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      Effect of bladder volume on measured intravesical pressure: a prospective cohort study

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      1 , , 2
      Critical Care
      BioMed Central

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          Abstract

          Introduction

          Correct bedside measurement of intra-abdominal pressure (IAP) is important. The bladder method is considered as the gold standard for indirect IAP measurement, but the instillation volumes reported in the literature vary substantially. The aim of this study was to evaluate the effect of instillation volume on intra-bladder pressure (IBP) as an estimation for IAP in critically ill patients.

          Methods

          In this prospective cohort study in 13 sedated and mechanically ventilated patients, we used a revised closed system repeated measurement technique for measurement of IBP. After the system was flushed, IBP was measured with 25 ml increments up to 300 ml. The absolute bias for each volume was calculated as IBP at a given volume minus IBP at zero volume.

          Results

          In total, 30 measurement sets were performed (mean 2.3 per patient). The median IBP at 25 ml was already significantly higher than IBP at zero volume (7.5 versus 6 mmHg). There was no correlation between IBP at zero volume and absolute IBP bias at any bladder volume. Median absolute IBP bias was 1.5 mmHg at 50 ml; 2.5 mmHg at 100 ml; 5.5 mmHg at 150 ml; and up to 11 mmHg at 300 ml.

          Conclusion

          Larger instillation volumes than the usually recommended 50 ml to estimate IAP by bladder pressure may cause clinically relevant overestimation of IAP. Small volumes to a maximum of 25 ml, enough to create a fluid column and to remove air, may be sufficient.

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          Most cited references12

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          Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal.

          The diagnosis of intra-abdominal hypertension (IAH) or abdominal compartment syndrome (ACS) is heavily dependent on the reproducibility of the intra-abdominal pressure (IAP) measurement technique. Recent studies have shown that a clinical estimation of IAP by abdominal girth or by examiner's feel of the tenseness of the abdomen is far from accurate, with a sensitivity of around 40%. Consequently, the IAP needs to be measured with a more accurate, reproducible and reliable tool. The role of the intra-vesical pressure (IVP) as the gold standard for IAP has become a matter of debate. This review will focus on the previously described indirect IAP measurement techniques and will suggest new revised methods of IVP measurement less prone to error. Cost-effective manometry screening techniques will be discussed, as well as some options for the future with microchip transducers.
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            Bench-to-bedside review: Chest wall elastance in acute lung injury/acute respiratory distress syndrome patients

            The importance of chest wall elastance in characterizing acute lung injury/acute respiratory distress syndrome patients and in setting mechanical ventilation is increasingly recognized. Nearly 30% of patients admitted to a general intensive care unit have an abnormal high intra-abdominal pressure (due to ascites, bowel edema, ileus), which leads to an increase in the chest wall elastance. At a given applied airway pressure, the pleural pressure increases according to (in the static condition) the equation: pleural pressure = airway pressure × (chest wall elastance/total respiratory system elastance). Consequently, for a given applied pressure, the increase in pleural pressure implies a decrease in transpulmonary pressure (airway pressure – pleural pressure), which is the distending force of the lung, implies a decrease of the strain and of ventilator-induced lung injury, implies the need to use a higher airway pressure during the recruitment maneuvers to reach a sufficient transpulmonary opening pressure, implies hemodynamic risk due to the reductions in venous return and heart size, and implies a possible increase of lung edema, partially due to the reduced edema clearance. It is always important in the most critically ill patients to assess the intra-abdominal pressure and the chest wall elastance.
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              Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure.

              Primary abdominal compartment syndrome (ACS) is a known complication of damage control. Recently secondary ACS has been reported in patients without abdominal injury who require aggressive resuscitation. The purpose of this study was to compare the epidemiology of primary and secondary ACS and develop early prediction models in a high-risk cohort who were treated in a similar fashion. Major torso trauma patients underwent standardized resuscitation and had prospective data collected including occurrence of ACS, demographics, ISS, urinary bladder pressure, gastric tonometry (GAP(CO2) = gastric regional CO(2) minus end tidal CO(2)), laboratory, respiratory, and hemodynamic data. With primary and secondary ACS as endpoints, variables were tested by uni- and multivariate logistic analysis (MLA). From 188 study patients during the 44-month period, 26 (14%) developed ACS-11 (6%) were primary ACS and 15 (8%) secondary ACS. Primary and secondary ACS had similar demographics, shock, and injury severity. Significant univariate differences included: time to decompression from ICU admit (600 +/- 112 vs. 360 +/- 48 min), Emergency Department (ED) crystalloid (4 +/- 1 vs. 7 +/- 1 L), preICU crystalloid (8 +/- 1 vs. 12 +/- 1L), ED blood administration (2 +/- 1 vs. 6 +/- 1 U), GAP(CO2) (24 +/- 3 vs. 36 +/- 3 mmHg), requiring pelvic embolization (9 vs. 47%), and emergency operation (82% vs. 40%). Early predictors identified by MLA of primary ACS included hemoglobin concentration, GAP(CO2), temperature, and base deficit; and for secondary ACS they included crystalloid, urinary output, and GAP(CO2). The areas under the receiver-operator characteristic curves calculated upon ICU admission are primary= 0.977 and secondary= 0.983. Primary and secondary ACS patients had similar poor outcomes compared with nonACS patients including ventilator days (primary= 13 +/- 3 vs. secondary= 14 +/- 3 vs. nonACS = 8 +/- 2), multiple organ failure (55% vs. 53% vs. 12%), and mortality (64% vs. 53% vs. 17%). Primary and secondary ACS have similar demographics, injury severity, time to decompression from hospital admit, and bad outcome. 2 degrees ACS is an earlier ICU event preceded by more crystalloid administration. With appropriate monitoring both could be accurately predicted upon ICU admission.
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                Author and article information

                Journal
                Crit Care
                Critical Care
                BioMed Central (London )
                1364-8535
                1466-609X
                2006
                6 July 2006
                : 10
                : 4
                : R98
                Affiliations
                [1 ]Intensive Care Unit, Ziekenhuisnetwerk Antwerpen Campus Stuivenberg, Lange Beeldekensstraat, B-2060 Antwerp, Belgium
                [2 ]Department of Internal Medicine and Intensive Care Medicine, Ziekenhuisnetwerk Antwerpen Campus Stuivenberg, Lange Beeldekensstraat, B-2060 Antwerp, Belgium
                Article
                cc4962
                10.1186/cc4962
                1750998
                16934130
                45c4cf75-d040-44b0-94e3-3e990bab3541
                Copyright © 2006 Malbrain and Deeren; licensee BioMed Central Ltd.

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 February 2006
                : 13 March 2006
                : 30 April 2006
                : 7 June 2006
                Categories
                Research

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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