank test for compari- be sent within 5 weeks to avoid lower response rates and false low problem son between and within groups, p(cid:8)0.05. scores. Results and Discussions: Demographic data showed no significant dif- References: ferences. Systolic blood pressure of G1 (112(cid:7)11mmHg) remained signifi- 1 Raspe H et al. Das Gesundheitswesen. 1998;60:75–79. cant higher compared to G2 (97(cid:7)9mmHg) and G3 (78(cid:7)9mmHg). LF/HF(I) 2 Ley P et al. Br J Soc Clin Psychol. 1976;15:403–413. 3 Heidegger T et al. Brit J Anaesth. 2002;89(6):863–872. was significant lower in G1 (1.4(cid:7)0.7) compared to G2 (3.3(cid:7)2.2) and G3 Acknowledgements: The study was supported by the Department of (3.2(cid:7)1.9). This findings were confirmed by a significant lower LF and higher Anaesthesia and the Quality Committee, Cantonal Hospital, St. Gallen, HF of G1 compared to G2 and G3 at event I. Within groups LF/HF decreased Switzerland. significantly after VP in G2 to 1.9(cid:7)0.9 whereas it decreased slightly in G3 after VP but decreased significantly after SPA (II: 2.6(cid:7)1.3; III: 1.4(cid:7)0.6). These data indicate a higher sympathetic drive preoperatively in patients A-5 with severe hypotension after SPA. Patients of G2 responded significantly to Return hospital contacts in two Danish day surgery units. VP in terms of decrease of sympathetic drive before SPA, thus alleviating hypotension. G3 did not respond to VP, sympatholysis after SPA leads to Readmission, morbidity and mortality severe hypotension. J. Engbaek, J. Bartholdy, N.C. Hjortsø, L.P. Jacobsen Conclusions: HRV might be a tool to detect patients at high risk for hypo- Department of Anaesthesiology and Intensive Care, Herlev Hospital, tension preoperatively and might be feasible to modulate preoperative VP. University of Copenhagen, Herlev, Denmark References: Background and Goal of Study: Large population studies show that day 1 Chestnut D: Obstetric anesthesia. Principles and practice, 1999. 2 Pomeranz B, et al.: Am J Physiol, 1985. surgery is a safe practice (1,2,3). Return hospital visit rates and associated 3 Pagani M, et al.: Circ Res, 1986. morbidity following discharge from day surgery may serve as a local indi- cator of outcome and quality. In a Danish population we examined the A-7 frequency of all day surgery related surgical and medical return hospital contacts and the related morbidity rates of specific diagnose groups. Pulmonary vascular reactivity: new insights from Materials and Methods: From two University Hospitals 13.906 patients transgenic mice with excessive erythrocytosis undergoing day surgery during 1996–2000 (gynecology, orthopedics, K. Wagner, J. Hasegawa, J. Shibata, D. Li, R. Depping, W. Jelkmann, urology, gastroenterology and mamma surgery) were retrospectively exam- S. Uhlig ined. Their individual civil identification number identified patients. Data of any hospital contact within 60 days after surgery were extracted from The Department of Anesthesiology and Critical Care Medicine, Danish National Registry of patients. The Register delivers informations University Lübeck, Lübeck, Germany about date, type of contact and locality (amb, emergency room (ER) or Background and Goal of Study: Pulmonary vascular remodeling during inpatient) and diagnosis according to ICD10 including death. The medical chronic hypoxia may be the result of either oxygen deprivation or erythro- records of all contacts with selected codes were assessed to decide cytosis. To examine the effect of a chronically elevated hematocrit uncon- whether the contact was definitely related, definitely not related or possibly nected to hypoxia on the pulmonary vascular reactivity, we investigated related to day surgery. transgenic mice over-expressing erythropoietin (1). These mice, reaching a Results and Discussions: Of 149 contacts 64 (0.5%) were definitely related hematocrit of 0.85 (2) without signs of thrombosis or embolism (3), had a sig- (amb 1:1986, ER 1:993, inpatients 1:323). The table shows diagnose groups nificantly increased pulmonary artery pressure (PAP) in vivo (transgenic: with N. No related deaths occurred. Sixty-five percent of the contacts hap- 22.4(cid:7)2.8mmHg, wild type: 14.4(cid:7)4mmHg). pened from the 5th–20th day. The most common diagnose was wound Materials and Methods: Since the significantly elevated blood viscosity of infection (1:356). transgenic mice could have masked the PAP decrease from pulmonary Abstracts 1-153....qxd 5/13/04 3:11 PM Page 3 Evidence-based practice and quality assurance 3 vasodilation, a saline perfused isolated lung setup was used to investigate adherence and phagocytosis. When PFH was present during E. colichal- pulmonary vascular reactivity. lenge, mean fluorescence of adherent bacteria was significantly decreased Results and Discussions: Under ex-vivo conditions, the significantly in neutrophils by about 20% compared to control (p(cid:8)0.05) and tended to reduced baseline PAP indicated that there was chronic pulmonary vasodila- be lower in monocytes (p(cid:1)0.11). However, in these groups, neutrophil tion in transgenic mice. When the thromboxane agonist U46619 was added phagocytic capacity was not impaired and monocytic phagocytosis of following inhibition of cyclooxygenase and/or endothelial nitric oxide syn- E. coliwas even promoted significantly (p(cid:8)0.05). Cell morphology of PFH thase (eNOS), transgenic mice were found to have a significantly smaller rise treated samples showed variable quantities of ingested PFH particles but in PAP compared to wild type mice, consistent with increased perfusate was equivalent to controls otherwise. prostacyclin concentrations (transgenic vs. wild type, 160(cid:7)112pg/ml vs. Conclusions: Perfluorohexane does not result in impaired leukocyte phago- 42(cid:7)37pg/ml) and eNOS protein on immunohistochemistry. cytosis capacity. This result provides further evidence for a safe pulmonary Conclusion(s): Surprisingly, in erythropoietin transgenic mice pulmonary administration of PFC and argues against concerns about PFC impairing vascular smooth muscle thickness was significantly reduced. The effects of host defense. an isolated chronic erythrocytosis on the pulmonary vascular bed consisted of an increased production of vasodilator substances and a reduced smooth A-9 muscle thickness in the pulmonary vessels. These findings indicate, that Cyclic GMP infusion prevents endothelial dysfunction and hypoxia and not erythrocytosis per se markedly contributes to the pulmonary acute lung injury induced by cardiopulmonary bypass vascular remodeling present in chronic obstructive lung disease. References: A. Ruiz, I. Rovira, J. Martinez, A. Puente, C. Ayats, S. Acero 1 Ruschitzka F. et al., PNAS 2000, 97: 11609–11613. Department of Anesthesiology, Hospital Clinic, Barcelona, Spain 2 Wagner K. et al., Blood 2001, 97: 536–542. Background and Goal of Study: Cardiopulmonary bypass (CPB) causes 3 Shibata J. et al., Blood 2003, 101: 4416–4422. dysfunction of the endothelium by reducing endogenous nitric oxide (NO) Acknowledgements: Supported in part by the DFG grant Uh 88/2-4 (SU) [1]. In the lung, endothelial dysfunction increases vascular permeability, and a grant from the Max Kade Foundation (KW). induces alveolar oedema, hypoxaemia and pulmonary hypertension. We investigated the effects cGMP, the second messengerof NO, on endothelial A-8 dysfunction and acute lung injury in an experimental model of CPB. Materials and Methods: Twelve anaesthetized and mechanically ventilated Perfluorohexane exposure does not result in impaired pigs were studied in two groups of six: Group 1 (control) and group 2 (cGMP). leukocyte phagocytosis in vitro All animals were on CPB for 2 hours. Group 1 received no treatment and D. Haufe, E. Koenigshausen, L. Knels, T. Koch group 2 received an infusion of 5(cid:2)gkgmin(cid:3)1of cGMP before, during and after CPB. Acute lung injury was assessed by arterial blood gases and pulmonary Clinic of Anesthesiology and Intensive Care Medicine, Technical University haemodynamics. Pulmonary vascular resistance change to acetylcholine of Dresden, Dresden, Germany (endothelial-dependent relaxation) and to sodium nitroprusside (endothelial- Background and Goal of Study: Liquid ventilation with perfluorocarbons independent relaxation) was used to assess endothelial function. All meas- (PFC) was successfully applied in experimental and human lung injury. urements were performed before and after 2 hours of CPB. Antiinflammatory properties of PFC may contribute to the beneficial effects Results: Pulmonary vascular resistance (PVR) changes, PaO, and mean but also raise concerns regarding a compromised host defense. Therefore, 2 pulmonary artery pressure are shown in the table. this study evaluated the phagocytosis capacity of PFC-exposed human leukocytes in an in vitromodel. Group 1 Group 2 Materials and Methods: Whole blood of human volunteers was pre- PVR change Before After CPB Before After CPB exposed to 25% [v/v] perfluorohexane (PFH) for 1 or 4h with and without ACH (%) (cid:3)31(cid:7)27 (cid:5)8(cid:7)7* (cid:3)52(cid:7)25 (cid:3)40(cid:7)9# subsequent PFH removal. Respective controls consisted of blood incubated SNP (%) (cid:3)33(cid:7)3 (cid:3)26(cid:7)9 (cid:3)44(cid:7)17 (cid:3)35(cid:7)15 in the absence of water-immiscible PFH. After samples were incubated for PaO2(mmHg) 214(cid:7)23 94(cid:7)11* 230(cid:7)22 217(cid:7)17# 10min with opsonized FITC-labeled E. coli, extracellular bacteria were mPAP (mmHg) 18(cid:7)2.0 23(cid:7)1.8* 16(cid:7)1.5 14(cid:7)1.3# quenched with a staining solution and phagocytosis was determined by flow Mean(cid:7)SD, ANOVA & Bonferroni, *P(cid:8)0.05 vs. before, #vs. group 1. ACH (acetylcholine), fluorocytometry. Additional aliquots not subjected to the quenching proce- SNP (sodium nitroprusside). dure were used to calculate the amount of bacteria bound to the cell surface membrane. Cell morphology of E. coli-stimulated leukocytes with and with- CPB impaired pulmonary endothelial-dependent relaxation, causing hypo- out PFH exposure was analyzed using fluorescence microscopy and elec- xaemia and pulmonary hypertension. All this effects were totally prevented tron microscopy. by cGMP infusion. Results and Discussions: During the incubation period, 82–95% of the Conclusions: In this experimental model of CPB the infusion of cGMP pre- neutrophils and 65–81% of the monocytes actively phagocytosed E. coli. In vented endothelial dysfunction and acute lung injury. all groups, there was no significant difference between PFH-exposed sam- Reference: ples and respective controls. PFH pre-exposure for 1 and 4h and removal of 1 Morita K, Ihnken K, Buckerg GD et al. Ann Thorac Surg1996; 61: 1775–1780. the agent prior to E. coliaddition did not influence the degree of bacterial Acknowledgements: Hospital Clinic Residents Grant. Evidence-Based Practice and Quality Assurance A-10 either iv dexamethasone 4 mg (Group DEX, n(cid:1)40), droperidol 1 mg (Group Comparison of prophylactic antiemetic efficacy of DRO, n(cid:1)37) or saline 1ml (Group C, n(cid:1)37). Nausea and vomiting on a dexamethasone and droperidol: a retrospective study 3-point ordinal scale (0(cid:1)none; 1(cid:1)nausea; 2(cid:1)vomiting) and the need for rescue antiemetic treatment were evaluated during 0–4h (early PONV) and R. Krobot, J. Premuzic, I. Bacak 4–24h (late PONV) periods postoperatively. Data were analysed by Kruskal- Department of Anesthesiology and Intensive Care, General Hospital Varazdin, Wallis and Fisher’s exact test (significance level P(cid:8)0.05). Varazdin, Croatia Results and Discussions: Groups were comparable with respect to Background and Goal of Study: Postoperative nausea and vomiting demographic data, anaesthesia time and anaesthetic drug dosage. Both (PONV) are frequent and disturbing adverse effects of laparoscopic chole- dexamethasone and droperidol significantly decreased the incidence of early cystectomy and the antiemetic prophylaxis is strongly recommended (1). PONV when compared to saline, with an incidence of 2%, 3% and 22%, Goal of this retrospective study was to compare prophylactic antiemetic respectively (P(cid:8)0.05). The incidence of late PONV was 43% in Group C effect of dexamethasone and droperidol in patients undergoing laparo- compared to 20% in Group DEX (P(cid:1)0.04) and 27% in Group DRO scopic cholecystectomy. (P(cid:1)0.22). Late nausea was experienced in 5%, 3% and 16% and late emetic Materials and Methods: A total of 114 ASA I or II patients undergoing laparo- episodes occurred in 15%, 24% and 27% patients in Group DEX, DRO and scopic cholecstectomy were included in study. All patients received TIVA with C, respectively. The proportion of patients who required antiemetic treatment propofol, fentanyl and rocuronium. After tracheal intubation, patients received during 24h-period was 19% in Group C compared to 3% in Group DEX Abstracts 1-153....qxd 5/13/04 3:11 PM Page 4 4 Evidence-based practice and quality assurance (P(cid:1)0.03) and 8% in Group DRO (P(cid:1)0.30). No clinically important side- significantly (p(cid:8)0,01) more hypothermic than in GA group. Surgical com- effects related to the use of dexamethasone and droperidol were found. plications occurred to 4 (8%) patients in GA group and 11 (22%) in GA(cid:5)EA Conclusion(s): Both dexamethasone and droperidol significantly reduced group (p(cid:1)0,07). early PONV (0–4h) but only dexamethasone significantly reduced the inci- Conclusions: Our study showed that: 1. Esophageal core temperature dence of late PONV (4–24h). The need for rescue antiemetic treatment dur- decreased in all patients, but heat lost was more profound in combined gen- ing 24-h period postoperatively was significantly lower in dexamethasone, eral and epidural anesthesia group. 2. Hypothermia might be an important but not in droperidol group. risk factor in postoperative surgical complications development after major Reference: abdominal surgery. 1 Thune A, Appelgren L, Haglind E. Eur J Surg 1995;161:265–268. A-13 A-11 Is it necessary to use ondansetron during a total intravenous Effect of oxygenation and suction in monitored anaesthesia anesthesia with propofol to reduce the incidence of care of eye surgery postoperative nausea and vomiting (PONV)? A. Turan, H. Esgin, S. Seker, Z. Pamukcu C. Aguila, P. Leyton, G. Volpato, P. Lagos, M. Cumsille Department of Anaesthesiology and Opthalmology, Trakya Univ. Medical Faculty, Edirne, Turkey Department of Anesthesiology, University of Chile, Santiago, Chile Background and Goal of Study: Hypoxia and carbondioxide rebreathing Background and Goal of Study: Anesthesia based in inhalation agents are the main factors effecting patient comfort in eye surgery. We aimed to present a high incidence of postoperative nausea and vomiting (PONV). The investigate the role and effect of oxygen application and suction of carbon- use of propofol decreases this problem. Our goal was to estimate the inci- dioxide rich air in monitored anesthesia care of eye surgery. dence of PONV in patients with propofol–remifentanil TIVA and to study if it Materials and Methods: Following ethic committee approval and written is necessary the use of ondansetron for the prevention of PONV after TIVA. informed consent, 100 patients (ASA I–II) scheduled for elective eye surgery Materials and Methods: 71 patients ASA I–II scheduled for lumbar or cervi- were randomly divided into four groups. In Group I patients suction under cal discectomy were included in this double blinded prospective study. drapes and nasal oxygen (2l/min), group II patients nasal oxygen (2l/min), Patients were randomly assigned to received ondansetron 4mg iv or placebo group III nothing and in group IV patients suction under drapes were used. at the end of the surgery. Ondansetron 4mg iv was used as rescue antiemetic Patients were first sedated by 2mg midazolam and according to ramsay agent. Both groups received propofol TCI combined with remifentanil infu- scale were given 1mg midazolam whenever required. Heart rate, mean arte- sion. PONV were recorded at different times (60min, 4, 8, 12 and 24 hours) rial pressure, SpO, Ramsay scale, midazolam consumption through opera- after the end of surgery. Statistical analysis: chi-square test. 2 tion and, Aldrete scale, patient satisfaction, side-effects were postoperatively Results and Discussion: 37 patients received ondansetron and 34 placebo. evaluated. Anova, Kruskal Wallis, Friedman, Student’s t test and chi square 58 patients had a lumbar discectomy and 13 cervical discectomy. Mean (SD) were used as appropriate. propofol consume was 1114mg (575.28) and for remifentanil 3.38mg (1.64). Results and Discussions: Patient demography, operation time, heart rate, Nausea incidence was 9.8% (7 patients) and vomiting was 5.6% (4 patients). mean arterial pressure, Ramsay scores, Aldrete scores and midazolam con- There were no significant differences between groups at different times. sumptions were similar in all groups. SpO values were found to be higher in 2 group I and in group II at first 10mins of operation when compared with Table 1. Incidence of PONV (nausea: n) (vomiting: v) group III and IV (p(cid:8)0.05). At 20mins to end of operation SpO2values were Times 60min 4hrs 8hrs 12hrs 24hrs higher in group I when compared with other groups, and in group II was Ondansetron 0 0 0 0 3 n(cid:5)1 v found to be higher when compared with groups III and IV (p(cid:8)0.05). Patient Placebo 0 2 n 1 v 0 2 n(cid:5)2 v satisfaction was found higher in groups I and II when compared with groups II and IV (p(cid:8)0.05). Conclusion(s): The incidence of PONV after lumbar and cervical discectomy Conclusions: Nasal oxygen was ineffective after 10mins of operation and with propofol anesthesia is low. Our study suggests there is no need to use only suction had no effect. Nasal oxygen with suction was the most effective ondansetron if general anesthesia is maintained with propofol–remifentanil through operation in preventing hypoxia with higher patient satisfaction. In TIVA. eye operations where patients face is covered with drapes we suggest nasal Reference: oxygen and suction to improve patient comfort and decrease hypoxia. 1 Tramèr MR. Efficacy, dose-response and safety of ondansetron in prevention of post- operative nauseas and vomiting. Anesthesiology 1997; 87: 1277–1289. A-12 Intraoperative core temperature changes and postoperative A-14 complications rate in colorectal cancer surgery. Comparison Continuous infusion of urapidil in ENT surgery of two different methods of anesthesia J.L. López-Berlanga, M. Zaballos, C. Benito, E. García de Lucas K. Rimaitis Dpto. Anestesia y Reanimación, Hospital Gregorio Marañón, Madrid, Spain Department of Anesthesia, Kaunas Medical University Hospital, Background and Goal of Study: A moderate degree of controlled hypo- Kaunas, Lithuania tension is recommended in ENT procedures. This method decreases bleed- Background and Goal of Study: The purpose of our study is to compare ing in the surgical site and improve operating conditions. We evaluated the combined general and epidural anesthesia with general anesthesia alone in effectiveness and safety of continuous infusion of urapidil associated with respect to core temperature changes intraoperatively and to evaluate post- remifentanil, to maintain MAP within 20–30% of baseline MAP. operative complication rate after major abdominal surgery. Materials and Methods: After written informed consent, 40 patients, Materials and Methods: One hundred patients scheduled to undergo elec- 43(cid:7)18yrs, ASA I–III, scheduled for elective ENT surgery were included tive colorectal cancer surgery were randomized to receive general anesthesia in this prospective study. The patients were randomly assigned to one of (GA group) or combined general and epidural anesthesia (GA(cid:5)EA group) 2 groups: Group U (urapidil, n(cid:1)20) received 0.3mgkg(cid:3)1of urapidil followed 50 patients in each group. Prior induction of anesthesia, thoracic epidural by a constant infusion of 2(cid:2)gkg(cid:3)1min(cid:3)1, and Group C (control, n(cid:1)20) catheter was inserted and block was established up to T4 level using bupiva- urapidil was substituted by saline. Anaesthesia was induced with propofol caine 2,5mg/ml and fentanyl 10(cid:2)g/ml mixture in GA(cid:5)EA group. Induction (TCI system) and remifentanil at 0,4(cid:2)gkg(cid:3)1min(cid:3)1, and reduced to and maintenance of general anesthesia were performed the same way in 0,2(cid:2)gkg(cid:3)1min(cid:3)1, after tracheal intubation. Urapidil infusion was titrated to both groups. Temperature in operating theatre was kept at 22(cid:7)2°C level in maintain hypotension. We use nitro-glycerine (NTG) as a rescue medication all cases. Intravenous infusion fluids were heated in thermostatic cupboard if hypotension was not achieved. Haemodynamic parameters, percentage of and their temperature was the same (36°C) in both groups. Core temperature patients with target MAP, percentage of dry operative field, and secondary in esophagus was started to measure every 5min after induction of anes- effects were recorded during all procedure. Statistical analysis: independent thesia until the end of surgery registering the stage of operation. All post- Student’s t-tests. Chi-square or Fisher’s exact test, as appropriate. SPSS operative complications were accurately registered. Results and Discussions: Both groups were similar in demographic, ASA, Results: There were no significant differences between the groups in respect preinduction haemodynamic parameters and surgical procedures. U Group to patients’ characteristics, operations carried out and duration of surgery. Core showed a statistically significant difference in percentage of Target MAP temperature decreased during surgery from 36,5(cid:7)0,4°C to 36,0(cid:7)0,5°C in (p(cid:8)0.002) respect C Group, and requested less NTG to get this target GA group as compared with 36,3(cid:7)0,4°C to 35,7(cid:7)0,6°C in GA(cid:5)EA (p(cid:8)0.0001). Both groups presented a non statistically significant difference group respectively (p(cid:8)0,01). Moreover, patients in GA(cid:5)EA group became in percentage of Dry Field and requests of Ephedrine.