Smooth muscle degeneration of the mesenteric and branching veins causing ischemic enteritis: a case report

Background Ischemic bowel injuries are generally caused by arteriosclerosis, thromboembolism, or vasculitis. Ischemic enteritis is less common than ischemic colitis because of the rich collateral arteries of the small intestine. In the present case, smooth muscle degeneration of the mesenteric to th...

Full description

Saved in:
Bibliographic Details
Published in:Surgical case reports Vol. 8; no. 1; p. 1
Main Authors: Sunakawa, Taiki, Ito, Nobuo, Moriyasu, Ryo, Seki, Nobuya, Takeuchi, Daisuke, Sasahara, Kotaro
Format: Journal Article
Language:English
Published: Berlin/Heidelberg Springer Berlin Heidelberg 04-01-2022
Springer Nature B.V
SpringerOpen
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background Ischemic bowel injuries are generally caused by arteriosclerosis, thromboembolism, or vasculitis. Ischemic enteritis is less common than ischemic colitis because of the rich collateral arteries of the small intestine. In the present case, smooth muscle degeneration of the mesenteric to the submucosal veins caused ischemic enteritis and small bowel obstruction. Case presentation An 85-year-old woman with recurrent enteritis eventually developed small bowel obstruction. We performed laparoscopic partial resection of the small intestine. The pathological findings revealed smooth muscle degeneration of the mesenteric veins that caused ischemic enteritis. Venous changes were detected not only in the injured region, but also in a part of the normal region of the resected specimen. She continued to experience some minor symptoms postoperatively; however, these symptoms subsided in a short period with medicine discontinuation. Conclusion This report shows the possibility that a disease causes ischemic enteritis with unique venous pathological changes and may recur postoperatively.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:2198-7793
2198-7793
DOI:10.1186/s40792-021-01353-x