Pulmonary aspiration of gastric contents results initially from reflux of stomach contents into the esophagus. Small-bore enteral feeding tubes are thought to result in less pulmonary aspiration and less reflux. We prospectively investigated the effect of nasogastric tube size upon gastroesophageal (GE) reflux in normal volunteers in a randomized crossover trial. Reflux was assessed by gastroesophageal scintiscanning, a radioisotopic technique that detects and quantitates GE reflux. A total of 11 subjects were studied three times: control, no nasogastric tube, small-bore (8F) nasogastric tube, and large-bore (14F) nasogastric tube. Reflux was assessed in each subject under each experimental condition by provocative testing in which abdominal pressure was increased from 0 to 100 mm Hg by 20-mm Hg increments with an abdominal pressure device. GE reflux indices were calculated for each measurement and the groups compared. A positive indicator of reflux was defined as a > or = 4% reflux index. Gastroesophageal reflux was not detected at any level of abdominal pressure regardless of the presence or size of a nasogastric tube. With maximum 100 mm Hg abdominal pressure, the reflux index was control, 1.75 +/- 0.45%; small-bore tube, 1.67 +/- 0.28%; and large-bore tube, 1.88 +/- 0.35% (NS). The reflux index was not different between small-bore and large-bore nasogastric tubes. Our data suggest the size of a nasogastric tube is not an important determinant of GE reflux in normal subjects during short-term intubation. Large-bore tubes did not cause more reflux than small-bore tubes. The presence of a nasogastric tube did not cause reflux in normal subjects. These data suggest that factors other than the size of nasogastric tube are more important in GE reflux in normal subjects.

The effects of malnutrition and refeeding on nutritional indices, pulmonary function, and diaphragmatic contractile properties were studied in severely malnourished patients with anorexia nervosa. Fifteen patients were evaluated upon hospital admission (Day 0) and on Days 7, 30, and 45 after starting feeding. Spirometry, lung volumes, and arterial blood gases were measured at each time interval, as were contractile properties of the diaphragm as assessed by transdiaphragmatic pressure generated during electrical phrenic nerve stimulation (Pdistim) and a maximal sniff maneuver (Pdisniff). Anthropomorphic and biochemical measurements were performed at each time interval. Patients were severely malnourished upon admission; mean body weight was 37.1 +/- 4.7 kg (63% ideal body weight). During nutritional support, body weight increased significantly to 42.9 +/- 4.6 kg on Day 45 (p < 0.01), as did muscle mass: 11.2 +/- 4.1 kg on Day 0, to 16.6 +/- 4.9 kg on Day 45 (p < 0.01). Vital capacity and FEV1 increased significantly by Day 30 (p < 0.05). Lung volumes were unchanged. Mean arterial blood gas values were also within the normal range at Day 0; PaO2, 92.6 +/- 2.4 mm Hg and PacO2, 41.0 +/- 1.5 mm Hg. Four patients, however, had an increased PacO2 (> 42 mm Hg) at Day 0, which returned to normal by Day 30. Diaphragmatic contractility was severely depressed initially; Pdistim, 15.9 +/- 1.4 cm H2O; Pdisniff, 65.4 +/- 5 cm H2O; but it significantly increased with nutritional support by Day 30 to 22.5 +/- 1.9 and 84.6 +/- 4.7 cm H2O, respectively. We conclude that diaphragmatic function is severely impaired in malnuorished patients free of other coexisting

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