Beta-lactam antibiotics can be measured in the exhaled breath condensate in mechanically ventilated patients : a pilot study

202408 bcchVersion of RecordOthersFacultad de Medicina de la Pontificia Universidad Católica de Chile; “Fondo Nacional de Desarrollo Científico y Tecnológico” FONDECYTPublishedC

Non-lobar atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation

Introduction When alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation. Methods A total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (VT) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH2O (VT10/PEEP3); and 2) VT = 20 ml/kg and PEEP = 0 cmH2O (VT20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls. Results Atelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm3. There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the VT20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1β and cytokine-induced neutrophil chemoattractant-1 between regions. Conclusions The present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue

Update on management of acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a frequent and life-threatening condition in intensive care units (ICUs). Management of ARDS remains challenging despite years of research. Morbidity and mortality are not only caused by the syndrome itself but can also be the result of ventilator-induced lung injury. In this article, an update on ARDS management including ventilator strategies, rescue therapies, pharmacological treatments, ICU supportive care, and rehabilitation is proposed. While lung protective ventilation remains the standard option for patients with ARDS, neuromuscular blockade and prone positioning are gaining support after successful trials. Helmet non-invasive ventilation and high-flow nasal cannula might be useful for mild-to-moderate ARDS. Extracorporeal membrane oxygenation and carbon dioxide removal are not recommended in standard practice although they might be useful in severe ARDS