Ventilator Associated Pneumonia Clinical Trial
Official title:
Gastrointestinal Complications in Association With Oropharyngeal and Respiratory Infections in Mechanical Ventilation
Detection of gastrointestinal complications in mechanically ventilated critically ill patients and its relation to oropharyngeal and respiratory infections in relation to oropharyngeal and gastric PH.
Hospital acquired or nosocomial infections continue to be an important cause of morbidity and
mortality. The critically ill patient is at particular risk of developing intensive care unit
acquired infection, with the lungs being especially vulnerable. Nosocomial bacterial
pneumonia occurring after two days of mechanical ventilation is referred to as ventilator
associated pneumonia, and is the most common nosocomial infection seen in the intensive care
unit. Intubation of the trachea and mechanical ventilation is associated with a 7-fold to
21-fold increase in the incidence of pneumonia and up to 28% of patients receiving mechanical
ventilation will develop this complication. Its development is associated with an
attributable increase in morbidity and mortality. Ventilator associated pneumonia (VAP) is
defined as nosocomial pneumonia occurring in a patient after 48 hours of mechanical
ventilation via a tracheal or tracheostomy tube. It is commonly classified as either early
onset (occurring within 96 hours of start of mechanical ventilation) or late onset (.96 hours
after start of mechanical ventilation). It is a common condition, difficult to diagnose
accurately, and expensive to treat. Its development prolongs a patient's stay in the
intensive care unit (ICU), and is associated with significant morbidity and mortality. Most
cases seem to result from aspiration of pathogenic material that commonly colonises the
oropharyngeal airways of the critically ill. Simple measures to decrease the incidence of
aspiration or reduce the burden of colonisation of the oropharynx may aid in the prevention
of ventilator associated pneumonia. VAP is the infection that occurs 48 hours after
intubation, which was not incubated during the period of the patient's admission, and 72
hours after extubation.
The gastrointestinal tract is believed to play an important role in ventilator-associated
pneumonia (VAP), because during critical illness the stomach often is colonized with enteric
Gram-negative bacteria. These are the same bacteria that frequently are isolated from the
sputum of patients with VAP.
This is known as the "gastropulmonary hypothesis" and it postulates the following sequence.
First, the stomach is colonized by potentially pathogenic microorganisms, either from an
exogenous source (contaminated liquid injected into a nasogastric tube), or from an
endogenous source (Detection of gastrointestinal complications in mechanically ventilated
critically ill patients and its relation to oropharyngeal and respiratory infections in
relation to oropharyngeal and gastric PH duodenogastric reflux). This is followed by
retrograde colonization of the oropharynx . Finally, the lower respiratory tract is colonized
from sustained microaspiration of contaminated oropharyngeal (or gastric) secretions around
the endotracheal tube cuff.
The Role of Gastric pH on the Incidence of VAP
Under fasting conditions, gastric sterility is maintained by an acidic pH. Clinical evidence
suggests that a gastric pH of 3.5 prevents bacterial colonization, whereas a pH 4.0 is
associated with clinically important bacterial colonization and a higher incidence of
nosocomial pneumonia.
Critically-ill patients with either respiratory failure requiring mechanical ventilation or
coagulopathy are at increased risk for clinically important, stress-related GI bleeding .This
has been associated with a significantly higher mortality rate, compared to patients without
evidence of bleeding (48.5 vs 9.1%, p _ 0.001).
Giving that such patients show an increasing risk of important gastrointestinal (GI)
bleeding, stress-ulcer prophylaxis (SUP) has been recommended for the prevention of upper GI
hemorrhage. SUP strategy rely on drugs that block the secretion of gastric acid and increase
the gastric pH (histamine-2-receptor antagonists - H2RA, and proton pump inhibitor - PPI) and
those that does not alter gastric pH (sucralfate). The increase of gastric pH leads to
bacterial overgrowth and potential colonization of trachea determining a higher risk of VAP.
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