Asthma

Bei Asthmaanfällen hatte ich ein Spray verwendet aber dann darauf verzichtet und mich zusammen gerafft. Bei Asthma heiligt der Zweck keineswegs die chemische Keule als Mittel, weil Akupressur (Lppendruck aber nicht Lippenbremse) ehrlicher und wirksamer ist. Soweit es geht, will ich naturverbunden leben und nicht überstürzt zu Pillen greifen. Meine beendete Asthmalaufbahn fing mit Mundatmung an. Hier muss eine Mutter aufpassen.

Das freut mich, dass das bei Ihnen gut funktioniert hat! Ich gehe aber davon aus, dass Sie zu den rund 35% “Asthma“-Patienten gehörten, die eine vorschnelle Diagnose erhalten hatten. Gerade bei reinen Bronchialkrämpfen kommen diverse Differenzialdiagnosen in Betracht. Bei einem echten Asthma reichen solche Methoden - leider! nicht aus und es ist schlimm, wenn so etwas immer wieder öffentlich behauptet wird, das verunsichert Eltern und Patienten gleichermaßen. Sie stellen Ihre Behauptung seit Jahren in diversen Foren immer mal wieder auf. “Ei des Kolumbus “ usw. Ähnlich wie bei der Buteyko-Methode glaube ich, dass es durchaus mal ein, zwei Glückstreffer gibt, bei denen Asthma nach Anwendung der Methode verschwindet. Placebo (und in Ihrem Fall kontinuierliches Training der Atemhilfsmuskulatur) kann unheimliche Heilungserfolge erzielen, das weiß auch jeder Mediziner. Bleibt nur, Ihnen zu wünschen, dass Ihr Erfolg von Dauer ist. Sollte es tatsächlich echtes Asthma gewesen sein, kann die nächste heftige Atemwegsinfektion (Influenza o.ä.) die Krankheit aber wieder aktivieren. Hier muss ein Patient aufpassen.

Asthma war gar nicht so schwerwiegend in der Vergangenheit. Die heutige Behandlung ist blinder Aktionismus. Siehe A HISTORICAL ACCOUNT OF DEATH FROlVI ASTHMA Il. I,. Alexander, X.D.,* St. Louis, Xo. ENOUGH material has now accumulated on the subject of death from asthma to formulate an appraisal of it. The history of bronchial asthma dates back to the ancients. The literature is characterized by periods in which observers presented concise descriptions of the disease as well as intervals in which it could not be distinguished from many disorders to which the designation “asthma” had been applied. However, clear records hare been available since the latter half of the last century, a time when extensive anatomical and physiological experimentation on bronchial occlusion was performed, particularly in Germany and in France. One may now recognize three periods during which the occurrence of death from asthma showed a characteristic trend. The first is measured by a century, the second by a few decades, and the third by a few years. In assembling available material on the subject, it became necessary at the outset to establish a precise definition of death from asthma. Some asthmaties die eventually from a complication of the disease. A small number succumb from the immediate lesions of asthma during a paroxysm, and these are the cases with which this report is concerned. At first, patients were limited to those in whom lesions were revealed at postmortem examination. Some who died during a paroxysm and on whom no autopsy had been performed were then compared to the first group in terms of age, age of onset, and duration of the diseasr. The two groups were almost identical in these respects, so they were combined. Although it is realized that, in the absence of post,mortcm examinations, there mny have been concealed factors that contributed to death, t,hese would not contradict the findings of this report. Cases in which death inadvertently was due to drugs, to the administration of excessive amounts of allergens, or to other causes that did not reflect t,he natural history of the disease were excluded. THE FIRST PERIOD Of the recognizable periods into which fatalities have been separated, thtb first ended about the year 1930. Prior to this date, death during an asthmatic: attack was almost unknown. To be sure, in that era there was less clinical material in terms of hospital populations, fewer autopsies, fewer medical periodicals, and fewer opportunities to present cases at medical meetings, compared to facilities of the present day. Moreover, in the earlier years there were no allergists with a particular interest in asthma. Nevertheless, the evidence that death during an asthmatic paroxysm was exceedingly uncommon is overwhelming. Perhaps the earliest recorded recognition of this phenomenon is the often quoted remark of Trousseau who lived during the first half of the last century, “Asthme n’est pas fata,le.” Andral in his Cours de Pathologie, published in 1839, made the quaint statement that asthma is a brevet of long life. Oliver Wendell Holmes, commenting on his own symptoms, said essentially the same thing, and there is an aphorism of Osler, “The asthmatic pants into old age. ” This belief was amply documented in textbooks and didactic teaching of the day, both in this country and abroad. In Riegel and Fraentzel’s Handbuch der Respirations, published in 1877, the statement is made that rarely is life threatened during an asthmatic attack. No mention of death is made in the chapter on asthma by Hyde Salter in Reynolds System of Medicine that appeared in 1880. Strtimpell’s Textbook of Medicine published in 1888 states, “There is hardly ever any danger to life, even in the most intense paroxysms.” In Stedman’s extensive Twentieth Century Practice of Medicine of 1896, the following appears: “Although paroxysms of asthmatic dyspnea are so alarming to witness, death rarely, if ever, occurs during a fit.” Andral’s Practice of Medicine, 1899, states, “There is rarely any danger to life excepting emphysema.” In Albutt and Rolleston’s System of Medicine, published 10 years later, the chapter on asthma, written by Goodhart and Springgs, does not mention death. Ameville and Bordet wrote the chapter on asthma in Trait4 Pathologia Me’ditale et Therapeutique Applique’e compiled by Rabideau and Babonneix and published in 1922. They stated, “Asthmatic paroxysms by themselves do not lead to any danger.” In the earlier years of this century, this doctrine was adhered to in leading medical schools in this country. Particularly important, with one minor exception,l is the absence of any other point of view in the literature of the day. In 1922 a classical article by Huber and Roessler2 appeared. These authors had assembled all of the published autopsy reports of death from asthma in which microscopical examinations had been made. There were but 15 in all to which they added 7 more. A review of these cases3 indicated that most of the patients did not die primarily from asthma, but from causes such as acute complications of cardiac and renal diseases, disseminated cancer of t,he lung, and, in one case, drowning. With this revision, there were but eleven deaths primarily from asthma recorded by the year 1926. Some new reports were published before 1930, but by that year no more than 30 cases of death occurring during an asthmatic paroxysm are on record. THE SECOND PERIOD During the succeeding 25 years there was, at first, a gradual increase in the number of reported deaths from asthma (187 instances had been assembled in 1937, without distinguishing those in which death occurred in status asthmaticus), and after that there was an acceleration in the number of fatalities. Experiences in several hospitals and clinics were published where death during a paroxysm of asthma was recorded. There were 19 such instances at the Massachusetts General Hospital (1944) ,4 37 at Barnes Hospital in St. Louis, 36 at the Mayo Clinic, 5 101 reported from Cardiff, Wales6 and 49 at the Westminster Hospital in London,’ including some previously reported cases. These instances averaged approximately 20 per cent of the total deat’hs from asthma which included deaths from complications. According to the National Vital Statistics Division of the United States Public Health Service, under the designation “Deaths from Asthma,” the peak occurred between the years 1951 and 1953. During the latter year there were 6,737 such deaths, and in this period the death rate rose from 2.5 per 100,000 population in 1937 to 4.5 in 1951. More dramatic still was the New Zealand experience where the death rate from asthma rose from 1.7 in 1939 to 10.4 in 1953. Although no distinction was made concerning those which occurred during a paroxysm, in view of the average percentage stated in other series, the actual numbers of such deal,hx may have been considerable. Comparative data between the first and second periods were found to be of a wholly different order of magnitude.8 THE THIRD PERIOD Approximately after the year 1953, there appeared to be a decided diminution in the number of asthmatic deaths. It is difficult to estimate how great the decline may have been for there is little literature on the subject. Perhaps so much had been published previously about deaths from asthma that further accounts were no longer newsworthy, or there may have been too few deaths to report. In one of the few publications on the subject,D the decrease in fatal cases is noted and, according to vital statistics, deaths from asthma dropped from a rate of 4.5 in 1951 t,o 3.6 in 1955 and 2.8 in 1959. The apparent abrupt decline in fatalities appeared at a time when cortisone and related hormones were coming to be used extensively in the treatment of asthma. It seems probable, and this is the opinion of others,” that these products were largely responsible for reversing the trend. At the Barnes Hospital, where 4 asthmatics on the medical wards succumbed during paroxysms in 1949, such deaths have been negligible since 1951 when hormone therapy was instituted. Time alone will tell whether the decreased death rate will continue. There well may be other reasons for the apparent diminution of fatalities in comparison to the incidence during the second period, but expla.nations for this must be postponed until the cause of the acceleration during that period is revealed. POSTMORTEM OBSERVATIONS Until some 25 years ago there were few decisive observations concerning the cause of death in bronchial asthma. The prevailing theory implicated bronchial constriction from contraction of the bronchial musculature. There was considerable experimental support for this presumption, dating back to the last century. Hubcr and Koessler2 found hypertrophy of the bronchial muscles in asthmatics that came to autopsy, and this they interpreted as an indication of frequent contraction. These authors described, although without emphasis, other postmortem lesions. It was later realized that several of the anatomical findings described by Huber and Koessler were not specific for asthma, and other theories of etiology were debated. In 1930, Coke”’ wrote, “Pure asthma, no matter how severe the spasm leaves little to be found post-mortem and no evidence on which the condition can be diagnosed or which in the absence of a clinical history, the patient can be said to have died from asthma.” In Coca, Walzer, and Thommen’s classical treatise Asthma and Hay Fever in Theory and Practice published in 1931, it is stated that the reason so few deaths had been reported was that no pathological entity existed. Tuft, in the 1937 edition of his Clinical Allergy, said essentially the same thing, but he recognized a few lesions that appeared consistently in reported cases. Moreover, he listed one group of fatal cases in which suffocation had been attributed to excessive mucus, a significant observation. As more autopsy material became available, it was increasingly evident in cases in which death occurred during a paroxysm that the conspicuous lesion was partial or complete occlusion of bronchioles by mucus. It was Mallory who demonstrated this fact conclusively in a lecture before the Society for the Study of Ast,hma and Allied Conditions in 1941. Although abundant mucus has been reported in a large majority of autopsies in which death occurred during a paroxysm, it has not been observed in some cases. Although other lesions, such as the accumulation of products of infection which is frequently present along with probable bronchospasm, may encroach upon the airways, it is difficult to assess their contribution to the suffocation that occurs during an asthmatic attack. It may be noted that the distribution of mucus can be irregular so that it is seen only in some sections of bronchioles. In these instances, it becomes necessary to examine sections of bronchi at various levels before the participation of mucus can be excluded. The presence of emphysema or car pulmonale has not been regarded as important in contributing to immediate death, since in many cases these lesions were present to no more than a moderate degree, if at all. This was particularly true where the duration of symptoms was short. In view of the importance of bronchial mucus in status asthmaticus, it seems remarkable tha.t until the past decade no systematic study of this material or of the mucous glands in asthma had been published. One recent significant observation revealed the distinction between normal bronchial mucus and that which appears in asthma and chronic bronchitis. The former contains a mucoprotein in the form of a mucous gel. The mucus in asthma contains, in addition, desoxyribonucleoprotein (DNP) derived largely7 from the nuclei of desquamated and inflammatory cells. The DNP is thought to be drawn out into thick tough bundles by respiratory and ciliary movements. With infec- DEATH FROM ASTHMA 30!4 tion, the large numbers of inflammatory cells greatly enhance t,his effecat. An early observation, which later was rtgardetl of much importance. was made by Moore” in 1925. He was concerned with ciliated bronchial rpithelium in asthma. Moore referred to the studies of Moffatt, then in press. Both t,hese authors pointed out that cilia which have a rrmarkable ability to move mucus may be impaired in bronchial asthma. The cells t,o which these bodies a~*(~ attached form the outermost cpithelial layer ant1 may bc tlisplaccd easily. If asthma is not, intmse, regeneration may OWUI’ ; but, when scvcrc, thcrcl may be actual loss of cilia with degeneration of the epithclial cell. Some 20 years later, Hiltlig” enlarged upon these observations and demonstrated clearly thts degeneration and tlcsquamation of ciliated cpithclium in the prcscnct~ 01 excessive mucus. These findings wcrc t~laborat&l further by Houston and his a.ssociates.‘” They found instances where thcrc was a continuous mass of mucus extending from the major bronchi to the bronchiol(~s with some separation from the walls. These authors stated it is not genc>rally apl)rcciated that widcspread detachment of ciliated epithelium is a constant finding in death l’rom status asthmaticus. They believe the dcstructiol) of the ciliary mechanism permits mucus to accumulate and thus cause suffocation. From a historical point of view, mention should be tnade of a substantial literature in which death during a paroxysm of asthma had been attributecl to opiates to a point where, at one time, it was considered essentially the solo cause of exitus. Undoubtedly many fatalities have occurred -from ovcrsedation. but no good systematic study of the problem is available. It is of some int,rrtbst that, before the introduction of rpinephrint~, tnorphinc was the trratmcnt OI choice for asthmatic paroxysms, and addiction was not uncommon ; and this was at a time when deaths from asthnta w(‘rc .1’ow. CLINICAL DATA In several reported series of deaths during status asi,hmaticus,“, :, 14 there is close agreement with ages at death and ages at onset, of symptoms, from which the duration of the disease was derived. Average figures indicate that some 10 per cent of fat,alities occurred in infants and rhildren under 2 years of age, and a few more up to the age of 5 years. Then there was a long period of comparative immunity during the following 30 years wherein less than 15 per cent ol the total deaths occurred. ,4t the age of 35, the rat,e began to climb and somt’- what over 50 per cent of the fatalities appeared bet,wcen the fortieth and sixtieth year of life. Excluding t,hose under 2 years of age, statistics indicate that, over 15 pet cent of those who died during status asthmaticus had asthma less than one year. This highly malignant process is matched by few chronic diseases. Thirty-t,hrer per cent had symptoms no more than 2 years and in some 50 per cent, thcl diseascl was apparent less than 5 years. In these instances, asthma was scarcely “a brevet of long life. ” There was a striking difference between the images of most of those who died in an acute attack and those who had the familiar syndrome of asthma ant1 July-August, 1963 bronchitis for many years and died eventually from emphysema, infection, or of something else. Although detailed descriptive case reports are not abundant, it appears that, in addition to onset in middle age and comparatively short duration of symptoms, very many patients had an initial respiratory infection, and a similar process ushered in subsequent acute asthmatic attacks. It was not possible to assess the participation of atopic factors, other than the frequent statement that none was found. This pattern conforms to the criteria described as “intrinsic” or “infectious” asthma. The associat.ion of apparent infectious asthma with many immediate deaths led to a review of this type of the disease, particularly in the earlier years when deaths were few. From available case histories, the majority of fatalities at that period seemed to be in patients with infectious asthma. However, there is reason to believe that there was a decided increase in this syndrome in subsequent years, at the time that the death rate was accelerating. Although this type of the disease existed, certainly, it was not recognized in the early years of clinical allergy. Classifications of asthma at that time by Cooke,15 Walker,“j and RackemanrP separated those who were sensitive to extrinsic allergens from those who were not. The latter group was ident,ified with designations such as “intrinsic,” “bacterial,” “reflex,” “ unclassified,” etc., and in one series this group had the highest incidence before the age of 10 years. It was not until 1940 that the pattern of infectious asthma was clearly presented. Rackemann I8 then described the syndrome (he used the term “intrinsic asthma”) and pointed out its seriousness. He recorded in a later series 283 such cases with 20 deaths whereas there were no fatalities in 2,000 instances of atopic asthma. He described two expressions of infectious asthma in which the duration was not short. One was typical “extrinsic” asthma in early years of life, followed by a free interval of many years. When asthma recurred in middle age, the atopic element no longer could be detected and the case took on the pattern of “intrinsic” asthma, namely, its appearance in the middle decades, the tendency to increased severity of symptoms, association with respiratory infections, and resistance to specific treatment. There were also instances of continual asthma in which hypersensitivity to specific allergens in earlier years seemingly became lost and intrinsic asthma ensued. Soon after Rackemann’s communication, there were others who described the syndrome.ls, 2o That it was not well known at the time is reflected in three textbooks on asthma that appeared a few years later in which intrinsic asthma received scant attention and there were prominent allergists who questioned its existence and attributed specific etiologies in terms of allergy to. these cases. An apparent increase in the incidence of infectious asthma during the ensuing years, when fatalities rose, is indicated in the Barnes Hospital experience. The records of all patients who entered with a primary diagnosis of bronchial asthma over a period of 35 consecutive years (1924-1958) were reviewed. There was a striking contrast between the number of admissions identified with infectious asthma in the earlier period when compared to that of the later years of the series. In 1924 they constituted 20 per cent. Although the hospital had been in operation at that time for 8 years, no deaths from asthma had occurred. Most of the patients were young ancl specific hypersensitivity was commonly found. (Adults only are admitted.) There was a gradual increase of cases identified as infectious asthma which in 1958 constituted slightly over 70 per cent of admissions. The average age was 51 years. After factors such as an aging population and more available beds for older patients arc taken into account, the difference in the incidence of admissions of cases of infectious asthma seen in the earlier years and that of the later periods is evident. DISCUSSION From the data presented, it would appear that t,he characterization of bronchial asthma was transformed from a benign to a malignant disease during the past few decades. The symptoms of the disorder do not appear to have changed except in their intensity. There is reason to believe that in the first period, when deaths were Sew, most cases of asthma were atopic. In the Barnes Hospital series a large majority of asthmatics admitted in 1924 had this type of the disease. Had infectious asthma been prevalent at the time, patients with it would have sought hospital care just as they did in the following decades. Death in uncomplicated atopic asthma is a very unusual event if one excludes infants and accidents, such as occur in drug hypersensitivity. Few deaths have been described, and Rackemann’s observations on 2,000 consecutive cases of this type of asthma without fatality is impressive. The recognition of the clinical pattern of infectious asthma came later. According to a few early case histories of death from asthma, this type of the disease apparently existed. That it was not prevalent at the time, however, is indicated by its omission from several early classifications of asthma. The designation “intrinsic” then referred, in part, to the chronic asthmatic with emphysema and bronchitis (who panted into old age), a familiar figure, particularly in out-patient clinics. Not only were there differences in clinical patterns and in death rates t,o be observed in the first and later periods, there was also a marked discrepancy in autopsy observations. The repeated statements 30 years ago that there was no discernible lesion, post mortem, in cases of bronchial asthma is in sharp contrast to t,he striking appearance of bronchial occlusion by mucus seen suhscquently in most cases in which death occurred during paroxysm. The recognition of infectious asthma with which most fatalities arc associated and the identification of excessive mucus as the cause of suffocation during an asthmatic paroxysm were both reported approxirnat,ely the same year. A relationship between the two phenomena is no more than suggestive since the underlying factors that mediate infectious asthma remain unknown. From the standpoint of etiology, one consistent factor is its identification with infection of the respiratory tract. Bronchial infection, however, has long been recognized as a common complication of asthma so that. one might inquire whether the patterns of infections may have changed. This seems to be the case. 312 ALEXANDER J. Allergy July-August, 1963 The years that marked the apparent increase of infectious asthma were also historical ones in the field of infectious diseases. With the expanding use of chemotherapeutic agents, particularly of antibiotics, certain bacterial infections susceptible to these products gave way to disorders dominated by gram-negative organismsZ1 ; viral pneumonia and unrecognized diseases of the respiratory tract became clinical ent,ities; and, with newer culture methods, an ever widening spectrum of virus infections continues to unfold. One scarcely can speculate whether death from asthma may have been influenced by these changes. There is little evidence that allergy to bacteria or viruses plays an important role. However, certain possibilities suggest themselves. One is related to the discovery that destruction of cilia, the presumable cause of death during status asthmaticus, occurs in some virus infections of the respiratory tract. Hers and MuldaZ2 clearly showed this in influenza1 infection in man. Likewise, denudation of cilia-bearing cells, ciliocytophthorea, has been found in many cases of respiratory infections identified with adenoviruses.Z3 Moreover, some respiratory infections add DNP to asthmatic sputum and thus make it more difficult to discharge the mucus. These off-hand suggestions merely serve to indicate how much remains to be learned about why patients with asthma died, some so quickly, during the years under consideration. REFERENCES Walzer, M.: Coca, Walzer, and Thommen in Asthma in Theory and Practice, Springfield, Ill. 1931, Charles C Thomas, Publisher, p. 136. Huber k., and Koessler, K. K.: .‘,‘m The Pathology of Asthma, Arch. Int. Med. 30: 689, .lYijZ. Rackemann, F. M.: Fatal Asthma. Report. of a Case With Autopsy, Boston M. & S. J. 167: 809 1926. Rackemann, F. M.: Death From Bronchial Asthma J. ALLERGY 15: 249 1944. Messer J. W Peters J. A and Bennett W. A.: ‘Causes of Death and Pathological F$dinas”in 304 %ases zf Bronchial Asthma. Dis. Chest 38: 616. 1960. Williams, 6. A., and Leopold, J. G.: Death F&m Asthma, Tr. 3rd Internat. Gong. Allergol., Paris, 1958, p. 119. Earle. B. V.: Fatal Asthma. A Series of 15 Cases With a Review Frbm the Literature, Thorax 8: 195, 1953. Bachelor, J.: Statistician, Consultant, Operations research. Personal communication. Sheldon, J. M.: An Allergist’s Rebuttal to Oliver Wendell Holmes, Proc. Medical Section of American Life Convention, 46th Meet., 1958, p. 105. Coke, F.: Asthma, Baltimore, 1930, Williams & Wilkins Co., p. 89. Moore. W. F.: Ciliarv Inhibition or Destruction in Tracheobronchial Asthma. Am. J. id. SC. 169: 799 1925. , Hildig, A. C.: The Relation of Ciliary Insufficiency to Death From Asthma and Other Respiratory Diseases, Ann. Otol., Rhinol. & Laryngol. 52: 5> 1943. Houston. J. C.. de Navesauez. S.. and Trounce. J. R.: A Clinical and Pathological Study of Fatal Cases-of ‘Status Asthmatic&, Thorax 8: 207, 1953. Alexander, H. L.: Death From Bronchial Asthma, Tr. 3rd Internat. Cong. Allergol., Paris; 1958, p. 109. Cooke, R. A.: Studies in Hypersensitiveness. New Etiologieal Factors in Bronchial Asthma, J. Immunol. 7: 147, 1922. Walker. I. C.: A Clinical Studv of 400 Cases of Bronchial Asthma, Boston M. & 5. J. 159: 288, 1918. 17. Rackemann, F. M.: ‘A Clinical Classification of Asthma, Am. J. M. SC. 162: 202, 1921. 18. Rackemann, F. M.: Intrinsic Asthma, J. ALLERGY 11: 147, 1940. 19. Alexander, H. L.: Allergic Syndromes in the Absence of Allergens, J. ALLERGY 11: 163, 1940. 20. Cohen, M. B.: Bronchial Asthma. Classification Based on Etiological and Pathogenic Factors, Ann. Int. Med. 20: 590, 1944. 21. Finland, M., Jones, W. F., and Branes! M. u’.: Occurrence of Serious Bacterial In22. Hers, fections Since Introduction of Antibacterial Agents, J. A. M. A. 170: 2188, 1959. J. F., and Mulder, J.: Broad Aspects of thP Pathology and Pathogpnesis of Human Influenza, Am. Rev. Resp. Dis. 83: 84, 1961. 23. Pierce, C. H., and Hirsch, J. G.: Ciliocytophthorea. Relationship to Viral Respiratory Infections in Humans, Proc. Sot. Blol. &- Med. 104: 492, 1960. With the author’s approval, a number of interested people were asked to comment on Dr. Alexander’s stimulating and challenging article. The following are being published in the order of their receipt in the hope that it will increase interest in this type of article and result in the submission to the Journal of others of equal caliber. EDITOR COMMENTS ON PRECEDING ARTICLE D R. ALEXANDER’S paper is an excellent review, and it contains a number of interesting implications. Fkst, he finds that the incidence of death from asthma varies according to three periods of history. In the first period, ending about 1930, all the textbooks of that epoch agree that deaths from asthma do not occur. After that time, however, deaths were recognized. Is there reason to think that in the nineteenth century asthma was different from what we see of it in the twentieth century? Can we assume that in “the old days” people were more exposed to “house dust” of various kinds than they are in this modern time? It is true that bathtubs were scarce--people were dirty ; streets were dusty ; animals-horses as well as dogs and cats-were everywhere. I can recall that in 1.920 asthma causetl by horses was a common affliction. It is quit,e proper to assume t,hat extrinsic asthma due to a sensitiveness to dusts in the environment was more common then than it is today, and now we know that this type of asthma is not often dangerous. On the other hand, older people must have had asthma then as now, and presumably it was quite as serious and as dangerous then as it is boday. Was it called asthma? The sudden onset of difficult breathing at the age of 50 was probably ascribed to heart disease, or emphysema, or perhaps “fibrinous bronchit,&,” but it was very likely the same disease that today I call “intrinsic ast,hma” ; it was due to infection. In Dr. Alexander’s second period-after 1930-deaths from asthma were recognized and described, but in the third period, beginning about 1953, t,hey fell off again. It is obvious that this later cha.nge has depended upon t,he use of cortisone and its relatives in treatment. (~‘ertainly the steroid drugs have done much to remove the terrors of status asthmaticus. As for the lesion in asthma, there is, first of all, good evidence that asthma-the wheezing-is a symptom of a constitutional disease, the tendency to which is inherited. Besides asthma, the disease includes eczema of the atopic

Ein Artikel aus 1963, der auf “Studien“ aus den 20ern und 30ern referenziert und auch “Medizinbücher“ von 1880 miteinbezieht? Darüberhinaus in grauenhafter Rechtschreibung und Grammatik... Asthma war damals nicht gefährlich.... Bis Mitte des 20. Jahrhunderts wurde unter “Asthma“ vorwiegend das Cardiale Asthma verstanden, oder die psychisch bedingten Atemnotzustände (Asthma nervosum). Solange ist es noch gar nicht her, dass man Asthma nach der heutigen Definition (s.o) betrachtet. Die meisten schweren Asthmatiker wurden auch nicht alt. Babys starben am schlimmen Husten, mein Großonkel schaffte es dank viel Kaffee (in dem eine Art Bronchienerweiterer enthalten ist) immerhin knapp 20 Jahre alt zu werden und starb in den 30ern an einem Asthmaanfall. Einer unserer Ärzte erzählte, dass er mit 10 Jahren kaum die Treppe hochkam und blitzblaue Lippen bekam. Er begann zu leben, als er mit 15 Jahren Kortison bekam, erst in Tablettenform, dann viele Jahrzehnte inhalativ. Er freute sich auf die Rente, die er ohne Medikation nie und nimmer erlebt hätte. Auch von Allergien hatte man 1963 und erst recht 1922 ... oder 1880 keine Ahnung. Aber da Sie ja anscheinend gern lesen, hier noch ein Artikel zu ihrer Fragestellung. https://www.aerzteblatt.de/archiv/277/Umwelt-und-Lunge Ergo... bestimmte Formen von Atemnotszuständen bekommt man mit gewissen Atemtechniken gut in den Griff (vgl. z.B. VCD ) , richtiges diagnostiziertes Asthma kann man auch mit Atemtherapien und einigen Kniffen verbessern, wir können aber dankbar sein, dass es für die schlimmeren Fälle gute Medikamente gibt.

Deinen Beitrag empfinde ich als Schlag ins Gesicht. Wenn es Deine persönliche Meinung ist, ist das ok. Das aber propagieren zu wollen, finde ich fahrlässig. Meine Tochter lag - wenige Monate alt - mehrmals wg. Asthma (das wissen wir heute) auf der Intensivstation, Sättigung unter 80%. Mit Lippenbremse und Kutschersitz allein als Therapie würde sie heute wahrscheinlich nicht mehr leben.

... Die Wirkung des Faustballens ist durch Akupressur, die Schulmediziner jetzt nicht auf dem Schirm haben. Zum Thema Asthma in der sprayfreien Vergangenheit siehe https://www.jacionline.org/article/0091-6749(87)90075-3/pdf von Dr. Sheldon Siegal.

... Was meinen Sie als Sachverständige mit den schicksalhaften Erfahrungen? Das so wichtige Ballen der Fäuste dabei entspannt die Bronchien. Außerdem drückt das kräftige Einatmen durch die Nase die Lippen zusammen ebenfalls durch Akupressur. Das diese Binsenweisheit über gesunde Atmung in der Asthmawelt keine Beachtung findet, ist paradox.