table 1). Each predictor was assigned a score of 1 (present) or 0 (absent), except for eMRCD score which could be 0, 1 or 2, giving a maximum DECAF score of 6. The DECAF score showed good performance for the prediction of in-hospital mortality (area under ROC curve¼0.858, 95% CI 0.82 to 0.89), and was a stronger predictor (p<0.0001) than either the APACHE (AUROC¼0.727) or CAPS (AUROC¼0.710) prognostic scores. In patients with coexistent consolidation (n¼299), DECAF was a stronger predictor of mortality than CURB-65 (AUROC¼0.77 vs 0.66, p¼0.0064). Conclusion The DECAF score is a strong predictor of in-hospital mortality and may improve the prognostication of patients hospitalised with AECOPD. External validation is required before recommending widespread application. We have investigated whether this trend has continued until 2009, and explored whether this can be explained by change in mean age at diagnosis and death. Methods We identified all patients aged between 35 and 89 years (n¼2 173 494, mean age ¼56, 49% male) in The Health Improvement Network (THIN) primary care database. From this cohort of patients we identified patients with a diagnosis of COPD using the criteria for QOF. We calculated annual incidence and prevalence rates, and mean age of patients with COPD, first COPD diagnosis and death between 2000 and 2009. Results In total, 53 379 (2.5%) of the patients were diagnosed with COPD. The prevalence of COPD increased by 50% over the 10-year period, from 24 cases per 1000 patient years in 2000 to 36 in 2009 (Abstract P213 figure 1A). However, the diagnosis of new COPD cases remained fairly constant (p¼0.295), at 3.5 cases per 1000 patient years (Abstract P213 figure 1A). The mean age at first COPD diagnosis (incidence) decreased significantly (p<0.001) by 2 years and 5 months from 69 years and 1 months in 2000 to 66 years and 8 months in 2009 (Abstract P213 figure 1B). The mean age at death of COPD patients increased significantly (p¼0.008) by 9 months from 76 years and 2 months in 2000 to 76 years and 11 months in 2009 (Abstract P213 figure 1B). Whereas the mean age of prevalent patients remained fairly constant (p¼0.098) over the period, varying between 70 years and 70 years and 8 months (Abstract P213 figure 1B). Conclusion We found that over the last decade, the average age of patients with COPD has remained relatively constant at around 70 years. COPD is increasingly being diagnosed at a younger age and patients are living longer, which may in part explain the 50% rise in COPD prevalence. Introduction Acute exacerbations of COPD are among the most common reasons for hospital admission in the UK. Exacerbations can lead to respiratory failure requiring ventilatory support, and so decisions regarding "escalation" or "ceilings" of treatment are often made early in admission. Such decisions on intubation are inevitably linked to decisions regarding resuscitation status. Prognostic factors should be used when making these decisions and FEV 1 should not be used exclusively. We reviewed admissions with ...
IntroductionChronic mucus hypersecretion (CMH) is associated with COPD development and progression. CMH presence across adult life is dynamic, influenced by factors such as smoking behaviour. CMH is usually considered a binary phenotype and the potential influence of longitudinal CMH pattern on concurrent FEV1 decline has not been explored. We investigated how longitudinal prevalence of CMH relates to concurrent FEV1 decline.MethodsThe MRC National Survey of Health and Development consists of a sample of men and women born in one week in March 1946 within England, Scotland and Wales. Smoking behaviour, MRC questionnaire defined CMH, height, weight and pre-bronchodilator spirometry were recorded at three ages: 43, 53 and (60–64) years.We used the number occasions that CMH was positively reported (0–3) as a measure of longitudinal prevalence of CMH. Multilevel models adjusted for sex were used to analyse the relationship between longitudinal prevalence of CMH and concurrent FEV1 decline (between ages 43 and (60–64)), allowing both intercept and slope to vary according to the longitudinal prevalence of CMH score. Height, weight and mean FEV1 at age 43 years were then included in the model. Smoking status (current, ex and never-smoker) and number of cigarettes smoked daily were included as time-varying covariates capable of influencing both intercept and slope.Results1960 individuals contributed data to the multilevel model: 46% male; 59% ever-smoker and mean FEV1 at age 43 years = 3.00 L. 13% reported CMH ≥ once between ages 43 and 60–64 years. After full adjustment, longitudinal prevalence of CMH was significantly associated with both a lower FEV1 at age 43 (intercept p < 0.001) and a faster decline (slope p = 0.003) (See Table 1). For each additional occasion CMH was reported there was an additional 3.2 ml/yr decline in FEV1 (p = 0.003) i.e. presence of CMH on all three occasions was associated with an additional 9.6 ml/year FEV1 decline compared with those without CMH on any occasion.Abstract P217 Table 1The association between longitudinal prevalence of CMH (number of occasions CMH reported) and FEV1 between ages 43 and 60–64 years. Multilevel model includes 1960 individualsConclusionLongitudinal prevalence of CMH is associated with concurrent FEV1 decline independent of concurrent smoking history. Rather than CMH being solely an airway disease phenotype, the longitudinal course of CMH may represent a biomarker of concurrent disease activity.
Poster sessions A156Thorax 2012;67(Suppl 2):A1-A204 symptom being major (dyspnoea, sputum purulence or volume) and the other a major or minor symptom (wheeze, cold, sore throat, cough). Reverse-transcription quantitative PCR was used to detect rhinovirus and real-time quantitative PCR was utilised to identify typical bacteria in sputum samples collected at exacerbation presentation (median 2 days after symptom onset), and at days 3, 7, 14 and 35 post-presentation. Results Nineteen patients with moderate to severe COPD (mean age 68.8 years (SD±8.1); FEV 1 48.4% predicted (±19.2%); current smoker 37%; FEV 1 /FVC 0.46 (SD±0.14); FEV 1 1.2L (SD±0.4); male gender 74%) provided 89 of 110 potential sputum samples at 5 time points during 22 exacerbations. Rhinovirus prevalence progressively fell from 71.4% at exacerbation presentation to 0% at day 35 with significant decreases in prevalence between presentation and days 7, 14 and 35 (all p<0.002) (Figure 1). No exacerbation was negative for rhinovirus detection at presentation but positive at later time points. For typical bacteria, 64.7% of samples taken at presentation were positive. This proportion fell at days 3 and 7 but these falls were non-significant (p=0.08 and p=0.09, respectively) -all events were treated with antibiotics. Seven of the 22 exacerbations (31.8%) were positive for both CRMs at presentation. Conclusion The prevalence of CRMs varies during recovery from a COPD exacerbation. Rhinovirus prevalence steadily decreases over 2 weeks whilst bacterial prevalence is more variable, presumably due to the background effects of lower airway bacterial colonisation. This emphasises the importance of rhinovirus as a major exacerbation trigger. ASSESSING THE REPEATABILITY OF BACTERIAL DETECTION IN STABLE COPD USING SEVERAL METHODS
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