ABSTRACT
OBJECTIVES: We aimed to characterise and quantify the incidence of common infectious agents in acute exacerbations of chronic obstructive pulmonary disease (COPD) requiring ventilation, with a focus on respiratory viruses. DESIGN: An epidemiological study conducted over 3 years. SETTING: A 12-bed intensive care unit (ICU). PARTICIPANTS: ICU patients over 45 years of age with a primary diagnosis of COPD exacerbation requiring non-invasive ventilation (NIV) or ventilation via endotracheal tube (ETT). MATERIALS AND METHODS: Nasopharyngeal aspirates (NPA) and posterior pharyngeal swabs (PS) were tested for viruses with immunofluorescence assay (IFA), virus culture (VC) and polymerase chain reaction (PCR). Paired virus and atypical pneumonia serology assays were taken. Blood, sputum and endotracheal aspirates were cultured for bacteria. RESULTS: 107 episodes in 105 patients were recorded. Twenty-three (21%) died within 28[Symbol: see text]days. A probable infectious aetiology was found in 69 patient episodes (64%). A virus was identified in 46 cases (43%), being the sole organism in 35 cases (33%) and part of a mixed infection in 11 cases (10%). A probable bacterial aetiology was found in 25 cases (23%). There was no statistically significant difference in clinical characteristics or outcomes between the group with virus infections and that without. CONCLUSION: Forty-six (43%) of the patients with COPD exacerbation requiring mechanical ventilation had a probable viral pathogen. Prodromal, clinical and outcome parameters did not distinguish virus from non-virus illness. PCR was the most sensitive whilst virus culture was the least of virus assays.
Subject(s)
Pulmonary Disease, Chronic Obstructive/therapy , Pulmonary Disease, Chronic Obstructive/virology , Respiration, Artificial , Virus Diseases/complications , Aged , Chi-Square Distribution , Female , Humans , Incidence , Intubation, Intratracheal , Male , Middle Aged , Polymerase Chain Reaction , Statistics, Nonparametric , Virus Diseases/diagnosis , Virus Diseases/epidemiologyABSTRACT
The relationship between reduced pulmonary function in early life and persistent wheeze (PW) in school-aged children remains uncertain. In this study, VmaxFRC was assessed at 1 month of age, and the presence of wheeze up to 11 years of age was prospectively identified. At 11 years of age, airway responsiveness (AR) to inhaled histamine and atopy were assessed. Recent wheeze at 11 years of age was associated with a reduced mean z score for VmaxFRC at 1 month of age (-0.41 [SD 0.91], n = 31) compared with no recent wheeze (0.04 [SD 1.00], n = 153, p = 0.03). Wheeze between 4 and 6 years that persisted at 11 years (PW) was most prevalent among those with reduced VmaxFRC at 1 month and atopy aged 11 years (p = 0.002) or reduced VmaxFRC and increased AR aged 11 years (p = 0.015). When all factors were considered, reduced VmaxFRC at 1 month (p = 0.03) and increased AR aged 11 years (p < 0.001) were independently associated with PW (n = 17) compared with other outcomes (n = 129). Reduced airway function present in early infancy is associated with PW at 11 years of age, and this relationship is independent of the effect of increased AR and atopy in childhood.
Subject(s)
Asthma/physiopathology , Bronchial Hyperreactivity/physiopathology , Lung/physiopathology , Respiratory Sounds/etiology , Child , Child, Preschool , Cohort Studies , Cross-Sectional Studies , Female , Functional Residual Capacity , Humans , Infant , Male , Prognosis , Respiratory Sounds/physiopathology , Risk FactorsABSTRACT
Within a longitudinal study of lung function in 243 infants, we identified a group of 23 individuals with flow limitation in tidal expiration. In infancy, flow-limited children have reduced lung function and increased airway responsiveness (AR), and at 2 years of age they are diagnosed with asthma more frequently. We hypothesized that these observations would persist throughout childhood. Data from ages 3 to 11 years were analyzed. Only at 4 years of age did the flow-limited group have increased wheeze compared with other cohort members (odds ratio, 4.25; 95% confidence interval [CI], 1.11 to 16.2; p = 0.04; n = 114). At 6 years of age, 117 cohort members were seen. The flow-limited group (n = 14) had greater AR (p = 0.009) and reduced mean FEV(1) (131 ml; 95% CI, 16 to 246; p = 0.03) and FEF(25-75) (0.28 L/second; 95% CI, 0.05 to 0.52; p = 0.02). At 11 years of age, 183 children were seen and the flow-limited group (n = 18) had greater AR (p = 0.02) and a trend toward reduced mean FEF(25-75) (0.24 L/second; 95% CI, -0.02 to 0.49; p = 0.08). Atopy and parental asthma were not increased in the flow-limited group. We suggest that the physiologic abnormality that causes flow limitation in early infancy may identify an at-risk group, different from asthma, who have reduced lung function and increased airway responsiveness in later life.
