1. Postpartum voiding difficulty and urinary retention (PPUR).
Overt urinary retention
Covert urinary retention
2. Postpartum urinary incontinence (PPUI).
Stress urinary incontinence (SUI)
Urgency urinary incontinence (UUI)
Mixed urinary incontinence (MUI)
3. Urinary tract injury:
Acute complications:
Iatrogenic bladder injury/laceration
Iatrogenic ureteric injury/laceration
Bladder rupture
Chronic complications: genitourinary fistulas
Postpartum Voiding Difficulty and Urinary Retention (PPUR)
Voiding difficulty and urinary retention are relatively common puerperal conditions among women in the immediate postpartum period. To ensure a rapid recovery and return to normal bladder function after delivery, it is important to accurately diagnose and properly manage this potentially serious condition [9].
Definition
PPUR is defined as inability to void, with a painful (usually), palpable or percussable bladder and need for catheterization to provide relief [6]. In the postpartum period, there are two main types of urinary retention:
Overt (acute, painful or symptomatic) urinary retention: it refers to sudden onset of inability to pass urine spontaneously within 6 h of vaginal birth. Typically it is characterized by suprapubic pain, palpable or percussable bladder and patients usually need catheterization.
Covert (chronic, painless or asymptomatic) urinary retention: it refers to increased post void residual volumes (PVR) of more than 150 ml measured by ultrasound or catheterization and no symptoms of urinary retention [10–12]. However, ultrasound measurement of postpartum bladder volumes can be inaccurate. Sometimes patients with covert urinary retention may present with frequency and feeling of incomplete emptying. However, it is usually a self-limiting condition, which often resolves within a few days [13].
Persistent PPUR may be defined as the inability to void spontaneously despite the use of an indwelling catheter for 3 days [6].
Incidence
The exact incidence of PPUR is uncertain and its range varies widely. Estimated PPUR incidences range from 0.05 to 37 % (Table 11.1) [6, 14]. This could be explained by the inconsistency in PPUR definitions and method of diagnosis. Moreover, most studies’ figures are different depending on whether these studies comment either on overt or covert urinary retention or both types.
Table 11.1
The incidence of PPUR among women
Authors | Number of patients in study | Number of patients with PPUR | Incidence (%) |
|---|---|---|---|
Groutz et al. (2001) [6] | 8402 | 4 | 0.05 |
Kekre et al. (2011) [12] | 771 | 82 | 10.6 |
Yip et al. (1997) [13] | 164 | 19 | 11 |
Ismail and Emery (2008) [14] | 100 | 37 | 37 |
Andolf et al. (1994) [15] | 539 | 8 | 1.5 |
Liang et al. (2002) [16] | 605 | 101 | 16.7 |
Hee et al. (1992) [17] | 51 | 23 | 45 |
Demaria et al. (2004) [18] | 154 | 55 | 36 |
Yip et al. (2005) [19] | 691 | 101 | 14.6 |
Saultz et al. (1991) [20] | – | – | 1.7–17.9 |
Although in most patients urinary function improves with time, a small number (0.05 % [6] up to 1 % [15]) continue to have persistent PPUR, beyond the early puerperium. These women, if not recognized and adequately treated in the early postnatal period, may develop acute prolonged bladder overdistension (ApBO) and risk of significant long-term bladder dysfunction.
Mechanism and Pathophysiology
Several mechanisms have been suggested to explain the pathophysiology of PPUR.
Hormonal Effect on the Bladder
In the postpartum period the bladder is hypotonic, and this is a result of the physiological hormonal changes such as elevated progesterone levels during normal pregnancy and puerperium, affecting the normal bladder function, as it is a hormone-responsive organ [21]. This reduction in smooth muscle tone usually starts after the third month of pregnancy with the bladder gradually increasing in capacity as pregnancy progresses and remaining so for a number of days following birth [22]. In a small number of patients these changes may persist for days or longer especially in those patients with risk of developing PPUR (see risk factors below).
Regional Anaesthesia
Spinal, epidural and pudendal nerve block are common causes of PPUR. This may be due to suppression of the sensory stimuli from the bladder to the pontine micturition centre after afferent neural blockade, followed by inhibition of the reflex micturition mechanism, which may result in reduction of bladder contractility and urinary retention [9]. In a retrospective case controlled study of 11,322 women, 51 women (0.46 %) had overt signs of PPUR following vaginal delivery and 98 % of these were associated with epidural anaesthesia [11].
Acute Prolonged Bladder Overdistension (ApBO)
Sometimes in a woman with an epidural or following spinal anaesthesia the discomfort associated with bladder overdistension is masked and if not recognized and treated properly, ApBO occurs. One episode of overdistension is considered enough to cause bladder damage [23]. ApBO pathogenesis likely consists of 2 consecutive stages. A primary temporary neurogenic dysfunction leads to acute urinary retention; if neglected and not treated properly postnatally, it will be followed by secondary myogenic detrusor damage. Recovery depends on whether reversible or irreversible damage has occurred [24]. With irreversible damage, the detrusor becomes atonic and unable to respond; this leads to long term voiding difficulties [25].
Prolonged Labour and Instrumental Delivery
Prolonged labout and delivery may lead to PPUR by two mechanisms:
Denervation pudendal nerve injury: The pudendal nerve (S2–4) travels along the posterior wall of the pelvis and exits the pelvis to innervate the external genitalia. Due to its length and position, it becomes more vulnerable to compression, pelvic floor tissue overstretching and damage when the fetal head is compressed against the pelvic floor for a long time during vaginal delivery. Pudendal nerve damage results in diminished reflex and voluntary mechanism required for normal voiding [11, 13]. Some studies described the status of pudendal nerve injury after vaginal delivery using electrophysiological tests and showed a significant increase in pudendal nerve terminal motor latencies, which may take a few months to recover post-delivery [26–28].
Mechanical obstruction: Another possible mechanism that may lead to transient PPUR is extensive tissue oedema around the urogenital area which results from prolonged compression of the fetal presenting part onto the birth canal or instrumental/assisted delivery or extensive vaginal and perineal laceration. As tissue oedema resolves within few days of delivery, PPUR gradually improves.
In a prospective observational study of 2866 women, instrumental delivery accounted for 16.7 % of the retention group compared with 4.7 % of the control group [4].
Risk Factors for PPUR
It is difficult to accurately predict the group of women who are more at risk of PPUR. However, in a large systematic review and meta-analysis including 23 observational studies with original data Mulder et al. concluded that “instrumental delivery, epidural analgesia, primiparity and episiotomy” can be identified as the main four clinical risk factors for development of overt or covert PPUR [29].
Therefore, special attention and careful follow-up should be offered to this group of high-risk women. They must be educated to seek a review and advice if they develop any symptoms suggestive of voiding difficulties in the early postpartum period.
Clinical Presentation of PPUR
Symptoms of PPUR differ according to its type. In patients with overt PPUR symptoms are much more obvious than in those with covert type, as they are not able to void and they usually experience associated suprapubic bladder pain.
Symptoms of overt “acute” PPUR include:
Pain (should not be misdiagnosed as caesarean wound pain)
Hesitancy
Slow or intermittent stream
Straining to void
Sensation of incomplete bladder emptying
Symptoms of covert urinary retention include:
Lack of pain or other symptoms of overt urinary retention
No urgency to void – reduced bladder sensation
Overflow incontinence [19]
Symptoms may be masked and patients may be asymptomatic especially if they had epidural anaesthesia. On the other hand, some patients may present with overflow UI owing to overdistension of the bladder and be misdiagnosed with SUI.
Diagnosis of PPUR
The diagnosis of PPUR can be difficult especially if a woman is asymptomatic. It is important to have a high level of suspicion if a patient develops any symptoms of overt or covert retention. Sometimes absence or presence of symptoms may be misleading and make the diagnosis challenging. This necessitates targeted clinical investigations and further evaluation. In a study by Groutz et al. up to 45 % of women complain of significant voiding symptoms in early puerperium, however, of these patients, only 22 % will have low flow rates. Pain was the most common symptom (63 %) followed by weak stream, intermittent stream and hesitancy (44, 38, and 33 %, respectively). In this study, the symptomatic group had significantly longer 2nd stage of labour and more instrumental deliveries (ventouse) [30]. Ramsay et al. showed that 43 % of patients in the immediate post-partum period had abnormal flow rates, although, the majority of them were asymptomatic [31].
On examination some patients may have suprapubic tenderness and bulge and a palpable and percussable bladder. Clinically, the diagnosis of overt PPUR could be made if the woman is unable to void in the first 6 h after delivery and requires urethral catheterization to drain >600 ml [32]. On the other hand, covert PPUR diagnosis could be made if the patient have PVR >150 ml and is unable to void adequate amount of urine (>50 % of normal bladder capacity) [13].
Postvoid residual (PVR) volume measurements could be carried out by two methods, either by catheterization or bladder ultrasound. Catheterization is more accurate than bladder scan; however, it potentially carries increased risks of UTI. Bladder scanning is a popular non-invasive method of measuring PVR and although its accuracy has been debated, some authors believe that ultrasound assessment is highly accurate even in the postpartum period as the bladder maintains an ellipsoid shape [33].
Management and Prevention of PPUR
The bladder management during the early postpartum period is aimed to:
Maintain the normal bladder function
Minimize the risk of damage to the urethra and bladder
Provide adequate management strategies for women who have problems with bladder emptying
Prevent long-term complications associated with bladder emptying
Postpartum Bladder Care
In the first days after birth the production of urine is increased, as extracellular fluid is excreted. The following instructions are recommended in the early postpartum period to prevent the development of PPUR [20, 23, 25, 34–36]:
The timing and volume of the first voided urine should be monitored.
Timed voiding should be encouraged every 3–4 h.
PVR should be measured.
Frequency volume charts should be filled with strict follow-up for urinary input and output to ensure adequate fluid balance in the first 24 h post-delivery.
Women should be counseled to report any of the following problems if occur: insentience episode, lack of awareness or desire to void urine, hesitancy, inability to empty her bladder fully; urinary frequency; pain on voiding; any other related concerns.
If urine has not been passed within 6 h after birth, efforts to assist urination should be advised, such as taking a warm bath or shower.
If bladder emptying has still not occurred, then either the bladder must be emptied by catheterization and the volume of urine recorded, or bladder volume estimated by ultrasound, followed by catheterization as appropriate.
What to Do if PPUR Is Suspected or Confirmed?
If the voided volume is <150 ml or PVR is >150 ml by ultrasound, the patient should be managed with in/out catheterization and PVR should be accurately measured. PVR of at least 150 ml may imply a degree of bladder dysfunction. At this stage a fluid balance chart is mandatory [32].
If Still Unable to Void after a Further 6 h, Insert an Indwelling Catheter
If urinary drainage is >500 ml in 1 h, leave the catheter for 24 h. If urinary drainage is >1000 ml in 1 h, leave the catheter for 48 h. Some authors advocate for the catheter to remain in situ for 1 week [32]. We should rule out UTI by sending a midstream or catheter urine sample for culture and if UTI is documented prescribe appropriate antibiotics [37]. Intermittent self-catheterization or indwelling catheter is recommended if a trial without catheter failed or there is persistent high PVR in the absence of infection. The urine volume drained initially can be used as a predictor for repeat catheterization. In a study by Burkhart et al. it was found that if the initial volume of PVR was <700 ml, patients did not require repeat catheterization, however, if PVR was >1000 ml, 20 % of patients required repeat catheterization [38].
Discharge Planning
After delivery all women should void of ≥400 ml before discharge. Women with risk factors and who develop PPUR must have three documented voids with normal voiding parameters post removal of catheter before discharge. Women who require bladder retraining and management should be counselled and referred to a health professional with appropriate training and expertise in the treatment options for urinary retention.
Postpartum Urinary Incontinence (PPUI)
Urinary incontinence (UI) is a common problem among adult women. It is more frequent during pregnancy and the postnatal period, which may be the first time that many women experience UI. The presence of incontinence during pregnancy may be predictive of PPUI [39]. Moreover, PPUI in the short term may be predictive of longer-term problems. Women with persistent postpartum SUI at 3 months have a 92 % risk of having stress urinary incontinence at 5 years [40].
Definitions
There is no exact definition for the term PPUI; however, various definitions of UI types are standardized according to the International Continence Society (ICS) and International Urogynecological Association (IUGA). In general UI is defined as “any complaint of involuntary leakage of urine” [41].
There are three main types of UI:
Stress urinary incontinence (SUI) is defined as “the complaint of involuntary leakage on effort or exertion or on sneezing or coughing.”
Urgency urinary incontinence (UUI) is defined as “the complaint of involuntary leakage preceded by urgency.”
Mixed urinary incontinence (MUI), combination of SUI and UUI [41]
Epidemiology
The prevalence of UI in adult women over 20 years is 25 % and increases with age [45]. Pregnancy and parity are considered the main risk factors for developing UI in women. Both could have a significant impact on the pelvic floor, leading to damage of the pelvic floor support (muscles, ligaments, fascias and peripheral nerves) and result in pelvic floor dysfunction with undesired sequelae regarding urogenital tract.
The prevalence of UI in women seems to increase during pregnancy and decrease following delivery; however, the prevalence of UI during the postpartum period is still higher than before pregnancy [46, 47]. The prevalence of UI during pregnancy and postpartum varies, and reports show a wide range of 7–64 % during pregnancy [48–50], while PPUI ranges from 3 to 40 % [46, 51, 52]. It is important to estimate the prevalence of PPUI to accurately assess the public health burden of this problem and also to calculate sample sizes when designing research studies.
A Norwegian large population-based study of 12,679 primiparous women found the prevalence of PPUI at 6 months to be as high as 31 %. Incontinence was most common among women with an instrumental delivery (36 %) or spontaneous vaginal delivery (34 %) and lowest among women with emergency CS (17 %) or elective CS (13 %). The prevalence of SUI was twice that of UUI in this study (Tables 11.2 and 11.3) [51]. In 2009, another large population-based cross-sectional study from the United States (Boyles et al.) estimated the incidence of PPUI among 5599 primiparous women. The incidence of PPUI at 6 months after delivery was 10 % (see Tables 11.2 and 11.3) [53].
Table 11.2
The incidence of PPUI among primiparous and multiparous women
Author | Number of patients | Postpartum assessment time (month) | Parity |
|---|---|---|---|
Wilson et al. (1996) [44] | 1505 | 3 | 12 % Primiparous 21 % Multiparous |
Wesnes et al. (2009) [51] | 12,679 | 6 | 21 % Primiparous |
Boyles et al. (2009) [53] | 5599 | 6 | 10 % Primiparous |
Eliasson et al. (2005) [54] | 665 | 12 | 21 % Primiparous |
Farrell et al. (2001) [55] | 595 | 6 | 26 % Primiparous |
Glazener et al. (2006) [56] | 3405 | 3 | 15 % Primiparous |
Solans-Domenech et al. (2010) [57] | 1128 | 2 | 5 % Primiparous |
Burgio et al. (2003) [58] | 523 | 3 | 10 % Multiparous |
Foldspang et al. (2004) [39] | 1232 | >12 | 14 % Multiparous |
Iosif (1981) [59] | 1411 | 6–12 | 19 % SUI Multiparous |
Dimpfl et al. (1992) [60] | 350 | 3 | 4 % SUI Primiparous 4 % Multiparous |
Table 11.3
The prevalence of PPUR among primiparous and multiparous women
Author | Number of patients | Postpartum assessment time (month) | Parity |
|---|---|---|---|
Wesnes et al. (2009) [51] | 12,679 | 6 | 31 % Primiparous |
Boyles et al. (2009) [53] | 5599 | 6 | 17 % Primiparous |
Ekstrom et al. (2008) [61] | 389 | 3 | 13 % SUI, 4 % UUI Primiparous |
Eliasson et al. (2005) [54] | 665 | 12 | 49 % Primiparous |
Foldspang et al. (2004) [39] | 1232 | >12 | 26 % Primiparous |
Sampselle et al. (1996) [62] | 59 | 6 | 67 % SUI Primiparous |
Thomason et al. (2007) [63] | 121 | 6 | 45 % Primiparous |
Yang et al. (2010) [64] | 1889 | 6 | 10 % Multiparous |
Ege et al. (2008) [65] | 1749 | 12 | 20 % Multiparous |
Ewings et al. (2005) [66] | 723 | 6 | 45 % Multiparous |
Hvidman et al. (2003) [78] | 642 | 3 | 3 % Multiparous |
Mason et al. (1999) [68] | 717 | 3 | 10 % Primiparous 31 % SUI Multiparous |
Raza-Khan et al. (2006) [69] | 113 | – | 46 % Primiparous 43 % Multiparous |
Schytt et al. (2004) [70] | 2390 | 12 | 18 % SUI Primiparous 24 % SUI Multiparous |
In a systematic review and meta-analysis of 33 population-based studies, Thom and Rortveit reported that the pooled prevalence of PPUI is 33 % in all women during the first 3 months postpartum. The mean prevalence of weekly and daily incontinence was 12 and 3 %, respectively. The mean prevalence was double in the vaginal delivery group (31 %) compared to the CS group (15 %) [7].
Mechanism and Pathogenesis
Stress Urinary Incontinence (SUI)
Most studies reported that the main underlying mechanism for development of SUI in women is the presence of intrinsic sphincter deficiency and/or bladder neck and urethral hypermobility with evidence that both pathologies are present together in most of patients with SUI. Pregnancy and childbirth are the main risk factors that predispose to both pathologies based on the hypothesis that pelvic organ support can be impaired by vaginal childbirth [71]. Peschers et al. demonstrated an impaired strength of PFM immediately after vaginal birth, which improves gradually with time [72]. Persistent PPUI could be the result of partial irreversible functional and anatomical changes of the PFM, which have a more serious prognosis than SUI developing during pregnancy [43].
The main underlying changes that occur after vaginal delivery and have a role in the development of PPUI are levator ani trauma, bladder neck and urethral hypermobility, and urethral sphincter injury.
Levator Ani Trauma
The PFM (the pubococcygeus–puborectalis complex) insert on the pelvic sidewall from the pubic rami to the ischial spine and form a V-shaped or U-shaped sling around the anorectal junction. The levator hiatus is the space bordered by this sling which contains the urethra anteriorly, the vagina centrally, and the anorectum posteriorly [73]. In nulliparous women, the levator hiatus varies from 6 to 36 cm2 on valsalva manoeuvre [74]. During labour, the average fetal head measures 60–90 cm2 in the plane of minimal diameters, requiring marked distension and deformation of the levator complex. Lien et al. showed that the most inferior and medial parts of the levator complex may have to increase in length by a factor of 3 or more during crowning of the fetal head [75], which explain that 36 % of women after vaginal delivery have a levator ani avulsion [73, 74]. Hoyte et al. found a significant decrease in levator muscle volume and levator hiatus widening in women with SUI [76]. An MRI study showed that nulliparous women do not have defects of the levator ani musculature, while up to 20 % of primiparous women have levator ani defects after vaginal birth [77].
Bladder Neck and Urethral Hypermobility
Both have been assessed as predictors of postpartum SUI. King and Freeman found that increased bladder neck mobility antenatally was predictive of postpartum SUI and they suggest that collagen susceptibility to changes during pregnancy, measured by changes in bladder neck mobility, might predict PPUI [78]. DeLancey et al. reported that low maximum urethral closure pressure was the most common factor associated with SUI in primiparous women followed by bladder neck hypermobility [79]. Toozs-Hobson and colleagues stated that bladder neck mobility was significantly greater in women who delivered vaginally compared to women with CS [80].
Urethral Sphincter Injury
The normal urethral sphincter function may be adversely affected after prolonged labour or instrumental vaginal delivery because of pressure-induced ischaemic injury [81]. In addition, in multiparous women there may be repeated urethral injury and greater urethral dysfunction following each vaginal birth [82]. Cannon et al. observed histologically in rats that prolonged vaginal distension results in extensive disruption and marked thinning of the urethral skeletal muscle fibres and regarding urethral sphincter function, there was associated lower leak point pressure with increased severity of SUI [83]. These findings suggest that ischaemic injury to the urethral sphincter is important in the development of SUI after prolonged vaginal distension.
Risk Factors
Several risk factors are found to be associated with the development of postpartum SUI and the persistence of symptoms such as:
Preconception UI, chronic cough and smoking [84]
Weak pelvic floor collagen, which might be relevant during pregnancy where connective tissue is weaker than in the non-pregnant [86]
Joint hypermobility has been proposed as a marker for connective tissue weakness and subsequent development of SUI and prolapse [87]. However, in other studies no differences were found except for elbow hyperextension [88].
Obesity is known to be a possible risk factor for postpartum SUI [89].
Urgency Urinary Incontinence
Diagnosis of urinary incontinence (UI)
History: For diagnosis a full history should be taken to evaluate patients’ pattern of voiding and leakage, which may determine the type of incontinence. Obstetric history including difficult deliveries, grand multiparity, forceps use, obstetric lacerations, and large babies, history of pelvic surgery especially prior incontinence procedures, hysterectomy, or pelvic floor reconstructive procedures should be asked about. In addition, the patient should be asked if she takes medications that affect LUT function.
Physical examination: Adequate physical examination is essential for the diagnosis of women with UI. If possible, it is optimal to examine the patient with a comfortably full bladder. This may aid confirmation of leakage of urine with a cough test during examination (cough-stress test). Pelvic examination by vaginal speculum and bimanual examination may reveal vaginal atrophy, vulvo-vaginitis, POP or pelvic masses. In addition, weakness of the PFM could be assessed. Spinal reflex activity of L5–S5 is assessed by bulbocavernosus reflex testing (squeezing of the clitoris induces anal sphincter contraction) and spinal reflex activity of S4–S5 nerve roots by anal reflex testing.
Urinalysis and culture: A urine dipstick assessment should be performed to exclude a urinary tract infection (UTI) and a specimen sent for microscopy and culture if abnormal. UTI should be excluded and treated first before shifting to other test.
Non-invasive urodynamic testing:
Bladder diary: the patient should keep a bladder diary form (3–7 days), record the times of urination, voided volumes, daily fluid intake, episodes of urine leakage, and estimated amounts of leakage.
Uroflowmetry and PVR measurement: provides information about the voiding pattern “continuous, fluctuating or interrupted” and numerical values (maximum flow rate “Qmax,” average flow rate, voided volume and PVR).
Invasive urodynamic studies: These studies include many tests such as cystometry, pressure flow study, urethral pressure profilometry, videourodynamics. These tests evaluate the bladder dynamics during the filling and voiding phases. They may be indicated for diagnosis if MUI is suspected, before surgical intervention, refractory cases, failed previous surgery or in the setting of research work.
Treatment and Prevention of Urinary Incontinence (UI)
Successful treatment of UI must be tailored to the specific type of incontinence and its cause. Patient symptoms, age and any underlying medical problems may also affect the treatment outcomes. A wide range of treatment options has been successfully used in the treatment of UI (SUI, UUI and MUI) and many guidelines and recommendations in the literature have described extensively the appropriate line of therapy for each type according to patient clinical presentation and diagnosis [91].
The following treatments could be considered for the treatment of UI:
- 1.
Conservative interventions: such as physical therapies (e.g. pelvic floor muscle training [PFMT] and biofeedback), lifestyle modification (e.g. weight loss, caffeine and alcohol restriction, weight reduction and smoking cessation), behavioural training (e.g. timed voiding and bladder training). According to several guidelines conservative treatment should be tried as the first line of therapy for all patients with UI.
- 2.
Pharmaceutical therapies: such as anticholinergics, alpha-adrenergic agonists, topical oestrogens, duloxetine.
- 3.
Surgical therapies: for SUI: midurethral tapes, bulking agents, Burch colposuspension and pubovaginal sling and for UUI: botulinum toxin injections, sacral neuromodulation and bladder augmentation.
Role of PFMT During Pregnancy and Puerperium
Physiotherapy such as pelvic floor muscle training (PFMT) is more appropriate during pregnancy and puerperium than drugs or surgery for the treatment of UI. Some drugs are contraindicated or best avoided during pregnancy and breastfeeding, while surgery is not recommended until a woman has completed her family [92].
PFMT was first popularized by Arnold Kegel for the treatment of UI [93], and is recommended as the first treatment of choice for UI [91]. The rationale for PFMT is based on two functions of the PFM; support of the pelvic organs and a contribution to the sphincteric closure mechanism of the urethra [94, 95].
In a Cochrane Database Systematic Review Hay-Smith et al. determined the effect of PFMT for the prevention and treatment of UI in antenatal and postnatal women. They found that pregnant women without prior UI who were randomized to intensive antenatal PFMT were less likely to report UI than women randomized to no PFMT or usual antenatal care in late pregnancy (about 56 % less) and up to 6 months postpartum (about 30 % less). Postnatal women with persistent UI 3 months after delivery and who received PFMT were less likely to report UI than women who did not receive treatment or received usual postnatal care (about 20 % less) 12 months after delivery. The authors concluded that there is some evidence that PFMT in women having their first baby can prevent UI in late pregnancy and postpartum and that PFMT is an appropriate treatment for women with persistent PPUI [92].
Does CS Reduce PPUI?
The impact of delivery mode and controversy over CS versus vaginal delivery with regard to pelvic floor trauma and subsequent development of UI has been discussed and debated. Damage to important pelvic floor muscles and nerves is primarily attributable to vaginal delivery [96]. Many reviews conclude that CS may be more protective against PPUI. However, these commonly held perceptions have been challenged in recent years [42]. The protective role of CS against injury to the pelvic floor cannot be justified because pregnancy itself may increase the prevalence of UI as a result of mechanical compression on the pelvic floor [97–99]. On the other hand, some studies found that there was no significant difference between CS and vaginal delivery in the protection against SUI suggesting that the labour process, rather than vaginal birth itself, may be implicated in pelvic floor damage [100, 101].
Related posts:
Pelvic Floor Physiotherapy for the Prevention and Management of Childbirth Trauma
Prediction, Risk Assessment, and Prevention of Childbirth Trauma
The Effect of Pregnancy on the Pelvic Floor
Female Pelvic Anatomy
Healing Process and Complications
Further Investigations and Follow-Up: Pelvic Floor Ultrasound
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