Pelvic floor disorders including lower urinary tract dysfunction are common, and may be evaluated by urodynamic tests, such as cystometry, uroflowmetry, pressure flow studies, electromyography, and video-urodynamics. These urodynamic tests provide objective information regarding the normal and abnormal function of the urinary tract and pelvic floor, and provide a better understanding of the pathophysiologic processes that cause lower urinary tract symptoms. This article describes typical urodynamic studies and their roles in the evaluation of common pelvic floor disorders, including stress urinary incontinence, overactive bladder, and pelvic organ prolapse.
The female pelvic floor is remarkable for the close functional relationships between its gastrointestinal, genital, and urologic structures. Because of anatomic factors, shared pelvic organ vascular supply and nervous system control, and overlapping environmental and biologic risk factors, pelvic floor disorders often overlap in individual patients. For instance, epidemiologic studies have confirmed a link between fecal and urinary incontinence in women. Obstructive defecation and vaginal prolapse are associated, although it is unclear whether defecatory dysfunction is more often a cause or result of vaginal prolapse. Similarly, rectal prolapse and uterine and vaginal prolapse result from defects in pelvic floor support, and may coexist or share similar risk factors. Given the high frequency of overlapping pelvic floor conditions and symptoms, the evaluation and treatment of women with anorectal dysfunction and other pelvic floor disorders often require a multidisciplinary approach.
Pelvic floor disorders that result in urinary symptoms are frequently evaluated using a set of tests collectively called “urodynamic testing.” Urodynamic tests evaluate lower urinary tract and pelvic floor function and dysfunction, and provide objective information about manometric, sensorimotor, and neurophysiologic parameters related to the bladder and pelvic floor. This article describes urodynamic tests and their parameters and discusses the role that urodynamic testing plays in the evaluation of common pelvic floor disorders.
Anatomy and innervation of the bladder and pelvic floor
Before discussing the urodynamic tests and their parameters, it is important to have a basic understanding of the anatomy and physiology of the bladder and pelvic floor. The lower urinary tract, including the bladder and urethra, must carry out both urine storage (bladder filling) and evacuation (micturition or bladder emptying) functions. The smooth muscle of the bladder walls (detrusor muscle) must relax during the filling phase and contract during micturition; and conversely, the smooth and striated portions of the urethra must contract during filling and relax during emptying. The bladder and urethra are intimately related to structures of the pelvic floor; consequently, optimal bladder function depends not only on an intact lower urinary neuromuscular system, but also on a well-functioning pelvic floor that provides adequate anatomic support.
The supportive functions of the pelvic floor are performed by both muscular and connective tissue components. The pelvic floor muscles are the levator ani (including the puborectalis, pubococcygeus, and iliococcygeus) and coccygeus muscles. These muscles are attached laterally along the pelvic sidewalls, creating a hammock-like sling between the pubis and coccyx. The levator ani muscle is tonically contracted, providing a firm posterior shelf to support the pelvic contents and aid with urinary continence. The connective tissue of the pelvic floor, sometimes called “endopelvic fascia,” is a loose network of connective tissue, small vessels, lymphatics, and nerves, which surrounds and supports the pelvic organs and the vagina through its connections to the pelvic floor muscles.
Bladder filling and voiding functions are controlled by closely coordinated autonomic and somatic neurologic pathways. The autonomic controls of the bladder include sympathetic and parasympathetic functions. The sympathetic (thoracolumbar) nerves promote urine storage by relaxing the detrusor muscle and contracting smooth muscle in the bladder neck and urethra. These nerves are inhibited during voiding. In contrast, parasympathetic (sacral) nerves cause the detrusor muscle to contract and are stimulated during micturition. The somatic nervous system controls the striated external urethral sphincter and levator ani muscle through the pudendal nerve and the sacral nerve roots (S2–S4). Inhibition of these nerves causes relaxation of the bladder outlet and pelvic floor, which must occur during voiding. The central nervous system provides voluntary control and modification of micturition reflexes.
Components of urodynamics
Lower urinary tract dysfunction is often categorized into disorders of bladder storage and disorders of bladder emptying. Various urodynamic tests may aid in the evaluation of one or both functions. Individual urodynamic tests include cystometry, uroflowmetry, pressure flow studies, electromyography (EMG), and videourodynamics. In practice, several or all of these components are often combined and performed together as “urodynamic testing.”
Cystometry
Cystometry refers to the measurement of intravesical bladder pressure during bladder filling, and most consider it the cornerstone of urodynamic testing. Several standard parameters are evaluated during a cystometrogram including bladder storage pressure, capacity, sensation, bladder stability, and compliance.
In preparation for this phase of urodynamics, both urethral and rectal (or vaginal) catheters are placed. The bladder is then filled with contrast, saline, or water through the urethral catheter, and several parameters are continuously measured. The direct measurement of bladder pressure during cystometry, or intra vesical pressure (Pves), reflects the total pressure within the bladder. This is defined as the sum of the pressure within the bladder caused by “bladder wall events,” or detrusor pressure (Pdet), and the pressure exerted on the bladder by external sources, or intra-abdominal pressure (Pabd). Pabd is measured by the rectal catheter. The actual pressure within the bladder caused by “bladder wall events,” or Pdet, is not a directly measurable entity, and is calculated by subtracting Pabd from Pves. A typical videourodynamic setup illustrating these parameters is shown in Fig. 1 .
Bladder sensation during filling is studied by questioning the patient during the test. Sensation during cystometry is subjective, and can be influenced by the rate of filling; temperature of the fluid medium; position of the patient (supine versus upright); and the patient’s level of concentration. Determining the volumes at which different degrees of fullness occur, and the report of pain during filling, and evidence of decreased sensation during filling may all be subtle predictors of disease processes. The greatest value of the cystometrogram with respect to sensation occurs when a symptom arises, and sensation is correlated to actual Pves changes.
Bladder capacity that is measured during urodynamics, or the maximum cystometric capacity, reflects the volume at which a subject with normal bladder sensation can no longer delay voiding. This measurement is different from the functional bladder capacity, which is usually determined by the voiding diary, and the maximum anesthetic capacity, which is obtained under anesthesia.
A “stable” bladder refers to the accommodation of increasing bladder volumes without evidence of an involuntary detrusor contraction, or detrusor overactivity. According to the most recent definition from the International Continence Society (ICS), detrusor overactivity is an observation of involuntary detrusor contractions during urodynamics, which may be either spontaneous or provoked. Detrusor overactivity is demonstrated on a cystometrogram tracing in Fig. 2 .
Bladder compliance is another important parameter that can be measured during cystometry. Compliance (C) has been described simply as the “inverse of stiffness,” and is formally defined as the change in bladder pressure for a given change in volume. Compliance is calculated by dividing the volume change (V) by the Pdet (C = V/Pdet) and is expressed as milliliter per centimeter of H 2 O. A normal bladder displays low pressures during filling because of its spherical shape and viscoelastic properties. Loss of elasticity results from replacement of the muscle with collagen, and can be caused by a number of disease processes including neurologic conditions, prolonged catheter drainage, radiation therapy, prior pelvic or urethral surgery, interstitial cystitis, and obstructive uropathy. A poorly compliant bladder displays an abnormal, often linear increase in Pdet during filling ( Fig. 3 ). This can result in dangerously high detrusor storage pressures. High storage pressures can distort the normal detrusor anatomy resulting in the development of vesicoureteral reflux, and can be transmitted to the upper tracts, causing the development of hydronephrosis and renal failure. Early studies by McGuire and associates have shown that sustained Pdet greater than 40 cm H 2 O is specifically linked to renal or upper tract damage.
Lastly, bladder compliance can be calculated using two standard points: the Pdet at the start of filling with the corresponding bladder volume; and the Pdet and volume at cystometric capacity, or before the start of any detrusor contraction that causes any significant leakage. Many clinicians, however, rely less on the actual calculated value of compliance and more on the actual bladder pressure during filling, because compliance can vary depending on the volume over which it is calculated.
Uroflowmetry
Uroflowmetry is one of the most commonly used forms of urodynamic testing. It is a noninvasive test that measures the rate of urine flow over time. Uroflowmetry involves a well-hydrated patient voiding into a uroflowmeter, which in turn generates a “flow curve.” The flow curve is plotted with the urine flow on the y-axis and time on the x-axis. Fig. 4 demonstrates a typical uroflowmetry curve. Uroflowmetry is extremely useful as a screening test, especially to determine which patients may need further testing with more formal urodynamics, although it cannot determine the exact cause of a patient’s voiding dysfunction.
There are several important variables to consider when interpreting the results of a uroflow test. First, the voided volume influences the validity of the test, because peak flow rates vary with the volume voided. For example, a voided volume less than 150 mL may indicate an invalid test, because flow patterns and parameters are inaccurate below this volume. Also, the voiding of a very large volume may lead to an abnormal flow test result in a patient with no significant pathology. This results from overstretching of the detrusor muscle, which can cause an inefficient contraction.
Next, maximum flow, or Qmax, is the maximum measured rate of flow, and can be determined by evaluating the flow curve during uroflowmetry (see Fig. 4 ). Qmax can be influenced by a number of factors, including age, gender, and volume voided. One must interpret this value in the setting of additional clinical information. For example, flow rates in men decrease with age. Also, women generate higher flow rates on average than men because of the presence of a shorter urethra, which offers less resistance. Finally, there can be variability among uroflow tests in the same patient, depending on several factors, including time of day, hydration status, and even “learning” by repetition. It is important to repeat an abnormal test on a patient who is being considered for surgery or invasive therapy.
Finally, the pattern of flow is also important to consider when evaluating uroflow data, although this may be subject to the interpretation of the individual clinician because there is no standard against which to compare these patterns. Flow patterns can be described in various ways, such as “intermittent,” which may indicate obstruction. Abnormal uroflowmetry results are often further evaluated using a more invasive test, typically a pressure flow study.
Pressure Flow Studies
Although uroflow studies are good screening tests for identifying patients with low flow rates or abnormal voiding patterns, they cannot identify whether this is caused by outlet obstruction or poor detrusor contractility. Pressure flow studies are useful in determining a patient’s voiding mechanism and the cause that underlies abnormal voiding. Pressure flow studies combine uroflowmetry with simultaneous measurement of Pdet, and require placement of a rectal (or vaginal) catheter for Pabd measurement, and a urethral catheter, which measures Pves and allows the calculation of Pdet during voiding. The bladder is filled until the patient feels sufficiently full, and then the patient is asked to void. By measuring the Pdet during voiding, specifically at maximum flow, one can determine whether poor flow is caused by obstruction (high pressures) or whether it is caused by detrusor failure (low or absent Pdet). Similar to noninvasive uroflowmetry, flow rates (including Qmax) and the pattern of flow are also evaluated during pressure flow studies.
Whereas outlet obstruction may be seen frequently in men because of an enlarged prostate, in women it is most likely caused by pelvic organ prolapse, as a complication after surgery for stress incontinence, or from pelvic floor or external sphincter pathology, such as detrusor sphincter dyssynergia. Fig. 5 is a pressure flow study from a female patient demonstrating bladder outlet obstruction occurring after a pubovaginal sling procedure performed for stress incontinence.
Electromyography
EMG is an additional part of standard urodynamic testing that can be performed during cystometry and during the pressure flow study to evaluate the striated urethral sphincter and pelvic floor. EMG monitoring is most commonly done with either perineal surface-patch electrodes or needle electrodes. Needle electrodes (the gold standard) are able to isolate electrical activity from specific muscle fibers within a 0.5-mm radius of the tip. They are, however, invasive, uncomfortable, and can be easily dislodged with movement. Use of patch electrodes has the benefit of being essentially noninvasive, with a patch being placed on the perineum, but some argue that the signal source may be inferior.
Although the striated urethral sphincter and levator ani are located in close proximity, they are anatomically and neurologically discontinuous. Perineal surface measurements may not accurately reflect striated sphincter activity, but a compounding of motor unit signals from all muscles of the pelvic floor. A recent study evaluated patch versus needle electrodes during pressure flow studies, and found that needle electrode EMG was more often interpretable, and showed motor unit quiescence of the external sphincter more often, suggesting that the signal obtained from the pelvic floor musculature in the region may mask the actual signal obtained from the external sphincter. Needle electrodes have been found to be more reliable in evaluating the urethral sphincter.
As with other aspects of urodynamics, it is important to recognize normal findings on EMG to interpret abnormal findings. A normal EMG study essentially rules out a neurologic cause in a patient’s voiding dysfunction; however, an abnormal EMG study may signify that further work-up is warranted. For example, low-level firing of EMG is seen in normal subjects at rest, and it increases in amplitude and frequency with increases in Pabd, such as with coughing and laughing, and with bladder filling. Patients may also exhibit an increased EMG activity during an involuntary detrusor contraction if they voluntarily try to contract their pelvic muscles to prevent leakage. Silence of the EMG signals is believed to be the first recognizable sign of the onset of micturition and should remain that way throughout flow.
Evaluation of the pelvic floor and external sphincter musculature by EMG is an integral component of the work-up of patients with obstructive voiding complaints to rule out sphincter or pelvic floor muscle dysfunction. Dysfunctional voiding is characterized by an intermittent flow rate caused by involuntary intermittent contractions of the periurethral striated muscle or pelvic floor during voiding in neurologically normal individuals. In those patients with suspected bladder outlet obstruction caused by an anatomic source (eg, pelvic organ prolapse), evaluation with EMG during voiding is important to rule out sphincteric dysfunction. Patients with an underlying and undiagnosed neurologic disorder may also display urethral sphincter dysfunction, and may present with either irritative or obstructive voiding complaints. In the setting of neurologic disease, this abnormal EMG finding is termed “detrusor sphincter dyssynergia,” and is defined as a detrusor contraction concurrent with an involuntary contraction of the urethral or periurethral striated muscle, which may prevent flow of urine. Urodynamically, detrusor sphincter dyssynergia is seen as a confluence of large amplitude EMG spikes during flow, and can occur in patients with neurologic disorders, such as multiple sclerosis and suprasacral spinal cord injury. In a patient without a known neurologic diagnosis, suspected detrusor sphincter dyssynergia should signal the physician that further work-up is warranted to exclude a neurologic etiology.
Video Urodynamics
Videourodynamic evaluation, which combines the use of fluoroscopy with the measurement of bladder and urethral pressures during cystometry or the pressure flow study, is desirable when simultaneous evaluation of structure and function is necessary to make a precise diagnosis. Videourodynamics may be especially helpful in the work-up of urinary incontinence associated with pelvic organ prolapse (discussed later). It is also useful in the evaluation of voiding dysfunction, specifically to identify the presence of vesicoureteral reflux caused by poor bladder compliance. If reflux occurs at low volumes, it may act as a “pop-off mechanism,” which may prevent elevation of a patient’s Pdet on the urodynamic tracing. This phenomenon may go unnoticed without use of fluoroscopy. Bladder diverticula caused by chronic bladder outlet obstruction may also result in an artificially low Pdet during voiding and may not be recognized during urodynamics without fluoroscopy.