Rectal prolapse pathophysiology
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Rectal prolapse Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shaghayegh Habibi, M.D.[2]
Overview
Pathophysiology
Pathogenesis
The evolution of rectal prolapse starts from excessive straining over time that leads to the weakness of pelvic floor muscles and connective tissue injury (including nerve injury and neuropathy of the pelvic floor) thereby leading to rectal intussusception initially, followed by external mucosal prolapse, and eventually a full protrusion of all layers of the rectal wall through the anus.
In severe cases, the large mass cannot reduce spontaneously, and may become incarcerated or strangulatied. Both complete rectal prolapse and internal intussusception can occur independently or can be associated with the descent of other pelvic organs, e.g., uterine or vaginal vault prolapse. Pre-existing dyssynergic defecation that cause chronic excessive straining may coexist.
Associated Conditions
Rectal prolapse is associated with several coexisting anatomic abnormalities:[1]
- Diastasis of the levator ani
- Abnormally deep cul-de-sac
- Redundant sigmoid colon
- Patulous anal sphincter
- Loss or attenuation of the rectal sacral attachments
References
- ↑ Bordeianou L, Paquette I, Johnson E, Holubar SD, Gaertner W, Feingold DL, Steele SR (2017). "Clinical Practice Guidelines for the Treatment of Rectal Prolapse". Dis. Colon Rectum. 60 (11): 1121–1131. doi:10.1097/DCR.0000000000000889. PMID 28991074.