Pelvic floor muscle fibers are divided into two types: type I muscle fibers (slow muscle fibers) and type II muscle fibers (fast muscle fibers) [26]. The interaction among pelvic floor muscles, fascia, and ligaments is essential to support the normal physiological state and function of pelvic organs [27]. Damage to the pelvic floor muscle fibers can lead to structural defects and dysfunction of the pelvic floor, which in turn can lead to postpartum UI and POP [28–31]. We found that abnormal postpartum vaginal dynamic pressure and injuries to the pelvic floor type I and II muscle fibers were common phenomena in the twin pregnancy population regardless of whether GWG was adequate or excessive. Excessive GWG further increased the risk of pelvic floor muscle damage, with a high rate of abnormal vaginal dynamic pressure of 95% (19/20) and severely damaged postpartum type I muscle fibers of 80% (16/20) in this group.
This study also found that, just as there was a higher proportion of abnormal dynamic vaginal pressure and severe damage to type I muscle fibers in the excessive GWG group, there was also a higher incidence of postpartum anterior vaginal wall prolapse and SUI in this group, the mechanism of which may be related to pelvic floor muscle damage due to excessive GWG [32]. During pregnancy, in the absence of pathological edema such as preeclampsia, heart failure, or nephropathy, excessive GWG is mainly associated with excessive maternal fat gain [13]. Excessive fat accumulation can create increasing and continuous pressure on the pelvic floor muscles and bladder, resulting in increased intra-abdominal pressure, leading to weakening of the pelvic floor muscle strength and destruction of fascia, causing damage to ligaments, nerves, blood vessels, and other tissues, thus changing the normal structure and anatomical position of the urethra and bladder and causing them to lose their original support, which are the pathophysiological reasons for the occurrence of POP and SUI [33–35].
We found that the prevalence of postpartum anterior vaginal wall prolapse in twin primipara was 71.20% by the POP-Q examination, and the rate was as high as 90% in the group with excessive GWG. The occurrence of anterior vaginal wall prolapse was significantly associated with excessive GWG (OR = 4.705, 95% CI: 1.004–22.054). A review of the literature by Lee [33] found that the prevalence of POP showed an increasing trend with increasing BMI. A randomized double-blind study [36] investigated 16608 women and found that POP progressed with weight gain, but prolapse did not improve with weight loss. Another randomized controlled study of overweight/obese women assessed subjects by the POP-Q system and reached the same conclusion [37]. These findings may indicate that the pelvic floor damage caused by excessive weight gain is irreversible. From this, we can infer that preventing excessive GWG and keeping GWG within reasonable limits may reduce the occurrence of irreversible POP.
UI is a common disease that affects women's quality of life. SUI, UUI, and MUI are the main types, among which SUI is most common in postpartum women [38]. The results of this study showed that the incidence of postpartum SUI, UUI and MUI in twin primiparas was 23.37%, 13.59%, and 5.98%, respectively, which was similar to the findings of a prospective longitudinal study conducted by KarenNg et al on singleton women [39]. We also found that SUI occurred in up to 50% (10/20) of twin primiparous women in the excessive GWG group, which was significantly higher than that in the group with suitable GWG (P < 0.009). The prevalence of SUI was significantly positively correlated with GWG excess (OR = 4.424, 95% CI: 1.578–12.403). A systematic review and meta-analysis that included 46 studies with 73010 subjects came to a similar conclusion: excessive GWG was associated with postpartum SUI [12]. We thus speculated that excessive GWG may play an etiological role in the development of SUI in twin primiparas.
Some studies have reported that the prevalence of postpartum SUI gradually decreases over time [40, 41]. Possibly due to differences in study populations and follow-up time, more studies have found the opposite: the effects of postpartum SUI on women's health are sustained, and over time, the cumulative incidence of SUI increases significantly [39, 42–46]. Other studies have found that the persistence of postpartum SUI is caused by higher BMI and excessive GWG in pregnant women [14, 39, 47, 48]. From these results, it is clear that control of excessive GWG is essential for the prevention of postpartum SUI. Preventive care for SUI should be provided throughout the life span of adult females, in addition to covering pregnancy and the puerperium period.
A study assessing the correlation between obesity and POP symptoms in Korean women found no significant correlation between obesity and the severity of POP symptoms [49]. This finding corroborates our results. This study found that although excessive GWG increased the prevalence of PFDs, it did not further exacerbate pelvic floor symptoms in twin primiparas. This may be related to the small sample size of the excessive GWG group in this study and may be the reason why the effect of excessive GWG on pelvic floor symptoms no longer increases after reaching a critical threshold level. The results of this study remind us that although excessive GWG does not exacerbate pelvic floor symptoms, pelvic floor injury and anatomical changes have occurred, and the negative impact of excessive GWG on the pelvic floor should not be overlooked as a result.
Although the birth rate of twins has increased significantly in recent decades, access to the sample is still limited compared to that of singletons. The above study sample was only from one tertiary teaching hospital in China, and there is still a need for a multicenter, large sample study to minimize bias. In assessing the effect of GWG on pelvic floor function, we only focused on the total growth of GWG and did not pay attention to the effect of the rate of weight gain at different periods of pregnancy. Additionally, this study did not explore postpartum pelvic floor function in the prepregnancy underweight and insufficient GWG groups, which will be the direction of follow-up research. The present study on the relationship between excessive GWG and pelvic floor function in twin primiparas is retrospective, and the argument for causality needs to be further confirmed by prospective cohort studies and randomized controlled trials.