• Mediastinal (interstitial) emphysema is caused by entry of air into the interstitium of the lung, from where it may track to the mediastinum and sometimes the subcutaneous tissue. It may occur spontaneously if a sudden increase in intraalveolar pressure (as with vomiting or violent coughing) produces alveolar rupture, which allows air to dissect into the interstitium. Sometimes it develops in children with whooping cough. 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). When the interstitial air gets into the subcutaneous tissue, the patient may literally blow up like a balloon, with marked swelling of the head and neck and crackling crepitation over the chest (subcutaneous emphysema). In most instances the air is resorbed spontaneously after the site of entry seals.
Emphysemaisachronicobstructiveairwaydiseasecharacterizedbyenlargementofairspacesdistaltoterminalbronchioles.
Subtypesincludecentriacinar(mostcommon:smoking-related),panacinar(seeninα1-anti-trypsindeficiency),distalacinar,andirregular.
Smokingandinhaledpollutantscauseongoingaccumulationofinflammatorycells,whicharethesourceofproteasessuchaselastasesthatirreversiblydamagealveolarwalls.
Patientswithuncomplicatedemphysemapresentwithincreasedchestvolumes,dyspnea,andrelativelynormalbloodoxygenationatrest(“pinkpuffers”).
Mostpatientswithemphysemaalsohavesignsandsymptomsofconcurrentchronicbronchitis,sincecigarettesmokingisariskfactorforboth.
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Chronic bronchitis is diagnosed on clinical grounds: it is defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. It is common among cigarette smokers and urban dwellers in smog-ridden cities; some studies indicate that 20% to 25% of men in the 40to 65-year-old age group have the disease. In early stages of the disease, the cough raises 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 bronchitic patients, especially heavy smokers, develop chronic outflow obstruction, usually with associated emphysema (COPD).
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 hypertrophy of mucous glands in the trachea and bronchi as well as an increase in mucin-secreting goblet cells in the epithelial surfaces of smaller bronchi and bronchioles. These irritants also cause inflammation marked by the infiltration of macrophages, neutrophils, and lymphocytes. In contrast with asthma, eosinophils are not seen in chronic bronchitis. Whereas the defining mucus hypersecretion is primarily a reflection of involvement of large bronchi, the airflow obstruction in chronic bronchitis results from (1) small airway disease, induced by mucous plugging of the bronchiolar lumen, inflammation, and bronchiolar wall fibrosis, and (2) coexistent emphysema. In general, while small airway disease (chronic bronchiolitis) is an important component of early, mild airflow obstruction, chronic bronchitis with significant airflow obstruction almost always is complicated by emphysema.