Bonten M J, Gaillard C A, van Tiel F H, van der Geest S, Stobberingh E E
Department of Internal Medicine, University Hospital Maastricht, The Netherlands.
Crit Care Med. 1994 Jun;22(6):939-44. doi: 10.1097/00003246-199406000-00010.
To test the influence of continuously administered enteral feeding on gastric pH and gastric colonization in patients receiving or not receiving topical antimicrobial prophylaxis of the oropharynx and stomach, including sucralfate as stress ulcer prophylaxis.
Prospective, open trial.
Two university hospital general intensive care units (ICUs).
Patients (n = 95) with an ICU stay for at least 5 days.
Thirty-one patients received antimicrobial agents into the stomach and oropharynx in combination with sucralfate (1 g/6 hrs) as stress ulcer prophylaxis. Sixty-four other patients did not receive antimicrobial prophylaxis or sucralfate, but instead received gastric pH-increasing stress ulcer prophylactic agents, if indicated. Gastric colonization and gastric pH were measured on admission and subsequently at least two times a week. Forty-eight patients (14 receiving and 34 not receiving antimicrobial prophylaxis) received enteral feeding.
Both enteral feeding and gastric pH-increasing stress ulcer prophylaxis independently increased gastric pH: the risks for a gastric pH of > 3.5 were, respectively, 4.54 and 2.04 (odds ratios). Enteral feeding also increased the risk for gastric colonization by potentially pathogenic microorganisms (odds ratio = 4.52). Patients receiving both topical antimicrobial prophylaxis and sucralfate remained free of gastric colonization for a longer period than those patients receiving gastric pH-increasing stress ulcer prophylaxis. In these two groups, patients without enteral feeding remained free of gastric colonization for a longer period than those patients receiving enteral feeding.
Topical antimicrobial prophylaxis, including sucralfate, successfully prevented gastric colonization with potentially pathogenic microorganisms and was correlated with lower gastric pH values. However, the efficacy was markedly decreased when continuous enteral feeding was administered simultaneously.
测试持续肠内喂养对接受或未接受口咽和胃部局部抗菌预防（包括使用硫糖铝预防应激性溃疡）的患者胃pH值和胃定植的影响。
前瞻性开放试验。
两家大学医院的综合重症监护病房（ICU）。
入住ICU至少5天的患者（n = 95）。
31名患者接受胃内和口咽抗菌药物联合硫糖铝（1 g/6小时）预防应激性溃疡。另外64名患者未接受抗菌预防或硫糖铝，而是根据需要接受提高胃pH值的应激性溃疡预防药物。入院时及随后每周至少两次测量胃定植和胃pH值。48名患者（14名接受抗菌预防，34名未接受抗菌预防）接受肠内喂养。
肠内喂养和提高胃pH值的应激性溃疡预防均独立提高胃pH值：胃pH值> 3.5的风险分别为4.54和2.04（比值比）。肠内喂养还增加了潜在致病微生物引起胃定植的风险（比值比 = 4.52）。接受局部抗菌预防和硫糖铝的患者胃定植阴性持续时间长于接受提高胃pH值的应激性溃疡预防的患者。在这两组中，未接受肠内喂养的患者胃定植阴性持续时间长于接受肠内喂养的患者。
包括硫糖铝在内的局部抗菌预防成功预防了潜在致病微生物的胃定植，并与较低的胃pH值相关。然而，同时进行持续肠内喂养时，疗效明显降低。
