Innovation for Pelvic Health

The goal of urodynamics testing is to provide objective confi rmation of the signs and symptoms of incontinence and
voiding dysfunction. While diagnosis and optimal treatment of lower urinary tract dysfunction require a careful history and objective evaluation, it has been demonstrated that urinary symptoms alone are not specifi c in predicting the type of dysfunction (15%–40% of diagnoses will be wrong without urodynamics testing, and 25%–30% of patients will have multiple diagnoses).

 The dilemma facing physicians treating urinary dysfunction is that symptoms, patient questionnaires, physical examination fi ndings, voiding diaries, and pad testing do not correlate well with the fi nal diagnosis. Urodynamics testing must be interpreted in combination with other fi ndings as part of an intelligent decision-making process.1-3
Naturally, there remains a level of uncertainty about the role of urodynamics. Some feel that it is not cost effective and is helpful under certain circumstances only. Others consider urodynamics essential in assessing urinary incontinence to confi rm defi nitive and objective diagnosis 4-6 and have advocated its use in all patients prior to surgical intervention. 7-10

 Urodynamics can detect detrusor overactivity that may or may not be clinically relevant. It will also detect neurological pathophysiology such as detrusor sphincter dyssynergia and urethral instability, which is a subtle but powerful cause of frequency and urgency syndromes. With new advances in urodynamics technologies, it is hoped that the results will correlate more closely to true clinical fi ndings and further help with clinical outcome prediction and proper choices of therapy.

Accurate diagnosis
The definition of urethral instability is a variation of the proximal urethra (Pura) baseline pressure of ±15 cm H2O. In our lab I consistently use a dual-pressure sensor, circumferential air-charged catheter for diagnosing urethral instability. The finding of urethral instability— and, for that matter, most urethral pathophysiology—has been difficult to obtain with traditional, point-sensor technology using water with microtip and fiberoptic catheters. Tanago and Ulmsten have taught that one should measure pressures within the urethra in a circumferential area for accurate pathophysiology, and they used a fluid-filled balloon in some of their research. Using an air-charged rather than fluid-filled balloon alleviates the difficulty caused by gravitational effects on the water, air bubbles in the water, and thermal changes of the water.

 For best results, I place one sensor into the bladder with the second sensor at the midurethra. I watch the pressures during the filling phase of the complex cystometrogram. To avoid false readings, I place the urethral sensor just to the bladder side of the maximum urethral pressure and use both tape and handholding of the catheter to prevent the migration of the pressure sensor. If the pressure sensor is too close to either the ureterovesical junction or the urethral meatus, the pathophysiological changes can be missed. Looking at figure 1, you can see the variations in pressure, with a saw-toothed pattern only at the midurethral area.
 
The significance of this urethral data was demonstrated in the case of a 19-year-old female patient who presented with a frequency-urgency syndrome characterized by voiding 50 times daily and every 20 minutes at night. The patient had had a prior complex cystometrogram, without a urethral pressure recording, that showed normal pressures; her electromyogram showed no detrusor instability. She also had a negative workup for interstitial cystitis. This patient had been treated over a 4-year period with anticholinergics as well as biofeedback and other conservative therapies, with no success. She had been referred to a psychiatrist and was taking sedatives. She had made two suicide attempts.

 My lab repeated the urodynamics testing but used a urethral pressure sensor. The patient demonstrated severe urethral instability (figure 2), and attempts at urethral stabilization with the alpha-receptor antagonist tamsulosin and then with alpha agonists failed. I then placed a sacral nerve stimulator. After the InterStim unit placement we repeated her urodynamics tests, which showed an absence of the urethral instability. The patient had complete reversal of her symptoms.

Sacral nerve stimulation
This is the first documented finding that I know of showing an objective change in urodynamics that led to a reversal of a patient’s physical symptoms. This phenomenon was our impetus to do a retrospective chart review to see if we had similar results with other patients who had been treated with InterStim sacral nerve stimulation (SNS) therapy. The chart review showed an interesting correlation on urodynamics testing between urethral instability and the success of SNS. Of 30 cases treated with SNS implants, 26 (86.7%) were successful. Urethral instability had been urodynamically demonstrated in 23 (88.4%) out of the 26 successful cases. Of the remaining 3 cases, 2 did not have a good cystometrogram with the Pura sensor in the right location; therefore, correlation was not possible to discern but could have existed. One of the failed SNS cases had no urethral instability on urodynamics testing. Furthermore, 11 patients had diagnoses of both interstitial cystitis (IC) and urethral instability, with severe symptoms of frequency and urgency that affected quality of life. Conservative therapy for IC had failed for these compromised patients, and they had undergone SNS implantation, with success for 10 out of 11.

 Interstitial cystitis appears to have a neurologic component; at the very least it may have a subtype that originates from overstimulation of the sacral nerves that stimulate the release of mast cells, contributing to the symptoms. Therefore, as part of our algorithm for treatment of IC, we favor SNS if there are urodynamics findings consistent with urethral instability.

 Our ongoing prospective study, approved by our institutional review board, has so far treated 15 patients who had urethral instability as the sole finding of urodynamics testing. All have received implants for InterStim therapy, with a 100% success rate. It would be of great benefit to run a large prospective study to validate the signifi cance of this urodynamics finding, and to verify that neurologic downregulation of the sacral nerves can lead to stabilization of urethral pressures.

In our experience, patients with frequency-urgency problems who demonstrate urethral instability and no detrusor instability on urodynamics testing do not respond well to common anticholinergic and antimuscarinic therapies for the overactive bladder. These patients appear to be better served by medications affecting the urethra, which has mainly norepinephrine and serotonergic receptors. Therefore, medications to stabilize the urethra—such as alpha agonists (e.g., pseudoephedrine, cetirizine plus pseudoephedrine) and antagonists (e.g., tamsulosin, terazosin)—may be more helpful, although we still try drugs in the anticholinergic category. A significant number of our patients have benefited from this unusual conservative protocol and have not progressed to sacral nerve stimulation. With this in mind we created an algorithm for the workup and treatment of frequency-urgency problems as shown in figure 3.

Conclusion
Urodynamics has a signifi cant role in urology, urogynecology, and female pelvic medicine. It is argued that urodynamics testing is not cost effective, limits access to specialty care, and requires specialized and expensive equipment, special training, and interpretation skills.11  Despite certain limitations, however, urodynamics testing continues to be the gold standard for defi ning the pathophysiology of lower urinary tract dysfunction.

It is proposed that urodynamics is not necessary when straightforward stress urinary incontinence is the clinical diagnosis. Unfortunately, misdiagnosis with the potential for improper treatment is possible. The effects of unnecessary or inappropriate surgery, prolonged ineffective medical treatment, recurrent or persistent incontinence (particularly if a less-effective surgery has been done), and postoperative voiding dysfunction can lead to prolonged patient suffering with potential medico-legal ramifications.

 Symptoms, questionnaires, voiding diaries, physical examination, and pad testing are not predictive of the final diagnosis and may lead to misdiagnosis. Urodynamics testing is an essential component of the workup of the incontinent and voiding-dysfunctional patient. Looking at the total picture and all findings, including urethral pressures during filling cystometry, can shed some light on the frequency-urgency patient who does not have detrusor instability or other neurologic findings.

References