Mickey Karram, MD

Slings abound, entering the market faster than research can evaluate every new modification as exhaustively as we would like. How should we determine what is best for a particular patient? That is the question we examine in this discussion—the first in a series of roundtables, Controversies in Pelvic Surgery.

Future topics in the series focus on other unsettled issues:

• Preventing and managing lower urinary tract injury
• How best to correct vaginal vault prolapse
• Choosing the right hysterectomy route
• Mesh augmentation in prolapse repair

We decided on a roundtable format for the series because it seems well suited to a review of sometimes spotty data, not to mention the onslaught of new products and procedures that, ironically enough, are intended to simplify our lives.

Choosing a sling for “uncomplicated” cases

DR. KARRAM: What is your sling procedure of choice for the uncomplicated patient who has primary stress urinary incontinence (SUI), urethral hypermobility, and what appears to be a healthy urethra?

DR. BLAIVAS: I prefer an old-fashioned, autologous, rectus fascial sling, or one made of soft prolene mesh, as described by Rodriguez and Raz¹—although I place the sling a bit more proximal than most and dissect into the retropubic space. The autologous rectus fascial sling has a long-term success rate at least as good as any other procedure. Even though it requires at least a small suprapubic incision, the possibility of serious complication (vascular or bowel injury, urethral or vaginal erosion) is almost nil.

Allograft and xenograft slings do not have as good a long-term success rate, but the chance of serious complication is nearly nil. If I do use a synthetic, I prefer the technique developed by Dr. Raz because it utilizes a time-honored, safe technique and avoids the unnecessary expense of the disposable midurethral sling kits.

I place the autologous sling at the bladder neck because long-term studies confirm its safety and efficacy.

DR. WALTERS: I use the literature as a guide and perform either Burch colposuspension or a synthetic midurethral sling procedure.Although its popularity has waned slightly, the Burch operation—either open or laparoscopic—is very effective.

My midurethral sling of choice for the simplest cases, as well as those with coexistent prolapse, is the Monarc transobturator sling (American Medical Systems, Minnetonka, Minn). The outcome data for this procedure are preliminary, and it has not yet been shown to equal a classic tension-free vaginal tape (TVT) technique, but I find that it causes less voiding dysfunction and urgency in my hands.

KARRAM: I would probably use a conventional TVT sling procedure. The reason: There is a tremendous amount of data to support the use of TVT for all types of SUI. The data and our experience supports a very low erosion or excursion rate with the TVT tape. Since it is really the only synthetic midurethral sling that has been shown to be as effective as—if not more effective than—conventional repairs, it remains my procedure of choice in uncomplicated cases.

Preop evaluation

KARRAM: Do you use the same sling procedure for all patients? If so, do you test preoperatively to help determine appropriate tension? If not, how do you decide which sling to use on which patient?

WALTERS: I use 3 types of slings:

• the Monarc transobturator sling for simple primary SUI, SUI with prolapse, and potential SUI,
• TVT placed very loosely for recurrent SUI with leak point pressures over 60 cm H₂O, and
• TVT placed with a little more tension under the urethra for patients who have recurrent SUI with leak point pressures under 60 cm H₂O, but who lack a complete “drainpipe” urethra.

Technically, I also use a fourth sling—a full fascial sling for severe intrinsic sphincter deficiency (ISD)—although I haven’t done one of these procedures in over a year.

BLAIVAS: For the uncomplicated case, I use either an autologous rectus fascial sling, an allograft or xenograft, or one made of soft prolene mesh, depending on the patient’s preference. zenograft

If I suspect she is at risk for erosion of a synthetic sling due to prior sling erosion, previous pelvic radiation, concomitant urethral diverticulectomy, or pelvic/urethral reconstructive surgery, I avoid synthetics.

BLAIVAS: Preoperatively, in addition to a focused history, questionnaire and examination, I make use of diaries, pad tests, video-urodynamics, pressure flow studies, cystoscopy, leak point pressure tests, and the Q-tip test whenever possible.

If the patient has significant urethral hypermobility and a relatively high leak point pressure, I use a bladder neck sling without any added tension. If there is little urethral mobility and a low leak point pressure, I make the sling a bit tighter.

If the woman has impaired detrusor contractility or urethral obstruction according to detrusor pressure uroflow data, I make the sling a bit looser.

I must emphasize that these are all “touchy, feely” things, unsupported by any meaningful data.

I also adjust the tension, depending on the patient’s feelings about intermittent catheterization versus persistent sphincteric incontinence.

That said, there is still a lot more art than science to this issue. I almost always tie the slings very loosely, compared with what I see others saying or doing. I do this because, in my own learning curve, I quickly encountered problems of urethral obstruction but almost never made a sling too loose. As I gained experience, I tied them looser and looser without ever losing clinical efficacy.

KARRAM: I don’t use the same sling for every patient. Like both of you, I first look at the leak point pressure and review the patient’s subjective complaints. I also consider any chronic systemic disorders, such as asthma or chronic obstructive lung disease, that may put a patient at high risk for failure. The findings help me adjust the tension intraoperatively.

I also try to reproduce the stress incontinence with a cough or Valsalva maneuver if the surgery is performed under local anesthesia, or using suprapubic pressure if it is done under general anesthesia.

Most of my sling procedures involve TVT. Although I recently began to selectively utilize a transobturator approach for women with occult incontinence or mild disease, I am not fully convinced it will be as efficacious as a traditional TVT for SUI.

KARRAM: Industry aggressively promotes new sling procedures—new materials, new placement techniques, new needles to pass the sling material. There are so many products and procedures that it is difficult to compare them all. Do you think this will become a serious problem, with many procedures lumped together and each assumed as effective as a similar product?

BLAIVAS: Emphatically, yes. Each new sling, no matter how slight the modification seems to be, is encumbered by a new learning curve. That means that the first batch of patients each surgeon operates on will be subjected to a higher complication rate or lower efficacy.

There have been unexpected (and unpublished) deaths due to vascular and bowel injuries and a 1% to 9% vaginal or urethral erosion rate with synthetic slings. Disappointing medium-term efficacy of allograft and zenograft slings were recently published, and recent abstracts suggest that transobturator slings are less efficacious for women with ISD.

WALTERS: This problem not only exists, it has been worsening over the past several years. We still don’t know if the transobturator sling is as effective as TVT, for example, yet we are slowly adopting it because it is easier and probably safer.

The various instruments required for these operations may not be that different, but the absorbable and nonabsorbable prosthetic sling materials are. They should be evaluated constantly and compared with the TVT procedure.

In medicine, we can’t control what industry does, but we can continue to study and test the new procedures before we consider them standards.

KARRAM: I agree that the problem already exists. Although we have a substantial amount of data on the TVT mechanism and the Gynecare material (Ethicon, Somerville, NJ), we need to derive data for other slings. This may be very difficult, given the number of different materials and kits already on the market.

KARRAM: The current rage is the transobturator approach, although we have very little data about it. Theoretically, it is safer than TVT, since there is no need to pass the needles through the retropubic space, and thus it is unlikely to lead to vascular and bowel, or bladder and urethral injury.

Should go ahead and adopt it as a primary procedure, or do you recommend waiting for more data on its efficacy?

BLAIVAS: I do not recommend that it be adopted until it is proven safe and effective, but I feel the same way about most of the other slings as well. When performed by experts, almost all these procedures are very safe, but we don’t know very much about long-term efficacy. If someone selects the transobturator approach out of fear of complications from a different procedure, he or she is probably not skilled enough to perform these operations in the first place.

KARRAM: I agree that we need to wait until efficacy data are established. As slings become less and less invasive, industry is aggressively pushing them into the hands of novices. Most of the time these are gynecologists who have not performed antiincontinence surgery and may even lack cystoscopy privileges. Do you think this will be a problem down the road?

BLAIVAS: Yes, unless the procedures are dumbed down enough and they are truly safe and effective.

Transobturator and TVT learning curves and outcomes

WALTERS: As for the transobturator approach, I am convinced, based on my surgical experience over the past 2 years, that it is easier than TVT and results in less voiding difficulty and urgency.

However, I am not convinced that it is equivalent to retropubic TVT in cure rates for SUI. This issue especially needs to be rigorously tested.

In my experience, TVT has a very high cure rate for SUI, but can cause urgency, including intractable urge and voiding dysfunction requiring transection of the polypropylene tape. This rarely occurs with the transobturator sling, making it attractive for simple SUI.

The transobturator sling also is easier than TVT to learn and teach, and completely avoids any risk of retropubic hematoma and bowel perforation. Also, unless there is extensive prolapse, the risk of entering the bladder and urethra is practically nil, assuming you are able to pass the needle and touch your finger from the lateral side.

The next big, important study will likely be a randomized comparison of transobturator and TVT slings, similar to the way TVT was compared with the open Burch procedure.

WALTERS: For their own protection, I don’t think gynecologists should be doing surgery for prolapse and incontinence if they do not have privileges for cystoscopy.

KARRAM: I agree. It is very important that the gynecologists performing these procedures evaluate the patient thoroughly enough to decide wisely between surgical and nonsurgical management. Certainly they should have the ability to evaluate the lower urinary tract with cystoscopy before doing these procedures.

WALTERS: I perform cystoscopy on virtually every pelvic reconstructive surgery and find abnormalities in the bladder, urethra, or ureters in 2% to 4% of cases a year. Although I encourage gynecologists to learn these operations, cystoscopy is crucial, so an effort should be made to obtain training and privileges for it.

KARRAM: You mentioned the Burch procedure, Dr. Walters. Do you think there is still a role for retropubic urethropexy—done laparoscopically or via an open technique?

WALTERS: I perform an open Burch procedure if I have already made a laparotomy incision for another reason, such as abdominal sacrocolpopexy or hysterectomy. I occasionally perform laparoscopic Burch procedures in younger women undergoing laparoscopy for other reasons, such as tubal sterilization or ovarian disease.

KARRAM: I perform retropubic urethropexy if operating in the abdomen for another reason, provided the patient has SUI, urethral hypermobility, and vaginal pliability.

BLAIVAS: Retropubic urethropexy has a proven track record, but requires skill and experience.

With uncomplicated incontinence, long-term success appears as good as any operation. If a surgeon is skilled, this procedure should be part of his or her armamentarium.

KARRAM: You are correct. Data suggest the retropubic operation and TVT procedure are equally effective.^2,3

WALTERS: I find it somewhat amusing that I am increasingly considered “old-style” when I continue to recommend the Burch procedure.

All I can say is that I’m glad my partners, fellows, and I have the ability to perform this operation when necessary.

KARRAM: Unfortunately, since retropubic urethropexy is performed much less frequently in the past, residents no longer learn retropubic anatomy.

This has become a problem because a many synthetic midurethral slings require blind passage of a needle through the retropubic space.

KARRAM: Are we going to see more complications with these procedures because of a lack of clear understanding of the anatomy? If so, how do you think this can be resolved?

WALTERS: Although TVT works very well for SUI, I think our specialty abandoned Burch colposuspension prematurely, ignoring all the evidence supporting its efficacy. I wish residents were still being taught Burch procedures on open cases. I can see that general Ob/Gyns are slowly forgetting how to do the operation, making it more difficult for them to manage complications such as hematomas and infections.

That said, I don’t think TVT complications will occur more often because of this lack of experience with the Burch procedure. On the contrary, I expect them to remain rare. Use of transobturator slings avoids retropubic anatomy completely, but we need more outcome data before making a wholesale switch from TVT.

KARRAM: More injuries to blood vessels and other structures are inevitable when novice surgeons unfamiliar with anatomy attempt to blindly pass large needles.

BLAIVAS: I agree, but the developers of the new techniques are trying to make them idiot-proof—and maybe they will! It’s a sad day, though, when surgeons don’t know anatomy. Too many don’t!

KARRAM: The only solution is to aggressively teach anatomy in residency and demand preceptorships that teach anatomy before allowing inexperienced surgeons to adopt the procedure.

BLAIVAS: If enough mistakes are made, we’ll be forced to teach anatomy again. The best solution, in my judgment, is sub-specialization to the point where all surgeons doing these procedures have sufficient experience.

KARRAM: Intrinsic sphincter deficiency has become a common term for severe forms of stress incontinence, although there is no widely accepted definition.

How do you define ISD? Is it important to detect it preoperatively? If so, how does ISD alter surgical management?

BLAIVAS: ISD was initially used to describe weakened sphincter mechanism, as distinct from incontinence because of urethral hypermobility.

For practical purposes, all patients with sphincteric incontinence have some degree of “intrinsic sphincter deficiency,” but I no longer use the term. Instead, I characterize the sphincter by vesical leak point pressure and the degree of urethral mobility as measured by a simple Q-tip test. The lower the leak point pressure, the weaker the sphincter, the more likely it will be designated ISD.

WALTERS: I still follow the rough guidelines I was taught: ISD exists at leak point pressures below 60 cm H₂O on cystometrogram., although this is probably not that accurate. There is no cutoff defining ISD, but a gradually increasing weakness of the urethral sphincter that correlates roughly with severity of symptoms.

I doubt the concept of ISD would hold up to rigorous scientific scrutiny as a condition or prognostic factor. However, I still use it.

KARRAM: Although intrinsic sphincter deficiency is a vague concept, I believe there are cases that exhibit it—eg, patients who have had multiple operations, been radiated, or have neurologic disease, who essentially have a urethra that is open at rest, doesn’t move, and leaks urine with minimal increases in intraabdominal pressure. In situations such as these, I select procedures that bulk up or obstruct the urethra to correct or improve the incontinence.

Most cases identified as having ISD are based on a urethral function test that measures either leak point pressure or static urethral closure pressure. Unfortunately, little data prove that these tests truly measure urethral function.

There are no definitive data suggesting that a procedure needs to be done any differently based on these tests. So I think the term is presently used in a very cavalier fashion and requires a more objective mechanism to define the condition. Only then can its potential impact on clinical management be evaluated.

Dr. Karram has received research support from American Medical Systems, Yamounouchi, and Gynecare, and serves on the speakers bureau for Gynecare, Ortho-McNeil, Watson, and Indevus. Dr. Blaivas reports no relevant financial relationships. Dr. Walters is a consultant for American Medical Systems and a lecturer for Boston Scientific.

Slings abound, entering the market faster than research can evaluate every new modification as exhaustively as we would like. How should we determine what is best for a particular patient? That is the question we examine in this discussion—the first in a series of roundtables, Controversies in Pelvic Surgery.

Future topics in the series focus on other unsettled issues:

• Preventing and managing lower urinary tract injury
• How best to correct vaginal vault prolapse
• Choosing the right hysterectomy route
• Mesh augmentation in prolapse repair

We decided on a roundtable format for the series because it seems well suited to a review of sometimes spotty data, not to mention the onslaught of new products and procedures that, ironically enough, are intended to simplify our lives.

Choosing a sling for “uncomplicated” cases

DR. KARRAM: What is your sling procedure of choice for the uncomplicated patient who has primary stress urinary incontinence (SUI), urethral hypermobility, and what appears to be a healthy urethra?

DR. BLAIVAS: I prefer an old-fashioned, autologous, rectus fascial sling, or one made of soft prolene mesh, as described by Rodriguez and Raz¹—although I place the sling a bit more proximal than most and dissect into the retropubic space. The autologous rectus fascial sling has a long-term success rate at least as good as any other procedure. Even though it requires at least a small suprapubic incision, the possibility of serious complication (vascular or bowel injury, urethral or vaginal erosion) is almost nil.

Allograft and xenograft slings do not have as good a long-term success rate, but the chance of serious complication is nearly nil. If I do use a synthetic, I prefer the technique developed by Dr. Raz because it utilizes a time-honored, safe technique and avoids the unnecessary expense of the disposable midurethral sling kits.

I place the autologous sling at the bladder neck because long-term studies confirm its safety and efficacy.

DR. WALTERS: I use the literature as a guide and perform either Burch colposuspension or a synthetic midurethral sling procedure.Although its popularity has waned slightly, the Burch operation—either open or laparoscopic—is very effective.

My midurethral sling of choice for the simplest cases, as well as those with coexistent prolapse, is the Monarc transobturator sling (American Medical Systems, Minnetonka, Minn). The outcome data for this procedure are preliminary, and it has not yet been shown to equal a classic tension-free vaginal tape (TVT) technique, but I find that it causes less voiding dysfunction and urgency in my hands.

KARRAM: I would probably use a conventional TVT sling procedure. The reason: There is a tremendous amount of data to support the use of TVT for all types of SUI. The data and our experience supports a very low erosion or excursion rate with the TVT tape. Since it is really the only synthetic midurethral sling that has been shown to be as effective as—if not more effective than—conventional repairs, it remains my procedure of choice in uncomplicated cases.

Preop evaluation

KARRAM: Do you use the same sling procedure for all patients? If so, do you test preoperatively to help determine appropriate tension? If not, how do you decide which sling to use on which patient?

WALTERS: I use 3 types of slings:

• the Monarc transobturator sling for simple primary SUI, SUI with prolapse, and potential SUI,
• TVT placed very loosely for recurrent SUI with leak point pressures over 60 cm H₂O, and
• TVT placed with a little more tension under the urethra for patients who have recurrent SUI with leak point pressures under 60 cm H₂O, but who lack a complete “drainpipe” urethra.

Technically, I also use a fourth sling—a full fascial sling for severe intrinsic sphincter deficiency (ISD)—although I haven’t done one of these procedures in over a year.

BLAIVAS: For the uncomplicated case, I use either an autologous rectus fascial sling, an allograft or xenograft, or one made of soft prolene mesh, depending on the patient’s preference. zenograft

If I suspect she is at risk for erosion of a synthetic sling due to prior sling erosion, previous pelvic radiation, concomitant urethral diverticulectomy, or pelvic/urethral reconstructive surgery, I avoid synthetics.

BLAIVAS: Preoperatively, in addition to a focused history, questionnaire and examination, I make use of diaries, pad tests, video-urodynamics, pressure flow studies, cystoscopy, leak point pressure tests, and the Q-tip test whenever possible.

If the patient has significant urethral hypermobility and a relatively high leak point pressure, I use a bladder neck sling without any added tension. If there is little urethral mobility and a low leak point pressure, I make the sling a bit tighter.

If the woman has impaired detrusor contractility or urethral obstruction according to detrusor pressure uroflow data, I make the sling a bit looser.

I must emphasize that these are all “touchy, feely” things, unsupported by any meaningful data.

I also adjust the tension, depending on the patient’s feelings about intermittent catheterization versus persistent sphincteric incontinence.

That said, there is still a lot more art than science to this issue. I almost always tie the slings very loosely, compared with what I see others saying or doing. I do this because, in my own learning curve, I quickly encountered problems of urethral obstruction but almost never made a sling too loose. As I gained experience, I tied them looser and looser without ever losing clinical efficacy.

KARRAM: I don’t use the same sling for every patient. Like both of you, I first look at the leak point pressure and review the patient’s subjective complaints. I also consider any chronic systemic disorders, such as asthma or chronic obstructive lung disease, that may put a patient at high risk for failure. The findings help me adjust the tension intraoperatively.

I also try to reproduce the stress incontinence with a cough or Valsalva maneuver if the surgery is performed under local anesthesia, or using suprapubic pressure if it is done under general anesthesia.

Most of my sling procedures involve TVT. Although I recently began to selectively utilize a transobturator approach for women with occult incontinence or mild disease, I am not fully convinced it will be as efficacious as a traditional TVT for SUI.

KARRAM: Industry aggressively promotes new sling procedures—new materials, new placement techniques, new needles to pass the sling material. There are so many products and procedures that it is difficult to compare them all. Do you think this will become a serious problem, with many procedures lumped together and each assumed as effective as a similar product?

BLAIVAS: Emphatically, yes. Each new sling, no matter how slight the modification seems to be, is encumbered by a new learning curve. That means that the first batch of patients each surgeon operates on will be subjected to a higher complication rate or lower efficacy.

There have been unexpected (and unpublished) deaths due to vascular and bowel injuries and a 1% to 9% vaginal or urethral erosion rate with synthetic slings. Disappointing medium-term efficacy of allograft and zenograft slings were recently published, and recent abstracts suggest that transobturator slings are less efficacious for women with ISD.

WALTERS: This problem not only exists, it has been worsening over the past several years. We still don’t know if the transobturator sling is as effective as TVT, for example, yet we are slowly adopting it because it is easier and probably safer.

The various instruments required for these operations may not be that different, but the absorbable and nonabsorbable prosthetic sling materials are. They should be evaluated constantly and compared with the TVT procedure.

In medicine, we can’t control what industry does, but we can continue to study and test the new procedures before we consider them standards.

KARRAM: I agree that the problem already exists. Although we have a substantial amount of data on the TVT mechanism and the Gynecare material (Ethicon, Somerville, NJ), we need to derive data for other slings. This may be very difficult, given the number of different materials and kits already on the market.

KARRAM: The current rage is the transobturator approach, although we have very little data about it. Theoretically, it is safer than TVT, since there is no need to pass the needles through the retropubic space, and thus it is unlikely to lead to vascular and bowel, or bladder and urethral injury.

Should go ahead and adopt it as a primary procedure, or do you recommend waiting for more data on its efficacy?

BLAIVAS: I do not recommend that it be adopted until it is proven safe and effective, but I feel the same way about most of the other slings as well. When performed by experts, almost all these procedures are very safe, but we don’t know very much about long-term efficacy. If someone selects the transobturator approach out of fear of complications from a different procedure, he or she is probably not skilled enough to perform these operations in the first place.

KARRAM: I agree that we need to wait until efficacy data are established. As slings become less and less invasive, industry is aggressively pushing them into the hands of novices. Most of the time these are gynecologists who have not performed antiincontinence surgery and may even lack cystoscopy privileges. Do you think this will be a problem down the road?

BLAIVAS: Yes, unless the procedures are dumbed down enough and they are truly safe and effective.

Transobturator and TVT learning curves and outcomes

WALTERS: As for the transobturator approach, I am convinced, based on my surgical experience over the past 2 years, that it is easier than TVT and results in less voiding difficulty and urgency.

However, I am not convinced that it is equivalent to retropubic TVT in cure rates for SUI. This issue especially needs to be rigorously tested.

In my experience, TVT has a very high cure rate for SUI, but can cause urgency, including intractable urge and voiding dysfunction requiring transection of the polypropylene tape. This rarely occurs with the transobturator sling, making it attractive for simple SUI.

The transobturator sling also is easier than TVT to learn and teach, and completely avoids any risk of retropubic hematoma and bowel perforation. Also, unless there is extensive prolapse, the risk of entering the bladder and urethra is practically nil, assuming you are able to pass the needle and touch your finger from the lateral side.

The next big, important study will likely be a randomized comparison of transobturator and TVT slings, similar to the way TVT was compared with the open Burch procedure.

WALTERS: For their own protection, I don’t think gynecologists should be doing surgery for prolapse and incontinence if they do not have privileges for cystoscopy.

KARRAM: I agree. It is very important that the gynecologists performing these procedures evaluate the patient thoroughly enough to decide wisely between surgical and nonsurgical management. Certainly they should have the ability to evaluate the lower urinary tract with cystoscopy before doing these procedures.

WALTERS: I perform cystoscopy on virtually every pelvic reconstructive surgery and find abnormalities in the bladder, urethra, or ureters in 2% to 4% of cases a year. Although I encourage gynecologists to learn these operations, cystoscopy is crucial, so an effort should be made to obtain training and privileges for it.

KARRAM: You mentioned the Burch procedure, Dr. Walters. Do you think there is still a role for retropubic urethropexy—done laparoscopically or via an open technique?

WALTERS: I perform an open Burch procedure if I have already made a laparotomy incision for another reason, such as abdominal sacrocolpopexy or hysterectomy. I occasionally perform laparoscopic Burch procedures in younger women undergoing laparoscopy for other reasons, such as tubal sterilization or ovarian disease.

KARRAM: I perform retropubic urethropexy if operating in the abdomen for another reason, provided the patient has SUI, urethral hypermobility, and vaginal pliability.

BLAIVAS: Retropubic urethropexy has a proven track record, but requires skill and experience.

With uncomplicated incontinence, long-term success appears as good as any operation. If a surgeon is skilled, this procedure should be part of his or her armamentarium.

KARRAM: You are correct. Data suggest the retropubic operation and TVT procedure are equally effective.^2,3

WALTERS: I find it somewhat amusing that I am increasingly considered “old-style” when I continue to recommend the Burch procedure.

All I can say is that I’m glad my partners, fellows, and I have the ability to perform this operation when necessary.

KARRAM: Unfortunately, since retropubic urethropexy is performed much less frequently in the past, residents no longer learn retropubic anatomy.

This has become a problem because a many synthetic midurethral slings require blind passage of a needle through the retropubic space.

KARRAM: Are we going to see more complications with these procedures because of a lack of clear understanding of the anatomy? If so, how do you think this can be resolved?

WALTERS: Although TVT works very well for SUI, I think our specialty abandoned Burch colposuspension prematurely, ignoring all the evidence supporting its efficacy. I wish residents were still being taught Burch procedures on open cases. I can see that general Ob/Gyns are slowly forgetting how to do the operation, making it more difficult for them to manage complications such as hematomas and infections.

That said, I don’t think TVT complications will occur more often because of this lack of experience with the Burch procedure. On the contrary, I expect them to remain rare. Use of transobturator slings avoids retropubic anatomy completely, but we need more outcome data before making a wholesale switch from TVT.

KARRAM: More injuries to blood vessels and other structures are inevitable when novice surgeons unfamiliar with anatomy attempt to blindly pass large needles.

BLAIVAS: I agree, but the developers of the new techniques are trying to make them idiot-proof—and maybe they will! It’s a sad day, though, when surgeons don’t know anatomy. Too many don’t!

KARRAM: The only solution is to aggressively teach anatomy in residency and demand preceptorships that teach anatomy before allowing inexperienced surgeons to adopt the procedure.

BLAIVAS: If enough mistakes are made, we’ll be forced to teach anatomy again. The best solution, in my judgment, is sub-specialization to the point where all surgeons doing these procedures have sufficient experience.

KARRAM: Intrinsic sphincter deficiency has become a common term for severe forms of stress incontinence, although there is no widely accepted definition.

How do you define ISD? Is it important to detect it preoperatively? If so, how does ISD alter surgical management?

BLAIVAS: ISD was initially used to describe weakened sphincter mechanism, as distinct from incontinence because of urethral hypermobility.

For practical purposes, all patients with sphincteric incontinence have some degree of “intrinsic sphincter deficiency,” but I no longer use the term. Instead, I characterize the sphincter by vesical leak point pressure and the degree of urethral mobility as measured by a simple Q-tip test. The lower the leak point pressure, the weaker the sphincter, the more likely it will be designated ISD.

WALTERS: I still follow the rough guidelines I was taught: ISD exists at leak point pressures below 60 cm H₂O on cystometrogram., although this is probably not that accurate. There is no cutoff defining ISD, but a gradually increasing weakness of the urethral sphincter that correlates roughly with severity of symptoms.

I doubt the concept of ISD would hold up to rigorous scientific scrutiny as a condition or prognostic factor. However, I still use it.

KARRAM: Although intrinsic sphincter deficiency is a vague concept, I believe there are cases that exhibit it—eg, patients who have had multiple operations, been radiated, or have neurologic disease, who essentially have a urethra that is open at rest, doesn’t move, and leaks urine with minimal increases in intraabdominal pressure. In situations such as these, I select procedures that bulk up or obstruct the urethra to correct or improve the incontinence.

Most cases identified as having ISD are based on a urethral function test that measures either leak point pressure or static urethral closure pressure. Unfortunately, little data prove that these tests truly measure urethral function.

There are no definitive data suggesting that a procedure needs to be done any differently based on these tests. So I think the term is presently used in a very cavalier fashion and requires a more objective mechanism to define the condition. Only then can its potential impact on clinical management be evaluated.

Dr. Karram has received research support from American Medical Systems, Yamounouchi, and Gynecare, and serves on the speakers bureau for Gynecare, Ortho-McNeil, Watson, and Indevus. Dr. Blaivas reports no relevant financial relationships. Dr. Walters is a consultant for American Medical Systems and a lecturer for Boston Scientific.

Slings abound, entering the market faster than research can evaluate every new modification as exhaustively as we would like. How should we determine what is best for a particular patient? That is the question we examine in this discussion—the first in a series of roundtables, Controversies in Pelvic Surgery.

Future topics in the series focus on other unsettled issues:

• Preventing and managing lower urinary tract injury
• How best to correct vaginal vault prolapse
• Choosing the right hysterectomy route
• Mesh augmentation in prolapse repair

We decided on a roundtable format for the series because it seems well suited to a review of sometimes spotty data, not to mention the onslaught of new products and procedures that, ironically enough, are intended to simplify our lives.

Choosing a sling for “uncomplicated” cases

DR. KARRAM: What is your sling procedure of choice for the uncomplicated patient who has primary stress urinary incontinence (SUI), urethral hypermobility, and what appears to be a healthy urethra?

DR. BLAIVAS: I prefer an old-fashioned, autologous, rectus fascial sling, or one made of soft prolene mesh, as described by Rodriguez and Raz¹—although I place the sling a bit more proximal than most and dissect into the retropubic space. The autologous rectus fascial sling has a long-term success rate at least as good as any other procedure. Even though it requires at least a small suprapubic incision, the possibility of serious complication (vascular or bowel injury, urethral or vaginal erosion) is almost nil.

Allograft and xenograft slings do not have as good a long-term success rate, but the chance of serious complication is nearly nil. If I do use a synthetic, I prefer the technique developed by Dr. Raz because it utilizes a time-honored, safe technique and avoids the unnecessary expense of the disposable midurethral sling kits.

I place the autologous sling at the bladder neck because long-term studies confirm its safety and efficacy.

DR. WALTERS: I use the literature as a guide and perform either Burch colposuspension or a synthetic midurethral sling procedure.Although its popularity has waned slightly, the Burch operation—either open or laparoscopic—is very effective.

My midurethral sling of choice for the simplest cases, as well as those with coexistent prolapse, is the Monarc transobturator sling (American Medical Systems, Minnetonka, Minn). The outcome data for this procedure are preliminary, and it has not yet been shown to equal a classic tension-free vaginal tape (TVT) technique, but I find that it causes less voiding dysfunction and urgency in my hands.

KARRAM: I would probably use a conventional TVT sling procedure. The reason: There is a tremendous amount of data to support the use of TVT for all types of SUI. The data and our experience supports a very low erosion or excursion rate with the TVT tape. Since it is really the only synthetic midurethral sling that has been shown to be as effective as—if not more effective than—conventional repairs, it remains my procedure of choice in uncomplicated cases.

Preop evaluation

KARRAM: Do you use the same sling procedure for all patients? If so, do you test preoperatively to help determine appropriate tension? If not, how do you decide which sling to use on which patient?

WALTERS: I use 3 types of slings:

• the Monarc transobturator sling for simple primary SUI, SUI with prolapse, and potential SUI,
• TVT placed very loosely for recurrent SUI with leak point pressures over 60 cm H₂O, and
• TVT placed with a little more tension under the urethra for patients who have recurrent SUI with leak point pressures under 60 cm H₂O, but who lack a complete “drainpipe” urethra.

Technically, I also use a fourth sling—a full fascial sling for severe intrinsic sphincter deficiency (ISD)—although I haven’t done one of these procedures in over a year.

BLAIVAS: For the uncomplicated case, I use either an autologous rectus fascial sling, an allograft or xenograft, or one made of soft prolene mesh, depending on the patient’s preference. zenograft

If I suspect she is at risk for erosion of a synthetic sling due to prior sling erosion, previous pelvic radiation, concomitant urethral diverticulectomy, or pelvic/urethral reconstructive surgery, I avoid synthetics.

BLAIVAS: Preoperatively, in addition to a focused history, questionnaire and examination, I make use of diaries, pad tests, video-urodynamics, pressure flow studies, cystoscopy, leak point pressure tests, and the Q-tip test whenever possible.

If the patient has significant urethral hypermobility and a relatively high leak point pressure, I use a bladder neck sling without any added tension. If there is little urethral mobility and a low leak point pressure, I make the sling a bit tighter.

If the woman has impaired detrusor contractility or urethral obstruction according to detrusor pressure uroflow data, I make the sling a bit looser.

I must emphasize that these are all “touchy, feely” things, unsupported by any meaningful data.

I also adjust the tension, depending on the patient’s feelings about intermittent catheterization versus persistent sphincteric incontinence.

That said, there is still a lot more art than science to this issue. I almost always tie the slings very loosely, compared with what I see others saying or doing. I do this because, in my own learning curve, I quickly encountered problems of urethral obstruction but almost never made a sling too loose. As I gained experience, I tied them looser and looser without ever losing clinical efficacy.

KARRAM: I don’t use the same sling for every patient. Like both of you, I first look at the leak point pressure and review the patient’s subjective complaints. I also consider any chronic systemic disorders, such as asthma or chronic obstructive lung disease, that may put a patient at high risk for failure. The findings help me adjust the tension intraoperatively.

I also try to reproduce the stress incontinence with a cough or Valsalva maneuver if the surgery is performed under local anesthesia, or using suprapubic pressure if it is done under general anesthesia.

Most of my sling procedures involve TVT. Although I recently began to selectively utilize a transobturator approach for women with occult incontinence or mild disease, I am not fully convinced it will be as efficacious as a traditional TVT for SUI.

KARRAM: Industry aggressively promotes new sling procedures—new materials, new placement techniques, new needles to pass the sling material. There are so many products and procedures that it is difficult to compare them all. Do you think this will become a serious problem, with many procedures lumped together and each assumed as effective as a similar product?

BLAIVAS: Emphatically, yes. Each new sling, no matter how slight the modification seems to be, is encumbered by a new learning curve. That means that the first batch of patients each surgeon operates on will be subjected to a higher complication rate or lower efficacy.

There have been unexpected (and unpublished) deaths due to vascular and bowel injuries and a 1% to 9% vaginal or urethral erosion rate with synthetic slings. Disappointing medium-term efficacy of allograft and zenograft slings were recently published, and recent abstracts suggest that transobturator slings are less efficacious for women with ISD.

WALTERS: This problem not only exists, it has been worsening over the past several years. We still don’t know if the transobturator sling is as effective as TVT, for example, yet we are slowly adopting it because it is easier and probably safer.

The various instruments required for these operations may not be that different, but the absorbable and nonabsorbable prosthetic sling materials are. They should be evaluated constantly and compared with the TVT procedure.

In medicine, we can’t control what industry does, but we can continue to study and test the new procedures before we consider them standards.

KARRAM: I agree that the problem already exists. Although we have a substantial amount of data on the TVT mechanism and the Gynecare material (Ethicon, Somerville, NJ), we need to derive data for other slings. This may be very difficult, given the number of different materials and kits already on the market.

KARRAM: The current rage is the transobturator approach, although we have very little data about it. Theoretically, it is safer than TVT, since there is no need to pass the needles through the retropubic space, and thus it is unlikely to lead to vascular and bowel, or bladder and urethral injury.

Should go ahead and adopt it as a primary procedure, or do you recommend waiting for more data on its efficacy?

BLAIVAS: I do not recommend that it be adopted until it is proven safe and effective, but I feel the same way about most of the other slings as well. When performed by experts, almost all these procedures are very safe, but we don’t know very much about long-term efficacy. If someone selects the transobturator approach out of fear of complications from a different procedure, he or she is probably not skilled enough to perform these operations in the first place.

KARRAM: I agree that we need to wait until efficacy data are established. As slings become less and less invasive, industry is aggressively pushing them into the hands of novices. Most of the time these are gynecologists who have not performed antiincontinence surgery and may even lack cystoscopy privileges. Do you think this will be a problem down the road?

BLAIVAS: Yes, unless the procedures are dumbed down enough and they are truly safe and effective.

Transobturator and TVT learning curves and outcomes

WALTERS: As for the transobturator approach, I am convinced, based on my surgical experience over the past 2 years, that it is easier than TVT and results in less voiding difficulty and urgency.

However, I am not convinced that it is equivalent to retropubic TVT in cure rates for SUI. This issue especially needs to be rigorously tested.

In my experience, TVT has a very high cure rate for SUI, but can cause urgency, including intractable urge and voiding dysfunction requiring transection of the polypropylene tape. This rarely occurs with the transobturator sling, making it attractive for simple SUI.

The transobturator sling also is easier than TVT to learn and teach, and completely avoids any risk of retropubic hematoma and bowel perforation. Also, unless there is extensive prolapse, the risk of entering the bladder and urethra is practically nil, assuming you are able to pass the needle and touch your finger from the lateral side.

The next big, important study will likely be a randomized comparison of transobturator and TVT slings, similar to the way TVT was compared with the open Burch procedure.

WALTERS: For their own protection, I don’t think gynecologists should be doing surgery for prolapse and incontinence if they do not have privileges for cystoscopy.

KARRAM: I agree. It is very important that the gynecologists performing these procedures evaluate the patient thoroughly enough to decide wisely between surgical and nonsurgical management. Certainly they should have the ability to evaluate the lower urinary tract with cystoscopy before doing these procedures.

WALTERS: I perform cystoscopy on virtually every pelvic reconstructive surgery and find abnormalities in the bladder, urethra, or ureters in 2% to 4% of cases a year. Although I encourage gynecologists to learn these operations, cystoscopy is crucial, so an effort should be made to obtain training and privileges for it.

KARRAM: You mentioned the Burch procedure, Dr. Walters. Do you think there is still a role for retropubic urethropexy—done laparoscopically or via an open technique?

WALTERS: I perform an open Burch procedure if I have already made a laparotomy incision for another reason, such as abdominal sacrocolpopexy or hysterectomy. I occasionally perform laparoscopic Burch procedures in younger women undergoing laparoscopy for other reasons, such as tubal sterilization or ovarian disease.

KARRAM: I perform retropubic urethropexy if operating in the abdomen for another reason, provided the patient has SUI, urethral hypermobility, and vaginal pliability.

BLAIVAS: Retropubic urethropexy has a proven track record, but requires skill and experience.

With uncomplicated incontinence, long-term success appears as good as any operation. If a surgeon is skilled, this procedure should be part of his or her armamentarium.

KARRAM: You are correct. Data suggest the retropubic operation and TVT procedure are equally effective.^2,3

WALTERS: I find it somewhat amusing that I am increasingly considered “old-style” when I continue to recommend the Burch procedure.

All I can say is that I’m glad my partners, fellows, and I have the ability to perform this operation when necessary.

KARRAM: Unfortunately, since retropubic urethropexy is performed much less frequently in the past, residents no longer learn retropubic anatomy.

This has become a problem because a many synthetic midurethral slings require blind passage of a needle through the retropubic space.

KARRAM: Are we going to see more complications with these procedures because of a lack of clear understanding of the anatomy? If so, how do you think this can be resolved?

WALTERS: Although TVT works very well for SUI, I think our specialty abandoned Burch colposuspension prematurely, ignoring all the evidence supporting its efficacy. I wish residents were still being taught Burch procedures on open cases. I can see that general Ob/Gyns are slowly forgetting how to do the operation, making it more difficult for them to manage complications such as hematomas and infections.

That said, I don’t think TVT complications will occur more often because of this lack of experience with the Burch procedure. On the contrary, I expect them to remain rare. Use of transobturator slings avoids retropubic anatomy completely, but we need more outcome data before making a wholesale switch from TVT.

KARRAM: More injuries to blood vessels and other structures are inevitable when novice surgeons unfamiliar with anatomy attempt to blindly pass large needles.

BLAIVAS: I agree, but the developers of the new techniques are trying to make them idiot-proof—and maybe they will! It’s a sad day, though, when surgeons don’t know anatomy. Too many don’t!

KARRAM: The only solution is to aggressively teach anatomy in residency and demand preceptorships that teach anatomy before allowing inexperienced surgeons to adopt the procedure.

BLAIVAS: If enough mistakes are made, we’ll be forced to teach anatomy again. The best solution, in my judgment, is sub-specialization to the point where all surgeons doing these procedures have sufficient experience.

KARRAM: Intrinsic sphincter deficiency has become a common term for severe forms of stress incontinence, although there is no widely accepted definition.

How do you define ISD? Is it important to detect it preoperatively? If so, how does ISD alter surgical management?

BLAIVAS: ISD was initially used to describe weakened sphincter mechanism, as distinct from incontinence because of urethral hypermobility.

For practical purposes, all patients with sphincteric incontinence have some degree of “intrinsic sphincter deficiency,” but I no longer use the term. Instead, I characterize the sphincter by vesical leak point pressure and the degree of urethral mobility as measured by a simple Q-tip test. The lower the leak point pressure, the weaker the sphincter, the more likely it will be designated ISD.

WALTERS: I still follow the rough guidelines I was taught: ISD exists at leak point pressures below 60 cm H₂O on cystometrogram., although this is probably not that accurate. There is no cutoff defining ISD, but a gradually increasing weakness of the urethral sphincter that correlates roughly with severity of symptoms.

I doubt the concept of ISD would hold up to rigorous scientific scrutiny as a condition or prognostic factor. However, I still use it.

KARRAM: Although intrinsic sphincter deficiency is a vague concept, I believe there are cases that exhibit it—eg, patients who have had multiple operations, been radiated, or have neurologic disease, who essentially have a urethra that is open at rest, doesn’t move, and leaks urine with minimal increases in intraabdominal pressure. In situations such as these, I select procedures that bulk up or obstruct the urethra to correct or improve the incontinence.

Most cases identified as having ISD are based on a urethral function test that measures either leak point pressure or static urethral closure pressure. Unfortunately, little data prove that these tests truly measure urethral function.

There are no definitive data suggesting that a procedure needs to be done any differently based on these tests. So I think the term is presently used in a very cavalier fashion and requires a more objective mechanism to define the condition. Only then can its potential impact on clinical management be evaluated.

Dr. Karram has received research support from American Medical Systems, Yamounouchi, and Gynecare, and serves on the speakers bureau for Gynecare, Ortho-McNeil, Watson, and Indevus. Dr. Blaivas reports no relevant financial relationships. Dr. Walters is a consultant for American Medical Systems and a lecturer for Boston Scientific.

A 66-year-old woman complains of urinary urgency, frequency, and incontinence, and estimates that she voids 15 or more times within a typical 24-hour period. So far, she has lost only small amounts of urine—because she hurries to void at the first sense of urgency—but she is distressed and worried that she will have a major accident.

Sound familiar? Overactive bladder affects 17 to 33 million US women.¹ Thanks to greater awareness and openness, more women today are seeking medical help for their troubling symptoms, although only a fraction have done so up to now.² Ob/Gyns who are prepared to quickly evaluate the problem and initiate effective management can help restore the quality of life these patients enjoyed before onset of symptoms. This article:

• reviews the pathophysiology of “overactive bladder”
  
• describes a 4-step evaluation and management routine that should be feasible for any gynecology office setting;
  
• discusses the action and the efficacy of available and forthcoming drugs;
  
• uses newly revised terminology that reflects greater sensitivity to the patient.
  

Revised terminology

One of the most notable changes in the terms used to describe lower urinary tract dysfunction, proposed by the International Continence Society,³ is organization of the terminology into 3 categories: symptoms, signs, and urodynamic observations.

Symptoms are now defined to more closely reflect the way the patient perceives her problem, and are set forth without specifying the volume of urine required for a diagnosis of “abnormal” sensation or urgency.

Signs can be observed by the physician, such as leakage of urine when the patient coughs.

Urodynamic observations are made during urodynamic studies.

Overall, the new and revised terms are relatively vague to allow for patient-to-patient variability. Here are a few examples:

• Overactive bladder is a syndrome of symptoms that suggest dysfunction of the lower urinary tract. It is characterized by urgency with or without urge incontinence, usually involving frequency and nocturia.
  
• Urinary incontinence is any involuntary leakage of urine.
  
• Daytime frequency. The patient feels she voids more frequently than she should during the day.
  
• Nocturia. The patient wakes 1 or more times at night to void.
  
• Urgency. The patient feels a sudden, compelling desire to pass urine.
  
• Urge urinary incontinence is involuntary leakage accompanied by or immediately preceded by urgency.
  
• Bladder sensation is identified during history taking: normal, increased, reduced, absent, and nonspecific.
  
• Detrusor overactivity replaces the term “detrusor instability” or “hyperreflexia.” It is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase, and may be spontaneous or provoked. It may be further qualified as neurogenic (if a neurologic condition underlies the problem) or as idiopathic.
  

What is abnormal bladder function?

Any actual incontinence should be considered abnormal, whether diurnal or nocturnal.

Frequency: More than 8 voids in 24 hours. Although an ordinary voiding pattern is not fully defined, most experts agree that a frequency of 8 or fewer voids in 24 hours is “normal.”

Urgency: Patient’s opinion determines. The sensation of urgency is more difficult to objectively define; hence, the need to rely on the patient’s perceptions. If a patient is voiding more frequently than normal because she has an uncomfortable, sudden desire to pass urine, she is considered to have urgency. In contrast, a woman who voids frequently because she has stress incontinence and wants to keep her bladder as empty as possible to avoid leakage has frequency without urgency. Urgency is best classified as being sensory or motor in nature.

• Sensory urgency is a strong, uncomfortable need to void without fear of impending leakage; for whatever reason, the bladder has become hypersensitive. Delaying voiding may result in pain but rarely leads to incontinence.
  
• Patients with motor urgency urinate frequently because they are afraid of experiencing a complete or partial involuntary void as a result of an involuntary bladder contraction.
  

How the normal bladder functions

The process of bladder storage and evacuation can be visualized as a complex of neurocircuits in the brain and spinal cord that coordinate the activity of smooth muscle in the bladder and urethra (FIGURE). These circuits act as “on/off” switches in the lower urinary tract, alternating between the 2 modes of operation: storage and elimination.

As the bladder gradually fills with urine, a woman initially perceives a first sensation of filling between 75 and 125 cc of urine, feels the first need to void at approximately 300 cc, and reaches maximum capacity and a strong urge to void at 400 to 700 cc.

Since the bladder is a low-pressure reservoir, intravesical bladder pressure typically rises very little despite increasing amounts of urine and distention of the smooth muscle or detrusor muscle of the bladder. Pressure ranges from 2 to 6 cm of water in an empty state and rarely exceeds 10 cm of water at maximum capacity.

At maximum capacity, a woman should be able to get to the toilet easily, initiate voluntary bladder contraction with complete relaxation of her pelvic floor, and void to completion.

Urge incontinence is more detrimental to quality of life

Of women who complain of urinary incontinence, more than 90% have either loss of detrusor muscle control (urge incontinence) or urethral sphincteric incompetence (stress incontinence).⁴ In addition, 30% to 50% of women with stress incontinence have coexistent urge incontinence. ¹

Urge incontinence has a much more dramatic impact on a woman’s quality of life than stress incontinence, because stress incontinence is predictable and controllable. The patient understands she will leak urine only with increases in intraabdominal pressure associated with exercise, coughing, etc. These leakages tend to occur in small spurts that are easily absorbed by protective wear. In contrast, urge incontinence manifests as an unpredictable, involuntary void in which urine is released in a gushing stream, often in quantities large enough to soak through heavy absorbent pads.

Although one might assume that subjective complaints would readily distinguish the 2 conditions, the bladder is a very poor “witness.” What the patient perceives often fails to correlate with the true mechanism of incontinence. Since therapies for these 2 conditions are completely different, the evaluation of incontinence is very important.

In aging women, the prevalence of frequency, urgency, and urge incontinence is much higher than that of stress incontinence. Among women 60 to 80 years of age—growth-wise, the largest segment of our population—as many as 50% experience frequency, urgency, and urge incontinence.

High economic cost. The tremendous expense of urinary incontinence is increasingly recognized. In 1995, for example, the economic cost in the United States was $26.3 billion, or $3,565 per person 65 years or older with the condition.^5,6 Of these resources, 48%, or $12.53 billion, were drawn directly from the economy to diagnose, treat, care for, and rehabilitate patients with incontinence.

Contributing factors and causes of overactive bladder

Overactive bladder is thought to be multifactorial. Symptoms often occur in the absence of any obvious pathology, which makes it difficult to pinpoint a cause. Coexisting conditions may also contribute to symptoms or may even be the sole cause.

Examples include infection or inflammation of the lower urinary tract, such as a simple case of cystitis, or a foreign body in the bladder.

Injury or diseases of the nervous system can disrupt voluntary control of voiding in adults, triggering the reemergence of reflex voiding, which leads to bladder hyperactivity and urge incontinence. At a local level, urge incontinence can develop secondary to intrinsic detrusor myogenic abnormalities.

Outlet obstruction can result in urge incontinence such as the well recognized symptoms of urethral obstruction in men with benign prostatic hyperplasia.

Detrusor sphincter dysnergia, most commonly secondary to spinal cord injury or multiple sclerosis, may affect younger men and women.

A deficient urethral sphincter in women with stress incontinence may induce urge incontinence, as urine leaking into the urethra secondary to the stress incontinence stimulates urethral afferents that induce involuntary voiding reflexes.⁷

Women with stress incontinence may unwittingly contribute to overactive bladder by voiding more and more often, hoping to prevent any involuntary urine loss. As a result of the frequent voiding, they develop frequency and urgency symptoms. That is, over time, this frequent, voluntary voiding leads to decreased bladder compliance. Thus begins a vicious cycle that ultimately leads to more frequency and urgency.

Urogenital atrophy. Irritative symptoms of the lower urinary tract in the form of frequency, urgency, and dysuria can result from lack of estrogen, leading to urogenital atrophy.

Pelvic organ prolapse is another common coexisting condition. Although the correlation between anatomic descent of pelvic organs and lower urinary tract symptoms is poorly understood, frequency and urgency—with or without urge incontinence—coexist with symptomatic pelvic organ prolapse in approximately 30% to 50% of cases.

An enlarged uterus or adnexal mass may cause external compression of the bladder and lead to lower urinary tract symptoms.

Previous surgery of the anterior vaginal wall or bladder neck may sometimes trigger de novo symptoms of frequency, urgency, and urge incontinence. In women who have undergone a previous antiincontinence procedure, these symptoms may be related to some form of outlet obstruction. In some cases these patients have no increase in the postvoid residual, and only subtle urodynamic testing elicits evidence of obstruction.

Step 1Ask the right questions, get voiding diary, assess quality of life

Most women can be thoroughly evaluated within the clinical practice setting of any gynecologist. The first and most important aspect of this assessment is understanding and appreciating the severity of a patient’s lower urinary tract symptoms. This can be done by asking pointed questions, in the following approximate sequence:

1. Do you have problems with accidental loss of urine?
   
2. How many months or years have you had leakage?
   
3. Do you have to wear pads or protective clothing to prevent or help with urinary loss? If so, how many pads do you wear a day?
   
4. How many trips do you make to the bathroom during the day? At night?
   
5. Do you ever wet the bed while sleeping?
   
6. Are you bothered by a strong sense of urgency to void? Can you overcome it?
   
7. Do you sometimes fail to reach the bathroom in time?
   
8. Does the sound, sight, or feel of running water cause you to lose urine?
   
9. Do you lose urine when you cough, sneeze, run, or lift heavy objects?
   
10. Do you lose urine with posture changes, standing, or walking?
    
11. Do you feel as though you are constantly wet?
    
12. Do you feel as though your bladder is completely empty after passing urine?
    
13. Do you have difficulty starting a stream of urine?
    

Take a thorough medical history, as well as a surgical history with emphasison previous bladder or gynecologic procedures.

Also review all prescription medications.

48-hour voiding diary. Give the patient a voiding diary to fill out 48 hours prior to her office visit. The reason: The diary often reveals more information than can be elicited from the patient’s history. For example, it may highlight daily activities associated with voiding, such as excessive consumption of liquids, high caffeine intake, high-impact exercise, and so on.

Quality-of-life assessment. An objective means of quantifying the effects of incontinence on the woman’s quality of life is recommended. We use the short form of the Incontinence Impact Questionnaire and the Urinary Distress Inventory.

Step 2Perform ‘eyeball’ cystometry, a simple and revealing office test

Ask the patient to go to the restroom and comfortably empty her bladder into a urine-collection device to determine the amount voided. Have a nurse measure the postvoid residual using a soft red rubber catheter. A sample can be taken for urinalysis and, if necessary, sent for culture.

Next, perform a simple filling or “eyeball” cystometry. Connect a Toomey syringe to the end of the red rubber catheter and pour sterile water into it. Ask the patient to tell you when she feels the first sensation of filling, first desire to void, strong urge to void, and maximum capacity, recording the levels at which each occurs. During filling, any evidence of bladder contraction will be revealed by a rise in the column of water. Record any significant discomfort or other observations during the filling portion of the study. When maximum capacity is reached, remove the catheter.

Step 3Conduct a thorough physical assessment

With the patient in the supine position, separate the labia and ask her to cough forcefully and perform the Valsalva maneuver 3 times, recording any evidence of water or urine loss through the urethral meatus. (If the patient has advanced pelvic organ prolapse, try to reduce the prolapse to eliminate any anatomic distortion of the urethra.)

Then ask the patient to stand with a full bladder and to squat, again having her cough forcefully 3 times. Record any additional urinary loss. Finally, ask the patient to void and again record the amount voided.

After the patient has emptied her bladder, again ask her to cough forcefully 3 times in the supine position, noting any evidence of leakage from the urethra (empty supine stress test).

Perform an overall inspection of the perineum and external genitalia and record a description in the patient’s chart.

Attempt to elicit an anal wink, and perform a brief neurological examination to ensure that spinal cord segments S2, S3, and S4 are intact. Next, gently insert a finger into the vagina and ask the patient to forcefully squeeze around it. Record the forcefulness of the squeeze on a scale of 0 to 5, with 0 being no appreciable movement and 5 being the most forceful squeeze possible. During this portion of the exam, instruct the patient on how to perform a Kegel exercise without recruiting the muscles of the buttocks and the abdominal wall.

Next, use a finger to gently massage the urethra, looking for any possible discharge from the urethral meatus that would be consistent with urethral diverticulum. Also note any tenderness or pain elicited during the exam.

Inserting a half-speculum into the vagina, displace the rectum away from the bladder. As the patient performs a Valsalva maneuver or coughs forcefully, evaluate the support of the anterior vaginal wall. Then turn the speculum 180 degrees and displace the bladder anteriorly, examining the posterior pelvic wall for any signs of prolapse. Also note any urogenital atrophy.

Finally, use a full speculum to evaluate the vaginal apex and cervix (if the patient has not had a hysterectomy). Bimanual and abdominal examinations also are important to rule out any abdominal or pelvic mass that could be irritating or causing pressure on the bladder.

Reexamine the patient for evidence of prolapse when she is standing. Some cases are difficult to detect when the patient is supine.

Step 4Begin multipronged therapy

Bladder retraining. Review the patient’s history, voiding diary, and findings from the physical exam to identify an appropriate treatment. After sharing all findings with the patient, instruct the patient on bladder retraining, which has 3 main components: education, scheduled voiding, and positive reinforcement. (Bladder retraining can be an extremely successful modality.)

Education consists of explaining the pathophysiology of overactive bladder and answering any questions the patient may have, so she understands why she is having the problem.

For scheduled voiding—also known as bladder retraining—examine the voiding diary to determine the approximate length of time between voids in a day. For instance, if the patient voids every hour, we generally ask her to continue doing so for the first week of retraining. The following week, we increase the interval to an hour and 15 minutes, the third week to 1.5 hours, and so on, with an ultimate goal of 3 hours between voids.

We also give instructions on pelvic floor rehabilitation or Kegel exercises. If the patient is able to voluntarily contract her pelvic floor muscles adequately, we recommend an exercise regimen that involves contracting her muscles numerous times a day for at least 10 seconds each time. If she is unable to contract her muscles or has a “dead” pelvic floor, she is referred to a physical therapist for biofeedback and possibly electrical stimulation.

We also instruct the patient to avoid racing to the bathroom when she feels an urge to void. Instead, have her stop, contract her pelvic floor muscles, and allow the urge to pass. She can then walk comfortably to the bathroom.

As mentioned earlier, the voiding diary may highlight problems such as excessive intake of fluids.

Local estrogen therapy can be added if there are signs of urogenital atrophy.

Medical therapy. In addition to education, timed voids, pelvic floor rehabilitation, and estrogen therapy, we usually start the extended-release form of tolterodine (4 mg) or oxybutynin (10 mg), which are antimuscarinic agents. (See “Treating overactive bladder: An expanding ‘pharmacopeia’”).

We ask her to return for a follow-up visit in 4 to 6 weeks to inquire about her symptoms and any significant side effects. We ask the patient to prepare another voiding diary for that visit so we can objectively measure decreases in frequency, urgency, and urge incontinence.

Dose adjustment is very important in patients with overactive bladder. If the woman is experiencing minimal effect with no side effects, titrate the dosage upward. If she is having good effect with significant side effects, decrease the dosage or consider switching to the transdermal form of oxybutynin.

When all these conditions are met and the patient remains severely affected, we perform multichannel urodynamic testing along with cystoscopy. If the testing supports the diagnosis of overactive bladder, and all other mechanisms for improvement have been exhausted, we counsel the patient about intravesical administration of botulism toxin, which relaxes skeletal and smooth muscle by preventing release of acetocholine from nerve terminal endings. Another option is sacroneuromodulation (InterStim therapy).

Implications of the placebo effect

We lack a complete understanding of how all the parts of this process interact and why. Most of the medications in use affect only 1 part of the complex process that governs urine storage and elimination.

In controlled trials, patients on placebo have experienced 30% improvement—or greater—in their symptoms. This would seem to suggest that education, behavioral retraining, and attention from physicians are responsible for some of the improvement. Indeed, in a recent systematic review of 32 trials involving 6,800 participants, Herbison et al⁸ found significant but relatively small differences between anticholinergic medications and placebo for many of the outcomes studied. Obviously, we have more to learn about the intricacies of this condition before we can eliminate it completely.

A 66-year-old woman complains of urinary urgency, frequency, and incontinence, and estimates that she voids 15 or more times within a typical 24-hour period. So far, she has lost only small amounts of urine—because she hurries to void at the first sense of urgency—but she is distressed and worried that she will have a major accident.

Sound familiar? Overactive bladder affects 17 to 33 million US women.¹ Thanks to greater awareness and openness, more women today are seeking medical help for their troubling symptoms, although only a fraction have done so up to now.² Ob/Gyns who are prepared to quickly evaluate the problem and initiate effective management can help restore the quality of life these patients enjoyed before onset of symptoms. This article:

• reviews the pathophysiology of “overactive bladder”
  
• describes a 4-step evaluation and management routine that should be feasible for any gynecology office setting;
  
• discusses the action and the efficacy of available and forthcoming drugs;
  
• uses newly revised terminology that reflects greater sensitivity to the patient.
  

Revised terminology

One of the most notable changes in the terms used to describe lower urinary tract dysfunction, proposed by the International Continence Society,³ is organization of the terminology into 3 categories: symptoms, signs, and urodynamic observations.

Symptoms are now defined to more closely reflect the way the patient perceives her problem, and are set forth without specifying the volume of urine required for a diagnosis of “abnormal” sensation or urgency.

Signs can be observed by the physician, such as leakage of urine when the patient coughs.

Urodynamic observations are made during urodynamic studies.

Overall, the new and revised terms are relatively vague to allow for patient-to-patient variability. Here are a few examples:

• Overactive bladder is a syndrome of symptoms that suggest dysfunction of the lower urinary tract. It is characterized by urgency with or without urge incontinence, usually involving frequency and nocturia.
  
• Urinary incontinence is any involuntary leakage of urine.
  
• Daytime frequency. The patient feels she voids more frequently than she should during the day.
  
• Nocturia. The patient wakes 1 or more times at night to void.
  
• Urgency. The patient feels a sudden, compelling desire to pass urine.
  
• Urge urinary incontinence is involuntary leakage accompanied by or immediately preceded by urgency.
  
• Bladder sensation is identified during history taking: normal, increased, reduced, absent, and nonspecific.
  
• Detrusor overactivity replaces the term “detrusor instability” or “hyperreflexia.” It is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase, and may be spontaneous or provoked. It may be further qualified as neurogenic (if a neurologic condition underlies the problem) or as idiopathic.
  

What is abnormal bladder function?

Any actual incontinence should be considered abnormal, whether diurnal or nocturnal.

Frequency: More than 8 voids in 24 hours. Although an ordinary voiding pattern is not fully defined, most experts agree that a frequency of 8 or fewer voids in 24 hours is “normal.”

Urgency: Patient’s opinion determines. The sensation of urgency is more difficult to objectively define; hence, the need to rely on the patient’s perceptions. If a patient is voiding more frequently than normal because she has an uncomfortable, sudden desire to pass urine, she is considered to have urgency. In contrast, a woman who voids frequently because she has stress incontinence and wants to keep her bladder as empty as possible to avoid leakage has frequency without urgency. Urgency is best classified as being sensory or motor in nature.

• Sensory urgency is a strong, uncomfortable need to void without fear of impending leakage; for whatever reason, the bladder has become hypersensitive. Delaying voiding may result in pain but rarely leads to incontinence.
  
• Patients with motor urgency urinate frequently because they are afraid of experiencing a complete or partial involuntary void as a result of an involuntary bladder contraction.
  

How the normal bladder functions

The process of bladder storage and evacuation can be visualized as a complex of neurocircuits in the brain and spinal cord that coordinate the activity of smooth muscle in the bladder and urethra (FIGURE). These circuits act as “on/off” switches in the lower urinary tract, alternating between the 2 modes of operation: storage and elimination.

As the bladder gradually fills with urine, a woman initially perceives a first sensation of filling between 75 and 125 cc of urine, feels the first need to void at approximately 300 cc, and reaches maximum capacity and a strong urge to void at 400 to 700 cc.

Since the bladder is a low-pressure reservoir, intravesical bladder pressure typically rises very little despite increasing amounts of urine and distention of the smooth muscle or detrusor muscle of the bladder. Pressure ranges from 2 to 6 cm of water in an empty state and rarely exceeds 10 cm of water at maximum capacity.

At maximum capacity, a woman should be able to get to the toilet easily, initiate voluntary bladder contraction with complete relaxation of her pelvic floor, and void to completion.

Urge incontinence is more detrimental to quality of life

Of women who complain of urinary incontinence, more than 90% have either loss of detrusor muscle control (urge incontinence) or urethral sphincteric incompetence (stress incontinence).⁴ In addition, 30% to 50% of women with stress incontinence have coexistent urge incontinence. ¹

Urge incontinence has a much more dramatic impact on a woman’s quality of life than stress incontinence, because stress incontinence is predictable and controllable. The patient understands she will leak urine only with increases in intraabdominal pressure associated with exercise, coughing, etc. These leakages tend to occur in small spurts that are easily absorbed by protective wear. In contrast, urge incontinence manifests as an unpredictable, involuntary void in which urine is released in a gushing stream, often in quantities large enough to soak through heavy absorbent pads.

Although one might assume that subjective complaints would readily distinguish the 2 conditions, the bladder is a very poor “witness.” What the patient perceives often fails to correlate with the true mechanism of incontinence. Since therapies for these 2 conditions are completely different, the evaluation of incontinence is very important.

In aging women, the prevalence of frequency, urgency, and urge incontinence is much higher than that of stress incontinence. Among women 60 to 80 years of age—growth-wise, the largest segment of our population—as many as 50% experience frequency, urgency, and urge incontinence.

High economic cost. The tremendous expense of urinary incontinence is increasingly recognized. In 1995, for example, the economic cost in the United States was $26.3 billion, or $3,565 per person 65 years or older with the condition.^5,6 Of these resources, 48%, or $12.53 billion, were drawn directly from the economy to diagnose, treat, care for, and rehabilitate patients with incontinence.

Contributing factors and causes of overactive bladder

Overactive bladder is thought to be multifactorial. Symptoms often occur in the absence of any obvious pathology, which makes it difficult to pinpoint a cause. Coexisting conditions may also contribute to symptoms or may even be the sole cause.

Examples include infection or inflammation of the lower urinary tract, such as a simple case of cystitis, or a foreign body in the bladder.

Injury or diseases of the nervous system can disrupt voluntary control of voiding in adults, triggering the reemergence of reflex voiding, which leads to bladder hyperactivity and urge incontinence. At a local level, urge incontinence can develop secondary to intrinsic detrusor myogenic abnormalities.

Outlet obstruction can result in urge incontinence such as the well recognized symptoms of urethral obstruction in men with benign prostatic hyperplasia.

Detrusor sphincter dysnergia, most commonly secondary to spinal cord injury or multiple sclerosis, may affect younger men and women.

A deficient urethral sphincter in women with stress incontinence may induce urge incontinence, as urine leaking into the urethra secondary to the stress incontinence stimulates urethral afferents that induce involuntary voiding reflexes.⁷

Women with stress incontinence may unwittingly contribute to overactive bladder by voiding more and more often, hoping to prevent any involuntary urine loss. As a result of the frequent voiding, they develop frequency and urgency symptoms. That is, over time, this frequent, voluntary voiding leads to decreased bladder compliance. Thus begins a vicious cycle that ultimately leads to more frequency and urgency.

Urogenital atrophy. Irritative symptoms of the lower urinary tract in the form of frequency, urgency, and dysuria can result from lack of estrogen, leading to urogenital atrophy.

Pelvic organ prolapse is another common coexisting condition. Although the correlation between anatomic descent of pelvic organs and lower urinary tract symptoms is poorly understood, frequency and urgency—with or without urge incontinence—coexist with symptomatic pelvic organ prolapse in approximately 30% to 50% of cases.

An enlarged uterus or adnexal mass may cause external compression of the bladder and lead to lower urinary tract symptoms.

Previous surgery of the anterior vaginal wall or bladder neck may sometimes trigger de novo symptoms of frequency, urgency, and urge incontinence. In women who have undergone a previous antiincontinence procedure, these symptoms may be related to some form of outlet obstruction. In some cases these patients have no increase in the postvoid residual, and only subtle urodynamic testing elicits evidence of obstruction.

Step 1Ask the right questions, get voiding diary, assess quality of life

Most women can be thoroughly evaluated within the clinical practice setting of any gynecologist. The first and most important aspect of this assessment is understanding and appreciating the severity of a patient’s lower urinary tract symptoms. This can be done by asking pointed questions, in the following approximate sequence:

1. Do you have problems with accidental loss of urine?
   
2. How many months or years have you had leakage?
   
3. Do you have to wear pads or protective clothing to prevent or help with urinary loss? If so, how many pads do you wear a day?
   
4. How many trips do you make to the bathroom during the day? At night?
   
5. Do you ever wet the bed while sleeping?
   
6. Are you bothered by a strong sense of urgency to void? Can you overcome it?
   
7. Do you sometimes fail to reach the bathroom in time?
   
8. Does the sound, sight, or feel of running water cause you to lose urine?
   
9. Do you lose urine when you cough, sneeze, run, or lift heavy objects?
   
10. Do you lose urine with posture changes, standing, or walking?
    
11. Do you feel as though you are constantly wet?
    
12. Do you feel as though your bladder is completely empty after passing urine?
    
13. Do you have difficulty starting a stream of urine?
    

Take a thorough medical history, as well as a surgical history with emphasison previous bladder or gynecologic procedures.

Also review all prescription medications.

48-hour voiding diary. Give the patient a voiding diary to fill out 48 hours prior to her office visit. The reason: The diary often reveals more information than can be elicited from the patient’s history. For example, it may highlight daily activities associated with voiding, such as excessive consumption of liquids, high caffeine intake, high-impact exercise, and so on.

Quality-of-life assessment. An objective means of quantifying the effects of incontinence on the woman’s quality of life is recommended. We use the short form of the Incontinence Impact Questionnaire and the Urinary Distress Inventory.

Step 2Perform ‘eyeball’ cystometry, a simple and revealing office test

Ask the patient to go to the restroom and comfortably empty her bladder into a urine-collection device to determine the amount voided. Have a nurse measure the postvoid residual using a soft red rubber catheter. A sample can be taken for urinalysis and, if necessary, sent for culture.

Next, perform a simple filling or “eyeball” cystometry. Connect a Toomey syringe to the end of the red rubber catheter and pour sterile water into it. Ask the patient to tell you when she feels the first sensation of filling, first desire to void, strong urge to void, and maximum capacity, recording the levels at which each occurs. During filling, any evidence of bladder contraction will be revealed by a rise in the column of water. Record any significant discomfort or other observations during the filling portion of the study. When maximum capacity is reached, remove the catheter.

Step 3Conduct a thorough physical assessment

With the patient in the supine position, separate the labia and ask her to cough forcefully and perform the Valsalva maneuver 3 times, recording any evidence of water or urine loss through the urethral meatus. (If the patient has advanced pelvic organ prolapse, try to reduce the prolapse to eliminate any anatomic distortion of the urethra.)

Then ask the patient to stand with a full bladder and to squat, again having her cough forcefully 3 times. Record any additional urinary loss. Finally, ask the patient to void and again record the amount voided.

After the patient has emptied her bladder, again ask her to cough forcefully 3 times in the supine position, noting any evidence of leakage from the urethra (empty supine stress test).

Perform an overall inspection of the perineum and external genitalia and record a description in the patient’s chart.

Attempt to elicit an anal wink, and perform a brief neurological examination to ensure that spinal cord segments S2, S3, and S4 are intact. Next, gently insert a finger into the vagina and ask the patient to forcefully squeeze around it. Record the forcefulness of the squeeze on a scale of 0 to 5, with 0 being no appreciable movement and 5 being the most forceful squeeze possible. During this portion of the exam, instruct the patient on how to perform a Kegel exercise without recruiting the muscles of the buttocks and the abdominal wall.

Next, use a finger to gently massage the urethra, looking for any possible discharge from the urethral meatus that would be consistent with urethral diverticulum. Also note any tenderness or pain elicited during the exam.

Inserting a half-speculum into the vagina, displace the rectum away from the bladder. As the patient performs a Valsalva maneuver or coughs forcefully, evaluate the support of the anterior vaginal wall. Then turn the speculum 180 degrees and displace the bladder anteriorly, examining the posterior pelvic wall for any signs of prolapse. Also note any urogenital atrophy.

Finally, use a full speculum to evaluate the vaginal apex and cervix (if the patient has not had a hysterectomy). Bimanual and abdominal examinations also are important to rule out any abdominal or pelvic mass that could be irritating or causing pressure on the bladder.

Reexamine the patient for evidence of prolapse when she is standing. Some cases are difficult to detect when the patient is supine.

Step 4Begin multipronged therapy

Bladder retraining. Review the patient’s history, voiding diary, and findings from the physical exam to identify an appropriate treatment. After sharing all findings with the patient, instruct the patient on bladder retraining, which has 3 main components: education, scheduled voiding, and positive reinforcement. (Bladder retraining can be an extremely successful modality.)

Education consists of explaining the pathophysiology of overactive bladder and answering any questions the patient may have, so she understands why she is having the problem.

For scheduled voiding—also known as bladder retraining—examine the voiding diary to determine the approximate length of time between voids in a day. For instance, if the patient voids every hour, we generally ask her to continue doing so for the first week of retraining. The following week, we increase the interval to an hour and 15 minutes, the third week to 1.5 hours, and so on, with an ultimate goal of 3 hours between voids.

We also give instructions on pelvic floor rehabilitation or Kegel exercises. If the patient is able to voluntarily contract her pelvic floor muscles adequately, we recommend an exercise regimen that involves contracting her muscles numerous times a day for at least 10 seconds each time. If she is unable to contract her muscles or has a “dead” pelvic floor, she is referred to a physical therapist for biofeedback and possibly electrical stimulation.

We also instruct the patient to avoid racing to the bathroom when she feels an urge to void. Instead, have her stop, contract her pelvic floor muscles, and allow the urge to pass. She can then walk comfortably to the bathroom.

As mentioned earlier, the voiding diary may highlight problems such as excessive intake of fluids.

Local estrogen therapy can be added if there are signs of urogenital atrophy.

Medical therapy. In addition to education, timed voids, pelvic floor rehabilitation, and estrogen therapy, we usually start the extended-release form of tolterodine (4 mg) or oxybutynin (10 mg), which are antimuscarinic agents. (See “Treating overactive bladder: An expanding ‘pharmacopeia’”).

We ask her to return for a follow-up visit in 4 to 6 weeks to inquire about her symptoms and any significant side effects. We ask the patient to prepare another voiding diary for that visit so we can objectively measure decreases in frequency, urgency, and urge incontinence.

Dose adjustment is very important in patients with overactive bladder. If the woman is experiencing minimal effect with no side effects, titrate the dosage upward. If she is having good effect with significant side effects, decrease the dosage or consider switching to the transdermal form of oxybutynin.

When all these conditions are met and the patient remains severely affected, we perform multichannel urodynamic testing along with cystoscopy. If the testing supports the diagnosis of overactive bladder, and all other mechanisms for improvement have been exhausted, we counsel the patient about intravesical administration of botulism toxin, which relaxes skeletal and smooth muscle by preventing release of acetocholine from nerve terminal endings. Another option is sacroneuromodulation (InterStim therapy).

Implications of the placebo effect

We lack a complete understanding of how all the parts of this process interact and why. Most of the medications in use affect only 1 part of the complex process that governs urine storage and elimination.

In controlled trials, patients on placebo have experienced 30% improvement—or greater—in their symptoms. This would seem to suggest that education, behavioral retraining, and attention from physicians are responsible for some of the improvement. Indeed, in a recent systematic review of 32 trials involving 6,800 participants, Herbison et al⁸ found significant but relatively small differences between anticholinergic medications and placebo for many of the outcomes studied. Obviously, we have more to learn about the intricacies of this condition before we can eliminate it completely.

A 66-year-old woman complains of urinary urgency, frequency, and incontinence, and estimates that she voids 15 or more times within a typical 24-hour period. So far, she has lost only small amounts of urine—because she hurries to void at the first sense of urgency—but she is distressed and worried that she will have a major accident.

Sound familiar? Overactive bladder affects 17 to 33 million US women.¹ Thanks to greater awareness and openness, more women today are seeking medical help for their troubling symptoms, although only a fraction have done so up to now.² Ob/Gyns who are prepared to quickly evaluate the problem and initiate effective management can help restore the quality of life these patients enjoyed before onset of symptoms. This article:

• reviews the pathophysiology of “overactive bladder”
  
• describes a 4-step evaluation and management routine that should be feasible for any gynecology office setting;
  
• discusses the action and the efficacy of available and forthcoming drugs;
  
• uses newly revised terminology that reflects greater sensitivity to the patient.
  

Revised terminology

One of the most notable changes in the terms used to describe lower urinary tract dysfunction, proposed by the International Continence Society,³ is organization of the terminology into 3 categories: symptoms, signs, and urodynamic observations.

Symptoms are now defined to more closely reflect the way the patient perceives her problem, and are set forth without specifying the volume of urine required for a diagnosis of “abnormal” sensation or urgency.

Signs can be observed by the physician, such as leakage of urine when the patient coughs.

Urodynamic observations are made during urodynamic studies.

Overall, the new and revised terms are relatively vague to allow for patient-to-patient variability. Here are a few examples:

• Overactive bladder is a syndrome of symptoms that suggest dysfunction of the lower urinary tract. It is characterized by urgency with or without urge incontinence, usually involving frequency and nocturia.
  
• Urinary incontinence is any involuntary leakage of urine.
  
• Daytime frequency. The patient feels she voids more frequently than she should during the day.
  
• Nocturia. The patient wakes 1 or more times at night to void.
  
• Urgency. The patient feels a sudden, compelling desire to pass urine.
  
• Urge urinary incontinence is involuntary leakage accompanied by or immediately preceded by urgency.
  
• Bladder sensation is identified during history taking: normal, increased, reduced, absent, and nonspecific.
  
• Detrusor overactivity replaces the term “detrusor instability” or “hyperreflexia.” It is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase, and may be spontaneous or provoked. It may be further qualified as neurogenic (if a neurologic condition underlies the problem) or as idiopathic.
  

What is abnormal bladder function?

Any actual incontinence should be considered abnormal, whether diurnal or nocturnal.

Frequency: More than 8 voids in 24 hours. Although an ordinary voiding pattern is not fully defined, most experts agree that a frequency of 8 or fewer voids in 24 hours is “normal.”

Urgency: Patient’s opinion determines. The sensation of urgency is more difficult to objectively define; hence, the need to rely on the patient’s perceptions. If a patient is voiding more frequently than normal because she has an uncomfortable, sudden desire to pass urine, she is considered to have urgency. In contrast, a woman who voids frequently because she has stress incontinence and wants to keep her bladder as empty as possible to avoid leakage has frequency without urgency. Urgency is best classified as being sensory or motor in nature.

• Sensory urgency is a strong, uncomfortable need to void without fear of impending leakage; for whatever reason, the bladder has become hypersensitive. Delaying voiding may result in pain but rarely leads to incontinence.
  
• Patients with motor urgency urinate frequently because they are afraid of experiencing a complete or partial involuntary void as a result of an involuntary bladder contraction.
  

How the normal bladder functions

The process of bladder storage and evacuation can be visualized as a complex of neurocircuits in the brain and spinal cord that coordinate the activity of smooth muscle in the bladder and urethra (FIGURE). These circuits act as “on/off” switches in the lower urinary tract, alternating between the 2 modes of operation: storage and elimination.

As the bladder gradually fills with urine, a woman initially perceives a first sensation of filling between 75 and 125 cc of urine, feels the first need to void at approximately 300 cc, and reaches maximum capacity and a strong urge to void at 400 to 700 cc.

Since the bladder is a low-pressure reservoir, intravesical bladder pressure typically rises very little despite increasing amounts of urine and distention of the smooth muscle or detrusor muscle of the bladder. Pressure ranges from 2 to 6 cm of water in an empty state and rarely exceeds 10 cm of water at maximum capacity.

At maximum capacity, a woman should be able to get to the toilet easily, initiate voluntary bladder contraction with complete relaxation of her pelvic floor, and void to completion.

Urge incontinence is more detrimental to quality of life

Of women who complain of urinary incontinence, more than 90% have either loss of detrusor muscle control (urge incontinence) or urethral sphincteric incompetence (stress incontinence).⁴ In addition, 30% to 50% of women with stress incontinence have coexistent urge incontinence. ¹

Urge incontinence has a much more dramatic impact on a woman’s quality of life than stress incontinence, because stress incontinence is predictable and controllable. The patient understands she will leak urine only with increases in intraabdominal pressure associated with exercise, coughing, etc. These leakages tend to occur in small spurts that are easily absorbed by protective wear. In contrast, urge incontinence manifests as an unpredictable, involuntary void in which urine is released in a gushing stream, often in quantities large enough to soak through heavy absorbent pads.

Although one might assume that subjective complaints would readily distinguish the 2 conditions, the bladder is a very poor “witness.” What the patient perceives often fails to correlate with the true mechanism of incontinence. Since therapies for these 2 conditions are completely different, the evaluation of incontinence is very important.

In aging women, the prevalence of frequency, urgency, and urge incontinence is much higher than that of stress incontinence. Among women 60 to 80 years of age—growth-wise, the largest segment of our population—as many as 50% experience frequency, urgency, and urge incontinence.

High economic cost. The tremendous expense of urinary incontinence is increasingly recognized. In 1995, for example, the economic cost in the United States was $26.3 billion, or $3,565 per person 65 years or older with the condition.^5,6 Of these resources, 48%, or $12.53 billion, were drawn directly from the economy to diagnose, treat, care for, and rehabilitate patients with incontinence.

Contributing factors and causes of overactive bladder

Overactive bladder is thought to be multifactorial. Symptoms often occur in the absence of any obvious pathology, which makes it difficult to pinpoint a cause. Coexisting conditions may also contribute to symptoms or may even be the sole cause.

Examples include infection or inflammation of the lower urinary tract, such as a simple case of cystitis, or a foreign body in the bladder.

Injury or diseases of the nervous system can disrupt voluntary control of voiding in adults, triggering the reemergence of reflex voiding, which leads to bladder hyperactivity and urge incontinence. At a local level, urge incontinence can develop secondary to intrinsic detrusor myogenic abnormalities.

Outlet obstruction can result in urge incontinence such as the well recognized symptoms of urethral obstruction in men with benign prostatic hyperplasia.

Detrusor sphincter dysnergia, most commonly secondary to spinal cord injury or multiple sclerosis, may affect younger men and women.

A deficient urethral sphincter in women with stress incontinence may induce urge incontinence, as urine leaking into the urethra secondary to the stress incontinence stimulates urethral afferents that induce involuntary voiding reflexes.⁷

Women with stress incontinence may unwittingly contribute to overactive bladder by voiding more and more often, hoping to prevent any involuntary urine loss. As a result of the frequent voiding, they develop frequency and urgency symptoms. That is, over time, this frequent, voluntary voiding leads to decreased bladder compliance. Thus begins a vicious cycle that ultimately leads to more frequency and urgency.

Urogenital atrophy. Irritative symptoms of the lower urinary tract in the form of frequency, urgency, and dysuria can result from lack of estrogen, leading to urogenital atrophy.

Pelvic organ prolapse is another common coexisting condition. Although the correlation between anatomic descent of pelvic organs and lower urinary tract symptoms is poorly understood, frequency and urgency—with or without urge incontinence—coexist with symptomatic pelvic organ prolapse in approximately 30% to 50% of cases.

An enlarged uterus or adnexal mass may cause external compression of the bladder and lead to lower urinary tract symptoms.

Previous surgery of the anterior vaginal wall or bladder neck may sometimes trigger de novo symptoms of frequency, urgency, and urge incontinence. In women who have undergone a previous antiincontinence procedure, these symptoms may be related to some form of outlet obstruction. In some cases these patients have no increase in the postvoid residual, and only subtle urodynamic testing elicits evidence of obstruction.

Step 1Ask the right questions, get voiding diary, assess quality of life

Most women can be thoroughly evaluated within the clinical practice setting of any gynecologist. The first and most important aspect of this assessment is understanding and appreciating the severity of a patient’s lower urinary tract symptoms. This can be done by asking pointed questions, in the following approximate sequence:

1. Do you have problems with accidental loss of urine?
   
2. How many months or years have you had leakage?
   
3. Do you have to wear pads or protective clothing to prevent or help with urinary loss? If so, how many pads do you wear a day?
   
4. How many trips do you make to the bathroom during the day? At night?
   
5. Do you ever wet the bed while sleeping?
   
6. Are you bothered by a strong sense of urgency to void? Can you overcome it?
   
7. Do you sometimes fail to reach the bathroom in time?
   
8. Does the sound, sight, or feel of running water cause you to lose urine?
   
9. Do you lose urine when you cough, sneeze, run, or lift heavy objects?
   
10. Do you lose urine with posture changes, standing, or walking?
    
11. Do you feel as though you are constantly wet?
    
12. Do you feel as though your bladder is completely empty after passing urine?
    
13. Do you have difficulty starting a stream of urine?
    

Take a thorough medical history, as well as a surgical history with emphasison previous bladder or gynecologic procedures.

Also review all prescription medications.

48-hour voiding diary. Give the patient a voiding diary to fill out 48 hours prior to her office visit. The reason: The diary often reveals more information than can be elicited from the patient’s history. For example, it may highlight daily activities associated with voiding, such as excessive consumption of liquids, high caffeine intake, high-impact exercise, and so on.

Quality-of-life assessment. An objective means of quantifying the effects of incontinence on the woman’s quality of life is recommended. We use the short form of the Incontinence Impact Questionnaire and the Urinary Distress Inventory.

Step 2Perform ‘eyeball’ cystometry, a simple and revealing office test

Ask the patient to go to the restroom and comfortably empty her bladder into a urine-collection device to determine the amount voided. Have a nurse measure the postvoid residual using a soft red rubber catheter. A sample can be taken for urinalysis and, if necessary, sent for culture.

Next, perform a simple filling or “eyeball” cystometry. Connect a Toomey syringe to the end of the red rubber catheter and pour sterile water into it. Ask the patient to tell you when she feels the first sensation of filling, first desire to void, strong urge to void, and maximum capacity, recording the levels at which each occurs. During filling, any evidence of bladder contraction will be revealed by a rise in the column of water. Record any significant discomfort or other observations during the filling portion of the study. When maximum capacity is reached, remove the catheter.

Step 3Conduct a thorough physical assessment

With the patient in the supine position, separate the labia and ask her to cough forcefully and perform the Valsalva maneuver 3 times, recording any evidence of water or urine loss through the urethral meatus. (If the patient has advanced pelvic organ prolapse, try to reduce the prolapse to eliminate any anatomic distortion of the urethra.)

Then ask the patient to stand with a full bladder and to squat, again having her cough forcefully 3 times. Record any additional urinary loss. Finally, ask the patient to void and again record the amount voided.

After the patient has emptied her bladder, again ask her to cough forcefully 3 times in the supine position, noting any evidence of leakage from the urethra (empty supine stress test).

Perform an overall inspection of the perineum and external genitalia and record a description in the patient’s chart.

Attempt to elicit an anal wink, and perform a brief neurological examination to ensure that spinal cord segments S2, S3, and S4 are intact. Next, gently insert a finger into the vagina and ask the patient to forcefully squeeze around it. Record the forcefulness of the squeeze on a scale of 0 to 5, with 0 being no appreciable movement and 5 being the most forceful squeeze possible. During this portion of the exam, instruct the patient on how to perform a Kegel exercise without recruiting the muscles of the buttocks and the abdominal wall.

Next, use a finger to gently massage the urethra, looking for any possible discharge from the urethral meatus that would be consistent with urethral diverticulum. Also note any tenderness or pain elicited during the exam.

Inserting a half-speculum into the vagina, displace the rectum away from the bladder. As the patient performs a Valsalva maneuver or coughs forcefully, evaluate the support of the anterior vaginal wall. Then turn the speculum 180 degrees and displace the bladder anteriorly, examining the posterior pelvic wall for any signs of prolapse. Also note any urogenital atrophy.

Finally, use a full speculum to evaluate the vaginal apex and cervix (if the patient has not had a hysterectomy). Bimanual and abdominal examinations also are important to rule out any abdominal or pelvic mass that could be irritating or causing pressure on the bladder.

Reexamine the patient for evidence of prolapse when she is standing. Some cases are difficult to detect when the patient is supine.

Step 4Begin multipronged therapy

Bladder retraining. Review the patient’s history, voiding diary, and findings from the physical exam to identify an appropriate treatment. After sharing all findings with the patient, instruct the patient on bladder retraining, which has 3 main components: education, scheduled voiding, and positive reinforcement. (Bladder retraining can be an extremely successful modality.)

Education consists of explaining the pathophysiology of overactive bladder and answering any questions the patient may have, so she understands why she is having the problem.

For scheduled voiding—also known as bladder retraining—examine the voiding diary to determine the approximate length of time between voids in a day. For instance, if the patient voids every hour, we generally ask her to continue doing so for the first week of retraining. The following week, we increase the interval to an hour and 15 minutes, the third week to 1.5 hours, and so on, with an ultimate goal of 3 hours between voids.

We also give instructions on pelvic floor rehabilitation or Kegel exercises. If the patient is able to voluntarily contract her pelvic floor muscles adequately, we recommend an exercise regimen that involves contracting her muscles numerous times a day for at least 10 seconds each time. If she is unable to contract her muscles or has a “dead” pelvic floor, she is referred to a physical therapist for biofeedback and possibly electrical stimulation.

We also instruct the patient to avoid racing to the bathroom when she feels an urge to void. Instead, have her stop, contract her pelvic floor muscles, and allow the urge to pass. She can then walk comfortably to the bathroom.

As mentioned earlier, the voiding diary may highlight problems such as excessive intake of fluids.

Local estrogen therapy can be added if there are signs of urogenital atrophy.

Medical therapy. In addition to education, timed voids, pelvic floor rehabilitation, and estrogen therapy, we usually start the extended-release form of tolterodine (4 mg) or oxybutynin (10 mg), which are antimuscarinic agents. (See “Treating overactive bladder: An expanding ‘pharmacopeia’”).

We ask her to return for a follow-up visit in 4 to 6 weeks to inquire about her symptoms and any significant side effects. We ask the patient to prepare another voiding diary for that visit so we can objectively measure decreases in frequency, urgency, and urge incontinence.

Dose adjustment is very important in patients with overactive bladder. If the woman is experiencing minimal effect with no side effects, titrate the dosage upward. If she is having good effect with significant side effects, decrease the dosage or consider switching to the transdermal form of oxybutynin.

When all these conditions are met and the patient remains severely affected, we perform multichannel urodynamic testing along with cystoscopy. If the testing supports the diagnosis of overactive bladder, and all other mechanisms for improvement have been exhausted, we counsel the patient about intravesical administration of botulism toxin, which relaxes skeletal and smooth muscle by preventing release of acetocholine from nerve terminal endings. Another option is sacroneuromodulation (InterStim therapy).

Implications of the placebo effect

We lack a complete understanding of how all the parts of this process interact and why. Most of the medications in use affect only 1 part of the complex process that governs urine storage and elimination.

In controlled trials, patients on placebo have experienced 30% improvement—or greater—in their symptoms. This would seem to suggest that education, behavioral retraining, and attention from physicians are responsible for some of the improvement. Indeed, in a recent systematic review of 32 trials involving 6,800 participants, Herbison et al⁸ found significant but relatively small differences between anticholinergic medications and placebo for many of the outcomes studied. Obviously, we have more to learn about the intricacies of this condition before we can eliminate it completely.