Patient participation in medication safety during an acute care admission

Background

Patient participation in medication management during hospitalization is thought to reduce medication errors and, following discharge, improve adherence and therapeutic use of medications. There is, however, limited understanding of how patients participate in their medication management while hospitalized.

Objective

To explore patient participation in the context of medication management during a hospital admission for a cardiac surgical intervention of patients with cardiovascular disease.

Design

Single institution, case study design. The unit of analysis was a cardiothoracic ward of a major metropolitan, tertiary referral hospital in Melbourne, Australia. Multiple methods of data collection were used including pre‐admission and pre‐discharge patient interviews (n = 98), naturalistic observations (n = 48) and focus group interviews (n = 2).

Results

All patients had changes made to their pre‐operative cardiovascular medications as a consequence of surgery. More patients were able to list and state the purpose and side‐effects of their cardiovascular medications at pre‐admission than prior to discharge from hospital. There was very little evidence that nurses used opportunities such as medication administration times to engage patients in medication management during hospital admission.

Discussion and Conclusions

Failure to engage patients in medication management and provide opportunities for patients to learn about changes to their medications has implications for the quality and safety of care patients receive in hospital and when managing their medications once discharged. To increase the opportunity for patients to participate in medication management, a fundamental shift in the way nurses currently provide care is required.     

White matter tract signatures of the progressive aphasias

The primary progressive aphasias (PPA) are a heterogeneous group of language-led neurodegenerative diseases resulting from large-scale brain network degeneration. White matter (WM) pathways bind networks together, and might therefore hold information about PPA pathogenesis. Here we used diffusion tensor imaging and tract-based spatial statistics to compare WM tract changes between PPA syndromes and with respect to Alzheimer's disease and healthy controls in 33 patients with PPA (13 nonfluent/agrammatic PPA); 10 logopenic variant PPA; and 10 semantic variant PPA. Nonfluent/agrammatic PPA was associated with predominantly left-sided and anterior tract alterations including uncinate fasciculus (UF) and subcortical projections; semantic variant PPA with bilateral alterations in inferior longitudinal fasciculus and UF; and logopenic variant PPA with bilateral but predominantly left-sided alterations in inferior longitudinal fasciculus, UF, superior longitudinal fasciculus, and subcortical projections. Tract alterations were more extensive than gray matter alterations, and the extent of alteration across tracts and PPA syndromes varied between diffusivity metrics. These WM signatures of PPA syndromes illustrate the selective vulnerability of brain language networks in these diseases and might have some pathologic specificity.     

Protective effect of chronic caffeine intake on gene expression of brain derived neurotrophic factor signaling and the immunoreactivity of glial fibrillary acidic protein and Ki-67 in Alzheimer’s disease

Alzheimer’s disease (AD) is a neurodegenerative disorder with progressive degeneration of the hippocampal and cortical neurons. This study was designed to demonstrate the protective effect of caffeine on gene expression of brain derived neurotrophic factor (BDNF) and its receptor neural receptor protein-tyrosine kinase-β (TrkB) as well as glial fibrillary acidic protein (GFAP) and Ki-67 immunoreactivity in Aluminum chloride (AlCl₃) induced animal model of AD. Fifty adult rats included in this study were classified into 5 group (10 rats each); negative and positive control groups (I&II), AD model group (III), group treated with caffeine from the start of AD induction (IV) and group treated with caffeine two weeks before AD induction (V). Hippocampal tissue BDNF and its receptor (TrkB) gene expression by real time RT-PCR in addition to immunohistochemical study of GFAP and Ki67 immunoreactivity were performed for all rats in the study. The results of this study revealed that caffeine has protective effect through improving the histological and immunohistochemical findings induced by AlCl₃ as well as BDNF and its receptor gene expression. It could be concluded from the current study, that chronic caffeine consumption in a dose of 1.5 mg/kg body weight daily has a potentially good protective effect against AD.     

Assessing quality of life in dementia: Preliminary psychometric testing of the Quality of Life Assessment Schedule (QOLAS)

We adapted a generic, individualised, patient-centred quality of life (QOL) assessment technique, the Quality of Life Assessment Schedule (QOLAS) for use with patients with dementia. The QOLAS was administered to a group of patients with mild to moderate dementia alongside a number of other measures of well-being to assess its psychometric properties. Each patient's main carer also completed the QOLAS, giving a proxy rating of the QOL of the patient. The patients understood the interview and were able to describe their quality of life both qualitatively and quantitatively. In this preliminary study the QOLAS was demonstrated to have good validity (content, construct, and criterion) and good internal reliability. The carers rated the patients as having a worse QOL than did the patients themselves on all subdomains of the QOLAS. The results suggest that patients with mild to moderate dementia can rate their own QOL and that the QOLAS is a promising method for assessing QOL in this patient group. The discrepancy between the patients' own views and the views of their carers raises important issues about whether the patient or a proxy is the best judge of QOL in patients with dementia.     

Atrophy rates of the cingulate gyrus and hippocampus in AD and FTLD

This study explores the diagnostic utility of atrophy rates of the cingulate gyrus, its subdivisions and the hippocampus in Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). Regions were manually outlined on MR images of a group of pathologically or genetically confirmed patients with AD (n=19), FTLD (n=8) and age-matched controls (n=11). Mean (S.D.) atrophy rates (%year(-1)) in the cingulate in controls, AD and FTLD were -0.3 (1.2), 5.9 (3.5), and 8.6 (4.1), respectively. Hippocampal atrophy rates in controls, AD and FTLD were -0.1 (0.8), 3.4 (2.2), and 5.2 (5.4), respectively. Atrophy rates were significantly higher in the cingulate and hippocampi in AD and FTLD compared with controls (p<0.01). There was evidence of a difference in trends of atrophy in the cingulate (more anterior in FTLD and more posterior in AD) between the disease groups (p=0.03). Cingulate atrophy rates discriminated perfectly between FTLD and controls. Significantly better discrimination between AD and controls was obtained by hippocampal rather than cingulate rates. In conclusion, cingulate atrophy is as significant a feature of AD and FTLD as hippocampal atrophy.