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Migratory atelectasis
CORRESPONDENCE
Migratory
atelectasis
To the Editor: In the May issue of the JOURNAL or1 ALLERGY, Hughes and &isrtlan report the C:W of a 12year-old ssthmat,ic child with migratory atelectasis following steroid withdrawal. ‘l’he article as well as the title implies that the atelectasis either resulted from or was provoked by the steroid withdrawal, but no proof is offered to support this implication. I was especially interested in this article because it recalled to mind a similar case recorded in the first editiou of my book, Clinic& allergy (as Fig. 35, p. 286), published in 1937. The patient wax a R-year-old girl, whom I saw for the first time in January, 1933, with a history of recurrwt attacks of severe, life-threatening asthma following what was diagnosed as “bronchopnwmania.” The patient remained in the hospital for more than 6 months, during which she hacl attacks of increasing severity about every 3 weeks; in fact, shortly after being taken out of the hospital by the parents, she died during an attack mhile en route to Arizona where they thought she might benefit from climatic change. \Vithout repeating the details which :I I’(’ available in the case report, we were able to demonst,rate during her attacks definite evidenw of atelectasis, involviug the right middle lobe on one occasion and the base of the right upper lobe ou another, and also to shorn in the latter instance clearing up of the atelectesis a week after the attack subsided. During the attack, the patient received epinephrine, sub cutaneously and even intravenously (this was before aminophylline was being used intrave nously in these patients), as well as other measurw (oxygen, intravenous glucose, and brow choscopic aspiration of the thick viscid secretion), all with little or no beneficial effect. When a11 seemed hopeless, the cough became looser, expectoration freer, and the patient’s condition improved rapidly so that no medication was needed until the next attack. Here, then, was a child with segmental atelectasis, similar to that observed and reported later by others, which could not be controlled or prevented by the therapy at our disposal nt that time. n-e theorized then that perhaps because of poor development or a congenital defwl, the narrowed bronchioles became obstructed by a mucous plug resulting in subscquettt atelcctasis. If an effective remedy like the corticosteroids had been available at t.hnt time, v(: might have been able to control the asthma during the interval and perhaps to prewut rccurrenco of the atelectasis during the acute attacks. The withdrawal of the steroids irr the case reported by Hughes and Reisman merely permitted the obstructive factors rcspou sible for the ntelectnsis to become operative and did not actually cause the atelectasis. li is not unlikely that, if their patient had received sufficient epinephrine (perhaps of tln~t “slow type”) over the 24 hour period to control the nsthrlln and the epinephrine thou LWY stopped, the segmental nteleetasis likewise would have occurred. It seems to me unfair, therefore’, to blame the steroid withdrawal, as the title of t,he pttper implies, for the atelec:tnsi::. LOGS Tuft, M.1). I’kilndelphicr,
1’11.
Reply
To the Editor: The occurrence of segmental atelectasis in association with symptovnntic asthma, as dwcrihed by Dr. Tuft, is certainly well recognized and was briefly revielved in the oprninK paragraph and in the discussion section of our report. The unique feature of the patient whom we described was the presence, followirr~ steroid ~vithdramal, of atelectasis involving various lung segments without clinical or hro,r choscopic cridence of mucous plugs or bronchospasm. Obstructive factors could not bc ~Io,-u-
Migratory
atelectasis
To the Editor: In the May issue of the JOURNAL or1 ALLERGY, Hughes and &isrtlan report the C:W of a 12year-old ssthmat,ic child with migratory atelectasis following steroid withdrawal. ‘l’he article as well as the title implies that the atelectasis either resulted from or was provoked by the steroid withdrawal, but no proof is offered to support this implication. I was especially interested in this article because it recalled to mind a similar case recorded in the first editiou of my book, Clinic& allergy (as Fig. 35, p. 286), published in 1937. The patient wax a R-year-old girl, whom I saw for the first time in January, 1933, with a history of recurrwt attacks of severe, life-threatening asthma following what was diagnosed as “bronchopnwmania.” The patient remained in the hospital for more than 6 months, during which she hacl attacks of increasing severity about every 3 weeks; in fact, shortly after being taken out of the hospital by the parents, she died during an attack mhile en route to Arizona where they thought she might benefit from climatic change. \Vithout repeating the details which :I I’(’ available in the case report, we were able to demonst,rate during her attacks definite evidenw of atelectasis, involviug the right middle lobe on one occasion and the base of the right upper lobe ou another, and also to shorn in the latter instance clearing up of the atelectesis a week after the attack subsided. During the attack, the patient received epinephrine, sub cutaneously and even intravenously (this was before aminophylline was being used intrave nously in these patients), as well as other measurw (oxygen, intravenous glucose, and brow choscopic aspiration of the thick viscid secretion), all with little or no beneficial effect. When a11 seemed hopeless, the cough became looser, expectoration freer, and the patient’s condition improved rapidly so that no medication was needed until the next attack. Here, then, was a child with segmental atelectasis, similar to that observed and reported later by others, which could not be controlled or prevented by the therapy at our disposal nt that time. n-e theorized then that perhaps because of poor development or a congenital defwl, the narrowed bronchioles became obstructed by a mucous plug resulting in subscquettt atelcctasis. If an effective remedy like the corticosteroids had been available at t.hnt time, v(: might have been able to control the asthma during the interval and perhaps to prewut rccurrenco of the atelectasis during the acute attacks. The withdrawal of the steroids irr the case reported by Hughes and Reisman merely permitted the obstructive factors rcspou sible for the ntelectnsis to become operative and did not actually cause the atelectasis. li is not unlikely that, if their patient had received sufficient epinephrine (perhaps of tln~t “slow type”) over the 24 hour period to control the nsthrlln and the epinephrine thou LWY stopped, the segmental nteleetasis likewise would have occurred. It seems to me unfair, therefore’, to blame the steroid withdrawal, as the title of t,he pttper implies, for the atelec:tnsi::. LOGS Tuft, M.1). I’kilndelphicr,
1’11.
Reply
To the Editor: The occurrence of segmental atelectasis in association with symptovnntic asthma, as dwcrihed by Dr. Tuft, is certainly well recognized and was briefly revielved in the oprninK paragraph and in the discussion section of our report. The unique feature of the patient whom we described was the presence, followirr~ steroid ~vithdramal, of atelectasis involving various lung segments without clinical or hro,r choscopic cridence of mucous plugs or bronchospasm. Obstructive factors could not bc ~Io,-u-