Etiology and management of fecal incontinence :

Skeletal muscle undergoes profound changes in morphological, physiological, and biochemical character when subjected to prolonged periods of increased use. Although increased use may be brought about in a variety of ways, the results show consistent features. In particular, endurance exercise and chronic stimulation differ only in degree: the properties which change in response to exercise are also those which change at an early stage of stimulation; the properties which are resistant to change under exercise conditions change only after prolonged stimulation. There is therefore a hierarchy of stability in the properties of skeletal muscle which is revealed in its response to changing functional demands. The adaptive potential of muscle provides a logical framework for understanding neural influences on the emergence of fiber types during muscle development. It is also relevant to the study of pathological conditions which may involve a sustained departure from normal postural and locomotor patterns of activity.

Biopsies of the external anal sphincter, puborectalis, and levator ani muscles have been examined in 24 women and one man with long-standing anorectal incontinence, 18 of whom also had rectal prolapse, and in two men with rectal prolapse alone. In 16 of the women anorectal incontinence was of unknown cause, but in eight there was a history of difficult labour. Similar biopsies were examined in six control subjects. In all the incontinent patients there was histological evidence of denervation, which was most prominent in the external anal sphincter muscle biopsies, and least prominent in the levator ani muscles. Myopathic features, which were thought to be secondary, were present in the more abnormal biopsies. There were severe histological abnormalities in small nerves supplying the external anal sphincter muscle in the three cases in which material was available for study. We suggest that idiopathic anorectal incontinence may be the result of denervation of the muscles of the anorectal sling, and of the anal sphincter mechanism. This could result from entrapment or stretch injury of the pudendal or perineal nerves occurring as a consequence of rectal descent induced during repeated defaecation straining, or from injuries to these nerves associated with childbirth.

The function of the anal sphincters has been studied by obtaining continuous recordings of the pressure in the anal canal and the electromyographic activity in the striated sphincter muscles during expansion of the ampulla recti by means of an air balloon. Ten healthy subjects were examined before and after the striated muscles had been entirely paralysed by bilateral pudendal block, making it possible to record the activity from the internal sphincter alone. The results show that the internal sphincter contributes about 85% of the pressure in the anal canal at rest but only about 40% after a sudden substantial distension of the rectum. During constant substantial rectal distension, the internal sphincter accounts for about 65% of the anal pressure. It is concluded that the internal sphincter in the adult is chiefly responsible for anal continence at rest. In the event of sudden substantial distension of the rectum, continence is maintained by the striated sphincter muscles, whereas both sphincter systems probably have an important function during constant distension of the rectum.