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Chapter 29. Urodynamic Studies

Sherif R. Absoeif, MD; Emil A. Tanagho, MD

Urodynamic Studies: Introduction

Urodynamic study is an important part of the evaluation of patients with lower urinary tract obstruction, voiding dysfunctions, urinary incontinence, and neuropathic disorders involving the lower urinary tract. Formerly, the examiner simply observed the act of voiding, noting the strength of the urinary stream, and drawing inferences about the possibility of obstruction of the bladder outlet. In the 1950s, it became possible to observe the lower urinary tract by fluoroscopy during the act of voiding, and in the 1960s, the principles of hydrodynamics were applied to lower urinary tract physiology. In the 1970s, videourodynamic was introduced, where fluoroscopy was incorporated with the pressure measurements to adequately assess both anatomy and function.

The field of urodynamic now has clinical applications in evaluating voiding problems resulting from lower urinary tract disease.

The nomenclature of the tests used in urodynamic studies is not yet settled, and the meanings of urodynamic terms are sometimes overlapping or confusing. In spite of these difficulties, urodynamic tests are extremely valuable. Symptoms elicited by the history or by physical, endoscopic, or even radiographic examination usually delineate the anatomic findings, but the function often must be investigated further by urodynamic tests so that therapy can be devised that is based on an understanding of the altered physiology of the lower urinary tract.

As is true of many high-technology testing procedures (eg, electrocardiography, electroencephalography), urodynamic tests have the greatest clinical validity when their interpretation is left to the treating physician, who should either perform or closely supervise the study or be responsible for correlating all of the findings with personal clinical observations.

Functions Relevant to Urodynamics and Tests Applicable to Each

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Urodynamic studies in concert with an accurate history and physical examination are the most useful clinical tools available for the evaluation of the lower urinary tract and can provide useful clinical information about the function of the urinary bladder, the sphincteric mechanism, and the voiding pattern itself.

Bladder function. This can be evaluated by simple cystometrogram (CMG) that measures vesical pressure as a function of bladder volume. This can provide important information on cystometric bladder capacity, bladder sensation, bladder compliance, and the presence of involuntary bladder contraction and bladder contractility.

Sphincteric function depends on two elements: the smooth muscle sphincter and the voluntary sphincter. The activity of both elements can be recorded urodynamically by measuring urethral pressure profile or by recording sphincter electromyography.

The act of voiding is a function of the interaction between bladder and sphincter, and the result is the flow rate. The flow rate is one major aspect of the total function of the lower urinary tract. It is generally recorded in milliliters per second as well as by total urine volume voided. The simultaneous recording of bladder activity (by intraluminal pressure measurements), sphincteric activity (by electromyography or intraluminal urethral pressure measurements), and flow rate reveals interrelationships among the three elements. Each measurement may give useful information about the normality or abnormality of one specific aspect of lower urinary tract function. A more complete picture is provided by integrating all the three lower tract elements for simultaneous comparison. This comprehensive approach may involve synchronous recordings of variable pressures, flow rate, volume voided, and electrical activity of skeletal musculature around the urinary sphincter (electromyography), along with fluoroscopic imaging of the lower urinary tract. The multiple pressures recorded are quite variable and usually include intravesical pressure, intraurethral pressure at several levels, intra-abdominal pressure, and anal sphincteric pressure as a function of muscular activity of the pelvic floor.

The techniques of urodynamic study must be tailored to the needs of specific patients. Each method has advantages and limitations depending on the requirements of the study. In one patient, results of a single test might be sufficient to establish the diagnosis and suggest appropriate therapy; in another, many more studies might be necessary.

Physiologic and Hydrodynamic Considerations

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Urinary Flow Rate

Because urinary flow rate is the product of detrusor action against outlet resistance, a variation from the normal flow rate might reflect dysfunction of either. The normal flow rate from a full bladder is about 20–25 mL/s in men and 25–30 mL/s in women. These variations are directly related to the volume voided and the person's age. Obstruction or detrusor dysfunction should be suspected in any adult voiding with a full bladder at a rate of <15 mL/s. A flow rate <10 mL/s is considered definite evidence of obstruction or detrusor dysfunction. Occasionally, one encounters “supervoiders” with flow rates far above the normal range. This may signify low outlet resistance but is of less concern clinically than obstruction. This phenomenon is more commonly seen in women.

Outlet Resistance

Outlet resistance is the primary determinant of flow rate and varies according to mechanical or functional factors.

Functional, outlet resistance is primarily related to sphincteric activity, which is controlled by both the smooth sphincter and the voluntary sphincter. Overactivity of the smooth sphincter is very rare and essentially nonexistent in females. It is rarely seen in men in association with hypertrophy of the bladder neck due to neurogenic dysfunction or distal obstruction. However, such cases must be evaluated before this conclusion is reached.

On the other hand, increased voluntary sphincteric activity is not uncommon. It is often neglected as a primary underlying cause of increased sphincteric resistance. It is manifested either as lack of relaxation or as actual overactivity during voiding. The normal voluntary sphincter provides adequate resistance, along with the smooth sphincter, to prevent escape of urine from the bladder, but it should completely relax during the act of voiding. If the voluntary sphincter does not relax during detrusor contraction, partial functional obstruction occurs. Overactivity of the sphincter, resulting in increased outlet resistance, is usually a neuropathic phenomenon. However, it can also be functional, resulting from irritative phenomena such as infection or other factors—chemical, bacterial, hormonal, or, even more commonly and often not appreciated, psychological and in patients who are infrequent voiders. This is commonly referred to as pelvic floor dysfunction. This is a spectrum of disease that varies from mild difficulty in voiding associated with incomplete emptying and some pelvic/perineal and genital discomfort to extreme cases of urinary retention known as Fowler's syndrome.

Mechanical Outlet Resistance

Mechanical factors resulting in obstruction to urine flow are the easiest to identify by conventional methods. In women, they may take the form of large cystoceles, urethral kinks, or, most commonly, iatrogenic scarring, fibrosis, and compression from previous vaginal or periurethral operative procedures. Mechanical factors in men are well known to all urologists; the classic form is benign prostatic hypertrophy. Urethral stricture from various causes and posterior urethral valves are other common causes of urinary obstruction in men, and there are many others.

Normal voiding with a normal flow rate is the product of both detrusor activity and outlet resistance. Complete sphincteric relaxation usually precedes detrusor contraction by a few seconds, and when relaxation is maximal, detrusor activity starts and is sustained until the bladder is empty. A high intravesical pressure resulting from detrusor contraction is usually an indication of increased outlet resistance and is not necessary to initiate normal voiding.

Variations in Normal Flow Rate

The sequence just described is not essential for normal flow rates. The flow rate may be normal in the absence of any detrusor contraction if sphincteric relaxation is assisted by increased intra-abdominal pressure from straining. Persons with weak outlet resistance and weak sphincteric control can achieve a normal flow rate by complete voluntary sphincteric relaxation without detrusor contraction or straining. A normal flow rate can be achieved in spite of increased sphincteric activity or lack of complete relaxation if detrusor contraction is increased to overcome outlet resistance.

Because a normal flow rate can be achieved in spite of abnormalities of one or more of the mechanisms involved, recording the flow rate alone does not provide insight into the precise mechanisms by which it occurs. Distinction between patterns of flow can be difficult. For practical purposes, if the flow rate is adequate and the recorded pattern and configuration of the flow curve are normal, these variations may not be clinically significant except in rare cases.

Nomenclature

The study of urinary flow rate itself is usually called uroflowmetry. The flow rate is generally identified as maximum flow rate, average flow rate, flow time, maximum flow time (the time elapsed before maximum flow rate is reached), and total flow time (the aggregate of flow time if the flow has been interrupted by periods of no voiding) (Figure 29–1). The flow rate pattern is characterized as continuous or intermittent, etc.

Figure 29–1.

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Uroflowmetry. Basic elements of maximum flow, average flow, total flow time, and total volume voided.

Pattern Measurement of Flow Rate

A normal flow pattern is represented by a bell-shaped curve (Figure 29–1). However, the curve is rarely completely smooth; it may vary within limits and still be normal. Flow rate can be determined by measuring a 5 seconds' collection at the peak of flow and dividing the amount obtained by 5 to arrive at the average rate per second. This rough estimate is useful, especially if the flow rate is normal and the values are above 20 mL/s.

In modern practice, the flow rate is more often recorded electronically: The patient voids into a container on top of a measuring device that is connected to a transducer, the weight being converted to volume and recorded on a chart in milliliters per second. Figure 29–2 is an example of such a recording from a normal man. The general bell-shaped curve is quite clear, and the tracing shows all of the values discussed previously: total flow time, maximum flow time, maximum flow rate, average flow rate, and total volume voided. Occasional supervoiders can exceed the limits of the chart, but this is usually not of clinical concern (Figure 29–3). A possible variation in the bell appearance is seen in Figure 29–4.

Figure 29–2.

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Classic normal flow rate, with peak of about 30 mL/s and average of about 20 mL/s. On the horizontal scale, one large square equals 5 seconds.

Figure 29–3.

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Flow rate of “supervoider.” Maximum flow rate exceeds limits of chart. Tracing shows fast buildup and complete bladder emptying of large volume of urine in a very short period. On the horizontal scale, one large square equals 5 seconds.

Figure 29–4.

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Normal flow rate with some variation in appearance of curve. Note the rapid pressure rise but progressive increase to maximum, followed by a sharp drop. There is also fluctuation in ascending limb of tracing. On the horizontal scale, one large square equals 5 seconds.

The overall appearance of the flow curve may disclose unsuspected abnormalities. In Figure 29–5, for example, flow time is greatly prolonged. Maximum flow rate may not be low, but the average flow rate is very low—though the maximum flow rate is at one point within the normal range. Such fluctuation in flow rate is most commonly related to variations in voluntary sphincteric activity. In Figure 29–6, this pattern is extreme: Maximum flow rate never exceeds 15 mL/s, and average flow rate is about 10 mL/s, which is indicative of obstruction. (Again, this fluctuation in pattern probably reflects sphincteric hyperactivity.)

Figure 29–5.

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Rather low flow rate (not exceeding 10 mL/s), yet at one point, the peak reaches 27–32 mL/s. Note again fluctuation in flow. On the horizontal scale, one large square equals 5 seconds.

Figure 29–6.

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Very low flow rate of short duration and small volume. Note that maximum flow is not >15 mL/s; however, flow average is <10 mL/s, and flow is almost completely interrupted in the middle. On the horizontal scale, one large square equals 5 seconds.

The flow rate pattern reveals a great deal about the forces involved. For example, if the patient is voiding without the aid of detrusor contractions—primarily by straining—this can be easily deduced from the pattern of the flow rate. Figure 29–7 shows an example of intermittent voiding, primarily by straining, with no detrusor activity, and at a rate that sometimes does not reach the usual peaks. With experience, one becomes expert at detecting the mechanisms underlying abnormalities in flow rate. For example, in Figure 29–5, the maximum flow rate is in the normal range, the average flow rate is slightly low, and the curve has a general bell pattern, yet brief partial intermittent obstructions to flow can be readily interpreted as due to overactivity of the voluntary sphincter, a mild form of detrusor/sphincter dyssynergia (see discussion following).

Figure 29–7.

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Classic flow rate due to abdominal straining with no detrusor activity. See effect of spurts of urine with complete interruption between them; patient cannot sustain increased intra-abdominal pressure. On the horizontal scale, one large square equals 5 seconds.

Flow rates in mechanical obstruction are totally different, classically in the range of 5–6 mL/s; flow time is greatly prolonged, and there is sustained low flow with minimal variation (Figure 29–8). Figure 29–9 is a striking example of a curve for a patient with benign prostatic hypertrophy. No simultaneous studies are needed with such a pattern, since the pattern is obviously one of mechanical obstructions.

Figure 29–8.

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Flow rate in a case of urinary obstruction showing very low average flow rate (not above 5 or 6 mL/s). Prolonged duration of flow is associated with incomplete emptying. On the horizontal scale, one large square equals 5 seconds.

Figure 29–9.

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Classic low flow rate of bladder outlet obstruction (benign prostatic hypertrophy), markedly prolonged flow time, and fluctuation due to attempt at improving flow by increasing intra-abdominal pressure. On the horizontal scale, one large square equals 5 seconds.

Reduced flow rate in the absence of mechanical obstruction is due to some impairment of sphincteric or detrusor activity. This is seen in a variety of conditions, for example, normal detrusor contraction with no associated sphincteric relaxation and normal detrusor contraction with sphincteric overactivity, which is more serious. These two entities are commonly referred to as detrusor/sphincter dyssynergia. If with detrusor contraction the sphincter does not relax and open up or (worse) if it becomes overactive, urine flow is obstructed (ie, flow rate is reduced and of abnormal pattern). Reduced flow rate may occur even with increased detrusor activity if the latter is not adequate to overcome sphincteric resistance.

So many variations are possible in the shape of the flow curve—no matter how accurately the flow is recorded or how often the study is repeated to confirm abnormal findings—that it is beneficial to relate it to simultaneous recordings, such as of bladder pressure, pelvic floor electromyography, urethral pressure profile, or simply cinefluoroscopy. Nevertheless, by itself it can be one of the most valuable urodynamic studies undertaken to evaluate a specific type of voiding dysfunction. Flowmetry is not only of diagnostic value but also of valuable in follow-up studies and in deciding on treatment. In some cases, however, flowmetry alone does not provide enough data about the abnormality in the voiding mechanism. More information must then be obtained by evaluation of bladder function.

Bladder Function

The basic factors of normal bladder function are bladder capacity, compliance, sensation, contractility, voluntary control, and response to drugs. All of them can be evaluated by cystometry. If all are within the normal range, bladder physiology can be assumed to be normal. Evaluation of every factor has its own implication and, before a definitive conclusion is reached, must be examined in the light of associated manifestations and findings.

Cystometry can be done by either of two basic methods: (1) allowing physiologic filling of the bladder with secreted urine and continuously recording the intravesical pressure throughout a voiding cycle (starting the recording when the patient's bladder is empty and continuing it until the bladder has been filled—at which time the patient is asked to urinate—and voiding begins) or (2) by filling the bladder with water and recording the intravesical pressure against the volume of water introduced into the bladder.

With the first (physiologic filling) method, the assessment of bladder function is based on voided volume (assuming that the presence of residual urine has been ruled out). The second method permits accurate determination of the volume distending the bladder and of the pressures at each level of filling, yet it has inherent defects: fluid is introduced rather than naturally secreted, and bladder filling occurs more rapidly than it normally does.

Bladder Capacity, Compliance, and Sensation

Bladder capacity: The maximum cystometric bladder capacity is the volume at which the patient feels he/she can no longer delay micturition, uninhibited detrusor contraction occurs leading to micturition or the intravesical pressure rises and the patient leaks. This is different from functional bladder capacity which is the maximum volume that the patient normally void. This is usually more relevant and is assessed from a voiding diary.

Bladder Compliance (Accommodation)

Bladder compliance reflects the ability of the bladder wall to expand to capacity with minimal changes in intravesical pressure. This expansile capability is contributed to by the smooth muscular, collagenous, and elastic components of the bladder submucosa and muscularis. The normally innervated bladder without any coexistent pathologic lesions retains this vesicoelastic capability during the storage phase of bladder activity.

The CMG (Figure 29–10) is obtained during the phase of bladder filling; the volume of fluid in the bladder is plotted against the intravesical pressure to show bladder wall compliance to filling. The normal cystometric curve shows a fairly constant low intravesical pressure until the bladder nears capacity, then a moderate rise until capacity is reached, and then a sharp rise as voiding is initiated. Normally, the sensation of fullness is first perceived when the bladder contains 100–200 mL of fluid and strongly felt as the bladder nears capacity; the desire to void occurs when the bladder is full (normal capacity, 400–500 mL). However, the bladder has a power of accommodation; that is, it can maintain an almost constant low intraluminal pressure throughout its filling phase regardless of the volume of fluid present, and this directly influences compliance. As the bladder progressively accommodates larger volumes with no change in intraluminal pressure, the compliance values become higher (compliance = volume/pressure) (Figure 29–10).

Figure 29–10.

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Cystometrogram of patient with normal bladder capacity. Note the stable intravesical pressure during filling phase; slight rise at end of filling phase, indicating bladder capacity perceived as sense of fullness; and sharp rise at end (voiding contraction).

Contractility and Voluntary Control

The bladder normally shows no evidence of contractility or activity during the filling phase. However, once it is filled to capacity and the patient perceives the desire to urinate and consciously allows urination to proceed, strong bladder contractions occur and are sustained until the bladder is empty. The patient can of course consciously inhibit detrusor contraction. Both of these aspects of voluntary detrusor control must be assessed during cystometric study in order to rule out uninhibited bladder activity and to determine whether the patient can inhibit urination with a full bladder and initiate urination when asked to do so. The latter is occasionally difficult to verify clinically because of conscious inhibition by a patient who may be embarrassed by the unnatural circumstances.

Responses to Drugs

Drugs are being used with increasing frequency in the evaluation of detrusor function. They can help to diagnose underlying neuropathy and to determine whether drug treatment might be of value in individual cases. Study of the relationship of bladder capacity to intravesical pressure and bladder contractility gives a rough evaluation of the patient's bladder function. Low intravesical pressure with normal bladder capacity might not be significant, whereas low pressure with a very large capacity might imply sensory loss or a flaccid lower motor neuron lesion, a chronically distended bladder, or a large bladder due to myogenic damage. High pressure (usually associated with reduced capacity) that rises rapidly with bladder filling is most commonly due to inflammation, enuresis, or reduced bladder capacity. However, uninhibited bladder activity during this high-pressure filling phase might indicate neuropathic bladder or an upper motor neuron lesion.

The parasympathetic drug bethanechol chloride (Urecholine) is often used to assess bladder muscle function in patients with low bladder pressure associated with lack of detrusor contraction. No response to bethanechol suggests myogenic damage; a normal response indicates a bladder of large capacity with normal musculature; and an exaggerated response indicates a lower motor neuron lesion. The test has so many variables that it must be done meticulously to give reliable results.

Testing with anticholinergic drugs or muscle depressants may be helpful in the evaluation of uninhibited detrusor contraction or increased bladder tonus and low compliance. The information thus obtained can be useful in choosing drugs for treatment.

Recording of Intravesical Pressure

Intravesical pressure can be measured directly from the vesical cavity, either by a suprapubic approach or via a transurethral catheter. The pressure inside the bladder is actually a function of both intra-abdominal and intravesical pressure. Thus, true detrusor pressure is the pressure recorded from the bladder cavity (intravesical pressure) minus intra-abdominal pressure. This point is important because variations in intra-abdominal pressure may alter the recorded intravesical pressure, and if the recorded intravesical pressure is mistakenly considered to reflect only detrusor pressure and not increased intra-abdominal pressure due to straining as well, erroneous conclusions may be reached.

Whenever possible, intra-abdominal pressure should be recorded simultaneously with intravesical pressure, since there is no other way to determine the true detrusor pressure. Intra-abdominal pressure is usually recorded by a small balloon catheter inserted high in the rectum and connected to a separate transducer.

The most valuable part of the cystometric study is the determination of voiding activity or voiding contraction. The characteristics of intravesical pressure can be quite significant. Normally, voiding contractions are not high (20–40 cm of water); this magnitude of intravesical pressure is generally adequate to deliver a normal flow rate of 20–30 mL/s and completely empty the bladder if it is well sustained. A higher voiding pressure is indicative of possible increase in outlet resistance yet denotes an overactive, healthy detrusor musculature. Figure 29–11 shows a normal flow rate associated with normal detrusor contraction at a magnitude of 20 cm of water that is well sustained and of short duration and results in complete bladder emptying.

Figure 29–11.

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Simultaneous recording of voiding contraction and resulting flow rate. Note the normal range of intravesical pressure during voiding phase as well as adequate normal flow rate (shown in Figure 29–4). On the horizontal scale, one large square equals 5 seconds.

The quality of bladder pressure can also be informative, even without simultaneous recording of flow rate. In such cases, however, it is preferable to record flow rate under normal circumstances. A well-sustained detrusor contraction, high at initiation and sustained at normal values, is seen in Figure 29–12. In Figure 29–13, the voiding pressure is too high—there is an element of sphincteric dyssynergia triggering variations in voiding pressures and flow rate. Simultaneous recording of bladder and intra-abdominal pressures would provide more information. As suggested previously, recording the intravesical pressure alone does not give as much information as may be required, and increased intra-abdominal pressure might be mistaken for detrusor action. This situation is illustrated in Figure 29–14. The bladder pressure appears to indicate good detrusor function; nevertheless, simultaneous recording of intra-abdominal pressure makes it clear that all of the apparent changes in vesical intraluminal pressure in fact represent variations in intra-abdominal pressure.

Figure 29–12.

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Recording of bladder pressure simultaneously with flow rate. Note the slightly higher intravesical pressure with high flow rate, which, at its maximum, is that of a supervoider (see Figure 29–3). On the horizontal scale, one large square equals 5 seconds.

Figure 29–13.

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Simultaneous recording of flow rate and intra-abdominal pressure; intravesical pressure overlap in top recording. Note the very high voiding pressure. However, flow rate is relatively low, with some interruption most likely due to sphincteric overactivity. On the horizontal scale, one large square equals 5 seconds.

Figure 29–14.

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Simultaneous recording of intra-abdominal and intravesical pressures. If one considers only intravesical pressure (upper recording), one might assume adequate detrusor contraction. Comparison with intra-abdominal pressure (lower recording) shows that they are almost identical and that there is no detrusor contraction at all.

Figure 29–15 shows the two pressures recorded on the same chart, on the same channel, by having the writing pen share the time between two transducers—one recording intra-abdominal pressure; the other, intravesical pressure.

Figure 29–15.

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Simultaneous recording of two measurements—intravesical pressure (top) and intra-abdominal pressure (bottom)—on a single channel. The difference between the two can be clearly seen as pure detrusor contraction.

Pathologic Changes in Bladder Capacity

The bladder capacity is normally 400–500 mL, but it can be reduced or increased in a variety of disorders and lesions (Table 29–1). Some common causes of reduced bladder capacity are enuresis, urinary tract infection, contracted bladder, upper motor neuron lesion, and defunctionalized bladder. Reduced capacity also may occur in association with incontinence and in postsurgical bladder. Increased bladder capacity is not uncommon in women who have trained themselves to retain large volumes of urine. Bladder capacity is increased also in sensory neuropathic disorders, lower motor neuron lesions, and chronic obstruction from myogenic damage. It is important to relate bladder capacity to the intravesical pressure (Table 29–2). Slight variations in bladder capacity with no change in bladder pressure might be of less significance than the reverse. What is usually of greatest significance is the bladder with reduced capacity associated with normal pressure or, more important, with increased pressure, or the bladder with large capacity associated with decreased pressure.

Table 29–1. Causes of Reduced or Increased Bladder Capacity.

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Table 29–1. Causes of Reduced or Increased Bladder Capacity.

Causes of reduced bladder capacity

Enuresis or incontinence

Bladder infections

Bladder contracture due to fibrosis (from tuberculosis, interstitial cystitis, etc)

Upper motor neuron lesions

Defunctionalized bladder

Postsurgical bladder

Neuropathic disorders

Lower motor neuron lesions

Megacystis (congenital)

Chronic urinary tract obstruction

Note: Normal capacity in adults is 400–500 mL.

Table 29–2. Relationship between Intravesical Pressure and Capacity in Various Diseases.

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Table 29–2. Relationship between Intravesical Pressure and Capacity in Various Diseases.

Low intravesical pressure

Normal capacity

Large capacity

Sensory deficits (diabetes mellitus, tabes dorsalis)

Flaccid lower motor neuron lesions

Large bladder (due to repeated stretching)

High intravesical pressure

Rapidly rising

Reduced capacity

Inflammation

Enuresis

Uninhibited contraction

Uninhibited neurogenic bladder

Upper motor neuron lesions

Pathologic Changes in Accommodation (Compliance)

Compliance is a measurement of the elasticity of the bladder wall and usually reflects change in intravesical pressure in response to filling. In a bladder with normal compliance—in which case the micturition center of the spinal cord is controlled by the central nervous system—intravesical pressure does not vary with progressive bladder filling until capacity is reached; in other words, when compliance is reduced secondary to fibrosis of the bladder wall, there will be a progressive increase in intravesical pressure and loss of accommodation. This usually occurs at smaller volumes and with reduced capacity. Poor compliance can be seen in cases of long-standing urinary obstruction or iatrogenically after extensive pelvic surgery.

The patient being studied by cystometry can always note the presence or absence of a sensation of fullness. One normally does not sense volumes in the bladder but only changes in pressure.

Compliance plays a crucial role in the long-term function of the upper urinary tract. The direct effect of intravesical pressure on ureteral urine transport and the long-term effects from the elevated pressure are significant.

Pathologic Changes in Sensation

A slight rise in intravesical pressure on cystometry signifies that the bladder is full to normal capacity and that the patient is perceiving it. This sign is usually absent in pure sensory neuropathy and in mixed sensory and motor loss. (Other sensations can be tested for in different ways; see Chapter 26.)

Pathologic Changes in Contractility

The bladder is normally capable of sustaining contraction until it is empty. Absence of residual urine after voiding usually denotes well-sustained contractions. Neuropathic dysfunction is usually associated with residual urine of variable amount depending on the type of dysfunction. Significant outlet resistance—mechanical or functional—is also a cause of residual urine.

Cystometric study may disclose complete absence of detrusor contractility due to motor or sensory deficits or conscious inhibition of detrusor activity (Table 29–3). Detrusor hyperactivity is shown as uninhibited activity, usually due to interruption of the neural connection between spinal cord centers and the higher inhibitory midbrain and cortical centers.

Table 29–3. Variations in Detrusor Contractility in Various Diseases.

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Table 29–3. Variations in Detrusor Contractility in Various Diseases.

Normal contractions

Normal volume

Well-sustained contractions

Absent or weak contractions

Sensory neuropathic disorders

Conscious inhibition of contractions

Lower motor neuron lesions

Uninhibited contractions

Upper motor neuron lesions

Cerebrovascular lesions

An integrated picture of bladder capacity, intravesical pressure, and contractility is useful for general assessment of the basic physiologic mechanisms of the bladder. Low intravesical pressure in a patient with normal bladder capacity may have no clinical significance, whereas low pressure with a very large capacity may signify sensory loss or a flaccid lower motor neuron lesion, a chronically distended bladder, or a large bladder due to myogenic damage. High pressure (usually associated with reduced capacity) that rises rapidly with bladder filling is most commonly associated with inflammation, enuresis, or reduced bladder capacity. However, uninhibited activity during the interval of rising pressure that occurs with bladder filling may indicate a neurogenic bladder or an upper motor neuron lesion.

Sphincteric Function

Urinary sphincteric function can be evaluated either by recording the electromyographic activity of the voluntary component of the sphincteric mechanism or by recording the activity of both smooth and voluntary components by measuring the intraurethral pressure of the sphincteric unit. The latter method is called pressure profile measurement (profilometry). With the use of videourodynamic, abdominal/Valsalva leak point pressure (ALPP) is another way to evaluate the sphincteric function: This test measures the ability of the urethra to resist abdominal pressure as an expulsive force. This will be discussed more in Section “Videourodynamic.”

Profilometry

The urethral pressure profile is determined by recording the pressure in the urethra at every level of the sphincteric unit from the internal meatus to the end of the sphincteric segment. Water profilometry, which requires a flow rate of about 2 mL/min, gives fairly accurate results. It may be used for screening patients with incontinence or functional obstruction, but it is not very sensitive and only provides information about total urethral pressure. The membrane catheter and microtransducer techniques of profilometry described in the following sections provide much more accurate and detailed information.

Membrane Catheter Technique

Membrane catheters used for recording pressure profiles usually have several channels, so several measurements can be obtained simultaneously. One such catheter used at UCSF has four lumens and an outside diameter of 7F. Two of the four lumens are open at the end, one for bladder filling and the other for recording bladder pressure; the other two lumens, which are situated 7 cm and 8 cm from the catheter tip, are covered by a thin membrane with a small chamber underneath (Figure 29–16). The space under the membrane and the lumen connected to it are filled with fluid, free of any gas, and connected to a pressure transducer. The pressure under this membrane should be zero at the level of the transducer so that it can register any pressure applied to the membrane whatever its level at any time. The catheter also has radiopaque markers at 1-cm intervals starting at the tip, with a heavier marker every 5 cm; it also has a special marker showing the site of each membrane. The markers permit fluoroscopic visualization of the catheter and the membrane levels during the entire study.

Figure 29–16.

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Membrane catheter showing radiopaque markers. Note the two membrane chambers for urethral pressure measurements and four separate channels—two channels for urethral pressure recording, one for bladder pressure recording, and one for bladder filling—each of which is connected to a separate ending. (Reproduced, with permission, from Tanagho EA, Jonas U: Membrane catheter: Effective for recording pressure in lower urinary tract. Urology 1977;10:173.)

Microtransducer Technique

The results of microtransducer profilometry are as accurate as those obtained with the membrane catheter. Two microtransducers can be mounted on the same catheter, one at the tip for recording of bladder pressure and the other about 5–7 cm from the tip to record the urethral pressure profile as the catheter is gradually withdrawn from the bladder cavity to below the sphincteric segment.

Electromyographic Study of Sphincteric Function

Electromyography alone gives useful information about sphincteric function, but it is most valuable when done in conjunction with cystometry. There are several techniques for electromyographic studies of the urinary sphincter: either surface electrodes or needle electrodes are used. Surface electrode recordings can be obtained either from the lumen of the urethra in the region of the voluntary sphincter or, preferably, from the anal sphincter by using an anal plug electrode. Recording via needle electrodes can be obtained from the anal sphincter, from the bulk of the musculature of the pelvic floor, or from the external sphincter itself, though in the latter case, the placement is difficult and the accuracy of the results is questionable.

Direct needle electromyography of the urethral sphincter provides the most accurate information. Because the technique is difficult, however, simpler approaches are generally used. The anal sphincter is readily accessible for electromyographic testing, and testing of any area of the pelvic floor musculature generally reflects the overall electrical activity of the pelvic floor, including the external sphincter. Electromyography is not simple, and the assistance of an experienced electromyographer is probably essential. Electromyographic study makes use of the electrical activity that is constantly present within the pelvic floor and external urinary sphincter at rest and that increases progressively with bladder filling. If the bladder contracts for voiding, electrical activity ceases completely, permitting free flow of urine, and is resumed at the termination of detrusor contraction to secure closure of the bladder outlet (Figure 29–17). Electromyography is important in showing this effect and, along with bladder pressure measurement, can pinpoint the exact time of detrusor contraction. Persistence of electromyographic activity during the phase of detrusor contraction for voiding—or, even worse, its overactivity during that phase—interferes with the voiding mechanism and leads to in coordination between detrusor and sphincter (detrusor/sphincter dyssynergia). During the interval of detrusor contraction, increased electromyographic activity interferes with the free flow of urine, as can be shown by simultaneous recording of flow rate.

Figure 29–17.

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Simultaneous recording of bladder pressure, flow rate, and electromyography of anal sphincter. With rise in bladder pressure for voiding, start of flow rate has a smooth, continuous, bell-shaped curve. Note also the complete absence of electromyographic activity of the anal sphincter throughout the voiding act. On the horizontal scale, one large square equals 5 seconds.

Electromyographic recording shows only the activity of the voluntary component of the urinary sphincteric mechanism and the overall activity of the pelvic floor. More information is gained when the electromyogram is recorded simultaneously with detrusor pressure or flow rate. However, this method gives no information about the smooth component of the urinary sphincter.

Pressure Measurement for Evaluation of Sphincteric Function

Perfusion profilometry, usually performed with the patient supine and with an empty bladder, provides a simple pressure profile that allows determination of the maximum pressure within the urethra. This is adequate for screening patients with incontinence or functional obstruction. However, in order to determine the maximum closure pressure (see section following), the bladder pressure must be recorded simultaneously with the urethral pressure profile. Such simultaneous recording is not possible with perfusion profilometry.

The membrane catheter and microtransducer techniques of profilometry, because they use multichannel recording, routinely provide much more detailed information; at least four distinct sets of measurements can be obtained from the simplest pressure profile made using the membrane catheter or microtransducer (Figure 29–18): (1) the maximum pressure exerted around the sphincteric segment, (2) the net closure pressure of the urethra, (3) the distribution of this closure pressure along the entire length of the sphincter, and (4) the exact functional length of the sphincteric unit and its relation to the anatomic length.

Figure 29–18.

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Urethral pressure profile and its components. Note the functional length, anatomic length, and the shape of the profile, with maximum closure pressure in the middle segment of the urethra rather than at the level of the internal meatus. (Reproduced, with permission, from Bradley W: Cystometry and sphincter electromyography. Mayo Clin Proc 1976;329:335.)

Total Pressure

The urethral pressure profile recording shows the pressure directly recorded within the urethral lumen along the entire length of the urethra from internal to external meatus. From this measurement, the maximum pressure exerted around the sphincteric segment can be determined.

Closure Pressure

The urethral closure pressure is the difference between intravesical pressure (bladder pressure) and urethral pressure, that is, the net closure pressure. The maximum closure pressure is the most important measurement in evaluating the activity of the sphincteric unit and its responses to various factors.

Distribution of Closure Pressure

As the catheter is withdrawn down the urethra, the closure pressure at various levels along the entire length of the sphincteric segment is recorded.

Functional Length of Sphincteric Unit

The functional length of the sphincteric unit is the portion with positive closure pressure, that is, where urethral pressure is greater than bladder pressure. The distinction between anatomic length and functional length is important. Regardless of the anatomic length, the effectiveness of the urethral sphincter may be limited to a shorter segment. In women, the pressure is normally rather low at the level of the internal meatus but builds up gradually until it reaches its maximum in the midurethra, where the voluntary sphincter is concentrated; it slowly drops until it is at its lowest at the external meatus. On the basis of these measurements, it is clear that the anatomic and functional lengths of the normal urethra in women are about the same and that the maximum closure pressure is at about the center of the urethra—not at the level of the internal meatus. In men, the pressure profile is slightly different: the functional length is longer, and the maximum closure pressure builds up in the prostatic segment, reaches a peak in the membranous urethra, and drops as it reaches the level of the bulbous urethra (Figure 29–19). The entire functional length in men is about 6–7 cm; in women, it is about 4 cm.

Figure 29–19.

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Normal male urethral pressure profile showing progressive rise throughout prostatic segment and peak being reached in membranous urethra. (Reproduced, with permission, from Tanagho EA: Membrane and microtransducer catheters: Their effectiveness for profilometry of the lower urinary tract. Urol Clin North Am 1979;6:110.)

Dynamic Changes in Pressure Profile

The usefulness of the pressure profile is enhanced if the examiner notes the sphincteric responses to various physiologic stimuli: (1) postural changes (supine, sitting, and standing), (2) changes in intra-abdominal pressure (sharp increase with coughing; sustained increase with bearing down), (3) voluntary contractions of the pelvic floor musculature to assess activity of the voluntary sphincter, and (4) bladder filling. The latter test consists of making baseline recordings with both an empty bladder and a full bladder and comparing these recordings with recordings made under conditions of stress (coughing, bearing down) and during voluntary contraction with an empty bladder and a full bladder.

A simple pressure profile is informative but does not provide data that will delineate and identify specific sites of sphincteric dysfunction. The advantage of using a membrane catheter or microtransducer is that the pressure profile can be expanded by slowing down the rate of withdrawal of the catheter and speeding up the motion of the recording paper. Since the catheter can be held at different levels for any length of time, other tests can be made and their effects monitored. Response to stress (particularly when standing), response to bladder distention, response to changes in position, the effects of drugs, and the effects of nerve stimulation can all be evaluated if needed. Bladder filling normally leads to increase in tonus of the sphincteric element, with some rise in closure pressure, especially when bladder filling approaches maximum capacity. Stress from coughing or straining also normally results in sustained or increased closure pressure (Figure 29–20). When the patient stands up, closure pressure is usually substantially increased (Figure 29–21). Testing for activity of the voluntary sphincter by the hold maneuver (asking the patient to actively contract the perineal muscles) produces a significant rise in urethral pressure (Figure 29–22). When the effects of all of these responses are recorded concomitantly with intravesical pressure, the data can be interrelated and the exact closure pressure at any given time can be ascertained.

Figure 29–20.

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Simultaneous recording of intraurethral (U) and intravesical (B) pressures and their responses to coughing and bearing down. Rise in intravesical pressure as a result of increase in intra-abdominal pressure is associated with simultaneous rise in intraurethral pressure, maintaining a constant closure pressure.

Figure 29–21.

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Urethral pressure profile of normal woman in sitting and standing positions. Note the marked improvement in closure pressure (in both functional length and magnitude) when patient stands up. (Reproduced, with permission, from Tanagho EA: Urodynamics of female urinary incontinence with emphasis on stress incontinence. J Urol 1979;122:200.)

Figure 29–22.

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Right: Urethral pressure profile in normal range. U, urethra; B, bladder. Left: Main point of effect of hold maneuver is significant increase in closure pressure of urethra (U) without change in bladder pressure (B)—act of voluntary sphincter.

The response to stress with the patient standing usually should also be recorded. Especially in cases of stress incontinence, weakness of the sphincteric mechanism may not be apparent with the patient sitting or supine but becomes clear when the patient stands up.

The effectiveness of drugs in increasing or reducing the urethral pressure profile can also be tested. For example, phenoxybenzamine (Regitine) can be administered and the urethral pressure profile recorded; a drop in pressure indicates that alpha-blockers may be an effective means of decreasing urethral resistance, with obvious implications for the management of urinary obstruction. Anticholinergic drugs can be tested for possible use as detrusor depressants. Detrusor activity can be investigated by administering bethanechol chloride (Urecholine) and simultaneously recording bladder and urethral pressures.

Characteristics of Normal Pressure Profile (Figure 29–23)

The basic features of the ideal pressure profile are not easily defined. In women, the normal urethral pressure profile has a peak of 100–120 cm of water and the closure pressure is in the range of 90–100 cm of water. Closure pressure is lowest at the level of the internal meatus, gradually builds up in the proximal 0.5 cm, and reaches its maximum about 1 cm below the internal meatus. It is sustained for another 2 cm and then starts to drop in the distal urethra. The functional length of a normal adult female urethra is about 4 cm. The response to stress with coughing and bearing down is sustained or augmented closure pressure. Standing up also increases this pressure, with maximum rise in the midsegment.

Figure 29–23.

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Recording of normal female urethral pressure profile, showing basic features and actual values, including anatomic as well as functional length. U, urethra; B, bladder. (Reproduced, with permission, from Tanagho EA: Membrane and microtransducer catheters: Their effectiveness for profilometry of the lower urinary tract. Urol Clin North Am 1979;6:110.)

Pressure Profile in Pathologic Conditions

Urinary Stress Incontinence

The classic pressure changes noted in this type of incontinence are as follows:

Low urethral closure pressure.
Short urethral functional length at the expense of the proximal segment.
Weak responses to stress.
Loss of urethral closure pressure with bladder filling.
Fall in closure pressure on assuming the upright position.
Weak responses to stress in the upright position.

Urinary Urge Incontinence

The most pertinent pressure changes in urinary urge incontinence are normal or high closure pressures with normal responses to stress, normal responses to bladder filling, and normal responses when the patient stands up. Urge incontinence can result from any of the following mechanisms (Figure 29–24):

Detrusor overactivity, with active detrusor contractions overcoming urethral resistance and leading to urine leakage.
The exact reverse, that is, a constant detrusor pressure with no evidence of detrusor overactivity but with urethral instability in that urethral pressure becomes less than bladder pressure, so that urine leakage occurs without any detrusor contraction.
A combination of the two preceding mechanisms (the most common form), that is, some drop in closure pressure and some rise in bladder pressure. In such cases, the drop in urethral pressure is often the initiating factor.

Figure 29–24.

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Three mechanisms of urinary urge incontinence. Left: Normal sphincter activity exceeded by hyperactive detrusor. Center: Normal detrusor, without any overactivity, yet unstable urethra with marked drop in urethral pressure leading to leakage. Right: Most common combination—some rise in intravesical pressure due to detrusor hyperirritability associated with drop in urethral pressure due to sphincteric relaxation. U, urethra; B, bladder.

Combination of Stress and Urge Incontinence

In this common clinical condition, profilometry is used to determine the magnitude of each component, that is, whether the incontinence is primarily urge, primarily stress, or both equally. As a guide to treatment, profilometric studies sometimes show that stress incontinence precipitates urge incontinence. The stress elements initiate urine leakage in the proximal urethra, exciting detrusor response and sphincteric relaxation and ending with complete urine leakage. Once the stress components are corrected, the urge element disappears. This combination cannot be detected clinically.

Postprostatectomy Incontinence

After prostatectomy, there is usually no positive pressure in the entire prostatic fossa, minimal closure pressure at the apex of the prostate, and normal or greater than normal pressure within the voluntary sphincteric segment of the membranous urethra. It is the functional length of the sphincteric segment above the genitourinary diaphragm that determines the degree of incontinence; the magnitude of closure pressure in the voluntary sphincteric segment has no bearing on the patient's symptoms. High pressure is almost always recorded within the voluntary sphincter despite the common belief that what someone termed “iatrogenically induced incontinence” is due to damage to the voluntary sphincter—which is definitely not the case.

Detrusor/Sphincter Dyssynergia

In this situation, findings of cystometric studies are normal at the filling phase, with possible closure pressure above average. However, the pathologic entity becomes clear when the patient attempts to void: Detrusor contraction is associated with a simultaneous increase in urethral closure pressure instead of a drop in pressure. This is a direct effect of overactivity of the voluntary component, leading to obstructive voiding or low flow rate and frequent interruption of voiding. This phenomenon is commonly seen in patients with supraspinal lesions. It can be encountered in several other conditions as well.

Value of Simultaneous Recordings

Measurement of each of the physiologic variables described previously gives useful clinical information. A rise in intravesical pressure has greater significance when related to intra-abdominal pressure. The urine flow rate is more significant if recorded in conjunction with the total volume voided as well as with evidence of detrusor contraction. The urethral pressure profile is more significant when related to bladder pressure and to variations in intra-abdominal pressure and voluntary muscular activity. And for greatest clinical usefulness, all data must be recorded simultaneously so that the investigator can analyze the activity involved in each sequence.

At a minimum, a proper urodynamic study should include recordings of intravesical pressure and intra-abdominal pressure (true detrusor pressure is intravesical pressure minus intra-abdominal pressure), urethral pressure or electromyography, flow rate, and, if possible, voided volume. For a complete study, the following are necessary: intra-abdominal pressure, intravesical pressure, urethral sphincteric pressure at various (usually 2) levels, flow rate, voided volume, anal sphincteric pressure (as a function of pelvic floor activity), and electromyography of the anal or urethral striated sphincter. These physiologic data are recorded with the patient quiet as well as during activity (ie, voluntary increase in intra-abdominal pressure, changes in the state of bladder filling, voluntary contraction of perineal muscles, or—more comprehensively—an entire voiding act starting from an empty bladder; continuing through complete filling of the bladder, and initiation of voiding; and ending when the bladder is empty).

The data derived from urodynamic studies are descriptive of urinary tract function. Simultaneous visualization of the lower urinary tract as multiple recordings are made gives more precise information about the pathologic changes underlying the symptoms. By means of cinefluoroscopy, the examiner can observe the configuration of the bladder, bladder base, and bladder outlet during bladder filling (usually with radiopaque medium). The information obtained can then be correlated with the level of catheters, with pressure recordings, and with changes in pelvic floor support during voiding. Combined cinefluoroscopy and pressure measurements thus represent the ultimate in urodynamic studies.

Videourodynamic

This involves the use of fluoroscopy with concurrent measurement of bladder and urethral pressure. Although simple urodynamic can make the diagnosis in many cases, the use of videourodynamic is essential when simultaneous evaluation of structure and function is necessary to make the diagnosis. The simultaneous pressure measurement with fluoroscopic visualization reduces the possibility of misinterpretation of findings because artifactual errors are minimized. In addition, the study is available on videotape, so it can be reviewed to restudy particular portions of the examination. McGuire et al have demonstrated that combination of radiographic imaging and urodynamic studies is extremely valuable in many situations, including male and female incontinence, neurologic conditions, assessment of bladder compliance, and bladder outlet obstruction. In neurologic or obstructive conditions, evaluation of bladder compliance is of great importance because poor compliance is associated with a direct risk to ureteral and renal function. During simple urodynamic, undetected leakage per urethra or vesicoureteral reflux can occur, both of which may allow detrusor compliance to appear better than it really is as they act as a vent to lower bladder pressure. Evaluating compliance with fluoroscopy obviates these problems (Figure 29–25).

Figure 29–25.

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Videourodynamic showing bilateral ureteral reflux and urinary incontinence in a small contracted bladder. The bladder compliance is poor; however, it is masked by both the reflux and urinary leakage.

Videourodynamic Equipment

Videourodynamic studies can be performed with almost any fluoroscopic unit as long as the table can be tilted to place the patient in the upright position. Fluoroscopy time is generally under 1 minute with minimal radiographic exposure. The urodynamic machine is equipped with a video capability that allows capturing and playing images slowly and correlating pressure and events as straining and coughing with fluoroscopic images.

Indications for Videourodynamic

A videourodynamic evaluation is indicated when the diagnosis cannot be achieved using standard urodynamic testing. Conditions in which videourodynamic is particularly helpful include the evaluation of incontinence in females and various neurologic and obstructive conditions.

In females with urinary incontinence, in addition to evaluation of bladder and sphincteric function, videourodynamic provides valuable information about anatomical findings, such as degree of urethral hypermobility, and any associated significant prolapse that may mask coexisting stress incontinence.

Diagnosis of urethral obstruction in females can be very difficult with standard urodynamic methods. The diagnosis can be derived much easier with the use of videourodynamic because in addition to high detrusor pressure during voiding, the level of obstruction can be documented (Figure 29–26).

Figure 29–26.

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Videourodynamic after pubovaginal sling in a patient with urinary retention showing high voiding pressure and dilation of proximal urethra above the sling during voiding.

In neurologic and obstructive conditions, evaluation of bladder compliance is considered to be the most important part of the bladder evaluation, as poor compliance is associated with direct risk to ureteral and kidney functions. Poor compliance with its detrimental effect on the renal function can be masked by the presence of vesicoureteral reflux or leakage per urethra. Both can be easily seen on fluoroscopy (Figure 29–25).

Leak Point Pressure

A great amount of credit should be given to Dr. McGuire and his colleagues who popularized the use of leak point pressure measurement. They developed and defined leak point pressure measurement based on videourodynamic studies done over many years in a broad cross section of patients with various types of incontinence and neurogenic conditions.

There are two leak point pressure tests that measure different aspects of lower urinary tract function. Bladder or detrusor leak point pressure (DLPP) and abdominal or Valsalva leak point pressure.

Detrusor Leak Point Pressure

This is a measurement of the detrusor pressure required to induce leakage across the urethra. It measures bladder compliance, and the higher the DLPP, the worse the compliance. It is not very useful to determine if obstruction exists or not, nor it is useful to characterize bladder contractility. Both are measured by pressure flow studies.

In late 1970s, McGuire and his group from Michigan noted that myelodysplastic children with detrusor leak pressure of 40 cm H2O or more at the instant of leakage invariably developed upper tract disease if not treated. These findings were later confirmed by another retrospective study by the same group that showed that all children with abnormal upper tracts demonstrated very poor bladder compliance. Because poor compliance was not likely to impair ureteral function unless outlet resistance was high, it seemed likely that elevated outlet resistance led to the development of poor compliance in the first place. Furthermore, it has been shown by Wang et al that control of detrusor pressure below 40 cm H2O prevented the development of upper urinary tract disease in myelodysplastic children.

In children with high DLPP and poor compliance, urethral dilation resulted in an immediate fall in leak point pressure and surprisingly a gradual but significant improvement in bladder compliance.

Abdominal/Valsalva Leak Point Pressure

This test measures the ability of the urethra to resist abdominal pressure as an expulsive force. This is usually equal to detrusor pressure plus the abdominal pressure generated by the Valsalva maneuver. McGuire et al have shown that low ALPP is associated with poor intrinsic sphincteric function (intrinsic sphincteric deficiency); however, this has no or poor relationship to simultaneously measured maximum urethral closure pressure. They believed that measuring the urethral intraluminal pressure, particularly in the high-pressure zone, cannot tell how good or bad the urethra is.

The abdominal pressure required to induce leakage appears to be inversely proportional to urethral weakness. A normal urethra does not leak at any achievable pressure, whereas a very bad urethra leaks at a very low pressure. Between these two points, lie most of incontinent patients.

Although this test is widely used to assess patients with urinary incontinence, it has inherent flaws that need to be addressed including volume in the bladder, pelvic organ prolapse, and ability of the individual to generate the required pressure to complete the testing.

Volume in the bladder is very important, as an empty bladder will not leak and a very full bladder can induce a pronounced detrusor component that can make a good urethra look very bad. Measuring the ALPP should be done at moderate volume, between 200 and 250 mL.

Pelvic organ prolapse can dissipate the effect of the abdominal pressure on the urethra and mask the stress incontinence. It is very important to determine whether genital prolapse exists and if present, the prolapse should be reduced in order to properly interpret the leak point pressure.

How to Measure the Abdominal Leak Point Pressure

The bladder is filled slowly to approximately 200 mL while the patient is in the upright position. The patient is asked to do a progressive Valsalva maneuver until he or she leaks. If no leakage can be demonstrated with the Valsalva maneuver, then repetitive coughing may be tried. If still no leakage is seen, the same is repeated at a higher volume. In the absence of significant pelvic organ prolapse, low leak point pressure of 65 cm H2O or less indicates intrinsic sphincteric deficiency. A high leak point pressure of 100 or more usually associated with urethral hypermobility.

Bibliography

Urethra and Bladder

Aboseif SR et al: Continence mechanism of the ileal neobladder in women. A urodynamic study. World J Urol 1998;16(6):400–404. [PubMed: 9870288]

Abrams P: Managing lower urinary tract symptoms in older men. Br Med J 1995;310:1113. [PubMed: 7742679]

Abrams P: Objective evaluation of bladder outlet obstruction. Br J Urol 1995;76(Suppl 1):11.

Abrams P: Lower urinary tract symptoms in women: Who to investigate and how. Br J Urol 1997;80(Suppl 1):43.

Abrams P et al; Standardisation Sub-Committee of the International Continence Society: The standardisation of terminology in lower urinary tract function: Report from the standardisation sub-committee of the International Continence Society. Urology 2003;61(1):37–49. [PubMed: 12559262]

Artibani W: Diagnosis and significance of idiopathic overactive bladder. Urology 1997;50(6A, Suppl):25.

Awad SA et al: Urethral pressure profile in female stress incontinence. J Urol 1978;120:475. [PubMed: 568183]

Bazeed MA et al: Histochemical study of urethral striated musculature in the dog. J Urol 1982;128:406. [PubMed: 6213791]

Beck RP et al: Intraurethral-intravesical cough-pressure spike differences in 267 patients surgically cured of genuine stress incontinence of urine. Obstet Gynecol 1988;72:302. [PubMed: 3405548]

Berger Y et al: Urodynamic findings in Parkinson's disease. J Urol 1987;138:836. [PubMed: 3656541]

Borirakchanyavat S et al: Continence mechanism of the isolated female urethra. An anatomical study of the intrapelvic somatic nerves. J Urol 1997;158(3, Pt 1):822–826.

Bruschini H et al: Effect of urethral stretch on urethral pressure profile. Invest Urol 1977;15:107. [PubMed: 561766]

Bruskewitz R, Raz S: Urethral pressure profile using microtip catheter in females. Urology 1979;14:303. [PubMed: 573517]

Bump RC et al: Dynamic urethral pressure profilometry pressure transmission ratio determinations after continence surgery: Understanding the mechanism of success, failure, and complications. Obstet Gynecol 1988;72:870. [PubMed: 3186096]

Cameron AP et al: Combination drug therapy improves compliance of the neurogenic bladder. J Urol 2009;182(3):1062–1067. [PubMed: 19616807]

Cardenas DD et al: Residual urine volumes in patients with spinal cord injury: Measurement with a portable ultrasound instrument. Arch Phys Med Rehabil 1988;69:514. [PubMed: 3291820]

Cho SY et al: The clinical significance of poor bladder compliance. Neurourol Urodyn 2009;28(8):1010–1014. [PubMed: 19260082]

Coolsaet B: Bladder compliance and detrusor activity during the collection phase. Neurourol Urodyn 1985;4:263.

DeGroat WC: A neurologic basis for the overactive bladder. Urology 1997;50(6A, Suppl):36.

Desai P: Bladder pressure studies combined with micturating cystourethrography. Radiography 1985;52:2.

Desmond AD, Ramayya GR: The adaptation of urethral pressure profiles to detect sphincter incompetence and sphincter obstruction using a microcomputer. J Urol 1987;137:457. [PubMed: 3820375]

Dwyer PL, Rosamilia A: Evaluation and diagnosis of the overactive bladder. Clin Obstet Gynecol 2002;45:193. [PubMed: 11862072]

Glen ES et al: Urethral closure pressure profile measurements in female urinary incontinence. Acta Urol Belg 1984;52:174. [PubMed: 6539048]

Gosling JA et al: A comparative study of the human external sphincter and periurethral levator ani muscles. Br J Urol 1981;53:35. [PubMed: 6451256]

Graber P et al: Effect of abdominal pressure rise on the urethral profile: An experimental study on dogs. Invest Urol 1974;12:57. [PubMed: 4858146]

Griffiths D: Clinical aspects of detrusor instability and the value of urodynamics: A review of the evidence. Eur Urol 1998;34(Suppl 1):13.

Harvey MA, Versi E: Predictive value of clinical evaluation of stress urinary incontinence: A summary of the published literature. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:31. [PubMed: 11294529]

Henriksson L et al: The urethral pressure profiles in continent and stress-incontinent women. Scand J Urol Nephrol 1979;13:5.

Henriksson L et al: Combined urethrocystometry and cinefluorography in continent and incontinent women. Radiology 1979;130:607. [PubMed: 570716]

Jepsen JV, Bruskewitz RC: Comprehensive patient evaluation for benign prostatic hyperplasia. Urology 1998;51(4A, Suppl):13.

Jonas U, Klotter HJ: Study of three urethral pressure recording devices: Theoretical considerations. Urol Res 1978;6:119. [PubMed: 568336]

Kelly MJ et al: Transurethral incision of the prostate: A preoperative and postoperative analysis of symptoms and urodynamic findings. J Urol 1989;142:1507. [PubMed: 2585625]

Kim YH et al: Bladder leak point pressure: The measure for sphincterotomy success in spinal cord injured patients with external detrusor-sphincter dyssynergia. J Urol 1998;159:493. [PubMed: 9649270]

Koefoot RB Jr, Webster GD: Urodynamic evaluation in women with frequency, urgency symptoms. Urology 1983;21:648. [PubMed: 6868242]

Koelbl H, Bernaschek G: A new method for sonographic urethrocystography and simultaneous pressure-flow measurements. Obstet Gynecol 1989;74:417. [PubMed: 2668819]

Langer R et al: Detrusor instability following colposuspension for urinary stress incontinence. Br J Obstet Gynaecol 1988;95:607. [PubMed: 3390403]

Lim CS, Abrams P: The Abrams-Griffiths nomogram. World J Urol 1995;13:34. [PubMed: 7539679]

Lose G: Urethral pressure measurement. Acta Obstet Gynecol Scand Suppl 1997;166:39. [PubMed: 9253377]

McGuire EJ: The role of urodynamic investigation in the assessment of benign prostatic hypertrophy. J Urol 1992;148:1133. [PubMed: 1383572]

McGuire EJ et al: Leak-point pressures. Urol Clin North Am 1996;23:253. [PubMed: 8659025]

Narayan P et al: Neuroanatomy of the external urethral sphincter implications for urinary continence preservation during radical prostate surgery. J Urol 1995;153(2):337–341. [PubMed: 7815577]

Nevéus T et al: The standardization of terminology of lower urinary tract function in children and adolescents: report from the Standardisation Committee of the International Children's Continence Society. J Urol 2006;176(1):314–324. [PubMed: 23107910]

Nørgaard JP et al: Standardization and definitions in lower urinary tract dysfunction in children. International Children's Continence Society. Br J Urol 1998;81(Suppl 3):1.

Ouslander J et al: Simple versus multichannel cystometry in the evaluation of bladder function in an incontinent geriatric population. J Urol 1988;140:1482. [PubMed: 3193520]

Saxton HM: Urodynamics: The appropriate modality for the investigation of frequency, urgency, incontinence, and voiding difficulties. Radiology 1990;175:307. [PubMed: 2183277]

Schafer W: Analysis of bladder-outlet function with the linearized passive urethral resistance relation, linPURR, and a disease-specific approach for grading obstruction: From complex to simple. World J Urol 1995;13:47. [PubMed: 7773317]

Schafer W: Principles and clinical application of advanced urodynamic analysis of voiding function. Urol Clin North Am 1990;17:553. [PubMed: 1695782]

Schmidt RA et al: Recording urethral pressure profile. Urology 1977; 10:390. [PubMed: 919127]

Schmidt RA et al: Urethral pressure profilometry with membrane catheter compared with perfusion catheter systems. Urol Int 1978;33:345. [PubMed: 705985]

Schmidt RA, Tanagho EA: Urethral syndrome or urinary tract infection? Urology 1981;18:424. [PubMed: 6974921]

Snyder JA, Lipsitz DU: Evaluation of female urinary incontinence. Urol Clin North Am 1991;18:197. [PubMed: 2017804]

Sullivan MP et al: Micturitional urethral pressure profilometry. Urol Clin North Am 1996;23:263. [PubMed: 8659026]

Tanagho EA et al: Urethral resistance: Its components and implications. 2. Striated muscle component. Invest Urol 1969;7:136. [PubMed: 4309609]

Tanagho EA: Interpretation of the physiology of micturition. In: Hinman F Jr (ed) Hydrodynamics. Thomas, 1971.

Tanagho EA: Vesicourethral dynamics. In: Lutzeyer W, Melchior H (eds) Urodynamics. Springer-Verlag, 1974.

Tanagho EA: Membrane and microtransducer catheters: Their effectiveness for profilometry of the lower urinary tract. Urol Clin North Am 1979;6:110. [PubMed: 571157]

Tanagho EA: Neurophysiology of urinary incontinence. In: Cantor EB (ed) Female Urinary Stress Incontinence. Thomas, 1979.

Tanagho EA: Urodynamics of female urinary incontinence with emphasis on stress incontinence. J Urol 1979;122:200. [PubMed: 572436]

Tanagho EA, Jones U: Membrane catheter: Effective for recording pressure in lower urinary tract. Urology 1977;10:173. [PubMed: 561471]

Tanagho EA, Miller ER: Functional considerations of urethral sphincteric dynamics. J Urol 1973;109:273. [PubMed: 4568313]

Turner WH, Brading AF: Smooth muscle of the bladder in the normal and the diseased state: Pathophysiology, diagnosis and treatment. Pharmacol Ther 1997;75:77. [PubMed: 9428000]

van Geelen JM et al: The clinical and urodynamic effects of anterior vaginal repair and Burch colposuspension. Am J Obstet Gynecol 1988;159:137.

Versi E: Discriminant analysis of urethral pressure profilometry data for the diagnosis of genuine stress incontinence. Br J Obstet Gynaecol 1990;97:251. [PubMed: 2334653]

Woodside JR, McGuire EJ: A simple inexpensive urodynamic catheter. J Urol 1979;122:788. [PubMed: 513224]

Yalla SV et al: Striated sphincter participation in distal passive urinary continence mechanisms: Studies in male subjects deprived of proximal sphincter mechanism. J Urol 1979;122:655. [PubMed: 501822]

Urinary Flow Rate

Bates CP et al: Synchronous cine-pressure-flow cystourethrography with special reference to stress and urge incontinence. Br J Urol 1970;42:714. [PubMed: 5491923]

Gleason DM, Bottaccini MR: Urodynamic norms in female voiding. 2. Flow modulation zone and voiding dysfunction. J Urol 1982;127:495. [PubMed: 7199581]

Griffiths D: Basics of pressure-flow studies. World J Urol 1995;13:30. [PubMed: 7773315]

Griffiths DJ: Pressure-flow studies of micturition. Urol Clin North Am 1996;23:279. [PubMed: 8659027]

Jensen KM-E et al: Relationship between uroflowmetry and prostatism. Proc Int Continence Soc 1985;15:134.

Jørgensen JB,Jensen KM: Uroflowmetry. Urol Clin North Am 1996; 23:237. [PubMed: 23185633]

Kavia RB et al: Urinary retention in women. BJU Int 2006;97(2):281–287. [PubMed: 16430630]

Kavia R et al: A functional magnetic resonance imaging study of the effect of sacral neuromodulation on brain responses in women with Fowler's syndrome. BJU Int 2010;105(3):366–372. [PubMed: 19735259]

Meyhoff HH et al: The effects of transurethral resection on the urodynamics of prostatism. J Urol 1989;142:785. [PubMed: 2475646]

Nording J: A clinical view of pressure-flow studies. World J Urol 1995;13:70.

Siroky MB et al: The flow rate nomogram. 2. Clinical correlation. J Urol 1980;23:208.

Siroky MB: Interpretation of urinary flow rates. Urol Clin North Am 1990;17:537. [PubMed: 2142839]

Stubbs AJ, Resnic MI: Office uroflowmetry using maximum flow rate purge meter. J Urol 1979;122:62. [PubMed: 156798]

Tanagho EA, McCurry E: Pressure and flow rate as related to lumen caliber and entrance configuration. J Urol 1971;105:583. [PubMed: 5104903]

van Mastrigt R, Kranse M: Analysis of pressure-flow data in terms of computer-derived urethral resistance parameters. World J Urol 1995;13:40.

Electromyography

Colstrup H et al: Urethral sphincter EMG activity registered with surface electrodes in the vagina. Neurourol Urodyn 1985;4:15.

King DG,Teague CT: Choice of electrode in electromyography of external urethral and anal sphincter. J Urol 1980;124:75. [PubMed: 7411727]

Koyanagi T et al: Experience with electromyography of the external urethral sphincter in spinal cord injury patients. J Urol 1982;127:272. [PubMed: 7062383]

Nielsen KK et al: A comparative study of various electrodes in electromyography of the striated urethral and anal sphincter in children. Br J Urol 1985;57:557. [PubMed: 4063736]

Siroky MB: Electromyography of the perineal floor. Urol Clin North Am 1996;23:299. [PubMed: 8659028]

Steward JE et al: Quantitative evaluation of electrodes for external urethral sphincter electromyography during bladder-to-urethral guarding reflex. World J Urol 2010;28(3):365–371. [PubMed: 19680661]

Urodynamic Testing

Barrent DM, Wein AJ: Flow evaluation and simultaneous external sphincter electromyography in clinical urodynamics. J Urol 1981;125:538.

Blaivas JG: Multichannel urodynamic studies. Urology 1984;23:421. [PubMed: 6719661]

Blaivas JG et al: The role of urodynamic testing in the evaluation of subtle neurologic lesions. Neurourol Urodyn 1985;4:211.

Blaivas JG: Multichannel urodynamic studies in men with benign prostatic hyperplasia: Indications and interpretation. Urol Clin North Am 1990;17:543. [PubMed: 1695781]

Blaivas JG, Fischer DM: Combined radiographic and urodynamic monitoring: Advances in technique. J Urol 1981;125:693. [PubMed: 7230340]

Cassidenti AP,Ostergard DR: Multichannel urodynamics: Ambulatory versus standard urodynamics. Curr Opin Obstet Gynecol 1999;11:485. [PubMed: 10526926]

Daneshgari F: Valsalva leak point pressure: Steps toward standardization. Curr Urol Rep 2001;2:388. [PubMed: 12084246]

Everaert K et al: Urodynamic assessment of voiding dysfunction and dysfunctional voiding in girls and women. Int Urogynecol J Pelvic Floor Dysfunct 2000;11:254. [PubMed: 11005479]

Gasthuisberg KU, Vereecken RL: A critical view on the value of urodynamics in non-neurogenic incontinence in women. Int Urogynecol J Pelvic Floor Dysfunct 2000;11:188.

Gerber GS: The role of urodynamic study in the evaluation and management of men with lower urinary tract symptoms secondary to benign prostatic hyperplasia. Urology 1996;48:668. [PubMed: 8911507]

Kulseng-Hanssen S: Reliability and validity of stationary cystometry, stationary cysto-urethrometry and ambulatory cysto-urethro-vaginometry. Acta Obstet Gynecol Scand Suppl 1997;166:33. [PubMed: 9253376]

Lane TM, Shah PJ: Leak-point pressures. BJU Int 2000;86:942. [PubMed: 11069431]

Lewis P, Abrams P: Urodynamic protocol and central review of data for clinical trials in lower urinary tract dysfunction. BJU Int 2000;85(Suppl 1):20.

Massey A, Abrams P: Urodynamics of the female lower urinary tract. Urol Clin North Am 1985;12:231. [PubMed: 4039485]

McGuire EJ, Woodside JR: Diagnostic advantages of fluoroscopic monitoring during urodynamic evaluation. J Urol 1981;125:830. [PubMed: 7241684]

McLellan A, Cardozo L: Urodynamic techniques. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:266. [PubMed: 11569657]

O'Donnell PD: Pitfalls of urodynamic testing. Urol Clin North Am 1991;18:257. [PubMed: 23145981]

Sand PK et al: Uninhibited urethral relaxation: An unusual cause of incontinence. Proc Int Continence Soc 1985;15:117.

Schafer W: Urethral resistance? Urodynamic concepts of physiological and pathological bladder outlet function during voiding. Neurourol Urodyn 1985;4:161.

Schafer W et al: Good urodynamic practices: Uroflowmetry, filling cystometry, and pressure-flow studies. Neurourol Urodyn 2002;21(3):261–274. [PubMed: 11948720]

Siroky MB: Urodynamic assessment of detrusor denervation and areflexia. World J Urol 1984;2:181.

Sutherst JR,Brown MC: Comparison of single and multichannel cystometry in diagnosing bladder instability. Br Med J 1984;288:1720. [PubMed: 6428513]

Tanagho EA: Membrane and microtransducer catheters: Their effectiveness for profilometry of the lower urinary tract. Urol Clin North Am 1979;6:110. [PubMed: 571157]

Thüroff JW: Mechanism of urinary continence: Animal model to study urethral responses to stress conditions. J Urol 1982;127:1202. [PubMed: 23185733]

Turner-Warwick R, Brown AD: A urodynamic evaluation of urinary incontinence in the female and its treatment. Urol Clin North Am 1979;6:203.

Turner-Warwick R, Milroy E: A reappraisal of the value of routine urological procedures in the assessment of urodynamic function. Urol Clin North Am 1979;6:63.

van Waalwijk van Doorn ES et al: Ambulatory urodynamics: Extramural testing of the lower and upper urinary tract by Holter monitoring of cystometrogram, uroflowmetry, and renal pelvic pressures. Urol Clin North Am 1996;23:345.

Wein AJ et al: Effects of bethanechol chloride on urodynamic parameters in normal women and in women with significant residual urine volumes. J Urol 1980;124:397. [PubMed: 7191909]

Videourodynamic

McGuire EJ et al: Upper urinary tract deterioration in patients with myelodysplasia and detrusor hypertonia: A follow up study. J Urol 1983;129:183.

McGuire EJ et al: Clinical assessment of urethral sphincter. J Urol 1993;150:1452–1454. [PubMed: 8411422]

McGuire EJ,Woodside JR: Diagnostic advantages of fluoroscopic monitoring during urodynamic evaluation. J Urol 1981;125: 830. [PubMed: 7241684]

Sinha D et al: Value of leak point pressure study in women with incontinence. J Urol 2006;176(1):186–188; discussion 188. [PubMed: 16753397]

Türker P et al: The presence of transurethral cystometry catheter and type of stress test affect the measurement of abdominal leak point pressure (ALPP) in women with stress urinary incontinence (SUI). Neurourol Urodyn 2010;29(4):536–539. [PubMed: 23185720]

Wang SC et al: A bladder pressure management system for myelodysplasia-clinical outcome. J Urol 1988;140:1499–1502. [PubMed: 3193522]

White T et al: Correlation of maximum urethral closure pressure with Valsalva leak point pressure using air-charged urodynamic catheters. Int Urogynecol J Pelvic Floor Dysfunct 2009;20(9): 1109–1112. [PubMed: 19444363]

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Urodynamic Studies: Introduction

Functions Relevant to Urodynamics and Tests Applicable to Each

Physiologic and Hydrodynamic Considerations

Urinary Flow Rate

Outlet Resistance

Mechanical Outlet Resistance

Variations in Normal Flow Rate

Nomenclature

Figure 29–1.

Pattern Measurement of Flow Rate

Figure 29–2.

Figure 29–3.

Figure 29–4.

Figure 29–5.

Figure 29–6.

Figure 29–7.

Figure 29–8.

Figure 29–9.

Bladder Function

Bladder Capacity, Compliance, and Sensation

Bladder Compliance (Accommodation)

Figure 29–10.

Contractility and Voluntary Control

Responses to Drugs

Recording of Intravesical Pressure

Figure 29–11.

Figure 29–12.

Figure 29–13.

Figure 29–14.

Figure 29–15.

Pathologic Changes in Bladder Capacity

Pathologic Changes in Accommodation (Compliance)

Pathologic Changes in Sensation

Pathologic Changes in Contractility

Sphincteric Function

Profilometry

Membrane Catheter Technique

Figure 29–16.

Microtransducer Technique

Electromyographic Study of Sphincteric Function

Figure 29–17.

Pressure Measurement for Evaluation of Sphincteric Function

Figure 29–18.

Total Pressure

Closure Pressure

Distribution of Closure Pressure

Functional Length of Sphincteric Unit

Figure 29–19.

Dynamic Changes in Pressure Profile

Figure 29–20.

Figure 29–21.

Figure 29–22.

Characteristics of Normal Pressure Profile (Figure 29–23)

Figure 29–23.

Pressure Profile in Pathologic Conditions

Urinary Stress Incontinence

Urinary Urge Incontinence

Figure 29–24.

Combination of Stress and Urge Incontinence

Postprostatectomy Incontinence

Detrusor/Sphincter Dyssynergia

Value of Simultaneous Recordings

Videourodynamic

Figure 29–25.

Videourodynamic Equipment

Indications for Videourodynamic

Figure 29–26.

Leak Point Pressure

Detrusor Leak Point Pressure

Abdominal/Valsalva Leak Point Pressure

How to Measure the Abdominal Leak Point Pressure

Bibliography

Urethra and Bladder

Urinary Flow Rate

Electromyography

Urodynamic Testing

Videourodynamic

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