High-flow nasal cannula therapy for infants with bronchiolitis (Review)

Aim:The study aims to investigate the prevalence of off-label prescribing in the general paediatric ward at a major teaching hospital in Tasmania, Australia. Method: The drug charts and medical records from two groups of 150 consecutive paediatric patients, admitted 6 months apart in July 2009 and January 2010, were studied retrospectively. Patients were required to spend at least one night in hospital and be aged less than 12 years. Each prescribed drug was compared with the approved product information to determine if the usage was off-label. Data concerning documented informed consent and adverse drug reactions were also recorded. Results: Three hundred patients were prescribed a total of 887 medicines. Of these, 31.8% were off-label and 57.3% of children received an off-label medication. There was no significant seasonal variation in patient characteristics or prescriptions. Drugs were most commonly off-label due to their dosage or frequency of administration. Of the 106 different drugs used, the use of 51 was off-label on at least one occasion, and for 30 drugs their use was off-label on more than 75% of occasions. The drugs most commonly used off-label were oxycodone, salbutamol and paracetamol. No informed consent documentation was identified, and two of five recorded adverse drug reactions were associated with off-label drug use. Conclusion: Off-label use of medicines occurred frequently in paediatric inpatients. The available evidence often supported off-label medication use. An improved system for the revision of approved drug information and an Australian guideline for paediatric prescribing are needed.

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BackgroundChildhood interstitial lung disease (chILD) represents a rare heterogeneous group of respiratory disorders. In the absence of randomized controlled clinical trials, global collaborations have utilized case series with an aim to standardising approaches to diagnosis and management. Australasian data are lacking. The aim of this study was to calculate prevalence and report the experience of chILD in Australasia over a decade.MethodsPaediatric pulmonologists in Australia and New Zealand involved in the care of patients aged 0–18 years with chILD completed a questionnaire on demographics, clinical features and outcomes, over a 10 year period. These data, together with data from the 2 reference genetics laboratories, were used to calculate prevalence.ResultsOne hundred fifteen cases were identified equating to a period prevalence (range) of 1.5 (0.8–2.1) cases/million for children aged 0–18years. Clinical data were provided on 106 patients: the <2 year group comprised 66 children, median age (range) 0.50 years (0.01–1.92); the ≥2 year group comprised 40 children, median age 8.2 years (2.0–18.0). Management approach was heterogeneous. Overall, 79% of patients had a good clinical outcome. Mortality rate was 7% in the study population.ConclusionchILD is rare in Australasia. This study demonstrates variation in the investigations and management of chILD cases across Australasia, however the general outcome is favorable. Further international collaboration will help finesse the understanding of these disorders.

What is known and objective Fever, one of the most common symptoms of illness experienced by children, often creates undue parental anxiety about the consequences of fever, which can lead to overtreatment. The full extent of this problem in Australia is not known. This study aimed to describe parents' knowledge, beliefs and perceptions about childhood fever and its management, and identify any predictors of the burden on parents when children are febrile. Methods This was a cross‐sectional web‐based survey of parents living in Australia. Parents with at least 1 child <6 years were recruited via Facebook. Demographic information, parental fever knowledge and beliefs and responses to the Parent Fever Management Scale, a measure of parental burden, were collected and analysed. Results and discussion Of the 12 179 parents who completed the survey, 42.0% knew that a temperature above 38°C constitutes a fever, with 33.4% underestimating the temperature of a fever. Parents believed that there were many harms associated with untreated fever, namely seizures (71.8%), dehydration (63.6%), serious illness (43.0%) and brain damage (36.8%). Phobic beliefs were more common among parents who underestimated the temperature of a fever. Identification of health professionals as a main information source about fever did not significantly improve knowledge or reduce fears. Up to 65.0% of respondents indicated that they practice non–evidence‐based strategies to reduce temperature. The belief that ‘every child with a fever should be treated with medication to lower temperature’ was the strongest predictor of parental burden (ß = 0.245, P < 0.001). What is new and conclusion Poor parental knowledge and misconceptions surrounding fever and its management are still common among parents throughout Australia. Large‐scale, sustainable educational interventions are needed to dispel misconceptions and concerns about fever, encourage appropriate and safe care of febrile children.

The Pseudomonas aeruginosa quorum sensing signal molecule N-3-oxododecanoyl-l-homoserine lactone (3OC12HSL) can inhibit function of the mammalian anti-inflammatory transcription factor peroxisome proliferator activated receptor (PPAR)γ, and can be degraded by human paraoxonase (PON)2. Because 3OC12HSL is detected in lungs of cystic fibrosis (CF) patients infected with P. aeruginosa, we investigated the relationship between P. aeruginosa infection and gene expression of PPARγ and PON2 in bronchoalveolar lavage fluid (BALF) of children with CF. Total RNA was extracted from cell pellets of BALF from 43 children aged 6 months–5 years and analyzed by reverse transcription–quantitative real time PCR for gene expression of PPARγ, PON2, and P. aeruginosa lasI, the 3OC12HSL synthase. Patients with culture-confirmed P. aeruginosa infection had significantly lower gene expression of PPARγ and PON2 than patients without P. aeruginosa infection. All samples that were culture-positive for P. aeruginosa were also positive for lasI expression. There was no significant difference in PPARγ or PON2 expression between patients without culture-detectable infection and those with non-Pseudomonal bacterial infection, so reduced expression was specifically associated with P. aeruginosa infection. Expression of both PPARγ and PON2 was inversely correlated with neutrophil counts in BALF, but showed no correlation with other variables evaluated. Thus, lower PPARγ and PON2 gene expression in the BALF of children with CF is associated specifically with P. aeruginosa infection and neutrophilia. We cannot differentiate whether this is a cause or the effect of P. aeruginosa infection, but propose that the level of expression of these genes may be a marker for susceptibility to early acquisition of P. aeruginosa in children with CF.

People with cystic fibrosis (CF) have been reported to make lung T cell responses that are biased towards T helper (Th) 2 or Th17. We hypothesized that CF-related T cell regulatory defects could be detected by analyzing CD4+ lymphocyte subsets in peripheral blood. Peripheral blood mononuclear cells from 42 CF patients (6 months–53 years old) and 78 healthy controls (2–61 years old) were analyzed for Th1 (IFN-γ+), Th2 (IL-4+), Th17 (IL-17+), Treg (FOXP3+), IL-10+ and TGF-β+ CD4+ cells. We observed higher proportions of Treg, IL-10+ and TGF-β+ CD4+ cells in CF adults (≥ 18 years old), but not children/adolescents, compared with controls. Within the CF group, high TGF-β+% was associated with chronic Pseudomonas aeruginosa lung infection (p < 0.006). We observed no significant differences between control and CF groups in the proportions of Th1, Th2 or Th17 cells, and no association within the CF group of any subset with sex, CFTR genotype, or clinical exacerbation. However, high Th17% was strongly associated with poor lung function (FEV1 % predicted) (p = 0.0008), and this association was strongest when both lung function testing and blood sampling were performed within one week. Our results are consistent with reports of CF as a Th17 disease and suggest that peripheral blood Th17 levels may be a surrogate marker of lung function in CF.

BackgroundEmpyema is a serious complication of pneumonia frequently caused by Streptococcus pneumoniae (SP). We assessed the impact of the 13-valent pneumococcal conjugate vaccine (13vPCV) on childhood pneumonia and empyema after inclusion in the Australian National Immunisation Program.MethodsFor bacterial pneumonia and empyema hospitalisations, we ascertained incidence rates (IRs) using the National Hospital Morbidity Database International Statistical Classification of Disease discharge codes and relevant population denominators, and calculated incidence rate ratios (IRR) comparing the 13vPCV period (June 2012–May 2017) with the 7vPCV period (June 2007–May 2011). Blood and pleural fluid (PF) cultures and PF PCR of 401 children with empyema from 11 Australian hospitals during the 13vPCV period were compared with our previous study in the 7vPCV period.FindingsAcross 7vPCV and 13vPCV periods, IRs per million children (95% CIs) were 1605 (1588 to 1621) and 1272 (1259 to 1285) for bacterial pneumonia, and 14.23 (12.67 to 15.79) and 17.89 (16.37 to 19.42) for empyema hospitalisations. IRRs were 0.79 (0.78 to 0.80) for bacterial pneumonia and 1.25 (1.09 to 1.44) for empyema. Of 161 empyema cases with SP serotypes, 147 (91.3%) were vaccine types. ST3 accounted for 76.4% of identified serotypes in the 13vPCV period, more than double than the 7vPCV period (p<0.001); ST19A decreased from 36.4% to 12.4%. No cases of ST1 empyema were identified in the 13vPCV period versus 14.5% in the 7vPCV period.Interpretation13vPCV resulted in a significant reduction in all-cause hospitalisations for bacterial pneumonia but empyema hospitalisations significantly increased, with emergence of pneumococcal ST3 as the dominant serotype in empyema.Trial registration numberAustralian and New Zealand Clinical Trial Registry ACTRN 12614000354684.