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numerous as are those which operate in bringing about subinvolu-
tion. I would like to make the statement still more emphatic
and claim that every case of prolonged subinvolution will with-
out exception pass over into chronic metritis unless treated
systematically and energetically.

I have never seen a true case of chronic metritis in a virgin.
By this I do not mean in a nulliparous woman, but I mean in a
virgin. In the former class, i.e., the nulliparous patients, re-
peated slight abortions may take place without amenorrhea
and without the knowledge of the patient, and there is no more
fruitful source of chronic metritis than abortion, just as there is no
more frequent cause of septic trouble than abortion. Shaw,(i2)
in a paper of three years ago, says he has seen several cases
in virgins and that they do not differ microscopically from those
in the parous women. But we have only to note that Shaw's
only stain was Van Giesen, which gives no differential staining
to the elastic tissue which is the all-important structure. Granted,
then, that subinvolution or defective sequelae of pregnancy are
the causative agents in chronic metritis, how can the microscopical
picture be accounted for?

A triple process is at work, though when thoroughly analyzed
the three resolve themselves into one. If we study a uterus
undergoing involution we find that it builds for itself a complete
new system of arteries throughout its whole walls during involu-
tion, and this takes place not only after the first, but after each
and every pregnancy. To be more emphatic, the blood after
delivery courses through an entirely new system of arteries from
that through which it flowed during pregnancy. The vessels
that supplied the placenta are replaced completely by a new sys-
tem. The old and very large vessel which supplied the placenta
atrophies and during its atrophy it builds for itself out of its

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goodall: climacteric hemorrhages. 37

constituent elements a new and smaller vessel in its lumen. I
regret that I can touch but lightly upon this interesting topic in
the time alloted.(i7)* In this placental area the disproportion
in size between the old and the new vessel is very great, so that
the old wall lies completely outside and beyond the new one which
it surrounds. In vessels which have to undergo such enormous
reduction in size the changes are readily understood, whereas
in the extraplacental portions of the uterus the reduction in
size which the vessel must undergo is not so great, so that the old
vessel may impinge in varying degrees upon the outer portion
of the media of the new one that is contained within its lumen,
and a portion of the media of the old vessel may be retained to
form part of the muscular wall of the new one.

In the first type, that is, in the subplacental areas, the old
vessel ought to undergo complete destruction and absorption,
and in the extraplacental portions the old vessels will undergo
varying degrees of atrophy and disappear, as much of them
being retained as is necessary to complete the new vessel wall.
The least resistant tissue of the old vessel to destructive processes
can be abundantly shown to be the musculature, and the more
resistant is the elastic tissue, and among elastic tissues the
elastica interna of the arteries is very resistant. Now, if the
involution of the uterus is rapid and normal in a young woman,
both these types of tissues in the wall of the old vessel undergo
rapid degeneration and absorption and leave no trace of their
former eixstence. But if involution is slow and retarded; if
chronic disease has sapped the vitality of the patient; if acute
disease has supervened during the puerperium, or if the most
frequent causes, sepsis and retained products, have come into
operation, remarkable and far-reaching changes take place in the
uterine wall. To put the matter tersely, structures that ought
to have been destroyed owing to their no longer having any
function to perform, remain in the various stages of degenerative
change, and the rule applies with all its vigor that the most
highly specialized tissues suffer the most and the less specialized
the least.

But the rule has also a second application which adds a great
deal to our understanding of the process, and that is that the
same causative factors which inhibited the degenerative and
absorptive processes also inhibit regeneration of tissue, and in
the same ratio, that where the most highly specialized cannot be

* See this Journal for December, 1909.

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regenerated a less specialized can be reproduced; that is, where
muscle regeneration is impossible, elastic tissue regeneration is
possible. Hence it is that in chronic metritic cases the uterus
contains a great deal of the old vessel wall that should have been
absorbed. Its musculature has almost completely disappeared,
but its elastic tissues have imdergone tremendous hypertrophy.
The new vessel which has been formed contains varying degrees
of deficiency of muscular tissue and a corresponding degree of
overgrowth of elastic. In other words, where nature cannot
regenerate a highly contractile tissue like muscle it supplies the
next best, namely, elastic tissue.

In the reduction of the veins a somewhat similar process is
at work. Hence it is that in diseased conditions which bring
about subinvolution the result is a hindrance to the normal
changes which take place in the uterus, and the end-product is a
large uterus containing a superabundance of muscle and fibrous
tissue and a relatively very large amount of perivascular elastic

Marchand(i3) and Jores(i4) have clearly shown that, generally
speaking, the thirty-fifth year of age marks an important turning-
point in tissue regenerative powers of the individual. I would
go still farther and say that, roughly speaking, the twenty-fifth
year introduces a much more important turning-point. In the
early years of life muscle is readily regenerated; to wit, how the
heart hypertrophies and compensates in the young, but how inju-
rious the same strenuous exercises of youth become to the athlete
over twenty-five years. In children and young adolescence the
arteries increase their media to meet the demands of the increas-
ing blood pressure. At a certain time in life, roughly speaking
twenty-five years, muscle regeneration becomes less active, but
elastic tissue development is now in the ascendant, and at
thirty-five years elastic regeneration grows less and less marked
and the less specialized fibrous tissue comes into play and is
found to step in where the others and more highly specialized
tissues fail. To me the Jores and Marchand conception is a
grand one which throws a new light upon the whole subject of
arteriosclerosis. In early years of life arteries increase their
strength by hypertrophy and hyperplasia of the muscular media
or by repeated layers of muscle and delicate elastica interna
between the intima and media. These are known as the hyper-
plastic layers of Jores, and take place in all arteries to meet
the demands of increased blood pressure. After twenty-five

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goodall: climacteric hemorrhages. 39

years of age regeneration of muscle becomes less and less com-
plete, but the increase in strength of the vessel wall is now made
up with increasingly greater amounts of elastic tissue, until after
thirty-five years even this specialized resilient tissue is no longer
producible and the less specialized fibrous tissue begins to make
its presence felt. So true is this that I have found even in
children of six to ten years of age who have suffered for years
with chronic rheumatism and chronic nephritis, that muscle
regeneration was almost at a standstill under such diseased con-
ditions, and the strengthening of the vessel walls to meet the
increased blood pressure was almost wholly by elastic tissue.

So it is with the uterus. In the normal young woman filled
with the vigor of health there is complete destruction of tissues
that no longer have a fimction to perform and a complete
regeneration of muscle and a complete return to the virgin state.
But how seldom the puerperium runs its course with all these
favorable circumstances! In eighty uteri of parous women that
I cut and examined during my work in Berlin, there were but two
that had returned to such a normal state that I think even the
most experienced microscopist would fail to detect the difference
between them and the uteri of the virgin. If, then, complete
return to the normal state is so seldom in the young woman, it is
a very rare finding in the woman who bears children after thirty-
five years. The older the women the less complete is her return
to the normal, and women, as men, are as old as their arteries.
Hence it is that women who are predisposed to arteriosclerosis
will be strongly predisposed to chronic metritis. This is quite
in accordance with our experience of cases at the Royal Victoria
Hospital. From this it will be readily gathered that there are
two types of arterial sclerosis in the uterus, just as there are two
types in the ovaries. These are a ftmctional sclerosis and a
true arteriosclerosis.

Therefore the causative agencies which produce subinvolution
operate in bringing about chronic metritis. Moreover, the long-
continued and hotly contested battle between the advocates of
infection and those of noninfective agencies has ceased, and
both sides have won their point. That the causative factor
may lie in the uterus, such as retained products, puerperal
infection, etc., one can readily understand; in fact, herein will
lie the chief cause of subinvolution. That the active agent can
also lie outside the uterus and yet be pelvic is seen in cases of
tuberculosis of the adnexa; and still further, that it may be still

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40 goodall: climacteric hemorrhages.

more remote and yet operate not through infection, but through
diminished vitality or toxemia, is seen in acute as well as
chronic diseases.

Many works have been produced to show — and here, gentle-
men, there is unanimity of opinion; I say many works have been
produced to show that acute disease supervening during the
puerperium, places a "block" upon involution, and the arrest of
involution will be proportionate in its completeness with the
severity of the infection. That infection alone in the virgin or
nullipara, be it gonorrheal or tuberculous, cannot give rise to
true metritis I am fully convinced, for in my experience the uterus
of a virgin or nullipara suffering from tuberculosis or gonorrhoeal
disease is in the first stages enlarged somewhat but is soft and
edematous, but in the later stage is always small, indurated, and

The changes in the endometrium in chronic metritis . will
depend, as you can readily understand, upon the source of the
causative agent, whether the trouble begins in the uterus or
whether it lies extrapelvic.

As to the causes of the hemorrhages, many explanations have
been advanced, none of which as yet seem thoroughly adequate.
Reinicke attributes this symptom to the lack of contractility of
the vessel walls; Theilhaber and Meyer(i5), to the lack of power
of the musculature of the uterus to contract and retract and
thereby arrest the hemorrhage. This weakness they attribute
to the inhibitory influence of the fibrous tissue. The question
is a difficult one and it seems that, from a functional point of
view, to separate the uterine vessel walls from the uterine
musculature is quite unjustifiable.

To me it appears that the uterine contractions and retractions
play the all-important part in the arrest of hemorrhage at labor
and during menstruation, otherwise the flow of blood at men-
struation and after labor would be continuous instead of being
intermittent. But I think also that we must assume that the
thick muscular walls of the arteries have a controlling influence
in arresting hemorrhages from the uterus. If we admit this,
and I think we must, we must also admit that in chronic metritis,
where both the arterial system is so loaded with elastic tissue and
the uterine muscle fibres so inhibited by noncontractile elements,
the controlling influence of both these great factors will be
partially or completely lost. It would be an impossibility to
even guess at the relative importance of these two controlling

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goodall: climacteric hemorrhages. 41

factors, for no two cases need be alike : in this one the arterial
system would be most at fault, in that one the vessels less and
the uterine musculature more culpable.

In Dr. Gardner's and my own work we considered another
important factor in the hemorrhage of chronic metritis, and that
is ovarian function or ovarian secretion. Here, gentlemen^
we are treading upon dangerous ground. My own modest
opinion is as follows: In the milder grades of chronic metritis
the hemorrhages amount to menorrhagia only; in the graver
cases metrorrhagia more or less intermittent comes on; in the
gravest cases metrorrhagia is constant.

In all cases the organ at fault is the uterus. I mean the uterus
broadly speaking, not limiting the meaning to either muscu-
lature or vessels. In the milder cases, where the loss of blood
amounts only to an increase at menstruation, the uterus cannot
control the amount of blood brought to it at the menstrual
pelvic congestion when all the organs are so engorged with
blood. In the graver cases of metrorrhagia the uterine walls
are so diseased that hemorrhage takes place quite independent
of the menstrual pelvic congestion ; that is, when the blood supply
to the pelvis is at its minimum. When looking over the litera-
ture, I find that where ovariotomy had been performed for the
relief of chronic metritis, a certain percentage of cures takes
place. It is in the milder cases that the cures are found, be-
cause the exciting cause of pelvic congestion is removed by
removal of the ovaries. But when hemorrhage continues in-
dependent of menstruation — in other words, where metrorrhagia
is pronounced — the result of ovariotomy was not encouraging.
Hence we may sum up in a few words that the part played by
the ovaries in the production of the hemorrhages of chronic
metritis is simply the marked exacerbations of the hemorrhage
brought about by the pelvic congestion incident to menstru-
ation. But the cause of the unnatural discharges of blood
must be sought in the uterus.

Symptoms and Signs. — ^The one prominent symptom for
which these patients seek relief is hemorrhage. But let me
state most emphatically that not all cases of chronic metritis are
necessarily bleeders. The menstrual flow may not be disturbed
in the slightest. The condition under such circumstances is
generally discovered accidentally. When hemorrhage becomes
a symptom, it may be a slight increase over the normal amount
or it may be very profuse menorrhagia. As a rule, the increase

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42 goodall: climacteric hemorrhages.

in the quantity of blood lost is a slowly progressive one and
may pass eventually through all the stages of menorrhagia, then
intermittent, and finally constant metrorrhagia. The loss of
blood may be alarming and leave the patient weak and almost
exsanguinated. The blood is of a very dark color and almost
free from mucus. As a rule, there is no pain whatever, except
possibly a slight dragging pain in the back. Leucorrhea is
very variable, but, as a rule, a very minor symptom. The pa-
tients are multipara, usually between thirty-five and forty-five
years of age. I have never seen hemorrhage from chronic
metritis supervene once menopause had been definitely estab-
lished; hence it is always before menopause. It is especially
common in women who have had repeated abortions or septic
puerperal troubles. I cannot pass on without a word about the
frequency of chronic metritis in women who have had repeated
abortions and have frequently born dead and macerated
syphilitic children.

On physical examination chronic diseases of the other systems
are frequently found, and especially to be mentioned are arterio-
sclerosis and nephritis. The perineum and vagina show signs
of multiparity; the cervix is almost invariably involved in the
same pathological state as that of the uterus. It is large,
cartilaginous in consistence, and contains numerous Nabothian
cysts. Lacerations are common. The uterine body is larger
than normal and is very firm. It is nearly always markedly
tender to pressure and not infrequently the whole of the genital
tract is involved in this hyperalgesic state. In uncomplicated
cases the uterus will be freely movable and lie in an otherwise
healthy pelvis. But in complicated cases it may be associated
with all degrees of chronic involvement of adnexa, perimetrium,
and parametrium.

Diagnosis. — ^The disease which offers the greatest difficulty
in diagnosis is the case of a submucous fibrous polypus of the
uterine body, which enlarges the uterus but does not destroy
its normal outline. Let the tumor be the size of a pigeon's or
hen's egg and the diagnosis cannot be other than tentative
until operation. Under such conditions the symptoms and
physical signs are exactly alike.

From chronic endometritis it is usually distinguished by
the age of the patient and by the softness of the uterus.

In cancer of the uterine body the consistence of the uterus

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GOOD all: climacteric hemorrhages. 43

is not so firm; moreover, cancer of the body occurs most fre-
quently in nulliparous patients.

From subinvolution the condition is readily differentiated
by the history of recent pregnancy or abortion and by the
softer consistence of the organ.

However, there will be many cases in which nothing but the
curette will clear up the diagnosis, and, gentlemen, in the curette
we have an infallible diagnostic means. In chronic metritis
the uterine cavity is always found very capacious. The tip
of the curette moves about in the uterine body as if in a large
empty space. The chief diagnostic sign lies in the fact that
in true chronic metritis the curette brings nothing but thin
blood away, and the uterus, instead of relaxing, as the normal
uterus does under the curette, presents resistant walls which
are firm, and the curette gives out a rasping sound when drawn
with pressure over the uterine mucosa. This, gentlemen, is
without doubt the diagnostic sign of greatest value.

Treatment, — ^Treatment will resolve itself into prophylactic,
palliative, and operative.

The prophylactic treatment will be directed toward the pre-
vention or removal of all the conditions which leave the uterus
in a state of subinvolution. That is, a more careful routine
examination of the placentas and membranes to see that every-
thing has come away; careful asepsis, and later a careful exami-
nation into the causes of a prolonged lochial discharge; and
finally, a careful examination of patients some weeks after labor
to ascertain that conditions are normal. A persistent retrover-
sion after labor I look upon as a very frequent cause of subinvolu-
tion and later of chronic metritis. But in spite of the greatest
care, in spite of ideal treatment, there will be a goodly percentage
of cases develop from causes over which the physician has no

Palliative treatment will consist in rest, both physiological as
well as physical, and the use of the various ecbolics and hemo-
statics. Among these may be mentioned, ergot, stypticine,
ergotine, suprarenal, viscum album, and gelatin. The most
I can say for these therapeutic measures is that I have seen little
or no effect except that which rest alone will bring about. Mas-
sage and tonics are indicated and not infrequently return of
general strength is associated with a diminution of the loss of

Operative treatment may be divided into minor operative

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44 goodall: climacteric hemorrhages.

measures and the radical cure. Inasmuch as chronic endometritis
may be associated with the chronic metritis, and inasmuch as
when present the diseased endometrium will tend to increase the
hemorrhage, and, moreover, owing to the fact that an associated
endometritis cannot be diagnosticated except by means of the
curette, curettage for the relief of chronic metritis has found
warm advocates. In certain types of cases doubtless the results
are very great, namely, just in those cases where the endometrium
is markedly hypertrophic. Shaw and Donald (i 6) advocate its
use in all cases and claim good results. But what they call
results are very doubtful results indeed. In one of my own cases,
which they take as indicative of the beneficial results of curettage,
the woman was worse after curettage and nearly bled to death
on several occasions before a bettering of the hemorrhages took
place exactly two years after curettage.

The course to be adopted will differ with the class of patients
with whom we have to deal. My own feelings are that among the
leisure classes the patient may be advised to undergo a curettage
and repair of the cervix in the hope of an improvement of the
symptoms. But the surgeon must never neglect to tell the
patient that he is adopting a less severe measure in the patient's
interest, but a measure that is not always followed by success.
If the curette yields but a little or no endometrium the chances
of improvement are indeed very slight and hysterectomy under
those conditions is imperatively demanded. The results from
hysterectomy are sure and satisfactory. As to whether the
procedure will be abdominal or vaginal will depend entirely
upon the nature of the case and the ability of the surgeon.


1. Scanzoni. Krankheiten der weiblichen Sexualorgane, Bd.
i, S. 360.

2. Seifert. Prager Vierieljahrschrifi, xxiii, 1-4, 1866.

3. Finn. Ceniralblati f. med. Wissenschafiy 1868, S. 564.

4. V. Klebs. Handbuch der patholog. Anatomic.

5. Birsch-Hirschfeld. Lehrbuch der patholog. Anatomic.

6. V. Klob. Path. Anatomic der weiblichen Sexualorgane.

7. Kiwisch. Klinische Vortrage, 4 Aufl., i, S. 580.

8. Virchow. Die krankhaf ten Geschwiilste, 1863.

9. Olshausen. Arch, f. Gynecologies 1870.

10. Cornil. Anatomic Patholog. des Metrites. Journal des
Connaissances Medicates, Juin, 1888.

11. Gardner and Goodall. British Medical Journal, Nov. 3,

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brothers: xtnicornate and bicornate uterus. 45

12. Shaw. Journal of Gyn, and ObsL of British Empire,
Feb., 1907.

13. Marchand. Verhandlungen der Gesellschaft fiir Pathol-
ogic, 1902.

14. Jores. Wesen und Entwicklung der Arteriosclerosis.
Wiesbaden, 1903.

15. Theilhaber and Meyer. Die Ursachen der praklimacter-
ischen Blutungen. Arch.f Gyn., Bd. Ixii, S. 415.

16. Donald. Jour, of Gyn. and ObsL of British Emp., Feb.,

17. Goodall. Amer. Jour. Obst. (December, 1909); Arch,
f Gyndkologie; Dec, 1909; Studies from the Royal Victoria




Associate Professor of G)mecology, N. Y. Post-Graduate Hospital;

Visiting Gynecologist, Beth Israel Hospital,

New York City.
(With two illustrations.)

The various malformations of the uterus have been classified
by P. Miiller as follows: a. complete absence of the uterus; b.
atrophy of the uterus; c. absence and atrophy of the uterine
neck; d. one-homed uterus; e. one-homed uterus with atro-
phied second horn; f. the two homed uterus; g. the two-chambered
uterus; h. the double uterus; i. faulty development of the uterus.

I have had the tmusual experience of unexpectedly coming
across two rare and interesting anomalies of the uterus on the
operating table in a short space of time from each other. The
one case was a two-homed uterus, and the other proved to be a
one-horned uterus with rudimentary second horn.

The normal development of the vagina, uterus, and Fallopian
tubes follows a fixed plan by which the ducts of Miiller, passing
downward from the WolflSan bodies and making a half turn on
their longitudinal axes, meet in the median line and, by aggluti-
nation of their walls with final absorption of the interior partitions,
• the single utero-vaginal canal is formed. Any error in this
process may result in congenital malformations. Thus, in the
case of complete absence of the uterus, it is possible that either
the ducts of Miiller were not formed or that they were destroyed.
The various grades or varieties of uterine malformation, in a
similar manner, correspond to the degree and nature of the

Online Libraryof Rhodes. Spurious works AndronicusThe American journal of obstetrics and diseases of women and children → online text (page 5 of 109)