SURVIVAL IN PATIENTS WITH NOSOCOMIAL PNEUMONIA - IMPACT OF THE SEVERITY OF ILLNESS AND THE ETIOLOGIC AGENT

Objective: To assess the impact of severity of illness at different ti mes, using the Mortality Probability Models (MPM II), and the impact o f etiologic agent on survival in patients with nosocomial pneumonia. D esign: Retrospective, observational study. Setting: Fourteen-bed medic al surgical intensive care unit (ICU) in a teaching hospital. Patients : Sixty-two patients with nosocomial pneumonia who were receiving earl y appropriate antibiotic treatment. Interventions: None. Measurements and Main Results: Severity of illness at the time of admission to the ICU (M-0), 24 hrs after admission (M-24), and at the time of pneumonia diagnosis (M-1) was determined using MPM II. Bacteriology was establi shed 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 % (M-0), 36.4% (M-24), and 52.2% (M-1). We observed significant differ ences in mean MPM II determinations between survivors and nonsurvivors at M-1 (39.3% vs. 60.9%, p =.001) but not at M-0, and M-24. In the un ivariate 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 ( M-1). Multivariate analysis showed that, in the absence of Pseudomo na s aeruginosa, an MPM II determination of >50% at M-1 was associated wi th 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 bo th populations with MPM II determinations at M-1 of <50% and >50%, res pectively. Conclusions: Severity of illness when pneumonia is diagnose d is the most important predictor of survival, and this determination should be used for therapeutic and prognostic stratification. In addit ion, the presence of P.aeruginosa contributed to an excess of mortalit y that could not be measured by MPM II alone, suggesting the importanc e of the pathogen in prognosis.