Dataset Information

Risk factors for adverse outcomes of Indigenous infants hospitalized with bronchiolitis.

ABSTRACT:

Background

Hospitalized bronchiolitis imposes a significant burden among infants, particularly among Indigenous children. Traditional or known risk factors for severe disease are well described, but there are limited data on risks for prolonged hospitalization and persistent symptoms. Our aims were to determine factors (clinical and microbiological) associated with (i) prolonged length of stay (LOS); (ii) persistent respiratory symptoms at 3 weeks; (iii) bronchiectasis up to ∼24 months post-hospitalisation; and (iv) risk of respiratory readmissions within 6 months.

Methods

Indigenous infants hospitalized with bronchiolitis were enrolled at Royal Darwin Hospital between 2008 and 2013. Standardized forms were used to record clinical data. A nasopharyngeal swab was collected at enrolment to identify respiratory viruses and bacteria.

Results

The median age of 232 infants was 5 months (interquartile range 3-9); 65% male. On multivariate regression, our 12 point severity score (including accessory muscle use) was the only factor associated with prolonged LOS but the effect was modest (+3.0 hr per point, 95%CI: 0.7, 5.1, P = 0.01). Presence of cough at 3 weeks increased the odds of bronchiectasis (OR 3.0, 95%CI: 1.1, 7.0, P = 0.03). Factors associated with respiratory readmissions were: previous respiratory hospitalization (OR 2.3, 95%CI: 1.0, 5.4, P = 0.05) and household smoke (OR 2.6, 95%CI: 1.0, 6.3, P = 0.04).

Conclusion

Increased severity score is associated with prolonged LOS in Indigenous children hospitalized with bronchiolitis. As persistent symptoms at 3 weeks post-hospitalization are associated with future diagnosis of bronchiectasis, optimising clinical care beyond hospitalization is needed to improve long-term respiratory outcomes for infants at risk of respiratory disease. Pediatr Pulmonol. 2016;51:613-623. © 2015 Wiley Periodicals, Inc.

SUBMITTER: McCallum GB

PROVIDER: S-EPMC7167668 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Micronutrient deficiencies and environmental exposures have been to known to adversely impact brain and nervous system functions in adults and children worldwide. However, few studies have examined the short and long-term impact of these risk factors on neurodevelopmental outcomes in children in low-income countries, where the effects are likely to be more pronounced due to limited resources for monitoring and insufficient regulations. Biological risk factors of relevance include micronutrient deficiencies such as zinc and exposure to heavy metals such as lead and mercury. Studies have suggested an association between neurodevelopmental impairment and micronutrient deficiency as well as exposure to a number of heavy metals and environmental toxins. Moreover, findings also suggest that risk factors for adverse developmental outcomes that are independently significant may have the potential for causing cumulative increases in adverse effects. In Sub-Saharan Africa, severe malaria is a leading risk factor for long-term neurocognitive impairment in children. Zinc deficiency or exposure to heavy metals could influence risk of severe malaria, modify the risk of neurocognitive impairment in children with severe malaria, or independently affect risk of neurocognitive impairment. Untargeted analyses for potential environmental exposures or metabolomic changes in children with cerebral malaria vs. without cognitive impairment or in children with higher vs. lower cognitive scores, could also identify new risk factors for neurodevelopmental impairment in Ugandan children with cerebral malaria.In our completed study in Kampala, we assessed neurologic and developmental impairment in children with cerebral malaria [CM] or severe malarial anemia [SMA], as compared to health community children from the same extended household as the children with CM or SMA. As an extension of this study, we are interested in determining levels of micronutrients such as zinc in the population, and in addition, determining exposure levels of heavy metals (lead, mercury, copper, manganese etc.) in samples collected from children with severe malaria and community controls. The primary hypotheses of this study is that nutrient deficiencies or exposure to heavy metals influence short and long term neurocognitive outcomes in healthy community children and in children with severe malaria, and that children with cerebral malaria have specific metabolomic changes that relate to long-term neurocognitive impairment. The specific aims of our study are:Aim 1: To determine levels of zinc, heavy metals, and biomarkers associated with inflammation in children presenting with different forms of severe malaria (SM) and in healthy community children (CC). The working hypothesis of this aim is that 1) children with SM will have lower zinc levels compared to CC; 2) children with SM will present with higher toxic metal exposure and higher levels of biomarkers associated with inflammation than CC.Aim 2: To investigate how micronutrient deficiency, toxic metal exposure and inflammatory biomarkers affect short and long term neurodevelopmental outcomes and growth in children with severe malaria and community children (CC).The working hypothesis of this aim is that the lower levels of zinc, and presence of toxic metals in high concentrations will independently contribute to worsening neurodevelopmental outcomes and worsening growth over time in children with severe malaria and in community children. An alternate hypothesis is that micronutrient deficiency, toxic metal exposure and inflammatory states may interact with each other and with severe malaria to produce greater neurodevelopmental impairment, i.e., that the contribution is not independent but interactive.Aim 3: To determine whether the CSF metabolome differs according to level of neurodevelopmental impairment in children with cerebral malaria. The working hypothesis of this aim is that neurodevelopmental impairment in children with cerebral malaria is associated with changes in the CSF metabolome.