Delayed transfer of care from NHS secondary care to primary care in England: its determinants, effect on hospital bed days, prevalence of acute medical conditions and deaths during delay, in older adults aged 65 years and over.

BACKGROUND: The delay in discharge or transfer of care back to the community following an acute admission to the hospital in older adults has long been a recognized challenge in the UK. We examined the determinants and outcomes of delayed transfer of care in older adults. METHODS: A prospective observational study was conducted in a district general hospital with a catchment population of 250,000 in England, UK. Those >or= 65 years admitted to two care of the elderly wards during February 2007 were identified and prospectively followed-up till their discharge. Data was presented descriptively. RESULTS: 36.7% (58/158) of patients had a delay in transfer of care. They tended to be older, had poorer pre-morbid mobility, and were more likely to be confused at the time of admission. Compared to the 2003 National Audit Report, a significantly higher percentage (29.3%vs.17%) awaited therapist assessments or (27.6%vs.9%) domiciliary care, with a lower percentage (< 1%vs.14%) awaiting further NHS care. Of 18 in-patient deaths, five occurred during the delay. Seven patients developed medical conditions during the delay making them unfit for discharge. The number of extra bed days attributable to delayed discharges in this study was 682 (mean = 4.8) days. CONCLUSION: Awaiting therapy and domiciliary care input were significant contributing factors in delayed transfer of care. Similar local assessments could provide valuable information in identifying areas for improvement. Based on available current evidence, efficacy driven changes to the organisation and provision of support, for example rapid response delayed discharge services at the time of "fit to discharge" may help to improve the situation.

Staphylococcal alpha-toxin causes increased tracheal epithelial permeability.

Staphylococcus aureus is an important cause of pulmonary infections. The role of S. aureus alpha-toxin as a virulence factor is unclear. We hypothesized that airway epithelium is a target of S. aureus alpha-toxin and that exposure of airway epithelium to alpha-toxin results in damage to the airway epithelium. To examine the hypothesis that alpha-toxin is capable of independently producing airway epithelium damage as measured by permeability and morphometry, an isolated whole mouse trachea test apparatus was developed. In vitro epithelial permeability (P) was calculated and digital micrographs were analyzed morphometrically. Purified S. aureus alpha-toxin produced a significant increase in tracheal epithelial P (P < 0.05). Morphometric analysis revealed the ratio of adherent tracheal epithelium attached to the basement membrane divided by the total length of the basement membrane decreased in a dose-dependent manner with 1 microg/ml alpha-toxin and 10 microg/ml alpha-toxin (P < 0.05). We developed a novel isolated whole mouse trachea test apparatus for the measurement of tracheal epithelium damage. Increased P and separation of the tracheal epithelium from the basement membrane occurred after S. aureus alpha-toxin exposure. We conclude that mammalian airway epithelium is a target of S. aureus alpha-toxin.

Peroxidase activity within circulating neutrophils correlates with pulmonary phenotype in cystic fibrosis.

Excess neutrophils are present in the airways of patients with cystic fibrosis (CF). Myeloperoxidase (MPO) activity of acid extracts of sputum is directly correlated with airflow obstruction in CF patients. We hypothesized that the sputum MPO was derived from the MPO of neutrophils that entered the airways from the circulation. Active MPO without protease activity injures airways. If MPO activity from circulating neutrophils that emigrate into the airways of these patients causes increased airway epithelial permeability and mucus-gland secretion, then (1) those patients with greater MPO activity per circulating neutrophil would be more likely to produce sputum and (2) the MPO activity per circulating neutrophil would positively correlate with airflow obstruction. We determined the MPO activity for both circulating and sputum neutrophils. Spirometry and respiratory cultures were obtained simultaneously with blood and sputum samples. CF patients with more MPO activity within their circulating neutrophils were more likely to produce sputum ( P =.001, chi 2 test), and the MPO activity per circulating neutrophil was positively correlated with airflow obstruction as measured on the basis of the ratio of 1-second forced expiratory volume to forced vital capacity ( P <. 03, Kruskal-Wallace test). These associations were independent of age, sex, the results of respiratory-tract culture, or protease activity in the circulating neutrophils. MPO activity in circulating neutrophils from CF patients homozygotic for the deletion of phenylalanine at position 508 in the CF transmembrane regulator protein is directly related to the severity of these patients' pulmonary disease. Our results are consistent with the hypothesis that circulating neutrophils deliver active MPO to the airway, producing airway injury and airflow obstruction in homozygotic delF508 CF patients.