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Causes of Dysuria after Prostatic Surgery1
CAUSES OF DYSURIA AFTER PROSTATIC SURGERY1 REX E. VAN DUZEN
With the increased popularity of transurethral resection in the treatment of obstructive lesions of the prostate more cases of postoperative dysuria are encountered. Early in this decade, the common practice was to remove only that part which projected into the bladder or elevated the floor the prostatic urethra. I recently saw a series of postoperative cystograms, which showed a slight funneling of the urethra at the internal vesical orifice but this did not extend to the region of the verurnontanum. I have seen other cystograms which showed the prostatic urethra transformed almost into an hourglass continuation of the bladder. Some resectionists state they do not hesitate to go external to the verumontanum if obstructing tissue is present. With this divergence of opinion on how much tissue should be removed, it is natural there are likewise divergent opinions on how to treat the cases of postoperative dysuria. Some have claimed that the cause is rigidity of the prostatic bed, and others consider every case due to insufficient removal of tissue. It is the intent of this paper to recite a few problems as they were presented to me. Case 1. McMo, aged 52 years, first consulted me because of marked dysuria. He had had a suprapubic removal of the median lobe of the prostate at the age of 45 years. One year before I saw him he underwent pros ta tic resection. When the catheter was removed, urination was difficult, and a second resection was performed. Urination was still difficult and shortly before he consulted me, he was advised to have a third resection. Cysto-urethroscopic examination revealed the most complete removal of prostatic tissue from verumontanum to the region of the internal vesical orifice that I have ever seen. The muscular wall of the prostatic bed resembled the posterior wall of a bladder with marked trabeculation. The bladder was separated from the prostatic cavity by a muscular diaphragm, which included the interureteric bar. The ureteral meati were seen on the edge of this diaphragm. The internal vesical orifice was high above the floor of the prostatic urethra and became smaller when the patient attempted to void. I found he had lost the normal downward pull of the trigone muscle. Because of the extensive resection, he had also lost the lateral muscular pull that was reported by Dr. Looney and myself 1 Read before annual meeting, South Central Section, American Urological Association, Excelsior Springs, Mo., Sept. 29, 1939.
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several years ago. As a result, attempt to void only produced contraction of the circular vesical fibers in the diaphragm, and resultant decrease in the size of the opening of the internal vesical orifice. What could one do to remedy this? There certainly was no more prostatic tissue to remove. If the interureteric mus.de was divided, the ureteral orifices would retract and produce lateral retraction of the cut edges of the diaphragm. However, this patient desired to avoid any surgical treatment if possible. I dilated the internal vesical orifice widelywith the Kollman dilator andadvised repeated passage of large urethral sounds. I saw the patient 6 months later and he was voiding freely. Cystoscopy showed a deep laceration in the diaphragm at 5 o'clock, and the diaphragm remained open when he attempted to void. Urethral dilatations were continued for 2 years, and the patient reports now, 5 years after the first observation, that the voiding is free. Case 2. D . F . R ., aged 46 years, consulted me first in 1934. He gave the history of having had a prostatic resection in 1933 fo r chronic prostatitis. Since that time he had had pain in the perineum and difficulty in voiding. Cystogram showed a stricture in the deep urethra and a large funnel neck bladder extending to the verumontanum. Examination of the prostatic urethra through the cystoscope showed a widely resected prostatic urethra. This patient has had extensive treatment of the prostatic urethra with no permanent relief. Treatment has included the passage of sounds, the Elliott heat treatment through the rectum, chemotherapy, and treatment of a spastic colon, with no avail. Injections of testosterone propionate and vitamin B aggravated the symptoms. He has visited several large clinics with no permanent relief. At present he receives the most relief by gentle massage of the remaining prostate, which is felt as a V, and lavage of the bladder with hot boric acid solution. In these cases the resection was most extensive. It might be noted that the resections were done in relatively young men. But we see after many years observation, no suggestion of growth of remaining prostatic tissue. In Case 1 we saw the formation of a diaphragm which causes the urinary obstruction. In Case 2 there was no diaphragm. We only noted that the posterior urethra was spastic. W henever the spastic colitis was aggravated, such as after taking a laxative, urination was more difficult. We have used antispasmodic drugs with no appreciable result. An English writer states the cause of dysuria is due to increased rigidity of the tissues around the prostatic urethra. In Case 2 I suspect there is both spasticity of the prostatic bed and the periprostatic tissues, which produce the same result as :fibrosis of the periurethral tissue. Nesbit has pointed out the frequency of fi.brotic stric-
CAUSES OF DYSURIA AFTER PROSTATIC SURGERY
247
tures in the urethra after resection. This patient had a stricture, but dilatation alone did not relieve him. It is not my intention to leave the impression that dysuria follows prostatic resection only. I have seen diaphragm formation after suprapubic enucleation of the prostate. In 1 case the tissue showed giant cells suggesting tuberculosis. Resection of this diaphragm gave complete relief. Another patient developed the dysuria 6 years after suprapubic enucleation of the prostate. Resection of the posterior portion of the diaphragm only gave relief for 1 month, but resection of tissue in the region of the anterior commissure gave complete and permanent relief. We must always remember the danger of malignancy in cases of dysuria. I recently saw a case of complete retention which developed 15 years after suprapubic enucleation of the prostate. Resection of tissue in region of the anterior commissure showed adenocarcinoma, Grade 4. This case illustrates that malignancy may develop from the compressed prostatic tissue after removal of the adenomatous portion of the prostate and also from the region of the anterior commissure, which has little glandular tissue. Another cause of dysuria after either resection or open surgery is spinal cord disease. In some cases it is difficult to determine the cause. Routine cystoscopic examination should be done before any prostatic surgery is attempted. I do not believe one is able to diagnose many neurogenic disorders of the bladder from cystograms. If one sees a funnel-neck bladder in a cystogram, the diagnosis is easy. However, these are rare, and it is most difficult to make a diagnosis when the bladder neck is hypertonic. The cystometer is a most useful ipstrument, but many urologists do not have access to one and the interpretation of the curve is still controversial. For the average urologist the cystoscope, if correctly used, will offer the best means of diagnqsis. It is not enough to learn the length of the urethra, the size and shape of the prostate, but what about the trigone? Is it hypertrophied? Does it depress the posterior lip of the vesical neck? Watch for lateral retraction of the vesical orifice at "4 and 8 o'clock." When the examining telescope is removed, one should observe whether the fluid escapes under pressure or requires suprapubic pressure to empty the bladder. Our most difficult cases are those of prostatic h:ypertrophy and neurogenic disturbance of bladder function combined. I have found this most frequently associated with diabetes or with primary anemia. In these cases postopera-
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tive stasis has been troublesome. This is often accompanied by infection. I have made it a rule to institute suprapubic drainage when the neurogenic involvement is diagnosed, and later do either a resection or suprapubic enucleation. I do not use the perineal operation in these cases although I prefer it in diabetics if no nerve lesion is demonstrable. I have not tried to discuss the cases of insufficient removal of tissue in this short resume. Everyone sees such cases and repeats the resection or does an open operation. Bladder calculi and bladder diverticula may be the cause of dysuria. Diverticula with wide necks usually are relieved after resection, but those with the small necks are not. It is debatable when one should resect a diverticulum. I believe we should mention the occurrence of carcinoma of the bladder associated with prostatic hypertrophy. It is not difficult to overlook a small carcinoma if there is a large hypertrophy of the prostate. I have seen several such cases in recent years. Such cases could only be diagnosed by a cystoscopic examination. This is especially true if the carcinoma is situated in the bas fond. During the resection, the carcinoma could easily be mistaken for a blood clot. CONCLUSIONS
Dysuria may be due to (1) a muscular or fibrous diaphragm at the internal vesical orifice; (2) fibrosis or spasticity of the prostatic bed; (3) malignancy; (4) neurogenic causes; (5) vesical calculi and diverticula; (6) insufficient removal of tissue; (7) vesical carcinoma.
721 Medical Arts Bldg., Dallas, Texas.
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With the increased popularity of transurethral resection in the treatment of obstructive lesions of the prostate more cases of postoperative dysuria are encountered. Early in this decade, the common practice was to remove only that part which projected into the bladder or elevated the floor the prostatic urethra. I recently saw a series of postoperative cystograms, which showed a slight funneling of the urethra at the internal vesical orifice but this did not extend to the region of the verurnontanum. I have seen other cystograms which showed the prostatic urethra transformed almost into an hourglass continuation of the bladder. Some resectionists state they do not hesitate to go external to the verumontanum if obstructing tissue is present. With this divergence of opinion on how much tissue should be removed, it is natural there are likewise divergent opinions on how to treat the cases of postoperative dysuria. Some have claimed that the cause is rigidity of the prostatic bed, and others consider every case due to insufficient removal of tissue. It is the intent of this paper to recite a few problems as they were presented to me. Case 1. McMo, aged 52 years, first consulted me because of marked dysuria. He had had a suprapubic removal of the median lobe of the prostate at the age of 45 years. One year before I saw him he underwent pros ta tic resection. When the catheter was removed, urination was difficult, and a second resection was performed. Urination was still difficult and shortly before he consulted me, he was advised to have a third resection. Cysto-urethroscopic examination revealed the most complete removal of prostatic tissue from verumontanum to the region of the internal vesical orifice that I have ever seen. The muscular wall of the prostatic bed resembled the posterior wall of a bladder with marked trabeculation. The bladder was separated from the prostatic cavity by a muscular diaphragm, which included the interureteric bar. The ureteral meati were seen on the edge of this diaphragm. The internal vesical orifice was high above the floor of the prostatic urethra and became smaller when the patient attempted to void. I found he had lost the normal downward pull of the trigone muscle. Because of the extensive resection, he had also lost the lateral muscular pull that was reported by Dr. Looney and myself 1 Read before annual meeting, South Central Section, American Urological Association, Excelsior Springs, Mo., Sept. 29, 1939.
245
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REX E . VAN DUZEN
several years ago. As a result, attempt to void only produced contraction of the circular vesical fibers in the diaphragm, and resultant decrease in the size of the opening of the internal vesical orifice. What could one do to remedy this? There certainly was no more prostatic tissue to remove. If the interureteric mus.de was divided, the ureteral orifices would retract and produce lateral retraction of the cut edges of the diaphragm. However, this patient desired to avoid any surgical treatment if possible. I dilated the internal vesical orifice widelywith the Kollman dilator andadvised repeated passage of large urethral sounds. I saw the patient 6 months later and he was voiding freely. Cystoscopy showed a deep laceration in the diaphragm at 5 o'clock, and the diaphragm remained open when he attempted to void. Urethral dilatations were continued for 2 years, and the patient reports now, 5 years after the first observation, that the voiding is free. Case 2. D . F . R ., aged 46 years, consulted me first in 1934. He gave the history of having had a prostatic resection in 1933 fo r chronic prostatitis. Since that time he had had pain in the perineum and difficulty in voiding. Cystogram showed a stricture in the deep urethra and a large funnel neck bladder extending to the verumontanum. Examination of the prostatic urethra through the cystoscope showed a widely resected prostatic urethra. This patient has had extensive treatment of the prostatic urethra with no permanent relief. Treatment has included the passage of sounds, the Elliott heat treatment through the rectum, chemotherapy, and treatment of a spastic colon, with no avail. Injections of testosterone propionate and vitamin B aggravated the symptoms. He has visited several large clinics with no permanent relief. At present he receives the most relief by gentle massage of the remaining prostate, which is felt as a V, and lavage of the bladder with hot boric acid solution. In these cases the resection was most extensive. It might be noted that the resections were done in relatively young men. But we see after many years observation, no suggestion of growth of remaining prostatic tissue. In Case 1 we saw the formation of a diaphragm which causes the urinary obstruction. In Case 2 there was no diaphragm. We only noted that the posterior urethra was spastic. W henever the spastic colitis was aggravated, such as after taking a laxative, urination was more difficult. We have used antispasmodic drugs with no appreciable result. An English writer states the cause of dysuria is due to increased rigidity of the tissues around the prostatic urethra. In Case 2 I suspect there is both spasticity of the prostatic bed and the periprostatic tissues, which produce the same result as :fibrosis of the periurethral tissue. Nesbit has pointed out the frequency of fi.brotic stric-
CAUSES OF DYSURIA AFTER PROSTATIC SURGERY
247
tures in the urethra after resection. This patient had a stricture, but dilatation alone did not relieve him. It is not my intention to leave the impression that dysuria follows prostatic resection only. I have seen diaphragm formation after suprapubic enucleation of the prostate. In 1 case the tissue showed giant cells suggesting tuberculosis. Resection of this diaphragm gave complete relief. Another patient developed the dysuria 6 years after suprapubic enucleation of the prostate. Resection of the posterior portion of the diaphragm only gave relief for 1 month, but resection of tissue in the region of the anterior commissure gave complete and permanent relief. We must always remember the danger of malignancy in cases of dysuria. I recently saw a case of complete retention which developed 15 years after suprapubic enucleation of the prostate. Resection of tissue in region of the anterior commissure showed adenocarcinoma, Grade 4. This case illustrates that malignancy may develop from the compressed prostatic tissue after removal of the adenomatous portion of the prostate and also from the region of the anterior commissure, which has little glandular tissue. Another cause of dysuria after either resection or open surgery is spinal cord disease. In some cases it is difficult to determine the cause. Routine cystoscopic examination should be done before any prostatic surgery is attempted. I do not believe one is able to diagnose many neurogenic disorders of the bladder from cystograms. If one sees a funnel-neck bladder in a cystogram, the diagnosis is easy. However, these are rare, and it is most difficult to make a diagnosis when the bladder neck is hypertonic. The cystometer is a most useful ipstrument, but many urologists do not have access to one and the interpretation of the curve is still controversial. For the average urologist the cystoscope, if correctly used, will offer the best means of diagnqsis. It is not enough to learn the length of the urethra, the size and shape of the prostate, but what about the trigone? Is it hypertrophied? Does it depress the posterior lip of the vesical neck? Watch for lateral retraction of the vesical orifice at "4 and 8 o'clock." When the examining telescope is removed, one should observe whether the fluid escapes under pressure or requires suprapubic pressure to empty the bladder. Our most difficult cases are those of prostatic h:ypertrophy and neurogenic disturbance of bladder function combined. I have found this most frequently associated with diabetes or with primary anemia. In these cases postopera-
248
REX E. VAN DUZEN
tive stasis has been troublesome. This is often accompanied by infection. I have made it a rule to institute suprapubic drainage when the neurogenic involvement is diagnosed, and later do either a resection or suprapubic enucleation. I do not use the perineal operation in these cases although I prefer it in diabetics if no nerve lesion is demonstrable. I have not tried to discuss the cases of insufficient removal of tissue in this short resume. Everyone sees such cases and repeats the resection or does an open operation. Bladder calculi and bladder diverticula may be the cause of dysuria. Diverticula with wide necks usually are relieved after resection, but those with the small necks are not. It is debatable when one should resect a diverticulum. I believe we should mention the occurrence of carcinoma of the bladder associated with prostatic hypertrophy. It is not difficult to overlook a small carcinoma if there is a large hypertrophy of the prostate. I have seen several such cases in recent years. Such cases could only be diagnosed by a cystoscopic examination. This is especially true if the carcinoma is situated in the bas fond. During the resection, the carcinoma could easily be mistaken for a blood clot. CONCLUSIONS
Dysuria may be due to (1) a muscular or fibrous diaphragm at the internal vesical orifice; (2) fibrosis or spasticity of the prostatic bed; (3) malignancy; (4) neurogenic causes; (5) vesical calculi and diverticula; (6) insufficient removal of tissue; (7) vesical carcinoma.
721 Medical Arts Bldg., Dallas, Texas.
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