Ogilvie syndrome pathophysiology: Difference between revisions
No edit summary |
|||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
Please help WikiDoc by adding content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing. | Please help WikiDoc by adding content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing. | ||
{{Ogilvie syndrome}} | {{Ogilvie syndrome}} | ||
| Line 5: | Line 6: | ||
==Overview== | ==Overview== | ||
==Pathophysiology== | ==Pathophysiology== | ||
The | |||
=== Pathogenesis === | |||
The precise mechanism by which colonic dilation occurs in patients with acute colonic pseudo-obstruction is unknown. The association with trauma, spinal anesthesia, and pharmacologic agents suggests an impairment of the autonomic nervous system. Interruption of the parasympathetic fibers from S2 to S4 leaves an atonic distal colon and a functional proximal obstruction . However, there is no proposed mechanism to explain colonic dilation in those patients without obvious involvement of the parasympathetic nerves. | |||
In patients with acute colonic pseudo-obstruction, increasing colonic diameter accelerates the rise in tension on the colonic wall, increasing the risk of colonic ischemia and perforation. The risk of colonic perforation increases when cecal diameter exceeds 10 to 12 cm and when the distention has been present for greater than six days [12]. The duration of dilation is probably more important than the absolute diameter of the colon. | |||
Rare cases have been reported in association with atrophic visceral myopathy with an extremely thin colonic wall, atrophic circular, and longitudinal muscularis propria without inflammation or fibrosis, and unaffected ganglion cells and myenteric plexus. The cause of the smooth muscle atrophy was unclear and the only potential association was with prior hypothyroidism. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
Revision as of 15:15, 26 January 2018
Please help WikiDoc by adding content here. It's easy! Click here to learn about editing.
| Ogilvie syndrome Microchapters
|
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Ogilvie syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Ogilvie syndrome pathophysiology |
|
Risk calculators and risk factors for Ogilvie syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Pathogenesis
The precise mechanism by which colonic dilation occurs in patients with acute colonic pseudo-obstruction is unknown. The association with trauma, spinal anesthesia, and pharmacologic agents suggests an impairment of the autonomic nervous system. Interruption of the parasympathetic fibers from S2 to S4 leaves an atonic distal colon and a functional proximal obstruction . However, there is no proposed mechanism to explain colonic dilation in those patients without obvious involvement of the parasympathetic nerves.
In patients with acute colonic pseudo-obstruction, increasing colonic diameter accelerates the rise in tension on the colonic wall, increasing the risk of colonic ischemia and perforation. The risk of colonic perforation increases when cecal diameter exceeds 10 to 12 cm and when the distention has been present for greater than six days [12]. The duration of dilation is probably more important than the absolute diameter of the colon.
Rare cases have been reported in association with atrophic visceral myopathy with an extremely thin colonic wall, atrophic circular, and longitudinal muscularis propria without inflammation or fibrosis, and unaffected ganglion cells and myenteric plexus. The cause of the smooth muscle atrophy was unclear and the only potential association was with prior hypothyroidism.