PATHOPHYSIOLOGY OF HOSPITAL-ACQUIRED PNEUMONIA

Citation
G. Gudmundsson et Db. Hornick, PATHOPHYSIOLOGY OF HOSPITAL-ACQUIRED PNEUMONIA, Seminars in respiratory and critical care medicine, 18(2), 1997, pp. 99-110
Citations number
109
Categorie Soggetti
Respiratory System
ISSN journal
10693424
Volume
18
Issue
2
Year of publication
1997
Pages
99 - 110
Database
ISI
SICI code
1069-3424(1997)18:2<99:POHP>2.0.ZU;2-Z
Abstract
Hospital-acquired pneumonia (HAP) is an important contributor to hospi tal morbidity, mortality, and increased hospital costs. We review the factors that identify groups of patients that are at risk for HAP, the mechanism by which bacteria enter the lung, and the interaction betwe en bacteria and the host defenses at the cellular level. Mechanical ve ntilation is the most significant risk factor. Other significant risk factors are discussed and categorized as intervention-related, patient -related, and infection control-related factors. Hospital-associated b acteria such as gram-negative bacilli and S. aureus commonly colonize the oropharynx of hospitalized patients and most commonly cause pneumo nia via aspiration into the lung. The lungs are protected from these p otential pathogens by physical barriers, mechanical clearance, and at the cellular level by the antimicrobial properties of airway surface f luid and inflammatory cells (e.g., pulmonary macrophages, neutrophils) . We review new data indicating that respiratory epithelial cells part icipate in regulating the inflammatory response. When the host defense s are handicapped in severe illness, hospital-associated bacteria, par ticularly P. aeruginosa, express multiple virulence factors that can f rustrate the crippled host defense mechanisms and propagate lung destr uction.