Fatal Bronchial Asthma

Craige, Branch

doi:10.1001/archinte.1941.00200020161010

Cited by 23 publications

(3 citation statements)

References 6 publications

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“…Huber and Koessler (1922) summarized those 15 cases together with six of their own. Since then at least six outstanding articles (Lamson and Butt, 1937;Thieme and Sheldon, 1938;Craige, 1941;Rackemann, 1944;Unger, 1945;Walton et al, 1951) have appeared, dealing with conjoint clinical and necropsy findings, the most recent of which stresses the low number of recorded cases and gives the opinion that this could be due to lack of recognition of the condition at necropsy.…”

Section: Discussionmentioning

confidence: 99%

Fatal Bronchial Asthma

Robertson¹,

Sinclair²

1954

BMJ

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Section: Discussionmentioning

confidence: 99%

Fatal Bronchial Asthma

Robertson¹,

Sinclair²

1954

BMJ

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“…Although several excellent case reports with postmortem examination appeared in the German literature in the late 19th century (9,34), Huber & Koessler's report in 1922 provided one of the earliest systematic studies of the morbid anatomy of asthma in English (26). Studies reported more recently have revealed that asthma mortality has increased and there is some evidence that this increase could be related to new therapeutic agents (1, 3, 4, 7,16,25,27,31,39,51,57,64).…”

mentioning

confidence: 99%

The pathology of asthma

Hogg¹

1997

APMIS

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Hogg, J. C. The pathology of asthma. Review article. APMIS 105: 735-745, 1997. Asthmatics respond with reversible airway narrowing when stimulated in ways that have no effect on non-asthmatic persons. Studies conducted at the turn of this century established that the pathology present in the airways of asthmatics is based on the inflammatory process. Recent work suggests that this inflammatory response may be driven by a particular group of T cells (Th2 response) that cause an overproduction of IL-4, IL-5 and other cytokines that produce an excessive infiltration of eosinophils and overproduction of IgE. The structural changes produced by the inflammatory process result in an overall thickening of the airway wall with changes in the epithelium, an increase in the interstitial matrix particularly the collagen types that contribute to the light microscopic appearance of the basement membrane, the vasculature, smooth muscle and mucous glands. Contraction of airway smooth muscle results in narrowing of the lumen particularly in the bronchioles where smooth muscle surrounds the entire lumen. An increase in wall tissue thickness as a result of asthma amplifies this normal effect producing a greater reduction in the airway lumen. Computer modelling of airway function and direct measurement of airway resistance in patients suggest that the smaller airways are the site of the greatest increase in airway resistance in asthma. These new data have shifted the emphasis away from the concept that abnormal airway smooth muscle function causes asthma toward the hypothesis that inflammatory-based changes in the airway wall act in series with normal smooth shortening to produce disease. The increased understanding of the role of the inflammatory process provides a basis for treatment of asthma with anti-inflammatory agents. LL 0 lJ!rL!-0 8 10 12 14 16 18 20 22 24

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“…THE ROLE OF DRUGS.-Morphine is generally incriminated as a precipitating cause of death. Clarke (1930), Thieme and Sheldon (1938), Craige (1941), Thomson (1945), Unger (1945, and Serafini (1950) all describe patients dying within a few hours of having morphine. Facquet and Claisse's patients (1939) died a few mihutes after having been given the drug.…”

Section: Present Series Of Fatal Casesmentioning

confidence: 99%

Fatal Bronchial Asthma: A Series of Fifteen Cases with a Review of the Literature

Earle¹

1953

Thorax

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Fatal Bronchial Asthma

Cited by 23 publications

References 6 publications

Fatal Bronchial Asthma

Fatal Bronchial Asthma

The pathology of asthma

Fatal Bronchial Asthma: A Series of Fifteen Cases with a Review of the Literature

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