Does childbirth alter the reflex pelvic floor response to coughing?

Ultrasound Obstet Gynecol (2012) Published online in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/uog.10083 Does childbirth alter the reflex pelvic floor response to coughing? H. P. DIETZ, V. BOND and K. L. SHEK Sydney Medical School Nepean, Penrith, Australia KEYWORDS: levator ani; pelvic floor; reflex; ultrasound; urinary stress incontinence ABSTRACT INTRODUCTION Objective To determine the prevalence of and to quantify the effect of reflex pelvic floor activation on coughing in nulliparous pregnant women, and to assess peripartal changes and any association with stress urinary incontinence. Methods Between April 2008 and March 2010, 131 nulliparous pregnant women were recruited from an antenatal clinic. All participants were interviewed and underwent four-dimensional translabial ultrasound examination at antepartum (35.8 (mean) weeks gestation) and postpartum (4.6 (mean) months) visits. Four-dimensional ultrasound volume datasets of the pelvic floor during coughs were obtained at a minimum frame rate of 16 Hz, usinga10 volume acquisition angle. To quantify a reflex levator contraction we measured the midsagittal hiatal diameter at multiple time points. Levator integrity was determined using tomographic ultrasound imaging. Results From 131 women recruited, 47 datasets were technically suboptimal, leaving 84. There was a visible pelvic floor reflex in 82 (98%) cases. At the postpartum visit this was reduced to 63/84, i.e. 75% (P < 0.001). The magnitude of a reflex contraction was markedly reduced postpartum, from 4.8 mm to 2.0 mm (P < 0.001), and this effect was associated with delivery mode (P = 0.042). There was a trend towards an association between lower reflex contraction magnitude and stress incontinence (0.87 ± 3.18 mm vs. 2.36 ± 3.5 mm; P = 0.08) at the postpartum follow-up visit. Conclusions Pelvic floor reflexes are altered by childbirth. This alteration may be associated with vaginal delivery. Reflex magnitude may be associated with postpartum stress urinary incontinence. The clinical significance of this finding is uncertain. Copyright 2012 ISUOG. Published by John Wiley & Sons, Ltd. The pathophysiology of stress urinary incontinence has eluded researchers for 100 years. It is likely that anatomical factors are involved; incontinence has long been assumed to be due to abnormal support of the bladder neck 1, or lately, to abnormal mid-urethral fixation 2. Partial denervation of the rhabdosphincter via pudendal nerve trauma has been proposed as a neurogenic etiology of stress urinary incontinence 3. However, other factors clearly play a role, since urethral mobility and urethral closure pressure explain only a small part of the variability of stress continence 4,5. Voluntary activation of the pelvic floor muscles results in elevation of the bladder neck 6 9, reduction of the anteroposterior diameter of the levator hiatus 10 and increased intravaginal 11,12 and intraurethral pressures 13 15. Clearly, these muscular structures can be activated also in the form of a reflex detectable by translabial ultrasound 16 18. In addition, activation of the urethral rhabdosphincter, whether voluntarily or reflexly, is thought to contribute to stress continence via augmentation of urethral closure pressure 19, an effect demonstrated by several authors 13 15,20. Such reflexes are clearly centrally mediated, influenced by learned responses 21,and may depend on bladder filling 22. There is some electromyographic evidence of altered activation patterns in women with urinary incontinence 23, although it is unclear whether such reflex alteration is a cause or an effect of clinical symptoms. The timing of reflex activity is likely relevant for the prevention of incontinence, and it has been claimed that delayed contraction of the levator ani is associated with urinary incontinence 24. It is likely that activation of the pelvic floor muscles and the urethral striated muscle normally occurs simultaneously, both acting to safeguard continence. These hypotheses provide the central justification for conservative treatment of urinary incontinence by pelvic floor muscle exercises 25. Correspondence to: Prof. H. P. Dietz, Sydney Medical School Nepean, Nepean Hospital, Penrith NSW 2750, Australia (e-mail: hpdietz@bigpond.com) Accepted: 16 August 2011 Copyright 2012 ISUOG. Published by John Wiley & Sons, Ltd. ORIGINAL PAPER

Dietz et al. In this study we prospectively obtained fourdimensional (4D) ultrasound volume data on coughing, allowing the detection and quantification of reflex activation of the levator ani muscle as identified by a reduction in the anteroposterior diameter of the levator hiatus which has been shown to be a valid and repeatable measure of pelvic floor muscle activity 10. The primary aim was to document such reflex activity in nulliparous pregnant women, repeating the assessment 3 months postpartum, and to investigate the effect of childbirth on this reflex. In addition, we aimed to test for any association between such reflex activity and stress urinary incontinence. METHODS Between April 2008 and March 2010, 131 nulliparous women with a singleton pregnancy at a mean gestation of 35.8 (range, 33 37) weeks were recruited from the antenatal clinic at two tertiary hospitals for an unrelated parent study. This was a sub-analysis of the pilot phase of a perinatal intervention trial that tested the effect of a vaginal dilator (the Epi-No device) on pelvic floor trauma. All patients were invited for a second assessment at least 3 months postpartum. All participants were interviewed and underwent 4D translabial ultrasound examination, after voiding, in the supine position as previously described 26 at both antepartum and postpartum visits. Ultrasound volume datasets were obtained at rest, on maximal Valsalva and pelvic floor muscle contraction, and at least one cough was registered at a minimum frame rate of 16 Hz, using a 10 volume acquisition angle (Figure 1). Analysis of the volume datasets was performed by one of the authors (V.B.) who was blinded to all other data, using 4D View v 5.0 (GE, Kretz Ultrasound, Zipf, Austria). To quantify a reflex contraction of the levator ani we measured the midsagittal hiatal diameter 27 at rest, on maximum cough, on maximum reflex levator contraction and immediately after coughing. We also determined the timing of the maximum levator contraction relative to maximum bladder neck displacement on coughing. This was achieved by slowly paging through all obtained volume data sets (usually at 50 ms per volume, maximum of 62.5 ms) and determining the timing of the first visible downwards displacement of the bladder neck (as evidence of a cough) relative to the first visible reduction of the anteroposterior hiatal diameter (as evidence of a reflex levator activation). For example, if volume 17 showed the first evidence of caudal displacement of the bladder neck, and volume 19 the first evidence of reflex levator activation, we recorded a latency of 2 50 ms = 100 ms. Figure 2 shows measurements of bladder neck descent and hiatal diameter during rest at the start of the cough cycle, during precough levator activation, at maximum cough impact and maximal levator activation, and after recovery. We rated a levator ani reflex contraction as present if there was a reduction in midsagittal hiatal diameter just prior to or during coughing. We did not assess the clitoral reflex, which also can be observed during a cough, since this is difficult to quantify and has been shown not to be associated with stress incontinence or urodynamic stress incontinence in a recent unrelated study conducted at this unit 16. Levator integrity was determined using tomographic ultrasound imaging as previously described 28. In short, a patient was rated as positive for avulsion of the puborectalis muscle if the plane of minimal hiatal dimensions, as well as slices 2.5 mm and 5 mm cranial to that plane, showed an abnormal muscle insertion. Our null hypothesis was that childbirth does not affect pelvic floor reflexes. This hypothesis was tested using both qualitative data (reflex present/not present) and quantitative data (reflex magnitude as determined Figure 1 Activation of external perineal muscles displaces the clitoris (vertical arrow) and activation of the levator ani accentuates the anorectal angle (horizontal arrow); both can be observed often during coughing. (a) Image taken at rest. (b) Vertical strip-like image taken at rest showing the axial plane as seen in a narrow rendered volume. (c) Image taken during maximum cough. (d) Vertical strip-like image taken during maximum cough showing the axial plane as seen in a narrow rendered volume. A, anal canal; B, bladder; L, levator ani; R, rectum; S, symphysis pubis; U, urethra.

Pelvic floor reflexes Figure 2 Measurements of bladder neck descent and hiatal diameter during a cough cycle, recorded at 20 volumes/s. (a) Image showing the situation at rest (start of cycle): the bladder neck is at 31.4 mm above the symphysis pubis; the hiatus measures 57 mm. (b) Image showing evidence of levator activation prior to first evidence of bladder neck displacement due to the cough: the bladder neck is at 31.3 mm; the hiatus is reduced to 51.9 mm (six volumes or 300 ms later). (c) Image demonstrating the moment of maximum cough impact: the bladder neck is displaced caudally by c.10 mm, to 21.1 mm above the symphysis pubis; at the same time there is maximum levator activation, with the hiatus reduced to 42.9 mm (10 volumes or 500 ms from start of cycle). (d) Image showing a return to (largely) precough resting conditions: the bladder neck is at 30.5 mm above the symphysis pubis; the hiatus is at 53.5 mm (26 volumes or 1300 ms from the start of the cycle). by a reduction in anteroposterior diameter of the levator hiatus on coughing). This was a pilot study and, lacking the necessary data, we did not undertake power calculations. Descriptive and comparative statistics (t-tests) were undertaken using Minitab v 13 (Minitab Inc, State College, PA, USA) after normality testing using the Kolmogorov Smirnov method. All parameters tested proved to be normally or near-normally distributed, with the exception of the length of the second stage of labor. For normally distributed data we utilized paired and unpaired t-tests, ANOVA and logistic regression analysis. To analyze an association between the second stage of labor and pelvic floor reflex presence and magnitude we used the Mann Whitney U-test and Spearman s correlation. A test retest series of midsagittal hiatal diameter measurements was performed by two examiners (V.B. and K.L.S.), with interobserver agreement assessed using the intraclass correlation coefficient (ICC). P < 0.05 was regarded as significant. This prospective study was approved as an extension of a previously approved study by the local Human Research Ethics Committee (SWAHS HREC 07 022). RESULTS The test retest series (n = 58) of midsagittal hiatal diameter measurements yielded an interobserver ICC of 0.93 (95% CI, 0.89 0.96), signifying excellent repeatability after a short period of training. Of 131 women recruited between April 2008 and March 2010, who had both antepartum and postpartum coughs registered, ultrasound volume datasets in 47 were technically suboptimal (acquired at less than 16 Hz or not showing the entire hiatus on coughing), leaving 84 cases. All subsequent analysis refers to this dataset. Mean age was 29.6 (range, 19.5 42.3) years and mean body mass index was 23.7 (range, 16.9 47.2) kg/m 2. Women were examined at a mean gestational age of 35.8 (range, 33.6 37.4) weeks and again at 4.6 (range, 2.3 9.7) months postpartum. Mean gestational age at delivery was 39.8 (range, 36.4 41.6) weeks. Delivery data for the study population are shown in Table 1. Twenty-six women complained of stress incontinence at the antepartum visit, and 20 reported stress incontinence at the postnatal visit. Levator defects were diagnosed by tomographic ultrasound examination at the postpartum visit in six women (9.4% of vaginally delivered patients). Of 84 women with coughs registered at the antenatal visit, there was a visible pelvic floor reflex in 82 (98%). At the postpartum visit this was reduced to 63/84, i.e. 75% (P < 0.001; chi-square test). The mean difference in midsagittal diameter between rest (mean ± SD, 50.1 ± 6.2 mm) and maximum contraction (45.3 ± 6.3 mm) was 4.8 (range 0 17.1, SD 4.8) mm antenatally. The magnitude of a reflex contraction was markedly reduced postpartum, from 4.8 to 2.0 mm (P < 0.001). This reduction was not associated with group allocation in the pilot randomized controlled trial, nor with follow-up time (P = 0.98), and on biostatistical advice we felt it permissible to merge the intervention and control groups. Vaginal delivery was associated with a trend towards greater reduction in reflex contraction magnitude (3.2 ± 4.2 vs.1.6 ± 3.2 mm; P = 0.07). Based on ANOVA, increasing the traumatic potential of delivery mode (Prelabor Cesarean section (CS), first-stage CS, second-stage CS, normal vaginal delivery, vacuum, forceps) was associated with a reduction Table 1 Obstetric data of the study group (n = 84) Parameter Value Normal vaginal delivery 46 (55) Vacuum extraction 15 (18) Forceps delivery 3 (4) Prelabor Cesarean section 2 (2) Cesarean section in first stage 12 (14) Cesarean section in second stage 6 (7) Use of epidural 39 (46) Use of Syntocinon 42 (50) Length of first stage (min) 410 (33 1209)* Length of second stage (min) 61 (5 231) Perineal tears 28 (33) Vaginal tears 8 (9) Birth weight (g) 3434 (2615 4455)* Data are given as n (%), mean (range)* or median (range).

Dietz et al. in reflex contraction magnitude (P = 0.042). Length of second stage, birth weight, head circumference, use of intrapartum epidural pain relief and levator trauma were not shown to be confounders of this association on multivariate logistic regression, although in the case of avulsion this may be due to a lack of power (2.74 ± 4.03 in women with avulsion mm vs. 4.02 ± 4.14 mm in those with intact pelvic floor; P = 0.5). The magnitude of a reflex levator contraction was not associated with antepartum stress incontinence; however, there was a trend towards an association between lower reflex contraction magnitude and stress incontinence (0.87 ± 3.18 mm vs. 2.36 ± 3.5 mm; P = 0.08) at the postpartum follow-up appointment. There was a nonsignificantly greater reduction in reflex contraction magnitude in those women complaining of postpartum stress incontinence (3.88 ± 4.27 mm vs. 2.51 ± 3.92 mm: P = 0.21). The timing of a levator reflex relative to the onset of downwards displacement of the bladder neck caused by the cough was not associated with stress incontinence, neither antepartum nor postpartum. DISCUSSION Reflex contraction of the levator ani and external perineal muscles can be observed on translabial ultrasound during sudden increases in intra-abdominal pressure 16. These reflex contractions are almost universally present in nulliparous pregnent women. There seems to be a reduction in reflex contraction magnitude after childbirth, and this reduction may be associated with delivery mode. This finding is consistent with the growing evidence of pelvic floor damage, both macroscopic and functional, or possibly ultrastructural, attributable to vaginal delivery 29 33. There was a trend towards weaker levator reflexes in women who complained of stress incontinence at the postpartum visit, but this study was insufficiently powered to examine obstetric factors in greater detail. A small study using perineal ultrasound, albeit employing a different methodology for the detection of reflex activity 17, suggests that reflex pelvic floor muscle activation may be less effective in stress incontinent women, an observation that seems to support our findings. Previous work from our unit, using a much simpler methodology based on the visual perception of a reflex muscle contraction, found visible reflex activity in only 57% of nulliparas in late gestation 34 ; the difference in prevalence is very likely due to the much more sensitive methodology used in the present study. There are several weaknesses of this study that have to be acknowledged. This is a small series, and some of the statistical results suggest a lack of power, in particular in view of the multiple analyses conducted. It may be preferable to repeat this study with a larger dataset. However, our numbers were sufficient to test our primary null hypothesis, i.e. that childbirth does not affect pelvic floor reflexes. This hypothesis was proven false. The main weakness of this study may be that we were able to assess the ultrasound datasets of fewer than two thirds of all originally recruited patients. This is mainly due to initial problems with the methodology, since the reliable registration of a levator reflex by 4D ultrasound requires a high temporal resolution. We achieved this by obtaining narrow 4D volume datasets at acquisition angles of 10. However, it is not always easy to guarantee the depiction of all relevant structures in such a narrow volume, since both the central symphysis pubis and the central aspect of the levator ani behind the anorectal junction must be included exactly in the midline. Even minor asymmetries can affect measurements substantially, which is why we excluded a high number of suboptimal datasets rather than compromise measurements. In some instances a lower temporal resolution had been employed, and we decided to exclude all datasets acquired at less than 16 Hz. Furthermore, it is acknowledged that the visibility of a reflex contraction will depend crucially on its magnitude. It is quite likely that women in whom we were unable to detect a reflex contraction did in fact produce such a reflex, although it may have been too weak to visualize. Evidently, electromyographic testing would be more likely to detect such weak reflexes. However, the likely lower sensitivity of ultrasound examination for the detection of reflex activity of the levator ani does not affect the testing of our hypothesis, nor its clinical implications. In order to obtain reliable electromyographic data, invasive means may be necessary, thus reducing compliance and raising ethical issues with regard to the antenatal component of our study. Furthermore, crosstalk between different pelvic floor structures may severely limit the usefulness of such a methodology. It is precisely because of these issues that the pathophysiology of female stress urinary incontinence remains a challenge for clinical research. It remains to be determined why childbirth would result in a reduction in reflex activation of the levator ani. Denervation may be one factor, although permanent denervation of the levator ani seems unlikely to play a major role 35 since our assessment was undertaken more than 3 months postpartum, when any temporary neuropathy should have resolved. On the other hand, there is ample evidence that childbirth can damage the puborectalis and iliococcygeus muscles 29 33, and any such trauma is likely to result in a weaker pelvic floor muscle contraction 36, whether due to macroscopic trauma, i.e. avulsion of the muscle from its insertion, or to microscopic or ultrastructural trauma following overdistension 30. The weaker a contraction, the harder it would be to detect on imaging, which may account for cases of visually absent reflexes postpartum. However, in this study we did not detect a statistically significant effect of avulsion, possibly because of a lack of power. In conclusion, pelvic floor reflexes are altered by childbirth. This alteration may be associated with vaginal delivery. Their magnitude may be associated with postpartum stress urinary incontinence. The clinical significance of this finding is uncertain.

Pelvic floor reflexes DISCLOSURES Prof. H.P. Dietz has received honoraria as a speaker from GE, Astellas and AMS and has acted as consultant for CCS and AMS. He has also received equipment loans from GE, Toshiba and Bruel and Kjaer. The other authors have no potential conflict of interest to declare. REFERENCES 1. Bonney V. The principles that should underlie all operations for prolapse. J Obstet Gynaecol Brit Empire 1934; 41: 669 683. 2. Pirpiris A, Shek K, Kay P, Dietz H. Urethral mobility and urinary incontinence. Ultrasound Obstet Gynecol 2010; 36: 507 511. 3. van Geelen JM. Delivery and Urethral sphincter incontinence. In Pelvic Floor Reeducation- Principles and Practice, Schuessler B, Laycock J, Norton P, Stanton SL (eds). Springer: London, 1994; 111 118. 4. Dietz HP, Clarke B. The urethral pressure profile and ultrasound imaging of the lower urinary tract. Int Urogynecol J 2001; 12: 38 41. 5. DeLancey JO, Ashton-Miller JA. Pathophysiology of adult urinary incontinence. 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