HOSPITAL-ACQUIRED PNEUMONIA: EPIDEMIOLOGY, ETIOLOGY, AND TREATMENT

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Despite continuing improvements in diagnostic testing, therapeutic agents, and supportive care, hospital-acquired pneumonia (HAP) remains a major health concern. HAP, which is defined as the development of pneumonia at least 48 hours after hospitalization and not incubating at the time of admission, is not a reportable disease; however, the current literature suggests that HAP is the second most frequent cause of hospital-acquired infection and the leading cause of morbidity and mortality from nosocomial infections.10, 24 HAP is estimated to occur at a rate of 5 to 10 cases per 1, 000 hospital admissions, accounting for approximately 13% to 18% of all nosocomial infections, or approximately 300, 000 cases annually. However, the incidence of HAP is not uniform, rather it varies depending upon a number of factors. HAP is also a major contributor to hospital costs, as it lengthens hospitalization by an additional 7 to 9 days and results in additional direct annual costs of $2 billion.11, 78

It is in the intensive care unit (ICU) where the incidence of HAP is highest and carries the greatest mortality, especially among mechanically ventilated patients. Some reports suggest that up to 25% of ICU patients receiving mechanical ventilation develop clinical evidence of pneumonia, an incidence which is 21 times greater than in the non-ICU patient.7, 13, 29 The reason for this increased incidence of pneumonia appears to relate more to the need for mechanical ventilation than simply residing in the ICU, since the median rate of pneumonia occurring among mechanically ventilated patients is reported to be 34.4 cases per 1, 000 ICU days versus a median rate of 3.2 cases per 1, 000 ICU days among nonventilated ICU patients.71 Because of its severity, and the fact that the mechanically ventilated population is much more likely to have significant underlying disease and receive more intensive therapy, many physicians have referred to HAP occurring in mechanically ventilated patients as ventilator-associated pneumonia (VAP).

The crude mortality for HAP is reported to range from 30% to 70%, but a number of patients succumb to their underlying disease, with HAP as an agonal event. Determining the incidence of mortality attributable to HAP itself, referred to as “attributable mortality”, is important since it determines the effect that appropriate management may have on outcome. Studies to date estimate that the attributable mortality of HAP is one third to one half of all deaths associated with HAP, and it may be higher among bacteremic patients and those infected with certain resistant gram-negative pathogens such as Pseudomonas aeruginosa or Acinetobacter spp.10, 19, 20, 21, 44

Attributable mortality can be reduced by the rapid initiation of appropriate antimicrobial therapy, but even when diagnostic tests are able to identify the offending pathogen, the results are not available for hours to days. Because of this delay, antimicrobial therapy is empiric. The literature suggests that the pathogens most commonly isolated in HAP are the enteric gram negative bacilli (GNB) and Staphylococcus aureus. Further complicating our understanding of HAP are the facts that an etiology is not identified in up to one half of all cases, and the role of viral, fungal, and certain atypical organisms, including Legionella spp. and Mycobacterium tuberculosis, are probably under appreciated.26, 33

This article reviews the epidemiology of HAP, discusses the spectrum of pathogens associated with HAP and identifies specific risk factors which expand this spectrum, and finally presents strategies for the initial empiric management of HAP in immunocompetent adults. Much of this information is included in a recent American Thoracic Society (ATS) statement on HAP, but additional information not available at the time of that report has been added.5 Because of its severity, where the literature is available, VAP is discussed separately from other forms of HAP.

Section snippets

Pathogenesis

While the incidence of HAP is estimated to be 5 to 10 cases per 1, 000 hospital admissions, this incidence is not uniform, but varies depending upon several factors. The incidence of HAP, as reported by the Centers for Disease Control and Prevention (CDC's) National Nosocomial Infection Surveillance, is much less common in community hospitals and among patients residing on obstetric or psychiatric wards than in large tertiary referral centers and among patients residing on medical and surgical

ETIOLOGY

Since S. aureus and GNB are the most commonly recovered pathogens from patients with HAP, the potential spectrum of pathogens is quite broad, and recent studies suggest that in up to one half of mechanically ventilated patients, the etiology of HAP is polymicrobial.19 It is appreciated that most HAP cases result from microaspiration of oropharyngeal secretions previously colonized with pathogenic bacteria and that the pathogens colonizing the oropharynx are influenced by specific factors.11, 18

TREATMENT

While the importance of early, appropriate antimicrobial therapy on outcome has been questioned, 67 more recent studies suggest that mortality can be reduced with early, appropriate empiric therapy.7, 73 Celis et al reported that the mortality rate for HAP was 30.5% when the appropriate treatment was instituted as compared to 91.6% when the therapy was inappropriate.7 Torres et al reported a similar increase in mortality when inappropriate therapy was given in ventilated patients.73 More

CONCLUSION

Annually in the United States, there are estimated to be 300, 000 cases of HAP, but the incidence of HAP varies considerably throughout the hospital, and is highest among patients receiving mechanical ventilation. While HAP is the most common cause of nosocomial death, early appropriate therapy is reported to reduce mortality. However, the results of most diagnostic tests, if positive, are not available for several hours or days, and initial therapy is by necessity, empiric. In selecting an

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    Address reprint requests to G. Douglas Campbell, Jr, MD, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Louisiana State University School of Medicine in Shreveport, 1501 Kings Highway, Shreveport, LA 71130

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    Division of Pulmonary and Critical Care Medicine, Louisiana State University School of Medicine, Shreveport, Louisiana

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