Interest in the diagnosis and appropriate repair of obstetric anal sphincter injuries (OASIS) has been rekindled in the last two decades by the advent of endoanal endosonography. However, many issues remain to be resolved. The authors of this manuscript deserve commendation as they have now added another spoke to this ever-turning wheel. The external anal sphincter (EAS) is a striated muscle and damage to this muscle is usually associated with urgency and urge fecal incontinence. The internal anal sphincter (IAS) is a smooth muscle that maintains most of the resting tone and is responsible for ‘fine tuning’; its function is largely to control flatus and prevent passive soiling. Both these muscles work in concert to orchestrate the mechanism of maintaining anal continence. In their paper, Norderval et al. aimed to determine whether a better outcome could be obtained when a full-length repair of the EAS was achieved combined with separate repair of the torn IAS. Ideally, a randomized controlled study would have provided the best evidence, but it would be ethically difficult to justify not repairing a disrupted ring of functional IAS. Instead, they compared the outcome to that in a control group from some years earlier when the IAS was not routinely reconstructed as a separate entity. They found that improved continence status was associated with better longitudinal reconstruction of the EAS. This is an important finding, as it has previously been shown in patients with fecal incontinence who have undergone a secondary sphincter repair that the single independent predictor for subsequent continence was restoration of anal sphincter length1. A full-length primary repair is indeed achievable as the EAS has a well-defined proximal border. Indeed, Norderval et al. have shown in a previous study that shorter anal length following primary anal sphincter repair is associated with poorer outcome2. In contrast to the EAS, the IAS is a continuation of the circular muscle of the rectum, which becomes thickened distally to form the IAS. Its proximal margins are less well defined. In general, as the IAS is enveloped by the EAS, the EAS would have to be disrupted first before the IAS can tear, except proximally as the EAS is shorter in its anterior aspect. However, although this phenomenon has been demonstrated using endoanal ultrasound, it is not a common finding and isolated partial length IAS damage appears to have no physiological or clinical significance. The use of a validated endoanal ultrasound scoring system has ensured standardized reporting. As not all anal sphincter defects are associated with functional compromise, it may have been useful for Norderval et al. to perform anal manometry (measuring anal length and resting and squeeze pressures) to complement the ultrasound findings. The authors did not find a difference in size or length of IAS defects between the groups. While this finding could have been different with larger numbers, it could also reflect obstetricians' lack of familiarity with the IAS, although its identification and separate repair was described over a decade ago3. Consequently, the full extent of the IAS tear may not be identified and repaired. This highlights a very important issue, as the best, and possibly only, opportunity to repair a freshly torn IAS is by an obstetrician following delivery. Once fibrosis has occurred, colorectal surgeons find it very difficult to repair the IAS defect and therefore most colorectal surgeons simply divide and overlap the fibrosed anterior sphincter bulk of tissue. In their study, women with a prior vaginal delivery had an inferior outcome regardless of the mode of repair. One explanation given is that OASIS may have been undiagnosed after the first vaginal delivery. This is very plausible, as it has been shown that a considerable number of anal sphincter tears are not diagnosed at delivery and focused training can improve the diagnostic yield4. However, as over 80% of anal sphincter tears occur with the first vaginal delivery, the incidence of such injuries in multiparous women should be low. Finally, the authors should be excused for being unable to reach the intended number of women in this study. The reason for this was that the number of women sustaining OASIS was dramatically reduced following an intervention program that was implemented in four different units in Norway5. Over the last two decades we have come a long way. Using endoanal endosonography we established that OASIS were being missed because clinical training was suboptimal. Studies conducted by Norderval and others have explored better surgical techniques. The time has now come to focus on preventative strategies and implement training sessions like the Norwegian intervention program at a global level. Only then can we minimize the occurrence of OASIS with its attendant morbidity on women's quality of life. A. H. Sultan*, * Department of Obstetrics and Gynaecology, Croydon University Hospital, London Road, Croydon CR7 7YE, Surrey, UK
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Apr 1, 2017
Kumaran Thiruppathy + 4
Open Access
