• M J Bonten, C A Gaillard, S van der Geest, F H van Tiel, A J Beysens, H G Smeets, and E E Stobberingh.
• Department of Internal Medicine, University Hospital Maastricht, The Netherlands.
• Am. J. Respir. Crit. Care Med. 1995 Dec 1; 152 (6 Pt 1): 1825-34.

UnlabelledThis study evaluates the effects of sucralfate and antacids on intragastric acidity, colonization of stomach, oropharynx and trachea, and the incidence of ventilator-associated pneumonia (VAP) in mechanically ventilated patients in intensive care units. We conducted a prospective randomized double-blind trial in which patients were stratified on initial gastric pH. Intragastric acidity was measured with computerized, continuous intragastric monitoring. The diagnosis of VAP was established with protected specimen brush and/or bronchoalveolar lavage. The study included consecutive eligible patients with mechanical ventilation and nasogastric tube.InterventionsAfter stratification on initial intragastric pH into two groups, patients from both groups were randomly assigned to receive either antacids (a suspension of aluminum hydroxide and magnesium hydroxide), 30 mL every 4 h, or sucralfate, 1 g every 4 h. Continuous intragastric pH monitoring was performed in 112 patients (58 antacids, 54 sucralfate). Using predetermined criteria, colonization of stomach, oropharynx, and trachea, and the incidence of VAP were assessed. Altogether, 141 patients were included (74 receiving antacids, 67 sucralfate) and continuous intragastric pH monitoring was performed in 112 patients, with a mean of 75 h per patient. The median pH and the percentage of time with a pH < 4.0 were calculated from each measurement. No significant differences in median pH values (4.7 +/- 2.2 and 4.5 +/- 2.0 for antacids and sucralfate, respectively) were observed. Median pH values were higher in patients with gastric bacterial colonization than in noncolonized patients (5.5 +/- 2.1 and 3.3 +/- 2.0, p < 0.01), but colonization of oropharynx and trachea was not related to intragastric acidity. Thirty-one patients (22%) developed VAP, with a similar incidence in both treatment groups. In addition, antibiotic use, duration of hospitalization, and mortality rates were similar in both groups. Enteral feeding did not change intragastric acidity significantly but increased gastric colonization with Enterobacteriaceae, without influencing oropharyngeal and tracheal colonization. Antacids and sucralfate had a similar effect on intragastric acidity, colonization rates, and incidence of VAP. Intragastric acidity influenced gastric colonization but not colonization of the upper respiratory tract or the incidence of VAP. Therefore, it is unlikely that the gastropulmonary route is important for the development of VAP.

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