Role of pudendal canal syndrome in the etiology of fecal incontinence in rectal prolapse.

BACKGROUND

The current communication investigates the role of pudendal canal syndrome in the genesis of fecal incontinence (FI) in complete rectal prolapse (CRP).

METHODS

89 patients with CRP (group A, 45 with FI, and group B, 44 without FI) were studied. Ten healthy volunteers in group C acted as controls. The subjects were assessed for rectal and rectal neck pressures, electromyographic (EMG) activity of the external anal sphincter (EAS) and levator ani, as well as for pudendal nerve terminal motor latency (PNTML).

RESULTS

Group-A patients manifested perianal hypo- or anesthesia, diminished rectal neck pressure (p < 0.05) and EMG activity of EAS and levator muscle and prolonged PNTML (p < 0.05). In group B, rectal neck pressure was diminished (p < 0.05) in all patients. The EMG activity of the EAS and PNTML (p > 0.05) were normal in 34 patients, while the EMG activity was reduced and the PNTML prolonged (p < 0.05) in the remaining 10. The levator ani muscle showed diminished activity in the 44 patients of this group.

CONCLUSION

The results of group A point to pudendal neuropathy as a cause of FI. In group B, 10 patients showed manifestations of subclinical pudendal neuropathy which may present later on with FI. The constant prolongation of PNTML in patients with FI postulates a relationship between the two. The cause of prolonged PNTML seems to be attributable to pudendal neuropathy due probably to pudendal nerve entrapment in the pudendal canal with a resulting pudendal canal syndrome. Therefore, pudendal canal syndrome is suggested to play a significant role in the genesis of FI in CRP.