Bonten M J, Gaillard C A, van der Geest S, van Tiel F H, Beysens A J, Smeets H G, Stobberingh E E
Department of Internal Medicine, University Hospital Maastricht, The Netherlands.
Am J Respir Crit Care Med. 1995 Dec;152(6 Pt 1):1825-34. doi: 10.1164/ajrccm.152.6.8520743.
This 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.
After 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.
本研究评估了硫糖铝和抗酸剂对重症监护病房中机械通气患者胃内酸度、胃、口咽和气管定植情况以及呼吸机相关性肺炎（VAP）发生率的影响。我们进行了一项前瞻性随机双盲试验，根据初始胃pH值对患者进行分层。采用计算机化连续胃内监测来测量胃内酸度。通过保护性标本刷和/或支气管肺泡灌洗来确诊VAP。该研究纳入了连续符合条件的机械通气且插有鼻胃管的患者。
根据初始胃内pH值分为两组后，两组患者被随机分配接受抗酸剂（氢氧化铝和氢氧化镁混悬液），每4小时30毫升，或硫糖铝，每4小时1克。对112例患者（58例接受抗酸剂，54例接受硫糖铝）进行了连续胃内pH监测。根据预定标准，评估胃、口咽和气管的定植情况以及VAP的发生率。总共纳入了141例患者（74例接受抗酸剂，67例接受硫糖铝），对112例患者进行了连续胃内pH监测，每位患者平均监测75小时。从每次测量中计算出pH中位数和pH<4.0的时间百分比。未观察到pH中位数有显著差异（抗酸剂组和硫糖铝组分别为4.7±2.2和4.5±2.0）。胃细菌定植患者的pH中位数高于未定植患者（5.5±2.1和3.3±2.0，p<0.01），但口咽和气管定植与胃内酸度无关。31例患者（22%）发生了VAP，两个治疗组的发生率相似。此外，两组的抗生素使用、住院时间和死亡率也相似。肠内喂养对胃内酸度无显著影响，但增加了肠杆菌科在胃内的定植，而不影响口咽和气管定植。抗酸剂和硫糖铝对胃内酸度、定植率和VAP发生率有相似的影响。胃内酸度影响胃内定植，但不影响上呼吸道定植或VAP的发生率。因此，胃肺途径对VAP发生的重要性不太可能。
