Endotracheal lactate reflects lower respiratory tract infections and inflammation in intubated patients.

The aim of this study was to assess L-lactate and D-lactate in endotracheal aspirate from intubated patients hospitalized at the intensive care unit and explore their use as diagnostic biomarkers for inflammation and lower respiratory tract infections (LRTI). Tracheal aspirates from 91 intubated patients were obtained at time of intubation and sent for microbiological analyses, neutrophil count, and colorimetric lactate measurements. We compared the concentration of lactate from patients with microbiological verified LRTI or clinical/radiological suspicion of LRTI with a control group. In addition, associations between inflammation and the lactate isomers were examined by correlating L-lactate and D-lactate with sputum neutrophils and clinical assessments. The concentration of L-lactate was increased in aspirates with verified or suspected LRTI (p < 0.001) relative to the control group at Day 0. Connections between L-lactate and inflammation were indicated by the correlation between neutrophils and L-lactate (p < 0.001). We found no increase in sputum D-lactate from patients with verified or suspected LRTI relative to the control group and D-lactate was not correlated with neutrophils. L-lactate was found to be a potential indicator for inflammation and LRTI at the time of intubation. An association was found between neutrophil count and L-lactate. Interestingly, the increase of L-lactate in the control group after intubation may suggest that intubation challenges the host response by inflicting tissue damage or by introducing infectious microbes.

The influence of active and passive air humidification on exhaled breath condensate volume.

Exhaled breath condensate (EBC) is safely collected in mechanically ventilated (MV) patients, but there are no guidelines regarding humidification of inhaled air during EBC collection. We investigated the influence of active and passive air humidification on EBC volumes obtained from MV patients. We collected 29 EBC samples from 21 critically ill MV patients with one condition of active humidification and four different conditions of non-humidification; 19 samples from 19 surgical MV patients with passive humidification and two samples from artificial lungs MV with active humidification. The main outcome was the obtained EBC volume per 100 L exhaled air. When collected with different conditions of non-humidification, mean [95% CI] EBC volumes did not differ significantly (1.35 [1.23; 1.46] versus 1.16 [1.05; 1.28] versus 1.27 [1.13; 1.41] versus 1.17 [1.00; 1.33] mL/100 L, p=0.114). EBC volumes were higher with active humidification than with non-humidification (2.05 [1.91; 2.19] versus 1.25 [1.17; 1.32] mL/100 L, p<0.001). The volume difference between these corresponded to the EBC volume obtained from artificial lungs (0.81 [0.62; 0.99] versus 0.89 mL/100 L, p=0.287). EBC volumes were lower for surgical MV patients with passive humidification compared to critically ill MV patients with non-humidification (0.55 [0.47; 0.63] versus 1.25 [1.17; 1.32] mL/100 L, p<0.001). While active humidification increases EBC volumes, passive humidification decreases EBC volumes and possibly influences EBC composition by other mechanisms. We propose that EBC should be collected from MV patients without air humidification to improve reproducibility and comparability across studies, and that humidification conditions should always be reported.