Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
296
pubmed:dateCreated
1993-12-1
pubmed:abstractText
Dysbaric osteonecrosis (DON) can occur in humans and sheep after a single hyperbaric air exposure with inadequate decompression. The authors hypothesize that DON does not result from primary embolic or compressive effects of nitrogen bubbles on the osseous vasculature, but by secondary injury to the marrow adipose tissue by rapidly expanding nitrogen gas that triggers local, and possibly systemic, intravascular coagulation. A 28-year-old scallop diver remained at a depth of 92 feet in sea water for 4.5 hours on surface-supplied compressed air. Decompression sickness occurred after a no-stop ascent to the surface, and he died 70 minutes later. Autopsy showed multiple gas bubbles, not only within the great vessels, but in the fatty marrow of his femoral and humeral heads. Lipid and platelet aggregates were found on the surface of marrow bubbles. Fibrin-platelet thrombi were detected within dilated venous sinusoids adjacent to bubbles, and in veins, capillaries, and arterioles. Since pulmonary, renal, and intraosseous (subchondral) fat embolism and fibrin thromboses were observed, it is suggested that injured marrow adipocytes can release liquid fat, thromboplastin, and other vasoactive substances, which conceivably can also play a systemic procoagulant role in triggering disseminated intravascular coagulation and additional DON.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0009-921X
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
256-64
pubmed:dateRevised
2005-3-3
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
The pathophysiologic role of fat in dysbaric osteonecrosis.
pubmed:affiliation
Diagnostic Osteonecrosis Center, Kelseyville, California.
pubmed:publicationType
Journal Article, Case Reports