Dyssynergic Vesicourethral Responses During Bladder Rehabilitation in Spinal Cord Injury Patients: Effects of Suprapubic Percussion, Credé Method and Bethanechol Chloride

Dyssynergic Vesicourethral Responses During Bladder Rehabilitation in Spinal Cord Injury Patients: Effects of Suprapubic Percussion, Credé Method and Bethanechol Chloride

V cl. l lb, rviay THE JmJRNf.L or UEOLOCY CopyI·ight © 1976 by The ~YVilliarns & V/ilkins Co. Printed in U.S.A. U rodynamics DYSSYNERGIC VESICOURE...

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V cl. l lb, rviay

THE JmJRNf.L or UEOLOCY

CopyI·ight © 1976 by The ~YVilliarns & V/ilkins Co.

Printed in U.S.A.

U rodynamics DYSSYNERGIC VESICOURETHRAL RESPONSES DURING BLADDER REHABILITATION IN SPINAL CORD INJURY PATIENTS: EFFECTS OF SUPRAPUBIC PERCUSSION, CREDE METHOD AND BETHANECHOL CHLORIDE SUBBARAO V. YALLA, ALAIN B. ROSSIER

AND

BUSHRA FAM

From the Harvard Medical School, Spinal Cord Injury and Urology Services, West Roxbury Veterans Administration Hospital, Boston, Massachusetts

ABSTRACT

Five normal men and 70 spinal cord injury male patients underwent 100 studies with the multiple pressure recording technique, incorporating the continuous infusion principle for sphincter pressure monitoring. Gross cystosphincteric dyssynergia was noted in the majority of patients with complete upper motor neuron bladders less than 2 years in duration. Some form of synergic voiding patterns was noted, mostly in patients with incomplete upper motor neuron bladders. The external sphincter tends to be synergic in late cases of upper motor neuron bladders. Internal sphincter dyssynergia is uncommon in cases of injuries less than 2 years in duration, with the exception of patients who have autonomic dysreflexia. Bladder neck obstruction seems to be more common in late lesions secondary to global hypertrophy of the bladder. Rehabilitation maneuvers and bethanechol chloride administration may exaggerate detrusor sphincter dyssynergia and injudicious use of such procedures could be detrimental to the urinary tract. Scott and Quesada and their associates were able to distinguish 3 main groups of micturitional patterns in spinal cord injury patients: 1) the coordinated micturitional reflex found in the normal healthy individual, 2) the discordant reflex pattern in which reflex activity exists except that the discordant action of sphincter and detrusor muscles causes bizzare changeable patterns and 3) the absent reflex pattern in which there is no vesical pressure other than that produced straining or bladder filling. 1• 2 These voiding patterns were demonstrated urodynamic studies, using voiding flow rates, intravesical pressure measurements and sphincter electromyography. Detrusor sphincter dyssynergia characterized by inappropriate contractions of the urethral sphincter coincident with detrusor contractions belongs to the discordant reflex patterns. of the external sphincter causing functional bladder obstruction has been clinically recognized other earlier investigators. 3- 6 Lack of synergism between detrusor and external sphincter has been mentioned by Rossier and Ott as a major cause of unbalanced bladder function in upper motor neuron lesions. 7 Dyssynergia between the bladder and external sphincter could be influenced by various rehabilitation maneuvers. The effects have been studied of some bladder rehabilitation techniques, namely straining, suprapubic percussion (tapping), the Crede method as well as the use of bethanechol chloride. Our technique of urodynamic evaluation in this study differs from that advocated by Scott and Quesada and their associates. 1 • 2 We have used radiologically monitored synchroAccepted for publication August 1, 1975. Read at annual meeting of American Urological Association, Miami Beach, Florida, May 11-15, 1975. 575

nous cystosphincteric pressure recordings, adopting the continuous urethral infusion principle. MATERIAL AND METHODS

We performed 100 urodynamic studies on 70 spinal cord injury male patients and 5 normal men. There were 56 patients with an upper motor neuron bladder (41 complete and 15 incomplete lesions), 11 with a lower motor neuron bladder (all complete lesions) and 3 with a mixed lesion. The patients ranged in age from 19 to 65 years and the lesions had been present for 72 hours to 30 years. The technique of urodynamic investigation essentially consisted of simultaneous recordings of intravesical and intrasphincteric activity (fig. 1). 8 The method of recording teric pressures is based on the constant flow principle advocated by Brown and Wickhamo 9 A special No. 12F tri-lumen plastic catheter* was used for this synchronous study. Two channels terminating at the catheter tip allowed transvesical pressure recording and filling. The third lumen, which terminates either 10 or 15 cm. away from the catheter tip, was used for urethral sphincter pressure monitoring during constant intraurethral infusion. A radiopaque marker located 10 or 15 cm. from the catheter tip indicated the site of urethral infusion. Details of this method, which includes the physical factors governing the interpretation, have been mentioned elsewhere. 8 Patients were kept in the supine position with about 15 degrees of obliquity and the complete study was monitored by an image intensifier and videotape whenever indicated. In each instance the bladder was emptied before initiating the study with a pressure monitored cystourethrogram. The intra-

* Portex Limited, Hythe, Kent, England, CT21, 6JL.

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200vesical pressure was recorded via a double lumen No. 14F plastic catheter during rapid bladder filling with a solution* at room temperature running freely by gravity and during voiding whenever obtainable. Continuous urethral pressure profile with manual withdrawal technique at about 1 cm. per 5 to 10 oseconds was recorded to give a preliminary indication of the site of internal and external sphincter zones. Withdrawal of the catheter was followed by fluoroscopy to accurately correlate sphincteric sites with the anatomical landmarks of the bony pelvis. Then simultaneous cystometrogram and sphincterometrogram were obtained during bladder filling at the rate of 4.4 cc per minute of a 30 per cent contrast material mixed with 60 cc furacin solution. t Distilled water was added to 360 cc of the solution until the total amount of this specially prepared solution was 450 cc (specific gravity 1,065); for 0~ urethral infusion, distilled water mixed with furacin solution (specific gravity 1,000) was used at the rate of 2.2 cc per 200-4::& minute. Pressure activity at the internal (vesicourethral junction) and external sphincter sites was individually recorded during various phases of bladder activity (fig. 1). Effects of various stimuli, namely cough, bulbocavernous reflex, suprapubic percussion, straining and the Crede maneuver, were recorded while the bladder was being filled. When the bladder was full, up to approximately 400 cc, unless the patient had already voided, further bladder filling was discontinued and the effects of the same stimuli and of subcutaneous injection of 2 mg. bethanechol chloride were recorded individually. During voiding it was necessary under fluoroscopic monitoring to manually steady the catheter at the appropriate sphincter site FIG. 2. Complete (C6 to C7) upper motor neuron lesion after as indicated by the position of the radiop:ique marker in recovery from spinal shock (2 months after injury) in 21-year-old man. relation to the fixed pelvic bony landmarks. With the catheter Interrupted voiding typical of dyssynergia between detrusor and tip in the bladder and the proximal radiopaque marker placed striated urethral sphincter. Electromyograph pattern of striated in the bulbous urethra, distal to the highest sphincteric sphincter and synchronous sphincteric pressure activity are clonic in nature. High residuals varying from 200 to 300 ml. pressure zone (U3) described by Rossier and Ott, 7 pressure gradients across internal and external sphincters could be recorded when voiding did take place. Residuals were mea- occurred 2 to 4 seconds before detrusor contractions appeared. A few seconds after the decrease in external sphincter pressure sured at the end of each study. uninterrupted voiding coincident with sustained detrusor contraction was noted. No uninhibited external sphincter contracRESULTS In the normal patient suprapubic percussion and/or the tions occurred throughout voiding. Before voiding pressures of Crede maneuver resulted in minimal contractile responses at 30 to 45 cm. water and 75 to 100 cm. water were noted at the the sphincter sites when the individual was advised to inhibit internal and external sphincter sites, respectively. During contractions of the pelvic floor muscles during those maneu- uninterrupted voiding pressures at corresponding sphincter vers. Bulbocavernous reflex was consistently elicited in a sites always became either equal to or less than the intravesical contractile response at the external sphincter region. When the pressure; there were no uninhibited sphincter contractions. bladder was filled to a volume that resulted in a desire to void, This pattern of response of the urethral sphincters to bladder the external sphincter exhibited an increase in pressure activ- activity is a synergic one. Such a synergic pattern was seen only ity during attempts to voluntarily inhibit voiding. When asked occasionally in upper motor neuron bladders, especially in to void, a decrease in pressure in the external sphincter region incomplete ones. Dyssynergic response of urethral sphincters characterized by inappropriate contractions would result in * Reno-M-Dip ™ (30 per cent), E. R. Squibb & Sons, Inc., New York, either interrupted voiding or non-voiding (figs. 2 and 3). Voiding sometimes took place under high intravesical presNew York. t Eaton Laboratories, Norwich, New York. sures. At rest there was a high pressure within the external

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urethral This latter form of might have been considered synergic had it not been for the excessive intravesical voiding pressure that compensatorily tended to overcome the initial high intrasphincteric resistance. Such patterns of dyssynergic cystosphincteric were often seen in upper motor neuron lesions. The incidence of 1 0 0 - ~

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and in relation to nature and duration of the lesion is shown m the table. With continuous pressure profile recordings internal sphincter spasms with a high pressure zone that tended to cause dyssynergia at the bladder neck were seen in 2 of the 33 early lesions and 5 of the 23 old lesions (fig. 4). Pressures in the bladder and bulbous urethra during voiding in normal subjects were about 50 to 60 and 30 to 40 cm. water, respectively, while a much greater disparity was noted in dyssynergic patterns of voiding whether that was interrupted or continuous. Rehabilitation maneuvers and subcutaneous injection of bethanechol chloride in cases with dyssynergia always resulted in an exaggerated form of incoordinated activity and never caused a synergia pattern of voiding (figs. 3 and 5). When voiding took place it always did so under high bladder and sphincter pressures. Whenever voiding cystourethrograms were

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FIG. 4. Same patient as in figure 3. Internal sphincter hyperactivity at vesical neck is demonstrated with continuous urethral profile. Elevated pressure aiso is encountered in external sphincter zone. Corresponding narrovv sphincter zones can be seen on cystog-ram.

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oCmli. in 1-\0 FIG. 5. C6 to C7 complete spastic lesion 13 weeks in duration in 47-year-old man. S.c. bethanechol chloride administration resulted in exaggeration of detrusor striated sphincter dyssynergia. Arrhythmic sphincteric activity and uninhibited detrusor contractions can be seen 8 to 9 minutes after administration of drug.

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YALLA, ROSSIER AND FAM

obtained, sometimes more than once in a single study, they most often corroborated the urodynamic findings. DISCUSSION

In normal micturition close coordination between bladder activity and urethral sphincters is essential for bladder emptying. Present observations on normal subjects with the aforementioned recording technique indicate that voiding is preceded by relaxation of the external urinary sphincter followed by bladder contraction. Similar observations have been made by Tanagho, 10 Abramson and associates, 11 and by Petersen and associates. 12 In spinal cord injury patients variation from the normal pattern is the rule. In the majority of complete upper motor neuron lesions gross detrusor external sphincter dyssynergia is typical and is characterized by total cessation of voiding with high intravesical pressure or interrupted spurts of voiding with usually large residuals in both cases. However, in some patients who recovered recently from spinal shock no uninhibited detrusor activity was demonstrated, although spastic activity of the external sphincter was encountered. Different views to explain this areflexic behavior of the bladder after the end of the period of spinal shock have been expressed, such as overdistension of the detrusor and/or infection. 13 Animal studies on the effect of pudenda! nerve and anal region stimulation on detrusor activity indicate an inhibitory effect on the latter, 14 whereas in spinal cord patients, perianal and rectal stimulation have been shown to facilitate rather than to inhibit detrusor responses. 4 Susset and associates also have indicated that anal dilatation resulted in marked activity of the external urinary sphincter in these patients. 15 Persistent bladder areflexia in conjunction with a spastic external urinary sphincter could be owing to various afferent impulses, including those originating from feedbacks of striated muscles-pelvic floor or extremities, causing secondary detrusor inhibition. The sacral segmental interplay existing between detrusor and striated muscles or vice versa has been well documented. 16 • 17 Dyssynergia with an areflexic bladder as well as the typical detrusor-sphincter incoordination were seen

in 80 per cent of the complete upper motor neuron lesions, wl!_ich consisted of recent and old lesions. Twenty of 21 recent (less than 2 years after recovery from spinal shock) complete upper motor neuron lesions demonstrated some form of dyssynergia versus 13 of 20 old complete lesions, indicating that striated sphincter dyssynergia probably abates with time. However, incomplete upper motor neuron lesions do not manifest such degrees of dyssynergia. In fact, most of them eventually adjust to some form of synergic voiding pressures. The same observation is noted in many of the late cases whose tendency to obstruction seems to be caused more by hypertrophy of the internal sphincter in response to an overload on the detrusor than by primary dyssynergia of the external sphincter. Excitability of the external sphincter to various stimuli is much less than in the more recent cases. This observation could be correlated with the histological findings of Cukier and associates, who showed fibrous and muscle fibers degeneration within the striated urinary sphincter. 18 Exaggerated dyssynergic activity in response to rehabilitative maneuvers and bethanechol chloride injection has been observed to be maximum in complete upper motor neuron lesions after recovery from spinal shock. The deleterious effects after such maneuvers were seen in T. P., a 50-year-old man with C6 to C7 spastic incomplete lesions, who had a smooth contoured bladder on a cystogram 2 months after injury. Cystosphincterometry during suprapubic tapping with 400 ml. in the bladder revealed areflexic bladder, slight opening of the bladder neck and a spastic striated sphincter that displayed dyssynergic contractions during these maneuvers. After having been on bethanechol chloride for 2 months the patient voided with no residuals. However, trabeculation, diverticula of the bladder and bilateral vesicoureteral reflux developed. A pressure study 4 months after injury showed high intravesical pressure. A few uninhibited sphincter contractions led to a voiding in successive spurts. The cystogram 2 months after bethanechol chloride was discontinued did not show vesicoureteral reflux. The bladder contour appeared smooth without diverticula.

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DYSSYNERGIC VESICOURETHRAL RESPONSES DURING BLADDER REHABILITATION

Dyssynergia at the level of the internal sphincter is rather uncommon. It is especially noted in patients prone to autonomic dysreflexia. Krane and Olsson have proposed that such a phenomenon is secondary to alteration of the sympathetic outflow in the region of the bladder neck. 1 • It was suggested that the effect of parasympathetic nerve fibers on sympathetic neurons in the internal sphincter is inhibitory and damage to the parasympathetic system could result in uninhibited sympathetic over discharge with the result of increased resistance in the internal sphincter region. However, such type of internal sphincter overactivity was noted only in 2 incomplete upper motor neuron bladders out of 33 recent upper motor neuron injuries. Per contra, in 5 of 23 old lesions this abnormal internal sphincter overactivity was noted in association with detrusor hypertrophy. Whether the Krane and Olsson hypothesis'" is correct must be weighed against the known fact that distal urethral obstruction per se leads to detrusor hypertrophy. Patients who demonstrated hypoactive or areflexic bladders usually have collapsed (closed) vesical neck with normal pressures but such high internal sphincter pressure activity was not encountered. The possible mechanisms underlying detrusor-urethral sphincter dyssynergia (internal and external) in response to various rehabilitative stimuli are outlined in figure 6. In lower motor neuron lesions, whether complete or incomplete, no spontaneous or induced external sphincter activity was noted. Rehabilitative maneuvers, such as the Crede method, create high intravesical pressure without necessarily increasing the external sphincter pressure. In those cases pressure at the internal sphincter region may be elevated passively during this maneuver and they may require some form of treatment. Urodynamic studies are valuable adjuncts in the urological evaluation of spinal cord injury patients. Dependence on residual measurement alone is not adequate since it fails to reflect the intravesical pressures under which voiding takes place. The amount of residual urine accepted as indicative of a balanced bladder again differs according to various investigators. Spinal cord injury patients are increasingly treated in specialized centers. Rehabilitation of the bladder is thought to be best achieved by early institution of intermittent catheterization as well as the application of various bladder rehabilitation maneuvers to train the bladder.2° In fact such maneuvers elicit different types of stimuli that have been shown by the authors to act adversely on either or both the detrusor and urethral sphincters. Such stimuli become effective only if there is no concomitant dyssynergia. Messrs. Anthony Costello, William Reilly and Joseph Cronin and Miss Rosemary Phillips provided technical assistance. REFERENCES

1. Scott, F. B., Quesada, E. M. and Cardus, D.: The use of combined uroflometry, cystometry and electromyography in evaluation of neurogenic bladder dysfunction. In: The Neurogenic Bladder. Edited by S. Boyarsky. Baltimore: The Williams & Wilkins Co.,

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pp. 106-114, 1967. 2. Quesada, E. M., Scott, F. B. and Cardus, D.: Functional classification of neurogenic bladder dysfunction. Arch. Phys. Med. Rehab., 49: 692, 1968. 3. Bors, E.: Rationale of anesthetic procedures in the rehabilitation of patients with cord bladder. Int. Coll. Surg., 42: 22, 1964. 4. Rossier, A. B. and Bors, E.: Detrusor responses to perianal and rectal stimulation in patients with spinal cord injuries. Urol. Int., 18: 181, 1964. 5. Emanuel, M.: Mechanomyography of the external urethral sphincter. J. Urol., 107: 795, 1972. 6. Ross, J. C., Damanski, M. and Gibbon, N.: Resection of the external urethral sphincter in the paraplegic-preliminary report. J. Urol., 79: 742, 1958. 7. Rossier, A. B. and Ott, R.: Urinary manometry in spinal cord injury: a follow-up study. Value of cysto-sphincterometrography as an indication for sphincterotomy. Brit. J. Urol., 46: 439, 1974. 8. Yalla, S. V., Rossier, A. B. and Fam, B. A.: Synchronous cysto-sphincterometry using continuous bladder and urethral infusions and physical factors influencing interpretation. Urology, 6: 777, 1975. 9. Brown, M. and Wickham, J.E. A.: The urethral pressure profile. Brit. J. Urol., 41: 211, 1969. 10. Tanagho, E. A.: Interpretation of the physiology of micturition. In: Hydrodynamics of Micturition. Edited by F. Hinman, Jr. Springfield, Illinois: Charles C Thomas, Publisher, pp. 18-40, 1971. 11. Abramson, A. S., Roussan, M. S. and D'Oronzio, G.: Method for evaluating function of the neurogenic bladder. J.A.M.A., 195: 146, 1966. 12. Petersen, I., Stener, I., Sellden, U. and Kollberg, S.: Investigation of urethral sphincter in women with simultaneous electromyography and micturition urethro-cystography. Acta Neurol. Scand., suppl. 3, 38: 145, 1962. 13. Bradley, W. E., Chou, S. and Markland, C.: Classifying neurologic dysfunction of the urinary bladder. In: The Neurogenic Bladder. Edited by S. Boyarsky. Baltimore: The Williams & Wilkins Co., pp. 139-146, 1971. 14. Sundin, T., Carlsson, C. A. and Kock, N. G.: Detrusor inhibition induced from mechanical stimulation on the anal region and from electrical stimulation of pudenda! nerve afferents. An experimental study in cats. Invest. Urol., 11: 374, 1974. 15. Susset, J. G., Rabinovitch, H. and MacKinnon, K. J.: Parameters ofmicturition: clinical study. J. Urol., 94: 113, 1965. 16. Bors, E., Comarr, A. E. and Moulton, S. H.: The role of nerve blocks in management of traumatic cord bladders: spinal anesthesia, subarachnoid alcohol injections, pudenda! nerve anesthesia and vesical neck anesthesia. J. Urol., 63: 653, 1950. 17. Bors, E. H. and Blinn, K. A.: Spinal reflex activity from the vesical mucosa in paraplegic patients. Arch. Neurol. Psychiat., 78: 339, 1957. 18. Cukier, J., Leger, P., Benhamou, G., Lacombe, M., Maury, M. and Couvelaire, R.: La myotomie chirurgicale du sphincter strie de l'urethre. Une nouvelle voie d'abord sous-pubienne. Contribution a l'etude de la pathologie du sphincter strie du paraplegique. J. Urol. Nephrol., 77: 27, 1971. 19. Krane, R. J. and Olsson, C. A.: Phenoxybenzamine in neurogenic bladder dysfunction. I. A theory of micturition. J. Urol., 110: 650, 1973. 20. Bors, E. and Comarr, A. E.: Neurological Urology, Physiology of Micturition. Its Neurological Disorders and Sequelae. New York: S. Karger, 1971.

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