Severe portal and systemic acidosis during CO2-laparoscopy compared to helium or gasless laparoscopy and laparotomy in a rodent model: an experimental study

Background and aims This experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and peripheral-arterial pH during experimental laparoscopy. Methods Firstly, 36 male WAG/Rij rats were randomized into six groups ( n  = 6) spontaneously bre...

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Published in:Surgical endoscopy Vol. 36; no. 7; pp. 4701 - 4711
Main Authors: Inderbitzin, Devdas T., Mueller, Tobias U., Marti, Grischa, Eichenberger, Simone, Fellay, Benoît, Magnin, Jean-Luc, Kraehenbuehl, Lukas
Format: Journal Article
Language:English
Published: New York Springer US 01-07-2022
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Abstract Background and aims This experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and peripheral-arterial pH during experimental laparoscopy. Methods Firstly, 36 male WAG/Rij rats were randomized into six groups ( n  = 6) spontaneously breathing during anaesthesia: laparoscopy using carbon dioxide or helium at 6 and 12 mmHg, gasless laparoscopy and laparotomy. 45 and 90 min after setup, blood was sampled from the portal vein, vena cava and the common femoral artery with immediate blood gas analysis. Secondly, 12 animals were mechanically ventilated at physiological arterial pH during 90 min of laparotomy ( n  = 6) or carbon dioxide laparoscopy at 12 mmHg ( n  = 6) with respective blood gas analyses. Results Over time, in spontaneously breathing rats, carbon dioxide laparoscopy caused significant insufflation pressure-dependent portal acidosis (pH at 6 mmHg, 6.99 [6.95–7.04] at 45 min and 6.95 [6.94–6.96] at 90 min, pH at 12 mmHg, 6.89 [6.82–6.90] at 45 min and 6.84 [6.81–6.87] at 90 min; p  < 0.05) compared to laparotomy (portal pH 7.29 [7.23–7.30] at 45 min and 7.29 [7.20–7.30] at 90 min; p  > 0.05). Central-venous and peripheral-arterial acidosis was significant but less severely reduced during carbon dioxide laparoscopy. Laparotomy, helium laparoscopy and gasless laparoscopy showed no comparable acidosis in all vessels. Portal and central-venous acidosis during carbon dioxide laparoscopy at 12 mmHg was not reversible by mechanical hyperventilation maintaining a physiological arterial pH (pH portal 6.85 [6.84–6.90] ( p  = 0.004), central-venous 6.93 [6.90–6.99] ( p  = 0.004), peripheral-arterial 7.29 [7.29–7.31] ( p  = 0.220) at 90 min; Wilcoxon–Mann–Whitney test). Conclusion Carbon dioxide laparoscopy led to insufflation pressure-dependent severe portal and less severe central-venous acidosis not reversible by mechanical hyperventilation.
AbstractList Background and aimsThis experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and peripheral-arterial pH during experimental laparoscopy.MethodsFirstly, 36 male WAG/Rij rats were randomized into six groups (n = 6) spontaneously breathing during anaesthesia: laparoscopy using carbon dioxide or helium at 6 and 12 mmHg, gasless laparoscopy and laparotomy. 45 and 90 min after setup, blood was sampled from the portal vein, vena cava and the common femoral artery with immediate blood gas analysis. Secondly, 12 animals were mechanically ventilated at physiological arterial pH during 90 min of laparotomy (n = 6) or carbon dioxide laparoscopy at 12 mmHg (n = 6) with respective blood gas analyses.ResultsOver time, in spontaneously breathing rats, carbon dioxide laparoscopy caused significant insufflation pressure-dependent portal acidosis (pH at 6 mmHg, 6.99 [6.95–7.04] at 45 min and 6.95 [6.94–6.96] at 90 min, pH at 12 mmHg, 6.89 [6.82–6.90] at 45 min and 6.84 [6.81–6.87] at 90 min; p < 0.05) compared to laparotomy (portal pH 7.29 [7.23–7.30] at 45 min and 7.29 [7.20–7.30] at 90 min; p > 0.05). Central-venous and peripheral-arterial acidosis was significant but less severely reduced during carbon dioxide laparoscopy. Laparotomy, helium laparoscopy and gasless laparoscopy showed no comparable acidosis in all vessels. Portal and central-venous acidosis during carbon dioxide laparoscopy at 12 mmHg was not reversible by mechanical hyperventilation maintaining a physiological arterial pH (pH portal 6.85 [6.84–6.90] (p = 0.004), central-venous 6.93 [6.90–6.99] (p = 0.004), peripheral-arterial 7.29 [7.29–7.31] (p = 0.220) at 90 min; Wilcoxon–Mann–Whitney test).ConclusionCarbon dioxide laparoscopy led to insufflation pressure-dependent severe portal and less severe central-venous acidosis not reversible by mechanical hyperventilation.
Background and aims This experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and peripheral-arterial pH during experimental laparoscopy. Methods Firstly, 36 male WAG/Rij rats were randomized into six groups ( n  = 6) spontaneously breathing during anaesthesia: laparoscopy using carbon dioxide or helium at 6 and 12 mmHg, gasless laparoscopy and laparotomy. 45 and 90 min after setup, blood was sampled from the portal vein, vena cava and the common femoral artery with immediate blood gas analysis. Secondly, 12 animals were mechanically ventilated at physiological arterial pH during 90 min of laparotomy ( n  = 6) or carbon dioxide laparoscopy at 12 mmHg ( n  = 6) with respective blood gas analyses. Results Over time, in spontaneously breathing rats, carbon dioxide laparoscopy caused significant insufflation pressure-dependent portal acidosis (pH at 6 mmHg, 6.99 [6.95–7.04] at 45 min and 6.95 [6.94–6.96] at 90 min, pH at 12 mmHg, 6.89 [6.82–6.90] at 45 min and 6.84 [6.81–6.87] at 90 min; p  < 0.05) compared to laparotomy (portal pH 7.29 [7.23–7.30] at 45 min and 7.29 [7.20–7.30] at 90 min; p  > 0.05). Central-venous and peripheral-arterial acidosis was significant but less severely reduced during carbon dioxide laparoscopy. Laparotomy, helium laparoscopy and gasless laparoscopy showed no comparable acidosis in all vessels. Portal and central-venous acidosis during carbon dioxide laparoscopy at 12 mmHg was not reversible by mechanical hyperventilation maintaining a physiological arterial pH (pH portal 6.85 [6.84–6.90] ( p  = 0.004), central-venous 6.93 [6.90–6.99] ( p  = 0.004), peripheral-arterial 7.29 [7.29–7.31] ( p  = 0.220) at 90 min; Wilcoxon–Mann–Whitney test). Conclusion Carbon dioxide laparoscopy led to insufflation pressure-dependent severe portal and less severe central-venous acidosis not reversible by mechanical hyperventilation.
Author Marti, Grischa
Inderbitzin, Devdas T.
Magnin, Jean-Luc
Mueller, Tobias U.
Fellay, Benoît
Kraehenbuehl, Lukas
Eichenberger, Simone
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  surname: Inderbitzin
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  organization: Department of Cardiac Surgery, University Hospital of Zurich, Department of Anatomy, Faculty of Science and Medicine, University of Fribourg
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  givenname: Tobias U.
  surname: Mueller
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  fullname: Kraehenbuehl, Lukas
  organization: Department of Surgery, Bauchzentrum Medical Center See-Spital
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Issue 7
Keywords Insufflation pressure
Blood gases
Laparoscopy
Insufflation gas
Acidosis
Language English
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PublicationSubtitle And Other Interventional Techniques
PublicationTitle Surgical endoscopy
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Snippet Background and aims This experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and...
Background and aimsThis experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and...
BACKGROUND AND AIMSThis experimental study assesses the influence of different gases and insufflation pressures on the portal, central-venous and...
SourceID pubmedcentral
proquest
crossref
springer
SourceType Open Access Repository
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Publisher
StartPage 4701
SubjectTerms Abdominal Surgery
Acidosis
Blood gas analysis
Carbon dioxide
Gastroenterology
Gynecology
Hepatology
Hyperventilation
Laparoscopy
Laparotomy
Medicine
Medicine & Public Health
Physiology
Proctology
Surgery
Title Severe portal and systemic acidosis during CO2-laparoscopy compared to helium or gasless laparoscopy and laparotomy in a rodent model: an experimental study
URI https://link.springer.com/article/10.1007/s00464-021-08810-6
https://www.proquest.com/docview/2672174294
https://search.proquest.com/docview/2594297528
https://pubmed.ncbi.nlm.nih.gov/PMC9160112
Volume 36
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