[Skip to Content]
[Skip to Content Landing]
February 1942


Author Affiliations

From the bronchoscopic clinics of Temple University Hospital, Hospital of the Women's Medical College of Pennsylvania and St. Christopher's Hospital for Children.

Am J Dis Child. 1942;63(2):217-224. doi:10.1001/archpedi.1942.02010020002001

Notwithstanding the tremendous amount of research that has been conducted in recent years on the subject of chronic allergic asthma, the precise pathologic physiology of the disease still continues to defy adequate explanation. Extensive postmortem studies1 made after fatal attacks have disclosed rather characteristic changes in the tissue, comprising hyalinization and thickening of the basement membrane of the bronchi, hyperplasia of the mucus-secreting cells, varying quantities of viscid mucoid material in the air passages, eosinophilic infiltration and edema of the bronchial wall, hypertrophy of the bronchial musculature and variable degrees of pulmonary emphysema. In a large number of autopsies performed on asthmatic patients who have died of an inter-current disease, however, such changes have not been found, suggesting that they probably represent merely the picture of excessively violent exacerbation rather than that of the underlying morbid process in its truly chronic state. According to Thieme and Sheldon,2 the