Stomach as a source of colonization of the respiratory tract during mechanical ventilation: association with ventilator-associated pneumonia

Abstract

The aetiopathogenesis of ventilator-associated pneumonia (VAP) requires abnormal oropharyngeal and gastric colonization and the further aspiration of their contents to the lower airways. VAP develops easily if aspiration or inoculation of microorganisms occur in patients with artificial airways, in whom mechanical, cellular and/or humoral defences are altered.Well-known risk factors for gastric colonization include: alterations in gastric juice secretion; alkalinization of gastric contents; administration of enteral nutrition; and the presence of bilirubin. However, the role of the colonized gastric reservoir in the development of VAP remains debatable.Evidence in favour of the role of the stomach in the development of VAP comes mainly from randomized, controlled trials of selective gut decontamination and stress ulcer prophylaxis in the intensive care unit (ICU), in which reducing the bacterial burden of the stomach decreases the incidence of nosocomial respiratory infections. However, at least three studies of flora have found an absence of stomach origin of pneumonia occurring during mechanical ventilation.Prophylactic measures suggested to prevent VAP in relation to the gastric reservoir include: treatment for stress ulcers with sucralfate; prevention of duodenal reflux with metoclopramide; reduction of gastric burden and bacterial translocation by selective digestive decontamination; acidification of enteral feeding; and jejunal feeding. Gastro-oesophageal reflux can be prevented by using small bore nasogastric tubes and jejunal feeding. The aspiration of gastric contents can be reduced by positioning patients in a semirecumbent position, checking the patency of the tube cuff, and aspiration of subglottic secretions.The role of the stomach as a reservoir for microorganisms causing ventilatorassociated pneumonia is still controversial but despite the debate, there is major evidence in the literature in favour of the gastric origin of part of these pulmonary infections.

Risk factors for Hospital-Acquired Pneumonia in nonventilated adults

“…It has been stated that alkalinization of the stomach provides an ideal environment for bacterial overgrowth -and, subsequently, to contamination Table 3. Microorganisms recovered from patients with nonventilator associated hospital acquired-pneumonia of the lower airways [14,18]. However, the importance of the "gastropulmonary route" for colonization and infection of the respiratory tract has been challenged.…”

“…Recent research suggests a predominant role for oropharyngeal colonization and micro-aspiration of microorganisms in the pathogenesis of hospital-acquired pneumonia [19]. Still, studies that favor either gastric or oropharyngeal colonization as a source of pathogens for hospital-acquired pneumonia enrolled patients under mechanical ventilation [18,19]. We can only hypothesize that, among nonventilated patients, contaminated gastric content could reach lower airways through reflux.…”

Bacteriological Aspects of Late Pneumonia in Ventilated Patient in Intensive Care Units: A Single Center Study in Morocco

“…The Gram-negative, nonfermenting bacteria accounted for 67.83% and the enterobacteria for 32.16%. This dominance could be explained by the VAP physiopathology; lung contamination being due in one hand by modified endogenous flora of oropharynx and gastric fluid, mainly represented by enteric Gram-negative bacteria and Pseudomonas aeruginosa [42][43][44] and in the second hand, by exogenous flora from respiratory instruments or aerosols [3,[42][43][44][45].…”

Ventilator‐associated pneumoniaDiagnosis, pathogenesis and prevention

“…Risk factors for gastric colonisation include duodenal [47] and gastric [48] enteral feeding. The importance of the gastropulmonary route for VAP pathogenesis remains controversial because studies of colonisation sequences prior to the development of VAP have failed to show consistently the stomach as an initial or preceding site of colonisation [48][49][50]. However, many of the organisms causing VAP do arise from the gastrointestinal tract and this is the basis for selective decontamination of the digestive tract (SDDT).…”