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Table of Contents
REVIEW ARTICLE
Year : 2021  |  Volume : 32  |  Issue : 3  |  Page : 94-101

Videourodynamic precision diagnosis and treatment of lower urinary tract symptoms in women


Department of Urology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, and Tzu Chi University, Hualien, Taiwan

Date of Submission17-Mar-2021
Date of Decision30-Apr-2021
Date of Acceptance03-Jun-2021
Date of Web Publication28-Sep-2021

Correspondence Address:
Hann-Chorng Kuo
Department of Urology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, No. 707, Section 3, Chung-Yang Road, Hualien 970
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/UROS.UROS_46_21

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  Abstract 


Lower urinary tract symptoms (LUTSs) in women are common in urological practice but are usually uninformative for diagnosing the underlying lower urinary tract dysfunction. To obtain a precise diagnosis and devise a precise treatment strategy, a videourodynamic study (VUDS) is an essential tool for investigating the bladder and bladder outlet dysfunction, especially when LUTS cannot be relieved after initial medical treatment. An accurate VUDS diagnosis can guide effective treatment and prevent unnecessary or incorrect surgical intervention. This article reviews updated applications of VUDS in the diagnosis and treatment of LUTS in women.

Keywords: Lower urinary tract symptoms, urinary bladder, urodynamics, woman


How to cite this article:
Kuo HC. Videourodynamic precision diagnosis and treatment of lower urinary tract symptoms in women. Urol Sci 2021;32:94-101

How to cite this URL:
Kuo HC. Videourodynamic precision diagnosis and treatment of lower urinary tract symptoms in women. Urol Sci [serial online] 2021 [cited 2021 Dec 2];32:94-101. Available from: https://www.e-urol-sci.com/text.asp?2021/32/3/94/326934




  Introduction Top


Lower urinary tract symptoms (LUTS) in women include storage and voiding symptoms. Several types of lower urinary tract dysfunction (LUTD) account for these LUTS. In women with storage LUTS, LUTDs include hypersensitive bladder, detrusor overactivity, detrusor overactivity with low contractility, interstitial cystitis/bladder pain syndrome (IC/BPS), stress urinary incontinence (SUI), contracted bladder and low bladder compliance, and detrusor overactivity with bladder outlet obstruction (BOO).[1] In women with voiding LUTS, LUTDs include bladder neck dysfunction (BND), dysfunctional voiding, urethral obstruction, poor relaxation of the pelvic floor muscles (PFMs), pelvic organ prolapse, and urethral meatus stricture.[2] In most cases, LUTS in women cannot be used to make an accurate clinical diagnosis of LUTD.[1] Therefore, when the treatment for the initial tentative diagnosis is ineffective, a detailed urodynamic study, especially a videourodynamic study (VUDS), can provide a precise diagnosis and guide management [Table 1].
Table 1: The pathophysiology of lower urinary tract dysfunction in women with storage and voiding lower urinary tract symptoms

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  Storage Lower Urinary Tract Symptoms Top


Hypersensitive bladder

Normally, women first perceive bladder filling at the level of 100 mL, a full bladder sensation at 300–350 mL, and urgency at 450–500 mL. The International Urogynecological Association and the International Continence Society defines the sensation of bladder fullness without reaching these levels as increased bladder sensation,[3] usually called “hypersensitive bladder.”[4] Women with a hypersensitive bladder may have both storage and voiding LUTS because the bladder is not fully distended, and detrusor contraction during voiding is not forceful. Affected patients can undergo VUDS with a distended bladder and exhibit a normal flow rate and voided volume. Using VUDS, clinicians can distinguish detrusor overactivity and BOO from a hypersensitive bladder. Changes in drinking habits (e.g., drinking more water), holding urine as long as possible, and biofeedback training may help improve these symptoms.

Interstitial cystitis/bladder pain syndrome

During urodynamic studies, it is essential to instill 30 mL of potassium chloride (KCl) of 0.4 M concentration to check for the absence of BOO and the presence of IC/BPS when the cystometric bladder capacity is lower than 350 mL.[5] The KCl test has a sensitivity of 85.5% and a specificity of 81.6% in diagnosing IC/BPS. Urothelial dysfunction with increased permeability is present if the KCl solution can elicit bladder pain or the sensation of urgency.[5] In this case, cystoscopic hydrodistension is usually a recommended assessment for glomerulation or Hunner's lesion. IC/BPS can be diagnosed[6] and managed with hyaluronic acid instillation, platelet-rich plasma injection, or botulinum toxin A injection.[7],[8] Patients with IC/BPS usually have a hypersensitive bladder and need to urinate at a small bladder capacity; therefore, they have difficulty urinating and using abdominal pressure to void [Figure 1]a. In patients with ulcerative IC/BPS, urothelial defects might induce terminal detrusor overactivity when the bladder capacity is reached. VUDS can help differentiate poor PFM relaxation, detrusor overactivity, and BOO [Figure 1]b.
Figure 1: (a) A patient with interstitial cystitis/bladder pain syndrome used abdominal pressure to void; there was no bladder outlet obstruction. (b) Ulcerative interstitial cystitis/bladder pain syndrome with terminal detrusor overactivity and a positive potassium chloride test during videourodynamic study. (c) In a woman with ketamine cystitis, videourodynamic study revealed detrusor overactivity, a contracted bladder, high-grade vesicoureteral reflux, and increased urethral sphincter activity during voiding (arrows), which resulted in high voiding pressure and severe bladder pain

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Patients with a hypersensitive bladder usually exhibit poor PFM relaxation during voiding.[9] Biofeedback with PFM training can help patients relax the PFMs and facilitate spontaneous detrusor contraction during voiding at a small bladder capacity.[10]

Ketamine cystitis

Ketamine cystitis is a newly defined type of chemical cystitis in women who abuse ketamine as a recreational drug. In severe cases, the urinary bladder exhibits severe inflammation and fibrosis with erosive urothelium. Patients usually develop detrusor overactivity with guarding external sphincter hyperactivity, decreased bladder capacity, vesicoureteral reflux, and lower ureteral obstruction [Figure 1]c. VUDS can reveal the pathophysiological features of LUTD and guide the management strategy, either conservative treatment or augmentation enterocystoplasty, for the diseased bladder.[11] In patients with ketamine cystitis, the bladder has contracted and has low capacity (<300 mL), and irreversible urinary tract changes are observed. In such cases, partial cystectomy and augmentation enterocystoplasty can help restore normal lower urinary tract function. However, the outcome of augmentation enterocystoplasty is better than that of conservative treatment.

Intrinsic sphincter deficiency and overactive bladder

Intrinsic sphincter deficiency may cause urine leakage into the proximal urethra, stimulate the urethral mucosa, and elicit the urethrovesical stimulating reflex, resulting in urethral distension and detrusor contraction.[12] During VUDS, coughing or abdominal straining may provoke detrusor overactivity, causing the sensation of urgency or urine leakage [Figure 2]a. This phenomenon mimics the sensation of urgency during walking or running with a full bladder. If storage LUTS does not improve after behavior modification, biofeedback with PFM training, medical treatment, or a suburethral sling in the proximal urethra, surgical interventions should be considered for intrinsic sphincter deficiency.
Figure 2: (a) In a woman with urgency and frequency, especially at the full bladder, videourodynamic study revealed provoked detrusor overactivity during Valsalva maneuver (arrow), and urine leak into the proximal urethra is noted. (b) Detrusor after-contraction after complete bladder emptying, the patient felt residual and difficulty in urination after initial voiding

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Detrusor after-contraction

Some women have a sensation of residual urine after voiding and may experience difficulty urinating after the initial voiding. In these cases, VUDS may reveal that the bladder continues to contract after complete emptying [Figure 2]b. The cause of such detrusor after-contraction has not been elucidated, but it might be attributed to detrusor hyperactivity. In a study involving women with these symptoms, ambulatory monitoring had demonstrated a relatively high prevalence of detrusor after-contraction and an association between detrusor overactivity and detrusor after-contraction.[13] PFM training after urination can relieve this condition and decrease the amplitude of after-contraction.

Detrusor overactivity with or without bladder outlet obstruction

The most common storage LUTS in women is detrusor overactivity, which can occur during the storage phase (phasic detrusor overactivity) or when the bladder capacity is reached (terminal detrusor overactivity) [Figure 3]a. Patients with urodynamic detrusor overactivity usually have the sensation of urgency. However, older women with central nervous system (CNS) disorders, such as stroke, Parkinson's disease, and early dementia, might not perceive the sensation of urgency when detrusor overactivity first occurs. Nevertheless, they may perceive it before reaching bladder capacity, leading to urgency urinary incontinence. Some patients might have guarding urethral sphincter hyperactivity, which causes dysfunctional voiding. During urination, the voiding detrusor pressure decreases because the external sphincter relaxes. Of interest is that some affected older women stop urination before bladder emptying is complete because they cannot perceive the sensation of residual urine, and a large amount of postvoid residual urine (PVR) remains [Figure 3]b. This is a common pathophysiological feature of detrusor overactivity and low contractility from reduced bladder sensation.[14] Women with SUI may have intrinsic sphincter deficiency while coughing, but detrusor overactivity may be provoked without intrinsic sphincter deficiency during coughing or straining, which mimics SUI. If VUDS does not identify urgency urinary incontinence, surgical intervention for SUI might fail to eradicate the symptoms[15] [Figure 3]c.
Figure 3: (a) Terminal detrusor overactivity in a 46-year-old woman presenting with urgency and urgency urinary incontinence. (b) An 80-year-old woman presented with urgency and urgency urinary incontinence and incomplete bladder emptying. A videourodynamic study revealed detrusor overactivity and low contractility because she did not perceive bladder fullness sensation after voiding a small amount of urine. (c) Stress test during videourodynamic study revealed urine leakage while coughing, provoking detrusor contraction and urination after heavy cough (arrow). (d) Videourodynamic study revealed terminal detrusor overactivity in a woman with bladder outlet obstruction due to a previous anti-incontinence operation. The voiding pressure was high, and the flow rate was low. A mid-urethral narrowing was noted during voiding

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Storage LUTS caused by detrusor overactivity may respond to antimuscarinic drugs, the beta-3 adrenergic agonist mirabegron, or a combination of these modalities.[16] If the therapeutic effect of an oral medication fails, intravesical injection of 100-U onabotulinumtoxin A usually improves overactive bladder symptoms, even in elderly patients with detrusor overactivity and low contractility.[17] In one study, onabotulinumtoxin A injection had reduced urgency and urinary incontinence in patients with overactive bladder, relieving bladder pain and reducing bladder oversensitivity in patients with IC/BPS.[18]

In women with overactive bladder symptoms refractory to medical treatment, the presence of BOO should also be evaluated. The diagnosis of BOO should be suspected if the voiding pressure during a pressure-flow study is >30 cm H2O, but VUDS should confirm the precise site of BOO.[19] Radiological evidence of bladder outlet narrowing, in addition to a voiding pressure of >35 cm H2O and a maximum flow rate of <15 mL/s or a voiding pressure of >40 cm H2O, confirms the diagnosis of BOO [Figure 3]d.[20]


  Voiding Lower Urinary Tract Symptoms Top


In a study involving women with voiding dysfunction, VUDS helped diagnose BOO in 42.3% of the patients and bladder dysfunction in 54.8% and yielded normal tracings in 2.9% of them. Anatomical BOOs include cystocele and urethral stricture. The common subtypes of bladder dysfunction included detrusor underactivity (in 17.6% of the patients), detrusor overactivity and low contractility (12.1%), and bladder oversensitivity (17.0%). Common functional BOOs included dysfunctional voiding (17.0%) and poor relaxation of the PFMs (17.6%).[21]

Detrusor underactivity

Detrusor underactivity commonly occurs during VUDS in women with voiding dysfunction. Women with low detrusor contractility might have detrusor acontractility or detrusor underactivity, with or without detrusor overactivity[14] [Figure 4]a. The dose of antimuscarinic drugs or mirabegron should be carefully tailored to prevent large amounts of PVR after treatment.[17] If medical treatment fails and urgency urinary incontinence is remarkable, intravesical onabotulinumtoxin A injection may be considered.[22] However, large amounts of PVR and loss of bladder fullness sensation should be managed cautiously, especially in elderly and frail women.[23] Patients with low detrusor contractility might also have poor PFM relaxation, resulting in incomplete bladder emptying. If VUDS confirms the absence of anatomical BOO, biofeedback and PFM training may reduce PFM hypertonicity and improve voiding efficiency.[9] In women with SUI and poor PFM relaxation, biofeedback and PFM training can improve both storage and voiding conditions.[24] In one study, more than half of the patients with detrusor underactivity and a tight bladder neck during voiding experienced an improvement in voiding efficiency after transurethral incision of the bladder neck.[25]
Figure 4: (a) A videourodynamic study in an 80-year-old woman with urgency and dysuria revealed terminal detrusor overactivity with incomplete bladder emptying. Detrusor overactivity with low contractility is the likely cause of her voiding lower urinary tract symptoms. (b) Videourodynamic study in a woman with a high-grade cystocele and stress urinary incontinence. The cystocele contracts during urination, and the detrusor pressure decreases when urination starts (arrow), suggesting the bladder outlet obstruction of cystocele in the initiation of urination can be eliminated during voiding

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Pelvic organ prolapse

Women with voiding dysfunction and the sensation of a vaginal lump should be examined for pelvic organ prolapse. In patients with severe cystocele, rectocele, or vault prolapse, the voiding condition can improve after manual prolapse reduction or insertion of a pessary. During VUDS, cystocele contractility should be carefully observed [Figure 4]b. Usually, BOO can be reduced during voiding and cystocele contraction. However, in some cases of high-grade cystocele, BOO develops during voiding. Furthermore, reducing the cystocele during VUDS and checking for urine leakage during stress tests are essential. During the reduction, concomitant anti-incontinence surgery should be performed for pelvic organ prolapse.

Urethral obstruction

Two decades ago, urethral obstruction was the most common cause of BOO in women. Since then, improvements in surgical skills and knowledge have helped reduce urethral obstruction after sling surgery. If BOO develops after sling surgery for SUI, a transvaginal sling incision effectively relieves urethral obstruction. Voiding dysfunction after suburethral sling surgery can be resolved using sling incision. In one series, approximately 85.7% of the patients who underwent this procedure maintained urinary continence and reported outcome satisfaction.[26]

VUDS is the best assessment for differentiating between the presence of urethral obstruction and poor relaxation of PFMs after anti-incontinence surgery.[27] A suburethral sling procedure should reestablish a hammock effect on the proximal urethra during abdominal straining without compromising urethral resistance. When patients who had normal voiding before surgery develop urination difficulties and large amounts of PVR after anti-incontinence surgery, BOO is the likely cause [Figure 5]a. Most patients with BOO have high-pressure, low-flow tracings on VUDS after sling surgery, but some have low-pressure, low-flow tracings [Figure 5]b.
Figure 5: A videourodynamic study in a woman with difficulty in urination after suburethral sling operation. (a) The voiding pressure was higher, and the maximal flow rate was lower than those in the preoperative study, indicating urethral obstruction developed after the sling operation. (b) Another woman with dysuria after anti-incontinence surgery, videourodynamic study revealed low voiding pressure. Still, the maximal flow rate was very low, and there was mid-urethral narrowing, suggesting bladder outlet obstruction due to sling operation

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In addition to urethral obstruction caused by previous anti-incontinence surgery, intrinsic and extrinsic urethral obstructions should be considered in women with voiding dysfunction. These obstructions include urethral diverticulum, urethral cancer, compression by a gynecological tumor, and urethral fibrosis. VUDS can provide characteristic pressure-flow tracings and voiding cystourethrographic images.


  Bladder Neck Dysfunction Top


A nonopening bladder neck is frequently observed in patients with detrusor underactivity or detrusor overactivity with low contractility.[28] BND is present in 12.3% of women with bladder outlet dysfunction. High-pressure BND can cause anatomical BOO, whereas low-pressure BND is likely to affect urination by inhibiting detrusor contractility. VUDS is the mainstay tool for diagnosing BND in women [Figure 6]a. Alpha-blocker therapy is indicated in female patients with BND with or without detrusor contractility. If medical treatment fails, transurethral incision of the bladder neck may be helpful.[29] In patients with detrusor underactivity, this procedure improved long-term voiding efficiency. Compared with lower intravesical pressure, higher intravesical pressure was predictive of satisfactory surgical outcomes.[29] Patients with stroke or early dementia might also have a tight bladder neck during voiding, suggesting that sympathetic tonicity is high in these patients [Figure 6]b. Transurethral incision of the bladder neck can also provide therapeutic efficacy in these patients.[25]
Figure 6: (a) A videourodynamic study in an 80-year-old woman with chronic urinary retention revealed detrusor overactivity and low contractility and a tight bladder neck (arrow). (b) Bladder neck dysfunction in a woman with detrusor overactivity and high voiding pressure low-flow tracing. These women urinated smoothly after transurethral incision of the bladder neck

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Dysfunctional voiding

Dysfunctional voiding is an abnormality of bladder emptying in neurologically normal individuals in which the external sphincter activity increases during voiding. Among 1,605 women with LUTS, 168 (10.5%) had dysfunctional voiding.[30] Patients with dysfunctional voiding had significantly lower cystometric bladder capacity, higher detrusor pressure, lower maximum flow rate, and larger PVR amounts than controls. Among the 168 patients with dysfunctional voiding, 114 (67.9%) had the chief complaint of storage LUTS and 54 (32.1%) had voiding LUTS, and urodynamic detrusor overactivity occurred in 116 (69%). VUDS has demonstrated that patients with a bladder base elevation in the filling phase had significantly higher voiding pressure and a higher incidence of dyscoordinated PFM electromyographic activities during voiding. This finding suggests that the incidence rates of BOO and PFM hypertonicity were higher in these patients.[31] Women with dysfunctional voiding also have a high incidence of recurrent urinary tract infections.[32]

No definitive treatment for dysfunctional voiding currently exists; biofeedback with PFM training, alpha-blockers and skeletal muscle relaxants, and urethral sphincter onabotulinumtoxin A injection have limited efficacy. A long-term follow-up study has revealed that medical treatment with or without urethral onabotulinumtoxin A injection reduced voiding pressure and the BOO index. More prominent obstruction demonstrated by baseline VUDS was associated with a higher BOO index.[33] Improvement after onabotulinumtoxin A injection in the urethral sphincter was subjectively reported by 61.1% of patients with voiding dysfunction caused by urethral sphincter hyperactivity. An open bladder neck during voiding at baseline is predictive of a successful outcome.[34] VUDS is the most important examination for diagnosing and treating dysfunctional voiding in women [Figure 7]a.
Figure 7: (a) Videourodynamic study in a woman with urgency frequency and dysuria revealed detrusor overactivity and dysfunctional voiding with a narrow mid-urethra during voiding (arrow). (b) Videourodynamic study in a woman with Parkinson's disease and voiding dysfunction revealed terminal detrusor overactivity (arrow), high voiding pressure, and urethral sphincter hyperactivity. (c) Videourodynamic study in a woman with poor relaxation of the pelvic floor muscles revealed low voiding pressure with abdominal pressure and intermittent low-flow rate (arrow). (d) Videourodynamic study in a woman with dementia and urinary incontinence revealed low bladder compliance and detrusor overactivity, (arrows) low contractility, and contracted bladder. The patient cannot adequately urinate and has large postvoid residual urine. (e) An 85-year-old woman with overactive bladder and dysuria. videourodynamic study revealed terminal detrusor overactivity, dilated urethra and urethral meatus stricture (arrow), and bladder outlet obstruction. After urethral dilatation, the patient resumed smooth voiding

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Central nervous system-related detrusor overactivity and dysfunctional voiding

Because 69% of women have urodynamic detrusor overactivity, long-term detrusor overactivity resulting in urethral sphincter hyperactivity is probably the fundamental cause of dysfunctional voiding. Patients with detrusor overactivity due to CNS diseases, such as stroke, Parkinson's disease, and dementia, might also have dysfunctional voiding [Figure 7]b. Antimuscarinic drugs are commonly prescribed in treating combined detrusor overactivity and dysfunctional voiding.[33]

Poor pelvic floor muscle relaxation

Poor PFM relaxation is another common cause of voiding dysfunction in women.[9] Among 1914 women with voiding dysfunction, 336 (17.6%) had poor PFM relaxation. In contrast with patients with dysfunctional voiding, the incidence of detrusor overactivity was only 5.7% in patients with poor PFM relaxation. Patients with this condition had significantly increased bladder sensation, lower cystometric bladder capacity, lower maximum flow rate, smaller voided volume, larger PVR, and lower voiding efficiency than control individuals. Patients with this condition usually void with the aid of abdominal pressure, and the flow pattern is intermittent with or without large PVRs. Patients usually have a low voiding pressure [Figure 7]c. A high percentage of women with recurrent urinary tract infections also have retroperitoneal and pelvic fibromatosis.[32] Poor PFM relaxation is also frequently observed in patients with CNS diseases, such as cerebrovascular accidents, Parkinson's disease, and early dementia. Biofeedback with PFM training is the treatment of choice, and an alpha-blocker regimen with skeletal muscle relaxants might also help affected patients.[9]

Low bladder compliance

In women with chronic cystitis and those who have undergone previous bladder surgery or pelvic irradiation, the bladder may become contracted and exhibit poor compliance. Detrusor contractility is usually low in individuals with poor bladder compliance. In some cases, detrusor overactivity may also be present and result in urgent urinary incontinence and incomplete bladder emptying [Figure 7]d. Treatment entails medication for overactive bladder or onabotulinumtoxin A injection to decrease intravesical pressure and reduce urinary incontinence, followed by clean intermittent catheterization.[35] If affected patients are otherwise healthy and have normal abdominal pressure, augmentation enterocystoplasty may improve storage function and voiding efficiency.[36]

Urethral meatus stricture

In older women with voiding dysfunction, urethral stricture should also be evaluated. Estrogen deficiency, trauma, and chronic inflammation resulting in periurethral fibrosis are the common causes of urethral stricture.[37] Patients with long-term urethral stricture and BOO may also develop detrusor overactivity and low detrusor contractility. Although most urethral meatal strictures are usually found on physical examination and cystoscopy, some women in whom storage LUTS are predominant have urethral meatal stricture only during VUDS [Figure 7]e. Urethral dilatation or meatoplasty helps relieve meatal stenosis and restore unobstructed voiding.


  Conclusion Top


LUTS in women include storage and voiding symptoms. In most affected women, clearly diagnosing the underlying bladder or bladder outlet dysfunctions is difficult. VUDS is a comprehensive investigation of LUTD that helps identify bladder and bladder outlet dysfunctions and helps prevent incorrect medical treatment or unnecessary surgical intervention.

Financial support and sponsorship

This study was supported by grants from the Buddhist Tzu Chi Medical Foundation (TCMF-SP 108-01 and TCMF-MP 107-02-01).

Conflicts of interest

Prof. Hann-Chorng Kuo, an editorial board member at Urological Science, had no role in the peer review process of or decision to publish this article.



 
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Abstract
Introduction
Storage Lower Ur...
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