Gastroesophageal Reflux And Ventilator Associated Pneumonia

Background： Ventilator-associated pneumonia (VAP) is a lung parenchymainfection seen in patients receiving mechanical ventilation for48hours, and is acommon complication of mechanical ventilation. According to the Canadian Society ofcritically ill patient VAP Guide: the rate of VAP infection in critically ill ICU patientsis40%-60%, respiratory infections account for30%-60%, the average ICU stayincreases by4.3days and the absolute risk of death increases by5.8%. Therefore,preventing and reducing the incidence of VAP can improve the therapeutic success rateof critically ill patients in an emergency and shorten the duration of mechanicalventilation. However, the strict measures taken so far to prevent exogenous infectionhave not achieved the expected effect of significantly reducing the incidence of VAP.These findings suggest that there is another mechanism in addition to the exogenouspathway involved in VAP, i.e., the endogenous mechanism of stomach-lung infection,and this pathway has attracted more and more attention in clinical practice. Recently, itwas suggested that the stomach-lung pathway of VAP is due to gastroesophageal reflux.Objective： To investigate the relationship between pepsin concentration in thepharynx and trachea and the severity of ventilator-associated pneumonia (VAP) inmechanically ventilated ICU patients.Methods： Samples (0.5mL) of pharyngeal and tracheal secretions were collectedfrom42patients following24-48hours,3-5days, and5-7days, respectively, ofmechanical ventilation. The quantity of pepsin was measured by ELISA, and theconcentration of pepsin was determined using a microplate reader. In addition, theclinical pulmonary infection score (CPIS) was determined in each patient. Rankcorrelation statistical methods were used to determine whether there was a correlationbetween pharyngeal and tracheal pepsin concentration and the CPIS.Results： After24-48hours,3-5days and5-7days on a ventilator,16.7%,54.8%, 78.6%patients, respectively, were positive for pepsin in the pharynx and the differencewas statistically significant. Following mechanical ventilation for48hours, patientswere automatically divided into VAP and non-VAP groups. There was no significantdifference in pharyngeal pepsin concentration in the two groups after24-48hours ofmechanical ventilation, however, statistically significant differences at3-5days and5-7days were observed. The tracheal pepsin concentration was significantly differentbetween the VAP and non-VAP groups at all three time points. There were significantdifferences in pepsin concentration in the pharynx and trachea at all three time pointsin the VAP group, but not in the non-VAP group. In the VAP group, correlationsbetween pharyngeal pepsin concentration and the CPIS were demonstrated at3-5daysand5-7days, and correlations between tracheal pepsin concentration and the CPIS atall three time points. No correlations between pharyngeal pepsin concentration and theCPIS were seen in the non-VAP group at any of the three time points.Conclusions：With extended duration of mechanical ventilation, pharyngeal andtracheal pepsin concentrations gradually increased, and were correlated with VAPseverity.