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Timely diagnosis of lung infection in critically ill patients is key to guide therapy and avoid futile antibiotic prescription. The gold standard for diagnosis is microbiological culture of bronchoalveolar lavage fluid (BALf). However, it takes up to 48 hours to disclose results. Pentraxin 3 (PTX3) is an acute phase mediator of infection that can be assayed in a few hours. We described a relationship between BALf PTX3 presence and lung infection in acute respiratory distress syndrome patients. The aim of this study was to validate BALf PTX3 as an early marker of lung infection in critically ill patients.

Positive end-expiratory pressure (PEEP) improves oxygenation in acute lung injury (ALI) patients by increasing end-expiratory lung volume (EELV). Electrical impedance tomography (EIT) is a relatively new non-invasive bedside method to monitor regional distribution of tidal ventilation and EELV changes, validated in preclinical studies. We tested EIT as a monitor of PEEP-induced tidal redistribution and EELV changes in ALI patients, and the relationship between EIT parameters and oxygenation.

Implementation of assisted mechanical ventilation in acute lung injury (ALI) patients may decrease ventilator-induced lung injury by redistribution of tidal ventilation towards dependent lung regions. Up to now, tidal ventilation regional distribution has been measured by expensive and complicated methods, not readily available at the bedside. Electrical impedance tomography (EIT) is a relatively new non-invasive bedside method to monitor tidal ventilation distribution, validated in preclinical studies. We verified the feasibility of using EIT to monitor tidal ventilation regional distribution in patients undergoing assisted ventilation and we describe the effect of different pressure support levels on regional ventilation.

Receptor for advanced glycation end products (RAGE) is an acute phase inflammatory mediator primarily expressed by alveolar type I cells in the lung. The association between circulating RAGE and severity of acute lung injury and acute respiratory distress syndrome (ALI/ARDS) has been recently suggested by both experimental and human studies. The purpose of our study is to study the significance of plasma RAGE levels over time and of bronchoalveolar lavage fluid (BALf ) RAGE in ALI/ARDS patients.

Severe acute respiratory distress syndrome (ARDS) patient transportation is an extremely high-risk procedure. We report our experience in transferring these patients to our centre while on extracorporeal membrane oxygenation (ECMO).

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is characterized by an important inflammatory reaction involving both lungs, often spreading systemically. Pentraxin 3 (PTX3) has recently been described as a mediator of the acute phase of innate immunity. It belongs, together with C-reactive protein (CRP), to the pentraxin superfamily. PTX3 is produced by endothelial cells, fibroblasts, mononuclear phagocytes and dendritic cells in response to primary inflammatory signals (IL-1, tumor necrosis factor, LPS). Its involvement in the pathogenesis of ALI/ARDS seems probable and potentially interesting for the pathophysiology, the diagnosis and possibly the therapy of the syndrome. We measured PTX3 levels, by an ELISA test, in the sera of 25 patients affected by ALI/ARDS. We also collected data related to etiology, pulmonary mechanics, gas exchange, systemic inflammatory involvement, microbiology, blood cells and the outcome of these patients. PTX3 was markedly elevated in all 25 patients (average 111.07 ± 192.01 ng/ml; range 4.94–922.91 ng/ml). In no patient were PTX3 levels lower or equal to the physiological threshold of 2 ng/ml. Levels of logPTX3 were significantly different between survivor and nonsurvivor patients (1.465 ± 0.529 log ng/ml vs 1.950 ± 0.643 log ng/ml; P = 0.05). Patients with two or more organ failures (besides the lung) also had logPTX3 levels significantly higher than patients with just one additional organ failure (1.936 ± 0.597 log ng/ml vs 1.423 ± 0.542 log ng/ml; P < 0.04). The same was true when PTX3 levels in patients with septic shock were compared with PTX3 levels in patients without shock (262.465 ± 350.727 ng/ml vs 63.257 ± 70.261 ng/ml; P < 0.03). PTX3 and logPTX3 were correlated with body temperature (r = 0.56 P < 0.01; r = 0.51 P = 0.01) and with arterial blood pH (r = -0.53 P < 0.01; r = -0.53 P < 0.01). We have underlined a relationship between circulating levels of PTX3 and some markers of the severity of systemic involvement. PTX3 could be an indicator of the gravity of the systemic inflammatory reaction and of unfavourable outcome in ALI/ARDS patients.