• Garry Nind, Wei-Hao Chen, Richard Protheroe, Katsuhiko Iwakiri, Robert Fraser, Robert Young, Marianne Chapman, Nam Nguyen, Daniel Sifrim, Rachael Rigda, and Richard H Holloway.
• Department of Gastroenterology, Hepatology and General Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
• Gastroenterology. 2005 Mar 1;128(3):600-6.

Background & AimsGastroesophageal reflux is a major problem in mechanically ventilated patients and may lead to pulmonary aspiration and erosive esophagitis. Transient lower esophageal sphincter relaxations are the most common mechanism underlying reflux in nonventilated patients. The mechanisms that underlie reflux in critically ill ventilated patients have not been studied. The aim of this study was to determine the mechanisms underlying gastroesophageal reflux in mechanically ventilated patients in the intensive care unit.MethodsIn 15 mechanically ventilated intensive care unit patients, esophageal motility, pH, and intraluminal impedance (11/15 patients) were recorded for 1 hour before and 5 hours during continuous nasogastric feeding.ResultsBasal lower esophageal sphincter pressure was uniformly low (2.2 +/- 0.4 mmHg). The median (interquartile range) acid exposure (pH <4) was 39.4% (0%-100%) fasting and 32% (7.5%-94.2%) fed. Acid reflux occurred in 10 patients, but slow drifts in esophageal pH were also an important contributor to acid exposure. If esophageal pH decreased to pH <4, it tended to remain so for prolonged periods. A total of 46 acid reflux events were identified. Most (55%) occurred because of absent lower esophageal sphincter pressure alone; 45% occurred during straining or coughing.ConclusionsGastroesophageal reflux in mechanically ventilated patients is predominantly due to very low or absent lower esophageal sphincter pressure, often with a superimposed cough or strain. These data suggest that measures that increase basal LES pressure may be useful to prevent reflux in ventilated patients.

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