Ventilator-associated pneumonia pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.D. [2] Template:Ventilator-associated pneumonia

Overview

Ventilator-associated pneumonia is primarily caused by the endotracheal or tracheostomy tube allowing free passage of bacteria into the lower segments of the lung in a person who often has underlying lung or immune problems. Bacteria travel in small droplets both through the endotracheal tube and around the cuff. Often, bacteria colonize the endotracheal or tracheostomy tube and are embolized into the lungs with each breath. Bacteria may also be brought down into the lungs with procedures such as deep suctioning or bronchoscopy. Whether bacteria also travel from the sinuses or the stomach into the lungs is, controversial. However, spread to the lungs from the blood stream or the gut is uncommon. Once inside the lungs, bacteria then take advantage of any deficiencies in the immune system (such as due to malnutrition or chemotherapy) and multiply. A combination of bacterial damage and consequences of the immune response lead to disruption of gas exchange with resulting symptoms.

Major Points for Pathogenesis of Adults with Hospital-Acquired, Ventilator-Associated, and Healthcare-Associated Pneumonia (DO NOT EDIT)

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Major Points for Pathogenesis 1 Sources of pathogens for HAP include healthcare devices, the environment (air, water, equipment, and fomites), and commonly the transfer of microorganisms between the patient and staff or other patients (Level II) . 2 A number of host- and treatment-related colonization factors, such as the severity of the patient's underlying disease, prior surgery, exposure to antibiotics, other medications, and exposure to invasive respiratory devices and equipment, are important in the pathogenesis of HAP and VAP (Level II). 3 Aspiration of oropharyngeal pathogens, or leakage of secretions containing bacteria around the endotracheal tube cuff, are the primary routes of bacterial entry into the lower respiratory tract (Level II). 4 Inhalation or direct inoculation of pathogens into the lower airway, hematogenous spread from infected intravenous catheters, and bacterial translocation from the gastrointestinal tract lumen are uncommon pathogenic mechanisms (Level II). 5 Infected biofilm in the endotracheal tube, with subsequent embolization to distal airways, may be important in the pathogenesis of VAP (Level III). 6 The stomach and sinuses may be potential reservoirs of nosocomial pathogens that contribute to bacterial colonization of the oropharynx, but their contribution is controversial, may vary by the population at risk, and may be decreasing with the changing natural history and management of HAP (Level II).

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