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      Prognostic impact of fecal pH in critically ill patients

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          Abstract

          Introduction

          We have reported that altered gut flora is associated with septic complications and eventual death in critically ill patients with systemic inflammatory response syndrome. It is unclear how fecal pH affects these patients. We sought to determine whether fecal pH can be used as an assessment tool for the clinical course of critically ill patients.

          Methods

          Four hundred ninety-one fecal samples were collected from 138 patients who were admitted to the Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, Japan. These patients were treated in the intensive care unit for more than 2 days. Fecal pH, fecal organic acids, and fecal bacteria counts were measured and compared by survived group and nonsurvived group, or nonbacteremia group and bacteremia group. Logistic regression was used to estimate relations between fecal pH, age, sex, or APACHE II score and mortality, and incidence of bacteremia. Differences in fecal organic acids or fecal bacteria counts among acidic, neutral, and alkaline feces were analyzed.

          Results

          The increase of fecal pH 6.6 was significantly associated with the increased mortality (odds ratio, 2.46; 95% confidence interval, 1.25 to 4.82) or incidence of bacteremia (3.25; 1.67 to 6.30). Total organic acid was increased in acidic feces and decreased in alkaline feces. Lactic acid, succinic acid, and formic acid were the main contributors to acidity in acidic feces. In alkaline feces, acetic acid was significantly decreased. Propionic acid was markedly decreased in both acidic and alkaline feces compared with neutral feces. No differences were noted among the groups in bacterial counts.

          Conclusions

          The data presented here demonstrate that the fecal pH range that extended beyond the normal range was associated with the clinical course and prognosis of critically ill patients.

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          Most cited references21

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          Intraluminal pH of the human gastrointestinal tract.

          After a short introduction (chapter 1) methods of measuring gastrointestinal pH are described in chapter 2. The methods are divided into intubation techniques and tubeless methods, and the advantages and disadvantages are discussed. Measurements with pH-sensitive, radiotransmitting capsules are highlighted, and methodological problems with these capsules are described. Chapter 3 concerns the gastrointestinal pH profile of healthy subjects. The intraluminal pH is rapidly changed from highly acid in the stomach to about pH 6 in the duodenum. The pH gradually increases in the small intestine from pH 6 to about pH 7.4 in the terminal ileum. The pH drops to 5.7 in the caecum, but again gradually increases, reaching pH 6.7 in the rectum. The physiological background of these pH values is discussed. Chapter 4 describes the effect of gastrointestinal pH on bacterial flora, absorption of vitamins and electrolytes, and on the activity of digestive enzymes. The pH-profile in children is described in chapter 5. The profile is identical with that of adults, and it is therefore concluded that the release of a drug from pH-dependent, controlled-release preparations is also probably identical with that of adults. Chapter 6 describes the correlation between certain diseases and the gastrointestinal pH. A resection of the colon and the creation of an ileostomy do not affect the pH of the remaining gut. An ileocaecal resection shortens the small intestinal transit time, increases pH of the proximal colon, but does not change the pH-profile of the small intestine. Chronic pancreatitis and cystic fibrosis seem to decrease pH of the proximal small intestine. Very low colonic pH values have been observed in severe active ulcerative colitis and in Crohn's disease, but the background and clinical implication of this phenomenon are not clear. Chapter 7 describes the modulating effect of diet and drugs on gastrointestinal pH. Diet primarily has an effect on the colonic pH, whereas drugs might affect both small intestinal and colonic pH. The different effects are described. Finally, chapter 8 summarizes the present knowledge about gastrointestinal pH, and future investigations are proposed.
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            Intestinal crosstalk: a new paradigm for understanding the gut as the "motor" of critical illness.

            For more than 20 years, the gut has been hypothesized to be the "motor" of multiple organ dysfunction syndrome. As critical care research has evolved, there have been multiple mechanisms by which the gastrointestinal tract has been proposed to drive systemic inflammation. Many of these disparate mechanisms have proved to be important in the origin and propagation of critical illness. However, this has led to an unusual situation where investigators describing the gut as a "motor" revving the systemic inflammatory response syndrome are frequently describing wholly different processes to support their claim (i.e., increased apoptosis, altered tight junctions, translocation, cytokine production, crosstalk with commensal bacteria, etc). The purpose of this review is to present a unifying theory as to how the gut drives critical illness. Although the gastrointestinal tract is frequently described simply as "the gut," it is actually made up of (1) an epithelium; (2) a diverse and robust immune arm, which contains most of the immune cells in the body; and (3) the commensal bacteria, which contain more cells than are present in the entire host organism. We propose that the intestinal epithelium, the intestinal immune system, and the intestine's endogenous bacteria all play vital roles driving multiple organ dysfunction syndrome, and the complex crosstalk between these three interrelated portions of the gastrointestinal tract is what cumulatively makes the gut a "motor" of critical illness.
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              Altered gut flora and environment in patients with severe SIRS.

              The gut is considered an important target organ of injury after severe insult such as sepsis, trauma, and shock. The impact of bacterial translocation or mesenteric lymph on systemic inflammatory response and multiple organ damage has been investigated in animals, but dynamic changes in the gut flora and environment have not been fully clarified in critically ill patients. In the present study, we quantitatively evaluated changes in the gut microflora and environment in patients with severe systemic inflammatory response syndrome (SIRS). Twenty-five patients with severe SIRS, who fulfilled the criteria for SIRS, had a serum CRP level >10 mg/dL, and were treated in the intensive care unit for more than 2 days, were included in our study. SIRS was a result of sepsis in 18 patients, trauma in 6, and burn in 1. A fecal sample was used for quantitative evaluation of microflora (bacterial counts of 10 key groups including Bifidobacterium and Lactobacillus) by plate or tube technique and of the gut environment (pH and 9 organic acids by high speed liquid chromatography). Data obtained from patients were compared with corresponding data from healthy volunteers. Analysis of fecal flora confirmed that patients with severe SIRS had significantly lower total anaerobic bacterial counts (especially 2-4 log fewer "beneficial" Bifidobacterium and Lactobacillus) and 2 log higher "pathogenic" Staphylococcus and Pseudomonas group counts than those of healthy volunteers. Concentrations of total organic acids (especially "beneficial" short-chain fatty acids such as acetic acid, propionic acid, and butyric acid) in the feces were significantly decreased in the patients, whereas pH was markedly increased. The gut flora and environment are significantly altered in patients with severe SIRS. Abnormal gut flora and environment may affect systemic inflammatory response after severe insult.
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                Author and article information

                Contributors
                Journal
                Crit Care
                Crit Care
                Critical Care
                BioMed Central
                1364-8535
                1466-609X
                2012
                10 July 2012
                : 16
                : 4
                : R119
                Affiliations
                [1 ]Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, 2-15 Yamadaoka, Suita, Osaka, 565-0871, Japan
                [2 ]Department of Clinical Quality Management, Osaka University Hospital, 2-15 Yamadaoka, Suita, Osaka, 565-0871, Japan
                [3 ]Department of Biomedical Statistics, Osaka University Graduate School of Medicine, 2-15 Yamadaoka, Suita, Osaka, 565-0871, Japan
                [4 ]Yakult Central Institute for Microbiological Research, 1796 Yaho, Kunitachi, Tokyo, 186-8650, Japan
                Article
                cc11413
                10.1186/cc11413
                3580696
                22776285
                e2cb7f31-b62f-4899-bdb6-61d8c9aaaa19
                Copyright ©2012 Osuka et al.; 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
                : 7 March 2012
                : 6 May 2012
                : 10 July 2012
                Categories
                Research

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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