Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by CHARR, R.
Right arrow Articles by SAVACOOL, J. W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by CHARR, R.
Right arrow Articles by SAVACOOL, J. W.
(Chest. 1944;10:103-114.)
© 1944 American College of Chest Physicians

Collapsed Lung—Postmortem Findings

ROBERT CHARR M.D., F.C.C.P.1 and J. WOODROW SAVACOOL M.D.1

1 From the Department for Diseases of the Chest, Jefferson Hospital, Philadelphia, and White Haven Sanatorium, White Haven, Pennsylvania

1) Pulmonary changes in collapse therapy were studied at autopsy in 49 cases.

2) Pleural inflammation with or without effusion was a constant finding and it was usually related to the tuberculous lesions in the underlying lung. Tuberculous empyema occurred from rupture of adhesions or of subpleural tubercles rather than from faulty operative technique.

3) Selective collapse was caused apparently by atelectasis resulting from occlusion of diseased bronchioles in the tuberculous areas.

4) Dilatation of the so-called giant or ball-valve cavities depended upon tuberculous changes of several types in the draining bronchi which permitted air to enter but prevented it from leaving the cavities.

5) Panarteritis, leading to thrombosis and sclerosis in the tuberculous areas was a constant finding and resulted in considerable loss of blood supply about the chronic fibrotic cavities. This appeared to be responsible for failure of such cavities to undergo healing even under satisfactory collapse.

6) Vascular changes around recent cavities were minimal, the blood supply being therefore practically unimpaired. This appeared to contribute to the healing of such cavities which occurred by concentric collapse and fibrosis.

7) Phrenic nerve paralysis caused extensive fibrosis of the paralyzed portion of the diaphragm and brought about relatively greater rise of the central and posterior portions of the diaphragm than of the anterior portion. Consequently the posterior and central cavities were more influenced by phrenic paralysis than the anterior ones.

8) It is suggested that collapse therapy in chronic pulmonary tuberculosis should be carried out before vascular and fibrotic changes are too great to permit concentric cavity closure and anatomic healing. Serious complications almost never occurred in early tuberculosis in which there was satisfactory collapse of the lesions.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1944 by the American College of Chest Physicians.