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The Influence of Prostatic Urethral Anesthesia in Overactive Detrusor in Patients with Benign Prostatic Hyperplasia
0022-534 7/94/1516-1554$03.00/0 THE JOURNAL OF UROLOGY Copyright© 1994 by AMERICAN UROLOGICAL ASSOCIATION, INC.
Vol. 151, 1554-1556, June 1994
Printed in U.S.A.
THE INFLUENCE OF PROSTATIC URETHRAL ANESTHESIA IN OVERACTIVE DETRUSOR IN PATIENTS WITH BENIGN PROSTATIC HYPERPLASIA OSAMU YOKOYAMA,* KEN-ICHI NAGANO, KOUHEI KAWAGUCHI, OSAMU UEKI MITSUO OHKAWA
AND
From the Department of Urology, School of Medicine, Kanazawa University, Kanazawa, Japan
ABSTRACT
We examined the effects of prostatic urethral anesthesia on cystometrography in benign prostatic hyperplasia (BPH) patients with or without neurological disorders. Although cystometrography after anesthesia showed no disappearance of involuntary detrusor contraction, it did demonstrate significant increases in first sensation volume and maximum cystometric capacity in BPH patients without neurological diseases, as well as BPH patients with a history but no physical evidence of neurological disease. Furthermore, the bladder might be augmented more efficaciously in patients with involuntary detrusor contractions. No significant differences were found in first sensation volume or maximum cystometric capacity before and after anesthesia in patients without infravesical obstruction who had documented neurological disease with physical evidence. Our results demonstrated that prostatic urethral anesthesia can be used preoperatively in patients with infravesical obstruction to discriminate whether 1· voluntary detrusor contractions are due to infravesical obstruction or to neurological disease. KEY
WORDS:
prostate, urethra, anest ,esia, prostatic hypertrophy
It is widely believed that more than 50% of the patients with obstruction secondary to benign prostatic hyperplasia (BPH) have involuntary detrusor contractions, defined as detrusor instability, and that in approximately 40% of these patients the instability persists after relief of the obstruction. 1- 3 It is believed to be difficult to avoid incontinence postoperatively when neurogenic disorders are present. In patients with infravesical obstruction and a history of cerebrovascular accident it is difficult, based only on cystometric examination, to ascertain whether involuntry detrusor contraction is due to infravesical obstruction or to the neurological disorder. Concerning the pathophysiology of detrusor instability in patients with infravesical obstruction, Chalfin et al revealed that a transperineal prostatic block with lidocaine eliminated involuntary detrusor contraction in 10 of 11 patients but had no effect in 4 with a normal cystometrogram. 4 They contended that sensory stimuli from an anatomically altered prostatic urethra induced involuntary detrusor contraction. Bors et al examined the effects of urethral and vesical anesthesia on cystometry of patients with spinal cord injuries. 5 The bladder capacity increased less frequently following urethral anesthesia than vesical anesthesia in these patients. These reports suggested that involuntary detrusor contraction caused by neurological disorders can not be restrained by prostatic urethral anesthesia. It is important to determine preoperatively whether involuntary detrusor contraction is due to infravesical obstruction or neurological disorders. Therefore, we examined the effects of prostatic urethral anesthesia on the cystometrogram in patients with BPH with or without neurological disorders.
disease, group 3-37 patients with BPH and documented neurological disease accompanied by physical evidence, and group 4-12 patients without infravesical obstruction who had documented neurological disease accompanied by physical evidence. The numbers and mean ages in the 4 groups are compared in table 1. The sites of neurological lesions that affect micturition are shown in table 2, with most of the patients in groups 2 to 4 having brain lesions, especially cerebrovascular disease. Cystometry before prostatic urethral anesthesia was performed 3 times at intervals of 5 minutes with carbon dioxide as the filling medium at a rate of 100 ml. per minute via a 12F catheter. After confirming that increasing or decreasing rates of bladder volumes remained within 15% on repeated cystometric studies, we began the examination. We defined an overactive detrusor as the presence of involuntary uninhibited detrusor contracTABLE 1. Classification of patients according to the presence or absence of BPH, history of neurological disease and physical evidence of neurological disease
PATIENTS AND METHODS
Group
1 2 3 4 Totals
BPH
History of Neurological Disease
Physical Evidence of Neurological Disease
Yes Yes Yes No
No Yes Yes Yes
No No Yes Yes
No. Pts.
64 20 37 12 133
Mean Age ±SD 71.1 72.5 71.2 69.3 71.2
± ± ± ± ±
6.9 7.4 6.5 9.5 7.2
TABLE 2. Site of neurological lesions in each group
The study was conducted on 133 patients between 54 and 88 years old (mean age 71.2 years) who were referred to our clinic with symptoms of voiding dysfunction. They were divided into the 4 groups: group 1-64 patients with BPH and no history of neurological disease, group 2-20 patients with BPH and a history of neurological disease but no physical evidence of the Accepted for publication November 24, 1993. * Requests for reprints: Department of Urology, School of Medicine, Kanazawa University, Takara-machi 13-1, Kanazawa, 920, Japan. 1554
Areas of Neurological Disease Brain lesions: Cerebrovascular disease Brain atrophy Brain contusion Others Spinal cord lesions Peripheral nerve lesions Total No. pts.
Group 2
Group 3
Group 4
7
22 4 1 3
9
7 1
6
20
1
1 1
37
12
0
1 4
1 0 0
URETHRAL
ANEST"HESIA AND O'VERACTIVE
MCC
FSV
r
A
200
200
-0--
Group
l
(n=64)
l
180
180
--0-
Group
(n=20)
°" u
-Ill--
Group
3 4
(n=37)
160
Group
"'
160
-.-
2
""'
140
140
120
120
100
100
80
80
CL
:'l
Before 50cmH,O [
(n=12)
5min
D D
:0
0
1555
DETRUSOR
50cmH,O [
B
,Y
~
;;f
~
Q)
u
C
"'~
>
10min
urge '"'-"\..
~
50cmH,o[~ 60
60 0
5
10
0
15
5
Time after prostatic ure1hral anesthesia
10
15
15min
(min.)
FIG. 1. Changes in first sensation volume (FSV) and maximum cystometric capacity (MCC) before and after prostatic urethral anesthesia in each group. Values represent means plus or mmus standard error.
urge
50cmH ,O [
~ 50
100
150
0
50
Volume (ml)
MCC
FSV 200
200
z °" u "'n_ :'l oi
180
180
160
160
140
140
-0---
Group
l
(n=37)
--0--
Group
2
(n=9)
Group
3
(n=24)
-
I
"'
MCC
FSV 200
200
180
180
160
160
120
120
0
~
1!
100
100
>
80
80
~
60
""ro :i5
·0
ro
140
©
0
5
10
15
--0--
Overactive
----$----
Normal and underactive
(na37) (na27)
~
"'~ 60
150
FIG. 3. A, cystometrogram from SO-year-old man with BPH and no history of neurological disease (group 1) shows urge to v01d at 4_5 ml. before anesthesia and overactive detrusor. Maximum cystometnc capacity increases significantly 10 and 15 minutes after anesthesia. B, cystometrogram from 81-year-old man with BPH and documented multiple cerebral infarction accompanied by physical evidence (group 3) shows no significant differences in maximum cystometnc capacity before and after anesthesia.
D D
:0
100
Volume (ml)
0
Time after prostatic urethral anesthesia
5
10
15
(min.)
FIG. 2. Changes in first sensation volume (FSV) and maximum cystometric capacity (MCC) before and after prostatic urethral anesthesia in patients with BPH who demonstrated overactive detr'.lsor function on cystometric findings. Values represent means plus or mmus standard error.
120
0
i
>
100 80
11
60
140 120 100
~]· *
80 -
P < 0.05
60 10
15
0
5
10
15
Time after prostatic urethral anesthesia (min.)
tions during cystometry that exceeded 15 cm. water. After measurement of the urethral pressure profile with the same catheter the catheter was fixed at the point of the maximal urethral' pressure. Urethral anesthesia was accomplished instilling 3 to 5 ml. of a mixture of 0.2% benoxinate hydrochloride jelly and 1 % lidocaine through the catheter into the prostatic urethra. Immediately after anesthesia the catheter was reinserted into the bladder to eliminate the urine and anesthetic agent. Cystometric investigations were repeated before, and 5, 10 and 15 minutes after anesthesia. With this method the influence of prostatic urethral anesthesia on cystometry was investigated, with special reference to the changes in first sensation volume and maximum cystometric capacity. All patients tolerated the investigation well and there were no local or systemic adverse reactions to the local anesthesia. Differences between values obtained before and after anesthesia were analyzed by Fisher's direct probability test and Student's t test. RESULTS
Concerning the variations in first sensation volume and maximum cystometric capacity among the patients, we regarded the volume before anesthesia as 100% in each individual,
FIG. 4. Changes Hl first sensat10n volume and maximum cystometric capacity (MCC) before and after . . methral anesthesia in patients with BPH (group 1) who were d1v1ded mto 2 groups according~ to presence or absence of involuntary detrusor contraction. Values represent means plus or minus standard error.
with the volumes after anesthesia expressed as a percentage of the pre-anesthesia volumes. Although cystometrography after anesthesia showed no disappearance of involuntary detrusor contraction, the first sensation volume and maximum cystometric capacity increased significantly 5, 10 and 15 minutes after anesthesia in group 1 compared to the volume before anesthesia (p <0.01, fig. 1). In group 2 first sensation volume increased significantly 5, 10 and 15 minutes after anesthesia (p <0.01) and maximum cystometric capacity increased significantly at 5 and 10 minutes (p <0.05). In groups 3 and 4 no significant differences were found in first sensation volume or maximum cystometric capacity before and after anesthesia, and these values decreased significantly 5 minutes after anesthesia in group 4 (p <0.05). The same examinations were done in 70 patients with BPH and an overactive detrusor (37 in group 1, 9 in group 2 and 24 in group 3, fig. 2). The volumes 5, 10 and 15 minutes after anesthesia in group 3 did not differ significantly from those
1556
PROSTATIC URETHRAL ANESTHESIA AND OVERACTIVE DETRUSOR
before anesthesia. It was noted, however, that the volumes after anesthesia in group 1 increased significantly compared to those before anesthesia. In group 2 first sensation volume increased significantly 5, 10 and 15 minutes after anesthesia (p <0.01), and maximum cystometric capacity increased significantly at 10 minutes (p <0.05). The rates of increased bladder capacity did not differ between groups 1 and 2 but they differed significantly between groups 1 and 3, and between groups 2 and 3 (p <0.01). Representative examples of the response of overactive detrusor to prostatic urethral anesthesia are shown in figure 3. Group 1 patients with BPH and no history of neurological disease were subdivided into 2 groups according to the presence or absence of involuntary detrusor contraction (fig. 4). Compared to before anesthesia, significant increases in first sensation volume and maximum cystometric capacity were observed at all times in patients with overactive detrusor function (p <0.05), while significant increases in only first sensation volume were found after 5, 10 and 15 minutes in the patients with normal and underactive detrusor function (p <0.05). Maximum cystometric capacity 15 minutes after anesthesia in patients with overactive detrusor function differed significantly from that in patients with normal and underactive detrusor function (p <0.05). DISCUSSION
The etiology of detrusor instability in infravesical obstruction is not clearly understood. Various theories have been proposed, including increased sensory stimulation from the prostatic urethra and trigone of the bladder. 4·6 In our study prostatic urethral anesthesia resulted in significant increases in first sensation volume and maximum cystometric capacity among the BPH patients without neurological diseases and those who had a history but no physical evidence of neurological disease. However, in BPH patients and patients without BPH but with obvious neurological diseases no significant differences were found in first sensation volume or maximum cystometric capacity before and after prostatic urethral anesthesia. These results indicate that the bladder might be augmented more effectively in BPH patients than in patients who have neurological disease affecting micturition. Furthermore, the bladder might be augmented more efficaciously in patients with involuntary detrusor contractions. Because intravesical lignocaine had an effect on detrusor instability caused by infravesical obstruction, Reuther et al reported that lignocaine was useful to determine whether detrusor instability was due to infravesical obstruction. 7 By measurement of trigonal sensitivity using a balloon catheter traction technique, Klein suggested that the pressure sensitive receptors in the mucosa or submucosa of the bladder base and posterior urethra had a role in micturition. 8 Mahony et al reported that the most potent facilitative receptors for the micturition reflex were in the posterior urethra. 9 Although there is a possibility that the anesthetic effect extended from the prostatic urethra to the bladder in our study, anesthesia of the prostatic urethra is believed to be more effective than that of only the bladder. We hypothesized that the onset of the micturition reflex was triggered by detrusor contractions induced by increased sensory input from the prostatic urethra in the patients with infravesical obstruction. Accordingly, it was believed that decreasing sensory input from the prostatic urethra might induce enlargement of bladder capacity. Barrington's second reflex, urethral detrusor facilitative reflex, is believed to exist in the cat but its existence in man is uncertain. 9 - 11 Sutherst and Brown examined the effect on bladder pressure of the sudden entry of fluid into the posterior urethra and reported that there was no change in intrinsic bladder pressure following injection, even in patients with an unstable bladder. 11 Chalfin and Bradley postulated that this reflex might exist in man and might even become a significant force in various states of proximal urethral disease, that is BPH resulting in an anatomically altered proximal urethra. 4
They speculated that sensory stimuli from the altered urethra induced detrusor instability, which was eliminated by transperineal prostatic block with lidocaine. While involuntary detrusor contraction could not be eliminated in our study, sensory nerve afferents were imperfectly ablated by prostatic urethral anesthesia. Tissue penetration by lidocaine as a local anesthetic solution is considered to be poor. Previously, we reported that overdistension and increased wall tension of the bladder caused by infravesical obstruction resulted in nerve degeneration with subsequent supersensitivity of the detrusor muscle to acetylcholine in dogs and human subjects, which was considered to be denervation supersensitivity.12-14 There is evidence that increased maximal response of smooth muscle is the result of enhanced synchronization of contraction by virtue of improved smooth muscle cell coupling in the denervated tissues. 15 These findings suggest that in patients with infravesical obstruction nerve degeneration of the bladder wall may have an important role in the persistence and augmentation of involuntary detrusor contraction. Furthermore, considering our evidence, sensory input from the prostatic urethra might be related to initiation of involuntary detrusor contraction. Detrusor instability is believed to be a manifestation of easy irritability of the anatomically altered prostatic urethra and partially denervated detrusor muscle. We found that pro static urethral anesthesia could be used preoperatively in patients with infravesical obstruction to differentiate between involuntary detrusor contractions caused by infravesical obstruction and those caused by neurological disorders. Our results suggest that prostatic urethral anesthesia can predict persistent involuntary detrusor contraction postoperatively at least in patients with neurological disorders. REFERENCES
1. Leppanen, M. K.: A cystometric study of the function of the urinary bladder in prostatic patients. Urol. Int., 14: 226, 1962. 2. Andersen, J. T.: Detrusor hyperreflexia in benign infravesical obstruction. A cystometric study. J. Urol., 115: 532, 1976. 3. Price, D. A., Ramsden, P. D. and Stobbart, D.: The unstable bladder and prostatectomy. Brit. J. Urol., 52: 529, 1980. 4. Chalfin, S. A. and Bradley, W. E.: The etiology of detrusor hyperreflexia in patients with infravesical obstruction. J. Urol., 127: 938, 1982. 5. Bors, E., Rossier, A. and Sullivan, F. J.: Urological and neurological observations following anesthetic procedures of patients with spinal cord injuries. II. Cystometric and electromyographic effects of topical anesthesias. Urol. Survey, 12: 205, 1962. 6. Andersen, J. T. and Bradley, W. E.: Detrusor and urethral dysfunction in prostatic hypertrophy. Brit. J. Urol., 48: 493, 1976. 7. Reuther, K., Aagaard, J. and Sander Jensen, K.: Lignocaine test and detrusor instability. Brit. J. Urol., 55: 493, 1983. 8. Klein, L. A.: Measurement of trigonal sensitivity as a test of bladder function. J. Urol., 137: 245, 1987. 9. Mahony, D. T., Laferte, R. 0. and Blais, D. J.: Integral storage and voiding reflexes. Neurophysiologic concept of continence and micturition. Urology, 9: 95, 1977. 10. Barrington, F. J. F.: Component reflexes of micturition in cat. Brain, 64: 239, 1941. 11. Sutherst, J. R. and Brown, M.: The effect on the bladder pressure of sudden entry of fluid into the posterior urethra. Brit. J. Urol., 50: 406, 1978. 12. Yokoyama, 0., Kawaguchi, K. and Hisazumi, H.: Denervation supersensitivity of the detrusor muscle due to prolonged bladder overdistension. Acta Urol. Jap., 30: 1, 1984. 13. Yokoyama, 0., Kawaguchi, K. and Hisazumi, H.: Denervation supersensitivity of the detrusor muscle due to bladder overdistension, with special reference to the relationship between supersensitivity, and changes in the connective tissue. Acta Urol. Jap., 31: 2127, 1985. 14. Yokoyama, 0., Nagano, K., Kawaguchi, K. and Hisazumi, H.: The response of the detrusor muscle to acetylcholine in patients with infravesical obstruction. Urol. Res., 19: 117, 1991. 15. Goto, K., Masuda, Y. and Kasuya, Y.: The effect of denervation on the synchronization of contraction of the rat vas deferens. Eur. J. Pharmacol., 36: 395, 1976.
Vol. 151, 1554-1556, June 1994
Printed in U.S.A.
THE INFLUENCE OF PROSTATIC URETHRAL ANESTHESIA IN OVERACTIVE DETRUSOR IN PATIENTS WITH BENIGN PROSTATIC HYPERPLASIA OSAMU YOKOYAMA,* KEN-ICHI NAGANO, KOUHEI KAWAGUCHI, OSAMU UEKI MITSUO OHKAWA
AND
From the Department of Urology, School of Medicine, Kanazawa University, Kanazawa, Japan
ABSTRACT
We examined the effects of prostatic urethral anesthesia on cystometrography in benign prostatic hyperplasia (BPH) patients with or without neurological disorders. Although cystometrography after anesthesia showed no disappearance of involuntary detrusor contraction, it did demonstrate significant increases in first sensation volume and maximum cystometric capacity in BPH patients without neurological diseases, as well as BPH patients with a history but no physical evidence of neurological disease. Furthermore, the bladder might be augmented more efficaciously in patients with involuntary detrusor contractions. No significant differences were found in first sensation volume or maximum cystometric capacity before and after anesthesia in patients without infravesical obstruction who had documented neurological disease with physical evidence. Our results demonstrated that prostatic urethral anesthesia can be used preoperatively in patients with infravesical obstruction to discriminate whether 1· voluntary detrusor contractions are due to infravesical obstruction or to neurological disease. KEY
WORDS:
prostate, urethra, anest ,esia, prostatic hypertrophy
It is widely believed that more than 50% of the patients with obstruction secondary to benign prostatic hyperplasia (BPH) have involuntary detrusor contractions, defined as detrusor instability, and that in approximately 40% of these patients the instability persists after relief of the obstruction. 1- 3 It is believed to be difficult to avoid incontinence postoperatively when neurogenic disorders are present. In patients with infravesical obstruction and a history of cerebrovascular accident it is difficult, based only on cystometric examination, to ascertain whether involuntry detrusor contraction is due to infravesical obstruction or to the neurological disorder. Concerning the pathophysiology of detrusor instability in patients with infravesical obstruction, Chalfin et al revealed that a transperineal prostatic block with lidocaine eliminated involuntary detrusor contraction in 10 of 11 patients but had no effect in 4 with a normal cystometrogram. 4 They contended that sensory stimuli from an anatomically altered prostatic urethra induced involuntary detrusor contraction. Bors et al examined the effects of urethral and vesical anesthesia on cystometry of patients with spinal cord injuries. 5 The bladder capacity increased less frequently following urethral anesthesia than vesical anesthesia in these patients. These reports suggested that involuntary detrusor contraction caused by neurological disorders can not be restrained by prostatic urethral anesthesia. It is important to determine preoperatively whether involuntary detrusor contraction is due to infravesical obstruction or neurological disorders. Therefore, we examined the effects of prostatic urethral anesthesia on the cystometrogram in patients with BPH with or without neurological disorders.
disease, group 3-37 patients with BPH and documented neurological disease accompanied by physical evidence, and group 4-12 patients without infravesical obstruction who had documented neurological disease accompanied by physical evidence. The numbers and mean ages in the 4 groups are compared in table 1. The sites of neurological lesions that affect micturition are shown in table 2, with most of the patients in groups 2 to 4 having brain lesions, especially cerebrovascular disease. Cystometry before prostatic urethral anesthesia was performed 3 times at intervals of 5 minutes with carbon dioxide as the filling medium at a rate of 100 ml. per minute via a 12F catheter. After confirming that increasing or decreasing rates of bladder volumes remained within 15% on repeated cystometric studies, we began the examination. We defined an overactive detrusor as the presence of involuntary uninhibited detrusor contracTABLE 1. Classification of patients according to the presence or absence of BPH, history of neurological disease and physical evidence of neurological disease
PATIENTS AND METHODS
Group
1 2 3 4 Totals
BPH
History of Neurological Disease
Physical Evidence of Neurological Disease
Yes Yes Yes No
No Yes Yes Yes
No No Yes Yes
No. Pts.
64 20 37 12 133
Mean Age ±SD 71.1 72.5 71.2 69.3 71.2
± ± ± ± ±
6.9 7.4 6.5 9.5 7.2
TABLE 2. Site of neurological lesions in each group
The study was conducted on 133 patients between 54 and 88 years old (mean age 71.2 years) who were referred to our clinic with symptoms of voiding dysfunction. They were divided into the 4 groups: group 1-64 patients with BPH and no history of neurological disease, group 2-20 patients with BPH and a history of neurological disease but no physical evidence of the Accepted for publication November 24, 1993. * Requests for reprints: Department of Urology, School of Medicine, Kanazawa University, Takara-machi 13-1, Kanazawa, 920, Japan. 1554
Areas of Neurological Disease Brain lesions: Cerebrovascular disease Brain atrophy Brain contusion Others Spinal cord lesions Peripheral nerve lesions Total No. pts.
Group 2
Group 3
Group 4
7
22 4 1 3
9
7 1
6
20
1
1 1
37
12
0
1 4
1 0 0
URETHRAL
ANEST"HESIA AND O'VERACTIVE
MCC
FSV
r
A
200
200
-0--
Group
l
(n=64)
l
180
180
--0-
Group
(n=20)
°" u
-Ill--
Group
3 4
(n=37)
160
Group
"'
160
-.-
2
""'
140
140
120
120
100
100
80
80
CL
:'l
Before 50cmH,O [
(n=12)
5min
D D
:0
0
1555
DETRUSOR
50cmH,O [
B
,Y
~
;;f
~
Q)
u
C
"'~
>
10min
urge '"'-"\..
~
50cmH,o[~ 60
60 0
5
10
0
15
5
Time after prostatic ure1hral anesthesia
10
15
15min
(min.)
FIG. 1. Changes in first sensation volume (FSV) and maximum cystometric capacity (MCC) before and after prostatic urethral anesthesia in each group. Values represent means plus or mmus standard error.
urge
50cmH ,O [
~ 50
100
150
0
50
Volume (ml)
MCC
FSV 200
200
z °" u "'n_ :'l oi
180
180
160
160
140
140
-0---
Group
l
(n=37)
--0--
Group
2
(n=9)
Group
3
(n=24)
-
I
"'
MCC
FSV 200
200
180
180
160
160
120
120
0
~
1!
100
100
>
80
80
~
60
""ro :i5
·0
ro
140
©
0
5
10
15
--0--
Overactive
----$----
Normal and underactive
(na37) (na27)
~
"'~ 60
150
FIG. 3. A, cystometrogram from SO-year-old man with BPH and no history of neurological disease (group 1) shows urge to v01d at 4_5 ml. before anesthesia and overactive detrusor. Maximum cystometnc capacity increases significantly 10 and 15 minutes after anesthesia. B, cystometrogram from 81-year-old man with BPH and documented multiple cerebral infarction accompanied by physical evidence (group 3) shows no significant differences in maximum cystometnc capacity before and after anesthesia.
D D
:0
100
Volume (ml)
0
Time after prostatic urethral anesthesia
5
10
15
(min.)
FIG. 2. Changes in first sensation volume (FSV) and maximum cystometric capacity (MCC) before and after prostatic urethral anesthesia in patients with BPH who demonstrated overactive detr'.lsor function on cystometric findings. Values represent means plus or mmus standard error.
120
0
i
>
100 80
11
60
140 120 100
~]· *
80 -
P < 0.05
60 10
15
0
5
10
15
Time after prostatic urethral anesthesia (min.)
tions during cystometry that exceeded 15 cm. water. After measurement of the urethral pressure profile with the same catheter the catheter was fixed at the point of the maximal urethral' pressure. Urethral anesthesia was accomplished instilling 3 to 5 ml. of a mixture of 0.2% benoxinate hydrochloride jelly and 1 % lidocaine through the catheter into the prostatic urethra. Immediately after anesthesia the catheter was reinserted into the bladder to eliminate the urine and anesthetic agent. Cystometric investigations were repeated before, and 5, 10 and 15 minutes after anesthesia. With this method the influence of prostatic urethral anesthesia on cystometry was investigated, with special reference to the changes in first sensation volume and maximum cystometric capacity. All patients tolerated the investigation well and there were no local or systemic adverse reactions to the local anesthesia. Differences between values obtained before and after anesthesia were analyzed by Fisher's direct probability test and Student's t test. RESULTS
Concerning the variations in first sensation volume and maximum cystometric capacity among the patients, we regarded the volume before anesthesia as 100% in each individual,
FIG. 4. Changes Hl first sensat10n volume and maximum cystometric capacity (MCC) before and after . . methral anesthesia in patients with BPH (group 1) who were d1v1ded mto 2 groups according~ to presence or absence of involuntary detrusor contraction. Values represent means plus or minus standard error.
with the volumes after anesthesia expressed as a percentage of the pre-anesthesia volumes. Although cystometrography after anesthesia showed no disappearance of involuntary detrusor contraction, the first sensation volume and maximum cystometric capacity increased significantly 5, 10 and 15 minutes after anesthesia in group 1 compared to the volume before anesthesia (p <0.01, fig. 1). In group 2 first sensation volume increased significantly 5, 10 and 15 minutes after anesthesia (p <0.01) and maximum cystometric capacity increased significantly at 5 and 10 minutes (p <0.05). In groups 3 and 4 no significant differences were found in first sensation volume or maximum cystometric capacity before and after anesthesia, and these values decreased significantly 5 minutes after anesthesia in group 4 (p <0.05). The same examinations were done in 70 patients with BPH and an overactive detrusor (37 in group 1, 9 in group 2 and 24 in group 3, fig. 2). The volumes 5, 10 and 15 minutes after anesthesia in group 3 did not differ significantly from those
1556
PROSTATIC URETHRAL ANESTHESIA AND OVERACTIVE DETRUSOR
before anesthesia. It was noted, however, that the volumes after anesthesia in group 1 increased significantly compared to those before anesthesia. In group 2 first sensation volume increased significantly 5, 10 and 15 minutes after anesthesia (p <0.01), and maximum cystometric capacity increased significantly at 10 minutes (p <0.05). The rates of increased bladder capacity did not differ between groups 1 and 2 but they differed significantly between groups 1 and 3, and between groups 2 and 3 (p <0.01). Representative examples of the response of overactive detrusor to prostatic urethral anesthesia are shown in figure 3. Group 1 patients with BPH and no history of neurological disease were subdivided into 2 groups according to the presence or absence of involuntary detrusor contraction (fig. 4). Compared to before anesthesia, significant increases in first sensation volume and maximum cystometric capacity were observed at all times in patients with overactive detrusor function (p <0.05), while significant increases in only first sensation volume were found after 5, 10 and 15 minutes in the patients with normal and underactive detrusor function (p <0.05). Maximum cystometric capacity 15 minutes after anesthesia in patients with overactive detrusor function differed significantly from that in patients with normal and underactive detrusor function (p <0.05). DISCUSSION
The etiology of detrusor instability in infravesical obstruction is not clearly understood. Various theories have been proposed, including increased sensory stimulation from the prostatic urethra and trigone of the bladder. 4·6 In our study prostatic urethral anesthesia resulted in significant increases in first sensation volume and maximum cystometric capacity among the BPH patients without neurological diseases and those who had a history but no physical evidence of neurological disease. However, in BPH patients and patients without BPH but with obvious neurological diseases no significant differences were found in first sensation volume or maximum cystometric capacity before and after prostatic urethral anesthesia. These results indicate that the bladder might be augmented more effectively in BPH patients than in patients who have neurological disease affecting micturition. Furthermore, the bladder might be augmented more efficaciously in patients with involuntary detrusor contractions. Because intravesical lignocaine had an effect on detrusor instability caused by infravesical obstruction, Reuther et al reported that lignocaine was useful to determine whether detrusor instability was due to infravesical obstruction. 7 By measurement of trigonal sensitivity using a balloon catheter traction technique, Klein suggested that the pressure sensitive receptors in the mucosa or submucosa of the bladder base and posterior urethra had a role in micturition. 8 Mahony et al reported that the most potent facilitative receptors for the micturition reflex were in the posterior urethra. 9 Although there is a possibility that the anesthetic effect extended from the prostatic urethra to the bladder in our study, anesthesia of the prostatic urethra is believed to be more effective than that of only the bladder. We hypothesized that the onset of the micturition reflex was triggered by detrusor contractions induced by increased sensory input from the prostatic urethra in the patients with infravesical obstruction. Accordingly, it was believed that decreasing sensory input from the prostatic urethra might induce enlargement of bladder capacity. Barrington's second reflex, urethral detrusor facilitative reflex, is believed to exist in the cat but its existence in man is uncertain. 9 - 11 Sutherst and Brown examined the effect on bladder pressure of the sudden entry of fluid into the posterior urethra and reported that there was no change in intrinsic bladder pressure following injection, even in patients with an unstable bladder. 11 Chalfin and Bradley postulated that this reflex might exist in man and might even become a significant force in various states of proximal urethral disease, that is BPH resulting in an anatomically altered proximal urethra. 4
They speculated that sensory stimuli from the altered urethra induced detrusor instability, which was eliminated by transperineal prostatic block with lidocaine. While involuntary detrusor contraction could not be eliminated in our study, sensory nerve afferents were imperfectly ablated by prostatic urethral anesthesia. Tissue penetration by lidocaine as a local anesthetic solution is considered to be poor. Previously, we reported that overdistension and increased wall tension of the bladder caused by infravesical obstruction resulted in nerve degeneration with subsequent supersensitivity of the detrusor muscle to acetylcholine in dogs and human subjects, which was considered to be denervation supersensitivity.12-14 There is evidence that increased maximal response of smooth muscle is the result of enhanced synchronization of contraction by virtue of improved smooth muscle cell coupling in the denervated tissues. 15 These findings suggest that in patients with infravesical obstruction nerve degeneration of the bladder wall may have an important role in the persistence and augmentation of involuntary detrusor contraction. Furthermore, considering our evidence, sensory input from the prostatic urethra might be related to initiation of involuntary detrusor contraction. Detrusor instability is believed to be a manifestation of easy irritability of the anatomically altered prostatic urethra and partially denervated detrusor muscle. We found that pro static urethral anesthesia could be used preoperatively in patients with infravesical obstruction to differentiate between involuntary detrusor contractions caused by infravesical obstruction and those caused by neurological disorders. Our results suggest that prostatic urethral anesthesia can predict persistent involuntary detrusor contraction postoperatively at least in patients with neurological disorders. REFERENCES
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