You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 108 No. 2, Aug 1961 TABLE OF CONTENTS
  Archives
  •  Online Features
  ARTICLES
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati
What's this?

A Study of Pulmonary Embolism

Part II. The Mechanism of Death; Based on a Clinicopathological Investigation of 100 Cases of Massive and 285 Cases of Minor Embolism of the Pulmonary Artery

L. WHITTINGTON GORHAM, M.D.

Arch Intern Med. 1961;108(2):189-207.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

An obstructive embolus in the main stem or in one of the two principal branches of the pulmonary artery almost invariably causes sudden death as has been shown in the 100 cases of massive pulmonary embolism described in Part I. A large coiled-up embolus originating in a femoral vein produces only minimal pathologic changes in the lungs, such as edema and atelectasis. By contrast, when a medium-sized artery is blocked, characteristic changes take place in the lung parenchyma supplied by this vessel. As a result of the stoppage of blood flow, the alveoli and capillaries become markedly distended with red blood cells, and a red infarct forms. Pulmonary infarcts are seldom white or anemic but are almost always hemorrhagic, because of the rapid anastomosis which develops between the pulmonary and bronchial vessels, when obstruction occurs in the former. Later if the patient recovers the red cells degenerate, and the alveolar . . . [Full Text PDF of this Article]


Author Affiliations

NEW YORK

From the Department of Pathology, New York Hospital-Cornell Medical Center.; Research Associate in the Department of Pathology; Research Consultant, Goldwater Memorial Hospital, First Research Service of the College of Physicians and Surgeons, Columbia University; Professor of Medicine (Emeritus), Albany Medical College of Union University; Director (Emeritus) of the Public Health Research Institute of the City of New York, Inc.


Footnotes

Submitted for publication Aug. 19, 1960.

Editor's Note.—Only Part II of this excellent monograph appears in this issue of the Archives. Part I appeared in the previous issue. Part III will appear in the next issue. The tables are quite extensive, so only selected cases from the longer ones will appear in these pages. Full tables will be included in the author's reprints.



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati     What's this?





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1961 American Medical Association. All Rights Reserved.