Annette M Bourgault1, Rui Xie2, Steven Talbert3, Mary Lou Sole3. 1. University of Central Florida, College of Nursing, USA. Electronic address: annette.bourgault@ucf.edu. 2. University of Central Florida, Statistics and Data Science, USA. 3. University of Central Florida, College of Nursing, USA.
Abstract
AIM: This study explored relationships between enteral feeding and tracheal pepsin A. BACKGROUND: Mechanically ventilated (MV) patients receiving enteral feeding are at risk for microaspiration. Tracheal pepsin A, an enzyme specific to gastric cells, was a proxy for microaspiration of gastric secretions. METHODS: Secondary analysis of RCT data from critically ill, MV adults was conducted. Microaspiration prevention included elevated head of bed, endotracheal tube cuff pressure management, and regular oral care. Tracheal secretions for pepsin A were collected every 12 h. Microaspiration was defined as pepsin A ≥ 6.25 ng/mL. Positive pepsin A in >30 % of individual tracheal samples was defined as abundant microaspiration (frequent aspirator). Chi-squared, Fisher's Exact test, and generalized linear model (GLM) were used. RESULTS: Tracheal pepsin A was present in 111/283 (39 %) mechanically ventilated patients and 48 (17 %) had abundant microaspiration. Enteral feeding was associated with tracheal pepsin A, which occurred within 24 h of enteral feeding. Of the patients who aspirated, the majority received some enteral feeding 96/111 (86 %), compared to only 15/111 (14 %) who received no feeding. A greater number of positive pepsin A events occurred with post-pyloric feeding tube location (55.6 %) vs. gastric (48.6 %), although significant only at the event-level. Frequent aspirators (abundant pepsin A) had higher pepsin A levels compared to infrequent aspirators. CONCLUSIONS: Our findings confirmed the stomach as the microaspiration source. Contrary to other studies, distal feeding tube location did not mitigate microaspiration. Timing for first positive pepsin A should be studied for possible association with enteral feeding intolerance.
AIM: This study explored relationships between enteral feeding and tracheal pepsin A. BACKGROUND: Mechanically ventilated (MV) patients receiving enteral feeding are at risk for microaspiration. Tracheal pepsin A, an enzyme specific to gastric cells, was a proxy for microaspiration of gastric secretions. METHODS: Secondary analysis of RCT data from critically ill, MV adults was conducted. Microaspiration prevention included elevated head of bed, endotracheal tube cuff pressure management, and regular oral care. Tracheal secretions for pepsin A were collected every 12 h. Microaspiration was defined as pepsin A ≥ 6.25 ng/mL. Positive pepsin A in >30 % of individual tracheal samples was defined as abundant microaspiration (frequent aspirator). Chi-squared, Fisher's Exact test, and generalized linear model (GLM) were used. RESULTS: Tracheal pepsin A was present in 111/283 (39 %) mechanically ventilated patients and 48 (17 %) had abundant microaspiration. Enteral feeding was associated with tracheal pepsin A, which occurred within 24 h of enteral feeding. Of the patients who aspirated, the majority received some enteral feeding 96/111 (86 %), compared to only 15/111 (14 %) who received no feeding. A greater number of positive pepsin A events occurred with post-pyloric feeding tube location (55.6 %) vs. gastric (48.6 %), although significant only at the event-level. Frequent aspirators (abundant pepsin A) had higher pepsin A levels compared to infrequent aspirators. CONCLUSIONS: Our findings confirmed the stomach as the microaspiration source. Contrary to other studies, distal feeding tube location did not mitigate microaspiration. Timing for first positive pepsin A should be studied for possible association with enteral feeding intolerance.
Authors: Usha Gungabissoon; Kimberley Hacquoil; Chanchal Bains; Michael Irizarry; George Dukes; Russell Williamson; Adam M Deane; Daren K Heyland Journal: JPEN J Parenter Enteral Nutr Date: 2014-03-17 Impact factor: 4.016
Authors: Pierre Singer; Annika Reintam Blaser; Mette M Berger; Waleed Alhazzani; Philip C Calder; Michael P Casaer; Michael Hiesmayr; Konstantin Mayer; Juan Carlos Montejo; Claude Pichard; Jean-Charles Preiser; Arthur R H van Zanten; Simon Oczkowski; Wojciech Szczeklik; Stephan C Bischoff Journal: Clin Nutr Date: 2018-09-29 Impact factor: 7.324
Authors: Annika Reintam Blaser; Adam M Deane; Jean-Charles Preiser; Yaseen M Arabi; Stephan M Jakob Journal: Nutr Clin Pract Date: 2020-11-26 Impact factor: 3.080
Authors: Michael Klompas; Kathleen Speck; Michael D Howell; Linda R Greene; Sean M Berenholtz Journal: JAMA Intern Med Date: 2014-05 Impact factor: 21.873