Chronic Obstructive Pulmonary Disease



Chronic Obstructive Pulmonary Disease





Introduction

Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation as a result of small airway disease and parenchymal destruction (emphysema), most commonly related to cigarette smoking. The condition is a major cause of morbidity and mortality; in the UK COPD is the fifth leading cause of death and results in 240,000 hospital admissions annually, at a cost of £486 million (US$778 million). Exacerbations of COPD precipitating admission may be the result of lung infection but the airways of these patients are often chronically colonized with common bacterial pathogens and the significance of the organisms to worsening of respiratory symptoms may be difficult to define. The clinical, radiological, and microbiological aspects of COPD exacerbations are reviewed in this chapter.


Aetiology

Exacerbation of COPD is defined as a deterioration in symptoms from when the patient is clinically stable. Usually patients present with increased breathlessness, wheeze, and chest tightness. In addition, some patients have increased sputum volume and sputum purulence. Both infection (viral and/or bacterial) and air pollution can precipitate an exacerbation. Secondary causes of an exacerbation include pneumonia, pulmonary embolism, pneumothorax, rib fractures, inappropriate medication such as β-blockers or excess sedatives, cardiac arrhythmias, cardiac failure, or other diseases such as gastrointestinal bleeding.

The bronchial tree in patients with COPD is often chronically colonized with potential pathogens. These include Streptococcus pneumoniae and Haemophilus influenzae (capsulate and noncapsulate strains). Exacerbations are associated with a marked increase in pathogen numbers, detected by quantitative sputum culture. Moraxella catarrhalis is associated with acute purulent exacerbations. Other organisms which may colonize the airways and contribute to exacerbation include antibiotic-resistant Gram-negative bacilli such as Pseudomonas aeruginosa.


Illustrative cases

Figure 5.1 presents a chest radiograph from a 68-year-old man with severe COPD (FEV1: 0.8 l, 27% predicted) with hyperinflated lung fields, flattened widely spaced ribs, and flattening of the hemidiaphragms. In this case the patient had a noninfective exacerbation of COPD.

Figures 5.2, 5.3 are high resolution CT chest scans (lung window setting) from patients with severe COPD (both FEV1 <30% predicted). The scan in 5.2 shows focal areas of low attenuation without discernable walls. This is most noticeable in the upper lobes and is consistent with centrilobular emphysema. 5.3 is a scan from a 54-year-old male with α1-antitrypsin deficiency, revealing confluence of low attenuation areas without discernable walls and sparse lung vascular markings. This is most noticeable in the lower lobes and is consistent with pan-acinar emphysema.

A macroscopic picture of an inflated lung slice is shown (5.4) demonstrating the presence of centri-acinar emphysema. The enlarged airspaces are seen as ‘holes’ within the lung parenchyma. As only the central part of the acinar unit around the respiratory bronchioles is affected in centriacinar emphysema, uninvolved normal lung parenchyma is seen around the emphysematous spaces. This is the classical pattern of emphysema seen in smokers and typically affects the upper lobes.

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Sep 12, 2016 | Posted by in RESPIRATORY | Comments Off on Chronic Obstructive Pulmonary Disease

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