Chronic obstructive pulmonary disease (COPD) is a common cause of acute medical hospital admission, and the prevalence of undiagnosed COPD in the community is high. The impact of undiagnosed COPD on presentation to secondary care services is not currently known. We therefore set out to characterise patients at first admission with an acute exacerbation of COPD, and to identify potential areas for improvement in earlier diagnosis and further management. A retrospective case review of patients first admitted to a district teaching hospital with an acute exacerbation of COPD over a 1-year period was carried out. Forty-one patients with a first admission with an acute exacerbation of COPD were identified, 14 (34%) of whom had not been previously diagnosed and were diagnosed with COPD as a result of the admission. At presentation, this group of patients had severe disease, with mean (SD) FEV(1) 1.02 (0.32) L, and a respiratory acidosis in eight (20%) patients, even though this was their first admission for an acute exacerbation of COPD. Missed potential opportunities to intervene in community and inpatient management were identified, including earlier diagnosis, pre-hospital corticosteroid therapy, inpatient respiratory team input, provision of smoking cessation advice and consideration of pulmonary rehabilitation. Patients with a first hospital admission with an acute exacerbation of COPD frequently have severe disease at presentation. Despite having severe disease, a diagnosis of COPD had not been made in the community prior to admission in one-third of patients. Future work should be directed at earlier identification of patients who are symptomatic from COPD and ensuring that the interventions of proven benefit in COPD are systematically offered to patients in both primary and secondary care.

Background: There is evidence that platelet activation occurs in allergic inflammation and asthma, but little is known about the role platelets play in airway inflammation associated with asthma. Objectives: In the present study, we have investigated the kinetics of platelet activation following allergen provocation of allergic asthmatics to determine the dynamics of platelet activation relative to changes in lung function and changes in airway inflammation. Methods: Changes in platelet count and haematocrit from baseline were measured during the early asthmatic response (EAR), late asthmatic response (LAR; or at corresponding time points) and at 24 h were compared between allergen- and saline-challenged groups. A subgroup of allergen-challenged asthmatics, a group of 7 challenged asthmatics and 7 controls were bronchoscoped, and BAL fluid was collected and analysed for levels of histamine and eosinophil cationic protein. Results: There was a fall in circulating platelet count, but not haematocrit after allergen challenge when compared with saline during the LAR or at 24 h. At 24 h FEV₁ had returned to within 20% of baseline in all subjects, although the thrombocytopaenia and airway inflammation persisted. Conclusions: Our results suggest that persistent thrombocytopaenia accompanies allergen exposure and persists beyond changes in airway obstruction at a time when airway inflammation is present. Our results provide further evidence that platelets may be involved in allergic disease.

Background -Leukotrienes are inflammatory mediators implicated in the pathogenesis of asthma. The capacity of inflammatory cells within the airways to generate leukotrienes may be altered in asthma. This hypothesis was tested using bronchoalveolar lavage (BAL) to sample cells within the airways from atopic asthmatic and normal subjects, and by measuring their Asthma is characterised by reversible airflow obstruction, bronchial reactivity, and airways inflammation in which a range of mediators, including leukotrienes, is implicated.' Leukotriene B4 (LTB4) is chemotactic for neutrophils, eosinophils, and mononuclear cells, and activates neutrophils and eosinophils, but also stimulates T suppressor cell function.' The cysteinyl leukotrienes -leukotriene C4 (LTC4), leukotriene D4 (LTD4), and leukotriene E4 (LTE4)-cause bronchoconstriction, increased vascular permeability, and increased mucus secretion.3 The leukotrienes are derived from arachidonic acid by the 5-lipoxygenase pathway and their involvement in asthma is suggested by their increased levels in body fluids of asthmatic patients -for example, LTB4 and LTC4 in bronchoalveolar lavage (BAL) fluid4 and LTE4 in urine.' The most convincing evidence comes from studies of leukotriene antagonists and 5-lipoxygenase inhibitors in asthmatic subjects. These agents reduce bronchoconstriction induced by exercise6 and cold air7 and improve lung function in chronic asthma.8Leukotrienes are produced by a range of cells present in the airways, including eosinophils, mast cells, macrophages/monocytes, and neutrophils.9 Leukotriene generation independent of receptor-associated processes can be studied in vitro using calcium ionophore (A23187). Leukotriene generation by peripheral blood leucocytes from atopic asthmatic subjects is increased in response to ionophore compared with that in normal subjects.'0 We postulated that the capacity of inflammatory cells in the bronchi of asthmatic subjects to generate leukotrienes might also be increased. Inflammatory cells within the bronchi -most of which are alveolar macrophages -can be sampled by BAL and their function studied in vitro. The aim of this study was to investigate whether the capacity of BAL cells to generate leukotrienes when stimulated with ionophore is altered in asthmatic subjects. Methods SUBJECTSTwelve mild asymptomatic atopic asthmatic subjects and 12 normal human volunteers were studied. Between two and seven days before fibreoptic bronchoscopy each subject was assessed for the presence and severity of asthma. Clinical history and examination, standard skin prick tests (Bencard, Idis, Kingston, Surrey, UK), full blood count and differential white blood count, serum IgE, biochemical screen, chest radiography (if not performed within the previous year), spirometry and methacholine challenge were performed. Forced expiratory volume in one second (FEVy) was measured using a Vitallograph dry wedge bellows spirometer; baseline FEV, was recorded after three reproducible values were obtained. Methacholine challe...

No abstract

Poster sessions A168Thorax 2012;67(Suppl 2):A1-A204reflection that since the BTS emergency oxygen guidelines production, teaching on emergency oxygen has now become an integral part of medical student teaching which more senior doctors will not have benefited from. Education on oxygen therapy should be mandatory in medical schools and also to doctors in all grades throughout the trust. We believe that this reflects the undergraduate teaching focus on oxygen in COPD. We recommend introducing a compulsory undergraduate e-learning module on oxygen delivery and prescribing as newly-qualified doctors need to be able to prescribe oxygen safely. JUNIOR DOCTORS PERFORMANCE AND INTERPRETATION OF SPIROMETRY