{"paper_id":"04e0f841-b1e6-49ba-a440-cbed652cf882","body_text":"Vol.:(0123456789)\nInternational Urogynecology Journal \nhttps://doi.org/10.1007/s00192-026-06752-y\nORIGINAL ARTICLE\nDifferences in Pelvic Floor Morphometry for Women with Persistent \nPelvic Pain and Deep Infiltrating Endometriosis—A Cross‑Sectional \nStudy\nErin M. Nesbitt‑Hawes1,2  · Hans Peter Dietz3 · William L. Ledger1,2 · Jason A. Abbott1,2\nReceived: 4 November 2025 / Accepted: 12 May 2026 \n© Crown 2026\nAbstract\nIntroduction and Hypothesis This study is aimed at describing the morphometry of the pelvic floor for a large population \nof women with persistent pelvic pain (PPP) compared with those without pain.\nMethods A prospective cross-sectional study was performed between January 2013 and November 2015, recruiting women \nattending a general gynaecology clinic. Demographic data were collected and translabial four-dimensional ultrasound (4DUS) \nwas performed on all participants. Morphometric assessment of pelvic floor muscles was undertaken at rest, with contraction \nand Valsalva, and analysed by an assessor blinded to demographic details.\nResults Of the 747 participants, 469 (62.8%) had PPP and 278 (37.2%) reported no pelvic pain. Levator hiatal (LH) area \n(14.4 vs 18.6  cm2, p = 0.009) and left–right (LR) diameter (3.9 vs 4.1 cm, p = 0.019) were smaller for women with PPP in \nthe Valsalva assessment than in participants with no pain. For women who were currently requiring treatment for pelvic pain \n(158 out of 747, 21.2%) compared with those not having treatment, there were differences in LH area and LR diameter in all \nphases of movement; at rest (11.4 vs 12.8  cm2, p = 0.017; 3.6 vs 3.8   cm2, p = 0.038), Valsalva (13.6 vs 16.4  cm2, p =  < 0.001, \n3.8 vs 4.2   cm2, p = 0.001) and contraction (9.3 vs 10.4  cm2, p = 0.021, 3.3 vs 3.6   cm2, p = 0.006). For women with deep infil-\ntrating endometriosis (DIE), smaller LH areas were seen on rest and Valsalva (adjusted mean 11.89 vs 12.75  cm2, p = 0.015, \n15.13 vs 16.98  cm2, p = 0.002) but not contraction (10.05 vs 10.48  cm2, p = 0.161) than in women without endometriosis.\nConclusion Pelvic floor morphometry differs for women when comparing groups with PPP and no pain, particularly in \nthe group of patients currently receiving treatment for their PPP, as well as the subgroup of DIE even when adjusting for \nconfounding variables such as mode of delivery, age and prolapse. This supports the hypothesis that women with PPP have \ndifferent PFM characteristics from women without pain symptoms. This study reports on mean measurements with likely \noverlapping distribution groups; therefore, we are unable to give a diagnostic criterion or measurement that could be used \nfor the ultrasound assessment of women with PPP. Further research could stratify severity using validated assessments and \ncompare clinical examination findings with the results seen on ultrasound.\nKeywords Biometry · Four-dimensional ultrasound · Morphometry · Pelvic floor · Pelvic pain\nIntroduction\nPersistent pelvic pain (PPP) in women has a high burden of \ndisease [1–3]. The connection between increased pelvic floor \nmuscle (PFM) tone and PPP has been investigated using \nnumerous tools [4–6]. Unfortunately, synthesis of the litera-\nture is difficult owing to design and methodological factors. \nDespite this, an association is suggested by digital palpation \nand dynamometry with a strong recommendation to research \nmore objective methods for diagnosis [7].\nThree- and four-dimensional ultrasound (3DUS, 4DUS) \nof the pelvic floor is increasingly utilised in gynaecological \nHandling Editor: Symphorosa Shing Chee Chan\nEditor in Chief: Maria A. Bortolini\n * Erin M. Nesbitt-Hawes \n e.nesbitt-hawes@unsw.edu.au\n1 Discipline of Women’s Health, School of Clinical Medicine, \nUNSW Sydney, Sydney, NSW, Australia\n2 Gynaecological Research and Clinical Evaluation (GRACE) \nGroup, Gynaecology Department, Royal Hospital \nfor Women, Randwick, NSW, Australia\n3 Sydney Urodynamic Centres, Sydney, NSW, Australia\n\n International Urogynecology Journal\ninvestigation, primarily in the diagnosis of obstetric trauma \nand pelvic organ prolapse [8 –10]. More recently, this has \nextended to the assessment of pelvic pain such as pelvic gir-\ndle pain [11], endometriosis [12, 13] and provoked vestibu-\nlodynia [14, 15]. Data from these small studies suggest that \nmorphometry (shape and dimensions) of the PFM might dif-\nfer in women with specific pelvic pain conditions (notably, \nsmaller hiatal areas and reduced PFM contraction); however, \nnone of these studies reflects a broader group of women with \nPPP [11–15, 15].\nPelvic floor physiotherapy is used to treat PPP related to \nincreased PFM tone [16, 17]. Changes in levator hiatal (LH) \narea and left–right diameter have been recorded when com-\nparing 3DUS measurements before and after physiotherapy \nsessions for participants with high-tone pelvic floor dysfunc-\ntion [18]. In addition to these measurements, we hypothe-\nsised that increased muscle tone would also create increased \nbulk, leading to the addition of PFM width measurements \nfor our cohort.\nWe previously reported on nulliparous patients, where \nobstetric trauma could not bias results. That study reported \nno difference in 4DUS biometric indices for women with \nand those without PPP [19]. This study is aimed at reporting \non a cohort of women, both nulliparous and multiparous, to \nidentify differences in morphometry between women with \nand those without PPP.\nMaterials and Methods\nStudy Population\nThis prospective cross-sectional study was conducted \nbetween January 2013 and November 2015 with institutional \nethical approval (HREC 12/194). The methodology has \nbeen previously reported and is summarised here [19]. All \nwomen presenting to either a public or private gynaecology \nclinic were invited to participate, regardless of their clini-\ncal presentation. Exclusion criteria included current preg-\nnancy, inability to understand written and spoken English \nand age lower than 18. The primary outcome of the study \nwas to compare the pelvic floor morphometry of women \nwith and those without PPP. The secondary outcome was to \nconsider the utility of 4DUS as a diagnostic tool for women \npresenting with PPP. We also performed a subgroup analysis \nin patients who had a diagnosis of endometriosis to allow \ncomparison with previous literature that has examined this \nassociation [12, 16].\nDemographic details were recorded by questionnaire \nfilled out by the researchers during interview at the time of \npatient enrolment, and a dynamic pelvic floor ultrasound \nwas performed for each woman enrolled. Data included the \npresence of PPP (defined as pain located in the pelvic region \nthat was constant or intermittent, cyclical or non-cyclical \npain that persisted for greater than 3 months) [20]. Visual \nanalogue scoring of pain intensity was not performed. Types \nof PPP experienced were categorised as dysmenorrhoea, \nnon-menstrual pelvic pain, dyspareunia, dysuria and dys-\nchezia. Current treatment(s) for pain, prior pelvic surgery \n(including endometriosis and/or hysterectomy) and obstet-\nric history were documented, with surgical data including \nendometriosis subtype (deep or superficial, but not location \nof lesions) extracted from operation reports where availa-\nble. Disease-specific validated questionnaires were not used \nowing to limited availability at the time of data collection.\nPelvic Floor Ultrasound\nThe technique of 3DUS and 4DUS of the pelvic floor is sum-\nmarised here and has been described previously [21]. All \npelvic floor ultrasounds were performed by a single opera-\ntor (gynaecologist with 5 years’ clinical experience at the \ncommencement of the study) following a 3-month period of \ntraining with an expert in the field. Inter-observer variability \nanalysis was performed on an initial cohort of 36 partici-\npants as reported in a previously published paper that dem-\nonstrated good to very good correlation [19]. Other studies \nexamining inter-observer repeatability of 3D and 4DUS of \nthe pelvic floor have also shown good to excellent correla-\ntion for all measurements used in this study [22–24].\nA Voluson 730Expert or E8 (GE Medical Ultrasound, \nZipf, Austria) and an 8.4-MHz curved array volume probe \n(acquisition angle 70–85%) was used to capture ultrasound \nvolumes. Participants emptied their bladder and bowel and \nremoved tampons and pessaries prior to the procedure. \nWith participants in the dorsal lithotomy position, the ultra-\nsound probe was placed on the perineum in the midsagittal \nplane. The PFMs were assessed at rest and with a functional \nassessment, including maximal pelvic floor contraction \n(three repetitions) and maximal Valsalva manoeuvre (three \nrepetitions).\nMeasurements\nAnalysis of the ultrasound volumes was performed offline \nat a later date (on average 6 months following ultrasound \nacquisition), with the assessor blinded to demographic and \nclinical data. Volumes were reviewed and measurements \nwere performed with the PFM at rest, maximal contraction \n(maximal narrowing of the LH area) and Valsalva (maxi-\nmal descent of organs). Volumes that were determined \nto be of insufficient quality for measurements to be per -\nformed were excluded from analysis. Standard measure-\nments for each volume included bladder-neck descent, LH \narea, pubovisceral-muscle (PVM) length (measured as the \nexternal length of the contour of the pubovisceral muscle), \n\nInternational Urogynecology Journal \nanterior–posterior (AP) and left–right (LR) diameters, and \nan average of the PVM width or thickness performed at four \nintervals along the muscle and averaged [23].\nStatistical Analysis\nStatistical analysis was conducted using SPSS version 27. Con-\ntinuous data are presented as mean values with their respective \nstandard deviations. The normality of the data was assessed \nusing the Shapiro–Wilk test and Q-Q plots. Student's t test and \nanalysis of variance (ANOVA) were used for normally distrib-\nuted data, whereas the Mann–Whitney U test (Wilcoxon rank-\nsum test) was used for non-parametric data. Inverse probability \nweighting and generalised linear models were used to control \nfor confounders. Inverse probability weights were calculated \nusing a logistic regression model including baseline covari-\nates. To evaluate covariate balance, we compared weighted and \nunweighted means and proportions and calculated standard-\nised mean differences. Where residual differences remained, \nthe covariates were included in the outcome model. Effective \nsample sizes after weighting were calculated using the Kish \napproximation. A significance level of p < 0.05 was considered \nstatistically significant for all tests.\nAn a priori sample size calculation was performed, to \ndetect a difference in the LH area for women with pain using \npublished data for provoked vestibulodynia [15], as no data \nspecific to this field were available. Using a difference of \n1.06  cm2 (SD 2.22), power of 80% with a p  < 0.05, a mini-\nmum of 140 patients were required. Owing to an expecta-\ntion of a wider variation in pelvic floor measurements for a \nnon-pain cohort, incomplete data sets and anticipated mul-\ntivariate regression for several factors (allowing as a rule of \nthumb 20–30 patients per factor), we calculated a sample \nsize of 700 women to detect a difference in pelvic muscle \nmorphometry.\nResults\nOf 830 women approached, 747 (90%) consented to the \nstudy and underwent translabial 4DUS. Of these, 469 out of \n747 (62.8%) reported PPP of any type.\nDemographic data are presented in Table 1. The mean age \nfor the study population was 41.2 years (standard deviation \n[SD]: 13.3 years). Women who described PPP were younger, \nwith a mean age of 36.9 years (SD 10.5 years), vs no PPP \n48.5 years (SD:14.2 years). Women experiencing PPP were \nalso more likely to be pre-menopausal (71.1% vs 28.9%) and \nhave had surgery for endometriosis (46.5% versus 11.9%). \nMost women reported being Australian born (64.5%). When \nasked about their current non-surgical treatment for pelvic \npain, 158 out of 747 women (21.2%) reported current use of \nanalgesic medications (10.1%), physiotherapy (5%), botuli-\nnum toxin injections to the pelvic floor (0.4%), other (0.7%) \nor a combination of treatments (5%).\nAmong the total number of women in the cohort \n(N = 747), 14.6% reported prolapse, with participants with \nprolapse less likely to report PPP symptoms than those with-\nout prolapse (32.1% vs 67.9%; p < 0.001).\nThree hundred and eighty (n = 380, 50.9%) women in the \nstudy were parous (with 486 individual births). There was a \nsignificant difference between women with and those without \nPPP when comparing those who had ever had a vaginal deliv-\nery (including instrumental and those who had both vaginal \nand caesarean delivery for different births) versus those who \nonly had caesarean deliveries. Women with PPP had a higher \nTable 1  Demographic \ncharacteristics of all women \n(persistent pelvic pain (PPP) \nversus no pain)\nMode of delivery is reported as n = all that apply, with the cumulative total accounting for more than the \nnumber of parous women owing to patients having more than one type of delivery\nPercentages use the denominator of parous women in that group rather than the group as a whole\n*Statistically significant\nBMI body mass index, IQR interquartile range, PPP persistent pelvic pain, SD standard deviation\nDemographics PPP, N = 469 (62.8%) No pain, N = 278 (37.2%) p value\nAge (years), mean (SD) 36.9 (10.58) 48.5 (14.29)  < 0.001*\nBMI (kg/m2), mean (SD) 24.9 (5.0) 24.6 (4.5) 0.46\nPost-menopausal, % 9.0 36.6  < 0.001*\nSurgery for endometriosis, % 46.5 11.9  < 0.004*\nProlapse, % 9 31.6  < 0.001*\nParity, median (IQR) 0 (0–2) 2 (0–2)  < 0.001*\nParous, n  (%) 39.2 70.2  < 0.001*\nSpontaneous vaginal delivery, n  (%) 111/184 (60.3) 147/195 (75.4) 0.002*\nCaesarean, n  (%) 70/184 (38.0) 47/195 (18.7)  < 0.001*\nForceps, n  (%) 34/184 (18.5) 43/195 (22.1) 0.402\nVentouse, n  (%) 18/184 (9.8) 13/195 (6.7) 0.262\n\n International Urogynecology Journal\nfrequency of having had only caesarean deliveries 29.3% ver-\nsus 12.2% (Chi-squared (1) = 17.02, p < 0.001) in the non-pain \ngroup. Reasons for the caesarean delivery or the status of PPP \nprior to pregnancy were not available.\nOf the 469 women (62.8%) reporting PPP, 345 out of \n469 (73.6%) women reported dysmenorrhea, 312 out of 469 \n(66.5%) non-menstrual pelvic pain, 281 out of 469 (59.9%) \ndyspareunia, 108 out of 469 (23.0%) dyschezia and 153 out \nof 469 (32.6%) dysuria.\nAfter applying inverse probability weights, the effective \nsample size was approximately 405 in the PPP group and 160 \nin the no pain group. Table 2 demonstrates the comparison of \nunweighted and weighted means. Comparative morphometry \ndata for women with and those without PPP at rest, Valsalva \nand on contraction are presented in Table 3, with significant \ndifferences seen in LH area and LR diameter on Valsalva, as \nwell as PVM width on contraction. To better understand the \nmore severe cohort of PPP, analysis of biometric data was per-\nformed for women who were currently receiving non-surgical \ntreatment for PPP (Table 4). In this group, significant differ-\nences were found in both LH area and LR diameter at rest, on \nValsalva and on contraction.\nOf the 253 out of 747 (33.9%) women who had surgery \nfor endometriosis, 61 out of 253 (24%) had deep infiltrating \nendometriosis (DIE). After adjusting for prolapse, vaginal \ndelivery, age and BMI, the presence of DIE was signifi-\ncantly associated with a smaller LH area at rest and Valsalva, \nalthough this was not seen for PFM contraction (Table  5). \nAdditionally, a shorter PVM was seen in DIE across all \nmeasures of rest, Valsalva and contraction.\nDynamic pelvic floor assessments were incomplete for 93 \nparticipants, primarily because of technical issues related to \nTable 2  Unweighted and weighted means and standardised mean difference for persistent pelvic pain (PPP) versus no pain groups\nBMI body mass index, PPP persistent pelvic pain, SD standard deviation, SMD standardised mean difference\nPPP (unweighted) No pain (unweighted) SMD PPP (weighted) No pain (weighted) SMD\nAge (years), mean (SD) 36.9 (10.58) 48.5 (14.29) 0.92 40.4 (13.29) 44.5 (14.02) 0.30\nBMI (kg/m2,) mean (SD) 24.9 (5.0) 24.6 (4.5) 0.004 24.7 (4.90) 24.8 (4.570 0.04\nSurgery for endometriosis, % 46.5 11.9 0.82 46.4 12 0.82\nProlapse, % 9 31.6 0.59 14.3 25 0.27\nParous, % 39.2 70.2 0.66 39.3 68.5 0.61\nTable 3  Biometric measurements of patients with persistent pelvic pain (PPP) versus no pelvic pain (inverse probability weighting was used to \nadjust for confounding factors of age, parity, vaginal delivery and endometriosis diagnosis)\nAP anterior–posterior, L–R left–right, PPP persistent pelvic pain, PVM pubovisceral muscle\n*Statistically significant\nPPP, mean (SD) No pain, mean (SD) B Standard error 95% CI p value\nRest\n  Levator hiatal area  (cm2) 11.8 (3.41) 13.8 (4.70) −0.668 0.3931 (−0.10, 1.43) 0.089\n  PVM length (cm) 11.0 (1.56) 11.50 (1.72) −0.109 0.1691 (0.22, 0.41) 0.521\n  AP diameter (cm) 4.7 (0.85) 5.2 (1.23) −0.171 0.1030 (0.03, 2.75) 0.097\n  L-R diameter (cm) 4.42 (16.10) 3.39 (0.72) 0.839 0.9091 (−0.94, 2.62) 0.356\n  PVM width (average cm) 1.02 (0.19) 1.05 (0.20) −0.019 0.0205 (−0.06, 0.02) 0.344\nValsalva\n  Levator hiatal area  (cm2) 14.4 (5.73) 18.6 (8.39) −1.673 0.6436 (−2.9, −0.41) 0.009 *\n  PVM length (cm) 11.6 (1.73) 12.2 (1.96) −0.172 0.1775 (−0.52, 0.18) 0.332\n  AP diameter (cm) 5.1 (1.14) 8.0 (38.2) −1.588 1.3608 (−4.26, 1.08) 0.243\n  L–R diameter (cm) 3.9 (0.71) 4.1 (0.97) −0.187 0.0796 (−0.34, −0.03) 0.019 *\n  PVM width (average cm) 1.1 (1.66) 1.0 (0.16) 0.094 0.0837 (−0.07, 0.26) 0.262\nContraction\n  Levator hiatal area  (cm2) 9.5 (2.97) 11.2 (4.05) −0.517 0.3163 (−1.14, 0.10) 0.102\n  PVM length (cm) 9.8 (1.37) 10.3 (1.50) −0.234 0.1324 (−0.49, 0.03) 0.077\n  AP diameter (cm) 4.0 (0.78) 4.3 (0.94) −0.109 0.0813 (−0.27, 0.05) 0.178\n  L–R diameter (cm) 3.4 (0.65) 3.7 (0.75) −0.088 0.0648 (−0.22, 0.04) 0.177\n  PVM width (average cm) 1.0 (0.18) 1.1 (0.19) −0.043 0.0179 (−0.08, −0.01) 0.015 *\n\nInternational Urogynecology Journal \nultrasound data capture and transfer rather than patient fac-\ntors. A comparison was performed within the incomplete \nand complete groups, with no differences in age, BMI, parity \nand prolapse, although there was a significant difference in \nendometriosis surgery (Table  6). To account for potential \nbias, inverse probability weighting was applied.\nDiscussion\nThis is to our knowledge the largest prospective study to \nassess the pelvic floor using 3/4DUS in a general population \npresenting for gynaecological care and stratifying by the pres-\nence or absence of PPP. This study demonstrates differences \nin biometric measurements during Valsalva with smaller LH \narea and LR diameter for women with PPP. In addition, in the \ngroup of women requiring current treatment for PPP, differ-\nences in LH area and LR diameter were seen across all move-\nment parameters of rest, Valsalva and contraction. Smaller \nLH areas were seen in participants with DIE across Valsalva \nand contraction manoeuvres as well as AP diameters. The \npresence of high PFM tone may explain these findings, with \nreduced movement of the PFMs in women with PPP. This \nassociation is supported by a 2023 systematic review and \nmeta-analysis suggesting that stiffness and reduced flexibility \nmight be more common in high-tone PFMs [6].\nPrevious studies of PFM ultrasound have focused on spe-\ncific conditions such as pelvic girdle pain [11], endometrio-\nsis [12, 13] and provoked vestibulodynia [14, 15], with small \nnumbers in each cohort. A case–control study examined 49 \nwomen with pelvic girdle pain and 49 age-matched controls, \nshowing a significantly smaller LH area at rest and on con-\ntraction in the pain group [11]. In a separate study with near-\nidentical methodology, 38 women with provoked vestibulo-\ndynia were compared with 39 asymptomatic controls [14], also \nreporting a difference between the groups, with smaller LH \nareas at rest, contraction and Valsalva.\nOur publication of the nulliparous subgroup failed to \nshow a significant difference in biometric properties of the \npelvic floor in women with PPP [19]. The current cohort \nincludes all study participants, adjusted for parity and vagi-\nnal delivery. This study demonstrates differences in meas-\nurements in the Valsalva and contraction phases, but not at \nrest in the PPP group. Given the published literature and \nour hypothesis, this was unexpected but may point to some \nlimitations of our study. Pain scales and validated sever -\nity scores were not included in the patient questionnaire, \nand this may result in heterogeneity within the PPP group \nwith the inclusion of self-reported, unscaled pelvic pain. In \norder to better assess severity within the limitations of the \nprotocol, analysis of the group of women requiring current \ntreatment for their PPP was performed and demonstrated a \nTable 4  Biometric measurements of patients receiving current treatment for persistent pelvic pain (PPP) versus no treatment for pelvic pain \n(inverse probability weighting was used to adjust for confounding factors of age, BMI, parity, vaginal delivery and endometriosis diagnosis)\nAP anterior–posterior, L–R left–right, PPP persistent pelvic pain, PVM pubovisceral muscle\n*Statistically significant\nTreatment for PPP, \nmean (SD)\nNo treatment for \nPPP, mean (SD)\nB Standard error 95% CI p value\nRest\n  Levator hiatal area  (cm2) 11.4 (3.24) 12.8 (4.11) −0.935 0.3914 (0.17, 1.70) 0.017*\n  PVM length (cm)) 10.9 (1.61) 11.3 (1.60) −0.165 0.1732 (−0.51, 0.17) 0.340\n  AP diameter (cm) 4.7 (0.85) 5.0 (1.07) −0.160 0.0957 (−0.35, 0.23) 0.095\n  L–R diameter (cm) 3.6 (0.58) 3.8 (0.70) −0.144 0.0695 (−0.28, −0.01) 0.038*\n  PVM width (average cm) 1.0 (0.18) 1.0 (0.19) 0.015 0.0208 (−0.03, 0.06) 0.465\nValsalva\n  Levator hiatal area  (cm2) 13.6 (4.66) 16.4 (7.15) −2.20 0.5901 (−3.36, −1.04) < 0.001*\n  PVM length (cm) 11.4 (1.72) 11.9 (1.85) −0.319 0.1833 (−0.67, 0.04) 0.082\n  AP diameter (cm) 5.0 (1.05) 6.6 (28.00) −1.221 0.9001 (−2.99, 0.54) 0.175\n  L–R diameter (cm) 3.8 (0.63) 4.2 (0.88) −0.254 0.0770 (−0.41, −0.10)  <0.001*\n  PVM width (average cm) 1.0 (0.16) 1.1 (1.6) −0.077 0.0565 (−0.19, 0.03) 0.174\nContraction\n  Levator hiatal area  (cm2) 9.3 (2.82) 10.4 (3.58) −0.705 0.3064 (−1.3, −0.11) 0.021*\n  PVM length (cm) 9.7 (1.44) 10.1 (1.42) −0.183 0.1402 (−0.46, 0.09) 0.193\n  AP diameter (cm) 4.0 (0.81) 4.1 (0.86) −0.092 0.0806 (−0.25, 0.07) 0.252\n  L–R diameter (cm) 3.3 (0.57) 3.6 (0.73) −0.173 0.0633 (−0.30, −0.05) 0.006*\n  PVM width (average cm) 1.0 (0.16) 1.0 (0.19) −0.026 0.0175 (−0.06, 0.01) 0.141*\n\n International Urogynecology Journal\nreduced hiatal area and LR diameter at rest, Valsalva and \ncontraction, which is more consistent with the findings of \nother studies. This result suggests a correlation between the \nseverity of the PPP and greater differences in PFM biometric \ncharacteristics, possibly due to stiffer, higher-tone PFM.\nSeveral studies have assessed nulliparous women with \nendometriosis and their PFM biometry. The first compared \n50 women with endometriosis with 35 women without [12], \nreporting significant differences for LH areas at rest (12.0 \nvs 13.2  cm2; p = 0.03) and on Valsalva (14.5 vs 17.3  cm2; \np < 0.01) as well as AP diameter on Valsalva but not contrac-\ntion [12]. In the second, 75 women with DIE were compared \nwith 39 who had ovarian disease [13]. Participants in the DIE \ngroup had a reduction in LH area at rest (10.8 vs 11.9  cm2; p \n= 0.03), contraction (8.8 vs 9.3  cm2; p = 0.03) and Valsalva \n(12.2 vs 14.2  cm2; p = 0.02) as well as LR diameter in all \ndegrees of movement, compared with the group with ovarian \ndisease [13]. Our findings also suggest a difference for women \nwith DIE with reduced LH area (rest and Valsalva although \nnot contraction), PVM length (rest, Valsalva and contraction) \nand PVM width (Valsalva). Unlike the above studies, we did \nnot find an association with LR diameter in any of the phases \nof movement, and it is possible that this relates to the inclu-\nsion of parous as well as nulliparous women, resulting in a \nTable 5  Comparison of deep infiltrating endometriosis (DIE) versus no endometriosis among women who had experienced PPP\nAP anterior–posterior, DIE deep infiltrating endometriosis, L–R left–right, PVM pubovisceral muscle\n*Statistically significant\nEndometriosis group Adjusted mean (95% CI) Mean difference vs no \nendometriosis (B)\np value\nRest\n  Levator hiatal area  (cm2) No endometriosis (reference) 12.75 (12.48, 13.03) – –\nDIE 11.89 (11.26, 12.57) −0.070 0.015*\n  PVM length (cm) No endometriosis (reference) 11.28 (11.15, 11.41) – –\nDIE 10.83 (10.53, 11.15) −0.040 0.006 *\n  AP diameter (cm) No endometriosis (reference) 4.98 (4.90, 5.06) – –\nDIE 4.80 (4.62, 4.99) −0.036 0.071\n  L–R diameter (cm) No endometriosis (reference) 3.75 (3.70, 3.81) – –\nDIE 3.63 (3.51, 3.78) −0.031 0.108\n  PVM width (average cm) No endometriosis (reference) 1.05 (1.03, 1.07) – –\nDIE 1.04 (1.00, 1.08) −0.010 0.614\nValsalva\n  Levator hiatal area  (cm2) No endometriosis (reference) 16.98 (16.51, 17.47) – –\nDIE 15.13 (14.06, 16.28) −0.116 0.002*\n  PVM length (cm) No endometriosis (reference) 11.99 (11.84, 12.13) – –\nDIE 11.49 (11.13, 11.85) −0.043 0.008*\n  AP diameter (cm) No endometriosis (reference) 7.72 (7.40, 8.05) – –\nDIE 7.15 (6.39, 8.00) −0.077 0.190\n  L–R diameter (cm) No endometriosis (reference) 4.27 (4.20, 4.33) – –\nDIE 4.11 (3.94, 4.28) −0.038 0.080\n  PVM width (average cm) No endometriosis (reference) 1.11 (1.07, 1.14) – –\nDIE 0.96 (0.89, 1.04) −0.143 0.001 *\nContraction\n  Levator hiatal area  (cm2) No endometriosis (reference) 10.48 (10.25, 10.71) – –\nDIE 10.05 (9.48, 10.65 −0.042 0.161\n  PVM length (cm) No endometriosis (reference) 10.11 (10.00, 10.22) – –\nDIE 9.80 (9.53, 10.07) −0.031 0.030 *\n  AP diameter (cm) No endometriosis (reference) 4.19 (4.13, 4.26) – –\nDIE 4.19 (4.02, 4.36) −0.001 0.958\n  L–R diameter (cm) No endometriosis (reference) 3.59 (3.53, 3.65) – –\nDIE 3.49 (3.34, 3.64) −0.029 0.191\n  PVM width (average cm) No endometriosis (reference) 1.01 (1.00, 1.03) – –\nDIE 0.98 (0.95, 1.02) −0.030 0.124\n\nInternational Urogynecology Journal \nwider range of measurements. Studies associating DIE and \nsmaller LH areas hypothesise that deeply infiltrating disease \nand inflammation may be more likely to cause both neural and \nmuscular effects, because of either direct injury or increased \nvisceral sensitivity resulting in changes to PFM dimensions \n[18]. This represents a limitation of our study owing to the \nabsence of information on the specific location of endometrio-\nsis lesions, thus limiting the capacity for a stratified analysis \nof morphometry to better address this hypothesis.\nA difference was demonstrated between the PPP and no \npain groups with regard to modes of delivery, with a higher \nfrequency of caesarean delivery in the PPP group. Although \nthis study was not designed to measure this outcome and \ntherefore cannot answer questions such as the presence of \nPPP prior to pregnancy and delivery, or the reasons for hav-\ning caesarean delivery, it documents a correlation that is \nworthy of future investigation. There is divergent evidence \nof pain outcomes for women after delivery and the cor -\nrelation with PPP is still not established. One long-term \nstudy reported that women with a prior vaginal delivery are \nmore likely to have dyspareunia at 6–11 years postpartum, \nalthough general pelvic pain rates were no different [25]. \nA separate longitudinal study reported reduced new onset \npain in the first 3 months postpartum for women who had a \ncaesarean delivery, with a history of pelvic pain being the \nonly risk factor associated with increasing pain scores over \ntime [26]. A link between caesarean delivery and pelvic pain \nhas been reported in a small longitudinal study, and other \nstudies report pelvic girdle pain to be more common after \ncaesarean, both early and at 6 months postnatally [27– 29].\nOur hypothesis is that of reverse causation, with pre-\nexisting PPP resulting in the outcome of caesarean delivery. \nThis could be due to higher-tone PFM at baseline resulting \nin factors that could affect mode of delivery, such as reduced \ndistensibility to allow for vaginal delivery, or that patients \nmay have self-selected caesarean section as their mode of \ndelivery. Further research in this area would be beneficial to \nfurther explore and test this hypothesis.\nThere are several limitations of this study. First, pain \nseverity in women with PPP was not assessed, limiting fur-\nther stratification. To adjust for this within the study, analysis \nof the treated subgroup was performed. Second, the sample-\nsize calculation in this study was based on available pub-\nlished data at the outset of the study. This was in a specific \npopulation (provoked vestibulodynia) and resulted in changes \nin all biometric measures. This range of biometric differences \nwas not supported in this study, where a purposefully broad \ninclusion criterion was designed for greater external validity. \nOur decision to use this benchmark instead of conducting a \npilot study may have affected sample-size calculations; how-\never, the allowances for contingencies were generous. Third, \nthe evaluation of PFM tone was not clinically assessed. Our \naim was to examine the value of an “objective” measure such \nas ultrasound, as the assessment of tone is variably reported \nand may not be widely used in a general setting; however, \nwe recognise that a formal PFM assessment via a palpation \ntechnique, which would have allowed better understanding \nof the correlation between high-tone muscles on palpation \nand biometry on ultrasound. The evolution of 3D/4D ultra-\nsound as an imaging modality over time has tended to be \ncomplementary to clinical examination rather than a replace-\nment and this is supported by our findings. Finally, although \nwe report on several ultrasound measurements, our primary \nanalysis was of LH area and LR diameter, consistent with our \naims. We did not adjust for multiple comparisons, and this \nmay increase type 1 error. Results should be interpreted with \ncaution, with emphasis placed on effect sizes and confidence \nintervals rather than on p values alone.\nThis study adds to the literature supporting differences \nin PFM biometric indices for women with PPP (particularly \nthose requiring current treatment) and DIE when assessed by \n3D/4DUS and adds weight to the hypothesis of increased PFM \ntone in patients with PPP and endometriosis. Although differ-\nences were seen, the distribution of measurements is such that \nthere will be overlap between women in the PPP and no pain \ngroups. For this reason, ultrasound measurements alone can-\nnot be used to diagnose a patient with increased PFM tone but \nmay have a role in predicting response to or effect of, treatment \nsuch as physiotherapy. Scoring scales have been proposed as an \noption for women with endometriosis to help to identify those \nwho would benefit from adjuvant physiotherapy [30]. Treat-\nment effect with physiotherapy has already been measured \nusing 3DUS and this may have further application in provid-\ning an objective measure to determine effect on the musculature \nover time [18]. Further research that includes validated pain \nscoring as well as a comparison of 3D/4DUS with digital palpa-\ntion of high-tone PFM may demonstrate a stronger association \nbetween symptomatology and PFM biometry on ultrasound.\nAppendix 1\nTable 6  Comparison of incomplete versus complete ultrasound\n*Statistically significant\nIncomplete \n(n = 93)\nComplete \n(n = 654)\np value\nAge, mean (SD) 42.4 (15.75) 41.1 (12.93) 0.45\nBMI, mean (SD) 25.4 (5.3) 24.7 (4.7) 0.20\nProlapse, % 14 18 0.55\nPelvic pain, % 62 63 0.93\nEndometriosis sur-\ngery, %\n24 35 0.02*\nParous, % 45 52 0.24\n\n International Urogynecology Journal\nAcknowledgements We would like to thank Nancy Briggs for her \nassistance with the statistical evaluation. We thank the Australasian \nGynaecological Endoscopy and Surgery Society (AGES), the Royal \nHospital for Women Foundation, Gynaecological Research and Clinical \nEvaluation (GRACE) grant and the Royal Australian and New Zealand \nCollege of Obstetricians and Gynaecologists (RANZCOG) for their \nsupport for this study through funding and scholarships.\nAuthors’ Contributions E.M.N.-H.: protocol/project development, eth-\nics, data collection and management, data analysis, manuscript writ -\ning/editing; H.P.D.: data analysis, manuscript writing/editing; W.L.L.: \nmanuscript writing/editing; J.A.A.: protocol/project development, \nmanuscript writing/editing.\nFunding Open Access funding enabled and organized by CAUL and \nits Member Institutions. This study was funded by grants from the \nAGES, the Royal Hospital for Women Foundation, GRACE grant and \na scholarship from the RANZCOG. None of the sources of funding was \ninvolved in the design, collection or composition of the manuscript.\nDeclarations \nEthical Approval Ethical approval for this study was obtained from the \nSouth Eastern Sydney Local Health District Human Research Ethics \nCommittee (HREC 12/194).\nInformed Consent to Participate Written informed consent was \nobtained from all subjects before the study.\nInformed Consent to Publish Written informed consent was obtained \nfrom the patient(s) for their anonymised information to be published \nin this article.\nConflicts of interest H.P.D. has received unrestricted educational \ngrants, travel support and lecture fees from GE Healthcare. The other \nauthors have no conflicts of interest to disclose.\nOpen Access This article is licensed under a Creative Commons Attri-\nbution 4.0 International License, which permits use, sharing, adapta-\ntion, distribution and reproduction in any medium or format, as long \nas you give appropriate credit to the original author(s) and the source, \nprovide a link to the Creative Commons licence, and indicate if changes \nwere made. The images or other third party material in this article are \nincluded in the article’s Creative Commons licence, unless indicated \notherwise in a credit line to the material. If material is not included in \nthe article’s Creative Commons licence and your intended use is not \npermitted by statutory regulation or exceeds the permitted use, you will \nneed to obtain permission directly from the copyright holder. To view a \ncopy of this licence, visit http://creativecommons.org/licenses/by/4.0/.\nReferences\n 1. Mathias SD, Kuppermann M, Liberman RF, Lipschutz RC, \nSteege JF. Chronic pelvic pain: prevalence, health-related \nquality of life, and economic correlates. Obstet Gynecol. \n1996;87(3):321–7.\n 2. Zondervan KT, Yudkin PL, Vessey MP, Jenkinson CP, Dawes \nMG, Barlow DH, et al. The community prevalence of chronic \npelvic pain in women and associated illness behaviour. Br J Gen \nPract. 2001;51(468):541.\n 3. Bachmann GA, Rosen R, Arnold LD, Burd I, Rhoads GG, Lei-\nblum SR, et al. Chronic vulvar and gynecologic pain: prevalence \nand characteristics in a self-reported survey. J Reprod Med. \n2006;51(1):3.\n 4. Worman RS, Stafford RE, Cowley D, Prudencio CB, Hodges PW. \nEvidence for increased tone or overactivity of pelvic floor mus-\ncles in pelvic health conditions: a systematic review. Am J Obstet \nGynecol. 2022;228(6):657-74.e91.\n 5. Kapurubandara SC, Lowes B, Sansom-Daly UM, Deans R, \nAbbott JA. A systematic review of diagnostic tests to detect pel-\nvic floor myofascial pain. Int Urogynecol J Pelvic Floor Dysfunct. \n2022;33(9):2379–89.\n 6. Kadah S, Soh S-E, Morin M, Schneider M, Heron E, Frawley H. Is \nthere a difference in pelvic floor muscle tone between women with \nand without pelvic pain? A systematic review and meta-analysis. \nJ Sex Med. 2023;20(1):65–96.\n 7. Kadah S, Soh S-E, Morin M, Schneider M, Ang WC, McPhate L, \net al. Are pelvic pain and increased pelvic floor muscle tone asso-\nciated in women with persistent noncancer pelvic pain? A system-\natic review and meta-analysis. J Sex Med. 2023;;20(9):1206–21. \nhttps:// doi. org/ 10. 1093/ jsxmed/ qdad0 89.\n 8. Blasi I, Fuchs I, D’ Amico R, Vinci V, La Sala GB, Mazza V, et al. \nIntrapartum translabial three-dimensional ultrasound visualization \nof levator trauma. Ultrasound Obstet Gynecol. 2011;37(1):88–92.\n 9. Hoyte L, Schierlitz L, Zou K, Flesh G, Fielding JR. Two- and \n3-dimensional MRI comparison of levator ani structure, volume, \nand integrity in women with stress incontinence and prolapse. Am \nJ Obstet Gynecol. 2001;185(1):11–9.\n 10. Dietz HP, Steensma AB. The prevalence of major abnormali-\nties of the levator ani in urogynaecological patients. BJOG. \n2006;113(2):225–30.\n 11. Stuge B, Saetre K, Braekken IH. The association between pelvic \nfloor muscle function and pelvic girdle pain—a matched case con-\ntrol 3D ultrasound study. Man Ther. 2012;17(2):150–6.\n 12. Raimondo D, Youssef A, Mabrouk M, Del Forno S, Martelli V, \nPilu G, et al. Pelvic floor muscle dysfunction on 3D/4D transper -\nineal ultrasound in patients with deep infiltrating endometriosis: \na pilot study. Ultrasound Obstet Gynecol. 2017;50(4):527–32.\n 13. Mabrouk M, Raimondo D, Del Forno S, Baruffini F, Arena A, \nBenfenati A, et al. Pelvic floor muscle assessment on three-and \nfour-dimensional transperineal ultrasound in women with ovar -\nian endometriosis with or without retroperitoneal infiltration: a \nstep towards complete functional assessment. Ultrasound Obstet \nGynecol. 2018;52(2):265–8.\n 14. Thibault-Gagnon S, McLean L, Goldfinger C, Pukall C, Cham-\nberlain S. Differences in the biometry of the levator hiatus at \nrest, during contraction, and during Valsalva maneuver between \nwomen with and without provoked vestibulodynia assessed by \ntransperineal ultrasound imaging. J Sex Med. 2016;13(2):243–52.\n 15. Morin M, Bergeron S, Khalife S, Mayrand MH, Binik YM. Mor-\nphometry of the pelvic floor muscles in women with and with-\nout provoked vestibulodynia using 4D ultrasound. J Sex Med. \n2014;11(3):776–85.\n 16. Van Reijn-Baggen DA, Han-Geurts IJ, Voorham-van der Zalm \nPJ, Pelger RC, Hagenaars-van Miert CH, Laan ET. Pelvic floor \nphysical therapy for pelvic floor hypertonicity: a systematic review \nof treatment efficacy. Sex Med Rev. 2022;10(2):209–30.\n 17. Schubert R, Song S, Everist R, Nesbitt-Hawes E, Abbott J. The \nimpact of multimodal physiotherapy in an interdisciplinary set-\nting for the management of women with persistent pelvic pain and \npelvic floor tension myalgia. Eur J Physiother. 2024;26(2):66–71.\n 18. Volpe LJ, Zugelder M, Kotarinos R, Kotarinos E, Kenton K, Gey-\nnisman-Tan J. Objective changes in pelvic floor muscle strength \nand length in women with high-tone pelvic floor dysfunction after \npelvic floor physical therapy (RELAX Trial). Urogynecology. \n2023. https:// doi. org/ 10. 1097/ spv. 00000 00000 001355.\n 19. Nesbitt-Hawes E, Dietz H, Abbott J. Morphometry of the nullipa-\nrous pelvic floor. Ultrasound Obstet Gynecol. 2018;52(5):672–6.\n\nInternational Urogynecology Journal \n 20. Treede R-D, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, \net al. Chronic pain as a symptom or a disease: the IASP Clas-\nsification of Chronic Pain for the International Classification of \nDiseases (ICD-11). Pain. 2019;160(1):19–27.\n 21. Dietz H. Ultrasound imaging of the pelvic floor. Part II. Three-\ndimensional or volume imaging. Ultrasound Obstet Gynecol. \n2004;23(6):615–25.\n 22. Majida M, Braekken IH, Umek W, Bo K, Saltyte Benth J, Ell-\nstrom Engh M. Interobserver repeatability of three- and four-\ndimensional transperineal ultrasound assessment of pelvic floor \nmuscle anatomy and function. Ultrasound Obstet Gynecol. \n2009;33(5):567–73.\n 23. Dietz HP, Shek C, Clarke B. Biometry of the pubovisceral muscle \nand levator hiatus by three-dimensional pelvic floor ultrasound. \nUltrasound Obstet Gynecol. 2005;25(6):580–5.\n 24. Tan L, Shek KL, Atan IK, Rojas RG, Dietz HP. The repeatability \nof sonographic measures of functional pelvic floor anatomy. Int \nUrogynecol J Pelvic Floor Dysfunct. 2015;26(11):1667–72.\n 25. Blomquist JL, McDermott K, Handa VL. Pelvic pain and mode \nof delivery. Am J Obstet Gynecol. 2014;210(5):423.e1-6.\n 26. Bjelland EK, Owe KM, Pingel R, Kristiansson P, Vangen S, Eber-\nhard-Gran M. Pelvic pain after childbirth: a longitudinal popula-\ntion study. Pain. 2016;157(3):710–6.\n 27. Li W-Y, Liabsuetrakul T, Stray-Pedersen B, Li Y-J, Guo L-J, Qin \nW-Z. The effects of mode of delivery and time since birth on \nchronic pelvic pain and health-related quality of life. Int J Gynae-\ncol Obstet. 2014;124(2):139–42.\n 28. Bjelland EK, Stuge B, Vangen S, Stray-Pedersen B, Eberhard-Gran \nM. Mode of delivery and persistence of pelvic girdle syndrome 6 \nmonths postpartum. Am J Obstet Gynecol. 2013;208(4):298.e1-7.\n 29. Mukkannavar P, Desai B, Mohanty U, Parvatikar V, Karwa D, \nDaiwajna S. Pelvic girdle pain after childbirth: the impact of mode \nof delivery. J Back Musculoskelet Rehabil. 2013;26(3):281–90.\n 30. Arena A, Degli Esposti E, Cocchi L, Orsini B, Lenzi J, Del Forno \nS, et al. Three-dimensional ultrasound evaluation of pelvic floor \nmuscle contraction in women affected by deep infiltrating endo-\nmetriosis: application of a quick contraction scale. J Ultrasound \nMed. 2022;41(12):2973–9.\nPublisher's Note Springer Nature remains neutral with regard to \njurisdictional claims in published maps and institutional affiliations.","source_license":"CC-BY-4.0","license_restricted":false}