THE ESSENTIAL FACTOR IN THE 
OF STRICTURE, AND 
ITS BEARING UPON THE 
QUESTION OF RADICAL 
CURE. 
BY 
JOHN P. BRYSON, M. D„ 
ST. LOUIS. 
REPRINTED FROM THE JOURNAL OF 
CUTANEOUS AND GENITO-URINARY DISEASES 
FOR AUGUST, 1889. THE ESSENTIAL FACTOR IN THE /ETIOLOGY OF STRICTURE, 
AND ITS BEARING UPON THE QUESTION OF RADICAL 
CURE.* 
By JOHN P. BRYSON, M. D., 
St. Louis. 
A STUDY of the aetiology and pathogenesis of urethral stricture in- 
volves, at the outset, a repudiation of that definition which makes 
of it a mere mechanical narrowing of the canal, for any such 
definition includes conditions which no one regards as stricture in the 
true sense of that term. Polypi and warty growths springing from the 
urethral wall cause unnatural narrowings, and are not in any sense strict- 
ures. The same is to be said of collections of fluid in the peri-urethral 
spaces, and of tumors pressing upon the duct. An acute inflammation of 
the prostate gland certainly causes a lessening of the dilatability of that 
part of the urethra, yet it is universally conceded that stricture, as a dis- 
ease, does not affect this part of the canal at all. It is only when one 
regards stricture as a pathological condition of the urethral wall and 
subjacent tissues that he is in a position to study, in a. rational, scientific 
manner, the factors concerned in its inception and development. It is, 
therefore, of stricture as a disease, and not as a mere mechanical narrowing 
of the duct, that I would speak here. 
If, now, we compare a stricture with one of those congenital narrow- 
ings not uncommonly met with in practice, and which is quite as much 
an unnatural narrowing of the canal, we easily note several differences 
both in structure and in pathological behavior. In the case of the 
* Read, in the discussion of " The Question of the Radical Cure of Deep Urethral 
Stricture," before the American Association of Genito-urinary Surgeons at its third 
annual meeting, May 21, 1889. 
vol. vii.-23 282 
Original Communications. 
stricture, we observe that it not only causes a narrowing of the duct, but 
that this constantly increases. In the case of congenital coarctation the 
canal is narrow, it is true, but that narrowing does not increase, but re- 
mains stationary. There is, then, an activity manifested by the former 
disease (stricture) which is totally absent in the latter condition (congeni- 
tal narrowing). We observe, secondly, an anatomical difference, and it is 
one of great importance. In the case of the malformation, the point of 
narrowing is lined by normal and healthy mucous membrane, while the 
stricturing bands are overlaid by a mucous membrane, which is altered 
by inflammation or otherwise diseased, or is totally absent (cicatricial 
stricture). If, now, we apply the same treatment to the two cases, we will 
observe a corresponding difference in the result obtained. Division of the 
congenital narrowing is not followed by recontraction, while in the case 
of the stricture the disposition to recontraction is so marked and distinct 
that to prevent it really constitutes the surgical problem the solution of 
which would rob this formidable disease of its terrors for surgeon and 
patient. 
One may say, then, that the definitive characteristic of stricture, as a 
disease, is the persistent tendency of its constituent elements to multiply, 
to become more dense, and to contract toward the axis of the affected 
canal. This would exclude congenital narrowings from the list of dis- 
eases, and leave them where they belong-among the obstructing conditions, 
they being malformations and lacking the essential element of activity. 
In studying the pathogenesis of this disease we must also make a dis- 
tinction between those conditions which permit the process to begin and 
to continue, and the stricture-building itself. An ulcer, for instance, is 
not a stricture, and can never become one while it remains an ulcer. It is 
when the ulcer heals, and the site is replaced by a cicatrix, that the patho- 
logical processes begin, the sum of which is stricture-building. In a 
word, it is the changed condition of the mucous membrane which permits 
the stricture-forming. Mere inflammation of the urethral mucous mem- 
brane, even in its chronic form, is not stricture, and it is only in certain 
cases that the urethral mucosa is so altered by it as to permit of that peri- 
urethral fibrous overgrowth which constitutes the disease we name strict- 
ure. Here, again, we have an altered condition of the mucous membrane 
preceding the stricture development. Any number of times we see both 
of these pathological processes (inflammation and ulceration) approaching, 
without involving the urethral mucous membrane, from another direction, 
and still no stricture-building is inaugurated. If, however, either of them, 
coming from whatever direction, reaches and modifies the mucosa, we 
seem invariably to see the inception of the stricture disease, provided 
always that this altered state remains for a sufficient length of time. The 
essential thing seems to be that the mucous membranes undergo some not The Essential Factor in the of Stricture. 
283 
yet clearly defined change. This necessary thing being once accom- 
plished, we have a steady and persistent growth of fibrous connective 
tissue underneath the affected portion of the membrane, pushing it more 
and more toward the axis on the one hand, and on the other involving in 
its meshes the underlying and adjacent spongy elements, causing their 
atrophic degeneration, and finally their total disappearance. Thus we see 
it is underneath the membrane that the pathological process is active; and 
even in those cases of cicatricial stricture, on the urethral side of which 
there is no mucous membrane whatever, it is in the peri-urethral tissues 
that development of new tissue goes on, the urethral side only undergoing 
a change marked by condensation. In other words, we have in all cases a 
chronic peri-urethritis, with a distinct tendency to contract toward the 
axis of the canal. 
I would therefore propose the name of chronic contracting peri-ure- 
thritis by which to designate the stricture disease. 
If we include under this designation all cases belonging there, we may 
at once eliminate the microbe as an essential factor in the aetiology. Cer- 
tainly no one will accuse the traumatic cases of being microbian in origin 
or the microbe of having any essential pathogenetic relation to them. The 
researches of Oberlander and Neelson very clearly show the manner in 
which the microbe of gonorrhoea may, as it so frequently does, play the 
principal part in that modification of the mucous membrane which is 
apparently necessary to the inception and continuation of the disease. In 
fact, the disease gonorrhoea has long been known to hold this relation, the 
great majority of inflammatory strictures having followed it in such a way 
as to leave no room for doubt. 
To an English surgeon is due the credit of making the most important 
contribution to our knowledge of the pathogenesis of chronic contracting 
peri-urethritis we have yet had. It was Mr. Reginald Harrison, of Liver- 
pool, who showed that the chronic, persistent deposition of the so-called 
stricture-tissue was really a reaction of the underlying tissues against the 
leakage of urine or some of its numerous constituent elements through 
the altered mucous membrane; and this luminous demonstration not 
only adequately accounts for the different steps in the pathology of the 
disease, but it points the direction which radical treatment should take. 
Under this conception of the pathogenesis of the disease we have the 
changed condition of the mucosa, which permits of urine leakage as the 
essential though passive factor, and the leakage as the active element, 
rousing and maintaining the antagonism of the underlying tissues. This 
does away with the old mechanical one completely and adequately clears 
the field for treatment. 
So long as the old mechanical conception held sway in the surgical 
mind it was but natural that a purely mechanical treatment should be 284 
Original Communications. 
resorted to in order to conquer it. In a certain sense great benefit has 
resulted from this, for surgeons were stimulated to increased and never- 
ceasing efforts to devise new and better apparatus and technique. It was 
out of these efforts and the opportunities which they afforded for observa- 
tion that our present admirable treatment known as " inflammatory atro- 
phic dilatation " grew, and we have learned from our predecessors how to 
apply this method in a rational, scientific manner to the merely obstruct- 
ive part of the disease. So well indeed has the mechanical side of the 
matter been met that it may be seriously questioned whether our present 
armamentarium will ever be improved upon in any essential particular, or 
whether there is need for such improvement. With the means at our 
present command and ordinary skill in their use, one can say that the 
mere obstruction to urination is, in the great majority of cases, capable of 
being easily, safely, and adequately overcome by the modern surgeon. 
Indeed, this does not constitute the difficulty any longer. Here, where 
we have under consideration the question of the radical cure, it is easily 
perceived that it is not a question of removal of the mechanical obstacle so 
much as it is one of permanency of result. It is that treatment which 
will forever prevent recontraction, or, in other words, which will inhibit 
the pathological changes whose activity constitutes the disease that chiefly 
concerns modern surgery, for in our day it is clearly recognized that here 
lies the danger to the patient. 
I can not help thinking that something may be gained by observing the 
manner in which " that cunningest pattern of excellence, Nature," goes 
about treating this disease on her own account. If we watch a case which 
has not been interfered with surgically, we will observe the following course 
of events: As the narrowing progresses there is a gradual dilatation of the 
uninvolved urethra immediately behind the stricture. The walls of this 
dilated portion are rather in a state of atrophy than of inflammation, for 
we get mucus and necrotic epithelia from its surface rather than pus, and 
we observe that it is in a state of venous congestion. There are thinning 
and devitalization; finally, an erosion or an ulcer forms. These changes are 
apt to be greatest at that part immediately posterior to the deeper edge of 
the stricturing band and on the inferior wall of the duct. So low are the 
normal reparative energies that no bands are thrown out to re-enforce it. 
Finally, we have urinary infiltration, or lower down, where there is yet 
enough energy remaining, an abscess cavity forms, points at the surface of 
the body, bursts or is opened, and gives exit to the urine, forming a fist- 
ula ; but at first this is a fistula with soft and yielding walls. Gradually 
energy is gained, the tissues begin to resist the urinary encroachments, 
and we have eventually a fistula with hard walls, this hardening being the 
result of the development of the same kind of tissue that in the beginning 
caused the urethral narrowing; and this tissue behaves in the same way- The Essential Factor in the of Stricture. 
285 
namely, increases in bulk, condenses, and tends to contract upon the open- 
ing so long as urine is permitted to flow through the tract. How of the 
stricture-band in the mean time ? At first, when the fistula has formed 
and has soft walls, there is no great obstruction offered by it, and all the 
urine passes through by the new channel; but, however wide the fistulous 
opening may be, some urine comes in contact with the posterior edge of 
the stricture, perhaps remains constantly in contact, and so there is the 
necessary condition for a continuation of the peri-urethral contraction of 
the stricture-band, and especially of its posterior edge. This answers to this 
stimulation just as the stricture did originally, and tightly seals the urethral 
outlet of the pouch, forcing the urine to pass by the new way. It takes 
time for hard walls to form about the fistula, and more time for them to 
contract to such a degree as to offer great resistance to the urine. When 
they do, we have what seems a battle between the urethral narrowing and 
the obstructive efforts on the part of the fistulous opening, and it is quite 
interesting to observe the successful way in which the peri-urethral bands 
hold their own even when they are, as often occurs, only a line or two in 
breadth, for they are often seen to keep the urethra tightly closed while 
forcing the formation of one, two, several new fistulous outlets, which 
latter have at first soft and yielding walls which offer a minimum of re- 
sistance. 
There is one other phenomenon in this series of changes which is of 
interest as well as of practical value, and that is the behavior of the an- 
terior portion of the stricturing band, off which all urine is kept. For a 
long time I have been in the habit of calling the attention of my assist- 
ants and others about me to the fact that, when I was operating upon a 
case of this kind, where for a long time all the urine had apparently 
passed by fistulous openings, and none by the urethra, we always had to 
deal, at the critical moment, with an extremely narrow stricturing ring, 
in many cases quite resembling a thin diaphragm, through which there 
was still a very small hole to pass a probe. And this was not all. In some 
of the cases it was apparent, on inserting the Avery's threads to hold 
asunder the parts, that there was a pouch, or rather an unnaturally dilata- 
ble condition of the urethral walls in front of the diaphragm-like coarcta- 
tion, as well as behind it, but presenting a different appearance upon 
inspection after the section was made; for the walls of the anterior 
pouch were pale pink and healthy-looking, while those of the one pos- 
terior to the coarctation were soft, friable, covered by necrotic epithelium, 
and with veins deeply injected. For a long time this state of things 
puzzled me, as did the fact that I never found a broad stricture-band 
encircling and compressing the urethra in these cases. I am now per- 
suaded that this condition is the result of the atrophy and disappearance 
of the anterior portion of what was once a broader stricture-band, without 286 
Original Communications. 
reproduction of the normal elements, which had undergone shrinkage 
from pressure of the previously existing connective-tissue elements. Such 
a state of things might be expected to come about after the withdrawal 
of the outer supports of the mucous membrane. And I am all the more 
persuaded that this is the real explanation by watching the changes 
taking place in the walls of the fistulas after the urine was made to pass 
by the natural way or was withdrawn through a catheter; for here we 
observe the atrophy and disappearance of the same kind of tissue as the 
stricturing bands, in a manner quite striking. This, in my observation, 
goes on quite as rapidly and satisfactorily in the cases of fistulas that are 
not as in those that are attacked by the knife. The essential thing seems 
to be the removal of urine from contact. 
Mr. Harrison (" Lettsomian Lectures," 1888, p. 14), in speaking of 
the intention manifested by the tissue development in stricture, says: " In 
this strengthening of the urethra we recognize, in the first instance, a 
conservative action; eventually, however, as in other compensating pro- 
cesses, certain inconveniences follow which constitute, as it were, an inde- 
pendent disease." With that part of this view which regards the develop- 
ment of the stricture-bands in support of the urine-tight state of the 
urethra as conservative I agree; but if I correctly interpret the author 
to mean that the effort of the process to close up the urethra is but an 
accidental and vicious one, or one not equally conservative, I must respect- 
fully dissent from that view. To my thinking, the intent to close up the 
canal at the point of narrowing is manifest from the very beginning, and 
it would seem to be quite as conservative as any other of these phenomena. 
For, if the mucous membrane is no longer functionally efficient, it is 
manifest very soon that, develop and condense as it may, neither is the 
stricturing neoplasm capable of preventing entirely urinary resorption. 
If the effort was solely to strengthen the urethra against the urine, the 
tissue development might just as well be eccentric, wdiereas it is in an 
opposite direction, and with an evident intention. In a word, Nature 
seems early to have realized that the affected mucous membrane is best 
protected and cared for by being squeezed together tightly enough to keep 
urine off it altogether. 
The rate at which this urethral narrowing goes on is another feature of 
practical importance as well as of theoretical interest. We all know that 
the stricture-building process is a distinctly chronic one, requiring months 
and even years in most cases to extensively interfere with the functions of 
the parts, and we can not help regarding this slow rate of progress as an 
important item of conservatism so far, at least, as the life of the affected 
individual is concerned, for it affords opportunity for the development of 
those changes in the tissues immediately posterior to the lesion in such a 
way as least to jeopardize other organs which may be necessarily affected. The Essential Factor in the EEtiology of Stricture. 
287 
It is only by this slow progress that the bladder, ureters, and kidneys are 
protected, even in a small way, by being allowed time for adjustment to the 
new order of things. One sees a different and far more dangerous condi- 
tion arising in those rapidly developing cases of traumatic lesion where 
the passages may be shut up in a few hours by the mere swelling and dis- 
tortion from laceration. 
It is universally conceded that the pathological process concerned in 
the development of the stricture-bands is one of the forms of inflamma- 
tion-contracting, non-suppurative inflammation. The modern pathology 
requires us to believe that we must have a factor at work which is in some 
degree commensurate with the duration of the disease, or, in other words, 
that the inflammation will exist only so long as the causative factor is 
present and efficient. Remove this aetiological factor and the process 
ceases at once, and at least and in many cases there is a retrogressive action 
in the newly formed elements which may and often does go on until 
they have totally disappeared. One of the methods of dealing with the 
purely obstructive part of the disease is to change the constructive into a 
suppurative inflammation. Atrophic, inflammatory dilatation of a strict- 
ure does this and nothing more. May we not accomplish the same retro- 
gressive change by simply removing the factor concerned in the develop- 
ment of the newly formed tissues? I believe we can, not perhaps as 
rapidly as is required in many cases ; but one is hardly permitted to doubt 
that it can be done when he watches the rapid and complete retrogression 
which takes place in the hardened walls of an old urinary fistula after he 
has removed the urine from contact. If we could, in the case of inflam- 
matory stricture where we still have mucous membrane left, restore that 
membrane to its normal condition in every respect, we would, I think, be 
able to cure the disease permanently without either dilatation, cutting, or 
splitting, and the cure or restoration of the normal state of the parts 
would in every respect resemble the changes we observe in the fistulous 
walls after diverting the urinary stream; and it would be just as perma- 
nent or radical. If, however, we should fail in this because of the devel- 
opment of a cicatricial mass incapable of absorption, we would at least 
arrest the process of stricture-building. In the case of cicatricial stricture 
we could accomplish a like result by covering the altered portion of the 
urethral wall with healthy normal mucous membrane (transplantation, 
urethroplasty), though not here to the same extent might the caliber of 
the canal be raised. We would rather in this instance bring about a state 
of things closely resembling those non-progressive and far less dangerous 
states known to us as congenital narrowings. We would then have mal- 
formation, but not stricture in the sense here intended. 
I conclude, then : 
1. That the essential aetiological factor in urethral stricture is a modi- 288 
Original Communications. 
fication of the mucous membrane in such a way as to permit of the leak- 
age of urine or of some of its constituents. 
2. That the surgical indications thus afforded are («) to restore the 
mucous membrane to its normal condition, if that be possible, as it often 
is in inflammatory stricture; or, (#) failing in all efforts to restore the 
membrane, to remove the urine from contact by providing an artificial 
channel for its escape.