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Urethral pressure changes in women with detrusor instability Bladder or urethral pathologic process?
5 OD. NA¥glCS
L RETHRAL PRESSURE CHANGES IN WOMEN /ITH DETRUSOR INSTABILITY 131adder or Urethral Pathologic Process? ] ~ U L E KOONINGS, M.D.
ti3:IE H BERGMAN, M.D. F~ om the Department of Obstetrics and Gynecology, Los Angeles CounW/University of Southern California Medical Center, L~.'.~Angeles, California
AB S '! 1[ ~~~7. -- ~r, e h u n d r e d and fourteen f e m a l e patients had clinical and urod~ det r t. '~' i:~~tLzbii'it~. They all received oxybutynin chloride (Ditropan ) 5 m g t.i.d. eve l~,~ ~.~c ~ :r~0 ealed. Sixty-six of the 114 patients (58 %) responded favorably tre, t;~7te ~t ~ hi,!e ,18 patients (42 %) did not. Based on urethrocystometry, t w o w e "e ~~!~,~~~l:ied: ('~roup I consisted of 73 w o m e n w i t h bladder contraction that p~ in ~'.r,~,~" ~! p~e,csu'e. Group 11 consisted of 41 patients w i t h urethral pressure dro i det,',~,~ cc ntract~on by a f e w seconds. Sixty-one of the 73 w o m e n (84%) in f a v ~r c b~!, ~.~ h)ur weeJ~s of anticholinergic therapy w h i l e 88 percent (36 of 41) of did nc ~ ~.~ < 0,0~!). Our results suggest that w o m e n w i t h bladder contraction ure ;ii~c'l :'~~iaxa~tion represent a different pathologic entity than w o m e n w i t h "cle bili ~.y"
Idic F,~ttl)[,.' 'pri:naelry" detrusor instability (not sect ~.~Iar ~ L,~ ce:atr al nervous system lesion) is a blac d ~r .::~~diition of unknown etiology. ~ Treatmet t [n ::~,~!:~t:xi:ag t he unstable bladder by anticholil3c~r~ljc medications, ~ prostaglandin inhibitors. 3 ~nd ~',aleittm channel blockers 4 is empiric wit[ 1-:ss tt~ariL optimal results. U ret hr~l pressure changes are known to trigger ir[na~ly urgency ~,6 or detrusor contractions eith~.,r in ! kt~. physiologic phenomenon of voiding 7 c,r in cases of tarethral instability. 6 In these case,, tire ch:,,tr~asor muscle contracts in response to u:re:3r~al pressure changes and is not a primar,, l~ladder phenomenon. The present study was uttdertaken in order to study urethral dyn~ rr.ics :ir~twomen with detrusor instability to see wI~eth,~r or not their uninhibited bladder contract:ions alway~; represent a detrusor pathologic l?t oc~s~s.
540
Material and Meth One hundred and twenty-six tients with primary detrusor dynamic evaluation in the uroc LAC/USC Medical Center be 1986, and October 1987. The mean agei~ia" tients was thirty-nine years (range 21-'~!~!~ i a ,:~ d: mean parity was 2 (range 0-12). Eighty 2~'"~oof these women were premenopausal and 4 Y~JJi.[V¢d postmenopausal. Evaluation included ~ega~ urine culture, history and phy ~'~! oY,rrll~N !0~ with special emphasis on neu tion of $2-$4 lower micturiti. urethroeystoseopy, standing p urethroeystometry (at filling min) and urethral pressure p1 during stress (repeat eoughin: in the abdomen (approxim
UROLOGY
/ JUNE 1991
/
VOLUM]
VAQINAL PRESSURE (CM H20)
BLADDER PRESSURE (CM H=O)
URETHRAL PRESSURE (CM H20)
FIGURE2.
Urethral pressure drop (arrow) precedes detrusor contraction.
Jninhibited detrusor contraction starts change in urethral pressure. Drop in rare occurs only after peak contraction.
bladder, and urethra (at point of ~thral pressure) were measured conusing two 4F microtip pressure (Model 20K 60 and 20K 62, Dantek ~!ectronics, New Jersey). All patients in this se~!eshad unstable bladder (uninhibited detrusor i~ntraction of > 15 cm water on standing pro~cative urethrocystometry) and negative findihagson neurologic screening test of $2-$4 lower ~icturition center. Patients with findings of }~Urethritis (on urethroscopy), cystitis (on cystosl~py), or combined stress incontinence and delirusor instability were not included in this i~udy, i Following clinical and urodynamic evalua!~0a confirming the diagnosis of detrusor insta!ibility,patients received anticholinergic medieaiiion in the form of o x y b u t y n i n chloride ~itropan) 5 mg t.i.d. (which is the drug of i;Choiee for detrusor instability on our service). ~Sideeffects were discussed with patients, and ithey were encouraged not to stop medication !0nee side effects occurred. Patients w i t h ~aucoma were excluded. Clinical and uro~ynarnic evaluations were repeated after four ~'eeks of medical treatment. Cure is defined as isi~ificant improvement or disappearance of ~liaical urinary symptoms and urodynamic :'~fiadings of stable bladder on repeat standing ipr0vocative urethroeystometry. One hundred and fourteen patients were available for post-treatment evaluation and are UROLOGY /
JUNE 1991
/
VOLUME XXXVII, NUMBER 6
the subject of this report. All terminology conforms to that proposed by the International Continence Society ~° except where specifically mentioned. The chi-square test was used for statistical analysis of the data. Results Two patterns of urethral pressure changes correlating with detrusor contraction were identified in women with detrusor instability. The first pattern (Croup I) in 73 of the 114 women (64 % ) demonstrated uninhibited detrusor contraction which started prior to any urethral pressure change (Fig. 1). The second pattern (Group II) in 41 of the 114 women (36 %) demonstrated urethral pressure drop (of 20 cm water or more u) that occurred prior to the detrusor contraction (Fig. 2). There was no difference in the mean age, parity, or menopausal status among women in both groups. Sixty-six of the 114 patients (58 %) with detrusor instability responded favorably to four weeks of anticholinergic therapy while 48 patients (42 %) did not. Most women in Group I (61/73, 84%) responded favorably to oxybutynin chloride while most women in Group II (36/41, 88%) failed to respond to anticholinergics (P < 0.01) (Table I). TABLEI.
Response to oxybutynin chloride in 114 women with detrusor instability
Group I Group II
.Response Good (N = 66) Poor (N = 68) "61 (81%) "12 (16%) 5 (12 %) 36 (88 % )
*P < 0.01 by Chi square test.
541
Comment Most women in this series (64 %) had detrusor contraction that preceded any change in urethral pressure (Group I). The majority of these women (84%) responded favorably to antieholinergie treatment. In fact most women in this series who responded favorably to anticholinergics (61/66, 92 %) were in this group. Forty-one women in this study had detrusor contraction which followed urethral pressure drop (Group II). Most of these women (88%) failed to respond to anticholinergics. These results suggest that women in Group II may have a different pathologic process than women in Group I. Bladder pressure changes may be secondary to urethral pressure changes. 5-7 Detrusor contractions is reflectory induced by urethral relaxation during normal micturition. 7 In women with urethral instability, the clinical symptoms of urinary urgency and frequency are most probably secondary to urethral pressure changes. 6 These cases represent p r i m a r y urethral phenomenon where the detrusor muscle responds to change in urethral pressure. It is possible that women with detrusor instability where bladder contraction is preceded by urethral pressure drop have a primary pathologic process in the urethra rather than in the bladder. The different response of women in both groups to anticholinergics suggests that they represent different pathologic processes. Further studies are needed on whether or not detrusor contractions can be inhibited by pre-
542
venting urethral pressure drop in won-detrusor instability that represents pathologic condition in the urethra. LAC/USC Medic 1240 North Miss Los Angeles, Califon (DR. BE: References 1. Turner-Warwick RT: Observation on the function and function of the sphincter and detrusor mechanism, Ur~l~ North America 6:13 (1979). 2. Blaivas JG, Labib KB, Miehalik SJ, and Zayed AAii metric response to propantheline in detrusor hyperreflexi~ i peutic implications, J Urol 124:259 ( 1 9 8 0 ) . . ! 3. Bultitude MI, Mills NH, and Shuttleworth KEDi~ and experimental studies on the action of prostaglandins a~i synthesis inhibitors on detrusor muscle in vitro and in VMi Urol 48:631 (1976). 4, Ulmsten U, Ekman G, and Anderson KE: The effe~ii~i diline treatment in women with motor urge ineontinen~g Obstet Gyneeol 153:619 (1985). .... 5. Bhatia NN, and Bergman A: Urinary urgency f~iil TRH administration during simultaneous urethrocys~6~ Urology 31:180 (1988). . . . :~: 6. Ulmsten U, Henrikson L, and Iosff S: The unstabig ~ Am J Obstet Gyneeol 144:93 (1982). 7. Bradley WE: Physiology of the urinary bladder, ifii~! PC, Gittes RF, Perlmutter AD, and Stamey TA (Eds)i ~hJ Urology, ed 5, Philadelphia, WB Saunders Co, 1986, p p i 8. Bradley WE: Urologic-oriented neurologic examina~l Ostegard DR (Ed): Gynecologic Urology and Urodynam~i ! more, Williams and Wilkins, 1985, pp 63-68. '.i. 9. nhatia NN, and Bergman A: Urodynamie apprais~ii ii!~ [ nal pressure recording as indication of intra abdomin~ ~! changes, Urology 27:482 (1986). 1O. Bates P, et al: Fourth report on the standar&zat!0~ minology(1981),of lower urinary tract function, Br l Ur6f~ 11. Bhatia NN, and Bergman A: Urodynamic predic[a i~ voiding following incontinence surgery, Obstet Gyne'0[: (1984).
UROLOGY / JUNE 1991
VOLUME XXXVII ! ~i:! : ! ~
L RETHRAL PRESSURE CHANGES IN WOMEN /ITH DETRUSOR INSTABILITY 131adder or Urethral Pathologic Process? ] ~ U L E KOONINGS, M.D.
ti3:IE H BERGMAN, M.D. F~ om the Department of Obstetrics and Gynecology, Los Angeles CounW/University of Southern California Medical Center, L~.'.~Angeles, California
AB S '! 1[ ~~~7. -- ~r, e h u n d r e d and fourteen f e m a l e patients had clinical and urod~ det r t. '~' i:~~tLzbii'it~. They all received oxybutynin chloride (Ditropan ) 5 m g t.i.d. eve l~,~ ~.~c ~ :r~0 ealed. Sixty-six of the 114 patients (58 %) responded favorably tre, t;~7te ~t ~ hi,!e ,18 patients (42 %) did not. Based on urethrocystometry, t w o w e "e ~~!~,~~~l:ied: ('~roup I consisted of 73 w o m e n w i t h bladder contraction that p~ in ~'.r,~,~" ~! p~e,csu'e. Group 11 consisted of 41 patients w i t h urethral pressure dro i det,',~,~ cc ntract~on by a f e w seconds. Sixty-one of the 73 w o m e n (84%) in f a v ~r c b~!, ~.~ h)ur weeJ~s of anticholinergic therapy w h i l e 88 percent (36 of 41) of did nc ~ ~.~ < 0,0~!). Our results suggest that w o m e n w i t h bladder contraction ure ;ii~c'l :'~~iaxa~tion represent a different pathologic entity than w o m e n w i t h "cle bili ~.y"
Idic F,~ttl)[,.' 'pri:naelry" detrusor instability (not sect ~.~Iar ~ L,~ ce:atr al nervous system lesion) is a blac d ~r .::~~diition of unknown etiology. ~ Treatmet t [n ::~,~!:~t:xi:ag t he unstable bladder by anticholil3c~r~ljc medications, ~ prostaglandin inhibitors. 3 ~nd ~',aleittm channel blockers 4 is empiric wit[ 1-:ss tt~ariL optimal results. U ret hr~l pressure changes are known to trigger ir[na~ly urgency ~,6 or detrusor contractions eith~.,r in ! kt~. physiologic phenomenon of voiding 7 c,r in cases of tarethral instability. 6 In these case,, tire ch:,,tr~asor muscle contracts in response to u:re:3r~al pressure changes and is not a primar,, l~ladder phenomenon. The present study was uttdertaken in order to study urethral dyn~ rr.ics :ir~twomen with detrusor instability to see wI~eth,~r or not their uninhibited bladder contract:ions alway~; represent a detrusor pathologic l?t oc~s~s.
540
Material and Meth One hundred and twenty-six tients with primary detrusor dynamic evaluation in the uroc LAC/USC Medical Center be 1986, and October 1987. The mean agei~ia" tients was thirty-nine years (range 21-'~!~!~ i a ,:~ d: mean parity was 2 (range 0-12). Eighty 2~'"~oof these women were premenopausal and 4 Y~JJi.[V¢d postmenopausal. Evaluation included ~ega~ urine culture, history and phy ~'~! oY,rrll~N !0~ with special emphasis on neu tion of $2-$4 lower micturiti. urethroeystoseopy, standing p urethroeystometry (at filling min) and urethral pressure p1 during stress (repeat eoughin: in the abdomen (approxim
UROLOGY
/ JUNE 1991
/
VOLUM]
VAQINAL PRESSURE (CM H20)
BLADDER PRESSURE (CM H=O)
URETHRAL PRESSURE (CM H20)
FIGURE2.
Urethral pressure drop (arrow) precedes detrusor contraction.
Jninhibited detrusor contraction starts change in urethral pressure. Drop in rare occurs only after peak contraction.
bladder, and urethra (at point of ~thral pressure) were measured conusing two 4F microtip pressure (Model 20K 60 and 20K 62, Dantek ~!ectronics, New Jersey). All patients in this se~!eshad unstable bladder (uninhibited detrusor i~ntraction of > 15 cm water on standing pro~cative urethrocystometry) and negative findihagson neurologic screening test of $2-$4 lower ~icturition center. Patients with findings of }~Urethritis (on urethroscopy), cystitis (on cystosl~py), or combined stress incontinence and delirusor instability were not included in this i~udy, i Following clinical and urodynamic evalua!~0a confirming the diagnosis of detrusor insta!ibility,patients received anticholinergic medieaiiion in the form of o x y b u t y n i n chloride ~itropan) 5 mg t.i.d. (which is the drug of i;Choiee for detrusor instability on our service). ~Sideeffects were discussed with patients, and ithey were encouraged not to stop medication !0nee side effects occurred. Patients w i t h ~aucoma were excluded. Clinical and uro~ynarnic evaluations were repeated after four ~'eeks of medical treatment. Cure is defined as isi~ificant improvement or disappearance of ~liaical urinary symptoms and urodynamic :'~fiadings of stable bladder on repeat standing ipr0vocative urethroeystometry. One hundred and fourteen patients were available for post-treatment evaluation and are UROLOGY /
JUNE 1991
/
VOLUME XXXVII, NUMBER 6
the subject of this report. All terminology conforms to that proposed by the International Continence Society ~° except where specifically mentioned. The chi-square test was used for statistical analysis of the data. Results Two patterns of urethral pressure changes correlating with detrusor contraction were identified in women with detrusor instability. The first pattern (Croup I) in 73 of the 114 women (64 % ) demonstrated uninhibited detrusor contraction which started prior to any urethral pressure change (Fig. 1). The second pattern (Group II) in 41 of the 114 women (36 %) demonstrated urethral pressure drop (of 20 cm water or more u) that occurred prior to the detrusor contraction (Fig. 2). There was no difference in the mean age, parity, or menopausal status among women in both groups. Sixty-six of the 114 patients (58 %) with detrusor instability responded favorably to four weeks of anticholinergic therapy while 48 patients (42 %) did not. Most women in Group I (61/73, 84%) responded favorably to oxybutynin chloride while most women in Group II (36/41, 88%) failed to respond to anticholinergics (P < 0.01) (Table I). TABLEI.
Response to oxybutynin chloride in 114 women with detrusor instability
Group I Group II
.Response Good (N = 66) Poor (N = 68) "61 (81%) "12 (16%) 5 (12 %) 36 (88 % )
*P < 0.01 by Chi square test.
541
Comment Most women in this series (64 %) had detrusor contraction that preceded any change in urethral pressure (Group I). The majority of these women (84%) responded favorably to antieholinergie treatment. In fact most women in this series who responded favorably to anticholinergics (61/66, 92 %) were in this group. Forty-one women in this study had detrusor contraction which followed urethral pressure drop (Group II). Most of these women (88%) failed to respond to anticholinergics. These results suggest that women in Group II may have a different pathologic process than women in Group I. Bladder pressure changes may be secondary to urethral pressure changes. 5-7 Detrusor contractions is reflectory induced by urethral relaxation during normal micturition. 7 In women with urethral instability, the clinical symptoms of urinary urgency and frequency are most probably secondary to urethral pressure changes. 6 These cases represent p r i m a r y urethral phenomenon where the detrusor muscle responds to change in urethral pressure. It is possible that women with detrusor instability where bladder contraction is preceded by urethral pressure drop have a primary pathologic process in the urethra rather than in the bladder. The different response of women in both groups to anticholinergics suggests that they represent different pathologic processes. Further studies are needed on whether or not detrusor contractions can be inhibited by pre-
542
venting urethral pressure drop in won-detrusor instability that represents pathologic condition in the urethra. LAC/USC Medic 1240 North Miss Los Angeles, Califon (DR. BE: References 1. Turner-Warwick RT: Observation on the function and function of the sphincter and detrusor mechanism, Ur~l~ North America 6:13 (1979). 2. Blaivas JG, Labib KB, Miehalik SJ, and Zayed AAii metric response to propantheline in detrusor hyperreflexi~ i peutic implications, J Urol 124:259 ( 1 9 8 0 ) . . ! 3. Bultitude MI, Mills NH, and Shuttleworth KEDi~ and experimental studies on the action of prostaglandins a~i synthesis inhibitors on detrusor muscle in vitro and in VMi Urol 48:631 (1976). 4, Ulmsten U, Ekman G, and Anderson KE: The effe~ii~i diline treatment in women with motor urge ineontinen~g Obstet Gyneeol 153:619 (1985). .... 5. Bhatia NN, and Bergman A: Urinary urgency f~iil TRH administration during simultaneous urethrocys~6~ Urology 31:180 (1988). . . . :~: 6. Ulmsten U, Henrikson L, and Iosff S: The unstabig ~ Am J Obstet Gyneeol 144:93 (1982). 7. Bradley WE: Physiology of the urinary bladder, ifii~! PC, Gittes RF, Perlmutter AD, and Stamey TA (Eds)i ~hJ Urology, ed 5, Philadelphia, WB Saunders Co, 1986, p p i 8. Bradley WE: Urologic-oriented neurologic examina~l Ostegard DR (Ed): Gynecologic Urology and Urodynam~i ! more, Williams and Wilkins, 1985, pp 63-68. '.i. 9. nhatia NN, and Bergman A: Urodynamie apprais~ii ii!~ [ nal pressure recording as indication of intra abdomin~ ~! changes, Urology 27:482 (1986). 1O. Bates P, et al: Fourth report on the standar&zat!0~ minology(1981),of lower urinary tract function, Br l Ur6f~ 11. Bhatia NN, and Bergman A: Urodynamic predic[a i~ voiding following incontinence surgery, Obstet Gyne'0[: (1984).
UROLOGY / JUNE 1991
VOLUME XXXVII ! ~i:! : ! ~