Cargando…

Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model

BACKGROUND: Intra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients. This study describes pathophysiologic effects of the acutely elevated intra-abdominal pressure on microvascular fluid exchange and mic...

Descripción completa

Detalles Bibliográficos
Autores principales: Elvevoll, Bjørg, Husby, Paul, Øvrebø, Kjell, Haugen, Oddbjørn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4216359/
https://www.ncbi.nlm.nih.gov/pubmed/25331782
http://dx.doi.org/10.1186/1756-0500-7-738
_version_ 1782342247840219136
author Elvevoll, Bjørg
Husby, Paul
Øvrebø, Kjell
Haugen, Oddbjørn
author_facet Elvevoll, Bjørg
Husby, Paul
Øvrebø, Kjell
Haugen, Oddbjørn
author_sort Elvevoll, Bjørg
collection PubMed
description BACKGROUND: Intra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients. This study describes pathophysiologic effects of the acutely elevated intra-abdominal pressure on microvascular fluid exchange and microcirculation. The resulting changes could contribute to development of organ dysfunction or failure. METHODS: 16 pigs were randomly allocated to a control-group (C-group) or an interventional group (P-group). After 60 min of stabilization, intra-abdominal pressure of the P-group animals was elevated to 15 mmHg by Helium insufflation and after 120 min to a level of 30 mmHg for two more hours. The C-group animals were observed without insufflation of gas. Laboratory and hemodynamic parameters, plasma volume, plasma colloid osmotic pressure, total tissue water content, tissue perfusion, markers of inflammation and cerebral energy metabolism were measured and net fluid balance and fluid extravasation rates calculated. Analysis of variance for repeated measurements with post-tests were used to evaluate the results with respect to differences within or between the groups. RESULTS: In the C-group hematocrit, net fluid balance, plasma volume and the fluid extravasation rate remained essentially unchanged throughout the study as opposed to the increase in hematocrit (P < 0.001), fluid extravasation rate (P < 0.05) and decrease in plasma volume (P < 0.001) of the P-group. Hemodynamic parameters remained stable or were slightly elevated in the C-group while the P-group demonstrated an increase in femoral venous pressure (P < 0.001), right atrial pressure (P < 0.001), pulmonary capillary wedge pressure (P < 0.01) and mean pulmonary arterial pressure (P < 0.001). The protein mass decreased in both study groups but was significantly lower in the P-group as compared with the C-group, after 240 min of intervention. The increased intra-abdominal pressure was associated with elevated intracranial pressure and reduced tissue perfusion of the pancreas and the gastric- and intestinal mucosa. CONCLUSION: Elevation of intra-abdominal pressure has an immediate impact on microvascular fluid extravasation leading to plasma volume contraction, reduced cardiac output and deranged perfusion of abdominal organs.
format Online
Article
Text
id pubmed-4216359
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-42163592014-11-02 Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model Elvevoll, Bjørg Husby, Paul Øvrebø, Kjell Haugen, Oddbjørn BMC Res Notes Research Article BACKGROUND: Intra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients. This study describes pathophysiologic effects of the acutely elevated intra-abdominal pressure on microvascular fluid exchange and microcirculation. The resulting changes could contribute to development of organ dysfunction or failure. METHODS: 16 pigs were randomly allocated to a control-group (C-group) or an interventional group (P-group). After 60 min of stabilization, intra-abdominal pressure of the P-group animals was elevated to 15 mmHg by Helium insufflation and after 120 min to a level of 30 mmHg for two more hours. The C-group animals were observed without insufflation of gas. Laboratory and hemodynamic parameters, plasma volume, plasma colloid osmotic pressure, total tissue water content, tissue perfusion, markers of inflammation and cerebral energy metabolism were measured and net fluid balance and fluid extravasation rates calculated. Analysis of variance for repeated measurements with post-tests were used to evaluate the results with respect to differences within or between the groups. RESULTS: In the C-group hematocrit, net fluid balance, plasma volume and the fluid extravasation rate remained essentially unchanged throughout the study as opposed to the increase in hematocrit (P < 0.001), fluid extravasation rate (P < 0.05) and decrease in plasma volume (P < 0.001) of the P-group. Hemodynamic parameters remained stable or were slightly elevated in the C-group while the P-group demonstrated an increase in femoral venous pressure (P < 0.001), right atrial pressure (P < 0.001), pulmonary capillary wedge pressure (P < 0.01) and mean pulmonary arterial pressure (P < 0.001). The protein mass decreased in both study groups but was significantly lower in the P-group as compared with the C-group, after 240 min of intervention. The increased intra-abdominal pressure was associated with elevated intracranial pressure and reduced tissue perfusion of the pancreas and the gastric- and intestinal mucosa. CONCLUSION: Elevation of intra-abdominal pressure has an immediate impact on microvascular fluid extravasation leading to plasma volume contraction, reduced cardiac output and deranged perfusion of abdominal organs. BioMed Central 2014-10-20 /pmc/articles/PMC4216359/ /pubmed/25331782 http://dx.doi.org/10.1186/1756-0500-7-738 Text en © Elvevoll et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Elvevoll, Bjørg
Husby, Paul
Øvrebø, Kjell
Haugen, Oddbjørn
Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
title Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
title_full Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
title_fullStr Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
title_full_unstemmed Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
title_short Acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
title_sort acute elevation of intra-abdominal pressure contributes to extravascular shift of fluid and proteins in an experimental porcine model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4216359/
https://www.ncbi.nlm.nih.gov/pubmed/25331782
http://dx.doi.org/10.1186/1756-0500-7-738
work_keys_str_mv AT elvevollbjørg acuteelevationofintraabdominalpressurecontributestoextravascularshiftoffluidandproteinsinanexperimentalporcinemodel
AT husbypaul acuteelevationofintraabdominalpressurecontributestoextravascularshiftoffluidandproteinsinanexperimentalporcinemodel
AT øvrebøkjell acuteelevationofintraabdominalpressurecontributestoextravascularshiftoffluidandproteinsinanexperimentalporcinemodel
AT haugenoddbjørn acuteelevationofintraabdominalpressurecontributestoextravascularshiftoffluidandproteinsinanexperimentalporcinemodel