The name asthma denotes a breathing difficulty of a special kind that occurs in the form of attacks, as a result of allergic reactions in the bronchial tree. Bronchial asthma is a manifestation of hypersensitive reactions of the respiratory tract to irritants that have penetrated into the lungs by air or blood, or both. The asthmatic crisis of dyspnea usually begins acutely, it is caused by the narrowing of the small bronchi and especially the bronchioles, resulting from a spasm of the bronchiolar and, possibly, bronchitis muscles, edema of the bronchiolar and bronchitis walls, especially the mucosa, and gradually as a result of increased bronchial gland mucus. The high tension of the inspiratory mechanisms to a certain extent is able to overcome the ventilation obstacles that arose due to the narrowing of the lumen of the bronchi and due to valve mechanisms. The alveoli, although with high voltage, receive air, but the expiratory forces and mechanisms are not able to ensure the removal of the same amount of air from the distribution and respiratory spaces. Thus, there is a restriction of gas exchange in the respiratory spaces with simultaneous acute overstretching of the alveoli. In this state, compression of the bronchial tree occurs, which, in turn, helps to narrow the lumen. The simultaneous compression of arterioles, slowing down blood circulation in the capillaries and venules cause a decrease in blood circulation and a slowdown in pulmonary circulation. Children from asthma die very rarely. Therefore, there is only a small number of pathomorphological studies. In the pathomorphological picture, the thickening of the walls of the middle and small bronchi and bronchioles is determined. Their walls are swollen, the gaps are reduced. The mucous bronchioles are relatively thicker than the bronchial mucosa, and in children is relatively thicker than in adults. The thicker the normal or pathological mucosa, the stronger the narrowing effect of the swelling and muscles of the walls. It should be borne in mind that with a maximum expiratory narrowing of the lumen of the large bronchi, the initial volume decreases by one fourth, in the middle and small bronchi – by 2/3 and even by 2/4. The contraction of muscle fibers located abruptly helically in the walls of the bronchioles can lead to narrowing of the lumen or completely block it (Hayek 1952). The epithelial layer of the bronchial wall in some places forms sack-shaped depressions. The smaller bronchi contain thick, compact mucus. Mucus can completely clog the bronchi. In the bronchioles, the mucus from the bronchi is not inhaled, but is excreted exclusively by the superficial epithelium of the bronchioles. With painful irritation, ciliated epithelial cells change into secreting ones. And in larger bronchi, the mucosa swells, soaks and becomes covered with a large amount of mucus. In some places, the desquamated epithelium is visible. In addition to bronchioles, mucous plugs can be found mainly in the small, sometimes in the middle bronchi. The epithelial lining is thickened, especially in chronic course. Metaplasia and small abscesses are also found. Some goblet cells of the bronchial mucosa and mucous glands are broken, others are in a state of increased activity. The bronchial glands, their tubules, are crowded and dilated with mucus, just like their excretory ducts and openings. There is a violation of the activity of the ciliated epithelium in the bronchi, a slowdown and even a complete stop of their movements. In the further stage of changes, the death of the ciliated epithelium and fatty cell infiltration occur. The basement membrane of the epithelial lining thickens and is hyalinized, especially in the middle bronchi. Similar changes are observed both in bronchioles and in large bronchi. The interstitial connective tissue of the wall of the bronchi, especially between muscle fibers and bundles, is infiltrated. Lymphatic foci located along the bronchi are enlarged. The thickened wall is penetrated by accumulations of lymphocytes, numerous fat cells (Marchand1918). After repeated attacks, with a longer course, in addition to these cellular reactions, eosinophilic infiltration of the bronchial wall, mainly the subepithelial layers and the rest of the bronchomural connective tissue, develops. These bronchomural infiltrations are not equally developed in every patient and are not distributed uniformly everywhere. In the submucous layer in some places moderate fibrotic changes are observed. Eosinophilic infiltration is sometimes observed in the alveoli and in the bronchomural lymph nodes. Everywhere here, eosinophils perform an important specific cleansing function. Parabronchial and paratracheal lymph nodes are enlarged, impregnated with fluid and softened. And in a chronic course, the musculature of the walls of the bronchi is hypertrophic. Bronchiolar and bronchial stenosis is caused by paroxysmal edema of the walls of small bronchi and bronchioles, especially their mucosa, paroxysmal tonic activity of the muscular system, the attachment of excessive mucous secretion and exudative processes, the presence of primary or secondary pathological mucus. The immediate pathomorphological consequence is acute lobar universal alveolar emphysema. In the chronic course of emphysema is stabilized. Some small or larger bronchi are so clogged with sticky compact mucus that more or less large polyobturation atelectases develop. Some bronchial glands gradually atrophy. Bag-shaped bronchiectasias develop in some places.