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Purpose The lateral Trendelenburg position (LTP) may hinder the primary pathophysiologic mechanism of ventilator-associated pneumonia (VAP). We investigated whether placing patients in the LTP would reduce the incidence of VAP in comparison with the semirecumbent position (SRP). Methods This was a randomized, multicenter, controlled study in invasively ventilated critically ill patients. Two preplanned interim analyses were performed. Patients were randomized to be placed in the LTP or the SRP. The primary outcome, assessed by intention-to-treat analysis, was incidence of microbiologically confirmed VAP. Major secondary outcomes included mortality, duration of mechanical ventilation, and intensive care unit length of stay. Results At the second interim analysis, the trial was stopped because of low incidence of VAP, lack of benefit in secondary outcomes, and occurrence of adverse events. A total of 194 patients in the LTP group and 201 in the SRP group were included in the final intention-to-treat analysis. The incidence of microbiologically confirmed VAP was 0.5% (1/194) and 4.0% (8/201) in LTP and SRP patients, respectively (relative risk 0.13, 95% CI 0.02-1.03, p = 0.04). The 28-day mortality was 30.9% (60/194) and 26.4% (53/201) in LTP and SRP patients, respectively (relative risk 1.17, 95% CI 0.86-1.60, p = 0.32). Likewise, no differences were found in other secondary outcomes. Six serious adverse events were described in LTP patients (p = 0.01 vs. SRP). Conclusions The LTP slightly decreased the incidence of microbiologically confirmed VAP. Nevertheless, given the early termination of the trial, the low incidence of VAP, and the adverse events associated with the LTP, the study failed to prove any significant benefit. Further clinical investigation is strongly warranted; however, at this time, the LTP cannot be recommended as a VAP preventive measure. ClinicalTrials.gov identifier NCT01138540., Author(s): Gianluigi Li Bassi [sup.1] [sup.2] [sup.3] [sup.4], Mauro Panigada [sup.5], Otavio T. Ranzani [sup.1] [sup.3] [sup.4] [sup.6], Alberto Zanella [sup.5], Lorenzo Berra [sup.7], Massimo Cressoni [sup.8], Vieri Parrini [sup.9], [...]

Purpose Open lung strategy during ARDS aims to decrease the ventilator-induced lung injury by minimizing the atelectrauma and stress/strain maldistribution. We aim to assess how much of the lung is opened and kept open within the limits of mechanical ventilation considered safe (i.e., plateau pressure 30 cmH.sub.2O, PEEP 15 cmH.sub.2O). Methods Prospective study from two university hospitals. Thirty-three ARDS patients (5 mild, 10 moderate, 9 severe without extracorporeal support, ECMO, and 9 severe with it) underwent two low-dose end-expiratory CT scans at PEEP 5 and 15 cmH.sub.2O and four end-inspiratory CT scans (from 19 to 40 cmH.sub.2O). Recruitment was defined as the fraction of lung tissue which regained inflation. The atelectrauma was estimated as the difference between the intratidal tissue collapse at 5 and 15 cmH.sub.2O PEEP. Lung ventilation inhomogeneities were estimated as the ratio of inflation between neighboring lung units. Results The lung tissue which is opened between 30 and 45 cmH.sub.2O (i.e., always closed at plateau 30 cmH.sub.2O) was 10 ± 29, 54 ± 86, 162 ± 92, and 185 ± 134 g in mild, moderate, and severe ARDS without and with ECMO, respectively (p < 0.05 mild versus severe without or with ECMO). The intratidal collapses were similar at PEEP 5 and 15 cmH.sub.2O (63 ± 26 vs 39 ± 32 g in mild ARDS, p = 0.23; 92 ± 53 vs 78 ± 142 g in moderate ARDS, p = 0.76; 110 ± 91 vs 89 ± 93, p = 0.57 in severe ARDS without ECMO; 135 ± 100 vs 104 ± 80, p = 0.32 in severe ARDS with ECMO). Increasing the applied airway pressure up to 45 cmH.sub.2O decreased the lung inhomogeneity slightly (but significantly) in mild and moderate ARDS, but not in severe ARDS. Conclusions Data show that the prerequisites of the open lung strategy are not satisfied using PEEP up to 15 cmH.sub.2O and plateau pressure up to 30 cmH.sub.2O. For an effective open lung strategy, higher pressures are required. Therefore, risks of atelectrauma must be weighted versus risks of volutrauma. Trial registration Clinicaltrials.gov identifier: NCT01670747 (www.clinicaltrials.gov)., Author(s): Massimo Cressoni [sup.1], Davide Chiumello [sup.2] [sup.3], Ilaria Algieri [sup.1], Matteo Brioni [sup.3], Chiara Chiurazzi [sup.1], Andrea Colombo [sup.1], Angelo Colombo [sup.4], Francesco Crimella [sup.1], Mariateresa Guanziroli [sup.1], Ivan [...]

Purpose The optimal method for estimating transpulmonary pressure (i.e. the fraction of the airway pressure transmitted to the lung) has not yet been established. Methods In this study on 44 patients with acute respiratory distress syndrome (ARDS), we computed the end-inspiratory transpulmonary pressure as the change in airway and esophageal pressure from end-inspiration to atmospheric pressure (i.e. release derived) and as the product of the end-inspiratory airway pressure and the ratio of lung to respiratory system elastance (i.e. elastance derived). The end-expiratory transpulmonary pressure was estimated as the product of positive end-expiratory pressure (PEEP) minus the direct measurement of esophageal pressure and by the release method. Results The mean elastance- and release-derived transpulmonary pressure were 14.4 ± 3.7 and 14.4 ± 3.8 cmH.sub.2O at 5 cmH.sub.2O of PEEP and 21.8 ± 5.1 and 21.8 ± 4.9 cmH.sub.2O at 15 cmH.sub.2O of PEEP, respectively (P = 0.32, P = 0.98, respectively), indicating that these parameters were significantly related (r.sup.2 = 0.98, P < 0.001 at 5 cmH.sub.2O of PEEP; r.sup.2 = 0.93, P < 0.001 at 15 cmH.sub.2O of PEEP). The percentage error was 5.6 and 12.0 %, respectively. The mean directly measured and release-derived transpulmonary pressure were -8.0 ± 3.8 and 3.9 ± 0.9 cmH.sub.2O at 5 cmH.sub.2O of PEEP and -1.2 ± 3.2 and 10.6 ± 2.2 cmH.sub.2O at 15 cmH.sub.2O of PEEP, respectively, indicating that these parameters were not related (r.sup.2 = 0.07, P = 0.08 at 5 cmH.sub.2O of PEEP; r.sup.2 = 0.10, P = 0.53 at 15 cmH.sub.2O of PEEP). Conclusions Based on our observations, elastance-derived transpulmonary pressure can be considered to be an adequate surrogate of the release-derived transpulmonary pressure, while the release-derived and directly measured end-expiratory transpulmonary pressure are not related., Author(s): Davide Chiumello [sup.1] [sup.2], Massimo Cressoni [sup.2], Andrea Colombo [sup.2], Giovanni Babini [sup.2], Matteo Brioni [sup.2], Francesco Crimella [sup.2], Stefan Lundin [sup.3], Ola Stenqvist [sup.3], Luciano Gattinoni [sup.1] [sup.2] [...]

Background: The acute respiratory distress syndrome (ARDS) and cardiogenic pulmonary edema (CPE) are both characterized by an increase in lung edema that can be measured by computed tomography (CT). The aim of this study was to compare possible differences between patients with ARDS and CPE in the morphologic pattern, the aeration, and the amount and distribution of edema within the lung. Methods: Lung CT was performed at a mean positive end-expiratory pressure level of 5 cm H2O in both groups. The morphological evaluation was performed by two radiologists, while the quantitative evaluation was performed by a dedicated software. Results: A total of 60 patients with ARDS (20 mild, 20 moderate, 20 severe) and 20 patients with CPE were enrolled. The ground-glass attenuation regions were similarly present among the groups, 8 (40%), 8 (40%), 14 (70%), and 10 (50%), while the airspace consolidations were significantly more present in ARDS. The lung gas volume was significantly lower in severe ARDS compared to CPE (830 [462] vs 1120 [832] mL). Moving from the nondependent to the dependent lung regions, the not inflated lung tissue significantly increased, while the well inflated tissue decreased (ρ = 0.96-1.00, P <.0001). Significant differences were found between ARDS and CPE mostly in dependent regions. In severe ARDS, the estimated edema was significantly higher, compared to CPE (757 [740] vs 532 [637] g). Conclusions: Both ARDS and CPE are characterized by a similar presence of ground-glass attenuation and different airspace consolidation regions. Acute respiratory distress syndrome has a higher amount of not inflated tissue and lower amount of well inflated tissue. However, the overall regional distribution is similar within the lung. [ABSTRACT FROM AUTHOR]