PA10†What i need you to know. building a collaborative communication tool.

BACKGROUND: During strategy consultation in Northern Ireland an "End of Life Care Passport" was suggested as a way to address myriad communication difficulties involved in living with evolving illness. AIM: To build a patient-owned communication tool to facilitate important conversations and capture key information as health changes. METHODS: Participatory action methods used to engage service users, carers, patient advocates, and healthcare professionals. Views harnessed via: face to face, email, telephone, via series of workshops. Iterative process of drafting, dissemination, evaluation, re drafting. Pilot version launched (350 disseminated): used for a 3 month evaluative period by 3 groups: living with dementia, with motor neurone disease, with advanced respiratory illness. Feedback widely sought from participating individuals and groups. RESULTS: The emergent tool(1) very different from originally envisaged. Key issues include widespread rejection of "End of Life Care Passport" (felt to be professionally based perspective); very high level of engagement with the process, imperative to develop a tool which focusses on language and communication needs of patient and carers rather than professionals. Emergent tool contains ten sections and brief explanatory content. Housed as A5 portable ring binder (e-version suggested), updated collaboratively by patient, carers, key supporters, professionals. CONCLUSION: Patients and carers face multiple communication difficulties negotiating changing health. At particular risk are those with rare illness and those whose capacity is limited due to illness, language or cultural barriers. There is a role for a communication tool which houses key evolving information, is completed collaboratively and patient owned and controlled. REFERENCE: http://www.rcgp.org.uk/rcgp-near-you/rcgp-northern-ireland/my-healthcare-passport.aspx.

Respiratory viral infection in exacerbations of COPD.

BACKGROUND: Patients with COPD have frequent exacerbations. The role of respiratory viral infection is just emerging. We wished to determine prospectively the incidence of viral infection in exacerbated and stable COPD patients as well as smokers who do not have airways obstruction. METHODS: Stable and exacerbated COPD patients were recruited along with a group of patients who had smoked but who did not have any airways obstruction. Spirometry was performed and sputum specimens were tested for a range of 12 different respiratory viruses using PCR. RESULTS: One hundred and thirty-six patients with exacerbations of COPD, 68 stable COPD patients and 16 non-obstructed smokers were recruited. A respiratory virus was detected in 37% of exacerbations, 12% of stable COPD patients and 12% of non-obstructed smokers, p<0.0005. Rhinovirus was most frequently detected. The symptom of fever was associated with virus detection, p<0.05. Infection with more than one virus was only found in the exacerbated COPD patients. CONCLUSION: Respiratory viral infection is associated with exacerbations of COPD. Rhinovirus was the most common infecting agent identified and in two cases human metapneumovirus was also detected. Dual infections were only seen amongst those patients admitted to hospital with acute exacerbations of COPD. Viruses were more commonly detected in those with more severe airways disease.

Acute and latent adenovirus in COPD.

INTRODUCTION: The COPD airway is infiltrated with CD8+ T cells, which has led to a virus being implicated in its pathogenesis. Some investigators have suggested a role for the persistence of the adenovirus E1A in bronchial epithelial cells. We examined respiratory tract specimens from COPD patients for the presence of E1A DNA and mRNA using real-time PCR. METHODS: Nucleic acid extraction was performed on sputum specimens from patients with COPD. Copy numbers for GAPDH, and adenovirus 5 E1A DNA and mRNA were determined using a quantitative real-time PCR assay. All samples were screened for the adenovirus hexon gene using nested PCR. RESULTS: One hundred and seventy-one patients, 80 male, aged 68.9+/-9.8 years with COPD were recruited. One hundred and thirty-six were seen during an exacerbation when admitted to hospital, 33 of whom were reviewed when clinically stable along with an additional 35 stable COPD patients. Ten patients in the exacerbation group were positive for the adenovirus hexon gene (7%), as were four in the stable group (6%). Only two patients in the exacerbation group were positive for adenovirus 5 E1A. Only one patient in the stable COPD group had detectable E1A DNA/mRNA and also tested positive for the adenovirus hexon gene. CONCLUSION: Adenovirus is detected in similar frequencies in exacerbated and stable COPD patients. Adenovirus E1A DNA is infrequently detected in respiratory secretions from patients with COPD. Our data suggest that the persistence of adenovirus 5 E1A in lung cells of sputum samples in patients with COPD occurs infrequently.