Abstract

Normal childbirth inevitably damages the pelvic floor, especially when non-evidence-based and potentially harmful obstetric practices are used during management of labor. Direct injury to the pelvic floor muscles significantly contributes to weakness of supportive function and development of support-related pelvic floor dysfunctions such as pelvic organ prolapse, urodynamic stress urinary incontinence (USI) and fecal incontinence (FI). Spontaneous perineal lacerations also commonly occur at vaginal delivery, particularly in primiparous women, causing either occult or recognized anal sphincter disruption with subsequent FI in 50% of cases [1]. Obstetric vesicoand rectovaginal fistulae represent the final “kiss of death” in a protracted labor scenario with ischemic necrosis and sloughing of the vaginal and bladder or rectal tissues interposed between the pelvic bones and presenting fetal part. Since the objective here is to focus on the earlier stages of birth trauma when recovery of pelvic floor supportive function is theoretically possible before loss of structural integrity of pelvic organs, obstetric fistulae will not be discussed further. Episiotomy has been traditionally performed by obstetric care providers to protect against direct trauma to the pelvic floor muscles during parturition. However, the value of this procedure is increasingly questioned by the urogynecologic community because of the associated postoperative morbidity in the absence of clearly defined evidence for efficacy [2]. In fact, episiotomy, particularly if median, is paradoxically associated with more anal sphincter injury and decreased perineal muscle strength and performance during the postpartum period than spontaneous perineal lacerations, because of greater tissue disruption [1, 2]. Moreover, the optimum ratio between the length of episiotomy and the length of perineum that can reliably predict minimal perineal damage is not known [1]. Despite the availability of this information, episiotomy, particularly the routine procedure, is performed more frequently in developing countries than in the West [3]. Over the past two decades, neurophysiological and experimental research has revealed that vaginal delivery damages the pelvic floor muscles through mechanisms unrelated to traumatic disruption [4–6]. During the second stage of labor, the pudendal nerve is compressed by the fetal head against the ischial spines, causing entrapment neuropathy and partial denervation of the striated pelvic floor muscles [4]. More importantly, in labor simulation computer and animal models, the fetal head and biomechanical labor forces cause direct stretch and compression injuries to the pelvic floor muscles during delivery that contributes to progressive deterioration in muscle function. Both muscle injuries were found to develop at a lower tissue elasticity threshold than that observed in normal Int Urogynecol J (2009) 20:615–617 DOI 10.1007/s00192-009-0891-0

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