DOI: 10.1097/CCM.0b013e3181935001

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PMID: 19112309

Issn Print: 0090-3493

Publication Date: 2009/01/01


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It’s all in the gut: Introducing the concept of acute bowel injury and acute intestinal distress syndrome …*

Manu L. N. G. Malbrain; Inneke De laet

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What this study tells us … In this issue of Critical Care Medicine, Olofsson et al (1) report the results of a study assessing gastric, intestinal, and renal cortex microcirculation parallel with central hemodynamics and respiratory function during intra-abdominal hypertension (IAH) in a large animal model. On first sight, this looks as a repeat of previously performed pathophysiologic studies in animals on the impact of IAH and abdominal compartment syndrome (ACS) on gut perfusion and cardiopulmonary function (2). Is this really the case? Data were collected prospectively in 26 swine. The authors performed 10 mm Hg stepwise increases of intra-abdominal pressure (IAP) at 10-min intervals up to 50 mm Hg via CO2 insufflation in 20 animals, whereas six animals without pneumoperitoneum served as controls. The microcirculation was measured via laser Doppler flowmetry at the mucosal level for the stomach, colon, and small bowel, at the seromuscular level for the colon and small bowel, and also at the level of the renal cortex. The authors observed a progressive drop in microvascular flow at all measurement sites during stepwise increase in IAP. However, when flow was compared relatively with the cardiac output no significant differences could be observed at the mucosal level. Classic effects on cardiac and respiratory function were observed. The authors also found a reasonable correlation between direct IAP and intravesical pressure in 140 paired measurements, although bias and limits of agreement were unacceptably high. The bottom line is that short-term increases in IAP to extreme levels decreased small bowel mucosal blood flow to a lesser extent than the seromuscular blood flow. However, no specific explanation could be given for this observation.
What this study adds… This animal study has a lot of similarities with previously published ones (3). Mucosal blood flow was more preserved during maximal IAP compared with seromuscular flow and this is a new finding (4). This “sparing” of the bowel mucosa suggests the presence of autoregulation/redistribution of microcirculatory (mucosal) blood flow in the small bowel during IAH, which has also been shown during sepsis and ischemia–reperfusion. The authors also successfully incorporated the new consensus definitions and recommendations recently published by the World Society on Abdominal Compartment Syndrome (WSACS, www.wsacs.org) (5, 6). With regard to the best IAP measurement method it remains unclear whether direct IAP measurement is a good standard with a bias of 5.6 mm Hg (compared with intravesical pressure) and unacceptable high limits of agreement ranging from −4.9 to 16.1 mm Hg (7)! Direct IAP measurement is prone to errors by flow dynamics resulting in rapid increases or decreases in pressure during insufflation. The Verres needle can be blocked leading to over- or underestimation of IAP. For study purposes, it is important that a reproducible IAP measurement is used, and recently fully automated continuous techniques have become available (www.spiegelberg.de or www.pulsion.com) (8). The article stresses the importance of a good animal model to study the implications of IAH on end-organ function (3). The best model should probably be “pathologic” in which IAH originates from a primary insult, capillary leak, resuscitation, and ischemia-reperfusion.
What this study does not tell us … To play the devil’s advocate one could argue that the questions that the authors tried to answer have already been addressed previously and some may even argue that the article is lacking some “novelty” value and the different effects on mucosal vs. seromuscular blood flow could be related to methodologic issues.
First, preload was not well defined because only central venous pressure was measured and although the pigs had a pulmonary artery flotation catheter no pulmonary artery occlusion pressures were given.
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