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After the first outbreak identified in Mexico in late March 2009, influenza A sustained by a modified H1N1 virus ("swine flu") rapidly spread to all continents. This article describes the first Italian case of life-threatening ARDS associated with H1N1 infection, treated with extracorporeal respiratory assistance (venovenous extracorporeal membrane oxygenation [ECMO]). A 24-year-old, previously healthy man was admitted to the Intensive Care Unit (ICU) of the local hospital for rapidly progressive respiratory failure with refractory impairment of gas exchange unresponsive to rescue therapies (recruitment manoeuvres, pronation and nitric oxide inhalation). An extracorporeal respiratory assistance (venovenous ECMO) was performed. It allowed a correction of the respiratory acidosis and made possible the transportation of the patient to the ICU (approximately 150 km from the first hospital). A nasal swab tested positive for H1N1 infection and treatment with oseltamivir was started. The chest computed tomography scan showed bilateral massive, patchy consolidation of lung parenchyma; lab tests showed leukopenia, elevated CPK levels and renal failure. The patient required high dosages of norepinephrine for septic shock and continuous renal replacement therapy. The clinical course was complicated by Pseudomonas aeruginosa superinfection, treated with intravenous and aerosolised colistin. ECMO was withheld after 15 days, while recovery of renal and respiratory function was slower. The patient was discharged from the ICU 34 days after admission. In this case, ECMO was life-saving and made the inter-hospital transfer of the patient possible

BACKGROUND AND OBJECTIVES: Acute respiratory distress syndrome (ARDS) is a frequent form of hypoxiemic respiratory failure caused by the acute development of diffuse lung inflammation. Dysregulated systemic inflammation with persistent elevation of circulating inflammatory cytokines is the pathogenetic mechanism for pulmonary and extrapulmonary organ dysfunction in patients with ARDS. Glucocorticoids (GCs) have a broad range of inhibitory inflammatory effects, including inhibition of cytokines transcription, cellular activation and growth factor production. They inhibit the inflammatory pathways through two specific intracellular glucocorticoid receptors (GRs), named GR alpha and GR beta. The aim of our study was to evaluate the histologic evidence of inflammatory injury and the GR alpha uptake of resident and inflammatory cells in different experimental models of acute lung injury (ALI). METHODS: We studied four groups of rats: three different experimental rat models of lung injury and a control group. The ALI was caused by barotrauma (due to an overventilation), oleic acid injection and mechanical ventilation. Results were compared to nonventilated rat control group. The duration of mechanical ventilation was of 2.5h. At the end of each experiment, rats were sacrificed. Lung biopsies were evaluated for morphologic changes. The immunohistochemistry was performed to study GR alpha expression. RESULTS: Histologic evidence of lung injury (alveolar and interstitial edema, vascular congestion, alveolar haemorrhage, emphysema, number of interstitial cells and neutrophils, and destruction of alveolar attachments) were present in all ventilated groups. Barotrauma lead to an additional inflammatory response. GR alpha expression significantly increased in the three ventilated groups compared with nonventilated groups. GR alpha expression was highest in barotrauma group. CONCLUSIONS: These data indicate that ALI is associated with diffuse alveolar damage, up-regulation of the