Prolonged moderate hyperoxia induces hyperresponsiveness and airway inflammation in newborn rats.

Bronchopulmonary dysplasia is the most common cause of chronic pulmonary disease in premature infants. Airway inflammation appears to play a major pathogenetic role together with barotrauma and oxygen toxicity. The aim of the present study was to determine the effect of a 15-d exposure to moderate hyperoxia (FiO2, 50%) on airway reactivity and inflammatory response in neonatal and adult rats. We studied in isolated tracheal rings the 1) isometric contraction to cumulative concentrations of carbachol (10(-8) to 10(-3) M); 2) epithelial, submucosal, smooth muscle, and connective tissue surface area; and 3) distribution of inflammatory cells (mastocytes, granulocytes, macrophages) by using MAb. Reactivity to carbachol was significantly increased in the hyperoxic pups, in which a 13% increase in tracheal smooth muscle surface area was observed. Type-I mast cells and macrophages (submucosa and connective tissue) and granulocytes (connective tissue) were increased in the neonatal hyperoxic group. Hyperoxia did not influence functional, morphometric, or cellular data in adult rats. In conclusion, exposure of newborn rats to moderate hyperoxia induces airway hyperresponsiveness and histologic changes similar to those reported in bronchopulmonary dysplasia. Hyperresponsiveness may be ascribed to an increase in smooth muscle related to the release of yet undetermined mediators by inflammatory cells infiltrating the airways. Lung immaturity definitely plays a role because similar alterations are not observed in adult rats.

Nosocomial pneumonia and tracheitis in a pediatric intensive care unit: a prospective study.

We conducted a prospective study in the multidisciplinary pediatric intensive care unit (pediatric ICU) of a tertiary-care university hospital in order to determine the incidence, risk markers, risk factors, and complications related to bacterial nosocomial pneumonia (BNP) and tracheitis (BNT) in children. A cohort of 1,114 consecutive admissions to the pediatric ICU was enrolled over a 56-wk period; 154 cases were excluded mostly (75%) because they already had a respiratory infection at entry. The final sample included 960 admissions (831 patients). Diagnosis of BNP or BNT was based on Centers for Disease Control of Atlanta criteria using a consensus method involving three experts, who also attributed complications to BNP and BNT. A total of 29 BNP and BNT (3.0%; 95% CI: 1.1 to 4.1%) were diagnosed (BNP: 1.2%, 95% CI: 0.7 to 1.9%; BNT: 1.8%, 95% CI: 0.8 to 2.6%). Three factors were retained by multivariate analysis as independent risk factors or markers for BNP (immunodeficiency, immunosuppression, and neuromuscular blockade), and two for BNT (head trauma and respiratory failure). Gram-negative bacteria and Staphylococcus aureus were the microorganisms most frequently found in the tracheal aspirates. Prescription of antibiotics was commonly attributable to BNP (75%) and BNT (59%). Death, as well as multiple organ system failure, resulted from BNP in 8% of cases, but never from BNT. In BNT, the reintubation rate was 24%. Nosocomial bacterial respiratory infections are rare in critically ill children. However, BNP causes significant complications, and more attention should be focused on BNT in the critically ill child.