Bronchial Asthma

BRONCHIAL ASTHMA, paroxysmal dyspnea, predominantly of expiratory type, usually beginning suddenly and for the most part ending suddenly, not associated with diseases of the cardiovascular (cardiac asthma) or excretory (uremic asthma) systems. Clinical Picture. The picture of a typical paroxysm: sometimes suddenly, sometimes in connection with emotional stress, heavy physical work, or after a sleepless night, the patient suddenly loses the ability to breathe evenly and begins to experience an agonizing feeling of lack of air; his attempts to struggle with the dyspnea lead to the fact that air increasingly accumulates in the chest cavity, since, with less difficult inspiration, expiration becomes increasingly difficult. In order to force expiration, the patient leans his hands on a nearby object or rests his elbows on his knees. The entire respiratory musculature participates in the act of breathing. The patient breathes slowly, inspiration is shortened, expiration is prolonged, accompanied by wheezing rales audible at a distance. The patient's face expresses suffering, is pale with a cyanotic tint, sometimes covered with cold sweat. The chest is distended, elevated, its excursions are insignificant, the head seems to have become stuck between the elevated shoulders. The lower borders of the lungs are lowered by one or two intercostal spaces, the absolute cardiac dullness is not determined due to the covering of the heart by the expanded lungs. A boxy sound is determined everywhere on percussion, on auscultation - wheezing rales occupying both respiratory phases (predominantly the second). The pulse during a paroxysm is rapid - 110-140 per minute. Sometimes patients experience palpitations. The sputum is characteristic during a paroxysm: it is viscous, clear, with difficulty separates from the vessel walls into which it is poured. At the beginning of the attack, there is little sputum, but then its quantity increases, it becomes less viscous and separates more easily. Blood is usually not present in the sputum. Sometimes the entire paroxysm occurs without sputum - 'dry asthma'. The duration of a paroxysm is extremely varied: from several minutes to many hours, and even days and weeks. In the latter cases, the intensity of the paroxysm changes periodically, sometimes weakening, sometimes intensifying. The attack ends either suddenly or the intensity of dyspnea gradually weakens, and little by little the attack ceases. The distention of the lungs becomes less distinct, the rales at a distance are not audible, they can only be detected upon direct auscultation - the patient can assume a comfortable position, appetite appears, which was absent during the paroxysm; in many patients, urine is secreted in abundance. Temperature during the attack may remain normal, but it can also show slight increases to 38°; sometimes it suddenly rises to 39°-40°, at which point the attack ceases. The cause of slight increases, some consider accompanying chronic processes in the bronchial glands, others - slight catarrhal inflammatory processes in the lungs (F. Hoffmann); finally, the cause of temperature elevation is also considered chronic bronchitis, exacerbating during the attack (Aryev). The cessation of the attack under the influence of high temperature can be explained by the antispasmodic effect of pyrogenic substances (tetrahydronaphthylamine, adrenaline, etc.), which are sympathicotropic. Sputum. Its quantity during the attack is small, from 50 to 100-200 cubic cm, sometimes up to 500. Upon examination (better with a magnifying glass), it is possible to confirm in the sputum threadlike formations of denser mucus, which branch in places, twist into spirals in others. From these threads are formed the spirals described by Curschmann. Their size is 0.25-1-2 cm, thickness from 1 mm. On the spirals, eosinophilic cells and Charcot-Leyden crystals are found. The mechanism of formation of spirals: due to the movement of air during the attack, mucus masses attached to the walls of the bronchi are stretched and twisted. Charcot-Leyden crystals are recommended to be sought at low magnification. These are needle-shaped crystals of octahedral form, of various sizes, from small ones visible only under immersion to large ones occupying most of the field of view. The crystals are colorless, may crumble into fragments upon pressure. Both spirals and crystals are not always found, but only in 30-35% of cases. Some assume that the crystals consist of crystallized mucin-like substance, others - that the crystals represent a phosphoric acid salt of some organic base. The third characteristic feature of asthmatic sputum - eosinophils. The latter probably have a relation to the Charcot-Leyden crystals: it is believed that the crystals come from protein bodies formed during the breakdown of eosinophils, with crystallization occurring at the expense of disappearing grains. Of the three specific elements of asthmatic sputum mentioned, eosinophils are the most frequently encountered. Blood. The morphology of blood in connection with an asthma attack has been more studied than its physicochemical properties. In most cases, the blood of an asthmatic outside of an attack, upon repeated examinations, shows eosinophilia. At the same time, both absolute and relative lymphocytosis can be noted. Outside of an attack, the absolute number of neutrophils is mostly within normal limits, the relative number is usually decreased. During an attack - the number of eosinophils in the blood decreases, especially in severe cases, lymphocytes also decrease in number at this time, while neutrophils increase. The latter is especially observed during severe attacks. The number of leukocytes in general remains within normal limits, increasing only during severe attacks due to neutrophils. Thus, the most characteristic morphological feature of asthmatic blood is eosinophilia and, to some extent, lymphocytosis. Since both phenomena are observed mainly during periods free from attacks, i.e., at a time when it is most difficult to diagnose bronchial asthma, these blood features acquire great diagnostic significance. As for the physicochemical properties of asthmatic blood, experiments by Widal, Abrami, and Brissaud showed that in humans during an attack, the so-called hemoclastic crisis occurs, blood coagulation slows down, the blood becomes diluted, its color becomes glossy, lacquered, the refractive index of serum decreases, the sedimentation of red blood cells accelerates. In addition, morphological changes in blood are also observed in the form of a decrease in the number of platelets, leukopenia and changes in the leukocyte formula. In view of existing views on the connection between bronchial asthma and constitutional peculiarities of the body, quantitative determinations of the components of blood serum become interesting, mainly uric acid and cholesterol, since bronchial asthma is associated with those metabolic disorders observed in arthritism. Determination of these components showed that the amount of uric acid (Grothel) and cholesterol (Myasnikov) in patients suffering from bronchial asthma is elevated: uric acid - up to 4-9.75‰ (normal - 2.5-4.0‰), cholesterol - up to 1.9-2.6‰ (normal - 1.2-1.8‰). Theories of Bronchial Asthma. It is necessary to distinguish the attack itself, i.e., that mechanism, those processes that take place in the respiratory tract (mainly in the bronchi), causing difficulty in breathing, and those still insufficiently studied general processes that create in the body such conditions under which the above-mentioned mechanism is activated. For a better understanding of the ideas about the origin of bronchial asthma, a brief characterization of the structure of the innervation apparatus of the musculature and mucous membrane of the bronchi is necessary. The bronchial musculature consists mainly of a powerful layer of circular muscles and weakly developed longitudinal ones. The circular musculature extends to the smallest bronchi. In the vagus and sympathetic nerves are located motor, secretory, and vasomotor fibers for the bronchial tree: irritation of the vagus nerve causes narrowing of the bronchial lumen, hyperemia and increased secretion of the mucous membrane. The sympathetic nerve is an antagonist to the vagus: upon irritation in animals of sympathetic fibers of the pulmonary plexus, the tone of bronchial musculature decreases; as for the secretory function as well as the vascular innervation of the bronchi, here too the sympathetic nerve is apparently an antagonist to the vagus nerve. Of the theories explaining the processes occurring during an attack in the respiratory apparatus, the most important are the following: 1) the theory of bronchospasm (Willis-Biermer, 1870), 2) the theory of diaphragm spasm (Wintrich, 1854) and 3) the vascular-secretory theory (Curschmann, Weber, 1872, and Shestopal, 1901). The theory of bronchospasm. The attack is the result of spasm of the circular muscles of small and medium bronchi. This spasm can explain the prolonged, forced expiration, wheezing rales, the sudden onset of the attack and its abrupt end. The spasm is the result of irritation of the vagus nerve reflexively from the mucous membrane of the respiratory tract. Biermer believed that, in addition to spasm, during an attack there is also increased secretion of the mucous membrane of the bronchi.

The swelling of the lungs during an attack is explained by the fact that spasmodically constricted bronchi experience unequal pressure during inhalation and exhalation: the narrowed lumen of the small bronchi, due to spasms, becomes even narrower during exhalation because of compression, whereas during inhalation, the pliable small bronchi, although narrowed, still expand somewhat. As a result, air enters the bronchi more easily than it exits, leading to its accumulation in the alveoli and the swelling of the lungs. The theory of diaphragm spasm, according to which an attack is the result of a tonic spasm of the diaphragm, currently has few adherents, because the clinical picture of diaphragm spasm is completely unlike the picture of an attack of bronchial asthma. Furthermore, X-ray observations of patients during an attack have shown that the diaphragm is not in a state of spasm but performs respiratory movements, albeit rather limited ones. The vascular-secretory theory. According to this theory, an attack is the result of acute swelling of the bronchial mucosa, both due to dilation of the vessels (angioneurosis) and due to abnormally increased secretion. As a result, narrowing of the lumen of the air passages occurs. According to this theory, processes occur in the bronchi during an attack that are analogous to those observed in some individuals in the nasal mucosa, which suddenly swells to the point of obstruction, and this swelling also ceases immediately. The vascular-secretory theory does not contradict the clinical features of an attack of bronchial asthma and finds confirmation in acute vascular-secretory processes that are also observed in other areas of our body. Based mainly on the first and third theories, it must be conceived that an attack of bronchial asthma, as far as the processes occurring in the respiratory apparatus itself, is the result of acute narrowing of the medium and small air passages due to a spastic or vascular-secretory process in the bronchi. At the same time, both the spasm of the musculature and the swelling of the bronchial mucosa depend on the acute irritation of the pulmonary branches of the vagus nerve. On the basis of clinical data, it must be assumed that in some cases spastic phenomena predominate (attacks with insignificant sputum), while in others vascular-secretory processes are in the forefront (attacks with abundant sputum). The mechanism of the attack, as far as the general processes that create the conditions leading to irritation of the parasympathetic section innervating the bronchi, is explained by various authors. The intoxication theory. French authors see the center of gravity in intoxication (and infection), with among intoxications arthritism occupying the main place, which is revealed by a number of functional diseases of an angioneurotic nature (acute edemas of the skin and mucous membranes, urticaria, acute swellings of the joints) and disturbances of carbohydrate, fat, and purine metabolism. Gout, obesity, and diabetes actually occur in the anamnesis of asthmatics: according to this theory, abnormal products of metabolism increase the sensitivity of the central nervous system, and it begins to react with attacks to such irritations that in persons not burdened by intoxication (auto-intoxication) do not cause any attack. The significance of intoxication as a factor creating general conditions under which attacks of bronchial asthma may appear cannot be denied, but there is no reason to place arthritism at the foundation of the intoxication theory, because statistics show that gout occurs by no means so frequently among asthmatics: See gives 3.8% (370 patients), Morawitz in 116 cases saw not a single gout sufferer, Aryan's material (142 patients) gives 4.1% gout sufferers. The reflex theory. According to this theory, the starting point that gives impetus to the development of an attack can be any organ, any point in the body, especially the mucous membrane of the respiratory passages, and there is no need for anatomical changes in the organs. These changes can, of course, be present (e.g., scars, inflammatory processes, tumors), there can be displacements of organs, bends, foreign bodies (parasites), but all this may also not be present—it is assumed that in various organs there are special points with increased sensitivity (asthmogenic points), from which through the central nervous system reflexes go to the pulmonary branches of the vagus nerve and cause asthma attacks. Indeed, many examples can be cited illustrating the connection between disturbances in the function of different organs and the appearance of asthma attacks (disappearance of attacks after elimination of coprostasis, after straightening a retroverted uterus, after removal of intestinal parasites, etc.). This circumstance should be a reason for the examination of all organs of the asthmatic, and also serves as an indication that the periphery is indeed one of the links that make up the chain of causes leading to the onset of an attack. The anaphylactic theory has developed over the last two decades, mainly thanks to the work of American authors. It is based on 1) some similarity between an attack of bronchial asthma and anaphylactic shock in animals (acute swelling of the lungs, eosinophilia, change in physical properties of the blood), 2) the very frequent possibility of establishing a connection between an attack of bronchial asthma and this or that protein bodies that enter the body through the respiratory or digestive tracts. (The anaphylactic theory was strengthened by observations of patients with so-called 'hay fever' and 'horse' asthma. The first occurs in some persons when inhaling flower pollen, the second, which occurs mainly in America, appears when inhaling keratinized scales separating from the horse's skin.) According to the anaphylactic theory, every asthmatic has his own protein, to which he suffers increased sensitivity. This increased sensitivity can be congenital or acquired through prolonged contact with this or that protein bodies. (Thus, 'horse' asthma is mainly suffered by persons who are often and for a long time near horses—grooms, coachmen; persons working in bakeries more often suffer attacks of asthma from inhaling flour dust. Cases of asthma from ipecacuanha powder are known in persons working in pharmacies.) The patient usually rarely knows which particular protein is the cause of his attacks. To find this protein, there are prepared from all kinds of proteins (animal, vegetable, and bacterial) the finest powders, with which the sensitivity of the patient to this or that protein substance is tested. For this, a drop of physiological solution is applied to the skin, to it is added this or that powder from the protein, and through the drop a superficial scarification of the skin is made. A positive skin reaction indicates the protein that is the cause of attacks of bronchial asthma (the test is performed with a whole series of proteins). In the USSR, and to some extent also in Western Europe, patients are rather rarely encountered who could serve as examples confirming the anaphylactic theory of bronchial asthma. It is possible that the cause is the different conditions of life and work in the New and Old Worlds. Thus, none of the proposed theories gives an exhaustive explanation of the general processes that create in the body the conditions under which the spastic and vaso-secretory processes in the bronchi occur, leading to attacks of suffocation. It must be admitted that both intoxication and auto-intoxication, as well as increased sensitivity to proteins, play a definite role in this respect. The periphery, which gives rise to the reflex leading to the above-mentioned processes in the bronchi, also has definite significance. From the review of all theories of bronchial asthma, as well as on the basis of clinical data, the conclusion must be drawn that the most diverse diseases of any organ, any system of the body—infections, intoxications, auto-intoxications, disturbances of metabolism, moments of nervous and mental order—can constitute a chain of causes, individual links of which, in different combinations, lead to the creation of such conditions under which an attack of bronchial asthma occurs. From this it follows that bronchial asthma cannot be considered as a nosological unit, as a special disease. Bronchial asthma is a symptom-complex that occurs with all sorts of diseases and hides behind it abnormalities in any area of the body. The question of why not all people, with the above-mentioned diseases, react with an attack of bronchial asthma must be decided in the sense that this depends on the constitutional peculiarities of the organism, consisting in the different state of the endocrine-nervous apparatus in different individuals. This also finds confirmation in the role of heredity in the origin of bronchial asthma. A special type of family anamnesis of patients with bronchial asthma can be noted. Here we have those diseases that are united by the concepts of exudative diathesis or arthritism: scrofula in childhood, eczemas, urticaria, psoriasis; in later periods of life—migraine, attacks of gout, angioneurotic edemas, colica mucosa; here also attacks of bronchial asthma. Along with this, the significance of heredity in bronchial asthma is revealed in the inherited neuropathic constitution (presence in the family anamnesis of psychoses, hysteria, neurasthenia, epilepsy). Bronchial asthma and profession.

As noted above, the profession has significance in some cases of bronchial asthma (asthma in bakers, grooms, and those working in pharmacies). To this can be added that work in a dusty atmosphere (stonecutters, millers, and those working in an atmosphere containing coal dust) can contribute to the appearance of asthma attacks, causing bronchitis, which often precedes attacks of bronchial asthma. Bronchial asthma has been observed in persons working for a long time with the same chemical substances, for example, dyes used in the production of furs (Urso paint). Bronchial asthma is quite often observed in lecturers, teachers, and those engaged in mental work. In such cases, the significance lies, apparently, in the insufficient stability of the nervous system, which reacts with attacks of bronchial asthma to such irritations, which in cases with a more stable nervous system may pass unnoticed. Although the significance of the profession is undeniable, it is nevertheless not primary, since attacks of bronchial asthma in a very large percentage of cases begin at an age when the role of the profession cannot be considered. Arev's material provides the following data: attacks of bronchial asthma appeared for the first time in 28% of cases before the age of 10. These data fully coincide with the data of American authors. Connection between bronchial asthma and other pathological and physiological conditions.-Bronchial asthma and emphysema of the lungs. During an attack, there is acute distension of the lungs. One might think that repeated attacks should eventually lead to persistent changes in lung tissue, to the development of emphysema. Clinical observations show, however, that if the periods free from attacks last for a more or less prolonged time, the phenomena of expansion of lung tissue disappear. These data are in agreement with observations over glassblowers, over musicians playing wind instruments; the walls of the alveoli in these persons daily experience great pressure, why one could expect the development of emphysema in them more often than in persons of other professions, however, this is not observed. Apparently, acute distensions of the lungs alone are not sufficient for the appearance of emphysema. In its origin, bronchitis, which accompanies many cases of bronchial asthma, plays an essential role; in addition, individual variations in the elastic properties of lung tissue, as well as the different state of the cartilaginous apparatus of the chest in different people, are of significance. The presence of emphysema in a patient suffering from attacks of bronchial asthma extremely complicates the clinical picture of the disease and creates great difficulties in evaluating attacks of difficult breathing in such patients. In these cases (often it is a matter of people over 40-45 years old), the attacks may depend on the insufficiency of cardiac activity, and therefore the question usually arises as to how far the attacks of suffocation are the result of cardiac insufficiency, i.e., whether there is cardiac asthma (a. cardiale) or the attacks of suffocation are the result of spastic (resp. angioneurotic) processes in the bronchi (a. bronchiale). This question can receive its resolution only upon detailed clinical examination of the patient; very often, however, the question remains open.-Bronchial asthma and bronchitis. In relation to bronchial asthma, one can distinguish primary bronchitis, preceding bronchial asthma, running for a long or more or less prolonged time without attacks of suffocation, with the latter joining the bronchitis only later, and secondary bronchitis, developing only after the patient has had attacks of bronchial asthma. In the first case, patients suffer from catarrhs of the upper respiratory tract, colds, tracheitis for a long time, often from childhood. Bronchitis in them often develops after measles, whooping cough, pneumonia. With the passage of time, in the presence of bronchitis, attacks of difficult breathing begin to develop, and then true attacks of bronchial asthma. Secondary bronchitis develops in connection with attacks of bronchial asthma in such patients in whom the attacks first appeared among complete health without any disease of the respiratory tract. Such patients initially, outside of attacks, have no symptoms of bronchitis. If the attacks become more frequent, their duration increases, and the periods free from attacks shorten, conditions are created under which the mucous membrane of the bronchi comes into a state of hyperemia and increased secretion, and persistent symptoms appear indicating that the mucous membrane of the bronchi has not returned to normal (cough, sputum, rales). With the passage of time, the phenomena of bronchitis (and at the same time the expansion of the lungs) become more and more persistent, and, finally, secondary bronchitis (and emphysema) develops, which in turn serves as a factor contributing to the appearance of attacks of bronchial asthma all the more so since the tendency to attacks is already present in these patients. Such cases are not particularly favorable in terms of prognosis.-Bronchial asthma and tuberculosis of the lungs. Opinions on the relationship between bronchial asthma and tuberculosis of the lungs are extremely contradictory: some believe that the presence of tuberculosis of the lungs excludes bronchial asthma, others closely connect bronchial asthma with tuberculosis of the lungs. Statistical data are as follows: Delthil found tuberculosis of the lungs among 3,400 asthmatics i:i:i only in 12, and in 8 of them the pulmonary process took a favorable course. Brugelmann, having material from several thousand patients with bronchial asthma, completely denies the connection between bronchial asthma and tbc of the lungs. On the other hand, Krez, on the basis of material from 2,000 cases of bronchial asthma, believes that in 75% of asthmatics it is possible to discover clinical signs of pulmonary tuberculosis; Marchand believes that tuberculosis predisposes to the disease bronchial asthma, especially in the presence of a neuropathic constitution. These seemingly contradictory data receive their explanation in the following: undoubtedly, tuberculous infection (including infection of the respiratory tract) is not foreign to persons suffering from bronchial asthma. This is indicated by the anamnesis of asthmatics (scrofula in childhood), tuberculin tests, and other data of clinical examination. But in persons prone to attacks of bronchial asthma, tuberculous infection of the respiratory tract apparently runs a very benign course, and the matter does not reach severe changes in lung tissue. Morawitz, in 116 patients with bronchial asthma, did not have a single case of open pulmonary tuberculosis. Thus, those authors who say that bronchial asthma and tuberculosis of the lungs exclude each other are right insofar as this concerns productive and exudative forms of pulmonary tuberculosis; those authors who say that bronchial asthma and tuberculosis of the lungs occur together are often right in relation to benign fibrous forms.-Bronchial asthma and bronchial glands. The relationship between bronchial asthma and bronchial glands deserves special consideration, since there is a view that attacks of bronchial asthma appear as a result of irritation of the vagus nerve by enlarged glands (mechanical theory of bronchial asthma). Despite the simplicity and attractiveness of such an explanation of attacks of bronchial asthma, there are no sufficiently convincing data to recognize the mechanical theory. It is difficult to imagine that prolonged pressure of a gland can give a relatively short attack. Further, even if a gland is enlarged, this does not yet mean that it presses on the vagus nerve. It is possible, of course, that sometimes, in tumors of the mediastinum, in enlargement of the thyroid gland, in aneurysms of the aorta, and also in some cases of enlargement of bronchial glands, the mechanical factor has a certain significance in the occurrence of attacks, but to believe that every bronchial asthma is the result of pressure of bronchial glands on the vagus nerve, there is no basis.-Bronchial asthma and glands of internal secretion. Clinic gives clear indications of the connection between the function of the glands of internal secretion and the creation of that state in which a tendency to attacks of bronchial asthma develops. If one turns to individual glands of internal secretion, one can see that the appearance or cessation, weakening or strengthening of attacks are connected with changes in the function of endocrine glands: attacks of bronchial asthma depend on menstrual periods, on pregnancy, on the climacteric (changes in ovarian function). In the literature there are examples illustrating the connection between dysfunction of the thyroid gland and attacks of bronchial asthma, and these attacks can occur simultaneously both in hyperthyroidism and hypothyroidism, and with improvement of one or the other state the attacks can disappear. There is no need to prove the influence of the adrenal gland hormone on an attack of bronchial asthma, since the usual means used for the purpose of stopping an attack is adrenaline. If to this is added the role of the endocrine system in the phenomena of anaphylaxis, which is the foundation of the most common theory of bronchial asthma at present, then the role of the glands of internal secretion in the origin of bronchial asthma will be understood. Pathological anatomy of bronchial asthma. Although bronchial asthma is not a nosological unit, but a syndrome, one can still speak of the path. anatomy of bronchial asthma, since with frequent and repeated attacks of bronchial asthma such changes occur in lung tissue as are already subject to anatomical research. The path-anat. material of bronchial asthma described in the literature is small, since death rarely coincides with an attack (about 20 cases).

Macroscopically, a more or less distinct picture of emphysema of the lungs is noted; in the bronchi, there are mucous fibrous formations and plugs of mucus; in some cases, the lumen of the bronchi is enlarged, in others it is narrowed. Microscopically, alveolar epithelium, cylindrical cells, and eosinophils are found in the bronchial secretion; in some cases, spirals are found. In 50% of cases, round-cell infiltration of the peri-bronchial tissue is noted; in some cases, thickening and hypertrophy of the circular muscles of the bronchi. In one patient, a severe spasm of the bronchial musculature was found, to the point of disappearance of the lumen. Of all these patho-anatomical data, the changes in the musculature of the bronchi are of particular importance, confirming the presence of spastic processes, and, in addition, the presence in 50% of cases of round-cell infiltration of the peri-bronchial tissue; the latter circumstance can be used to explain the rise in temperature observed during attacks of B. a. (see above). Differential diagnosis. A typical attack, with the symptoms described above, is recognized without particular difficulty. The case history is important, as it indicates the dependence of the attacks on such causes (e.g., climate, certain protein substances) that do not cause other forms of suffocation. Data on heredity can also assist in the diagnosis of B. a.: the presence in the family of nervous and mental diseases, the presence of B. a., attacks of migraine, urticaria, etc. The positive effect from the use of adrenaline or atropine during an attack of B. a. can also be utilized. The absence of pathological processes in the cardiovascular system or in the kidneys, and the absence of symptoms of narrowing of the upper respiratory tract must be taken into account in the differential diagnosis in the sense of recognizing 43G the attacks as bronchial-asthmatic. Great difficulties are presented by the differential diagnosis in those cases when in persons with signs of heart failure, especially in old age, attacks of suffocation occur, suggesting that their dependence is less on the insufficiency of cardiac activity than on spastic (and vaso-secretory) processes in the bronchi. In these cases, the presence of eosinophilia of sputum, Curschmann's spirals, and the positive effect from atropine, adrenaline, etc., can serve as proof of the presence of bronchial asthma. In some cases, however, the question of the nature of the asthmatic attacks must be left open. Prognosis. Since an attack of B. a. is a syndrome behind which various diseases and disorders of function of any organ, any system of the organism can be hidden, in prognosis it is not possible to use the points of support which we have when we predict the course of the disease in a. cardiale or in a. renale; in these latter cases we can be guided by the stage of the disease, the severity of the disease of the cardiovascular or renal systems. The prognosis in B. a. very often cannot be correlated with the observed frequency or strength of the attacks at a given time, since both frequency and strength of the attacks can change completely from unforeseen and unknown to us moments, while the general condition of the patient can also improve for the better. Thus, the prognosis in B. a. cannot be based on any definite data, and here one has to be guided by considerations of a general nature, by the state of the nervous system of the patient, his psyche, and, above all, by the state of those organs on which the attacks of B. a. particularly reflect—the state of the heart and the respiratory apparatus. This especially applies to elderly persons, as well as to younger persons who have organic lesions of the heart, since prolonged attacks can in such cases adversely affect the cardiovascular system and periodically cause phenomena of decompensation; in the most severe cases of B. a., the prognosis should be made with caution, since with the onset of prolonged intervals of remission the condition of patients can become quite satisfactory, and they can even return to their work. Death during an attack is rare; only a few such cases are described in the literature, but the cause of death in these cases must be considered infection, or disease of the heart, or accidental causes. Therapy of B. a. Treatment of the attack. In mild cases, it is not necessary to resort to special measures, since the attack stops quickly by itself; in other cases, it is sufficient to apply mustard plasters to the chest, or to immerse the hands or feet in hot water, for the attack to cease. In cases that are more severe, gradually developing from mild attacks, or in cases that are severe from the beginning, the patient himself resorts to measures that can be carried out before the arrival of the physician. These include, first of all, smoking powders or cigarettes. The composition of the most commonly used of them is as follows: 1) Pulv. Opii 3.0, Fol. Lobeliae 4.0, Fol. Belladon., Fol. Strammon. aa 6.0; Kalii nitrici 15.0, M.f. pulv. to burn and inhale. 2) Kalii nitrici 36.0, Fol. Strammon. pulv. 60.0, Bals. peruv. 1.5, Tragacant. 2.0, Sacch. albi 0.5, M.f. pulv. (Abyssinian powder—patent preparation). The action of the powders and cigarettes apparently consists of the following: part of the substances contained in them reaches the mucous membrane in an unchanged form and acts both as a local irritant and by absorption; possibly the psychological effect of these powders and cigarettes. Close to these methods of treatment is the arrest of the attack by inhaling atomized solutions containing cocaine, atropine, and adrenaline. For atomization, special apparatuses—atomizers (the atomizer has one or two tips, which are inserted into one or both nostrils; inhale separately, then take a break)—are constructed. The composition of the liquid according to Edens: Atropini sulfur. 0.03-0.05, Cocaini mur., Kalii sulfur, aa 0.3-0.5, Glycerini puri 3.0; Suprarenini hydrochl. 1:1,000 ad 25.0. The best effect is obtained from inhalation and smoking in fresh cases of B. a. With the passage of time, patients become accustomed to this method of treatment, and it becomes necessary to resort to the subcutaneous administration of medicinal substances (atropine, adrenaline, and morphine). Atropine was introduced for the treatment of B. a. in 1899 by Riegel on the grounds that it lowers the excitability of the vagus nerve. The effect of atropine sets in after a few minutes: breathing becomes freer, the whistling rales disappear, the distention of the lungs disappears. But in some cases the attack is not arrested by atropine. To arrest the attack, 1/2 to 3 cubic cm of Sol. Atropini sulf. 1:100 is injected under the skin. The best effect is given by adrenaline, proposed in 1909 by Jagich (von Jagic), for the purpose of exciting the antagonist of the vagus nerve—the sympathetic nerve. The dose of adrenaline is 1/2 to 1 cubic cm of a 1:1,000 solution under the skin. When taken internally, adrenaline is little effective. In some cases, adrenaline causes palpitations, extrasystoles, especially if patients abuse this medicinal substance. In some cases, adrenaline also has no effect. In some cases, a combination of adrenaline injections and pituitary preparations works well. A ready-made preparation is sold under the name asthmolysin. Morphine is injected under the skin in 1/2 to 1 cubic cm or more of a 1% solution. It most reliably interrupts the attack. The action of morphine is central: it decreases the excitability of the respiratory center, dulls the perception of unpleasant sensations associated with the attack, and calms the patient. In view of the fact that attacks of B. a. can recur periodically for many years, one should refrain from frequently prescribing morphine to patients with B. a. (danger of morphinism) and manage with the above-mentioned medicinal substances. All these substances can give complications in some individuals. Atropine even in a small dose can give a general excited state, palpitations, dryness of the mouth. Sometimes from atropine an intensification of suffocation occurs; this depends, possibly, on the dose, since small doses can excite the endings of the vagus nerve. Adrenaline in some can cause the above-mentioned unpleasant sensations in the area of the heart, palpitations, disturbances of rhythm. Some patients become accustomed to adrenaline and inject 2 cubic cm several times a day. For the purpose of arresting the attack, Pal (1913) recommends papaverine (Papaverini mur.), 1 cubic cm of a 2% solution under the skin. It can also be given internally in 0.03. During the attack, chloral hydrate 0.5-1.5 per dose, aspirin, antipyrine with caffeine, smearing the nasal mucous membrane with a 10% solution of cocaine (cotton swab with cocaine in the nose), faradization of the vagus nerve on the neck (both electrodes on both sides of the neck or 1 electrode on the neck, 2nd on the sternum) are recommended. Hot simple or mustard foot or hand baths, slapping with cold wet towels on the back of the head or back, cold douching of this area are recommended. Treatment of B. a. outside of attacks should be directed, on the one hand, to eliminating the increased excitability of the nervous system of patients, and on the other hand, to eliminating abnormalities on the periphery which can give rise to a reflex leading to an attack of B. a.

The treatment of bronchitis, diseases of the gastrointestinal tract, elimination of coprostasis, expulsion of worms, and regulation of disorders of the endocrine apparatus must be carried out with the aim of preventing the onset of attacks. A carefully collected history can provide much guidance for treatment: the appearance of attacks after acute diseases of the respiratory tract, the onset of attacks in connection with changes in lifestyle, change of residence, profession; the occurrence of attacks when consuming certain proteins, the connection of attacks with the presence of domestic animals (horses, cats, dogs) near the patient—must be taken into account in developing a treatment plan for patients with B. a. Only the most thorough and painstaking clinical or hospital examination and examination of living conditions (housing conditions, etc.) and working conditions of the patient can in some cases give the correct direction to therapeutic measures outside of attacks. In most cases, however, treatment proceeds as if by trial and error. Special attention is paid to iodine, considering it even a specific remedy for B. a. How it acts here is unknown (a liquefying effect on the secretions in the bronchi, an effect on the thyroid gland, the hormone of which acts to stimulate the adrenal glands?). Iodine is prescribed in small doses. Due to the antispasmodic and anti-exudative effect of calcium preparations, this remedy is now widely used in B. a. A 6-8% solution of Calcii chlorati is prescribed 6 times a day for 2-3 weeks. Due to its unpleasant taste, it should be prescribed with syrup. Calcium chloride can also be administered in the form of drop enemas of 100-200 cubic cm of a 2-4% solution. Intravenously, a 5-10% solution, 5-10 cubic cm, is administered. Among other methods of treatment, it is necessary to note roentgenotherapy, electrotherapy, treatment of the spleen with a quartz lamp, diathermy. All these methods of treatment give a favorable result in a certain percentage of cases. It is necessary to have all these methods of treatment in reserve, as with the passage of time the effect of them weakens and it becomes necessary to change the method of treatment. It is extremely difficult to state what the mechanism of action of these methods is. Treatment with quartz and X-rays is assumed to act on the enlarged bronchial glands, treatment with diathermy and X-ray irradiation of the spleen is assumed to cause increased antibody formation and thereby desensitize patients. Electrotherapy attempts to act on the altered tone of the respiratory musculature. But in these methods of treatment, a huge role is played by the effect on the psyche of patients, whose great impressionability and suggestibility are well known. The disciplining of the patient's breathing, both during an attack and in the clear intervals, undoubtedly has great importance. The method of Saenger is extremely suitable for this purpose. Its meaning is to shorten the inspiration and lengthen the expiration. For this, it is recommended to count, somewhat elongating the vowels, up to 4 or 5, then take a short inspiration through the nose and count again. These exercises require persistence on the part of the patient and physician and sufficient willpower. They are carried out in the clear intervals in order to learn to perform them even during an attack. Methods of treatment based on the anaphylactic theory.—Treatment with autovaccines. Statistical data indicate that in approximately 50% of cases, attacks are preceded by infectious diseases of the respiratory tract (pneumonia, acute bronchitis). It is assumed that during these infectious diseases, sensitization of the body occurs by bacterial bodies that caused the diseases. By isolating bacterial bodies from the sputum of asthmatics and injecting them under the skin, an attempt is made to desensitize patients and thereby free them from attacks. American authors have at their disposal a huge quantity (hundreds) of various protein bodies, with which they test the sensitivity of patients (by skin reaction) and, in case of a positive reaction, inject these protein bodies under the skin. According to their data, the results are very good. In the USSR, they have already begun to produce these protein bodies at the Mechnikov Institute in Moscow.—Treatment with tuberculin, which has not received widespread distribution, also belongs to these methods of treating bronchial asthma. Climatic treatment of B. a. The condition of patients suffering from bronchial asthma strongly depends on the peculiarities of the climate. As yet, there are no definite data that would allow one to speak about which particular peculiarities of the climate are of importance here. One can only point out that in a very large number of asthmatics, a connection can be observed between attacks of B. a. and the degree of humidity or dryness of the locality (even the apartment). The number of asthmatics usually increases in autumn and spring. Low temperature is also poorly tolerated by patients with asthma, and the combination of humidity and low temperature has an especially bad effect. But exceptions are also encountered, when attacks disappear in a humid locality or in a cold climate. Generally, one has to admit that there are apparently some peculiarities of the climate or locality, the nature of which has not yet been possible to grasp, but which are undoubtedly the cause causing the attacks. From this point of view, the research of Storm van Leeuwen and his colleagues is extremely interesting, who believe that in a certain percentage of cases, attacks are caused by climatic allergens. These allergens, entering the respiratory tract, cause attacks of B. a. For this purpose, Storm van Leeuwen has proposed placing asthmatic patients in special rooms, where air enters through filters that completely free it from all allergens. Such treatment gives, according to Storm van Leeuwen, an excellent result. All these considerations make understandable the importance that the climatic factor acquires in cases where other measures do not lead to improvement in the patient's condition and attacks do not disappear. In such cases, it is necessary to recommend the patient to change their place of residence and settle in a climate in which attacks cease to bother the patient. In this respect, the climate of mountainous regions with clean air, almost free from dust and bacterial particles, which, from the point of view of the anaphylactic theory, cause attacks, is especially favorable. A change of residence often remains the last remedy that can be recommended to the patient after the application of an infinite number of methods of treating B. a. Only in this way is it possible, in the end, to free the patient from attacks for a long time, if not forever, and restore their ability to work. It is necessary to note in this connection that the patient does not always immediately find such a favorable locality for themselves where they would feel well: sometimes it is necessary to move from place to place several times until it is possible to get into such climatic and local conditions in which attacks disappear. Lit.: Golubov N. F., On bronchial asthma and its treatment, M., 1905; Aryev M. Ya., Bronchial asthma (pathogenesis, clinic and treatment), L., 1926; Storm van Leeuwen V., Allergic diseases, Giz, 1927; Brugelmann W., Das Asthma, 5th ed., Wiesbaden, 1910; Soke R., Asthma, London, 1923; Deltheil Ed., L'asthme, Paris, 1917; De Walter, Beitrag zur Pathologie des Asthma bronchiale, Klinische Wochenschrift, 1927, № 30.

M. Aryev. Surgical treatment of bronchial asthma. Kummell in 1923, on the basis of empirical considerations, proposed sympathectomy of the cervicothoracic portion of the sympathetic nerve [to this day, according to the collective statistics of Hesse (1928), 212 cases have been published]. In 44.81% of these cases, an unsatisfactory result was observed and only in 19.34% cessation of attacks with an observation period of at least 5 months; mortality 2.45%. Thus, the results of cervical sympathectomy in B.A. are little satisfactory, and the long-term results are not encouraging. Late recurrences are sometimes observed. Sympathectomy is indicated only in the presence of signs of irritation of the sympathetic nervous system (asthma bronchiale sympathicotonicum). If sympathectomy is to be performed at all in B.A., it should be performed on the side where there are signs of nerve irritation. Most authors recommend total sympathectomy. The farther down the sympathectomy extends, the better the results. Hesse removed D II-D III. The results sometimes obtained after sympathectomy can be explained in various ways. From the point of view of experimental physiology, sympathectomy in B.A. is absurd, as this intervention should cause narrowing of the bronchial lumen and thereby lead not to improvement but to worsening. Meanwhile, it has been established that after sympathectomy, intensification of attacks has never been observed. Kummell, Mellendorff, and Braeucker point to the existence of intimate anastomoses between the n. sympat. and n. vagus. Some authors explain the effect of sympathectomy by a change in pulmonary circulation in the sense of some hyperemia. The most probable hypothesis is that of Glaser, who sees in the n. sympat. the centripetal part, and in the n. vagus the centrifugal part of one reflex arc. The center of the arc should be sought in the nuclei of the medulla oblongata, and the peripheral part in the bronchioles. Sympathectomy leads to weakening of the centrifugal conductivity of irritation of the n. vagi and thus causes relaxation of the spasm of the smooth musculature of the bronchioles. From the foregoing, it is clear that the theoretical justification for sympathectomy is based on weak foundations. It is much easier to explain the failures of sympathectomy. Bilateral disease should not be treated with unilateral surgery. After the operation, emphysema and bronchitis, accompanying asthma, remain unchanged. After cervical sympathectomy, the anastomoses of the pulmonary plexus with the spinal cord through the dorsal nerves (D III - D VII) remain undisturbed. Thus, even after cervical sympathectomy, pathways remain through which irritation of the bronchioles is possible. This is the main cause of failures. Cervical sympathectomy cannot promise success; in view of the above considerations, it must be recognized as an unsuitable operative procedure in the treatment of B.A. This explains the attempts to approach the solution of the problem from another point of view. Sauerbruch, following the theoretical considerations of Danielopolu, performed the severance of the 2nd-5th intercostal nerves directly at the spine and had success. Kappis proposed vagotomy in 1924. To this day, 128 cases of vagotomy in B.A. have been published. Cessation of attacks was achieved only in 15-16%. Even the author himself abandoned his proposal. The failures of vagotomy in B.A. are explained as follows: after severing the trunk of the n. vagi, all centrifugal fibers in its lower part, and therefore the bulbar bronchomotor fibers, undergo degeneration. But for conducting impulses, spinal fibers originating from the upper thoracic segments and going to the pulmonary plexuses remain; even after severing the trunk of the n. vagi, a large number of spinal fibers remain and communication with the central parts of the nervous system remains uninterrupted after vagotomy (Braeucker). The most suitable operative procedure for the treatment of B.A. is the severance of the pulmonary fibers of the vagus nerve directly at their transition to the bronchi. This idea was developed anatomically and experimentally by Braeucker and put into practice by Kummel and Sudeck. The anatomy of the bulbar bronchomotor fibers is known. They go from the trunk of the n. vagi through the anterior and posterior bronchial branches (rami bronchiales anteriores et posteriores) to the pulmonary plexus (plexus pulmonalis). The spinal bronchomotor fibers pass, according to Dixon and Ranson, through the rami communicantes D I - D IV. Braeucker proved that the spinal fibers do not go with the cardiac nerves. He severed the latter and, despite the severance of the cardiac nerves, could cause the same bronchomotor phenomena as before the severance. Braeucker proved by morphological studies that in the trunk of the thoracic portion of the vagus nerve, a fairly considerable number of sympathetic fibers pass, parts of which pass to all lateral branches of the n. vagus, including the rami bronchiales posteriores. On the basis of these data, Braeucker believes that the main mass of spinal bronchomotor fibers to the lung passes through the n. vagus and the aforementioned posterior bronchial branches. After severing the posterior bronchial nerves at their branching from the thoracic portion, irritation of the cervical vagosympathetic nerve in animals does not cause narrowing of the bronchioles (Braeucker). But even after removal of the posterior bronchial nerves, a considerable part of the pulmonary plexus (plexus pulmonalis anterior) remains as a conductor of bronchomotor impulses. In addition, fibers also go to the bronchi from the lower tracheal nerves. However, irritation of these branches does not cause spasm of the bronchioles. Experimental studies have proved that the asthmatic spasm occurs in the finest bronchioles. Studies by Braeucker have clarified that the anterior bronchial and lower tracheal nerves do not reach the bronchioles. The latter receive innervation only from the rami bronchiales posteriores. The anterior bronchial and lower tracheal nerves, however, innervate the large bronchi. After severing the posterior bronchial nerves, the bronchioles are deprived of their preganglionic fibers, and narrowing of the bronchioles by the nervous pathway becomes impossible. Braeucker performed the following convincing experiments on 6 dogs. He severed the posterior bronchial nerves and, after several weeks, exposed the medulla oblongata and irritated the area of the dorsal nucleus of the n. vagi. Bronchomotor phenomena were not obtained, consequently, in dogs the anterior bronchial and lower tracheal nerves do not reach the ganglia of the bronchioles. The fibers through which impulses for spasm of the bronchioles pass were reliably shut off by severing the posterior bronchial nerves. Braeucker further proved that the connection of bulbar and spinal bronchomotor fibers occurs in humans also in the posterior bronchial nerves. On the basis of these studies, it must be assumed that the severance of the posterior bronchial nerves is the only suitable procedure for denervation of the bronchioles. The operation of severing the posterior bronchial branches in humans was first performed by Kummel (1926). The operation is complex and not entirely safe. From the point of view of intervention on the autonomic nervous system, it is conservative, since only fibers going to the small bronchi are severed. The operation has so far been performed by Kummel in two cases. In both cases, the attacks completely disappeared, the observation period was 1 year. Sudeck severed all pulmonary branches (anterior and posterior bronchial branches) in two cases and obtained an excellent result. Further experiments by Braeucker clarified that substances introduced intravenously and having a direct effect on the smooth musculature of the bronchioles (muscarine) can cause spasm of the bronchioles even after severing the posterior bronchial nerves. If, therefore, in humans B.A. arises through the conduction of motor impulses along nerve pathways, then undoubtedly B.A. can be cured by resection of the posterior bronchial nerves. If, however, B.A. arises through the blood pathway and is caused by irritation of the postganglionic nerve apparatus by substances penetrating there with the blood flow, then any surgical method of treatment, including the severing of the posterior bronchial nerves, will give no result. The ganglia of the bronchioles are inaccessible to the knife: they lie in the lung substance itself. The practical results of the operation of severing the posterior bronchial nerves should shed some light on the etiology of B.A. in general. -Technique of the operation of severing the posterior bronchial branches: a flap incision on the anterior surface of the right half of the chest with resection of the IV and V ribs. Wide opening of the pleural cavity with the use of increased pressure (about apparatuses for increased pressure-Uberdruckapparat, see Thoracoplasty). The lung is pulled aside. Incision of the posterior leaf of the pleura above the right bronchus. Dissection of the trunk of the vagus nerve and severance of the four posterior bronchial nerves branching from it.

E. Hesse. Bronchial Asthma in children. In childhood, bronchial asthma occurs not infrequently. According to Persepier, out of 222 cases, the first attack occurred in the first year of life in 25 cases, in the period from 1 to 10 years in 118 cases, and from 10 to 20 years in 79 cases; most often the disease manifests itself in the 2nd-4th year of life. Children with bronchial asthma usually exhibit a number of constitutional deviations from the norm: these are more or less pronounced neuropaths, who also have signs of the so-called exudative or arthritic (gouty) diathesis; this includes a pastose habitus, prolonged dyspeptic stool or constant constipation in the first months of life, hypertrophy of adenoid tissue in the nasopharynx in older children with recurrent catarrhs of the nasopharynx and upper respiratory tract, sand in the urine, etc., and especially constitutional eczema, prurigo, and urticaria. In the anamnesis of the parents of sick children, the same phenomena are often noted, and sometimes bronchial asthma itself, i.e., a hereditary factor and a close connection between bronchial asthma and constitutional anomalies are revealed. The onset of a bronchial asthma attack in children is somewhat different than in adults. Sudden onset is rare; more often the attack develops after some acute disease of the respiratory tract (for example, a runny nose). For the infant age, it is characteristic that bronchial asthma most often occurs in the form of recurrent bronchitis, while the pure form of bronchial asthma is very rare. In these children, sometimes every bronchitis takes on an asthmatic character (bronchitis asthmatica). For bronchial asthma in early childhood, it is also very characteristic of the sometimes observed alternation of bronchial asthma with eczema: with the onset of an attack, eczema disappears, returning in the intervals between attacks. The duration of the attack is short—after several hours, at the latest after 1-2 days, the attack gradually passes. In infants, it is often possible to identify an alimentary factor (alimentary anaphylaxis). Skin tests with protein antigens are often positive but not specific, so no conclusions about etiology can be drawn from them; however, these tests can be used for differential diagnosis (presence or absence of an allergic condition). Among complications, only bronchopneumonia is sometimes noted, although it is often unclear whether the small focus determined 1-2 days after an acute attack is a consequence of asthma or its cause. The prognosis is favorable, although complete recovery does not occur quickly and not always. Marfan and others believe that the earlier asthma occurs, the sooner one can expect complete recovery, and it is noted that asthma often disappears by the time of puberty. When diagnosing bronchial asthma in a child, one must most often think of acute bronchitis, beginning bronchopneumonia, and also compression stridor (in infants); despite the presence of expiratory dyspnea, bronchial asthma is sometimes confused with diphtheria or false croup. One should also think about Lederer's broncho-tenia. The bronchitis fibrinosa sometimes described as a special form apparently represents a variety of bronchial asthma. The symptoms are generally similar; the characteristic feature is the expectoration of long, branched fibrinous casts—casts of the bronchial branches. In treatment, protein therapy sometimes helps: after 1-1 subcutaneous injections of 0.5-2.0 ml of milk, in intervals free from attacks, it is sometimes possible to completely eliminate the attacks or postpone them (desensitization method). Diet regulation is also important, according to the same principles as in constitutional eczema and other related processes. A stay on the shore of one of the northern seas is very beneficial. Lit.: Maslov M.S., Osnovy ucheniya o rebenke, t. II, 1927; Marfan A.B., Clinique des maladies de la premiere enfance, P., 1926; Engel St., Erkrankungen d. Respirationsorgane (Pfaundler M. und Schlossmann A., Handbuch der Kinderheilkunde, B. III, Leipzig, 1924).