Near-Fatal Asthma

By Mark D. Siegel, MD, FCCP

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Pathogenesis and Pathology

Autopsy studies have provided much of the information available on the pathology of severe asthma.¹³ Key features include mucus plugging in small and medium-sized airways, vascular dilatation, airway edema, increased volume and size of submucosal glands, desquamation of airway epithelial cells, an inflammatory cellular infiltrate, goblet cell hyperplasia, bronchial smooth muscle hypertrophy, and thickening of the epithelial basement membrane (Fig 1).^14,15 The degree of inflammation and changes in epithelial integrity, bronchial smooth muscle, and mucus glands parallel disease severity.¹⁵

Reports have traditionally emphasized the importance of eosinophils and their by-products, such as major basic protein.^16,17 More recent data highlight the central role of neutrophils and their mediators, particularly in severe asthma.^18-20 Unlike eosinophils, which decrease quickly with corticosteroid treatment, neutrophils persist in the airways of mechanically ventilated patients with NFA.¹⁹ Proinflammatory mediators predominate over anti-inflammatory ones, particularly cytokines and chemokines (tumor necrosis factor-a, interleukin-1b, interleukin-8, interleukin-5), leukotrienes, reactive oxygen species, and nitric oxide metabolites.^19,21-23

Most patients present after several days of symptoms, with extensive airway inflammation, epithelial desquamation, and mucus plugging. In contrast, the smaller group presenting with "sudden asphyxic asthma" tend to have fewer eosinophils, a predominance of neutrophils, and less mucus.^15,24

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