PubMed Health⌕ Search

PubMed · 17071575

Resource allocation for community-based therapy.

Abstract

PURPOSE: Adequate and equitable resourcing of services for children with disabilities and their families is a challenge that is faced by agencies as the growth in client numbers outstrips any increase in available funding. While funding models have been developed within the acute health care and education sectors, there have been few attempts to develop funding models for therapy (occupational therapy, physiotherapy, psychology, and speech pathology) provided within community-based, paediatric disability services. This paper outlines a model for allocating staff resources to provide therapy services for children with physical disabilities based on a project conducted by Novita Children's Services (formerly the Crippled Children's Association of South Australia, Inc.). METHOD: Services were mapped using a framework based on the International Classification of Function developed by the World Health Organization and adopted by the Australian Institute of Health and Welfare. An action research methodology was employed that included focus groups held with staff to identify potential resource drivers; collection of travel time data, client caseload numbers; and developing profiles of services and client groups. A model for allocating staff time was developed to reflect the differing service demands, travel time, leave allowances and time for activities to develop the social environment for individuals with disabilities. RESULTS AND CONCLUSIONS: Analysis indicated that the drivers of staff resources were the type of service delivery (early intervention versus school aged services), model specific (e.g., time required to provide community-based services and work within multi-disciplinary teams), and specific client (need for complex technology or equipment; school/preschool transition times; high health care needs due to dysphagia, deteriorating conditions with changing needs, or post surgery/medication rehabilitation) and family well-being issues. While further data collection and refinement of the model is needed, it provides the organization with more objective and equitable resource allocation and enables improved advocacy for client needs.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sonya Murchland, Wendy Wake-Dyster. 2006-11-30. Resource allocation for community-based therapy.. https://doi.org/10.1080/09638280600638281

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗

Extensive and differential platinum chemotherapy mutagenesis in livers of children.

Childhood cancer survivors often experience late adverse effects that may be linked to chemotherapy mutagenesis. We studied chemotherapy mutagenesis in normal pediatric tissues using duplex sequencing (NanoSeq) to enable the detection of mutations from single DNA molecules. We found that platinum chemotherapeutics increased the mutation burdens of normal pediatric tissues to levels seen in adults. In the liver, platinum agents imparted a tissue-specific mutational signature that was absent from other tissues. Gene-focused duplex sequencing revealed that chemotherapy mutagenesis generates a great diversity of nonsynonymous variants, some of which may have functional potential, such as leukemogenic variants in blood. Our findings demonstrate extensive chemotherapy mutagenesis in normal tissues of children, which may provide a plausible link between chemotherapy exposure and adverse effects in later life.

Child↗

Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.

TBK1 is a serine-tyrosine kinase protein that transmits signals from pattern recognition receptors to the NF-κB pathway leading to production of Type 1 Interferons. Mutations in this protein have been associated with arthritis, vasculitis, herpes simplex encephalitis and amyotrophic lateral sclerosis. In the current study, we characterized the functional consequences of a TBK1-variant bearing a truncation in exon 4 and 5 in a patient with poly arthritis resembling juvenile idiopathic arthritis and necrotizing encephalitis. The truncation was associated with reduced TBK1 protein abundance and altered phosphorylation. The variant was associated with increased basal/and or Poly-I: C induced IL-6, TNFα, IL-1β and IL-18 and type 1 Interferon ex vivo. Our findings expand the phenotypic spectrum of TBK1 loss-of-function variants and may provide insight into the management of immune dysregulation in affected patients.

Child↗