Euroanaesthesia 2004

228 Pages·2004·2.86 MB·English

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. Institutional: £599.00 (Europe), $985.00 (USA and Canada) and
Authorization to photocopy items for internal or personal use, or the
£639.00 (Rest of the World); Personal: £130.00 (Europe), $217.00 (USA
internal or personal use of specific clients, is granted by the European
and Canada), £135.00 (Rest of the World), in all cases post-free. Subscribers
Academy of Anaesthesiology for libraries and other users registered with
in Canada must add 7% to the subscription price, to allow for GST.
the Copyright Clearance Center (CCC) Transactional Reporting Service,
Subscribers in Europe must quote their VAT registration number or state
provided that the base fee of $15.00 per copy is paid directly to CCC, 222
that they are not registered. Subscribers in the following countries who are
Rosewood Drive, Suite 910, Danvers, MA 01923, USA. This consent
not VAT-registered must add VAT at the appropriate rate: Belgium (6%
does not extend to other kinds of copying, such as copying for general dis-
TVA/BTW), France (2.1% TVA), Germany (7% MWST), Spain (4% IVA),
tribution for advertising or promotional purposes, for creating new col-
The Netherlands (6% BTW). Orders for current subscriptions and back
lective works or for resale. Special requests should be addressed to the
issues should be sent to EJA Subscription Orders, Cambridge University
Editor. ISSN 0265-0215/01 $15.00.
Press, Edinburgh Building, Shaftesbury Road, Cambridge CB2 2RU, UK.
E-mail: [email protected].
The views expressed in this journal represent those of the authors only. In
The Publishers’ Policy is to use acid-free permanent paper, to the draft stan- no way can they be construed necessarily to reflect the view of either the
dard ISO/DIS 9706, made from sustainable forests using chlorine-free pulp. Editors or the Publishers.
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.