Chronic Bronchitis PDF

## Chronic Bronchitis Chronic bronchitis is defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. Thus its definition is based on clinical features, as opposed to emphysema which is defined anatomically. It is common among people...

## Chronic Bronchitis Chronic bronchitis is defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. Thus its definition is based on clinical features, as opposed to emphysema which is defined anatomically. It is common among people who smoke cigarettes and urban dwellers in smog-ridden cities. In early stages of chronic bronchitis, the cough produces mucoid sputum, but airflow is not obstructed. Some patients with chronic bronchitis have evidence of hyperresponsive airways, with intermittent bronchospasm and wheezing (asthmatic bronchitis), while other patients with bronchitis, especially those who smoke heavily, develop chronic outflow obstruction, usually with associated emphysema. ## Pathogenesis The distinctive feature of chronic bronchitis is hypersecretion of mucus, beginning in the large airways. Although the most important cause is cigarette smoking, other air pollutants, such as sulfur dioxide and nitrogen dioxide, may contribute. These environmental irritants induce (1) hypertrophy of mucous glands in the trachea and bronchi; (2) an increase in mucin-secreting goblet cells in the epithelial surfaces of smaller bronchi and bronchioles; and (3) inflammation marked by the infiltration of macrophages, neutrophils, and lymphocytes. In contrast with asthma (described later), eosinophils are not seen in chronic bronchitis. Whereas the mucus hypersecretion primarily involves the large bronchi, the airflow obstruction in chronic bronchitis results from small airway disease (chronic bronchiolitis) induced by mucous plugging of the bronchiolar lumen, inflammation, and bronchiolar wall fibrosis. It is postulated that many of the effects of environmental irritants on respiratory epithelium are mediated by local release of cytokines such as IL-13 from T cells. The expression of mucins in bronchial epithelium and the production of neutrophil elastase are also increased as a consequence of exposure to tobacco smoke. Microbial infection is often present but has a secondary role, chiefly by maintaining inflammation and exacerbating symptoms. ## Morphology Grossly, the mucosal lining of the larger airways is usually hyperemic and swollen by edema fluid and is covered by a layer of mucinous or mucopurulent secretions. The smaller bronchi and bronchioles may also be filled with secretions. The diagnostic feature of chronic bronchitis in the trachea and larger bronchi is enlargement of the mucus-secreting glands (Fig. 11.8). The magnitude of the increase in size is assessed by the ratio of the thickness of the submucosal gland layer to that of the bronchial wall (the Reid index-normally 0.4). Variable numbers of inflammatory cells, largely lymphocytes and macrophages but sometimes also admixed neutrophils, are frequently seen in the bronchial mucosa. Chronic bronchiolitis (small airway disease), characterized by goblet cell metaplasia, mucus plugging, inflammation, and fibrosis, is also seen. In severe cases, there may be complete obliteration of the lumen as a consequence of fibrosis (bronchiolitis obliterans). It is the submucosal fibrosis that leads to luminal narrowing and airway obstruction. Emphysematous changes often coexist. ## Clinical Features of Chronic Obstructive Pulmonary Disease Dyspnea is usually the first symptom; it begins insidiously but is often steadily progressive. In patients with underlying chronic bronchitis or chronic asthmatic bronchitis, cough and wheezing may be the initial symptoms. Weight loss is common and may be sufficiently severe to suggest an occult malignant tumor. Pulmonary function tests reveal reduced FEV1 with normal or near-normal FVC. Hence, the FEV1 to FVC ratio is reduced. The classic presentation of emphysema with no "bronchitic" component is one in which the patient is barrel-chested and dyspneic, with obviously prolonged expiration, sitting forward in a hunched-over position. Imaging studies show hyperinflated lungs that "flatten" the diaphragm. In such patients, air space enlargement is severe and diffusion capacity is low. Dyspnea and hyperventilation are prominent, so until very late in the disease, gas exchange is adequate and blood gas values are relatively normal. Hypoxia-induced vascular spasm and loss of capillary surface area from alveolar destruction cause the gradual development of secondary pulmonary hypertension, which in 20% to 30% of patients leads to right-sided congestive heart failure (cor pulmonale). At the other end of the clinical spectrum is a patient with pronounced chronic bronchitis and a history of recurrent infections. The course is quite variable. In some patients, cough and sputum production persist indefinitely without ventilatory dysfunction, while others develop significant outflow obstruction. Dyspnea is usually less prominent than in those with "pure" emphysema, and in the absence of increased respiratory drive the patient may retain carbon dioxide, becoming hypoxic and often cyanotic. The majority of patients with this type of COPD are overweight or obese, which may further decrease ventilation, particularly during sleep. Patients with severe chronic bronchitis have more frequent exacerbations, more rapid disease progression, and poorer outcomes than those with emphysema alone. Progressive COPD is marked by the development of pulmonary hypertension, sometimes leading to cardiac failure; recurrent infections; and ultimately respiratory failure. Approximately 10% to 30% of patients have obstructive sleep apnea; the pathogenic relationship between these two disorders is incompletely understood. ## Emphysematous Conditions Other Than COPD Several other conditions marked by abnormal air spaces or accumulations of air within the lungs or other tissues merit brief mention: * Compensatory emphysema is the dilation of residual alveoli in response to loss of lung substance elsewhere, such as through surgical removal of a diseased lung or lobe. * Obstructive overinflation is expansion of the lung due to air trapping. A common cause is subtotal obstruction of an airway by a tumor or foreign object. Obstructive overinflation may be life threatening if expansion of the affected portion produces compression of the remaining normal lung. * Bullous emphysema refers to large subpleural blebs or bullae (spaces >1 cm in diameter in the distended state). Such blebs stem from a localized accentuation of one of the four forms of pulmonary emphysema (discussed previously); most often the blebs are subpleural and prone to rupture, leading to pneumothorax. * Mediastinal (interstitial) emphysema is caused by entry of air into the interstitium of the lung, from where it may then track to the mediastinum and sometimes the subcutaneous tissue. It may occur when a sudden increase in intraalveolar pressure (as with vomiting or violent coughing) causes alveolar rupture, allowing air to dissect into the interstitium. It may also occur in patients on respirators who have partial bronchiolar obstruction or in individuals with a perforating injury (e.g., a fractured rib). If the interstitial air reaches the subcutaneous tissue, there can be marked swelling of the head and neck and crackling crepitation (subcutaneous emphysema) over the chest. In most instances the air is resorbed spontaneously after the site of entry seals.