Faecal incontinence after childbirth

Lacerations of the anal sphincter or injury to sphincter innervation during childbirth are major causes of fecal incontinence, but the incidence and importance of occult sphincter damage during routine vaginal delivery are unknown. We sought to determine the incidence of damage to the anal sphincter and the relation of injury to symptoms, anorectal physiologic function, and the mode of delivery. We studied 202 consecutive women six weeks before delivery, 150 of them six weeks after delivery, and 32 with abnormal findings six months after delivery. Symptoms of anal incontinence and fecal urgency were assessed, and anal endosonography, manometry, perineometry, and measurement of the terminal motor latency of the pudendal nerves were performed. Ten of the 79 primiparous women (13 percent) and 11 of the 48 multiparous women (23 percent) who delivered vaginally had anal incontinence or fecal urgency when studied six weeks after delivery. Twenty-eight of the 79 primiparous women (35 percent) had a sphincter defect on endosonography at six weeks; the defect persisted in all 22 women studied at six months. Of the 48 multiparous women, 19 (40 percent) had a sphincter defect before delivery and 21 (44 percent) afterward. None of the 23 women who underwent cesarean section had a new sphincter defect after delivery. Eight of the 10 women who underwent forceps delivery had sphincter defects, but none of the 5 women who underwent vacuum extractions had such defects. Internal-sphincter defects were associated with a significantly lower mean (+/- SD) resting anal pressure (61 +/- 11 vs. 48 +/- 10 mm Hg, P < 0.001) six weeks post partum, and external-sphincter defects were associated with a significantly lower squeeze pressure (increase above resting pressure, 70 +/- 38 vs. 44 +/- 13 mm Hg; P < 0.001). There was a strong association (P < 0.001) between sphincter defects and the development of bowel symptoms. Occult sphincter defects are common after vaginal delivery, especially forceps delivery, and are often associated with disturbance of bowel function.

71 women delivered at St Bartholomew's Hospital, London, were studied by electrophysiological tests of the innervation of the external anal sphincter muscle and by manometry. The investigations were done 2-3 days after delivery and again, in 70% of these women, 2 months later. Faecal and urinary incontinence developing after vaginal delivery has been thought to be due to direct sphincter division, or muscle stretching, but the results of the study suggest that in most cases this incontinence results from damage to the innervation of the pelvic floor muscles.

Anal incontinence for gas or faeces affects up to 11% of adults, and occurs frequently in 2%. The commonest cause in healthy women is unrecognised damage to the anal sphincter during childbirth; 13% of women having their first vaginal delivery develop incontinence or urgency, and 30% have structural changes shown by anal endosonography. The commonest predisposing cause of damage is the use of forceps. When a third-degree tear occurs, 85% of women have persistent structural sphincter defects and 50% remain symptomatic despite primary repair after delivery. Structural damage associated with childbirth is more important than neurological factors. The characterisation of this sphincter damage has led to improved treatment, including successful surgical repair.