This observational study of women with a history of OASI was designed to assess the impact of EAUS and anal manometry on their management in the postnatal and subsequent antenatal period. We found that in a subsequent pregnancy following OASI, there was a significant improvement in anal manometry pressures and reported anorectal symptoms compared to 3 months following OASI. To our knowledge, this is the first study to investigate the variation in outcomes using validated anal incontinence scores, anal manometry and EAUS at these two time points using a set protocol which aids clinicians in recommending the mode of subsequent delivery.
When endoanal ultrasound is completed postpartum following OASI by experienced clinicians, the interobserver agreement has been shown to be good [19, 20]. Starck et al. [19] previously investigated the interobserver agreement in the detection of anal sphincter defects using EAUS in asymptomatic women. In their study there was strong interobserver agreement in the detection of anal sphincter defects on EAUS. However, disagreement about the detection of anal sphincter defects occurred in 9 out of 97 women (9.3%), with the majority being due to disagreement surrounding the extent of an EAS defect (eight proximal partial EAS defects and one combined proximal EAS and IAS defect). It is therefore not surprising that in our study, although all scans were reviewed by one of the two consultants experienced in endoanal ultrasound, there was a discrepancy with the findings at the postpartum and subsequent antenatal period in 9.6% of scans, with most being due to disagreement with the extent of an EAS defect by 1 h, meaning their defect was now classified as > 1 h. This highlights that the size of an anal sphincter defect is unlikely to change with a subsequent pregnancy and most changes in scan findings noted are secondary to systematic interobserver error.
In our study, the average time between postpartum review following OASI and assessment in the subsequent pregnancy was 30 months. Injury to the anal sphincter during vaginal delivery can be mechanical, neuropathic or a combination of both [17] with each factor giving rise to anal incontinence. The pelvic floor musculature is innervated by the sacral nerves (S2-S4) from which the pudendal nerve also arises. The EAS is innervated by the inferior rectal branch of the pudendal nerve [21]. Injury to the pudendal nerve may be secondary to mechanical stretching and/or compression of the nerve by the foetal head, a large for gestational age foetus, prolonged second stage of labour or forceps delivery [21, 22]. However, the neuropraxia from stretch or compression injury usually recovers and muscle reinnervation occurs within 6 months [17, 23, 24]. This could explain why the iMSP, which correlates with anal sphincter function [18], increased significantly between the time period of 30 months following OASI and the subsequent pregnancy in those women with a sphincter defect ≤ 1 h. However, another reason for functional improvement is recovery of muscle strength with pelvic and anal sphincter exercises. In our dedicated perineal service, all women who have sustained an OASI are advised to start pelvic floor muscle training (PFMT) [25]. Information is provided using patient information leaflets and mobile health applications prior to discharge [26]. Women who are unable to contract their muscles effectively are referred to the colorectal nurse specialist for electrical muscle stimulation.
Up to 24% of women experience anal incontinence following OASI and repair by 2 months postpartum [27]. Women should be advised about the benefits of PFMT after OASI in reducing anorectal symptoms [28]. It has been shown that compared to initiation of PFMT 6 to 8 weeks after delivery, PFMT initiated within 4 weeks following OASI results in a significantly greater improvement in anorectal symptoms [28]. In particular, the risk of flatal incontinence and liquid stool incontinence was reduced by 50% and 80%, respectively, when PFMT was initiated early [26]. This may explain why anorectal symptoms had significantly improved during the period up to the subsequent pregnancy following OASI. However, although the mean follow-up time was 30 months, this may still be relatively short term with regard to the development and deterioration of anorectal symptoms. Women with a history of OASI tend to develop anal incontinence in their 50s because of additional factors such as ageing and menopause [29].
A recently published meta-analysis evaluating the risk of anal sphincter defects diagnosed on EAUS following OASI showed that 45% of women who had undergone primary repair of OASI did not have a residual defect [1]. At present, in our perineal clinic [4] we assess women who have sustained OASI both at 3 months postpartum and in the second half of a subsequent pregnancy. However, we showed that up to 77% of women (n = 76) with no residual defect on EAUS had normal anal manometry and were either asymptomatic or reported minor anorectal symptoms (SMIS ≤ 4) at 3 months following OASI. The proportion of these women with normal anal manometry and an SMIS ≤ 4 increased to 87% (n = 87) in subsequent pregnancy. In accordance with our perineal clinic protocol [4] as there was no EAUS defect (> 1 h), a vaginal delivery would have been recommended both at 3 months postpartum and in subsequent pregnancy. It is however important to note that the anal manometry pressures, a direct indicator of anal sphincter function [2] and reported SMIS, were significantly worse in women with a sphincter defect > 1 h compared to those ≤ 1 h. Our study therefore indicates that our current protocol needs re-appraisal for women who are asymptomatic and have normal anal manometry pressures and EAUS findings 3 months postpartum. Based on this study, if the protocol is modified, 76 (52.1%) women in this study could have had their mode of delivery recommendation made in the postnatal period and therefore these women would not require further review in their subsequent pregnancy. This new policy would avoid unnecessary intrusive investigations being repeated, with attendant financial savings.
The strengths of this study include, first, the use of a standardized protocol [4] and validated tools such as the SMIS [15] to assess anal sphincter function following OASI. Second, the study design comprised prospective collection of the data and independent review of EAUS images by two clinicians experienced in endoanal ultrasound. Third, there was relatively long-term reporting of anorectal symptoms (mean follow-up duration at the time of subsequent pregnancy of 30 months). The limitations include the lack of cost-benefit analysis, which would provide further evidence to support a policy change.
In conclusion, this study showed that following OASI the majority of women do not have a residual anal sphincter defect following a primary repair. Also, there is a significant improvement in reported anorectal symptoms and the incremental anal manometry pressure in a subsequent pregnancy. Therefore, women who remain asymptomatic and have normal anal manometry and no residual sphincter defects on EAUS at postnatal assessment do not need to have these investigations repeated in a subsequent pregnancy and can be recommended to have a vaginal delivery. However, as described previously, those postpartum women who are symptomatic, have compromised anal sphincter function or have anal sphincter defects should be reassessed with these investigations in subsequent pregnancy [4].