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Purpose Extent of lung contusion on initial computed tomography (CT) scan predicts the occurrence of acute respiratory distress syndrome (ARDS) in blunt chest trauma patients. We hypothesized that lung ultrasonography (LUS) on admission could also predict subsequent ARDS. Methods Forty-five blunt trauma patients were prospectively studied. Clinical examination, chest radiography, and LUS were performed on arrival at the emergency room. Lung contusion extent was quantified using a LUS score and compared to CT scan measurements. The ability of the LUS score to predict ARDS was tested using the area under the receiver operating characteristic curve (AUC-ROC). The diagnostic accuracy of LUS was compared to that of combined clinical examination and chest radiography for pneumothorax, lung contusion, and hemothorax, with thoracic CT scan as reference. Results Lung contusion extent assessed by LUS on admission was predictive of the occurrence of ARDS within 72 h (AUC-ROC = 0.78 [95 % CI 0.64-0.92]). The extent of lung contusion on LUS correlated well with CT scan measurements (Spearman's coefficient = 0.82). A LUS score of 6 out of 16 was the best threshold to predict ARDS, with a 58 % [95 % CI 36-77] sensitivity and a 96 % [95 % CI 76-100] specificity. The diagnostic accuracy of LUS was higher than that of combined clinical examination and chest radiography: (AUC-ROC) 0.81 [95 % CI 0.50-1.00] vs. 0.74 [0.48-1.00] (p = 0.24) for pneumothorax, 0.88 [0.76-1.00] vs. 0.69 [0.47-0.92] (p < 0.05) for lung contusion, and 0.84 [0.59-1.00] vs. 0.73 [0.51-0.94] (p < 0.05) for hemothorax. Conclusions LUS on admission identifies patients at risk of developing ARDS after blunt trauma. In addition, LUS allows rapid and accurate diagnosis of common traumatic thoracic injuries., Author(s): Damien Leblanc [sup.1], Clément Bouvet [sup.1], Franck Degiovanni [sup.1], Cosmina Nedelcu [sup.2], Guillaume Bouhours [sup.1], Emmanuel Rineau [sup.1], Catherine Ridereau-Zins [sup.2], Laurent Beydon [sup.1], Sigismond Lasocki [sup.1] Author Affiliations: [...]

Byline: J. Jane Pillow (1,5), Noah H. Hillman (2), Graeme R. Polglase (1), Timothy J. M. Moss (3), Suhas G. Kallapur (2), Fook-Choe Cheah (2), Boris W. Kramer (4), Alan H. Jobe (2) Keywords: Humidity; Temperature; Hyperoxia; Respiratory distress syndrome; Infant; Preterm Abstract: Purpose The relative contributions of factors influencing lung injury immediately after birth are poorly understood. We hypothesized that oxygen content and humidity of inspired air would influence markers of pulmonary inflammation in ventilated lambs. Methods Lambs delivered at 140 days gestation (term = 150 days) were assigned to one of five groups (n = 5--6/group): unventilated controls, or ventilation with 21 or 100% O.sub.2 that was either heated and humidified or cold and dry. Lambs were ventilated gently for 3 h: blood gases were recorded regularly. Bronchoalveolar lavage and samples of tracheal mucosa and lung were collected post mortem. Results Arterial pH was lower [mean difference (95% CI): -0.07 (-0.13, -0.03)], while there was an increase in PaCO.sub.2 [mean difference (95% CI): 10.2 (2.4, 17.9)] and fold change in lung pro-inflammatory IL-1[beta] cytokine mRNA [mean difference (95% CI): 28.3 (0.3, 56.2)] or IL-8 [mean difference (95% CI): 27.8 (7.9, 47.7)] cytokine mRNA expression with 100% O.sub.2 relative to 21% O.sub.2. Cold dry inspired gas did not influence gas exchange or dynamic mechanics at 3 h compared to heated humidified gas. Compared to 100% inspired O.sub.2, cold dry inspired gas had less marked effect on fold change in lung pro-inflammatory IL-1[beta] cytokine mRNA [mean difference (95% CI): 27.2 (-0/8, 55.1)] or IL-8 [mean difference (95% CI): 14.5 (5.5, 34.4)] cytokine mRNA expression, although cilial dysfunction/damage was evident on electron microscopy, especially when exposure to cold dry gas was combined with hyperoxia. Conclusions In near-term neonatal lambs ventilated for 3 h, hyperoxia was associated a more powerful stimulus for pulmonary dysfunction and upregulation of inflammatory cytokines than cold dry gas. Author Affiliation: (1) School of Women's and Infants' Health, The University of Western Australia, c/- 374 Bagot Rd, Subiaco, Perth, 6008, Australia (2) Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, 3333 Burnet Ave, Cincinnati, OH, 45229, USA (3) Department of Physiology, Monash University, Building 13F, Clayton, VIC, 3800, Australia (4) Department of Pediatrics, Maastricht University Medical Center, Postbus 5800, 6202 AZ, Maastricht, The Netherlands (5) Neonatal Clinical Care Unit, King Edward Memorial Hospital, 374 Bagot Rd, Subiaco, Perth, 6008, Australia Article History: Registration Date: 25/08/2009 Received Date: 07/10/2008 Accepted Date: 07/08/2009 Online Date: 15/09/2009 Article note: This research was presented at the annual conference of The Perinatal Society of Australia and New Zealand (April 2007) and the Pediatric Academic Societies Meeting (Toronto, 2007). Electronic supplementary material The online version of this article (doi: 10.1007/s00134-009-1624-z) contains supplementary material, which is available to authorized users.

Byline: Daniele Luca (1), Silvia Baroni (2), Giovanni Vento (1), Marco Piastra (3), Domenico Pietrini (3), Federica Romitelli (2), Ettore Capoluongo (2), Costantino Romagnoli (1), Giorgio Conti (3), Enrico Zecca (1) Keywords: Phospholipase A2; Lung injury; Newborn infants; Neonatal respiratory distress syndrome Abstract: Purposes Secretory phospholipase A2 hydrolyzes phosphoglycerides and it has been shown to be involved in alveolar inflammation and surfactant degradation. It plays an important role in acute lung injury but it has never been studied in newborn infants. We were aimed to investigate the phospholipase A2 activity in neonatal lung injury and its relationship with ventilatory findings. Setting Third level university hospital NICU. Methods We measured phospholipase activity in broncho-alveolar lavage fluid of 21 neonates with hyaline membrane disease, 10 with pneumonia or sepsis and 10 controls, ventilated for extrapulmonary reasons. Fluid was obtained before surfactant administration on the first day of life and phospholipase activity was measured using an ultrasensitive enzymatic method. Before lavage, lung mechanics in pressure controlled synchronized intermittent mandatory ventilation was analyzed. Results Phospholipase A2 was higher in babies ventilated for sepsis/pneumonia compared to hyaline membrane disease and to control babies. Phospholipase correlated negatively with dynamic compliance, positively with inspired oxygen fraction, mean airway pressure and oxygenation index. These correlations still remained significant after multivariate analysis, adjusting for possible confounding factors. Phospholipase was not correlated with blood and alveolar pH, gestational age, birth weight, blood gases, Apgar score, tidal volume, surfactant need and ventilation time. Conclusions These are the first data about phospholipase A2 in neonates. The enzyme plays a role in neonatal lung injury, especially in infection related respiratory failure. It is associated with lung stiffness, higher mean airway pressure and need for oxygen. Author Affiliation: (1) Neonatal Intensive Care Unit, Department of Pediatrics, University Hospital 'A. Gemelli', Catholic University of the Sacred Heart, L.go A. Gemelli 8, 00168, Rome, Italy (2) Institute of Clinical Biochemistry, University Hospital 'A. Gemelli', Catholic University of the Sacred Heart, Rome, Italy (3) Pediatric Intensive Care Unit, Department of Anaesthesiology and Intensive Care, University Hospital 'A. Gemelli', Catholic University of the Sacred Heart, Rome, Italy Article History: Registration Date: 11/07/2008 Received Date: 17/03/2008 Accepted Date: 10/07/2008 Online Date: 22/07/2008 Article note: This study has been partially presented to 48th Meeting of the European Society for Pediatric Research, selected for the Final Young Investigators Award Plenary Session (Prague, Czech Rep., October 6--8, 2007).

Byline: Tai-Fai Fok (1), Goldie Gu (1), Ka-Fai To (2), Feng Xu (1), Pak-Cheung Ng (1), Jane Yin (1) Keywords: Oxygen consumption Lung Rabbit Animal Chronic lung injury Acute lung injury Abstract: Objective: To study the oxygen consumption by lungs with acquired acute and chronic injury in a rabbit model. Design: A non-randomized controlled animal study. Subjects and method: Three groups of White New Zealand rabbits were studied to determine the oxygen consumption of the lungs. Group 1 (n=21, controls) consisted of healthy rabbits with normal lungs. The rabbits in group 2 (n=14) had sustained acute lung damage induced by subcutaneous N-nitroso-N-methylurethane and those in group 3 (n=9) had sustained chronic lung damage inflicted by a single dose of intra-tracheal bleomycin. Pulmonary oxygen consumption was estimated from the difference between the whole body oxygen consumption, measured by indirect calorimetry, and systemic oxygen consumption estimated by the Fick method. Measurements and results: Both acute and chronic lung-damaged groups had significantly greater pulmonary oxygen consumption than the control group, both as absolute values [control vs acute vs chronic: 0.25 (0.04) vs 0.76 (0.10) vs 1.77 (0.21) ml/kg per min, p Author Affiliation: (1) Department of Paediatrics, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong (2) Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong Article History: Received Date: 19/11/2000 Accepted Date: 15/06/2001 Article note: Final revision received: 22 May 2001 Electronic Publication

Byline: Eloisa Gitto (1), Russel J. Reiter (1), Malgorzata Karbownik (3), Dun Xian-Tan (1), Ignazio Barberi (2) Keywords: Distress respiratory syndrome Oxidative stress Antioxidants Abstract: Reactive oxygen and nitrogen species are generated by several inflammatory and structural cells of the airways. These oxidant species have important effects on a variety of lung cells as regulators of signal transduction, activators of key transcription factors and modulators of gene expression and apoptosis. Thus, increased oxidative stress accompanied by reduced endogenous antioxidant defenses may play a role in the pathogenesis of a number of inflammatory pulmonary diseases, including respiratory distress syndrome (RDS) in the newborn. There obviously are conflicting reports on the effect of oxygen, ventilation and nitric oxide (NO) on RDS and, thus, the question arises as what the neonatologist should do when confronted with a newborn with RDS. Clearly, utilizing lung protective strategies requires compromises between gas exchange goals and potential toxicities associated with over-distension, derecruitment of lung units and high oxygen concentrations. The results discussed in this brief review suggest rigorous clinical tests with antioxidants which may help to define the mechanisms associated with RDS and which could lead to new treatment strategies. Author Affiliation: (1) Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, Mail Code 7762, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900, USA (2) Institute of Medical Pediatrics, Neonatal Intensive Care Unit, University of Messina, Via Consolare Valeria, Messina, Italy (3) Department of Thyroidology, Institute of Endocrinology, Medical University of Lodz, 5 DR. Sterlinga St., 91-425 Lodz, Poland Article History: Received Date: 03/11/2000 Accepted Date: 06/04/2001 Article note: Final revision received: 15 March 2001 Electronic Publication

Byline: K. M. Smith (1), T. M. Wahlig (1), D. R. Bing (1), M. K. Georgieff (1), S. J. Boros (1), M. C. Mammel (1) Keywords: Key words Oxygen consumption; Mechanical ventilation; Synchronized ventilation; Respiratory distress syndrome Abstract: Objective: We tested the hypothesis that synchronization to patient effort during intermittent mandatory ventilation (SIMV), when compared to conventional unsynchronized intermittent mandatory ventilation (IMV), will decrease energy Author Affiliation: (1) Infant Diagnostic and Research Center, Children's Hospital of St. Paul, and the Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota, USA, US Article note: Received: 9 April 1996 Accepted: 13 November 1996