STOMACH AS A SOURCE OF COLONIZATION OF THE RESPIRATORY-TRACT DURING MECHANICAL VENTILATION - ASSOCIATION WITH VENTILATOR-ASSOCIATED PNEUMONIA

The aetiopathogenesis of ventilator-associated pneumonia (VAP) require s abnormal oropharyngeal and gastric colonization and the further aspi ration of their contents to the lower airways. VAP develops easily if aspiration or inoculation of microorganisms occur in patients with art ificial 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 con tents; administration of enteral nutrition; and the presence of biliru bin. However, the role of the colonized gastric reservoir in the devel opment of VAP remains debatable. Evidence in favour of the role of the stomach in the development of VAP comes mainly from randomized, contr olled trials of selective gut decontamination and stress ulcer prophyl axis in the intensive care unit (ICU), in which reducing the bacterial burden of the stomach decreases the incidence of nosocomial respirato ry infections, However, at least three studies of flora have found an absence of stomach origin of pneumonia occurring during mechanical ven tilation. Prophylactic measures suggested to prevent VAP in relation t o the gastric reservoir include: treatment for stress ulcers with sucr alfate; prevention of duodenal reflux with metoclopramide; reduction o f gastric burden and bacterial translocation by selective digestive de contamination; acidification of enteral feeding; and jejunal feeding, Gastro-oesophageal reflux can be prevented by using small bore nasogas tric tubes and jejunal feeding. The aspiration of gastric contents can be reduced by positioning patients in a semirecumbent position, check ing the patency of the tube cuff, and aspiration of subglottic secreti ons.The role of the stomach as a reservoir for microorganisms causing ventilator-associated pneumonia is still controversial but despite the debate, there is major evidence in the Literature in favour of the ga stric origin of part of these pulmonary infections.