Survival in patients with nosocomial pneumonia: impact of the severity of illness and the etiologic agent.

Overview

abstract

OBJECTIVE: To assess the impact of severity of illness at different times, using the Mortality Probability Models (MPM II), and the impact of etiologic agent on survival in patients with nosocomial pneumonia. DESIGN: Retrospective, observational study. SETTING: Fourteen-bed medical-surgical intensive care unit (ICU) in a teaching hospital. PATIENTS: Sixty-two patients with nosocomial pneumonia who were receiving early appropriate antibiotic treatment. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Severity of illness at the time of admission to the ICU (M0), 24 hrs after admission (M24), and at the time of pneumonia diagnosis (M1) was determined using MPM II. Bacteriology was established by quantitative cultures from bronchoscopic samples. The outcome measure was the crude mortality rate. The crude mortality rate in the ICU was 59.7%, compared with average predicted mortality rates of 43.5% (M0), 36.4% (M24), and 52.2% (M1). We observed significant differences in mean MPM II determinations between survivors and nonsurvivors at M1 (39.3% vs. 60.9%, p = .001) but not at M0 and M24. In the univariate analysis, the variables most predictive of mortality were the presence of coma (p = .02), inotropic medication use (p = .001), and an MPM II determination of > 50% (p = .001) when pneumonia was diagnosed (M1). Multivariate analysis showed that, in the absence of Pseudomonas aeruginosa, an MPM II determination of > 50% at M1 was associated with a relative risk of death of 4.8. The presence of P. aeruginosa was associated with an increase in the risk of death of 2.6 and 6.36 in both populations with MPM II determinations at M1 of < or = 50% and > 50%, respectively. CONCLUSIONS: Severity of illness when pneumonia is diagnosed is the most important predictor of survival, and this determination should be used for therapeutic and prognostic stratification. In addition, the presence of P. aeruginosa contributed to an excess of mortality that could not be measured by MPM II alone, suggesting the importance of the pathogen in prognosis.