Association of enteral feeding with microaspiration in critically ill adults.
Critical care
Enteral feeding
Mechanical ventilation
Microaspiration
Pepsin A
Journal
Applied nursing research : ANR
ISSN: 1532-8201
Titre abrégé: Appl Nurs Res
Pays: United States
ID NLM: 8901557
Informations de publication
Date de publication:
10 2022
10 2022
Historique:
received:
24
12
2021
revised:
25
05
2022
accepted:
27
06
2022
entrez:
18
9
2022
pubmed:
19
9
2022
medline:
21
9
2022
Statut:
ppublish
Résumé
This study explored relationships between enteral feeding and tracheal pepsin A. 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. 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. 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. 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.
Sections du résumé
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.
Identifiants
pubmed: 36116866
pii: S0897-1897(22)00053-2
doi: 10.1016/j.apnr.2022.151611
pmc: PMC9529068
mid: NIHMS1837299
pii:
doi:
Substances chimiques
Pepsin A
EC 3.4.23.1
Banques de données
ClinicalTrials.gov
['NCT02284178']
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
151611Subventions
Organisme : NINR NIH HHS
ID : R01 NR014508
Pays : United States
Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest None identified.
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