title: Duodenogastroesophageal reflux and esophageal mucosal injury in mechanically ventilated patients.
abstract: OBJECTIVE
  Esophagitis has been reported to be the most frequent cause of upper gastrointestinal bleeding in intensive care patients. The mechanisms causing esophagitis are unclear. The aim of this study was to measure esophageal acid and bile reflux and to examine the relationship between reflux and mucosal injury in mechanically ventilated patients.
  
  
  METHODS
  Twenty-five critically ill, mechanically ventilated patients with nasogastric tubes were prospectively included for 24-hour esophageal pH and duodenogastroesophageal bile reflux studies (Bilitec 2000 system). All patients received acid-suppressive therapy for stress ulcer prophylaxis with ranitidine. On the day before the study, patients underwent esophageal endoscopy to determine the presence or absence of esophagitis.
  
  
  RESULTS
  After approximately 5 days of mechanical ventilation, 12 patients (48%) had erosive esophagitis, 2 patients had pathological acid reflux, and 12 patients had pathological bile reflux. The presence of esophagitis was significantly associated with pathological bile reflux (P = 0.017, Fisher exact test). The severity of esophagitis was significantly correlated with the volume of gastric residual volume and with increasing times of bile reflux. The latter was significantly correlated with the number of organ failures.
  
  
  CONCLUSIONS
  Despite acid-suppressive therapy, esophagitis is a frequent finding in critically ill patients after less than a week of mechanical ventilation. In these patients, besides mechanical irritation by the nasogastric tube, chemical injury caused by duodenogastroesophageal reflux seems to have a major role in the pathogenesis of esophageal mucosal lesions.
authors.affiliation: Department of General Internal Medicine/Medical Intensive Care Unit, University Hospital Gasthuisberg, Catholic University of Leuven, Leuven, Belgium. alexander.wilmer@uz.kuleuven.ac.be
authors.forename: A
authors.initials: A
authors.lastname: Wilmer
authors.forename: J
authors.initials: J
authors.lastname: Tack
authors.forename: E
authors.initials: E
authors.lastname: Frans
authors.forename: H
authors.initials: H
authors.lastname: Dits
authors.forename: S
authors.initials: S
authors.lastname: Vanderschueren
authors.forename: A
authors.initials: A
authors.lastname: Gevers
authors.forename: H
authors.initials: H
authors.lastname: Bobbaers
mesh_terms: D000143:Acids / Q000378:metabolism; D000368:Aged; D001655:Bile Reflux / Q000209:etiology / Q000503:physiopathology; D004383:Duodenogastric Reflux / Q000209:etiology* / Q000378:metabolism; D004942:Esophagitis, Peptic / Q000209:etiology / Q000503:physiopathology; D004945:Esophagoscopy; D004947:Esophagus / Q000293:injuries*; D005260:Female; D005764:Gastroesophageal Reflux / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005773:Gastroscopy; D006801:Humans; D008297:Male; D008875:Middle Aged; D009092:Mucous Membrane / Q000293:injuries; D011446:Prospective Studies; D012121:Respiration, Artificial / Q000009:adverse effects*; D014947:Wounds and Injuries / Q000150:complications*
chemical_list: D000143:Acids