Sunday, April 8, 2012

Parity effects on the lower urogenital tract, pelvic floor and anorectal function

Parity effects on the lower urogenital tract, pelvic floor and anorectal function

Introduction
Parity effects on vesical continence and voiding function
The relevance of parity to ureteric dilatation
Parity effects on female genital organs
Parity effects on pelvic floor
Parity effects on anorectal functions



Introduction
            Gynecological and obstetric events (pregnancy, particularly previous vaginal delivery and hysterectomy) were the most prominent risk factors for SUI (Peyrat et al, 2002). Childbirth was found to be associated with a variety of muscular and neuromuscular injuries of the pelvic floor that are linked to the development of anal incontinence, UI and POP. Cesarean delivery appears to be protective, especially if the patient does not labor before delivery (Handa et al, 1996). Childbirth per se does not explain all cases of urinary and fecal incontinence (Weber and Walters, 1999). Urinary and faecal incontinence are problems that can severely limit the social, emotional and sexual being of the women (Wells, 1996).

          Relationship between first childbirth and obstetric trauma is strong but additional pregnancies and deliveries are aggravating factors as well as ageing and hormonal effects of the menopause (Fatton and Jacquetin, 1999).

Parity effects on vesical continence and voiding function
          Bladder dysfunction is a disorder often characterized by incontinence, urgency, patterns of dysfunctional voiding, incomplete emptying and so forth (Holmes et al, 2002). It has shown a higher rate of UI in parous women than in nulliparous women. Among types of incontinence, SUI consistently shows strongest associations with parity. Little or no association is found between urge incontinence and parity (Foldspang et al, 1992). Urinary incontinence, quite common during pregnancy, it occurs less frequently postpartum (5% in parous women) (Wijma et al, 2003).

          Vaginal delivery was associated with a higher incidence of UI (relative risk, 2.8) compared with cesarean. Cesarean delivery at any stage of labor reduces postpartum UI (Farrell et al, 2001). Vaginal delivery leads to loss of pelvic muscle strength in the immediate postpartum period, although most or all of this strength may be recovered with aggressive pelvic muscle exercises. Women who have had cesarean births demonstrate greater pelvic muscle strength during and after the postpartum period than women delivered vaginally (Sampselle, 1990).

            LUTS are common in women with genital prolapse. Voiding difficulty, bladder outlet obstruction and occult SUI may coexist and they are associated with prolapse (Romanzi et al, 1999).

The relevance of parity to ureteric dilatation
            There was a significant increase in the diameter of the right ureter in parous women with a history of proven UTI (Bradley et al, 1998). Procidentia may occasionally imprison the ureters, leading to hydroureter and hydronephrosis (McGuire et al, 1996).


Parity effects on pelvic floor
          The fetal head advancing through the hiatus genitals rips the vagina off its fascial anchoring, sliding it downward and outward. The rectum is torn from its attachment to the levator ani muscles and fascia. The fetal head tears or overstretches the levator muscles, causing their diastases. Anteriorly, the fascia between the vagina and bladder is stretched in a radial and downward fashion. This motion may tear the vagina and bladder off their anchorage to the upper surface of the endopelvic fascia or the levator ani and posterior surface of the pubic symphysis (Walters and Newton, 1999).
          Shape of the pelvis, preexisting pelvic muscle mass and strength of fascial supports, fetal presentation, position and size all contribute to different strains, stresses, and locations of particular injuries to pelvic floor and perineum (Nodine and Roberts, 1987).  

            Pelvic floor descent in both the primiparous and multiparous was significantly greater at rest and on squeezing than that in the nulliparous women. Furthermore, pelvic floor descent on straining was greater in the multiparous than in nulliparous women (Tsunoda et al, 1999). Perineal plane at straining was lower and the descent was larger in multigravidae than in primigravidae (Lee and Park, 2000).

Parity effects on anorectal functions
          Vaginal delivery may initiate damage to the anal continence mechanism by direct injury to the pelvic floor muscles, damage to their motor innervations, or both (Toglia and DeLancey, 1994). By using anal sonography in women before and after delivery, 35% of primiparous women sustained external or internal anal sphincter damage, although only 3% were recognized at the time of delivery (Sultan et al, 1993). None of the women delivered by cesarean birth sustained anal sphincter damage (Kamm, 1994). Only a third of women with sphincter defects had anal incontinence or fecal urgency, suggesting redundancy of function that maintains continence despite some damage (Sorensen et al, 1993).

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