Urinary incontinence is a common symptom in pregnancy and has been reported in up to 85% of women. Women reporting antenatal stress urinary incontinence (SUI) are at an increased risk for future SUI. De novo SUI has been reported to develop in 7% of primigravid women immediately following vaginal delivery but this only persisted in 3% at one year. The most likely mechanism is a combination of nerve and tissue damage. At five-year follow up, 19% of women without urinary symptoms after the first delivery reported SUI. In contrast 92% of women reporting stress incontinence three months after delivery, had SUI five years later. Antepartum incontinence has also been reported to strongly predict postpartum incontinence. It is remains unclear as to whether it is the pregnancy or specifically the vaginal delivery that is the risk factor for developing urinary incontinence. It would appear that vaginal delivery roughly doubles a woman’s chance of developing UI.
It is important to remember that after adjusting for other potential causes of pelvic floor damage, a woman’s risk for moderate to severe incontinence decreases from about 10% to 5% if all of her children are delivered by caesarean section. The protective effect of caesarean delivery and nulliparity dissipates around the sixth decade of life, such that the women have the same incidence of UI regardless of their delivery status.
AI is a distressing social handicap and vaginal delivery is a major etiological factor. AI occurs in as many as 29% of women nine months after delivery. The reported incidence of AI following anal sphincter rupture is in the region of 16-47%. There is some evidence to suggest that elective caesarean section is protective against AI but the impact of delivery mode appears to decline with age. The use of forceps is the single independent risk factor associated with anal sphincter damage and the development of AI. The first vaginal delivery has been suggested to be the most significant event leading to damage of the anal sphincter. Retrospective studies have reported that the prevalence of AI 30 years after delivery was comparable, regardless of mode of delivery.
Pelvic organ prolapse
Pelvic support defects appear to occur before delivery. Pregnant women have been shown to be more likely to have POP than their nulliparous counterparts. Parity increases the risk for POP and is the variable most strongly related to surgery for POP. We await prospective studies on the impact of vaginal delivery and intrapartum management, on the development and prevention of defects in the connective tissue and levator muscles that lead to pelvic organ prolapse.
There appears to be a strong association between the development of pelvic floor disorders including UI, AI and POP and pregnancy and childbirth. Mechanisms of injury include direct muscular trauma, disruption of connective tissues, and denervation injury. The first vaginal delivery is the most significant event impacting of the development on subsequent pelvic floor dysfunction. Other risk factors include advanced maternal age at first delivery, prolonged second stage of labour, delivery of a large baby, midline episiotomy, and the use of a forceps for delivery. Less pelvic floor damage may occur after elective caesarean section, but not necessarily with emergency caesarean section. The advantage of caesarean section appears, however, to dissipate in the long term in the majority of women and it is therefore not recommended in all women. It will not only be unnecessary in at least 50% of parturients, but many women desire the experience of vaginal delivery. Ideally, women should be offered strategies to reduce pelvic floor injury such as pelvic floor exercises. Adequate management of labour is essential and elective caesarean section should only be offered to women at high risk for pelvic floor damage.