Dive A, Michel I, Galanti L, Jamart J, Vander Borght T, Installé E
Intensive Care Unit, Mont-Godinne Hospital, Yvoir, Belgium.
Intensive Care Med. 1999 Jun;25(6):574-80. doi: 10.1007/s001340050905.
In order to prevent gastric microbial overgrowth, which may complicate nasogastric feeding, administration of nutrients more distally into the gut has been advocated in intensive care patients, as it offers the advantage of keeping the stomach empty and acid. In this study, we assessed the impact of jejunal feeding upon gastic pH in a group of mechanically ventilated, critically ill patients, with special focus on duodenogastric reflux as a possible cause of gastric alkalinization during jejunal nutrition.
Prospective experimental study.
Multidisciplinary intensive care unit of a university hospital.
Gastric pH was recorded by continuous pHmetry over a 4-h period of fasting followed by a 4-h period of nasojejunal feeding at 100 kcal/h in 21 mechanically ventilated, critically ill patients. To determine the contribution of duodenogastric reflux to modifications of gastric acidity, the diet was traced with [(111)In] DTPA (pentetic acid) in 11 of these 21 patients; gastric contents were aspirated every 30 min, then analysed for measurement of radioactivity, glucose, and bile acid concentration.
Median intragastric pH increased slightly from 1.59 (1.20-2.73; interquartile range) (fasting) to 2.33 (1.65-4.64) (feeding) (p = 0.013), and the length of time that the pH was 4 or above increased from 1 (0-24) to 9 (0-142) min (p = 0.026). The variability of pH values and the number of acute alkalinization episodes did not change between the two phases. In 10 of 11 patients in which the diet was labeled with [(111)In] DTPA, reflux was documented at a given time of the feeding period. Bile acid concentrations in the stomach increased from 392 (61-1076) (fasting) to 1446 (320-2770) micromol/l (feeding) (p = 0.010) and mean glucose concentration increased from 59 (28-95) to 164 (104-449) mg/dl (p = 0.006).
Duodenogastric reflux is common in mechanically ventilated critically ill patients with nasojejunal feeding tubes. It occurs both during fasting and during nasojejunal feeding. During nasojejunal feeding, moderate alkalinization of the gastric contents occurs as a result of bile and nutrient reflux.
为预防可能使鼻胃管喂养复杂化的胃微生物过度生长，在重症监护患者中提倡将营养物质更向肠道远端给药，因为这具有使胃保持排空和酸性的优点。在本研究中，我们评估了空肠喂养对一组机械通气的重症患者胃pH值的影响，特别关注十二指肠-胃反流作为空肠营养期间胃碱化的可能原因。
前瞻性实验研究。
大学医院的多学科重症监护病房。
对21名机械通气的重症患者在禁食4小时后通过连续pH监测记录胃pH值，随后以100千卡/小时的速度进行4小时的鼻空肠喂养。为确定十二指肠-胃反流对胃酸度改变的作用，在这21名患者中的11名患者中用[（111）铟]二乙三胺五乙酸（喷替酸）追踪饮食；每30分钟抽吸胃内容物，然后分析测量放射性、葡萄糖和胆汁酸浓度。
胃内pH值中位数从禁食时的1.59（1.20 - 2.73；四分位间距）略有增加至喂养时的2.33（1.65 - 4.64）（p = 0.013），pH值为4或更高的时间长度从1（0 - 24）分钟增加至9（0 - 142）分钟（p = 0.026）。两个阶段之间pH值的变异性和急性碱化发作次数没有变化。在11名用[（111）铟]二乙三胺五乙酸标记饮食的患者中的10名患者中，在喂养期的特定时间记录到反流。胃内胆汁酸浓度从禁食时的392（61 - 1076）微摩尔/升增加至喂养时的1446（320 - 2770）微摩尔/升（p = 0.010），平均葡萄糖浓度从59（28 - 95）毫克/分升增加至喂养时的164（104 - 449）毫克/分升（p = 0.006）。
十二指肠-胃反流在有鼻空肠喂养管的机械通气重症患者中很常见。它在禁食期间和鼻空肠喂养期间均会发生。在鼻空肠喂养期间，由于胆汁和营养物质反流，胃内容物会发生中度碱化。
