Experimental models of neuropathic fecal incontinence: an animal model of childbirth injury to the pudendal nerve and external anal sphincter.

Abstract

Childbirth is the most common cause of fecal incontinence and damage to the pudendal nerve is a major component of childbirth injury. This study was designed to develop an acute animal model of injury to the innervation of the external anal sphincter. Forty-eight female virgin wistar rats were studied. Two models of neuropathic injury were developed. Bilateral inferior rectal nerve crush (Group A) acted as a positive control. Prolonged intrapelvic retrouterine balloon inflation (Group B) simulated the pelvic compressive forces of labor. Quantitative analysis of external anal sphincter muscle function was performed by using electromyography, external anal sphincter specific force production, and stereologic calculation of external anal sphincter mass. Injury in both groups caused significant atrophy of the external anal sphincter (P = 0.002, ANOVA) and electromyographic evidence of reinnervation at one week. Specific force (mN force per mg mass) was not altered. External anal sphincter muscle mass recovered after four weeks in Group B. Balloon dilation within the boney pelvis results in denervation of the external anal sphincter and offers an experimental model of the effects of childbirth on the continence mechanism in humans.