Mucus plugging

Chest x-ray or chest computed tomography scan may reveal infiltrates, atelectasis, bronchiectasis, and mucus plugging. 

The causes of airway narrowing in acute asthmatic attacks (or "asthma exacerbations") include contraction of airway smooth muscle inspissation of viscid mucus plugs in the airway lumen and thickening of the bronchial mucosa from edema, cellular infiltration, and hyperplasia of secretory, vascular, and smooth muscle cells. Of these causes of airway obstruction, contraction of smooth muscle is most easily reversed by current therapy reversal of the edema and cellular infiltration requires sustained treatment with antiinflammatory agents. 

P. Greally. Human recombinant DNase for mucus plugging in status asthmatic us. Lancet 346 1423-1424 (1995). 

Disadvantages are that special apparatus is needed (some patients find pressurised aerosols difficult to use to best effect) and a drug must be nonirritant if the patient is conscious. Obstructed bronchi (mucus plugs in asthma) may cause therapy to fail. 

Asthma is a respiratory illness characterized by variable and reversible airflow obstruction. Over 100 years ago. Osier, in his influential Textbook of Medicine (Osier, 1892), concluded that airway wall edema, bronchoconstriaion and mucus plugging are responsible for the airflow obstruction in asthma. Since that time, edema of the airway mucosa has been assumed to be one of the central features of asthma, but comparatively few studies have addressed the issue directly. Therefore, there is litde information about the onset, duration, magnitude, location, mechanism, consequences and management of mucosal edema in asthma. 

FIGURE 26-1. Representative illustration of the pathology found in the asthmatic bronchus compared with a normal bronchus (upper right). Each section demonstrates how the lumen is narrowed. Hypertrophy of the basement membrane, mucus plugging, smooth muscle hypertrophy, and constriction contribute (/owersecf/on). Inflammatory cells infiltrate, producing submucosal edema, and epithelial desquamation fills the airway lumen with cellular debris and exposes the airway smooth muscle to other mediators (upper left). 

Inflammatory disease associated with bronchial hyperactivity (BHR), bronchospasm, T mucus secretion, edema, and cellular infiltration. Early asthmatic responses (EAR) lasting from 30 to 60 min are associated with bronchospasm from the actions of released histamine and leukotrienes late asthmatic responses (LAR) involve infiltration of eosinophils and lymphocytes into airways - > bronchoconstriction and inflammation with mucus plugging. 

Compared to CB, there is a paucity of mast cells seen in the tissue (16). The numbers of plasma cells may be increased in the submucosa. These bronchial epithelial cell changes and the inflammatory cell response are reflected in the sputum and the intrabronchial mucus plugs (17). Eosinophils account for 10 to 90% of the inflammatory cells, although neutrophils may be predominant when the asthmatic is stable. Mast cells are plentiful during stable phases of asthma but are difficult to find during an attack. Macrophages or histiocytes follow this same pattern. Plasma cells, however, are always difficult to identify. 

Although the reversibility of airways obstruction is an important characteristic of asthma, those asthmatics with chronic symptoms do not reverse completely. The chronic airways obstruction is probably related to mucus plugging of bronchi and hypertrophy of the bronchial smooth muscle. These changes are not reversible by bronchodilators, and it is not clear that they can be reversed with any specific therapy. Both types of obstruction contribute to an imbalance of the ventilation to perfusion ratio in the lung and can result in hypoxemia and hypocarbia. The decreased carbon dioxide content of the blood is the result of the asthmatic s hyperventilation and will persist until the respiratory muscles fatigue and hypoventilation becomes prominent. Asthmatics can die quite quickly when this occurs. 

A common complication of persistent hypersecretion and mucus plugging is a less effective mucociliary clearance mechanism. Inhaled bacteria which are normally quickly cleared from the bronchial system have greater opportunity for tissue invasion. Chronically affected asthmatics are more likely to develop bacterial bronchitis. It is not unusual for CB to become superimposed on the asthma as a consequence of these infections. Interestingly asthmatics who get an acute bacterial bronchitis will often note an improvement of their asthmatic symptoms. 

The prognosis in extrinsic asthma is generally excellent, but deaths do occur in otherwise uncomplicated cases. Those who die are usually the more chronic asthmatics. Over 90% will have extensive mucus plugs at autopsy, and hypertrophy of the bronchial smooth muscle is common. Sudden death in young asthmatics also occurs without a good explanation. The prognosis in intrinsic asthma is not as good and is likely similar to that for moderately severe chronic bronchitics. 

Secretion Therapy. Airways obstruction in asthma is almost always partially due to often clinically unsuspected excessive secretions and mucus plugs. The therapeutic regimen described to this point may decrease this problem. Unfortunately, the treatment of the asthmatic s secretions is often neglected. 

Radiology Airway wall thickening, mucus plugging, bronchiectasis Air trapping, consolidation... 

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