BACKGROUND:Postprandial gastric distention is frequently associated with transient lower esophageal sphincter relaxation and gastroesophageal reflux (GER). Since the role of nutrient perfusion into the jejunum in inducing GER is not well understood, we studied the effect of jejunal feeding on GER through a percutaneous gastrojejunal tube in patients with and without reflux esophagitis. METHODS:Nine stroke patients with reflux esophagitis were fed through a percutaneous gastrojejunal tube with either a liquid meal (2 kcal/2 ml/min) or saline for 2 h randomly on 2 separate days. An esophageal pH probe was placed 5 cm above the gastroesophageal junction to detect acid reflux. Six stroke patients without esophagitis were enrolled as controls. RESULTS: In both the patients with esophagitis and the controls, esophageal acid exposure (15.3% (4.9%-28.2%) versus 2.7% (0.0%-10.8%), P=0.003; 5.9% (0.5%-6.7%) versus 0.0% (0.0%-1.5%), P = 0.01) and events of acid reflux (5 (1-16) versus 2 (0-8), P = 0.02; 12 (3-17) versus 1 (0-4), P = 0.02) were significantly greater during jejunal meal feeding than during saline infusion. Furthermore, in the reflux patients, but not in the controls, acid clearance time was also greater during jejunal meal feeding than during saline infusion (2.9 min (0.5-9.6 min) versus 0.7 min (0.0-4.3 min), P = 0.04). CONCLUSIONS: We therefore conclude that jejunal nutrient infusion without gastric distention can induce GER in both patients with reflux esophagitis and controls. This implies that GER induced by jejununal nutrients may in part explain the incapability of jejunal tube feeding to prevent gastropulmonary aspiration in patients at risk.
RCT Entities:
BACKGROUND: Postprandial gastric distention is frequently associated with transient lower esophageal sphincter relaxation and gastroesophageal reflux (GER). Since the role of nutrient perfusion into the jejunum in inducing GER is not well understood, we studied the effect of jejunal feeding on GER through a percutaneous gastrojejunal tube in patients with and without reflux esophagitis. METHODS: Nine strokepatients with reflux esophagitis were fed through a percutaneous gastrojejunal tube with either a liquid meal (2 kcal/2 ml/min) or saline for 2 h randomly on 2 separate days. An esophageal pH probe was placed 5 cm above the gastroesophageal junction to detect acid reflux. Six strokepatients without esophagitis were enrolled as controls. RESULTS: In both the patients with esophagitis and the controls, esophageal acid exposure (15.3% (4.9%-28.2%) versus 2.7% (0.0%-10.8%), P=0.003; 5.9% (0.5%-6.7%) versus 0.0% (0.0%-1.5%), P = 0.01) and events of acid reflux (5 (1-16) versus 2 (0-8), P = 0.02; 12 (3-17) versus 1 (0-4), P = 0.02) were significantly greater during jejunal meal feeding than during saline infusion. Furthermore, in the reflux patients, but not in the controls, acid clearance time was also greater during jejunal meal feeding than during saline infusion (2.9 min (0.5-9.6 min) versus 0.7 min (0.0-4.3 min), P = 0.04). CONCLUSIONS: We therefore conclude that jejunal nutrient infusion without gastric distention can induce GER in both patients with reflux esophagitis and controls. This implies that GER induced by jejununal nutrients may in part explain the incapability of jejunal tube feeding to prevent gastropulmonary aspiration in patients at risk.