Vaginal delivery, notably the first, is strongly associated with pelvic organ prolapse and devastating long‐term consequences such as urinary and fecal incontinence. 1,2 Pelvic floor damage may occur either by direct support/ anatomic injury or indirectly by denervation injury. 3–7 It is known that postpartum pelvic muscles exercise results in fewer urinary incontinence symptoms, 8,9 but the successful implementation of rehabilitation still has not been determined in long‐term follow‐up studies. Moreover, the antepartum selection of puerperae at higher risk for developing pelvic floor damage is difficult because of the lack of selection criteria. Therefore, postpartum assessment of anatomic and functional status of pelvic floor structures can be useful for the admission of women to rehabilitative programs. The relation between visual evidence of perineal trauma in the immediate postpartum and pelvic floor dysfunctions in puerperium has not been determined. It might be expected that perineal trauma is associated with defective pelvic floor muscles function, stress urinary incontinence, and anal incontinence. Conversely, it seems important to know whether an intact perineum precludes the appearance of symptoms related to perineal trauma after vaginal delivery. The aim of this study was to determine the relation between the immediate postpartum perineal assessment and the occurrence of pelvic floor dysfunctions in puerperium.
MATERIALS AND METHODS
This prospective study was conducted on 218 consecutive primiparous women with singleton pregnancies and spontaneous vaginal delivery with the fetal head in occiput anterior position from January 2000 to December 2000. Institutional review board (I.R.C.C.S. Burlo Garofolo) approval was obtained for this study in 1999 (project no. 6/99). All the women were included in the study immediately after vaginal delivery. Exclusion criteria were cesarean delivery, episiotomy, breech delivery, and history of vaginal or anal surgery. The perineum was inspected by a group of obstetrics/gynecology physicians, and the position of any perineal tear was recorded before suture. Puerperae were divided in three groups according to the assessment of perineal trauma. The first group was identified as an intact perineum or superficial tears (group A: 171 women); the second group was identified as perineal muscle tears and intact anal sphincter (group B: 39 women); and the third group was identified as an anal sphincter tear with or without disruption of the rectal mucosa (group C: eight women). Each woman was questioned and examined by a separate single gynecologist, blinded to perineal inspection results, 2 months after vaginal delivery.
Anal incontinence was defined as incontinence of flatus, liquid or solid stool, stress urinary incontinence as involuntary loss of urine during physical exertion, and urge incontinence as the loss of urine associated with a strong desire to void. Frequency was defined as voiding seven or more times during the day and twice or more at night.
Careful histories were taken with particular attention to the development of urinary and/or anal incontinence in puerperium. A conventional clinical evaluation was then performed, and a digital scoring of pelvic floor contraction was carried out. Examination was performed with the woman in lithotomic position, with the knees semiflexed. A 0–5 score was given according to the previously validated Oxford Scale. 10 We considered digital test scores less than 3 as abnormal.
Vaginal manometry was performed with the woman in the same position using a silicone sensor perineometer (PFX Cardio Design Pty Ltd, Brisbane, Australia). Manometric values were expressed in cm H2O. We considered perineometric values less than 12 cm H2O as abnormal.
The urine stream interruption test (UST) was performed using a uroflowmeter (UroDesk 300, SI.EM Sistemi Elettromedicali s.r.l., Milano, Italy) according to the technique described by Sampselle et al. 11 The woman was asked to interrupt urine flow after a signal was given. The software of the uroflowmeter electronically measured the seconds from the signal to the complete cessation of urine flow (UST score). We considered the UST scores greater than 5 seconds abnormal.
Data collected were treated using different analysis methods. One‐way analysis of variance test and Dunnett multiple comparison test were used to compare age, maternal weight before pregnancy, neonatal weight, and weight gain in pregnancy among the three groups (Table 1). Fisher exact test was used to compare marital status and epidural analgesia, expressed in percentages (Table 1). Using a simple logistic regression model to test an estimate of relative risk, we expressed the odds ratios of every single variable considered with respect to the control population that we assumed was group A. Statistical evaluations were performed with the software program Stata 5.0 (Stata Corp., College Station, TX) and InStat2 (GraphPad Software, Inc., San Diego, CA). Statistical significance was set at P < .05.
Mean age of puerperae was 30.9 (standard deviation ± 4.2) years (range 21–43). Group A (n = 171) had intact perineal muscles or superficial tear; group B (n = 39) had perineal muscles tear and intact anal sphincter; and group C (n = 8) included seven women with anal sphincter tear and one with disruption of the rectal mucosa.
Of the 36 women who suffered from urinary symptoms (16.5%), 28 had stress incontinence (12.8% of the total, 77.8% of the symptomatic puerperae), six had frequency/urgency (2.7% of the total, 16.7% of the symptomatic puerperae), and two had urge incontinence (0.9% of the total, 5.6% of the symptomatic puerperae). None had mixed incontinence or dysuria. Of the six women with anal incontinence (2.7%), four had fecal incontinence (1.8%) and two had flatus incontinence (0.9%).
General characteristics of the 218 women are indicated in Table 1. No significant difference was found among the study groups with respect to age, marital status, maternal weight before pregnancy, and epidural analgesia. Weight gain in pregnancy was significantly higher in group B than in group A (15.1 ± 4.9 kg versus 13.2 ± 3.8 kg, P = .024) both with one‐way analysis of variance test and with Dunnett multiple comparison test, whereas neonatal weight was significantly higher in group C than in group A (3493.7 ± 475.4 g versus 3174.4 ± 418.7 g, P = .045) using one‐way analysis of variance test, but not using Dunnett multiple comparison test.
Table 2 shows the incidence of urinary and anal symptoms in the three study groups. No significant difference was found with regard to the incidence of stress incontinence, frequency/urgency, and urge incontinence, whereas anal incontinence was found more commonly in group C than in group A (relative risk 9.5, odds ratio 8.78, P = .003).
Abnormal results of pelvic floor muscle assessment are represented in Table 3. No significant differences were found with regard to the abnormal values of digital test, vaginal manometry, and urine stream interruption test among the groups.
Electrophysiologic studies of urethral and anal sphincters indicate that vaginal delivery may be important in the pathogenesis of anal and urinary incontinence. 4,5,12,13 Identification of variables that can increase the risk of postnatal symptoms might enable appropriate selection of candidates for pelvic floor rehabilitation programs. The relation between external evidence of perineal trauma and pelvic floor dysfunctions has not been investigated previously. Our study shows that the visual evidence of intact perineal muscles (intact perineum or superficial tear) does not preclude the appearance of symptoms related to perineal trauma after vaginal delivery.
Stress urinary incontinence was experienced in the 12.9% of the puerperae of group A (intact perineum or superficial tear). Iosif and Ingemarsson 14 reported stress urinary incontinence in 8.8% of women after elective cesarean delivery, suggesting a mechanism other than trauma sustained during vaginal delivery. On the other hand, we can suppose that pelvic floor integrity on clinical examination does not exclude urethral sphincter trauma.
As regards to anal incontinence (fecal and/or flatus incontinence), this condition was experienced by three women (1.8%) of group A, nearly half of the total patients. Therefore, clinical evidence of anal sphincter damage in the absence of visible pelvic floor muscle disruption may be considered possible even if uncommon.
The evidence of perineal muscle disruption (group B versus group A) does not seem to be associated with a higher incidence of urinary and anal dysfunctions. The evidence of anal sphincter damage (group C versus group A) seems associated with a significantly higher incidence of anal incontinence. Considering the small number of subjects in group C, the results power is low, so we can only hypothesize that immediate postpartum perineal examination could identify women at risk for anal dysfunctions. Finally, there is no relation between perineal inspection and the results of pelvic floor strength assessment (digital test, vaginal manometry, and urine stream interruption test).
We can conclude that immediate postpartum perineal examination is not a good predictor of pelvic floor weakness, stress urinary incontinence and, in general, lower urinary tract disorders.
Selection of candidates for perineal rehabilitation should not be based only on estimation of perineal damage. Further studies are necessary to investigate the role of delivery charts examination, clinical evaluation of postnatal symptoms related to perineal trauma, and clinical assessment of pelvic floor contraction.
Our findings seem very suggestive, but these conclusions should be considered preliminary and need further investigation to be confirmed in larger studies with adequate power.
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