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The detrusor muscle and urinary incontinence
The detrusor muscle and urinary incontinence R.
P.
BECK,
E.
A.
THOMAS,
G.
B.
MAUGHAN,
Montreal,
M.D.,
C.M.* M.D. M.D.,
C.M.,
M.Sc.
Quebec
1 N T E R E s T in detrusor muscle action has been stimulated by observations made during investigation into the problem of urinary stress incontinence at the Royal Victoria Hospital.1-4 A common type of stress incontinence due to pressure equalization between the urethra and bladder has been described.’ Clinically these patients lose a spurt of urine synchronously with cough when the intravesical pressure increases and equals the intraurethral pressure. Even with a full bladder the urine loss with cough is small in these cases. The incontinence ends abruptly with the cessation of the stress. It became obvious that there was another stress, lost large patient type who, with amounts of urine in a stream or gush as though voiding, frequently at the end of, or shortly after, cough. Often the patient gave a history of losing urine only after repeated coughing, and noted that the incontinence was worse in cold weather and when standing. This type of patient was not stress incontinent with resting urine volumes as was the former group. In these cases, simultaneous intraurethral and intravesical pressure studies
with a “non-full” bladder would indicate, with stress, an intraurethral pressure higher than the intravesical pressure, explaining continence under these conditions. When their bladders felt full these patients did not have urgency incontinence, but with coughing they lost large amounts of urine without warning. It appeared that the latter group of patients was stress incontinent as the result of an overactive detrusor muscle, whose action was triggered by stress. On the basis of this supposition, it was decided that the detrusor muscle in normal patients should be studied and compared with detrusor action in the latter group of incontinent patients. Method
by a grant from the Medical Council of Canada.
Presented at the Twenty-first Annual Meeting of the Society of Obstetricians and Gynaecologists of Canada, Halifax, Nooa Scotia, June 11-13, 1965. *Present address: Department Obstetrics an< Gynecology, $bne;pa Hospztal, Edmonton, a .
of University Alberta,
materials
Fifty-four patients without neurologic problems and without urinary symptoms, residual urine, demonstrable incontinence, or abnormal microscopic urine findings were chosen as suitable normal cases for the study of detrusor action. In order to create a starting point for these studies, each patient was asked to drink 1,500 C.C. of fluid over a half hour period and given a diuretic at the end of that time. When the patient felt a strong urge to void, a polyethylene catheter (outside diameter 4 mm.) with a terminal 6 mm. latex balloon was inserted into the bladder. The catheter had previously been connected to a transducer creating a fluid-filled, air-free system. The electromanometer of the Sanborn recording unit was calibrated to indicate pressure changes of 2 mm. Hg per small division on the recording graph paper. The paper speed was set at 2.5 mm. per second. After
From the Departments of Obstetrics and Gynaecology, McGill University and the Royal Victoria Hospital. Supported Research
and
of
483
484
February Am. J. Obst.
Beck, Thomas, and Maughan
taking a base-line pressure recording of the full bladder, the patient was asked to cough, to void, and then to strain at micturition but avoid urine loss by contracting the pelvic floor. Coughing, straining, and forceful heel-bouncing (to simulate walking) were carried out in the standing position. After 28 patients had been tested in this manner, another 26 were tested in the same way, and in addition were given a parasympathomimetic drug (carbamylcholine chloride,* 0.125 mg. subcutaneously) to observe its action on the detrusor muscle of a full bladder. After the drug had been given, the patients were asked to suppress micturition actively during the rest of the pressure testing. The bladder was then emptied by catheterization and the urine volume measured. Thirty-nine incontinent patients who failed to show a stress equalization-type incontinence with a “non-full” bladder but who, with a full bladder, either (a) lost urine spontaneously, i.e., had urgency incontinence, or (b) lost large amounts of urine with stress, were selected for detrusor activity studies. The same routine used in the normal series was followed except that no parasympathomimetic drug was given. It should be emphasized that all of these patients were asked to suppress the desire to void at all times. After 18 incontinent patients were tested to establish the pattern of an overactive detrusor muscle, another 21 similar patients were given a parasympatholytic ‘Carbachol.
15, 1966 & Gyncc.
drug (propantheline bromide,* 10 to 30 mg. intramuscularly) to determine its effect on the irritable detrusor. Microscopic urinalysis was done in all cases. Some, but not all, of the incontinent patients had urine cultures and cystoscopic examination at the time of pressure testing. Results The normal resting intravesical pressure with 200 C.C. of urine is 2 to 4 mm. Hg in the lithotomy position and 15 to 20 mm. Hg in the standing position. In the 54 normal patients with urine volumes of 500 to 1,200 cc. there was no elevation in the intravesical pressure above these base lines while voiding was suppressed. However, when voiding was in progress a smooth pressure curve elevation was described as result of detrusor contraction (Fig. 1) . Intra-abdominal pressure changes with coughing, deep breathing, and straining were, of course, reflected in the bladder pressure, but none produced the smooth curved elevation seen when the patient voided (Fig. 1). Parasympathomimetic drug administration to the 26 normal cases (with full bladders) spontaneous detrusor pressure produced curves and unavoidable urine loss in 8 cases (Fig. 2) ; a slight but constant rise in baseline pressure in 10 cases (Fig. 2) and no urine loss; no pressure changes whatsoever in 7 cases; and in one case an increase in the desire to void but no rise in intravesical pressure. In the 39 patients with incontinence, de*Probanthine.
Fig. 1. Normal bladder pressures in lithotomy and standing positions at cough and voiding. Intravesical pressure recording of a bladder containing 1,000 CL of fluid. Each fine division represents 2 mm. Hg. Arrow 1 points to pressure in lithotomy position. Arrow 2 shows cough pressure spike; note the prompt return to a constant pressure. Arrow 3 points to pressure rise on standing. Arrow 4 points to cough pressure spike preceded and followed by minor pressure fluctuations caused by deep breathing. Arrow 5 shows pressure rise caused by detrusor contraction at voiding.
Volume Number
94 4
Detrusor
muscle
and
urinary
incontinence
Fig. 2. Isotonic and isometric contraction of detrusor muscle. Top tracing shows isotonic contraction of detrusor muscle of full bladder 5 minutes after Carbachol injection. Arrow 1 points to intravesical pressure in lithotomy position. Arrows 2 and 3 point to detrusor contractions and urine loss. Bottom tracing shows isometric contraction of detrusor muscle of full bladder in another case. Arrow 4 points to base-line tracing of intravesical pressure, and Arrow 5 to a fairly sustained intravesical pressure increase 5 minutes after Carbachol injection.
Fig. 3. Hyperactive detrusor muscle stimulated by cough. Upper tracing is of the pressure ; lower tracing represents pressure at various points in the urethra. Arrows represent simultaneous intraurethral and intravesical pressures with a resting urine Patient was not incontinent at that time because intraurethral pressure was at all times than intravesical pressure. Arrow 3 indicates commencement of intravesical tracing lithotomy position after bladder felt full. Arrow 4 indicates cough pressure spike. The pressure which follows (Arrow 5) is caused by a detrusor contraction which resulted loss. Arrow 6 points to rise in pressure upon standing, and Arrow 7 to a heel-bounce by a detrusor contraction curve and urine loss.
bladder 1 and 2 volume. greater in the rise in in urine followed
485
486
Beck,
Thomas,
and
February Am. J. Obst.
Maughan
15, 1966 & Gynec.
Fig. 4. Parasympatholytic drug action on irritable detrusor muscle. Intravesical pressure tracing showing spontaneous detrusor contractions which responded to Probanthine injection. The drug was administered at Arrow I and two detrusor contractions were recorded. The graph paper was stopped at Arrow 2 until oscillations ceased (20 minutes), and then restarted to show the tranquilizing effect of the parasympatholytic drug on the irritable detrusor.
beyond volitional control were seen in all cases. In 8 cases, there were spontaneous detrusor contractions with urine loss while the patient was in the lithotomy position. In 14 cases, there were no detrusor contractions or urine loss while in the lithotomy position, but as soon as the patients stood up detrusor contractions with urine loss started. In the other 17 cases, detrusor contractions and incontinence were triggered by coughing or heel-bouncing (Fig. 3). When the simultaneous intraurethral and intravesical pressure studies of the latter 17 cases were reviewed, it was noted that in every case, although the intraurethral pressure was greater than the intravesical pressure with cough, the pressure differential between the two structures was small, as result of a low trusor
urethral
contractions
pressure
effect
in
one
case,
a scar
2 cases, and a high intraabdominal pressure effect in 14 cases.* Parasympatholytic drug administration to 21 of these 39 patients eliminated the desire to void and detrusor contractions in 7 cases (Fig. 4) ; it had no effect on the desire to void or on contractions in 9 cases; it reduced the magnitude of contractions but not the desire to void in 3 cases; it eliminated the desire to void but not detrusor contractions in one case; and in one case the effect of the drug was uncertain. tissue
effect
in
Comment The work of Denny-Brown and Robertson,S in 1933, on bladder physiology has been firmly entrenched in textbook? and the
minds of students of medicine. These workers reported that as the bladder filled there was a gradual but progressive increase in bladder pressure as 50 cc. lots of water were injected into the bladder. They also observed that an intense desire to pass urine was accompanied by a rise in intravesical pressure, and that when a patient decided to void there was a rise in intravesical pressure prior to the commencement of voiding. Our observations on the normal detrusor muscle would indicate that these three basic observations by Denny-Brown and Robertson” are incorrect. Our findings are more in agreement with those of Hodgkinson and associates.F, ’ The bladder appears capable of tremendous distention without any rise in intravesical pressure. The urge to void is not associated with any intravesical pressure rise. The intravesical pressure does rise, however, when the patient gives in to the desire to, and does, void. The likely reason for this disagreement with Denny-Brown and Robertson’s work” is the use of a more physiologic way to fill the bladder and the benefit of better pressure recording apparatus. The effect of ‘parasympathetic drug stimulation producing contraction pressure curves in some cases and a constant pressure rise in others indicates that the detrusor muscle can undergo isotonic and probably isometric contraction. The failure of the drug to produce detrusor contraction in spite of an intense desire to void indicates the tranquilizing effect that volitional control can exert over the detrusor.
Volume Number
94 4
Detrusor
The 8 patients who lost urine spontaneously in the lithotomy position certainly should be considered urgency incontinent cases. The 14 patients who stood up and immediately became incontinent, for practical purposes (i.e., clinical diagnostic purposes) also had urgency incontinence, but it should be remembered that these latter cases were actually subjected to the stress of an increased intravesical pressure (at least 15 to 20 mm. Hg) which normally occurs on standing. The other 17 cases were incontinent as result of detrusor activity being triggered by coughing or heel-bouncing (which cause intravesical pressure rises of up to 90 and 40 mm. Hg, respectively) acting in conjunction with a poor intraurethralintravesical pressure differential. These latter cases, therefore, present the combined clinical features of detrusor incontinence and pressure equalization (or “pure” stress) incontinence. The fact that some of these detrusor overactivity cases were tranquilized by a parasympatholytic drug may indicate that detrusor overactivity in some cases may be a neurogenic problem, produced by para-
Fig. 5. Pressure tracings of patient with abnormal detrusor muscle. Simultaneous intraurethral (lower) between ential to indicates bladder. operative 5). After as in Fig.
muscle
and
urinary
incontinence
487
sympathetic overactivity, like the spastic colon syndrome. Bladder infection is, undoubtedly, the most common cause of detrusor overactivity whether it is a detrusor overactivity incontinence triggered by stress or an urgency type of incontinence. We noted with great interest 2 patients with the detrusor overactivity type of stress incontinence in whom probantheline bromide was ineffective and in whom there was no evidence of bladder infection. The detrusor overactivity in these 2 cases was cured by the restoration of the bladder neck to proper position at anterior colporrhaphy for marked cystocele (Fig. 5). It may be that abnormal descent of the bladder neck, especially in the standing position, may trigger the detrusor muscle. Any patient coming to our clinic who demonstrates stress incontinence (without urgency incontinence) is first tested for a pressure type of incontinence which, if diagnosed, is treated accordingly. If the patient does not have a pressure type of incontinence, the bladder is “filled,” a detrusor pressure tracing is taken as described, and
descent
of bladder
and intravesical
neck
(upper)
and
an irritable
pressure tracing pressure differ-
Arrows I and 2 indicates a borderline but adequate urethral-vesical maintain continence. Note high intra-abdominal pressure effect at Arrow 2. Arrow 3 the start of an intravesical-intraurethral pressure tracing in the same case with full With each detrusor curve in the upper tracing, urine was lost. Arrow 4 shows posturethral-vesical pressure tracing in which there is less high pressure effect (Arrow operation the patient was no longer incontinent, and the detrusor tracing was normal 1.
488
February Am. J. Obst.
Beck, Thomas, and Maughan
the effect of a parasympatholytic drug is noted. A detrusor incontinent patient can be distinguished from a patient who voids because the latter does not show a detrusor contraction with cough during the testing. When the detrusor is found to be overactive, urinary infection is carefully looked for and cleared up by appropriate treatment. Should the parasympatholytic drug be effective, a trial on that drug is instituted. If there is no bladder infection and the parasympatholytic drug trial is unsuccessful, abnormal descent of the bladder neck is considered as a possible cause of the detrusor overactivity. Whenever restoration of the bladder neck reduces the detrusor to proper position anterior colporrhaphy is conoveractivity, sidered, and an all-out effort is made to correct the borderline urethral-bladder pressure ,gradient.4 Such surgery should never be carried out when there is a reduced
15, 1966 & Gym.
bladder capacity or neurogenic bladder. Treatment of urgency incontinence is directed to correction of a reduced bladder capacity and eradication of infection. In cases where parasympatholytic drugs tranquilize the irritable detrusor at pressure testing, use of these drugs should be considered at least as adjunctive therapy. Summary In addition to stress incontinence produced by urethral-bladder pressure equalization at stress, there is another type of incontinence wherein a hyperactive detrusor muscle, sensitized by stress, in the presence of a borderline urethral-vesical pressure differential, causes involuntary urine loss without warning. This latter incontinence is not urgency incontinence, although both are caused by an overactive detrusor muscle.
REFERENCES
Beck, OBST. Beck.
R. P., and Maughan. G. B.: AM. J. & GYNEC. 89: 746, 1964. R. P.. and Hsu. N.: AM. ”I. OBST. & GYN~C. 89: 738, 1964. ’ Beck, R. P., and Hsu, N.: AM. J. OBST. & GYNEC. 91: 820, 1965. Beck, R. P., Hsu, N., and Maughan, G. B.: AM. J. OBST. C GYNEC. 91: 314, 1965.
Denny-Brown, D., and Robertson, 56: 149, 1933. Hodgkinson, C. P., Ayers, M. A., B. H.: AM. T. OBST. & GYNEC. Hodgkinson,“C. P., and Cobert, OBST. & GYNEC. 79: 648, 1960. Wright, 8: Applied Physiology, 1952, Oxford University Press,
E. G.:
Brain
and Drukker, 87: 717. 1963. N.: AM. J. ed. 9, London, p. 767.
Discussion DR.
MICHEL
The ever-difficult
J. BERARD, therapeutic
Montreal, Quebec. problem of female
stress incontinence is confirmed by the many reports of procedures and hypotheses, suggestions, and fantasies devised to lower the incidence of surgical failures. More and more, the emphasis is on accurate diagnosis, resulting from meticulous investigations in all cases. The work of Denny-Brown and Robertson in 1933 seemed to answer many questions about the control of and their teaching prevailed for micturition, many years but some had doubts based on empirical and experimental observations. Hodgkinson challenged it conclusively around 1960 and Beck’s work renders a differential diagnosis more possible. We have nowadays to differentiate urgency incontinence, and stress incontinence, the incontinence due to the detrusor muscle. Urethrocystometry devised by Hodgkinson and
used by Beck seems to have gained its useful place in the work-up of the incontinent patient. Being no expert myself, I wonder this apparatus one can differentiate
if in using between the
contractions of the bladder itself and the contractions induced by the foreign body within the urethra, the balloon and catheter. A colleague in urology tells me that a small transmitter placed in the bladder is being used in a parallel study on the role of the detrusor. The methodology of Dr. Beck’s clinical investigation was well conceived and well controlled. Yet apart from my remark about the inherent contractions of the bladder and the possibly “balloon-induced” waves due to the foreign body, I wonder if another variable factor is not introduced. It seems to me that the pressure in the bladder is recorded through a direct system, whereas the pressure from the
Volume 94 Number 4
urethra is conducted through a closed circuit. Can we also consider as an entirely normal condition, the rapid excretion of urine secondary to the action of a diuretic after drinking 1,500 cc. in half an hour? Personally I think an artifact is introduced by injecting in addition to the diuretic, a parasympathomimetic drug, in order to observe its action on the detrusor muscle of a full bladder. The bladder, emptied by catheterization, is being tested for residual urine and not strictly speaking for detrusor activity, because it has been medically transformed. Hodgkinson has proved that “. . . the response to anticholinergic drugs is both unpredictable and unexplainable . . .” in cases he considered to be of the “dyssynergic detrusor dysfunction” variety. It is generally agreed that the motor function of the detrusor is through the pelvic parasympathetic nerves (S,, S,, and S,) . Bladder reflexes are mediated through the sacral cord at these neurologic levels. Clinical observations have shown that the patient with a normal function of her detrusor frequently cannot void or does with difficulty after atropine or atropine-like drugs which paralyze the bladder. There is agreement that the bladder and urethra in the active erect woman are subjected continuously to external pressure influences of unpredictable height and frequency. During walking gravitation has a positive and a negative influence, these balancing each other. Many researchers admit difficulties of interpretation with the accepted theories of micturition because of the variable relationship of the bladder and urethral pressures during voiding. Hodgkinson speculates that the urethral sphinc-
Detrusor
muscle and urinary
incontinence
489
teric closing mechanism is relatively passive, that it is probably opened by sustained elevation of intravesical pressure from any source and that, once open, it remains so until the pressure is lowered or the bladder emptied. I wonder, therefore, why coughing, walking, or squatting should not start this chain reaction in these patients with a “borderline” urethral-vesical pressure differential, without having to introduce a notion of dysfunction of the detrusor. On the other hand, Adler has observed that ‘L. . . only induction of urination is voluntary, once the sphincter is relaxed the further course is automatic. . . .” Do we wish, therefore, to explain incontinence due to an hyperactive detrusor muscle? I am tempted to offer a parallelism with the “reflex neurogenic bladder,” in which the complete removal of higher center control, reduces the status of the bladder to a simple reflex organ, whose activity is dependent solely upon the primary reflex arc through the sacral cord. Might it not be possible, in Dr. Beck’s cases, that we are confronted with patients suffering from latent degenerating disease of the multiple sclerosis type or of a minimally important damage to the pelvic parasympathetic nerves or plexus? I would have liked to have been told of the age and parity of these patients, because I could speculate that a degenerative process or “l’accouchement” having damaged the parasympathetic circuit might alIow a transitory reversion to a form of a “reflex neurogenic bladder.” Voluntary control might then still stop the chain reaction, once the stress is gone in those patients with a borderline urethral-vesical pressure differential.
P.
BECK,
E.
A.
THOMAS,
G.
B.
MAUGHAN,
Montreal,
M.D.,
C.M.* M.D. M.D.,
C.M.,
M.Sc.
Quebec
1 N T E R E s T in detrusor muscle action has been stimulated by observations made during investigation into the problem of urinary stress incontinence at the Royal Victoria Hospital.1-4 A common type of stress incontinence due to pressure equalization between the urethra and bladder has been described.’ Clinically these patients lose a spurt of urine synchronously with cough when the intravesical pressure increases and equals the intraurethral pressure. Even with a full bladder the urine loss with cough is small in these cases. The incontinence ends abruptly with the cessation of the stress. It became obvious that there was another stress, lost large patient type who, with amounts of urine in a stream or gush as though voiding, frequently at the end of, or shortly after, cough. Often the patient gave a history of losing urine only after repeated coughing, and noted that the incontinence was worse in cold weather and when standing. This type of patient was not stress incontinent with resting urine volumes as was the former group. In these cases, simultaneous intraurethral and intravesical pressure studies
with a “non-full” bladder would indicate, with stress, an intraurethral pressure higher than the intravesical pressure, explaining continence under these conditions. When their bladders felt full these patients did not have urgency incontinence, but with coughing they lost large amounts of urine without warning. It appeared that the latter group of patients was stress incontinent as the result of an overactive detrusor muscle, whose action was triggered by stress. On the basis of this supposition, it was decided that the detrusor muscle in normal patients should be studied and compared with detrusor action in the latter group of incontinent patients. Method
by a grant from the Medical Council of Canada.
Presented at the Twenty-first Annual Meeting of the Society of Obstetricians and Gynaecologists of Canada, Halifax, Nooa Scotia, June 11-13, 1965. *Present address: Department Obstetrics an< Gynecology, $bne;pa Hospztal, Edmonton, a .
of University Alberta,
materials
Fifty-four patients without neurologic problems and without urinary symptoms, residual urine, demonstrable incontinence, or abnormal microscopic urine findings were chosen as suitable normal cases for the study of detrusor action. In order to create a starting point for these studies, each patient was asked to drink 1,500 C.C. of fluid over a half hour period and given a diuretic at the end of that time. When the patient felt a strong urge to void, a polyethylene catheter (outside diameter 4 mm.) with a terminal 6 mm. latex balloon was inserted into the bladder. The catheter had previously been connected to a transducer creating a fluid-filled, air-free system. The electromanometer of the Sanborn recording unit was calibrated to indicate pressure changes of 2 mm. Hg per small division on the recording graph paper. The paper speed was set at 2.5 mm. per second. After
From the Departments of Obstetrics and Gynaecology, McGill University and the Royal Victoria Hospital. Supported Research
and
of
483
484
February Am. J. Obst.
Beck, Thomas, and Maughan
taking a base-line pressure recording of the full bladder, the patient was asked to cough, to void, and then to strain at micturition but avoid urine loss by contracting the pelvic floor. Coughing, straining, and forceful heel-bouncing (to simulate walking) were carried out in the standing position. After 28 patients had been tested in this manner, another 26 were tested in the same way, and in addition were given a parasympathomimetic drug (carbamylcholine chloride,* 0.125 mg. subcutaneously) to observe its action on the detrusor muscle of a full bladder. After the drug had been given, the patients were asked to suppress micturition actively during the rest of the pressure testing. The bladder was then emptied by catheterization and the urine volume measured. Thirty-nine incontinent patients who failed to show a stress equalization-type incontinence with a “non-full” bladder but who, with a full bladder, either (a) lost urine spontaneously, i.e., had urgency incontinence, or (b) lost large amounts of urine with stress, were selected for detrusor activity studies. The same routine used in the normal series was followed except that no parasympathomimetic drug was given. It should be emphasized that all of these patients were asked to suppress the desire to void at all times. After 18 incontinent patients were tested to establish the pattern of an overactive detrusor muscle, another 21 similar patients were given a parasympatholytic ‘Carbachol.
15, 1966 & Gyncc.
drug (propantheline bromide,* 10 to 30 mg. intramuscularly) to determine its effect on the irritable detrusor. Microscopic urinalysis was done in all cases. Some, but not all, of the incontinent patients had urine cultures and cystoscopic examination at the time of pressure testing. Results The normal resting intravesical pressure with 200 C.C. of urine is 2 to 4 mm. Hg in the lithotomy position and 15 to 20 mm. Hg in the standing position. In the 54 normal patients with urine volumes of 500 to 1,200 cc. there was no elevation in the intravesical pressure above these base lines while voiding was suppressed. However, when voiding was in progress a smooth pressure curve elevation was described as result of detrusor contraction (Fig. 1) . Intra-abdominal pressure changes with coughing, deep breathing, and straining were, of course, reflected in the bladder pressure, but none produced the smooth curved elevation seen when the patient voided (Fig. 1). Parasympathomimetic drug administration to the 26 normal cases (with full bladders) spontaneous detrusor pressure produced curves and unavoidable urine loss in 8 cases (Fig. 2) ; a slight but constant rise in baseline pressure in 10 cases (Fig. 2) and no urine loss; no pressure changes whatsoever in 7 cases; and in one case an increase in the desire to void but no rise in intravesical pressure. In the 39 patients with incontinence, de*Probanthine.
Fig. 1. Normal bladder pressures in lithotomy and standing positions at cough and voiding. Intravesical pressure recording of a bladder containing 1,000 CL of fluid. Each fine division represents 2 mm. Hg. Arrow 1 points to pressure in lithotomy position. Arrow 2 shows cough pressure spike; note the prompt return to a constant pressure. Arrow 3 points to pressure rise on standing. Arrow 4 points to cough pressure spike preceded and followed by minor pressure fluctuations caused by deep breathing. Arrow 5 shows pressure rise caused by detrusor contraction at voiding.
Volume Number
94 4
Detrusor
muscle
and
urinary
incontinence
Fig. 2. Isotonic and isometric contraction of detrusor muscle. Top tracing shows isotonic contraction of detrusor muscle of full bladder 5 minutes after Carbachol injection. Arrow 1 points to intravesical pressure in lithotomy position. Arrows 2 and 3 point to detrusor contractions and urine loss. Bottom tracing shows isometric contraction of detrusor muscle of full bladder in another case. Arrow 4 points to base-line tracing of intravesical pressure, and Arrow 5 to a fairly sustained intravesical pressure increase 5 minutes after Carbachol injection.
Fig. 3. Hyperactive detrusor muscle stimulated by cough. Upper tracing is of the pressure ; lower tracing represents pressure at various points in the urethra. Arrows represent simultaneous intraurethral and intravesical pressures with a resting urine Patient was not incontinent at that time because intraurethral pressure was at all times than intravesical pressure. Arrow 3 indicates commencement of intravesical tracing lithotomy position after bladder felt full. Arrow 4 indicates cough pressure spike. The pressure which follows (Arrow 5) is caused by a detrusor contraction which resulted loss. Arrow 6 points to rise in pressure upon standing, and Arrow 7 to a heel-bounce by a detrusor contraction curve and urine loss.
bladder 1 and 2 volume. greater in the rise in in urine followed
485
486
Beck,
Thomas,
and
February Am. J. Obst.
Maughan
15, 1966 & Gynec.
Fig. 4. Parasympatholytic drug action on irritable detrusor muscle. Intravesical pressure tracing showing spontaneous detrusor contractions which responded to Probanthine injection. The drug was administered at Arrow I and two detrusor contractions were recorded. The graph paper was stopped at Arrow 2 until oscillations ceased (20 minutes), and then restarted to show the tranquilizing effect of the parasympatholytic drug on the irritable detrusor.
beyond volitional control were seen in all cases. In 8 cases, there were spontaneous detrusor contractions with urine loss while the patient was in the lithotomy position. In 14 cases, there were no detrusor contractions or urine loss while in the lithotomy position, but as soon as the patients stood up detrusor contractions with urine loss started. In the other 17 cases, detrusor contractions and incontinence were triggered by coughing or heel-bouncing (Fig. 3). When the simultaneous intraurethral and intravesical pressure studies of the latter 17 cases were reviewed, it was noted that in every case, although the intraurethral pressure was greater than the intravesical pressure with cough, the pressure differential between the two structures was small, as result of a low trusor
urethral
contractions
pressure
effect
in
one
case,
a scar
2 cases, and a high intraabdominal pressure effect in 14 cases.* Parasympatholytic drug administration to 21 of these 39 patients eliminated the desire to void and detrusor contractions in 7 cases (Fig. 4) ; it had no effect on the desire to void or on contractions in 9 cases; it reduced the magnitude of contractions but not the desire to void in 3 cases; it eliminated the desire to void but not detrusor contractions in one case; and in one case the effect of the drug was uncertain. tissue
effect
in
Comment The work of Denny-Brown and Robertson,S in 1933, on bladder physiology has been firmly entrenched in textbook? and the
minds of students of medicine. These workers reported that as the bladder filled there was a gradual but progressive increase in bladder pressure as 50 cc. lots of water were injected into the bladder. They also observed that an intense desire to pass urine was accompanied by a rise in intravesical pressure, and that when a patient decided to void there was a rise in intravesical pressure prior to the commencement of voiding. Our observations on the normal detrusor muscle would indicate that these three basic observations by Denny-Brown and Robertson” are incorrect. Our findings are more in agreement with those of Hodgkinson and associates.F, ’ The bladder appears capable of tremendous distention without any rise in intravesical pressure. The urge to void is not associated with any intravesical pressure rise. The intravesical pressure does rise, however, when the patient gives in to the desire to, and does, void. The likely reason for this disagreement with Denny-Brown and Robertson’s work” is the use of a more physiologic way to fill the bladder and the benefit of better pressure recording apparatus. The effect of ‘parasympathetic drug stimulation producing contraction pressure curves in some cases and a constant pressure rise in others indicates that the detrusor muscle can undergo isotonic and probably isometric contraction. The failure of the drug to produce detrusor contraction in spite of an intense desire to void indicates the tranquilizing effect that volitional control can exert over the detrusor.
Volume Number
94 4
Detrusor
The 8 patients who lost urine spontaneously in the lithotomy position certainly should be considered urgency incontinent cases. The 14 patients who stood up and immediately became incontinent, for practical purposes (i.e., clinical diagnostic purposes) also had urgency incontinence, but it should be remembered that these latter cases were actually subjected to the stress of an increased intravesical pressure (at least 15 to 20 mm. Hg) which normally occurs on standing. The other 17 cases were incontinent as result of detrusor activity being triggered by coughing or heel-bouncing (which cause intravesical pressure rises of up to 90 and 40 mm. Hg, respectively) acting in conjunction with a poor intraurethralintravesical pressure differential. These latter cases, therefore, present the combined clinical features of detrusor incontinence and pressure equalization (or “pure” stress) incontinence. The fact that some of these detrusor overactivity cases were tranquilized by a parasympatholytic drug may indicate that detrusor overactivity in some cases may be a neurogenic problem, produced by para-
Fig. 5. Pressure tracings of patient with abnormal detrusor muscle. Simultaneous intraurethral (lower) between ential to indicates bladder. operative 5). After as in Fig.
muscle
and
urinary
incontinence
487
sympathetic overactivity, like the spastic colon syndrome. Bladder infection is, undoubtedly, the most common cause of detrusor overactivity whether it is a detrusor overactivity incontinence triggered by stress or an urgency type of incontinence. We noted with great interest 2 patients with the detrusor overactivity type of stress incontinence in whom probantheline bromide was ineffective and in whom there was no evidence of bladder infection. The detrusor overactivity in these 2 cases was cured by the restoration of the bladder neck to proper position at anterior colporrhaphy for marked cystocele (Fig. 5). It may be that abnormal descent of the bladder neck, especially in the standing position, may trigger the detrusor muscle. Any patient coming to our clinic who demonstrates stress incontinence (without urgency incontinence) is first tested for a pressure type of incontinence which, if diagnosed, is treated accordingly. If the patient does not have a pressure type of incontinence, the bladder is “filled,” a detrusor pressure tracing is taken as described, and
descent
of bladder
and intravesical
neck
(upper)
and
an irritable
pressure tracing pressure differ-
Arrows I and 2 indicates a borderline but adequate urethral-vesical maintain continence. Note high intra-abdominal pressure effect at Arrow 2. Arrow 3 the start of an intravesical-intraurethral pressure tracing in the same case with full With each detrusor curve in the upper tracing, urine was lost. Arrow 4 shows posturethral-vesical pressure tracing in which there is less high pressure effect (Arrow operation the patient was no longer incontinent, and the detrusor tracing was normal 1.
488
February Am. J. Obst.
Beck, Thomas, and Maughan
the effect of a parasympatholytic drug is noted. A detrusor incontinent patient can be distinguished from a patient who voids because the latter does not show a detrusor contraction with cough during the testing. When the detrusor is found to be overactive, urinary infection is carefully looked for and cleared up by appropriate treatment. Should the parasympatholytic drug be effective, a trial on that drug is instituted. If there is no bladder infection and the parasympatholytic drug trial is unsuccessful, abnormal descent of the bladder neck is considered as a possible cause of the detrusor overactivity. Whenever restoration of the bladder neck reduces the detrusor to proper position anterior colporrhaphy is conoveractivity, sidered, and an all-out effort is made to correct the borderline urethral-bladder pressure ,gradient.4 Such surgery should never be carried out when there is a reduced
15, 1966 & Gym.
bladder capacity or neurogenic bladder. Treatment of urgency incontinence is directed to correction of a reduced bladder capacity and eradication of infection. In cases where parasympatholytic drugs tranquilize the irritable detrusor at pressure testing, use of these drugs should be considered at least as adjunctive therapy. Summary In addition to stress incontinence produced by urethral-bladder pressure equalization at stress, there is another type of incontinence wherein a hyperactive detrusor muscle, sensitized by stress, in the presence of a borderline urethral-vesical pressure differential, causes involuntary urine loss without warning. This latter incontinence is not urgency incontinence, although both are caused by an overactive detrusor muscle.
REFERENCES
Beck, OBST. Beck.
R. P., and Maughan. G. B.: AM. J. & GYNEC. 89: 746, 1964. R. P.. and Hsu. N.: AM. ”I. OBST. & GYN~C. 89: 738, 1964. ’ Beck, R. P., and Hsu, N.: AM. J. OBST. & GYNEC. 91: 820, 1965. Beck, R. P., Hsu, N., and Maughan, G. B.: AM. J. OBST. C GYNEC. 91: 314, 1965.
Denny-Brown, D., and Robertson, 56: 149, 1933. Hodgkinson, C. P., Ayers, M. A., B. H.: AM. T. OBST. & GYNEC. Hodgkinson,“C. P., and Cobert, OBST. & GYNEC. 79: 648, 1960. Wright, 8: Applied Physiology, 1952, Oxford University Press,
E. G.:
Brain
and Drukker, 87: 717. 1963. N.: AM. J. ed. 9, London, p. 767.
Discussion DR.
MICHEL
The ever-difficult
J. BERARD, therapeutic
Montreal, Quebec. problem of female
stress incontinence is confirmed by the many reports of procedures and hypotheses, suggestions, and fantasies devised to lower the incidence of surgical failures. More and more, the emphasis is on accurate diagnosis, resulting from meticulous investigations in all cases. The work of Denny-Brown and Robertson in 1933 seemed to answer many questions about the control of and their teaching prevailed for micturition, many years but some had doubts based on empirical and experimental observations. Hodgkinson challenged it conclusively around 1960 and Beck’s work renders a differential diagnosis more possible. We have nowadays to differentiate urgency incontinence, and stress incontinence, the incontinence due to the detrusor muscle. Urethrocystometry devised by Hodgkinson and
used by Beck seems to have gained its useful place in the work-up of the incontinent patient. Being no expert myself, I wonder this apparatus one can differentiate
if in using between the
contractions of the bladder itself and the contractions induced by the foreign body within the urethra, the balloon and catheter. A colleague in urology tells me that a small transmitter placed in the bladder is being used in a parallel study on the role of the detrusor. The methodology of Dr. Beck’s clinical investigation was well conceived and well controlled. Yet apart from my remark about the inherent contractions of the bladder and the possibly “balloon-induced” waves due to the foreign body, I wonder if another variable factor is not introduced. It seems to me that the pressure in the bladder is recorded through a direct system, whereas the pressure from the
Volume 94 Number 4
urethra is conducted through a closed circuit. Can we also consider as an entirely normal condition, the rapid excretion of urine secondary to the action of a diuretic after drinking 1,500 cc. in half an hour? Personally I think an artifact is introduced by injecting in addition to the diuretic, a parasympathomimetic drug, in order to observe its action on the detrusor muscle of a full bladder. The bladder, emptied by catheterization, is being tested for residual urine and not strictly speaking for detrusor activity, because it has been medically transformed. Hodgkinson has proved that “. . . the response to anticholinergic drugs is both unpredictable and unexplainable . . .” in cases he considered to be of the “dyssynergic detrusor dysfunction” variety. It is generally agreed that the motor function of the detrusor is through the pelvic parasympathetic nerves (S,, S,, and S,) . Bladder reflexes are mediated through the sacral cord at these neurologic levels. Clinical observations have shown that the patient with a normal function of her detrusor frequently cannot void or does with difficulty after atropine or atropine-like drugs which paralyze the bladder. There is agreement that the bladder and urethra in the active erect woman are subjected continuously to external pressure influences of unpredictable height and frequency. During walking gravitation has a positive and a negative influence, these balancing each other. Many researchers admit difficulties of interpretation with the accepted theories of micturition because of the variable relationship of the bladder and urethral pressures during voiding. Hodgkinson speculates that the urethral sphinc-
Detrusor
muscle and urinary
incontinence
489
teric closing mechanism is relatively passive, that it is probably opened by sustained elevation of intravesical pressure from any source and that, once open, it remains so until the pressure is lowered or the bladder emptied. I wonder, therefore, why coughing, walking, or squatting should not start this chain reaction in these patients with a “borderline” urethral-vesical pressure differential, without having to introduce a notion of dysfunction of the detrusor. On the other hand, Adler has observed that ‘L. . . only induction of urination is voluntary, once the sphincter is relaxed the further course is automatic. . . .” Do we wish, therefore, to explain incontinence due to an hyperactive detrusor muscle? I am tempted to offer a parallelism with the “reflex neurogenic bladder,” in which the complete removal of higher center control, reduces the status of the bladder to a simple reflex organ, whose activity is dependent solely upon the primary reflex arc through the sacral cord. Might it not be possible, in Dr. Beck’s cases, that we are confronted with patients suffering from latent degenerating disease of the multiple sclerosis type or of a minimally important damage to the pelvic parasympathetic nerves or plexus? I would have liked to have been told of the age and parity of these patients, because I could speculate that a degenerative process or “l’accouchement” having damaged the parasympathetic circuit might alIow a transitory reversion to a form of a “reflex neurogenic bladder.” Voluntary control might then still stop the chain reaction, once the stress is gone in those patients with a borderline urethral-vesical pressure differential.