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Purpose To redress the paucity of studies evaluating non-invasive respiratory support in bronchiolitis patients. Methods Following ethics committee approval, the clinical database of a tertiary 23-bed paediatric intensive care unit (PICU) was reviewed for bronchiolitis admissions from January 2000 to December 2009. Length of stay (LOS), ventilatory requirements and risk factors, including prematurity, respiratory syncytial virus (RSV) status, chronic lung, neuromuscular, immune and congenital heart disease, were analysed. Results Of 8,288 admissions, 520 (6.27 %) had bronchiolitis with 343 (65.9 %) having RSV. Median (±SD) age and LOS were 2.78 months and 2.68 (±4.32) days. One (0.2 %) patient died. Assisted ventilation was required for 399 (76.7 %) patients. A total of 114 (28.6 %) patients were intubated directly and 285 (71.4 %) had a trial of non-invasive ventilation (NIV). Significant increase in the use of NIV was seen (2.8 %/year) with decline in intubation rates (1.9 %/ year) (p = 0.002). Of NIV patients, 237 (83.2 %) needed only NIV and 48 (16.8 %) failed and therefore needed intubation. The median LOS was shorter in those who succeeded NIV (2.38 ± 2.43 days) compared to those with invasive ventilation (5.19 ± 6.34 days) and those who failed NIV (8.41 ± 3.44 days). Presence of a risk factor increased the chances of failing NIV from 6 to 10 %. Conclusion NIV was successful in the vast majority of patients, particularly in those without risk factors and halved the LOS in intensive care. Failure of NIV was associated with increased duration of invasive ventilation and PICU LOS. A prospective study comparing different techniques of NIV will be helpful in defining the risks of failure of NIV., Author(s): Subodh Suhas Ganu [sup.1], Anil Gautam [sup.1], Barry Wilkins [sup.1], Jonathan Egan [sup.1] Author Affiliations: (1) grid.413973.b, 000000009690854X, Paediatric Intensive Care Unit, Sydney Medical School, The Children's Hospital at [...]

Byline: Louis Bont (1), Jan L. Kimpen (1) Keywords: Respiratory syncytial virus Artificial respiration Review Pathogenesis Immunity Abstract: Respiratory syncytial virus (RSV) bronchiolitis resulting in respiratory insufficiency is frequently encountered during the winter season in paediatric intensive care units. This review evaluates potential determinants described in severe RSV bronchiolitis with special attention to the role of immaturity of immune responses during infancy. Pre-existent cardiac or pulmonary compromises have been documented as clinical risk factors for severe RSV bronchiolitis. In addition to this group of infants with pre-morbidity, a large proportion of mechanically ventilated RSV bronchiolitis patients are previously healthy full-term infants or premature neonates without predisposing risk factors. In general, infants at this early age have maturation-related deficient cellular immunity. Several studies show an association between decreased cellular immunity and severe RSV bronchiolitis, indeed suggesting that a maturation-related defect of the cellular immune system facilitates severe RSV. In addition, low virus-specific antibody titres prior to RSV bronchiolitis have been shown to be a risk factor for severe RSV bronchiolitis. A low level of cellular and humoral immunity would explain that higher viral titres are found in infants with most severe illness. In conclusion, immaturity of the physiological functions in healthy pre-term infants and neonates, in particular the immune system, appears to be an important factor in the pathogenesis of RSV bronchiolitis resulting in mechanical ventilation. Author Affiliation: (1) Wilhelmina Children's Hospital, University Medical Center, POB 85090, 3508 AB Utrecht, The Netherlands Article History: Received Date: 07/03/2001 Accepted Date: 28/01/2002 Article note: Electronic Publication

Byline: Eric A.F. Simoes (1), Anthony R. Hayward (2), Esther M. Ponnuraj (1), John P. Straumanis (3), Kurt R. Stenmark (3), Harry L. Wilson (4), P. George Babu (5) Keywords: Key words: bronchiolitis, pneumonia, animal models, respiratory syncytial virus, bronchoalveolar lavage, Bonnet monkeys Abstract: The Bonnet monkey model of respiratory syncytial virus (RSV) infection may be a useful nonhuman primate model for studying RSV disease in humans because Bonnet monkeys can predictably be infected to obtain an orderly sequence of morphologic, cytologic, virologic, serologic, and inflammatory changes related to time of infection. Young feral Bonnet monkeys, Macaca radiata, were infected endotracheally with 10.sup.6 plaque-forming units (pfu) of the Long strain of RSV. RSV was recovered from the animals' lungs at necropsy on days 3, 5, and 7 with the highest viral titer obtained on day 3 (1.1 and 5.2x10.sup.3 pfu/g of tissue in the upper and lower lobes, respectively). RSV antigen and F protein mRNA were detected 3--5 days after infection in alveolar macrophages and in the epithelium of bronchi, terminal bronchioles, and alveoli. Histologic analysis of RSV-infected lungs at necropsy revealed progressive bronchiolar mucosal and submucosal inflammation, periarterial mononuclear interstitial inflammation, and focal alveolitis, with a maximal response at 7 days after infection. Cell counts in bronchoalveolar lavage (BAL) increased with time with neutrophils and macrophages predominating on day 3 (6.47 and 5.85x10.sup.5/mm.sup.3, respectively) and lymphocytes predominating on day 9 (4.18x10.sup.5/mm.sup.3). Serum-neutralizing antibody appeared on day 5 and IgG antibody to RSV was detected on day 9. This sequence of morphologic, cytologic, virologic, serologic, and inflammatory change following RSV infection creates a useful model in the study of experimentally induced RSV disease with a potential for testing future vaccine-induced alterations in RSV disease response. Author Affiliation: (1) Department of Pediatrics, Division of Pediatric Infectious Diseases, University of Colorado Health Sciences Center, Denver, CO 80262, USA , US (2) Department of Pediatrics, Division of Immunology, University of Colorado Health Sciences Center, Denver, CO 80262, USA , US (3) Department of Pediatrics, Developmental Lung Biology Laboratories, University of Colorado Health Sciences Center, Denver, CO 80262, USA , US (4) Department of Pathology, Providence Memorial Hospital, El Paso, TX 79902, USA , US (5) Department of Virology, Christian Medical College Hospital, Vellore, India 632004 , IN Article note: Received March 20, 1998 accepted September 7, 1998.