Abstract
IntroductionThe simple bedside method for sampling undiluted distal pulmonary edema fluid through a normal suction catheter (s-Cath) has been experimentally and clinically validated. However, there are no data comparing non-bronchoscopic bronchoalveolar lavage (mini-BAL) and s-Cath for assessing lung inflammation in acute hypoxaemic respiratory failure. We designed a prospective study in two groups of patients, those with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and those with acute cardiogenic lung edema (ACLE), designed to investigate the clinical feasibility of these techniques and to evaluate inflammation in both groups using undiluted sampling obtained by s-Cath. To test the interchangeability of the two methods in the same patient for studying the inflammation response, we further compared mini-BAL and s-Cath for agreement of protein concentration and percentage of polymorphonuclear cells (PMNs).MethodsMini-BAL and s-Cath sampling was assessed in 30 mechanically ventilated patients, 21 with ALI/ARDS and 9 with ACLE. To analyse agreement between the two sampling techniques, we considered only simultaneously collected mini-BAL and s-Cath paired samples. The protein concentration and polymorphonuclear cell (PMN) count comparisons were performed using undiluted sampling. Bland-Altman plots were used for assessing the mean bias and the limits of agreement between the two sampling techniques; comparison between groups was performed by using the non-parametric Mann-Whitney-U test; continuous variables were compared by using the Student t-test, Wilcoxon signed rank test, analysis of variance or Student-Newman-Keuls test; and categorical variables were compared by using chi-square analysis or Fisher exact test.ResultsUsing protein content and PMN percentage as parameters, we identified substantial variations between the two sampling techniques. When the protein concentration in the lung was high, the s-Cath was a more sensitive method; by contrast, as inflammation increased, both methods provided similar estimates of neutrophil percentages in the lung. The patients with ACLE showed an increased PMN count, suggesting that hydrostatic lung edema can be associated with a concomitant inflammatory process.ConclusionsThere are significant differences between the s-Cath and mini-BAL sampling techniques, indicating that these procedures cannot be used interchangeably for studying the lung inflammatory response in patients with acute hypoxaemic lung injury.
Highlights
The simple bedside method for sampling undiluted distal pulmonary edema fluid through a normal suction catheter (s-Cath) has been experimentally and clinically validated
The patients with acute cardiogenic lung edema (ACLE) showed an increased polymorphonuclear cells (PMNs) count, suggesting that hydrostatic lung edema can be associated with a concomitant inflammatory process
The clinical disorders associated with the development of primary acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) (n = 14) were pneumonia (n = 11), carmustine-induced lung injury (n = 1), methotrexate-induced lung injury (n = 1) and cryptogenic organising pneumonia (n = 1)
Summary
The simple bedside method for sampling undiluted distal pulmonary edema fluid through a normal suction catheter (s-Cath) has been experimentally and clinically validated. We designed a prospective study in two groups of patients, those with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and those with acute cardiogenic lung edema (ACLE), designed to investigate the clinical feasibility of these techniques and to evaluate inflammation in both groups using undiluted sampling obtained by s-Cath. In patients with acute hypoxaemic respiratory failure, acute respiratory distress syndrome (ARDS) represents the more severe form of acute lung injury (ALI) [1]. The inflammatory response of the lung is intense in the alveolar space, and the hallmark of ALI/ARDS in the early phase is severe damage of the alveolocapillary barrier, leading to increased permeability, development of protein-rich and biomarker-rich oedema fluid, and impaired clearance of the oedema [3,4,5]. Sequential sampling of oedema fluid is required for this purpose Another common cause of acute respiratory failure is acute cardiogenic lung oedema (ACLE). The mechanism of cardiogenic oedema is different from that of ALI/ARDS, recent studies have found that endothelial-derived and epithelialderived inflammatory mediators are released into the blood even during this form of hydrostatic oedema [6]
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