The urethral pressure profile in pregnancy and after delivery in healthy nulliparous women

Abstract Simultaneous urethrocystometry by means of a dual microtransducer catheter was performed occording to a precise, standardized technique serially at 8, 16, 28, and 36 weeks of pregnancy and at 8 weeks post partum in 43 healthy nulliparous women. The urethral pressure profile at rest and the effect of stress (cough) on the urethral pressure profile during pregnancy and after delivery were measured. At each recording session, blood was obtained for determination of 17β-estradiol (E 2 ), progesterone (P), and 17-alpha-hydroxyprogesterone (17-OH-P). The continence parameters functional urethral length and urethral closure pressure, as well as the urethral closure pressure response to stress, did not change systematically during the course of pregnancy. Engagement of the presenting part at 36 weeks did not influence the urethral pressure profile measurements. Alterations in hormone levels during pregnancy were not correlated with the changes in urethral pressure profile measurements. Both urethral pressure and length parameters in all women who underwent vaginal delivery were notably decreased 8 weeks post partum when compared with early pregnancy values and with values obtained in a group of healthy nulliparous women in the follicular phase of the cycle. 1 The decrease in length parameters was not observed in the six women in whom delivery was by cesarean section. The postpartum changes were not significantly correlated with the duration of the second stage of labor or with the presence or absence of an episiotomy. Also, no relationship with infant birth weight was found. Values of the urethral pressure profile parameters below the median value and defective transmission of pressure over the urethra were observed in almost all women who experienced stress incontinence during pregnancy and/or after delivery. These observations suggest that an inherent weakness of the urethral sphincter mechanism plays a key role in the pathogenesis of stress incontinence.