Urodynamic Assessment: Cystometry

WHEC Practice Bulletin and Clinical Management Guidelines for healthcare providers. Educational grant provided by Women's Health and Education Center (WHEC).

The cystometrogram (CMG) measures vesical pressure as a function of bladder volume. Cystometry is a test of detrusor function and can be used to assess bladder sensation, capacity, and compliance and to determine the presence and magnitude of both voluntary and involuntary detrusor contractions. Cystometry can be simple and office based or it can be multi-channel, including measurement of intraabdominal, bladder, and detrusor (bladder minus intraabdominal) pressures. The first cystometer dates back to 1872 when Schatz accidentally discovered a crude technique for measuring bladder pressure while trying to record intraabdominal pressure. Shortly thereafter, DuBois studied the effects changes in body position on intravesical and intrarectal pressures and observed that the desire to void was associated with contraction of the detrusor muscle. The currently popular water cystometer was designed by Lewis in 1939. The later use of air and carbon dioxide as filling media further simplified the procedure. Cystometry is an urodynamic test that measures the pressure and volume relationship of the bladder. It is used to assess detrusor activity, sensation, capacity, and compliance. Every factor has unique implications, and before any definitive conclusions can be reached, each parameter must be examined in association with symptoms and clinical findings. A normal bladder has the power of accommodation; it can maintain an almost constant low intravesical pressure throughout filling, regardless of volume. A normal woman should be able to suppress voiding even at maximum capacity. Then, in an acceptable environment, she should be able to initiate a voiding reflex of sufficient magnitude to empty her bladder.

The purpose of this document is to discuss basic principles of cystometry, indications, normal and abnormal cystometric parameters. A basic principle of cystometry is the coupling of a manometer to the bladder lumen. A filling medium is instilled into the bladder and, as it fills, intravesical pressure is measured against volume. Testing apparatuses range from simple single-channel methods, which are performed manually or electronically, to complex methods combining electronic measurements of bladder, abdominal, and urethral pressure, together with electromyography and fluoroscopy. A cystometrogram has two phases: a filling/storage phase and an emptying (voiding) phase. The filling phase is subdivided into a brief initial rise in pressure to achieve resting bladder pressure, followed by a tonus limb that reflects vesicoelastic properties of accommodation of the smooth muscle and collagen of the bladder wall. There may be a third increase in pressure, which is attributed to stretching of detrusor muscle and collagenous elements of the bladder wall beyond their limits at bladder capacity. During this third stage, the patient is still able to suppress voiding. A detrusor contraction then is initiated voluntarily and the patient voids.

Disorders of Micturition:

Disorders of micturition may be classified as storage problems, emptying problems and combination of two. The bladder and urethra are affected by neurologic conditions in only two generic ways, a loss of function or a release of function. This principle is critical to neuro-urology. Loss of function is exemplified by paralysis of the bladder in lower-motor lesion, whereas release of function is exemplified by detrusor overactivity in suprasacral spinal cord injury.

Failure to store: Because of the bladder -- detrusor hyperactivity; involuntary contractions; suprasacral neurologic disease; bladder outlet obstruction; idiopathic.

Decreased compliance -- fibrosis; idiopathic
Sensory urgency -- inflammatory; infections; neurologic; psychological; idiopathic
Because of outlet -- urethral hypermobility; intrinsic sphincter deficiency

Failure to empty: Because of the bladder -- detrusor aneflexia; impaired detrusor contractility; psychogenic learned behavior

Because of the outlet -- anatomic obstruction; detrusor sphincter; psychogenic learned behavior

Indications for Cystometry:

Each patient for cystometrogram (CMG) must be evaluated individually. Based on clinical findings and planned treatments, the physician must decide whether cystometry is indicated and, if it is, whether it should be performed via a simple office test or with more sophisticated electronic testing. Indications for single-channel cystometry have been debated extensively; however, few comparisons exist in the literature. Multichannel cystometry may have a higher sensitivity for recognizing low-pressure detrusor contractions, which have sometimes been called "sub-threshold detrusor instability". Multichannel techniques also improve the specificity of cystometry by avoiding false positive test results created by increases in abdominal pressure.

Indications for multichannel subtracted cystometry are: complicated history; inconclusive single-channel studies; stress incontinence before surgical correction; urge incontinence not responsive to therapy; recurrent urinary loss after previous surgery for stress incontinence; frequency, urgency, and pain syndromes not responsive to therapy; nocturnal enuresis not responsive to therapy; lower urinary tract dysfunction after pelvic radiation or radical pelvic surgery; neurologic disorders; continuous leakage; suspected voiding difficulties.

Cystometrogram (CMG):

The normal adult cystometrogram is divided into four phases.
Filling cystometry:
Phase I: Mild rise in pressure due to influence of initial fluid infusion. The initial pressure increase represents the initial response to filling and the level at which the bladder trace stabilizes is known as the initial filling pressure. The designation "resting pressure", though often used, is incorrect. The first phase of the curve is determined by the initial myogenic response to filling and by the elastic and viscoelastic response of the bladder wall to stretch. With more rapid rates of filling, there may be an initially higher peak, which then levels off. This peak type of initial response is common with gas cystometry.

Phase II: Minimal increase in pressure as bladder accommodates to continual increase in volume. It is called the tonus limb, and compliance is normally high and uninterrupted by phasic pressure increases. In practice, the compliance seen in the urodynamic laboratory is always lower than that existing during physiologic bladder filling. Normally, the increase is less than 10 cm H2O.

Phase III: Rise in pressure as bladder wall is stretched to its functional limit or capacity. Control over voiding is maintained with urgency. It is reached when the elastic and vesicoelastic properties of the bladder wall have reached their limit. Any further increase in volume generates a substantial increase in pressure. This increase in pressure is not the same as a detrusor contraction. If a voluntary or involuntary contraction occurs, phase III may be obstructed by the rise in the pressure so generated.

Voiding cystometry:
Phase IV: Voluntary detrusor contraction resulting in efficient voiding. It consists of the initiation of voluntary micturition. Many patients are unable to generate a voluntary detrusor contraction in the testing situation, especially in the supine position. This should not be called detrusor areflexia but, simply, absence of a detrusor contraction during cystometry, a finding that is not considered abnormal unless other clinical or urodynamic findings are present that substantiate the presence of neurologic or myogenic disease.

Involuntary Contractions:

It is not enough to determine or absence of involuntary detrusor contractions; rather, it must be determined whether the patient's symptoms are actually caused by the involuntary detrusor contractions. According to the International Continence Society (ICS), detrusor activity may be either normal or overactive. The overactive detrusor is characterized by involuntary detrusor contractions that may be spontaneous or provoked by rapid filling, coughing, or other triggering maneuvers. When involuntary detrusor contractions are caused by neurologic disorders, the condition is called detrusor hyperreflexia. In the absence of a demonstrable neurologic etiology, involuntary detrusor contractions are termed detrusor instability (DI). Thus, a spinal cord injury patient with involuntary bladder contractions is said to have detrusor hyperreflexia, whereas an elderly male with such a finding secondary to prostatic obstruction is said to have detrusor instability. Originally, the ICS had restricted the term unstable bladder to an involuntary phasic increase in detrusor pressure greater than 15 cm H2O, but in practice these contractions are often of lesser magnitude and are no less significant because of a lower magnitude. In some instances, unstable detrusor contractions may be of such small magnitude as to require electronic subtraction of intraabdominal pressure to be detectable.

Cystometry Abnormal Studies:

Any significant rise in true detrusor pressure during filling or provocation should be interpreted as abnormal detrusor activity or compliance. A pressure increase of 15 cm H2O has been used by the ICS to differentiate between normal and abnormal. It has currently become apparent that this cutoff is too arbitrary, and any pressure rise must be assessed in terms of the patient's symptoms. The most recent ICS recommendations have redefined detrusor overactivity to be any rise in true detrusor pressure that is felt not to be used by normal bladder compliance. Although it is useful to categorize pressure changes during cystometry, the different patterns that occur are not mutually exclusive. Detrusor overactivity may present as phasic contractions that return to baseline after each contraction or as phasic contractions in which there is a gradual rise in pressure. A steady rise in true detrusor pressure indicates a low-compliance bladder. When this type of pattern is noted, and organic reason for the poor bladder compliance, such as interstitial cystitis should be ruled out.

Sensory abnormalities are classified as either hypersensitive or hyposensitive. Hypersensitive bladder behavior is similar whether there is a definable cause, such as interstitial cystitis, or whether the cause is unknown. In these patients, catheterization is often painful. Volume at first sensation of bladder filling, first desire to void, and maximum capacity are reduced. Sensory urgency is present when the patient experiences a strong desire to void at abnormally low bladder volumes in the absence of any rise in true detrusor pressure. Bladder overactivity may be associated with hypersensitivity from causes such as radiation therapy and interstitial cystitis. Therapy may result in bladder stability; however, the symptoms of frequency and urgency may persist if the bladder remains hypersensitive. It is not meaningful to conduct Valsalva leak point pressure (VLPP) or urethral pressure profile (UPP) studies while the bladder is contracting.

Urodynamic Assessment: Patient demonstrates detrusor instability (DI); hyperreflexia with onset at low volume of infused saline.

Urodynamically, the hyposensitive bladder behaves similarly, whatever the cause. The bladder has large capacity and a flat cystometrogram. At maximum capacity, there may rarely be a rise in pressure as the limits of compliance are reached. This rise does not represent a detrusor contraction and there and there may be little or no sensation to filling up to this point. A hyposensitive, overdistended bladder, in itself, is not necessarily an indication of pathology. Detrusor instability (DI) is also diagnosed during filling cystometry and is characterized by involuntary, phasic detrusor contractions with urgency, often resulting in loss of fluid. It is this observation of involuntary phasic detrusor muscle contractions which separates classic DI from other bladder conditions such as low compliance, where the detrusor pressure increases abnormally without contractility.

Genuine Stress Incontinence (GSI); Detrusor Instability (DI); Intrinsic Sphincter Deficiency (ISD); Cystometrogram (CMG); Valsalva Leak Point Pressure (VLPP); Urethral Pressure Profile (UPP).

Genuine Stress Incontinence (GSI): The International Continence Society (ICS) defines GSI as "the involuntary loss of urine occurring when, in the absence of a detrusor contraction, intravesical pressure exceeds maximum urethral pressure". In other words, stress incontinence is the accidental loss of urine when laughing, sneezing, coughing or even standing up; this exertion causes abdominal pressure (transmitted to the bladder) to exceed the resistance generated by the urethra. Genuine stress incontinence (GSI) is characterized in two ways: hypermobility of the bladder neck; intrinsic sphincter deficiency (ISD).

Hypermobility of bladder neck: It is often due to weakened pelvic floor muscles and connective tissue. This laxity in the pelvic floor muscles is often seen in combination with pudendal nerve damage after childbirth, but occasionally can be noted in younger nulliparous women. In its natural position over the levator plate, the bladder is supported by pelvic muscles which act as a backboard to keep increases in abdominal pressure from exceeding urethral pressure. When this backboard is weakened or damaged, the bladder neck is displaced during abdominal "stress". The bladder neck funnels and the urethral closure pressure becomes inadequate to maintain continence. Loss of urine with hypermobility-related GSI occurs in spurts, and the volume of urine loss varies with the severity of the condition. Treatment for hypermobility can range from prescribing a variety of conservative therapies to surgical intervention. Surgery for incontinence is generally referred to as a "bladder neck suspension". The goal of surgery is to prevent descent of the bladder neck with rises in abdominal pressure.

Intrinsic sphincteric deficiency (ISD): It is a severe from of stress incontinence which occurs due to an intrinsic deficiency of the urethral closure mechanism or dysfunctional urethra. The bladder neck is open at rest. Worst-case ISD is referred to as a "stove pipe" urethra, resulting in continuous leakage of urine or leakage with minimal exertion. In ISD, the bladder neck can be fixed or hypermobile. ISD is often the result of urethral scarring from post incontinence surgeries. It can also be caused by pelvic radiation, other trauma or neurological conditions. A small percentage of patients with stress incontinence present with ISD. Standard treatments for GSI associated with hypermobility generally are not effective in treating ISD. Treatments for ISD include the suburethral sling, periurethral injections and the artificial sphincter. ISD can be managed also with a variety of palliative "urethral insert" products.

Clinical Relevance: Can the results of urodynamic studies change treatment strategy for patients? The ability of preoperative urodynamic studies to predict surgical outcome is hard to evaluate, and can be viewed from two perspectives. Firstly, if the urodynamic findings led to a change in treatment strategy, the patient's outcome could already be considered modified, as a more appropriate treatment option was chosen. Secondly, if the urodynamic results did not change the patient's management, is it possible that the test results could have helped predict treatment failure? Multiple studies have been performed that investigated the ability of urodynamic parameters to predict surgical failure. The results of studies that evaluated the persistence of preoperative detrusor overactivity in the post-operative period have been mixed. It has been reported that patients with high-amplitude detrusor overactivity (detrusor pressure greater than 25 cm H2O during an unstable contraction) are less likely to achieve surgical cure than those with lower detrusor pressures. As with detrusor overactivity, there seems to be variation in the ability of pressure-flow studies and observations of voiding mechanisms to predict postoperative urinary retention or the need for prolonged catheterization after surgical correction of GSI. Two studies that evaluated voiding after Burch urethropexy for correction of GSI reported prolonged times for patients to resume normal voiding in the presence of a low detrusor pressure (<15 cm H2O) associated with a low flow rate (maximum flow rate <20 mL/sec) on the pressure-flow study. Patients with a Valsalva voiding pattern (i.e. detrusor rise <15 cm H2O) also required prolonged catheterization. Another study that evaluated urodynamic findings in patients treated with a pubovaginal sling for GSI reported similar results. Patients who voided with an absent or low-amplitude detrusor contraction (<12 cm H2O) were more likely to develop postoperative urinary retention. These authors found that post-void residual urine (PVR) was a useful predictor of delay in the return to normal voiding.


We consider urodynamics to be a logical extension of the history and physical examination; it is an interactive process between patient and clinician. The best attempt to define and separate symptoms of bladder outlet obstruction from those of bladder dysfunction has not been successful. Abnormalities of the peripheral nervous system may be manifested by decreased perianal sensation, poor anal sphincter tone, and the absence of a bulbocavernosus reflex. The basic tool of the urodynamicist is the cystometrogram (CMG); no urodynamic evaluation is complete without CMG. In our opinion, an electronic single-channel study does not offer any more information than does a carefully performed non-electronic test. We believe the only reason to perform electronic urodynamic testing is to measure pressures from several anatomic sites, thus obtaining subtracted pressures of importance. Cystometry can be performed using either fluid (water, saline, or radiographic contrast) or gas (carbon dioxide) as the infusants; in our opinion, liquid is vastly superior to gas. Although urodynamic studies are clinically useful, its limitations should be recognized. Abnormalities of bladder filling are categorized into abnormal detrusor activity, compliance, sensation and capacity. Many patients have more than one cystometric abnormality. No single urodynamic finding should be taken in isolation.

Suggested Readings:

  1. Melville JL, Katon W, Delaney K et al. Urinary incontinence in US women: a population-based study. Arch Inter Med 2005;165:537-542
  2. Kenton K, Fitzgerald MP, Brubaker K. Striated urethral sphincter activity does not alter urethral pressure during filling cystometry. Am J Obstet Gynecol 2005;192:55-59
  3. Fallon B, Kreder KJ. Urodynamic assessment of sphincteric function in the incontinent female: which test, and does it matter anyway? Curr Uro Rep 2006;7:399-404
  4. Pfisterer MH, Griffiths DJ, Schaefer W et al. The effect of age on lower urinary tract function: a study in women. J Am Geriatr Soc 2006;54:405-412
  5. ACOG Practice Bulletin. Urinary incontinence in women. Number 63, June 2005
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  7. Weber AM. Leak point pressure measurement and stress urinary incontinence. Curr Womens Health Rep 2001;1:45-52 (Level III)
  8. Weber AM. Is urethral pressure profilometry a useful diagnostic test for stress incontinence? Obstet Gynecol Surv 2001;56:720-735. (Level III)
  9. Assessment and treatment of urinary incontinence. Scientific Committee of the First International Consultation on Incontinence. Lancet 2000;355:2153-2158. (Level III)
  10. Contreras Ortiz O. Stress urinary incontinence in the gynecological practice. Int J Gynecol Obstet 2004;86(suppl):S6-16. (Level III)
  11. Takacs EB, Zimmern PE. Recommendations for urodynamic assessment in the evaluation of women with stress urinary incontinence. Clinical Practice Urology 2006;3:544-550
  12. Weber AM, Walters MD. Cost-effectiveness of urodynamic testing before surgery for women with pelvic organ prolapse and stress urinary incontinence. Am J Obstet Gynecol 2000;183:1338-1346

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