Urinary symptoms and pelvic floor muscle function during the third trimester of pregnancy in nulliparous women

Abstract

Aim:  To evaluate pelvic floor muscle (PFM) function and its association with urinary symptoms in the third trimester of pregnancy.

Material and Methods:  A cross-sectional study was conducted among 91 nulliparous women at 30–34 weeks of pregnancy. PFM was evaluated by surface electromyography (sEMG) and manual muscle testing, while urinary symptoms were identified by interview. Chi-square and Fisher's exact tests were used to analyze proportions and Mann–Whitney test was used to analyze differences in means.

Results:  Average sEMG values were 4.8 µV for basic tonus (BT), 19.2 µV for maximum voluntary contraction (MVC), and 12.9 µV for average sustained contraction (ASC), and 48.4% presented muscle strength grade 3. Nocturia was reported by 80.2%, followed by increased daytime frequency (59.3%), stress urinary incontinence (50.5%), and urge urinary incontinence (25.3%). No association was found between urinary symptoms and MVC or ASC or PFM manual tested strength.

Conclusion:  No association was observed between PFM function and urinary incontinence, except decreased BT among late third trimester pregnant women with irritative bladder symptoms.

Introduction

The pelvic floor (PF) has a fundamental role in supporting the pelvic organs and in the mechanism of urinary continence.^1,2 The urethral structures, such as the vascular and submucosal plexus, combined with urethral sphincters muscle tonus maintain the coaptation of the urethral lumen during rest. Considering the sudden increase in intra-abdominal pressure, this closing mechanism needs the opposing PF muscle (PFM) contraction, keeping urethral pressure higher than vesical pressure.^1,2 Some factors may interfere in this mechanism, causing a prolonged increase of intra-abdominal pressure, overloading the PFM and its neural, fascial and fibromuscular structures. Among the main factors are obesity, constipation, senility, parity, chronic cough and pregnancy.^2,3 In the case of pregnancy, the supporting structures are believed to be overloaded due to the fetus weight and the progressive growth of the uterus, both in weight and size.³ Additionally, the pregnant uterus increases the angle between the vesical neck and urethra, which can contribute to urinary symptoms. Hormonal changes due to pregnancy can also cause changes in tissue, in the support, and in the continence mechanism.⁴ These changes become evident by the appearance of urinary incontinence (UI) and irritative bladder (IB) symptoms, which become more prevalent as pregnancy develops.^4–7 In non-pregnant women, there is a known relationship between lower PFM strength and presence of UI.⁸ During pregnancy, a similar relationship was observed by Morkved et al.,⁹ but not by Diez-Itza et al.¹⁰ We must highlight that the method used in both studies is validated and recommended for clinical practice, but as it is not a proper assessment method, with no standardization in equipment, probe size, and units used.¹¹ The evaluation of muscle activation by PFM surface electromyography (sEMG) is considered a reliable method. It can demonstrate basal tonus (BT), phasic muscle function (maximum voluntary contraction [MVC]), and tonic fibers (average sustained contraction [ASC]), providing a more complete functional muscle assessment, despite its lack of proper demonstration of the muscle movement.¹²

The role of the pelvic floor muscles in the development of urinary symptoms during pregnancy is still uncertain, so the aim of the present study was to assess the association between PFM function (by surface electromyography and manual grading of muscle strength) with the presence of urinary symptoms in nulliparous women in the third trimester of pregnancy.

Material and Methods

This was a cross-sectional study of nulliparous women in antenatal care at a reference center (CAISM–UNICAMP) or at primary health care units in Campinas, Brazil. Women were enrolled between October 2008 and April 2010. The project was approved by the Research Ethics Committee of the College of Medical Sciences UNICAMP.

Pregnant women aged 18–35 years of age, between 30 and 34 weeks of pregnancy, with one fetus, were invited to participate. Those who had difficultly understanding, had motor or neurological deficit of lower limbs, had been submitted to any surgery in the pelvic region, reported pelvic pain, had diabetes, or had previously exercised to reinforce PFM, and with contraindication for vaginal touch, were excluded. The goals of the study and the procedures indicated were explained to the candidates, and those who agreed to participate signed the written informed consent term.

Sociodemographic data were collected (age, height, weight, color of skin, schooling level, marital status, occupation), as well as knowledge of PFM, practice of physical exercises (unless PFM training), and presence of urinary symptoms.

In regard to physical exercises, participants were asked whether they had practiced physical exercises during the last six months and if so, how frequently and using which modality; they were considered regular if they practiced for more than 30 min, three or more times a week.

The presence of urinary symptoms during the previous week was questioned, and the following terminology proposed by the International Continence Society (ICS) was used:¹³ stress urinary incontinence (SUI); urge urinary incontinence (UUI); nocturnal enuresis; increased daytime frequency; urgency; and nocturia. Increased daytime frequency, urgency and nocturia were pooled as irritative bladder (IB) symptoms.^5,13 After completing the evaluation form, the volunteers were submitted to a physical exam, performed by the same physiotherapist (trained in pelvic floor muscle evaluation). The physical exam was realized in supine position (abducted semi-flexed hips and knees) and the objective was to check PFM function, grading the muscle strength and using surface electromyography (sEMG). The grading was done according to the validated, standardized modified Oxford Scale,¹⁴ which ranges from zero to five (zero, absence of muscle contraction; one, flicker of muscles; two, week contraction; three, medium contraction – slight lift of examiner's finger without resistance; four, strong contraction – elevation of examiner's finger against small resistance; five, very strong contraction – elevation of examiners finger against strong resistance). If a pregnant woman was graded with a zero, she was immediately discontinued from the research because it would not be possible to assess her muscular status using sEMG. Women were subsequently categorized as grades 1–2 or 3–4 for statistical analysis.

To perform sEMG, a sterile intravaginal electrode was used connected to an electromyograph (Miotool 200URO; Miotec, Porto Alegre-RS, Brazil), which converts the mioelectrical signal into continuous values expressed in microVolts (µV), viewed in graph format. sEMG assessment consisted of capturing the values of the average BT (muscle tension status during rest, which allows for a voluntary contraction immediately after receiving an impulse from the nervous centers), while resting (for 1 min); MCV value (highest value in three following repetitions); and average sustained contraction (ASC) for 10 s.

Statistical analysis was conducted using Epi Info version 3.5.1 and SAS version 9.02 and the assumed significance level was 5%. For the description of sociodemographic variables, muscle function and prevalence of urinary symptoms, we used frequency, average (±SD) and median measurements. Mann–Whitney test was used to evaluate the association between measurements of PFM, sEMG and urinary symptoms. Chi-square and Fisher's exact tests were used to analyze the association between PFM graded strength and urinary symptoms. To analyze possible factors associated with the presence of urinary symptoms the prevalence ratio (PR) was calculated with the respective 95% confidence interval (CI). This cross-sectional study is a secondary analysis of a cohort study aiming to evaluate the same women during the third trimester of pregnancy and 60 days postpartum. The sample size was calculated for the cohort study based on the difference of pelvic floor muscle strength pre- and postpartum.¹⁵

Results

One hundred and two nulliparous pregnant women were invited to participate, 11 refused. Therefore, the study was performed in 91 pregnant women with an average age of 24.3 years (±4.9), median gestational age of 32 weeks (30–34), and weight during pregnancy of 77.5 kg (±20.4). Over half (51 women) classified themselves as white (56%), 79.1% (72) were married or were in a stable relationship and 65.9% had studied beyond the eighth grade of fundamental school. Among the 18.7% who practiced in regular physical exercise, most walked. Most pregnant women (93.1%) had no information about pelvic floor, and the others could only point to the region.

Table 1 shows PFM function parameters, and average values for BT, MVC, and ASC were 4.8 µV, 19.2 µV, and 12.9 µV, respectively. Grade three was the highest muscle strength presented by pregnant women (48.4%).

Table 1. Pelvic floor muscle function of 91 pregnant women at 30–34 weeks of pregnancy

Electromyographic parameters in µV	Median (min-max)	Average (±SD)
Basal tonus	4.1 (0.6–24.6)	4.8 (3)
Maximum voluntary contraction	17.2 (3.5–50.1)	19.2 (8.7)
Average sustained contraction	11.7 (3.5–32.4)	12.9 (6.3)
Muscle strength grading	N	%
Grade 1	11	12.1
Grade 2	23	25.3
Grade 3	44	48.4
Grade 4	13	14.3
Grade 5	0	0

As shown in Table 2, 96.7% of pregnant women reported some urinary symptom, while IB symptoms were reported by 94.5%. Nocturia was prevalent among 80.2%, followed by increased daytime frequency (59.3%), and UUI (50.5%). SUI was related by 50.5% of women as the most prevalent symptom of incontinence. There was also a combination of complaints.

Table 2. Prevalence of urinary symptoms at 30–34 weeks of pregnancy

Urinary symptom	N	%
Any symptom	88	96.7
Stress urinary incontinence	46	50.5
Urge urinary incontinence	23	25.3
Nocturnal enuresis	5	5.5
Increased daytime frequency	54	59.3
Urgency	46	50.5
Nocturia	73	80.2

An association was noted between the presence of IB symptoms and lower BT (P < 0.05). A positive association was found between muscle strength grade and MVC and ASC (P < 0.05) (Table 3). No association was found between muscle strength grade and urinary symptoms (Table 4).

Table 3. Association between urinary symptoms and grading of muscle strength with PFM sEMG

	Basal tonus		Voluntary contraction		Sustained contraction
			Maximum		Average
	Average ± SD	P-value	Average ± SD	P-value	Average ± SD	P-value
Mann–Whitney test / †Power of the test 99%. PFM, pelvic floor muscle; sEMG, surface electromyography; SUI, stress urinary incontinence; UUI, urge urinary incontinence. Bold items indicate statistical significance.
SUI
Yes	4.4 (2)	0.4413	18.6 (7.5)	0.7299	11.9 (4.9)	0.4460
No	5.2 (3.8)		19.8 (9.7)		13.8 (7.4)
UUI
Yes	4 (1.9)	0.1623	20.6 (9)	0.4216	13.3 (7)	0.7771
No	5 (3.3)		18.8 (8.6)		12.7 (6.1)
Nocturnal enuresis
Yes	4.5 (2.5)	0.8074	16.2 (4.7)	0.5307	10.4 (3.6)	0.4032
No	4.8 (3.1)		19.4 (8.8)		13 (6.4)
Increased daytime frequency
Yes	4.4 (3.3)	0.0070	19.6 (9.1)	0.7252	12.8 (6.5)	0.7131
No	5.4 (2.5)		18.6 (8)		13 (6)
Urgency
Yes	4.3 (2.4)	0.0455	19.1 (8.3)	0.7964	12.7 (6.3)	0.8489
No	5.3 (3.5)		19.3 (9.1)		13.1 (6.4)
Nocturia
Yes	4.8 (3.2)	0.0485	19 (8.9)	0.6044	12.6 (6.6)	0.2478
No	5.1 (2.1)		19.9 (7.9)		13.9 (5.1)
Muscle strength grading
Grade 1–2	5.1 (2.5)	0.095	15.1 (5.6)	0.0003 †	10.3 (4.3)	0.0026 †
Grade 3–4	4.6 (3.3)		21.7 (9.3)		14.5 (6.8)

Table 4. Grading of muscle strength and urinary symptoms during pregnancy

	Total (91)	Grade 1–2	Grade 3–4	P-value
		n (%)	n (%)
Chi-square test / †Fisher's exact test. SUI, stress urinary incontinence; UUI, urge urinary incontinence.
SUI
Yes	46	20 (58.8)	26 (45.6)	0.2227
No	45	14 (41.2)	31 (54.4)
UUI
Yes	23	7 (20.6)	16 (28.1)	0.4369
No	68	27 (79.4)	41 (71.9)
Nocturnal enuresis
Yes	5	2 (5.9)	3 (5.3)	0.6211†
No	86	32 (94.1)	54 (94.7)
Increased daytime frequency
Yes	54	16 (47.1)	38 (66.7)	0.0654
No	37	18 (52.9)	19 (33.3)
Urgency
Yes	46	14 (41.2)	32 (56.1)	0.1672
No	45	20 (58.8)	25 (43.9)
Nocturia
Yes	73	26 (76.5)	47 (82.5)	0.488
No	18	8 (23.5)	10 (17.5)

The prevalence of SUI was almost twice (P = 0.0086; PR 1.79 [95% CI: 1.12–2.87]) as high among white pregnant women compared to non-white women (Table 5).

Table 5. Factors associated with stress urinary incontinence (SUI) and urge urinary incontinence (UUI) in pregnant women

	SUI				UUI
	Yes	No	Raw PR (95% CI)	P-value	Yes	No	PR (95% CI)	P-value
	n (%)	n (%)			n (%)	n (%)
Chi-square test / †Fisher's exact test; ‡Fundamental school. ASC, average sustained contraction; BMI, body mass index; BT, basic tonus; MVC, maximum voluntary contraction; PR, prevalence ratio.
Color
White	32 (62.8)	19 (37.2)	1.79 (1.12–2.87)	0.0086	12 (23.5)	39 (79.5)	0.86 (0.42–1.73)	0.6653
Not white	14 (35)	26 (65)			11 (27.5)	29 (72.5)
Schooling level
Up to 8th grade‡	12 (38.7)	19 (61.3)	0.68 (0.42–1.12)	0.1044	9 (29)	22 (71)	1.24 (0.61–2.55)	0.5533
Above 8th grade‡	34 (56.7)	26 (43.3)			14 (23.3)	46 (76.7)
Physical activity
None	39 (52.7)	35 (47.3)	1.28 (0.70–2.35)	0.3914	20 (27)	54 (73)	1.53 (0.52–4.57)	0.5450†
Regular	7 (41.2)	10 (58.8)			3 (17.7)	14 (82.3)
Gestational BMI
Overweight/obese	35 (51.5)	33 (48.5)	1.08 (0.66–1.75)	0.7625	17 (25)	51 (75)	0.96 (0.43–2.14)	0.9174
Normal/low weight	11 (47.8)	12 (52.2)			6 (26.1)	17 (73.9)
BT (µV)
≤4.11	25 (54.4)	21 (45.6)	1.16 (0.77–1.75)	0.4637	15 (32.6)	31 (67.4)	1.83 (0.86–3.89)	0.1036
>4.11	21 (46.7)	24 (53.3)			8 (17.8)	37 (82.2)
MVC
≤17.12	25 (54.4)	21 (45.6)	1.16 (0.77–1.75)	0.4637	10 (21.7)	36 (78.3)	0.75 (0.36–1.53)	0.4327
>17.12	21 (46.7)	24 (53.3)			13 (28.9)	32 (71.1)
ASC
≤11.72	22 (47.8)	24 (52.2)	0.90 (0.56–1.35)	0.5993	10 (21.7)	36 (78.3)	0.75 (0.36–1.53)	0.4327
>11.72	24 (53.3)	21 (46.7)			13 (28.9)	32 (71.1)
Muscle strength grading
Grade 1–2	20 (58.8)	14 (41.2)	1.29 (0.86–1.92)	0.2227	7 (20.6)	27 (79.4)	0.73 (0.33–1.60)	0.4269
Grade 3–4	26 (45.6)	31 (54.4)			16 (28.1)	41 (71.9)

Discussion

This study demonstrated a high prevalence of urinary symptoms in the late third trimester of nulliparous women, but no association was found between urinary symptoms and MVC, ASC and PFM strength, except basal tonus.

Increased daytime frequency was reported by 59.3% pregnant women, similar to Nel et al.,¹⁶ which was lower compared to two other studies.^5,6 Urinary urgency was the third most prevalent symptom, affecting 50.5% of pregnant women, while other studies showed prevalence varying from 27% to 68.2%.^5,6,16 Despite not being extensively studied during pregnancy, nocturia has a prevalence varying from 77.7% (nulliparous women, third trimester)⁵ to 87% (nulliparous and multiparous women),¹⁶ not different from the present study, being a highly prevalent symptom during pregnancy, regardless of parity. The prevalence of IB symptoms tends to increase as pregnancy develops.^5,6,16 A higher prevalence of IB symptoms was observed among women with a higher schooling level. Possibly, these women were better able to better understand the question or the concept of irritative urinary symptoms, which could increase their prevalence.⁶ SUI was the most prevalent UI symptom (50.5%), similar to Wijma et al.¹⁷ who had findings of 49%. However, most studies show a smaller prevalence.^6,7,10,17 Nocturnal enuresis was reported by 5.2% of pregnant women, a percentage that was similar to that described by Scarpa et al.⁵ But UUI was reported by 24.6% of nulliparous pregnant women, a prevalence above that reported by other studies,^5,6,18 which varied from 5.4% to 19%.

A large variation was observed in the prevalence of urinary symptoms in the different studies. The divergences seemed to be due to the heterogeneity of the populations studied, with racial, cultural, educational, social, and age group diversity, as well as in the difference of the method used to assess the symptoms, and the period of pregnancy when the study was performed.¹⁹

The pathophysiology of IB symptoms is still not entirely clear, both in pregnant as in non-pregnant women. A reasonable explanation for the increase in the number of daily voids (daytime frequency) and night voids (nocturia) during pregnancy would be the increased renal glomerular filtration rate, resulting in a greater urine production.²⁰ Another suggestion is that the increased weight and size of the uterus over the bladder decreases vesical capacity, causing these symptoms.²¹ This significant reduction in maximal cystometric capacity was observed by Nel et al.¹⁶ when performing urodynamic study in pregnant women. Other factors also seem to be involved in the development of these symptoms, such as hormonal changes due to pregnancy that would affect the biochemical composition of the tissues, altering the connective fibers, especially affecting the vaginal wall and pubovisceral muscles.¹ Therefore, the etiology of IB symptoms may be linked to PFM tissue modification.⁴ In the present study, an association was found between the presence of IB symptoms and decreased BT. Such a decrease in pregnant women may be explained by the action of the hormone relaxin, which enables connective tissues to remodel, reducing their tension. Therefore, the decrease of PFM activation during rest could cause this symptom.²² Even though PFM BT patterns have not been extensively studied, it is noticeable that some individuals with low resting tension, when requested to contract voluntarily, prove capable of contracting very efficiently.²² This could be the reason why a significant association between the presence of IB symptoms and MVC and ASC was not observed in the present study. Hence, there are indications that other factors have a stronger relation with the development of IB symptoms during pregnancy than the capacity for voluntary contraction of the PFM.

In SUI, the mechanism is different from IB symptoms. We know urinary continence is determined by the integrity and joint action of the PF structures.¹ Another factor that could contribute to SUI is growth of the uterus, which would increase the angle between the vesical neck and urethra.⁴ These changes would cause a compensation mechanism to maintain continence (increase in the urethral length and pressure), which would not happen in incontinent pregnant women, allowing the vesical pressure to exceed the urethral pressure.²³ This could also explain the cases of UUI in which the urethral sphincter would not stand the pressure exercised by the detrusor and would open, causing UI. The lack of compensation mechanism can also be linked to an intrinsic weakness of the urethral closure mechanism. Changes in tissue properties can be pre-existing and be responsible for the development of UI.^18,23

Besides the urethral mechanism the PFM also acts to prevent urine loss, overall in sudden increase of intra-abdominal pressure.^1,2 However, the ideal position of these structures can change during pregnancy, which may cause an inefficient urethral compression, leading to SUI.¹¹ Hence, the maximum and sustained contraction capacity would remain, even in cases of urine loss due to physical activity. This loss would cause a change in the ideal position of the contraction and not in the muscle itself. This could explain why no association was observed between graded muscle strength, MVC and ASC in the presence of UI.

In the present study, an association was observed between the presence of SUI and white women, suggesting this could be a risk factor for the development of this morbidity. Another study also observed a significantly higher prevalence of SUI among white women.²⁴ The reason for this difference is still not clear, both among pregnant and non-pregnant women;²⁴ however, Howard et al. demonstrated that black women have a higher urethral closing pressure and PFM strength, suggesting that this could be the reason for a lower prevalence of SUI, contrary to white women.²⁵ Other factors could also be involved.

Studies evaluating PFM training during pregnancy as a treatment for UI demonstrate that increased PF strength decreased the symptoms of UI.^26,27 However, these studies did not correlate symptoms with muscle contraction before physical exercises. Morkved et al.⁹ observed decreased PFM strength among pregnant women with UI, but Diez-Itza et al.¹⁰ did not. These studies used PFM pressure assessment, which is not much recommended for scientific goals, although it is a validated method.¹¹ Therefore, in the present study sEMG was chosen as the method for muscle assessment, which allows a more complete assessment. However, no significant difference was observed in the three electromyography parameters of pregnant women with or without UI symptoms.

Even though an association between muscle strength grading and UI symptoms was not observed in this study, there was a significant association between two (MVC and ASC) of three electromyographic parameters with the grading of muscle strength. Therefore, clinical assessment by grading PF strength must not be discharged as an assessment method, even being a subjective method, it allows the examiner to guarantee the correct contraction, has high intraexaminer reliability, is of low cost and is easy to execute.¹⁴ Therefore, if sEMG equipment cannot be used to evaluate PF muscles, grading of muscle strength can be used.

The present study offers a complete assessment of the rate of urinary symptoms in the third trimester of pregnancy and its association with muscle function; the study used urinary symptom definitions according to ICS recommendations.¹³ These definitions covered both IB and UI symptoms, offering a broad vision of urinary changes in the third trimester of pregnancy. However, the sample size limited the evaluation of associations. Another limitation is that the pre-gestational continence status of the participants was not evaluated. However, muscle function evaluation itself is not enough to assess other components responsible for supporting the PF (connective tissue, fascias and ligaments). During pregnancy, these components may have greater responsibility in the development of urinary symptoms.

Therefore, when clarifying the role of MAP during pregnancy, it is possible to analyze the expected impact. Muscle function could be improved, possibly reducing urinary complaints. However, it is important to educate all pregnant women to practice pelvic floor muscle training to prevent damage in supporting tissues and urinary symptoms. This information should be provided by health professionals who are involved in the gestational process.

We expect to know in the future the real mechanism for the development of the pregnancy urinary symptoms. Therefore, preventive measures that have proved to be efficient in decreasing UI prevalence,^26,27 such as training the PFM, must be used routinely and from the beginning of pregnancy to minimize the emergence of pregnancy symptoms.

This study did not demonstrate an association between PF muscle function, except by basal tonus with surface electromyography by Miotool and grading of muscle strength by Oxford Scale with the presence of urinary symptoms in nulliparous women in the third trimester of pregnancy.

Acknowledgment

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (project no. 2007/59378-1).

Disclosure

None.