Endwm&bsls as cause of dys-nhm To the Editors: In their article “New concepts in dysmenorrhea,” (AM. J. OBSTET. GYNECOL. 130: 833, 1978) Drs. Ylikorkala and Dawood made the statement: “There is almost always complete relief of dysmenorrhea with oral contraceptives, so that failure to respond would suggest an unusually large psychogenic component contributing to the pain,” If the authors use this criterion-a failure to respond to oral contraceptives-as an indicator of psychosomatic illness, then they are missing a great deal of organic disease. In my practice, in the past three years, I have performed laparoscopy on seven teen-age girls because of severe dysmenorrhea. In all cases, my principal criterion for recommending the operation was the failure of the oral contraceptive to completely or nearly completely relieve the dysmenorrhea. Four of these girls had definite endometriosis and one had probable endometriosis. No evidence of pelvic pathology was found in the remaining two patients. Endometriosis in young women is a common disease, far more so than has been previously recognized. Experience has shown that a failure of the oral contraceptive to relieve the patient’s dysmenorrhea is a cardinal symptom of endometriosis. Another prominent symptom is significant cul-de-sac tenderness when pelvic examination is carried out at the time of a menstrual period. Far too many patients have been labeled as having a psychosomatic disorder when indeed they have organic disease. Endometriosis is a common disease in my practice. It is common because I think of it and I look for it. I encourage my fellow gynecologists to do likewise. Michael D. Birnbaum, M.D. Section of Reproductive Endocrinology Division of Gynecology and Obstettics The Albert Einstein Medical Center Phitadel$hia, Pennsylvania 19141
Fk@y to Ck 4%Wum To the Editors: In his comment on our article “New concepts in dysmenorrhea,” Dr. Birnbaum directed attention to organic disease, including endometriosis, as a cause of dysmenorrhea, which is the secondary type. We wish to emphasize that the review was focused on primary 228
dysmenorrhea and this was stated at the beginning of the article. Secondary dysmenorrhea was briefly alluded to when the biochemical basis of the dysmenorrhea in such circumstances was similar to that in primary dysmenorrhea, namely, increased endometrial or menstrual fluid prostaglandins. We stated: “Irrespective of whether oral cdntraceptives exert their antidysmenorrheic effect throngh one or all of the above mechanisms, the clinical therapeutic effect of oral contraceptives in primary dysmenorrhea is well established . . There is almost always complete relief of dysmenorrhea with oral contraceptives, so that failure to respond would suggest an unusually large psychogenic component cont&buting to the pain.” We also pointed out, under “Symptoms and diagnosis of dysmenorrhea,” that: “Where it may be di%cult to differentiate primary dysmenorrhea from pelvic pains or secondary dysmenorrhea, the cause ofwhich is not clinically detectable, laparoscopy may be indicated.” Elence, contrary to Dr. Birnbaum’s conclusion, we do not use the criterion “failure to respond to oral contraceptives” as an indicator of psychosomatic illness unless pelvic organic disease has been ruled out. For thal matter, primary dysmenorrhea should not be diag nosed unless pelvic organic disease has been excluded. M. YusoJf Damood, M.D. Oh& Ylikarkala, M.D. Department of Obstetrics and Gynecology The New York Hos#&Corrzell Medical Center 525 East 68th Street New York, New York 10021
To the Editors: In their article, “Do static cystonrethrograms have a role in the mvestigation of female incontinence?” (AM. J. OBSTET. GYNECOL. 130: 516, 1978), Drs. Drutz, Shapiro, and Mandel recorded observations and rendered opinions so greatly at variance .with the experience of the vast majority of us working in this field during the past quarter century that I must .take strong issue with their interpretations and conclusions. I do so mainly on behalf of the countless present and future patients who do and will suffer fro’m the troublesome symptom of stress urinary incontinence .and whtih successful treatment will, as it always should, hinge on a careful and complete diagnostic evaluation, a vital segment of
Volume Number
132 2
which these authors groundlessly and cavalierly advocated should be discarded. Space does not allow a point-by-point discussion and rebuttal of what seem to be some erroneous concepts and fallacious conclusions regarding the general problem of the symptom of stress urinary incontinence expressed in this article, but a few items deserve brief comment. For example, it is not made clear in what way they found poor correlation between standard cystourethrograms in women with anatomic sphincterweakness (their phrase) stress urinary incontinence. This is very hard to understand and reconcile in view of the close correlation that we and many other groups working in this field during the past 25 years have consistently found to be the case. It should be noted that they used barium paste rather than a metallic bead chain to demonstrate the urethra and urethrovesical junction and recorded difficulties in outlining and identifying the urethra in a number of cases, so perhaps their technique was in part responsible for their “poor correlation.” And, as another example, their statement: “A detrusor contraction . . . cannot be distinguished from the classic SUI changes by static cystourethrography . .” has simply not been true in our experience. In carrying out cystourethrography with the metallic bead-chain technique in thousands of patients with the symptom of stress urinary incontinence during the past 25 years, we have only rarely observed detrusor contraction to occur during the course of the x-ray examination. In the few instances when it did occur it was easily recognized by the irregular, crenated outline of the contracting bladder, as seen on the x-ray film, and by the even more obvious loss of urine, and usually the metallic bead chain as well, while the films were being exposed. Such an event (the transient physiologic obliteration of the posterior urethrovesical (PUV) angle and rotational displacement of the urethral axis accompanying a detrusor contraction) can thus readily be distinguished from the permanent loss of the PUV angle and rotational descent of the urethra accompanying true anatomic stress incontinence due to deficient urethrovesical support. It will perhaps be more helpful to concentrate on just a few major examples of what seem to be misleading and unjustified conclusions drawn and opinions rendered and especially to comment on the two factors that could most likely account for their unusual experience-first, a seemingly unusual patient population and, second, quite possibly the manner in which the urodynamic studies were conducted. 1. In view of the very name of their clinic (Gynaecological Urology and Urodynamic Unit), it would be surprising if there were not an understandable difference in the referral pattern to such a combined urology-gynecology clinic, obviously specializing in complicated cases. The fact that pure stress urinary incontinence was rarely seen as the sole problem makes it almost certain that this unit is seeing an unusual and
Correspondence
229
highly selected population of women with urinary incontinence. Since their paper described only the techniques of study and did not include any clinical description of their patients, one has no way of knowing just what the symptoms were, how many had undergone one or more previous unsuccessful operations (such women are known to have a high incidence of urodynamic disorders, combinations of anatomic and urodynamic disorders, psychosomatic symptomatology, and iatrogenic urethral scarring and periurethral fibrosis, etc.), and how many previously had been studied and screened by their referring physicians and already were believed not to have straightforward true anatomic streSs incontinence. Year after year at our institution (The Massachusetts General Hospital, Boston, Massachusetts), 75 to 85 per cent of our patients suffering from the symptom of stress urinary incontinence prove to have true anatomic stress incontinence, unassociated with any urodynamic abnormality. The other 15 to 25 per cent have a variety of other mechanisms and disorders responsible for their symptoms-detrusor dyssynergia in 10 to 15 per cent and occasional fundamental neurological disorders, urethral diverticula, and urethral fibrosis in the remaining 5 to 10 per cent. In a recent personal series of 137 patients in the past four years, 78 per cent had pure anatomic stress incontinence, 17.5 per cent proved to have pure detrusor dyssynergia, and 4.5 per cent were found to have a combination of anatomic stress incontinence and detrusor dyssynergia. A report by McGuire and his associates’ is perhaps even more pertinent since it emanated from a combined gynecology-urology project established at Yale University Medical School that functioned in a manner quite like that of the unit of these authors. Using a similar detailed study program that included urodynamic and static cystourethrographic studies in all patients, they demonstrated 62 per cent of their patients to have pure anatomic stress incontinence, and an additional 22 per cent proved to have anatomic stress incontinence plus varying degrees of detrusor dyssynergia (almost all of this group were cured of anatomic stress incontinence by operation), and 9 per cent had pure detrusor dyssynergia. Parenthetically, Drutz, Shapiro, and Mandel seem to be unaware of the significance of this group of patients in whom both clear-cut anatomic stress incontinence and varying degrees of detrusor dyssynergia coexist. As experience accumulates, it is becoming clear that the detrusor dyssynergia in this special group disappears when, and only when, the anatomic weakness in the urethrovesical supporting mechanism is corrected surgically by the appropriate standard operative procedure for anatomic stress incontinence. In addition to the observations by McGuire and associates and our own recent parallel experience with this “combined problem” group, a similar experience has been recorded by Beck and co-workers* from the University of Alberta, Edmonton, Alberta, Canada.
230
Correspondence
2. It seems highly likely that the problems encountered by the authors in correlating information obwith their tained from “static cystourethrograms” “urodynamic studies” may also have stemmed in part from the inherent limitations and inaccuracies of the technique they used to evaluate the urodynamic situation in their patients, namely, the method of carbon dioxide gas retrograde urethrocystometry by means of the Browne-Robertson female carbon dioxide urethroscope and monitor. This technique has recently been criticized and the accuracy of the urodynamic observations made in this manner seriously questioned by several authorities. Hodgkinsong who, along with his urologic colleagues at Henry Ford Hospital in Detroit, Michigan abandoned its use after a careful trial, recently concisely summarized his reservations concerning retrograde carbon dioxide urethrocystometry. He pointed out that the information obtained in this way is no more helpful and probably less accurate than that provided by standard water cystometry, which also has its shortcomings and inaccuracies. He found that, in comparison with the far more physiologic direct electronic urethrocystometry, the retrograde carbon dioxide gas technique was not really an accurate or discriminating measure of the presence or absence or the degree of detrusor dyssynergia. Furthermore, he believes that in patients with a normal detrusor control mechanism the results of carbon dioxide gas urethrocystometry are often misleading and suggest detrusor irritability and dysfunction, when by all other parameters of study bladder function and its neurophysiologic control mechanisms are entirely normal. As a consequence he believes that in a number of recent publications, especially some emanating from Great Britain, an excessively high percentage of women have been reported to have “unstable bladders” among groups of women undergoing complete investigation for stress urinary incontinence and related bladder control disorders, this high incidence being erroneous and artifactual and simply incidental to the technique of urethrocystometry itself. In addition to the obvious potential problems with their technique of urethrocystometry, a technique that is not as accurate or infallible as they and others attempt to suggest, the authors actually do a disservice to the commendable progress made in the past decade toward a better understanding of the neurophysiologic mechanisms responsible for some types of female urinary incontinence by attempting to proclaim that the concept of urodynamics, and only urodynamics, explains everything. For those who wish to review again the facts of the other side of the coin, that is, the vast amount of evidence underlying the concepts of, the proper investigation of, and the appropriate treatment for the far more frequent and equally significant anatomic aspect of the problem (the one that gynecologic surgeons can successfully correct), along with a more realistic appraisal of the urodynamic side of the
September
1.5, 1978
Am. J. Obstet. C~WXO~.
coin, than that advanced by Drutz, Shapiro, and Mandel, reference could be made to a 1975 summary prepared for this same JOURNALS and especially to the publications of others working in this fascinating and challenging field included in the list of references at the end of that 1975 review article. What is needed in achieving proper understanding of some of the complexities of stress urinary iilcontinence and related disorders of micturitioil and its COW trol, and especially needed in the investigation and SUCcessful treatment of patients with the symptom of stress urinary incontinence, is not a tunnel vision that focuses only on the so-called “urodynamic” aspects. Rather, a broad vision is required, one that encompasses the all important urethrovesical anatomic support mechanism as well as the significant neurophysiologic and neuropharmacologic mechanisms (urodynamics) involved in producing the symptom of stress urinary incontinence. Fascinating and important as they are, these disorders of urodynamics, however, account for the symptom in only a relatively small percentage of the total population of patients with stress urinary incontinence. Since anatomic abnormalities of urethrovesical support are the fundamental cause in the vast majority of these women, and since the “static” cystourethrogram remains the one most accurate and highly objective means of assessing urethrovesical anatomic support, it should and will continue to play a very vital role, along with properly performed and carefulty interpreted urodynamic studies, in establishing the correct diagnosis, in selecting the optimal surgical procedure for those patients in whom operation is clearly indicated. and in assessing postoperatively whether or n~ot an adequate anatomic repair has been achieved. The final dogmatic recommendation of these authors that the use of cystourethrography in the study of female incontinence be abandoned is completely unjustified and cannot in any way contribute to, but rather is certain to prevent, a better understanding of and more successful efforts at correction of these troublesome disorders. Like one or two other authors who have criticized metallic bead-chain urethrocystograms during the past 15 years, these authors have stated the same clichk. a pseudoscientific one that is not as significant or meaningful as it might appear at first glance to the unwary, that it is a static measurement of dynamic function, and hence not of great value. It is revealing that they were able to cite only one reference that lends even limited support to their contention and chose to ignore the dozens of reports in the literature confirming that, where true anatomic stress incontinence is concerned, preoperative static urethrocystograms are highly accurate and valuable in establishing its presence and postoperative static cystourethrograms are equally reliable in demonstrating the anatomic reasons for success or failure of the surgical procedure to relieve the distressing symptom. Quite obviously they misunderstand the true purpose and vahle of rystoure-
Volume
132
Number
2
thrography, which is to evaluate the urethrovesical anatomic supporting mechanism, a mechanism that in the nonvoiding woman is fundamentally a constant and essentially static one. When defective, this mechanism can be exploited by the stress of a sudden increase in intra-abdominal pressure to produce abnormal urinary leakage, in the absence of any abnormal detrusor muscle activity whatsoever (i.e., in the absence of any abnormality of the patient’s so-called “urodynamics”) in the vast majority of instances. In point of fact, it is a failure of this static anatomic support mechanism that is the primary cause of the abnormal leakage of urine in 75 to 80 per cent of women with the symptom of stress urinary incontinence. And since our long-term cure rates following properly selected operations on patients with anatomic stress urinary incontinence, based on a minimum follow-up period of five years, continue to be in the 95 to 97 per cent range, we intend to continue to employ a balanced program of investigation and study of all women with the symptom of stress urinary incontinence. This will include both static cystourethrography to evaluate the status of the anatomic supports of the urethrovesical area and appropriate, carefully performed and interpreted urodynamic studies to evaluate the neurophysiologic aspects of the continence mechanism in our patients as well. Thomas H. Green, Jr., M.D. 8 Hawthorne Place Charles River Park Boston, Massachusetts 02114 REFERENCES
1. McGuire, E. J., Lytton, B., Pepe, V., and Kohorn, E. I.: Stress urinary incontinence, Obstet. Gynecol. 47: 255, 1976. 2. Beck, R. P., Arnusch, D., and King, C.: Results in treating 210 patients with detrusor overactivity incontinence of urine, AM. J. OBSTET. GYNECOL. 125: 593, 1976. 3. Hodgkinson, C. P.: Discussion of Fantl, J. A., Hurt, W. G., and Dunn, L. J.: Dysfunctional detrusor control, AM. J. OBSTET. GYNECOL. 129: 302, 197’7. 4. Green, T. H., Jr.: Urinary stress incontinence: Differential diagnosis, pathophysiology, and management, AM. J. OBSTET. GYNECOL. 122: 368, 1975.
Reply to Dr. Green To the Editors: Dr. Green’s letter, although emotionally based, neglects to appreciate that many current authors take strong issue with his interpretations and conclusions over the past quarter century. Although space is limited we are pleased to rebut the points raised by Dr. Green. The poor correlation between static cystourethrograms (CUG’s) and women with anatomic sphincterweakness stress urinary incontinence is clearly apparent in Table IIIB of our article. Approximately 82 per cent of patients whose problem was that of sensory
Correspondence
231
urgency alone or combined with unstable bladders had abnormal CUG’s, in keeping with Green’s radiographic criteria for stress urinary incontinence (SUI). On the other hand, only 69 per cent of patients with urodynamic and clinical evidence of SUI had CUG interpretations that confirmed this finding. This implies an 82 per cent false positive rate with Dr. Green’s radiographic technique. Although our article refers only to Greenwald’s paper* (1967) that strongly criticized Dr. Green’s technique, the literature contains ample other references (Crisp’and Mengert”) and specific statements we wish to quote. In chronologic order: Jones8 (1965) stated, “Any type of X-ray finding can occur in continent or incontinent patients”; Steinhausen and colleagues14 (1972) said, “An abnormal CUG does not necessarily indicate stress incontinence”; Kitzmiller and associates9 (1972) stated, “We conclude that no distinctive bladder neck abnormality as shown on chain cystourethrography is invariably or even usually associated with the presence or cure of stress incontinence.” Dr. Green criticized our use of barium paste rather than a metallic bead chain in performing static cystourethrography. Lowlo suggested the use of barium paste because it reduced distortion of anatomic detail caused by the chain to a minimum. Unnerus and coworkersls advocated the use of sterile barium sulfate suspension in their technique of urethrocystography. Dr. Shapiro recalls originally doing static cystourethrography with a metallic bead chain as advocated by Dr. Green and finding that the chain often fell out and that the use of barium paste was more reliable and gave more readily available “angles” to measure. Dr. Green thinks that he has only rarely observed detrusor contractions to occur during the course of the x-ray examination and that they were easily recognized by the irregular crenated outline of the contracting bladder. Bate? stated, “The first thing that happens when the bladder contracts is the same opening of the bladder neck with precisely the same loss of the angle. Jeffcoate himself makes this point and emphasizes the importance of ascertaining that the bladder is not contracting when the strain film is taken.” Finally, in a recent excellent monograph entitled Female Urinary Incontinence, StantonI has precisely summarized the distinct disadvantages of static CYStourethrography techniques as follows: “1) In normal women the posterior urethrovesical angle disappears when voiding commences, and the detrusor contracts. This sign, therefore, cannot be said to be present ‘at rest’ unless intrinsic bladder pressure measurements are made simultaneously with radiological screening to exclude detrusor contraction. Even when present, this sign may not be significant, as at rest some incontinent women have a normal posterior urethrovesical angle and some continent women have an abnormal angle; 2) *See reference 6 of original article.
Fk@y to Ck 4%Wum To the Editors: In his comment on our article “New concepts in dysmenorrhea,” Dr. Birnbaum directed attention to organic disease, including endometriosis, as a cause of dysmenorrhea, which is the secondary type. We wish to emphasize that the review was focused on primary 228
dysmenorrhea and this was stated at the beginning of the article. Secondary dysmenorrhea was briefly alluded to when the biochemical basis of the dysmenorrhea in such circumstances was similar to that in primary dysmenorrhea, namely, increased endometrial or menstrual fluid prostaglandins. We stated: “Irrespective of whether oral cdntraceptives exert their antidysmenorrheic effect throngh one or all of the above mechanisms, the clinical therapeutic effect of oral contraceptives in primary dysmenorrhea is well established . . There is almost always complete relief of dysmenorrhea with oral contraceptives, so that failure to respond would suggest an unusually large psychogenic component cont&buting to the pain.” We also pointed out, under “Symptoms and diagnosis of dysmenorrhea,” that: “Where it may be di%cult to differentiate primary dysmenorrhea from pelvic pains or secondary dysmenorrhea, the cause ofwhich is not clinically detectable, laparoscopy may be indicated.” Elence, contrary to Dr. Birnbaum’s conclusion, we do not use the criterion “failure to respond to oral contraceptives” as an indicator of psychosomatic illness unless pelvic organic disease has been ruled out. For thal matter, primary dysmenorrhea should not be diag nosed unless pelvic organic disease has been excluded. M. YusoJf Damood, M.D. Oh& Ylikarkala, M.D. Department of Obstetrics and Gynecology The New York Hos#&Corrzell Medical Center 525 East 68th Street New York, New York 10021
To the Editors: In their article, “Do static cystonrethrograms have a role in the mvestigation of female incontinence?” (AM. J. OBSTET. GYNECOL. 130: 516, 1978), Drs. Drutz, Shapiro, and Mandel recorded observations and rendered opinions so greatly at variance .with the experience of the vast majority of us working in this field during the past quarter century that I must .take strong issue with their interpretations and conclusions. I do so mainly on behalf of the countless present and future patients who do and will suffer fro’m the troublesome symptom of stress urinary incontinence .and whtih successful treatment will, as it always should, hinge on a careful and complete diagnostic evaluation, a vital segment of
Volume Number
132 2
which these authors groundlessly and cavalierly advocated should be discarded. Space does not allow a point-by-point discussion and rebuttal of what seem to be some erroneous concepts and fallacious conclusions regarding the general problem of the symptom of stress urinary incontinence expressed in this article, but a few items deserve brief comment. For example, it is not made clear in what way they found poor correlation between standard cystourethrograms in women with anatomic sphincterweakness (their phrase) stress urinary incontinence. This is very hard to understand and reconcile in view of the close correlation that we and many other groups working in this field during the past 25 years have consistently found to be the case. It should be noted that they used barium paste rather than a metallic bead chain to demonstrate the urethra and urethrovesical junction and recorded difficulties in outlining and identifying the urethra in a number of cases, so perhaps their technique was in part responsible for their “poor correlation.” And, as another example, their statement: “A detrusor contraction . . . cannot be distinguished from the classic SUI changes by static cystourethrography . .” has simply not been true in our experience. In carrying out cystourethrography with the metallic bead-chain technique in thousands of patients with the symptom of stress urinary incontinence during the past 25 years, we have only rarely observed detrusor contraction to occur during the course of the x-ray examination. In the few instances when it did occur it was easily recognized by the irregular, crenated outline of the contracting bladder, as seen on the x-ray film, and by the even more obvious loss of urine, and usually the metallic bead chain as well, while the films were being exposed. Such an event (the transient physiologic obliteration of the posterior urethrovesical (PUV) angle and rotational displacement of the urethral axis accompanying a detrusor contraction) can thus readily be distinguished from the permanent loss of the PUV angle and rotational descent of the urethra accompanying true anatomic stress incontinence due to deficient urethrovesical support. It will perhaps be more helpful to concentrate on just a few major examples of what seem to be misleading and unjustified conclusions drawn and opinions rendered and especially to comment on the two factors that could most likely account for their unusual experience-first, a seemingly unusual patient population and, second, quite possibly the manner in which the urodynamic studies were conducted. 1. In view of the very name of their clinic (Gynaecological Urology and Urodynamic Unit), it would be surprising if there were not an understandable difference in the referral pattern to such a combined urology-gynecology clinic, obviously specializing in complicated cases. The fact that pure stress urinary incontinence was rarely seen as the sole problem makes it almost certain that this unit is seeing an unusual and
Correspondence
229
highly selected population of women with urinary incontinence. Since their paper described only the techniques of study and did not include any clinical description of their patients, one has no way of knowing just what the symptoms were, how many had undergone one or more previous unsuccessful operations (such women are known to have a high incidence of urodynamic disorders, combinations of anatomic and urodynamic disorders, psychosomatic symptomatology, and iatrogenic urethral scarring and periurethral fibrosis, etc.), and how many previously had been studied and screened by their referring physicians and already were believed not to have straightforward true anatomic streSs incontinence. Year after year at our institution (The Massachusetts General Hospital, Boston, Massachusetts), 75 to 85 per cent of our patients suffering from the symptom of stress urinary incontinence prove to have true anatomic stress incontinence, unassociated with any urodynamic abnormality. The other 15 to 25 per cent have a variety of other mechanisms and disorders responsible for their symptoms-detrusor dyssynergia in 10 to 15 per cent and occasional fundamental neurological disorders, urethral diverticula, and urethral fibrosis in the remaining 5 to 10 per cent. In a recent personal series of 137 patients in the past four years, 78 per cent had pure anatomic stress incontinence, 17.5 per cent proved to have pure detrusor dyssynergia, and 4.5 per cent were found to have a combination of anatomic stress incontinence and detrusor dyssynergia. A report by McGuire and his associates’ is perhaps even more pertinent since it emanated from a combined gynecology-urology project established at Yale University Medical School that functioned in a manner quite like that of the unit of these authors. Using a similar detailed study program that included urodynamic and static cystourethrographic studies in all patients, they demonstrated 62 per cent of their patients to have pure anatomic stress incontinence, and an additional 22 per cent proved to have anatomic stress incontinence plus varying degrees of detrusor dyssynergia (almost all of this group were cured of anatomic stress incontinence by operation), and 9 per cent had pure detrusor dyssynergia. Parenthetically, Drutz, Shapiro, and Mandel seem to be unaware of the significance of this group of patients in whom both clear-cut anatomic stress incontinence and varying degrees of detrusor dyssynergia coexist. As experience accumulates, it is becoming clear that the detrusor dyssynergia in this special group disappears when, and only when, the anatomic weakness in the urethrovesical supporting mechanism is corrected surgically by the appropriate standard operative procedure for anatomic stress incontinence. In addition to the observations by McGuire and associates and our own recent parallel experience with this “combined problem” group, a similar experience has been recorded by Beck and co-workers* from the University of Alberta, Edmonton, Alberta, Canada.
230
Correspondence
2. It seems highly likely that the problems encountered by the authors in correlating information obwith their tained from “static cystourethrograms” “urodynamic studies” may also have stemmed in part from the inherent limitations and inaccuracies of the technique they used to evaluate the urodynamic situation in their patients, namely, the method of carbon dioxide gas retrograde urethrocystometry by means of the Browne-Robertson female carbon dioxide urethroscope and monitor. This technique has recently been criticized and the accuracy of the urodynamic observations made in this manner seriously questioned by several authorities. Hodgkinsong who, along with his urologic colleagues at Henry Ford Hospital in Detroit, Michigan abandoned its use after a careful trial, recently concisely summarized his reservations concerning retrograde carbon dioxide urethrocystometry. He pointed out that the information obtained in this way is no more helpful and probably less accurate than that provided by standard water cystometry, which also has its shortcomings and inaccuracies. He found that, in comparison with the far more physiologic direct electronic urethrocystometry, the retrograde carbon dioxide gas technique was not really an accurate or discriminating measure of the presence or absence or the degree of detrusor dyssynergia. Furthermore, he believes that in patients with a normal detrusor control mechanism the results of carbon dioxide gas urethrocystometry are often misleading and suggest detrusor irritability and dysfunction, when by all other parameters of study bladder function and its neurophysiologic control mechanisms are entirely normal. As a consequence he believes that in a number of recent publications, especially some emanating from Great Britain, an excessively high percentage of women have been reported to have “unstable bladders” among groups of women undergoing complete investigation for stress urinary incontinence and related bladder control disorders, this high incidence being erroneous and artifactual and simply incidental to the technique of urethrocystometry itself. In addition to the obvious potential problems with their technique of urethrocystometry, a technique that is not as accurate or infallible as they and others attempt to suggest, the authors actually do a disservice to the commendable progress made in the past decade toward a better understanding of the neurophysiologic mechanisms responsible for some types of female urinary incontinence by attempting to proclaim that the concept of urodynamics, and only urodynamics, explains everything. For those who wish to review again the facts of the other side of the coin, that is, the vast amount of evidence underlying the concepts of, the proper investigation of, and the appropriate treatment for the far more frequent and equally significant anatomic aspect of the problem (the one that gynecologic surgeons can successfully correct), along with a more realistic appraisal of the urodynamic side of the
September
1.5, 1978
Am. J. Obstet. C~WXO~.
coin, than that advanced by Drutz, Shapiro, and Mandel, reference could be made to a 1975 summary prepared for this same JOURNALS and especially to the publications of others working in this fascinating and challenging field included in the list of references at the end of that 1975 review article. What is needed in achieving proper understanding of some of the complexities of stress urinary iilcontinence and related disorders of micturitioil and its COW trol, and especially needed in the investigation and SUCcessful treatment of patients with the symptom of stress urinary incontinence, is not a tunnel vision that focuses only on the so-called “urodynamic” aspects. Rather, a broad vision is required, one that encompasses the all important urethrovesical anatomic support mechanism as well as the significant neurophysiologic and neuropharmacologic mechanisms (urodynamics) involved in producing the symptom of stress urinary incontinence. Fascinating and important as they are, these disorders of urodynamics, however, account for the symptom in only a relatively small percentage of the total population of patients with stress urinary incontinence. Since anatomic abnormalities of urethrovesical support are the fundamental cause in the vast majority of these women, and since the “static” cystourethrogram remains the one most accurate and highly objective means of assessing urethrovesical anatomic support, it should and will continue to play a very vital role, along with properly performed and carefulty interpreted urodynamic studies, in establishing the correct diagnosis, in selecting the optimal surgical procedure for those patients in whom operation is clearly indicated. and in assessing postoperatively whether or n~ot an adequate anatomic repair has been achieved. The final dogmatic recommendation of these authors that the use of cystourethrography in the study of female incontinence be abandoned is completely unjustified and cannot in any way contribute to, but rather is certain to prevent, a better understanding of and more successful efforts at correction of these troublesome disorders. Like one or two other authors who have criticized metallic bead-chain urethrocystograms during the past 15 years, these authors have stated the same clichk. a pseudoscientific one that is not as significant or meaningful as it might appear at first glance to the unwary, that it is a static measurement of dynamic function, and hence not of great value. It is revealing that they were able to cite only one reference that lends even limited support to their contention and chose to ignore the dozens of reports in the literature confirming that, where true anatomic stress incontinence is concerned, preoperative static urethrocystograms are highly accurate and valuable in establishing its presence and postoperative static cystourethrograms are equally reliable in demonstrating the anatomic reasons for success or failure of the surgical procedure to relieve the distressing symptom. Quite obviously they misunderstand the true purpose and vahle of rystoure-
Volume
132
Number
2
thrography, which is to evaluate the urethrovesical anatomic supporting mechanism, a mechanism that in the nonvoiding woman is fundamentally a constant and essentially static one. When defective, this mechanism can be exploited by the stress of a sudden increase in intra-abdominal pressure to produce abnormal urinary leakage, in the absence of any abnormal detrusor muscle activity whatsoever (i.e., in the absence of any abnormality of the patient’s so-called “urodynamics”) in the vast majority of instances. In point of fact, it is a failure of this static anatomic support mechanism that is the primary cause of the abnormal leakage of urine in 75 to 80 per cent of women with the symptom of stress urinary incontinence. And since our long-term cure rates following properly selected operations on patients with anatomic stress urinary incontinence, based on a minimum follow-up period of five years, continue to be in the 95 to 97 per cent range, we intend to continue to employ a balanced program of investigation and study of all women with the symptom of stress urinary incontinence. This will include both static cystourethrography to evaluate the status of the anatomic supports of the urethrovesical area and appropriate, carefully performed and interpreted urodynamic studies to evaluate the neurophysiologic aspects of the continence mechanism in our patients as well. Thomas H. Green, Jr., M.D. 8 Hawthorne Place Charles River Park Boston, Massachusetts 02114 REFERENCES
1. McGuire, E. J., Lytton, B., Pepe, V., and Kohorn, E. I.: Stress urinary incontinence, Obstet. Gynecol. 47: 255, 1976. 2. Beck, R. P., Arnusch, D., and King, C.: Results in treating 210 patients with detrusor overactivity incontinence of urine, AM. J. OBSTET. GYNECOL. 125: 593, 1976. 3. Hodgkinson, C. P.: Discussion of Fantl, J. A., Hurt, W. G., and Dunn, L. J.: Dysfunctional detrusor control, AM. J. OBSTET. GYNECOL. 129: 302, 197’7. 4. Green, T. H., Jr.: Urinary stress incontinence: Differential diagnosis, pathophysiology, and management, AM. J. OBSTET. GYNECOL. 122: 368, 1975.
Reply to Dr. Green To the Editors: Dr. Green’s letter, although emotionally based, neglects to appreciate that many current authors take strong issue with his interpretations and conclusions over the past quarter century. Although space is limited we are pleased to rebut the points raised by Dr. Green. The poor correlation between static cystourethrograms (CUG’s) and women with anatomic sphincterweakness stress urinary incontinence is clearly apparent in Table IIIB of our article. Approximately 82 per cent of patients whose problem was that of sensory
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urgency alone or combined with unstable bladders had abnormal CUG’s, in keeping with Green’s radiographic criteria for stress urinary incontinence (SUI). On the other hand, only 69 per cent of patients with urodynamic and clinical evidence of SUI had CUG interpretations that confirmed this finding. This implies an 82 per cent false positive rate with Dr. Green’s radiographic technique. Although our article refers only to Greenwald’s paper* (1967) that strongly criticized Dr. Green’s technique, the literature contains ample other references (Crisp’and Mengert”) and specific statements we wish to quote. In chronologic order: Jones8 (1965) stated, “Any type of X-ray finding can occur in continent or incontinent patients”; Steinhausen and colleagues14 (1972) said, “An abnormal CUG does not necessarily indicate stress incontinence”; Kitzmiller and associates9 (1972) stated, “We conclude that no distinctive bladder neck abnormality as shown on chain cystourethrography is invariably or even usually associated with the presence or cure of stress incontinence.” Dr. Green criticized our use of barium paste rather than a metallic bead chain in performing static cystourethrography. Lowlo suggested the use of barium paste because it reduced distortion of anatomic detail caused by the chain to a minimum. Unnerus and coworkersls advocated the use of sterile barium sulfate suspension in their technique of urethrocystography. Dr. Shapiro recalls originally doing static cystourethrography with a metallic bead chain as advocated by Dr. Green and finding that the chain often fell out and that the use of barium paste was more reliable and gave more readily available “angles” to measure. Dr. Green thinks that he has only rarely observed detrusor contractions to occur during the course of the x-ray examination and that they were easily recognized by the irregular crenated outline of the contracting bladder. Bate? stated, “The first thing that happens when the bladder contracts is the same opening of the bladder neck with precisely the same loss of the angle. Jeffcoate himself makes this point and emphasizes the importance of ascertaining that the bladder is not contracting when the strain film is taken.” Finally, in a recent excellent monograph entitled Female Urinary Incontinence, StantonI has precisely summarized the distinct disadvantages of static CYStourethrography techniques as follows: “1) In normal women the posterior urethrovesical angle disappears when voiding commences, and the detrusor contracts. This sign, therefore, cannot be said to be present ‘at rest’ unless intrinsic bladder pressure measurements are made simultaneously with radiological screening to exclude detrusor contraction. Even when present, this sign may not be significant, as at rest some incontinent women have a normal posterior urethrovesical angle and some continent women have an abnormal angle; 2) *See reference 6 of original article.
