A METHOD FOR EVALUATING THE STRESS OF URINARY INCONTINENCE ALLAN
c. BARNES, M.D., ANN ARBOR, MICH.
(FTom the Department of Obstetrics and Gynecology, University of Michigan Hospital)
HE importance of the problem of stress urinary incontinence in women is well recognized. The complaint is highly embarrassing or even incapacitating to the patient; it is met with frequently and its cure is difficult. The sizable literature which has appeared on this topic attests to the fact that this problem is far from settled. Many contributions have added new operations or new operative modifications to the already crowded list of therapeutic measures. However, a survey of some of the reported results of these operative procedures indicates that the percentage of patients cured ranges from 36 to 100 per cent, with an average for any particular procedure close to 80 per cent. 1 • 9 • 18 • 23 In general, the number of cures diminishes in direct ratio to the length of time allowed to elapse between operation and the follow-up studies. And the fact that from 6 to 14 per cent of the reported cures have been in patients subjected to repeated operations serves as a further indication that the therapeutic situation in respect to this complaint is not entirely satisfactory. It has been the opinion in this clinic that a sufficient number of wellestablished operative procedures are already available for the treatment of incontinent patients. It has been frequently demonstrated that certain of these can give satisfactory results when judiciously chosen and applied with a knowledge of the underlying disturbance of function. Therefore no new surgical procedures are described in this paper. It presents rather a clinical and investigative review of the fundamental factors in the pathologic physiology of stress urinary incontinence, together with a clinical test to serve as an aid in its correct evaluation and the selection of the proper operation.
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PHYSIOLOGIC CONSIDERATIONS In the normal female at rest, the involuntary urethral sphincter will retain urine in the bladder. This principle has been so clearly demonstrated by the excellent work of Denny-Brown and Robertson/ 0 that extensive discussion here is not necessary. It is well to bear in mind, however, the nature of involuntary sphincter action. With the bladder at rest the internal sphincter is firmly closed, but it is not in a state of continuous contraction. Involuntary sphincters do not maintain ''unmeaning contraction.' ' 11 If from its resting closed state an involuntary sphincter is gradually distended, it will exert a contractive 381
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force proportionate to the degree of distention. 1f nothing is disttmding it, the sphincter does not contract, but once it has been opened by trigonal action and stretched by fluid passing· through it, the muscle tends to close. "\Vhether this reaction is affected by nervous plexus or is a purely muscular phenomenon remains to be determined, but the loss of this "reactive contraction" meehanism undoubtedly contributes much to disability of the female bladder. ·with a cough, sneeze, or other strain which produces a rise in intraabdominal pressure, the voluntary sphincters are brought into play, and normally thesf.' are sufficient to provide the added barrier necessary to resist the associated rise in intracystic pressure. 12 ·with loss of internal sphincter tone, it is probable that the external voluntary sphincter is sufficient to preserve continence while the patient is quiet. 13 But the normal state of balance is disturbed, and the patient has no additional barrier to employ against the sudden (but not necessarily large) rise of bladder pressure associated with laughing, coughing, or sneezing. Since urinary incontinence, regardless of exact etiology, represents a momentary increase in the forces of urinary expulsion over the powers of urethral resistance, it would appear that incontinenee could r·esult from (a) an increase in urinary expulsive force or intravesical pressure, (b) a lowering of the powers of resistance or urethral . sphincter action, or (c) a combination of (a) and (b). (a) Increase in Urinary Expulsive Force.-The partial incontinence wllich so often develops in the last trimester of pregnancy, and that associated with large pressure·producing pelvic tumors are clear examples of incontinence chiefly on the basis of elevated intravesical pressure. But aside from these, the actual causative relationship between increases of intravesical pressure and diurnal incontinence is difficult to prove. In an effort to evaluate the role played by the forces of expulsion in stress incontinence, we have performed over 80 cystometric studies ou 32 patients with some degree of pelvic floor relaxation.H Fig. 1 is an illustration of three such curves obtained on the same patient. Curve B il-> a postoperative study, and represents a normal cystometric reading. Curve C is a preoperative study ob· tained in the traditional manner, and reveals a bladder of somewhat increased capacity with pressures slightly lower than normal. But the cystometrogram A i~ also a preoperative study on the same l)atient, and by comparison with C, this shows a relatively small capacity bladder of higher intnwesical pressure. The essential difference in the obtaining of these two readings was that in curve A, the patient's descensus was drawn down to the position it occupied while she was on her feet. In other words, the descensus uteri in this case could produce a relative increase of intravesical pressure while the patient was standing which would not have been indicated by the traditional cystometric reading performed with the patient recumbent.1G In like manner it can be .shown that pressure producing tumors (Fig. 2), and large rectoceles which press against the bladder result in relative rises in intravesical pressure. We are not suggesting that these conditions are frequent causes of stress urinary incontinence in women. Nevertheless, since the ultimate objective of treatment is to restore a balance in· wll.ich the powera of urethral. resistanee are greater than the forces of urinary expulsion, it is well to bear in :rniil.d that
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intravesical pressures may frequently be elevated, thereby making increased demands on the urethral sphincter mechanism. (b) Decrease in Urethral Resistance.-Damage to the sphincter mechanisms or their supporting structures may lower their efficiency to such an extent that they are unable to preserve continence. While this principle is a generally accepted one, the manner in which damage may occur, and the exact nature of such damage, has not been conclusively demonstrated. Most frequently the trauma of childbirth is assumed to be the chief cause of injury to the mechanism of urinary continence. While it is true that 150 patients with incontinence had a higher average parity than 140 continent parous women of the ward service at the University Hospital ( 4.8 children apiece compared to :l.6), we have also had two nulliparous patients with stress incontinence, and one of our most severe cases occurred in a para i who had a short easy labor, giving birth to a 5-pound child. The theories concerning the nature of the damage to the urethral sphincters are legion. .\ complete cataloguing of these theories would be of no value here. Suffice it to say that they all fall prindpally into two groups: those maintaining the primary damage to be on the
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Fig. 2. Fig. 1.-Three cyatometric curves from the same patient (see text). Fig. 2.-Preoperative (A) and postoperative (B) curves on patient with bilateral large ovarian fibroma. Cystometrics obtained with patient sittln;;· up.
urethra or its sphincters,16, 11 and those stating that the essential changes involve peri-urethral or supporting tissues.ts, 19 In all probability the problem is not one of ''either ... or,'' but of ''both ... and.' •zo, 21 The degree of the functional damage may be interpreted from the clinical history obtained. At onset the incontinence often seems to result from a failure on the patient's part to augment her sphincter mechanism rapidly enough. If she sneezes several times in succession, she will be incontinent only with the first sneeze. The reflex muscular tightening which reinforces the sphincter mechanism in the face of increased intra-abdominal pressure is delayed rather than com· pletely lost. Subsequently there may be incontinence associated with all coughing,· laughing or other relatively rapid changes in intra-abdominal pressure, while continence is preserved on lifting heavy objects, or in other situations where ample time may be taken to adjust the musculature to the increased strain. Finally there is complete incontinence on all activity or even incontinence while the patient is recumbent. ·
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The accurate diagnostic evaluation of patients with partial urinary incontinence has not in the past been easy. The patient's history and the physical examination do not tell the entire story, for seemingly mild cases will unpredictably resist every form of therapy attempted. More information than the degree of pelvic relaxation, if any, and the patient ',s description of her symptoms is necessary for the competent selection of the proper operative procedure. During the past year we have been employing in this clinic a test based on the physiologic principles outlined above, and designed to give additional diagnostic information necessary for the thorough evaluation of these cases. It consists essentially of three studies, all relatiVely easy to perform.
Fig. 3.-Normal anteroposterior sphinctometric. Balloon shadow obltterated by urethral resistance, leaving balloon dilated only inside internal and outside external meatus.
1. Measurement of Intravesical Pressure.-With a standard volume of fluid in the bladder, and with the patient standing, direct manometric readings are obtained.22 We have optionally selected 3¥2 ounces of physiologic saline solution, and have determined normal readings on a group of continent patients. For the occasional patient who cannot accommodate 3% ounces, the bladder is filled to eapacity and the reading (usually foundto be markedly elevated} is taken. Sinee most partial incontinence is suffered while the patients are active and on their feet, we feel that the standing position in which this reading is taken provides a more useful eomparative figure.
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2. Direct Measurement of Urethral Resistance.-The method we have adopted for measuring the strength of urethral resistance is a modification of an experiment performed some years ago by Kennedy. 23 A small balloon composed of two superimposed finger cots is inserted in the urethra, filled to a known manometric pressure with a 90 per cent sodium iodide solution, and an x-ray taken. Studies on normal patients indicate that under these conditions the entire urethra should remain closed and obliterate the balloon shadow at a pressure of 35 em. of fluid, and it is at this pressure that the x-ray is taken. The result in a normal patient is shown in Fig. 3. The bladder is filled with 180 c.c. of an 8 per cent solution of sterile sodium iodide, which is well tolerated, and the balloon is seen to be compressed throughout the length of the effective resistant force of the urethra. The essential point to be observed in this film is whether or not the dilatation of the balloon at its inner end lies
Fig. 4.
Fig. 5.
Figs. 4 and 5.-Two abnormal anteroposterior sphinctometrics, showing varying· degrees of weakness at internal sphincter area. Balloon dilates at inner end before urethrovesical junction is reached (A and B). Compare with Fig. 3.
within the bladder shadow. In other words, the effective urethral resistant force must reach the urethrovesical junction. Variations from this normal picture occurring in two patients with differing degrees of sphincteric weakening are shown in Figs. 4 and 5. 3. Indirect Measurement of Internal Sphincter Strength.-This determination is also made in conjunction with x-ray, the film being taken in the oblique, and an indwelling watch chain used to mark the course of the urethra as suggested by Stevens and Smith 24 (Fig. 6). As this film is exposed, the patient is asked to strain down as hard as she can. With straining intravesical pressures from 60 to 80 em. of water may be obtained, so that in this study the urethra is subjected to a much greater force than in the first film, but it is a force applied in a more physiologic manner, i.e., from within outward. In a normal person, a rise in intravesical pressure alone cannot force fluid through the internal sphincter without a detrussor contraction of
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the bladder. 10 Hence, in this x-l'ay ihe hladdPr floor· should he fl:Jt a1 the urethrovesical junction, and shoul
Fig. 6.-Normal oblique view, wHh watch chain in urethra. Despite the fact that the patient is straining, internal sphincter area (A) shows no funneling.
Fig. 7.
Fig. 8.
Figs. 7 and 8.-Two variations from the nonnal oblique view. l\larked relaxation C1) and minimal funneling (B). See also Fig. 1 0.
The information obtained from these studies permits a much better understanding of the patient's incontinence. With such information in mind, a complete program for the treatment of partial incontinence in women should include measures designed to (a) lower intracystic pres-
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sure where this is found to be increased, and (b) re-establish urethral resistance where this is diminished. (a) In a patient with pelvic relaxation ann descensus, plastic repair will lower the elevated intravesical pressure. Obtaining intravesical pressure readings pre- and postoperatively on 34 patients has Bhown that procedures which include plaiting of the pubovesicocervical muscle layer, correction of rectoceles, or operations for the removal of large uterine or ovarian tumors accomplish this result.
Fig. 9.-Preoperative (left) and postoperative (right) sphinctometric. Minimal relaxation indicated by dilatation of balloon at A outside bladder. Following Kelly .stitch this is corrected (B).
Fig. 10. Figs. 10 and 11.-Minimal funneling at .
Fig. 11. Bladder floor flat at B fol-
While causative relationship between increased forces of expulsion and stress incontinence cannot be completely demonstrated and is not here claimed, every gynecologist ha-s encountered cases of incontinence cured by nothing other than plastic repair, and the associated reduction in intravesical pressure may well be the explanation. Certainly it is asking much of a purely local procedure such as fulguration of the internal sphincter area, the Kelly stitch, or the ''direct muscle plastic'' of Stoeckel" to retain urine which may be at pressures 30 per eent above normal. (b) The re-establishment of functional urethral resistance has often been lost from view in attempts to re-establish urethral anatomy. Some writers have claimed a constant relationship between incontinence and changes in anatomic
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structure: d'Azevedo and Camposz" (los~ of angle of urethra to bladder fiooi·), 'raylor and Wattz• (descent of posterior methral wall), and Thumsen2H (loss of anterior angulation of urethra). Our x-rays have not confirmed a constant assor.•iation of these factors with incontinence, whereas continent patients have demoiJstrated wide variation in urethral angulation. To the patient, function rather than shape is important; a single band able to resist pre:-sure is 1110re valuable than a normally shaped urethra with no inherent powel' of effective resistance. Fig. 12.
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l<'ilil"S. 12 to 15.-Urethral resis.tance fails, as shown at A, outside bladder. Postoperatively internal sphincter area (B) resists pressure satisfactorily. l!'Unnellng ( 0) at Internal sphincter area corrected by p!a.stlc, restoring bladder ftoor and sphincter\() resistance (D). Compare postoperative view (Fig. 1.5) with normal (l!'ig. 6).
The same type of x-ray studies u~ed in the preoperative entluation of the patient's disability give a postoperativeindication of .whether or not effective urethral resistance has been restored. Fig, 9 is the pre- and postoperative antero· posterior view of a patient who had a Kelly stitch type of operation. In the view on the left, the dilatation of the inner end of the baUoon cttn be seen to begin just outside the bladder. Postoperatively, as shown in the film on the right, the urethral ability to contract extends, as it should normally, all the way to the urethrovesical junction. Figs. 10 and lJ are oblique studies before and after simple Kelly stitch. The funneling at the urethral vesical neck is minimal, hut postoperatively it is obliterated, and the patient is continent. In like manner, Figs. 12 to 15 give the preoperative (to the left) and postoperative studies of a patient who wag a candidate for a plastic operation. The
Fig. 16. Fig. 17.
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Fig. 16.-Preoperatlve view (compare with Fig. 3). Fig. 17.-Pcstoperative x-ray, with patient relaxed, shows marked improvement. Fig, 18.-Postoperatlve x-ray (with pyramidalis tightened) shows sphincteric action of transplant by increased obliteration of balloon shadow. (See text.)
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anteroposterior film reveals dilatation for a greater are:< <.1own the urethra; the oblique view demonstrates more marked funneling am1 the descent of the bladder floor. Postoperatively, these are correeted in a sati~faetory manner h;>~ repair, with particular care being taken of the internal "fihincter area. Fig. 16 reveals tl1e type of urethra which has no inherent resiBtance what· ever. Local tightening procedures al'e of uo avail in the fa.ee of ~uch complete lack of urethral resistance. 1-Vhatever the particular operation ~eleeted, it must he onP which brings the motive force to the meth1·a from elsewhere, and this stud~·. there· fore, indicates the necesRity for ~om<~ t,vpe of tran~plant operation. This par· tieular patient had a pyramidaliR nm:~cle-fascial transplant operation a~ de· scribed by Norman F. "!\1iller,zn and the po~toperative filmH reveal thE' re~ult. 'J'ht> film shown in Fig. J7 is in marked eontmst to the preopeJ·ati,-e film, and itl oll a new sphincteric acth•n is cleal'ly denwnstra ted. 1 t should perhaps he re·en1phasizcd that these x~rays are not primarily pktures of strul'lurP, hut indirate funetinnal ahilit.v to reHist force applied again~t i he sphincters. Sm
The difficulty of the accurate evaluation of stress urinary incontinence and the selection of the correct type of operative procedure fm· any given case is appreciated by all gynecologists. The principles which form the basis for the treatment of this complairlt are here presented, and a clinical test is reported which has been used and found satisfaetor.v as indicating the etiology, the operation of choice, and the results of operation for incontinence. It should be emphasized that this test i:; not intended to replace, but rather to complement, other methods nov\' in use for the evaluation of partial or stra"!s urinary ineont.inence in women. REt'ERENCJ;S
Riforma med. 52; 9i~l, 1936. (2) Douglass, Marion: AlL J. 0BST. &; GYNEe. 31: 268, 1936. (3) Davies, .1. W.: Surg. Gynee. Obst. 67: 273, 1938. (4) Frigyesi, Josef: Arch. f. Gynak. 160: 176, 1935. (5) Gomez, Carlos.: J. d 'urol. 45: 344, 1938. ( 6) Lmosley, 0. S.: J. Ural. 36: 400, 193ti. (7) Millin, T.: Proc. Royal Soc. Med. 32: 777, 1939. (8) Muret, M., an(l Cka11in, 0 ..J.: Gynefl. et abst. 36: 81 1 1937. (9) Schrattenbach, V.: Zentralbt f. Gyniik. 61: 1848, 1937. (10) Denny-Brown, D. E., and Robertson, E. G.: Brain 56: H!l, 193::1. (11) Denny· Brown, D. E.: New England J. Med. 215: 647, 1936. (12) Daviils.• .iL M., Newman, H. F., and Rubin, I. C.: ,T. Mt. Binai Hosp. 4: 861, 1938, (13) Yowng, H.: Quoted by Davids, Newman and Rubin. (14) Rose, D, K.: .T. Urol. 40: 248, 1938. (15) Idem: Ibid. 27: 207, 1932. (16) Johnston, H.: Surg. Gynec. Obst. 5lf: 96, 1931. (17) Stoeckel, W.: Zentralbl. f. Gynak. 61: 1224, 1937. (18) Kennedy, W. T,: AM . •T. 0BST. & GYNEO. 34: 576, 1937. (19) Wat.~on, B. P.: Brit. l\L J, 2: 566, 1929. (20) Thomsen, E.: Acta radial. 13: 433, 1932. (21) Nat<,ig, H.: No.rsk mag. f. laegevidensk. 92: 325, 1931. (22) Schwartz, 0.: Handbuch der Urologie, Berlin, 1926. (23) Kennedy, W. T.: A~r. J. 0BST. & GYNEC. 33: 19, 1937. (24) Stevens, W. E., and Smith, 8. P.: J. Urol. 37: 194, 1937. (25) Miller, J. D.: Ibid. 40: 612, 1938. ( 26) D 'Azevedo and Campos: Quoted by Steven& and Smith. ( 27) Taylor, H., an4 Watt, C.: Surg. Gynec. Obst. 24: 296, 1!H7. (28) Thomse~,,·E.: Acta radiol. 11: 527, 1930. (29) Miller. Norman];'.: J. A, M.A. 99: 628, 1932. (1) Bertone, Carlo: