Systemic inflammatory response after bronchoalveolar lavage in critically ill patients

Bronchoscopic bronchoalveolar lavage (BAL) may be followed by a systemic inflammatory response, Previous reports have suggested pneumonia as a predisposing condition and systemic cytokines as possible mediators. To test this hypothesis, systemic levels of interleukin (IL)-1 beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha) were studied before and at 12 h and 24 h after bronchoscopically guided BAL in 30 mechanically ventilated patients (median age 67 (range 54-76) yrs, simplified acute physiology score TT (SAPS II) 33 (12-56)), 20 of whom had pneumonia and 10 of whom were control patients without pneumonia, Arterial oxygen partial pressure to inspired oxygen fraction ratio (Pa2O2/FI,O-2), body temperature, mean arterial pressure, and cardiac frequency were recorded, The majority of patients (28/30, 93%) received antibiotic treatment prior to the procedure. Pa,O-2/FI,O-2 ratio was lower at 12 h compared to baseline in patients with pneumonia (baseline median 192 (range 65-256); 12 h 160 (66-190) mmHg, p < 0.001) and ventilated controls (baseline 293 (205-473); 12 h 226 (153-330) mm Hg p = 0.011), but returned to baseline levels at 24 h (pneumonia: 194 (92-312), p = 0.991; controls: 309 (173-487) mmHg, p = 0.785), No changes in other clinical variables were observed. Systemic TNF-<alpha> levels before BAL (pneumonia: 35 (10-88); controls: 17 (0-33) pg.mL(-1)) did not increase at 12 h (pneumonia: 35 (0-64); p = 0.735; controls: 16 (0-21) pg.mL(-1), p = 0.123 comparison to baseline) or 24 h (pneumonia: 31 (0-36), p = 0.464; controls: 19 (0-43) pg.mL(-1), p = 0.358), No changes of IL-1 beta (baseline: pneumonia 0 (0-13); controls 1 (0-32) pg.mL(-1)) or IL-6 (baseline: pneumonia, 226 (9-4300); controls, 53 (0-346) pg.mL(-1)) were detected. No deterioration of clinical variables and no increase in systemic cytokine release has been observed after bronchoalveolar lavage, in critically ill patients. The potential cytokine increase is probably too small, in relation to the pre-existing inflammatory response, to yield clinical significance in this population otherwise antibiotic therapy may have been protective.