PNEUMONIA IN THE SURGICAL INTENSIVE-CARE UNIT - IMMUNOLOGICAL KEYS TOTHE SILENT EPIDEMIC

Objective The authors undertook a prospective study of trauma victims in the intensive care unit (ICU) to investigate the clinical course of pneumonia and the local and systemic immune responses to the pneumoni a. Summary Background Data The silent epidemic of pneumonia has been a n ''unappreciated killer'' in terms of being overlooked in surgical IC Us for the past 5 years, and specifically, the most common major infec tion after severe trauma. Little is known about the immune response to an acute pulmonary infection. Methods The authors studied 50 consecut ive, critically ill trauma patients, with a mean injury severity score of 28 +/- 2, who developed pneumonia while ventilated mechanically. P atients were observed clinically, and specific immunologic parameters, including major histocompatibility antigen HLA-DR, complement recepto r (CR3), and Fc receptor (FcRIII), were measured in circulating and lo cal alveolar leukocytes for up to 30 days. Eleven patients provided un ique clinical data via bronchoscopy for unilateral pneumonia, with col lection of bronchoalveolar lavage (BAL) fluid from both the infected a nd uninfected sides. Results Patients developed clinical pneumonia 5.3 +/- 0.4 days after admission to the ICU. At diagnosis, mean temperatu re was 101.4 F, white blood cell count was 16,000/mm(3), arterial oxyg en tension was 104 +/- 14, fraction of inspired oxygen was 0.47, and p ositive end-expiratory pressure was 5. Thirty patients (Group A) recov ered relatively promptly; 20 patients had prolonged illnesses (Group 8 ), 15 of whom ultimately survived, and five of whom died. Patients wit h poor outcomes had greater leukocytosis (p < 0.05) and temperature el evation (p < 0.05) after 5 days of pneumonia. Immunologically, periphe ral leukocyte expression of HLA-DR, FcRIII, and CR3 was equivalent in both groups. However, the expression of all three antigens on local al veolar leukocytes was decreased to a greater extent in the poor outcom e group compared to the good outcome group, evident before any clinica l differentiation between the two outcome groups. Conclusions Pneumoni a prolonged duration of mechanical ventilation, ICU and hospital stay, and overall infectious morbidity. Although immune suppression has bee n recognized as a result of initial injury, the development of pneumon ia coincided with the nadir oi immune function. Poor outcome patients were clinically identifiable 5 days after pneumonia and immunologicall y identifiable within 2 days. Moreover, there was localized suppressio n of pulmonary leukocytes at the site of the infiltrate compared to th e uninfected lobes. This same alteration was noted in experimental Kle bsiella pneumoniae pneumonia. This evidence suggests that there is act ive immune participation within the respiratory system. It also sugges ts that there are predispositions to pulmonary infections, and it may allow immune modulation targeted to pulmonary leukocytes to hasten cli nical recovery and minimize pulmonary dysfunction.