At autopsy, the lungs from patients that die because of asthma are hyperinflated and tend not to collapse after the thorax is opened because the segmental and subsegmental airways and the bronchioles are filled with inflammatory mucus plugs. These plugs contain mucous, serous and cellular elements. The eosinophilic leukocyte is the cell which tends to predominate in these plugs, but other inflammatory cells and a large number of epithelial cells can also be found. The submucosa shows evidence of an inflammatory reaction which consists of a congested microvasculature and an edematous interstitial space containing the same inflammatory cellular infiltrate as the airways lumen.
The reason for the excess mucous in the airways is probably related to both increased production and decreased clearance, but the relative importance of these two mechanisms is unclear. The machinery for increased production is present in that there is both hypertrophy of the bronchial mucous glands, as well as goblet cell metaplasia and hyperplasia of the mucosal lining. The fact that these mucus plugs have a high protein content with much of this protein being albumin suggests that an inflammatory exudate may be important in their formation.
The importance of these mucus plugs in the pathogenesis of the disease is relatively unclear. While patients that die of asthma all have extensive mucus plugging of their airways,” the precise role in less severe forms of asthma is not known. Bronchographic studies of patients with chronic asthma showed that the airways of living asthmatic patients were often occluded by mucus, but this form of investigation is both unsuitable and unwise in these patients. While it has long been known that the sputum of asthmatic patients contains plugs, the study of sputum does not provide direct evidence on the severity of the airway obstruction caused by the plugs.
In summary, asthma is a disease characterized by muscle spasm, airway inflammation and mucus plugging of the airways, but the relative importance of these abnormalities varies with the state of the disease. For example, when an asthmatic attack is easily and completely reversible by drugfc that relax smooth muscle, it seems likely that smooth muscle spasm is the major cause of the airways obstruction. Similarly, when patients die of asthma and their airways are solidly plugged, it seems reasonable to conclude that the plugs are the cause of death. The transition between these two extremes represents the battleground between inconvenience and life-threatening disease and we believe that inflammation of the respiratory mucous membrane is the process that determines how this battle proceeds.
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