Mechanisms of decubitus ulcer formation — An hypothesis

Understanding of the etiology of decubitus ulcer formation is fragmentary and the existing literature contains much experimental data that are inconsistent with the idea that pressure sore formation is due extensively to depriving a tissue region of blood. In fact, there is substantial data that ill...

Full description

Saved in:
Bibliographic Details
Published inMedical hypotheses Vol. 4; no. 1; pp. 37 - 39
Main Authors Krouskop, Thomas A., Reddy, Narender P., Spencer, William A., Secor, John W.
Format Journal Article
LanguageEnglish
Published United States Elsevier Ltd 1978
Subjects
Animals
Dogs
Humans
Lymphatic System - physiopathology
Pressure
Pressure Ulcer - physiopathology
Rabbits
Rats
Online AccessGet full text

Cover

More Information
Summary:Understanding of the etiology of decubitus ulcer formation is fragmentary and the existing literature contains much experimental data that are inconsistent with the idea that pressure sore formation is due extensively to depriving a tissue region of blood. In fact, there is substantial data that illustrate that tissue can remain viable for very extended lengths of time, up to 13 hours, when subjected to externally applied pressures that collapse the blood microvasculature in a region. Based on these observations and on studies done in this laboratory on lymph propulsion and pressure sore prevention, an hypothesis has been formulated that is consistent with the published data and with clinical observations. The hypothesis states that a major contributing factor to pressure sores is the tissue necrosis that is caused by the accumulation of anaerobic metabolic waster products due to occlusion of the lymph vessels.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0306-9877
1532-2777
DOI:10.1016/0306-9877(78)90025-7