History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: September Supplement, 1938 Vancouver Medical Association Sep 15, 1938

Item Metadata

Download

Media
vma-1.0214360.pdf
Metadata
JSON: vma-1.0214360.json
JSON-LD: vma-1.0214360-ld.json
RDF/XML (Pretty): vma-1.0214360-rdf.xml
RDF/JSON: vma-1.0214360-rdf.json
Turtle: vma-1.0214360-turtle.txt
N-Triples: vma-1.0214360-rdf-ntriples.txt
Original Record: vma-1.0214360-source.json
Full Text
vma-1.0214360-fulltext.txt
Citation
vma-1.0214360.ris

Full Text

 SECTION   TWO
PAPERS READ AT THE ANNUAL MEETING OF THE
BRITISH COLUMBIA MEDICAL ASSOCIATION,
SEPTEMBER 15th to 17th, 1938. SPEAKERS:
Dr. E. G. Bannick, Seattle.
Dr. A. T. Bazin, Professor of Sur-
ery, McGill University, Montreal,
Que.
Dr. William Boyd, Professor of
Pathology, University of Toronto,
Toronto, Ont.
Dr. A. R. Kilgore, Associate Clinical
Professor of Surgery, University of
California, San Francisco, Cal.
Dr. Hans Lisser, Clinical Professor
of Medicine, University of California, San Francisco, Cal.
Dr. K. A. MacKenzie, President,
Canadian Medical Association,
Professor of Medicine, Dalhousie
University, Halifax, N. S.
Dr. L. H. Newburgh, Professor of
Internal Medicine, University of
Michigan, Ann Arbor, Mich. L
MASCULINIZING SYNDROMES;  A CONSIDERATION  OF
CUSHNG'S DISEASE; THE ADRENAL CORTICAL SYNDROME AND ARRHENOBLASTOMA OF THE OVARY
By Dr. Hans Lisser.
It is always a pleasure to come to Victoria and particularly to address this Association.
Every now and again a lady will come to you with a complaint of an embarrassing
excess of hair on the body, perhaps on the face. Frequently this will be the only disturbance, the only abnormal manifestation on examination, and, if such be the case, I quickly
tell you that as far as I know there is nothing to be done about it except to advise depilatory measures. Frankly, I know no organo-therapy that will cause this growth of hair
to vanish.
Now and again, in addition to this, which is, of course, the manifestation of masculin-
ization in the female, there may be some upset and perhaps some disturbance of menstruation. Even when these three facts are combined, the search for the underlying lesion
which may be responsible for this picture tends to be fruitless. Keep such a patient under
more or less periodical observation, on the chance that they may be developing a more
serious lesion, which, later, one can identify and which, if removed, results in a miraculous cure.
The differentiation problem will be taken up in the slides which follow.
You may have thought that I was dealing with just the adult, but the masculinizing
syndrome that occurs in little girls is of great interest. You see here a girl not quite two
years of age. This is so characteristic a syndrome that you can practically recognize it by
a picture or a glance at the patient. You will notice here that there is a protrusion of the
clitoris and so I suggest that a search be made for an adrenal cortical tumour, since this is
the only lesion, as far as I know, which causes this picture. This next picture shows the
patient two years after the removal of the tumour. Here is the clitoris still barely visible,
and here, two years after the lesion has been removed; and also you may note the accompanying absence of hairs. This is pseudo-sexual precocity. Accompanying that picture,
in true sexual precocity, is early menstruation, perhaps in, the first six months, at any rate
in the first six years of life. This is a sort of masculinization—there is practically never
menstruation in the early years of life. That constitutes a very important differential
syndrome. The internal genitalia are not developed. Here is the same picture, two years
after.
The next problem, of course, when you see such a girl and make the diagnosis and have
decided that you are dealing with a lesion of the adrenal cortex, which, of course, may be
a bilateral suprarenal cortical lesion, is to decide which adrenal is involved. This is very
difficult. I have seen a tumour the size of a large apple which could not be palpated even
under an anaesthetic.
One method is by pyelography. In this slide you will note there very decided changes.
The kidney is flattened from above from pressure of the tumour. Here is a picture taken
subsequently, after the tumour had been removed and with the kidney back in normal
position. Many times the tumour is not large enough to distort the pyelogram. You may
resort to the instillation of air through Pettit'si triangle, which is situated here. Through
this triangle you can put a lumbar puncture needle and pump air in, inserting the needle
upward and inward in the direction of the kidney* You go through the transversalis fascia
upwards and you get up into the fascia around the kidney, where, fortunately, there seem
co be no large blood vessels. You pump in 250 cc. of1 air and have pictures taken which
reveal the upper border of the kidney very sharply demarcated, and the lesion can be
localized. This was the tumour in this case and the next slide shows its microscopic appearance. It already shows malignant change. That is very important. These tumours frequently become malignant, but, as a rule, are very well encapsulated, so they are capable
of clean-cut surgical removal with a good opportunity of cure. This girl is alive and well
now, three years since the removal of the tumour. X-ray therapy had been given to
the region.
Here is another girl about three years of age. You will notice the pubic hair, no breast
development. You see this small penis which she has. Here is an example of the visualization
[73] of the adrenal by the insufflation of air in the fascia. You will see the shadow here, but it
is well to remember that the adrenal is not anatomically associated with the kidney. The
urologist will tell you that in operating on the kidney he must be scrupulously careful
where he cuts. Here is a combined picture of the .pyelogram and the air and you will see
here that from this pyelogram you would not recognize any enlargement of the adrenal,
but with the air above it you can visualize the adrenal as decidedly enlarged. This is not
a tumour but hyperplasia. Also note here the set-up of the femur, which, ordinarily, is not
present till 12 years of age. So that with this condition there is marked osseous development.
Going back to the adult woman, the syndrome known as virilism has been recognized
for a great many years. This woman was 3 5 when this picture was taken. She was perfectly
well; had menstruated normally; had had children and nursed them; and then two years
later she appeared this way. Such an appearance in two years made one suspicious of a
malignant lesion. We see here this abnormal growth of pubic hair, hair on the lower legs,
hair on the arms and hair on the face. We see the enlarged clitoris, and also, about a year
between those two pictures, she abruptly stopped menstruating. So with that picture
of abnormal hair growth and masculinization it was very easy to diagnose the picture as
one of adrenal cortical lesion. It was localized and diagnosed. She had a large tumour which
was inoperable. She died later. We saw her too late. Here again we saw someone too late,
and this, I think, is a very pathetic case and points- a lesson to us all in clinical medicine.
This woman was 33; had this beard, masculine breasts; had had four children and nursed
them. This mark here is to show a tumour that was even visible. Two years before
this picture was taken she began to note this growth of hair and she stopped menstruating.
She consulted a physician who did not even disrobe her. He prescribed some injections, but
a year after this treatment was started she had discomfort on the side where the tumour
was located. Here she is when we saw her first. Here is her enlarged clitoris. Here are the
pyelograms, which were not really necessary because the tumour was so large. I pleaded
with Dr. Hinman to operate on this woman even though she had demonstrable metastases
in the lung. He did operate and this tumour was removed. It was a huge thing. She had
a remarkable recovery. She began to menstruate regularly one month after the tumour
was removed. Here is a microscopic picture of the tumour. Here she is six months later,
but, unfortunately of course, it was too late. The improvement was only temporary and
the condition recurred and she died a year later. This was an unnecessary deSath. That
diagnosis should have been made before and her death would have been prevented. I stress
this because if you do encounter this type of case you will be able to recognize it and
save a life.
Here is another one which looks very much the same, but the patient had a very severe
diabetes. It was a case of diabetes of bearded women. She did not have a tumour which
could be visualized.
At the present time we don't know enough about the pathology of the adrenal in
frozen section and, therefore, it is sometimes hard to know how much to remove. I have
not any method of estimating the function of an adrenal. As you know, we need only
leave a small fragment of the adrenal to maintain life. However, in all this surgery it is
most important to prepare the patient properly before surgery with an ample salt intake
and low potassium and to be ready after surgery with an ample supply of salt. If carefully
done before and after, you can tend a patient over the crisis and get her in shape. This
patient had two-thirds of her adrenal removed. Perhaps the error was that, instead of
stopping at that, we turned her over and removed more of the gland. We went too far.
A piece of 'tissue was biopsied and declared to be normal, but later, in a frozen section, was
not normal. She got along very well for 36 hours but later went into shock and expired.
At autopsy we found that the piece we left in at operation was' the adenoma. That sounds
pretty shameful, but I think it is merely a frank statement which shows that not enough
adrenalectomies have been done to show how much to remove and to enable us to recognize
whether we are dealing with hyperplasias or tumours.
We were sorry to lose this case, as we were particularly anxious to see how the diabetes
would have acted after the operation. These pictures show other qases at different age
stages. This woman was quite well until she was 50 years of age and then developed
masculinizing syndromes. Were we dealing with an adrenal tumour or with Cushing's
disease?   In her case we were able to palpate the tumour in the pelvis.  We explored the
[74] pelvis and found the tumour to be a fibroid uterus. However, at operation we did find
another tumour, an arrhenoblastoma of the ovary. These tumours give masculinization of
the patient. There are now about 3 8 such cases on record and in many of them removal
of the tumour has been followed by a re-feminization of the patient. Size has nothing to
do with the case. Some of these tumours fill the entire abdomen. Some of them are
extremely small and impossible to palpate. This is the same woman six months later,
without any depilatory measures having been used. So that is the second condition that is
capable of masculinizing the female and must be borne in mind in differential diagnosis.
I don't think enough of these patients have had a glucose tolerance test to see if there
is any carbohydrate disturbance.
In the absence of a tumour that can be felt in the pelvis or visualized, I question
whether one can, on the basis of clinical endocrine manifestations, differentiate between
these three masculinizing conditions. Here we see this patient in three different stages.
We see the moon face, change in her physical development, abnormal growth of hair. Here
we see her again with the "buffalo" obesity and plethoric appearance. She had hypertension
at 2 8 years of age. She had amenorrhoea. She had a diabetic glucose tolerance curve. She
had everything that Dr. Cushing described in his original article. She came to us in the
fall of 1933 and we labelled her pituitary adenoma. Some of these patients had benefit
from x-ray therapy but nothing spectacular occurs as in the former conditions. The x-ray
of her skull showed a roomy sella turcica. As you know, this ordinarily appears normal,
perhaps small, in neuro-disease. This one, however, was roomy, but I advised an endocrine
investigation. I urged our surgeon to operate and he did, and removed six small fragments
of the hypophysis. I hasten to add that nothing else whatsoever was done for this patient.
Because we wished to keep our skirts olean, we did nothing else. She received no medication
of any kind, and you see her here, over a period of a year. I have heard of others who have
been operated on but these have unfortunately died.
My patient is still alive after five years since operation. We see a decided improvement
in her condition in these slides. You see the change in her face—the acne and redness have
disappeared. We see a change in her figure. Her blood pressure came down to normal and
the diabetic glucose test came down to normal. She menstruated regularly every month
since that operation. In other words, every symptom that she had demonstrated was
relieved. This went on for a year, but then some of her symptoms began to recur. She
has regained a good half of the weight she lost, the blood pressure has gone half way back,
and all the hair has grown back that had dropped out. We assumed that at the end of 1 l/z
years of watchful waiting that the condition in the hypophysis had recurred. We tried
x-ray without any improvement, so then we put her on a reasonable dietary regime. Here
we see her at the present time. Now, here we come to a very interesting point. Basophilic
adenoma was the diagnosis made, but after much investigation we found no basophilic
adenoma. There is nothing further to be done except to try further irradiation. However,
giving a high ootassium intake in the diet and a restriction of salt has had, in a few cases,
some beneficial results. This is the theory of a doctor in California who is now working on
Cushing's disease. She believes that this is the opposite of Addison's disease and that the
treatment, therefore, should be the opposite. This is a rather recent work, however, and
it is too early yet to tell the results.
ACUTE PANCREATITIS
Dr. E. G. Bannick.
I am honoured to have the privilege of addressing this Association. Being an internist,
I feel weak in talking on this suject. For the past thirteen years I have had an opportunity
of seeing a good many patients with acute abdominal disease admitted to the Mayo Clinic,
and during that time have become interested in the topic of acute pancreatitis. This was
for three reasons: (1) The condition was much more common than I had appreciated and
most cases were incorrectly diagnosed; (2) the clinical picture varied very greatly in
the different cases; (3) the prognosis in the majority of cases was a good deal better than
I had anticipated. For these reasons about three years ago I began to make a study of some
proven cases.  After going over the records of nearly 150 surgical or post-mortem cases,
[75 ] I was able to select 72 clear-cut cases. The others were thrown out chiefly because of
inadequate data of various kinds. These 72 cases constitute the basis for this study.
In this first slide I have listed some of the data which were obtained from the records
of these cases. There were 40 females and 32 males in the series. This is different from the
usually accepted figures—these mostly are to the effect that about 65% occur in females.
As to the ai:es, they were mostly middle-aged— between 50 and 65 years of age. However,
the extremes were from age 20 to age 70. There was obesity in 80% of cases; chronic
alcoholism in only 3% of the cases. As to the history of previous abdominal trouble—
76% of these patients had had previous attacks of acute abdominal pain; 90% of these
had been having some sort of trouble, either acute or chronic. The gall bladder had been
previously removed in two cases. In the other cases the gall bladder condition was present
without removal of the gall bladder.
In approaching the problem of differential diagnosis in any acute abdominal disease,
I think that we as physicians and surgeons usually make the mistake of promptly going in
and determining the temperature first and the leukocyte count, putting the hands on the
belly and arriving at a diagnosis. I think if we would take a little more time and survey
the possibilities, the previous data, and the possibilities of this individual having this or
that disease, sometimes we should not make some of the errors that we do make. The
erroneous diagnosis that is made in a considerable number of these cases is perforated
peptic ulcer.
Now, when you look at the data here we see some things which should help in a differential diagnosis. I have divided these 72 cases into 54 cases which I will call acute and 18
which I will call hyper-acute. The separation of these cases into these two clinical groups
makes me understand them much better. The ordinary acute cases were harder to recognize
than the hyper-acute cases. Two-thirds of the 18 cases were properly diagnosed. The
diagnosis in this particular group of cases was either correctly made or the error pointed to
an obscure peritonitis of some type. Now, in the ordinary acute cases* the correct unqualified diagnosis of 54 cases was only made in 2 cases. It was suspected in 7 others. That only
makes 9 cases out of the total.
Here we have quite a different clinical picture from the other group. I have here for
consideration some of the prominent symptoms in order to distinguish these two types of
pancreatitis. Pain is common in every case. It is acute, severe and prolonged in every case.
It required morphia in every case. In only 9 cases of this group was specific left upper
quadrant pain mentioned. However, we can see that it may not be present in these cases.
In some cases it is not crampy but a severe steady pain. Pain in both groups is an extremely
important symptom.
Vomiting is common in both groups. Frequently the vomitus was bloody. Severe pain
in the gall bladder area, unrelieved by the usual measures, associated with vomiting, sometimes gives us the first lead in these cases. There is tenderness in almost all cases, particularly in the hyper-acute cases. In some cases there is mentioned a left-sided pain. Generally
speaking, the tenderness is moderate. There may also be rigidity. In one-third of the hyperacute cases the rigidity was quite marked.
Abdominal distension.—Here we see a distinct difference. In the acute cases there is
usually only mild distension. In the hyper-acute cases, distension of the abdomen was a
general finding.
Shock.—In the. acute group shock was not a common feature. A little shock at the
onset of the attack should give us a lead, but in many cases this shock is a transitory feature.
The relatively infrequent occurrence of shock and distension in this acute group accounts
for the fact that the diagnosis has been overlooked. In the hyper-acute cases, however, the
shock is very marked.
Cyanosis also is more moderate in the acute cases than in the hyper-acute ones, as is
jaundice. The presence of jaundice is a symptom useful in the differentiation of these
cases. Glycosuria is a very significant finding. It is a rare finding, however, as a urinalysis
was not made often enough. Acute abdominal symptoms of the nature that I have
described, associated with glycosuria, give us a lead to acute pancreatitis.
[76] Fever was present in almost all the cases. Temperatures ranged from 99 to 102, usually
100 to 101. Leukocytosis was present in all the cases. Finally, I might mention that in
only 5 of these cases was a definitely enlarged pancreas found.
The mortality figures are interesting. In the hyper-acute cases the mortality is from
90% to 100% regardless of what kind of treatment is employed. The occasional case
that does survive is more apt to do so under conservative than under surgical treatment.
In the ordinary acute cases we tend to employ the more conservative type of treatment.
I hesitate to say anything about the surgical treatment of these cases; first of all, because
I am not a surgeon, and secondly, because there is such a wide variety of opinion. I doubt
if any hard-and-fast rule should be laid down as to conservative medical treatment or
surgical treatment in all cases, or as to the time for surgical treatment in all cases. My
observation is that these cases do better with early surgical than with delayed treatment.
This, however, is a problem.
Since I have completed this study I have seen 16 cases with proven acute pancreatitis
where the diagnosis was accurately made. This is because: (1) More interest in the problem of acute pancreatitis—the knowledge that this condition is not a great rarity and is
to be thought of constantly in the differentiation of acute abdomen; (2) the appreciation
of the clinical conditions of the disease, especially as to the two types; (3) more frequent
blood sugar determinations and urinalyses in suspected cases; (4) the determination of
serum lipase. This is a very valuable test in these cases. Anj elevation in the serum lipase
value is found in nearly all cases of acute pancreatitis and is a valuable test in differential
diagnosis.
PATHOLOGY OF THE GALL BLADDER
Dr. W. J. Boyd
The subject of the pathology of the gall bladder is obviously a big one. I will merely
just cover the subject, and as far as I know, nothing new has been contributed! to the
pathology of the gall bladder in the last ten or more years, so naturally I have nothing new
to give you. I merely wish to look at the subject of the gall bladder from the standpoint of
the pathology and to regard one or two points: (1) Structure and function; (2) inflammation.
If we knew enough, if we were clever enough, X suppose that we could tell, by considering the structure of an organ, what was its function; or if we were told the function
we could build up its structure. If you consider the microscopic appearance of the stomach
and of the small intenstine—the stomach with its great mass of branching glands and the
small intestine with its marvellous array of villi—we1 should, without knowing anything
about the physiology, say that the stomach was a secreting organ while the small intestine
was an absorbing organ. The same is true if we compare the structure of the gall bladder
and that of the urinary bladder. When we look at the structure of the urinary bladder
with a magnifying glass we see that its wall is smooth, it is lined by stratified epithelium,
and we would say that its function is that of storage, which, of course, is true. On the
other hand, if we look at the gall bladder we see that it is by no means smooth. It consists
of an infinite number of very delicate ridges, and when these are examined microscopically
we have an appearance as of villi. The picture which you see there on the slide is merely
a cross section of one of these ridges. We have the very antithesis of the structure of the
urinary bladder; we have the function of absorption here.
It is only owing to the kindness of the surgeon, who will remove, occasionally, a normal
gall bladder, that we can obtain such nice specimens as this. We don't get it at autopsy.
The reason I am stressing these points is that we now know that one of the functions of the
gall bladder is absorption and concentration. As you know, we have the very well known
radiological method—the dye method—of estimating gall bladder function.
With regard to inflammation—inflammation of the gall bladder (cholecystitis) is due
to bacteria, but at the present time there are a remarkable number of different opinions as
to the bacteriology of this condition.   Some years ago Wilkie found the streptococcus
[77] focemolyticus in a very high proportion of these cases. I think we can say with truth that
if a certain phase of work goes out from one university or clinic, and then a subsequent
paper appears from that same university, that confirmation is of comparatively little value;
but when the confirmation comes from some other university, then it is of much more
value. It is interesting to note that the contradiction of Wilkie's work came from Edinburgh University. The modern opinion seems to be that a considerable variety of different
bacteria can be responsible for cholecystitis. There are several routes through which the
bacteria can reach the gall bladder—mainly through the blood stream. The process of
inflammation is that with which you are all familiar. We may have acute or chronic
inflammation. In the gall bladder the pathologist very seldom sees the chronic form of
cholecystitis. In chronic inflammation we have fibrosis occurring. I will now show you
microscopic pictures of chronic inflammation of the gall bladder. There is one peculiarity
which is not usually emphasized in inflammation of the gall bladder—-that is, that it is
diffuse. In the appendix you will find localized inflammation, but here we see diffuse
involvement. We find, as in most chronic inflammations, marked proliferation of the
fibroblasts. In acute cholecystitis, the pathologist rarely sees that picture. We have something analogous to an infarction of the gall bladder. Here is the microscopical picture of
acute cholecystitis.
The strawberry gall bladder is the next condition. The condition is a very interesting
one, but still somewhat of a mystery to us. It is caused by the collection of cholesterol in
the gall bladder. Here we see microscopical slides of this condition. Now, what is this
cholesterol doing there and where is it going? There are two possibilities. One is that the
cholesterol is being absorbed by the bile, and the other, that it is being secreted into the
bile. My own feeling is that it is being absorbed by the bile. Here is a coloured slide which
shows clearly the collection of cholesterol. The meaning of this deposit of lipoid is obscure:
(1) The essential trouble may be a metabolic one; (2) what about the gall bladder wall
itself, quite apart from the cholesterol deposits? If you examine a markedly inflamed or
markedly thickened gall bladder wall, the chances are that you will see no cholesterol. The
best examples are when the gall bladder wall is only slightly thickened. One case I studied
some time ago showed three quarters of the wall chronically thickened and about one-
quarter very slightly thickened, and in this one-quarter we found quite a collection of
cholesterol.
The last feature is that of benign epithelial invasion. There are one or two places in
the body where this occurs. It is best seen, however, in the gall bladder wall and is, often
incorrectly called carcinoma of the gall bladder. It is of most interest to the pathologist,
of course. Here you see slides of this condition. This is a specimen of a gall bladder which
we had in the Museum at Winnipeg for several years. I never could understand it, because
at that time I was unfamiliar with this condition of benign epithelial invasion, but I now
know that that is a remarkable example' of that condition.
TREATMENT OF HIGH BLOOD PRESSURE
Dr. K. A. MacKenzie.
Someone has defined an expert as "an ordinary fellow who has wandered far from
home." Fascinating as it is to explore new fields, where one is occasionally rewarded by a
brilliant discovery, it often happens that the wanderer loses his way, sometimes enters a
blind alley, has to retrace his steps and, frequently, returns with grossly exaggerated
tales of what he has seen, heard or done. In dealing with this subject I disclaim the designation "expert," and wish to be considered a fellow who seldom wanders far from his
medical home, who listens to exaggerated tales with a healthy scepticism, and who labours
diligently, and I hope honestly, in his own fields with results which, in the aggregate, are
quite satisfactory.
High blood pressure is a common malady. It is estimated that there are 200,000 in
Canada; potentially there are many more. The average physician may see from fifty to
one hundred such patients each year.
[78] To simplify our problem we should exclude from this discussion those cases which,
after careful examination, are found to be secondary to definite causes, such as nephritis,
syphilis, gout hyperthyroidism, aortic regurgitation and the rare ardenal tumour. It will
be well to forget, for the time being, all academic discussions as to whether hypertension
is primary or secondary to arteriosclerosis. Etiology may be passed over by stating that the
only known causes, namely heredity and advancing years, are largely beyond control; that
certain alleged causes, such as alcohol, tobacco, obesity, overeating and a high protein diet,
are easily disproven; and that other alleged causes such as endocrine imbalance, intestinal
intoxication, focal infection and the stress and strain of modern life are so vague that
intelligent interpretation is impossible.
Attempts to treat high blood pressure on etiological grounds are, at the present time,
futile and disappointing.
Our therapeutic problem, shorn of its ambiguities, is to help a patient who has high
pressure through a period of inevitably declining vigour with the minimum of risk and
the maximum of safety, comfort and efficiency. There are good reasons why we should
cease to think, talk or act in terms of curing or reducing blood pressure. In the first place,
it cannot be done effectively. Blood pressure can be modified, it is true; but once hypertension develops it remains actually or potentially as long as the patient lives. Secondly,
the underlying organic changes, usually present, are not influenced by any form of treatment. In many instances, perhaps in all, an increased tension is essential for efficient circulation. And thirdly, undue stress on the importance of lowering the blood pressure leads
to disappointment, and tends to create and perpetuate a psychoneurosis which is far more
distressing and disabling than the basic defect. Since blood pressure reading has become
routine, a new disease has been created in the public mind, a blood-pressure phobia which
must be fully recognized in any scheme of treatment. In no other condition is it so fitting
that we should treat the patient and not the disease.
Today text books devote many pages to the discussion of physical agents, drugs, diet,
light and heat, electricity and even surgery. It is curious that the psychological aspects
are passed over as minor matters. One reads such vague advice as "take holidays," "avoid
worry," "go slow," etc. Such commonplace advice is good for all people whether they
have hypertension or not. One also reads that sedatives are advised in order to change a
man's philosophy of life. A man's philosophy is not changed by sedatives; but it can be
changed by conversation, explanation, and by persuasive talks. I am convinced that the
most valuable service which a physician can render to a hypertensive patient is to create a
state of mind which enables him to accept philosophically a condition which is as inevitable
and as incurable as grey hairs, premature baldness, or wrinkly skin. This is accomplished
by a leisurely conversation which may occupy an hour or longer, and during which time
various phases of the problem are discussed and explained in a frank, sympathetic manner,
always keeping in mind the part which fear plays in the production of symptoms. The
omission of this heart-to-heart talk may mar or wholly destroy the effect of excellent
advice.
In outlining the principle of treatment I shall attempt to lay proper stress on the mental
side of treatment. Psychotherapy, or whatever you wish to call it, which is a rational,
easily understood method of treatment, has a definite therapeutic value even if it is not
dispensed in pill, powder or potion. It is within the reach of all practitioners, free from
risk and undesirable effects which follow the injudicious use of drugs, diet, physical agents
of various kinds, and surgery. Every word, action and facial expression, from the preliminary handshake to the cheerful good-bye, should aim at keeping up the morale of the
patient, preventing, and if already present, eliminating the effects of fear.
The first step is a painstaking systematic and sympathetic examination which reveals
organic disease if present, and which introduces appropriate treatment. If hypertension is
the only defect, this examination has a definite value in winning the confidence of the
patient, creating a favourable soil for subsequent explanation and advice. During this
examination casual remarks have a subtle and real value. Such expressions as "You have a
good heart," "Your heart is regular," "You have many good points," 'Your lungs are
normal," "Your colour is good," have a favourable effect on the subconscious mind. You
may detect evidence of this good effect in the countenance of the patient, or in some
remark such as "Thank God for that much anyway."
[79 ] The history and examination completed, an excellent plan is for the doctor and patient
to seat themselves comfortably, facing each other, thus setting the stage for, a heart-to-
heart talk. The resources of the physician are unlimited. The main facts of the problem
are discussed frankly, honestly, and, as far as possible, clearly. Points on physiology may
be explained and will be usually followed witK great interest. One may discuss the physiology of the circulation or general health measures. The physiology of fear may be
described in terms which are easily understood. Fear, which is a mental thing, produces
many symptoms, some physical, some mental; such symptoms as tremors, rapid pulse, rapid
respiration, goose skin, dilated pupils, nausea, vomiting, sweating, even involuntary micturition. It may be pointed out that it matters not whether the cause of the fear is real
or otherwise; for instance, meeting a wild animal produces fear symptoms; seeing a stump
and believing it to be a wild animal has similar effects. Likewise fear of a disease such as
high blood pressure produces nervous symptoms, sleeplessness, etc. The cure is brought
about by taking a rational view of the problem. Many patients are hurt mentally by the
thought of being considered neurotic. Explanation helps them to overcome this distressing
state of mind. The nature and value of remedies may be discussed. The timei is past when
a physician can hand out a prescription with instructions to take it and ask no questions.
People today want to know a lot about remedies and disease; a frank explanation is
appreciated.
Pertinent questions will be asked; replies should be tactful, correct, and, above all,
convincing. Artifice is therapeutically sound and justifiable at times, but should be carefully concealed. Patients may be placed in three categories: The first is the placid individual who is not inclined to become neurotic and who will follow advice with great faithfulness, anxious to do everything that is reasonable. The second group includes those who
defy fate and ignore advice. It may be wise to use extreme frankness and even aim at
alarming the patient in order to persuade him to do the right thing. One should remember,
however, that an air of bravado may conceal a very sensitive nervous system: it is not
always the bully who makes the best soldier. The third group is large and includes those
with strong tendencies to overanxiety and the development of a psychoneurosis. These
tax the resources of the most tactful adviser, and require special care. A common question
is "How high is my pressure?" One should remember that the first reading, taken while
the patient is still excited by the fear of what will be found, is somewhat higher than readings taken after a rest or in the recumbent position. The lower reading is the proper one
to announce. Many patients do not insist on an accurate figure and are quite satisfied with
such a statement as "slightly above normal," "higher than it should be," thus relieving the
physician of making an alarming statement. In very high readings, 250 or over, it may
be wise to resort to a little bit of artifice and say "about 200" or "slightly over 200," both
statements quite true. In all instances there should be no indication of concern or alarm
on the part of the physician. At subsequent examinations a drop in pressure should be
announced with evident satisfaction, while a rise may be passed off with such an expression
as "quite satisfactory."
The question "Is it dangerous?" calls for an emphatic "No." The follow-up conversation should explain common risks which may be illustrated; motoring, sailing, jaywalking or flying are risks which are daily taken without undue regard to the occasional
accident. People accept daily such risks as operations and anaesthetics. The object of this
type of conversation is used to put the risk in the patient's mind at a true and not at an
inflated value. Most people are flattered by the suggestion that they are able to take risks
as soldiers and sailors do. The question "Can I be cured?" can only be answered honestly
in the negative; but one can state with confidence that they can be helped and that life
can be prolonged. It is helpful to explain that hypertension is inevitable in certain people;
that it is consistent with good health and efficiency; that it may, indeed, be beneficial and
necessary; and that they are better off with a raised pressure than with a normal one; that
they may outlive their neighbours (the neighbour may die next week); that they will
probably die of something else; all of which is told in order to convince the patient that
his pressure is not the main worry of his life. One is often asked if there is danger of a
stroke. The danger may be admitted; but it may also be pointed out that the risk of a
stroke in a man of fifty is only 7% while that of cancer' is 14% and pneumonia 12%. In
[80] some instances the mind may be diverted from worry by discussing irrelevant topics; even
an anecdote may prove useful.
The discussion of prognosis is still a part of treatment. Length of life can be forecast
in a group according to insurance statistics but it cannot be forecast in an individual. It
is therefore wrong to tell a patient that he has two or three years to live. To do so is bad
gambling and worse therapeutics. One of my patients has been making a joke of such a
prognosis, given fifteen years ago by a well-known clinician. It is quite wrong to suggest
to a patient that he is in danger of a stroke or of sudden death; that he can be patched up
for a while; or that he should make his will.
Some text books are at fault in stating that the treatment of hypertension is a "hopeless affair," "an almost hopeless task," "very discouraging." The words "hopeless" and
"discouraging" should not be spoken, written or implied. Many hypertensives live twenty
years. Some of my most happy experiences are concerned with this type of patient, and it
is no mean accomplishment to tide such people along in comfort.
At any stage in the conversation advice may be given on rest, diet, exercise and habits.
Instructions should be specific, usually oral, adapted to the individual requirements which
vary widely. Advice on rest and exercise is, as a rule, easy. Absolute rest is indicated for
a limited period when alarming symptoms are present. Work and play can be regulated
at a reasonably low level according to circumstances. Early retiring, longer hours in bed,
the midday nap, one day's rest in seven, and regulation of working hours may be intelligently discussed. Exercise in moderation is beneficial according to the tolerance of the
patient.   Severe restrictions are harmful, mentally and physically.
Diet is very important in the minds of most patients; many faulty diets have been
ordered in the past. One may say that the best diet is a normal one for the individual,
taking into account weight and activities. The average person requires about 2000 calories
daily to meet the ordinary waste of tissue activity. The protein content should not fall
below one gram per kilo. Any great departure from these two principles is probably wrong.
It is very little trouble to have a few specimen diets on hand and to supply the patient with
a written menu or give instructions verbally. To underfeed, is just as objectionable as to
overfeed. Diets too low in protein have been used too frequently in the past. There is no
place in therapy for a salt free diet; it is unpalatable and probably harmful. Salt in moderate
amounts is essential to life and health. Sufficient restrictions are supplied by not using the
salt shaker. Obese patients may have a diet lower than normal for the purpose of reducing
weight. Incidentally the pressure may fall at the same time. Most people eat too much and
definite instructions are necessary. It is quite wrong to tell a patient that he can eat anything he likes and as much as he likes. Alcohol is probably not good for anyone; but if it
is part of a patient's routine there is no good reason why it should be absolutely forbidden.
Tea and coffee in excess are probably harmful but a moderate amount is harmless.
And now we come to the story of specific therapy—of drugs, of Spas, of electricity,
light and heat, a long story of shattered hopes and bitter disappointments. We have in
turn placed reliance on iodides, nitrites, barbiturates, calcium lactate, potassium sulpho-
cyanate, watermellon seeds, mistletoe, ovarian extracts, thyroid and liver extracts, high
frequency currents, diathermy, violet rays, magnesium sulphate and many remedies
which are simply modifications of the above. We have searched for and eradicated focal
infections, and recently the bold inroads of the surgeon have brought us thyroidectomy,
sympathectomy, celiotomy and splanchnicectomy. The widely different nature of these
remedies should arouse suspicion. Frequently they are supported by a modicum of scientific
reasoning, but all the facts are rarely taken into account. They have all been supported
by clinical statistics, and the commercial interests have not been slow to take advantage
of their opportunity to sell their wares. Our offices are deluged with literature making
audacious claims. In the meantime the public is paying a big price for remedies of questionable value. It is not far from the truth to say that all these remedies may be safely omitted
from a sane scheme of treatment, with little or no injustice to patients. Faith in physical
remedies, so firmly planted in the minds of our predecessors, dies slowly, and too many are
still looking for magical cures. This does not mean that we should not continue to seek
new methods; but new remedies should be carefully assessed before they are foisted on a
defenceless public.
[81 ] Having discussed principles which are safe and sufficient for the great majority of
patients, it is now proper to say that there are many special circumstances which fully
justify the employment of physical remedies. One has many opportunities in the treatment
of symptoms. Headache, vertigo, sleeplessness and nervous symptoms can be definitely
helped by sedatives, of which we have a wide choice. Anginal distress is relieved by nitrites,
alcohol and sedatives. Constipation requires attention. Venesection may be a life-saving
measure in cedema of the lungs, some types of coma, severe headache or a threatened cerebral haemorrhage. In plethoric individuals with an unusually high pressure it may give
temporary relief. As a routine procedure it is not desirable. When congestive heart failure
supervenes digitalis is a proper remedy regardless of the level of the pressure. In fact, a
rise in pressure may go hand in hand with clinical improvement. I have a great deal of
sympathy with the physician who takes the line of least resistance and prescribes remedies
which are more or less in popular favour. He^ is honestly trying to do his best. The incidence of the use of drugs will, however, vary in proportion to the skill and the willingness
to spend time in outlining a system of correct living and in building up a state of mind
which enables the patients to accept the disability at its true value. "A glad heart doeth
good like a medicine," and the man who can make and keep the heart glad in the face of an
incurable disability is performing no mean service.
A NEW INTERPRETATION OF DIABETES MELLITUS IN
OBESE MIDDLE-AGED PERSONS; CURE BY
| REDUCTION IN WEIGHT
Dr. L. H. Newburgh.
You are all familiar with the general proposition that there is some important relationship between obesity and diabetes. I want to show you how really important this relationship is. We have made a statistical study of one year's experience at the hospital. We had
370 new admissions for diabetes mellitus. All of these patients who were seen for the first
time were divided into three groups according to age—patients who were less than 3 0 years
of age, middle-age groups (30 to 65), and patients over 65. Most of the patients occur in
this second age group—266 out of a total of 370 are 30 to 65 years of ago. That is the
usual experience of large clinics. In other words, 72% of all the cases are middle-aged.
There were 162 of these patients who were obese when they first came for treatment. This
does not include any patients who may have been obese earlier and who had come down to
normal weight when they came to us. They were definitely overweight at the time of the
first appearance. Roughly speaking about one-half of all individuals, including all of
these very young ones, are overweight when they first present themselves to the doctor for
treatment. This relationship has, of course, been discussed a great deal and the orthodox
statement is that diabetes is a hereditary incurable disease which, as the result of some predisposing cause (in this case adiposity) is brought to the surface. That is, that 50% of
this whole group were born with some fault which at some time or other would make itself
known and be given the term diabetes mellitus. I have come here this morning to try to
persuade you that that view is wrong.
Another definition of diabetes, from the laboratory point of view, is this: The diabetic
is an individual who is less able than normal to oxidize glucose. The patient, if he is a
diabetic, is held out as an individual who is not able to oxidize glucose in the normal
manner. The ability to oxidize glucose can be measured by an elaborate laboratory
apparatus. In order to carry out this kind of a study, the individual must be placed on
some very definite dietary plan for several days in order to get a uniform proportion and
in this first series the patients have been receiving a maintenance diet with the usual
amount of protein and 200 gm. of carbohydrates daily. After three days they are placed
in the apparatus. At the beginning of the period they drink water containing glucose and
for the next four hours the change is recorded, and from the effects one calculates how
much glucose has been oxidized during the three-hour period. Here are three controls
who oxidize glucose with an average of 48 gm. in 4 hours.
[ 82] Here are four middle-aged obese individuals who came to us because they had persistent glycosuria and who were found to have the standard diabetic glucose tolerance
curve. Compared with the normal, they oxidize at least as much glucose as the controls.
Here is another study—the same kind of thing with a slightly different proportion. Here
are the controls—average 43 gm. Here are the obese glycosurics—average 44 gm. No
one could detect any difference in either of these studies. Therefore, it seems to be true
that those individuals who have persistent glycosuria and who have the diabetic glucose
tolerance curve do not have this abnormality of high blood pressure because they are unable
to oxidize glucose. They do oxidize glucose normally and their inability to dispose of all
the glucose in the test must be attributed to some other fact. In normal individuals, as
the glucose is absorbed and passes through the portal vein to the liver, the glucose is
removed from the blood flowing through the liver, and laid down in an insoluble form as
glycogen. If the formation of glycogen is too slow then the blood sugar will be too high.
Unless the fault is in the oxidation of glucose, we are dealing with a condition which is
quite different from what occurs in the young severe diabetic. There it has been shown
over and over again that these young diabetics are actually less able to oxidize glucose than
normal children. Sometimes they are almost completely devoid of that capacity. But these
older persons are different from the younger ones. They have a fault which, strictly
speaking, is not diabetic in nature.
The next obvious thing to do was to see what would happen if the weight of these
people was reduced. They were, therefore, all placed on ordinary common reduction diets
and the glycosuria was completely ignored. We simply reduced their weight and did
nothing else. The next slide will show you the result of that effort. You will see that the
response is entirely normal after reduction of their weight. I will show you this same
response now in the form of a couple of diagrams. Here are a group of 21 individuals
presenting that glucose tolerance with glycosuria and still obese. Here is the result after
reduction of weight to normal, and you see that there is now a normal glucose tolerance.
The next slide will show you a group of patients who are still going through the mill.
Here they are at admission with a very high curve. Here they are when their weight has
been partly reduced, but they still have a considerable distance to go. They have shown
striking improvement, but the curve is still not normal. Many of these persons are now
down to the normal because their weight has come down since that chart was formed.
This sort of a response (slide shown) seems to be especially significant. It shows one
patient's glucose tolerance when she presented herself to us; then here it was after reducing
her weight to normal. Then she went away and gained some weight and you see here her
curve up again. Then we reduced her weight again and here she has a normal curve again.
All of this means to us the following: That about one-half of all the patients whom all
of us ever hear of and who are considered typical classical diabetics .are, in fact, middle-
aged obese individuals who are suffering from a disturbance in the metabolic carbohydrates,
which is different from what occurs in the classical juvenile diabetic—a disturbance which
is clearly a complication of adiposity since it can be removed by reducing the weight to
normal. This condition, then, cannot be a hereditary fault. It is probably of very secondary
importance. The main problem is to get the weight of these people down to normal and
keep it so, whereupon all of these features that we have in the past associated with the high
blood sugar and have called diabetic will disappear. This involves a huge number of individuals. There are statistics from the Metropolitan Life Insurance Company which indicate
that there are, in the United States, about two million of these obese glycosurics, for whom
we must find some term other than diabetics, and who should and can be brought under
control by getting their weight back to normal.
[83 ] CANCER OF THE BREAST
Dr. A. T. Bazin
In speaking on cancer, the points to be stressed are early diagnosis and prompt effective
treatment. Now, the title of my talk this morning is cancer of the breast. Cancer of the
breast is accessible, but it takes care, and meticulous care sometimes, to find cancer in some
breasts, not only because of the size of the breast but because of the character of the breast.
Breasts change their character at different stages. The nodular breast is a normal breast
and is often found if the breast is not well padded with fat, but the nodularity of a nodular
breast which is normal has a very definite regularity. Its nodules are small at the periphery,
gradually getting smaller. One must take that into consideration. All breasts that have
functioned in lactation are nodular after they go through the period of regression from
that activity, and so, in the examination of a breast, one must take into consideration the
age of the individual and the period of activity of that breast. It may be active as a premenstrual activity or as associated with ovarian disease or over-stimulation of the breast.
Of course, it may be active in pregnancy and lactation and then go through the period of
regression.
The early signs of cancer of the breast are three: (1) Lump or area of induration; (2)
discharge in the nipple; or (3) local persistent pain.
In most instances, local persistent pain in the breast, without any trauma immediately
preceding to account for it, is associated with an induration. That induration may be
superficial or it may be deep, but almost invaribly that local persistent pain and tenderness
means the beginning of an inflammatory type of carcinoma. While I am speaking of that
term, it is much better term in my opinion than "the carcinoma of lactation or pregnancy," since these are an inflammatory type. In my experience I have seen quite a few,
but only one was associated with an actively functioning breast—a young woman who
had a pain in her breast when she was nursing her child, and she was assured that it would
disappear after she stopped nursing her child, but it did not. It was inflammatory carcinoma. To finish with inflammatory carcinoma: it is weighty and the patient complains
bitterly of the weight. There is local heat and there is sometimes actually a slight rise in
general temperature. The treatment of this is certainly not operative; that is, not at the
first stage. It is radiation, and not traumatizing radiation. It is x-ray radiation—a
thorough course of this, extending over a period of anywhere from 14 to 21 days, according to the reaction the patient suffers and the amount of dosage they can stand in concentration. And after a lapse of time (five, six or seven weeks, according to the amount of
epidermic damage) then the breast is removed. You can do a radical removal or you can
be content with a simple mastectomy. The prognosis is very grave in any case. In all
probabiliy, distant metastases exist before the patient seeks advice.
Ordinarily, an induration means a definite pathological change. If it is a benign fibroadenoma it is freely mobile inside the breast tissue, but if it is associated with chronic
mastitis, if it is a cyst or a cystic dilatation of a duct, you will get the lump fixed to the
surrounding breast tissue, and, of course, if it is carcinoma it is fixed to the surrounding
breast tissue. It is said that early carcinoma is mobile in the breast. Well, it may be to the
hand but it never really is, because cancer is an invading tumour right from the very
beginning. So one is not absolutely fixing the diagnosis if one gets a mobility of the mass
within the immediately surrounding breast tissue, but that is a point that has to be kept
in mind.
Of course, the tissue of the breast that we are discussing pathologically is the specific
tissue of the breast, and tumours which arise in the epithelial lining of the duct and in that
special type of fibrous tissue are tumours of the breast, but, of course, there may be tumours
in the breast in and on the breast but not of the breast. Tumours of the skin overlying
the breast: tumours of the fat that is interspersed between the lobules of the breast,
tumours of the blood vessels. They occur in the breast but are not of the breast, and
tumours of those tissues do not vary from similar tumours in the same type of tissue elsewhere in the body.
[84] It is wise to adopt a routine in the examination of a patient so that you don't miss
anything. If you have this plan you are very much more secure than if you fly here and
there without any definite plan. So, have a definite plan of examination of the breast.
Establish your own plan and follow it routinely. My own plan in examination of the
breast is, first, get both breasts exposed, the patient sitting upright or standing, and insist
that any corselet or confining band be absolutely removed so that there is no roll of fat
being pushed up under the breast. Inspect for symmetry, variation in size, variation in
level of the nipple, etc., and then give careful attention to the nipple—whether it stands
out straight or upward or downward, whether it is tipped to one side or not. When you
come to palpation, if it is tipped you will find a little cord and that is very suspicious of
a thickening of the duct. If that is associated with discharge from the nipple, then your
suspicion is confirmed. Anchoring of the skin is another thing that is looked for, not only
by inspection but by palpation. If we get this, we have come to a carcinoma which has
gone out from its original site and into the lymphatic tissue. Then there may be peau
d'orange, which means a contraction of Cowper's ligaments, and that contraction is
brought about because carcinoma invades the lymphatic channels and causes a fibrosis of
these ligaments. Then there is, before that appears or perhaps quite independent of that,
a gross dimpling of the skin, especially when the breast is mobile or is mobilized. In change
of posture of the patient you may see a little dimpling of the skin. That can be brought
about by just moving the breast by the fingers and looking at it from different angles and
we get that gross puckering of the skin. Then there is the inability to pick the skin as
freely away from the underlying breast as should be. Flat hand palpation will bring out
the presence of any definite lump but it will not bring out the presence of an area of
induration, because the area of induration shelves gradually into the surrounding tissue of
the breast. Finger and thumb manipulation, picking up the breast and going through
every portion of that breast very carefully—you will get a great deal of information that
way. But all breasts should be palpated very gently because of the danger of rough handling
causing a spreading metastasis. Some surgeon some years ago brought that point out very
forcefully inasmuch as he had a hospital teaching service and had a large practice in1 that
hospital. He had a large number of breast carcinomas in that hospital and he made it a
rule that no one should examine those breasts but himself.
Now, as to transillumination. One would think that it is very easy to transillumine the
breast, but I must confess that I have never become expert at transillumination. In fact,
I have used, from time to time, the best available apparatus, and given it every opportunity
by using a perfectly dark room, and so forth, but I have not been able to satisfy myself
that I was getting any information from transillumination. This has disappointed me so
much that I have given it up. Two months ago I operated on the wife of a surgeon of
repute who has been very confident in the value of transillumination. Her husband examined this lump in the breast very frequently but said nothing about it because he said it
was a cyst by transillumination. Five months later I saw this woman and there was a mass
in the supraclavicular region, and on examination it proved to be carcinoma. The surrounding fat was involved and I am certain that that man was misled by transillumination
for five months. All our different methods of examination should be brought before us
as witnesses, and if the witnesses agree that is fine. If all but one agree, then any judge
would decide in favour of those in the majority.
There is another method of examination when you are in doubt, and that is biopsy.
Punch biopsy, I think, is wrong. First of all, it is not good enough. It is too much to ask
of a fellow to make a diagnosis from a few cells that you have beeni able to get out with
those side-cutting punch scissors; and traumatizing that tissue and giving it every opportunity to metastasize is not good. So I think this type of biopsy should not be done.
Exploration by removal of the tumour, or, if it is a lump, by the removal of the lump,
is best. The Thomas incision is an incision that is carried into the inframammary groove
and you go right down to the pectoral fascia, and if it proves to be a benign tumour, fine.
The breast drops back to position and the scar is practically invisible, but the difficulty
is that this incision interferes with1 radical amputation if the mass proves to be malignant.
So I have modified that incision, and I carry the incision across the lower portion of the
[85] breast and mark out on the lower contour of the breast what portion of that incision
for radical amputation would be just across the lower contour of the breast. I go through
the skin and take that flap down off the breast and then carry out the Thomas
manoeuvre. If it proves malignant, part of your incision is made and you have not interfered with the very valuable lower flap that can be brought out by under-cutting to such a
degree as to close the incision. If you are practically positive that you are dealing with a
benign tumour, then you can make this Thomas incision, but if you are suspicious more
than 5 0 % that you are dealing with a malignant thing, then I think the modified incision
is much better. Now, the question of biopsy. There is no doubt in the mind of anyone
that frozen section biopsy and immediate amputation for malignancy is the best plan.
Nipple leak.—Discharge can come from the nipple—different types of discharge. It
is not uncommon to have1 real milk a long time after lactation has ceased. Then a turbid
fluid will come from either type of inflammation of the breast. This is of very little
significance. Then there is the serous type of discharge and that can come from so-called
chronic mastitis or from duct carcinoma. The latter is much the most probable, and we
must not be too much influenced by authority: "chronic mastitis" is not often an inflammatory process, and is a misnomer for the real condition, a duct carcinoma. I believe there
is an addition to those two types of breast disease—a real chronic mastitis. Take anyone
who has been in practice for a long period of years and who can go back to various stages
in fashions for women. They will remember when the high bust was the fashion for women.
In those days we never saw that wedge-shaped area in the upper outer quadrant of the
breast, especially in young women. Then the fashion changed and it was fashionable to be
flat-breasted. The brassiere flattened the breast, and then it was very common to have
young girls with this pie-shaped, somewhat painful and tender area in the upper outer
quadrant. Those were very frequent in my experience. They disappeared, but now
they have appeared again. Why? Because in the last two or three years it is again fashionable for women to have prominent breasts and the brassieres are modelled to obtain that
effect, and again we don't see these areas of induration in the upper and outer quadrant.
I think that is a real chronic mastitis.
There may be an eczema of the nipple, but Paget's disease of the nipple does not start
on the skin. It always starts as a carcinoma in the nipple and in the duct. It may come to
the surface and along the lymphatics bordering Cowper's ligaments and produce histological Paget's disease of the skin.
There are some confusing conditions which arise in differential diagnosis. Remembering
the anatomy of the breast, you may have carcinoma of the breast originating out in the
axillary lymphatics. You can have supernumerary breasts or supernumerary nipples and
the common site for these is just below the normal breast. Another site for these is in the
axilla, and occasionally you will find a mass in the axilla that is breast without ny duct at
all, and it always gives trouble. When that woman bears children and her normal
breasts are preparing for lactation, this other breast will also undergo this change but will
give rise to a tumour. Another feature is quite a decided enlargement of the glands of the
axilla.   Careful examination of this breast will reveal no lesion.
Now, as to the male breast: It is a rudimentary breast, but it has ducts, and, in some
instances, it has acini and can undergo similar changes to the female breast and one of
these changes is carcinoma. I don't like to hear it said that carcinoma of the male breast
represents only 1 % of carcinomas of the breast. Carcinoma of the male breast occurs in
one out of every hundred of carcinomas of the breast—that is how I like to hear it said.
Now, as to treatment: Radiation first and then removal. Whenever you are in doubt
as to the diagnosis, necessarily you have to operate first. You can't consider preoperative
radiation then. In advanced cases, where there is no doubt about the diagnosis, I believe
that preoperative radiation is advisable, then radical amputation, then after a period of
two or three months another profuse irradiation. Palliation of an absolutely incurable
cancer can be achieved to a certain extent by irradiation. In fact, it is wrong to operate
on some carcinomas of the breast. It doesn't do any good. It threatens life as an operative
risk.
[86] Now, just a word about radiation of carcinoma of the breast. I don't like radium
implants. They are inadequate and are traumatizing. I don't think they are diffuse enough,
and I have given them up and use surface radiation altogether. I believe that x-ray is much
better and more economical than raduim implants of any kind. Of course, if one has
radium in sufficient quantity one can get the same diffuse surface radiation as in using
x-ray. X-radiation should be used with a good high voltage—200 to 250 volts, or, better
still, 400 volts is working out better than the low voltage. There is a very definite danger
in over-radiation. That is, damage to the lung and to the pleura, and many patients suffer
from considerable very irritating coughs, from attacks of fever and illness due to fibrosis
of the lung from an induced bronchiectasis. So care has to be taken in using such a
powerful thing as x-radiation. There has been devised, to overcome that difficulty, a
method of radiation so that the rays pass through the breast without penetrating the
chest wall.
EXTRA-ABDOMINAL DISEASES SIMULATING
| THE "ACUTE ABDOMEN"    §
By Dr. A. R. Kilgore.
Pain is referred from the region where it is produced to other regions where no disease
exists, by two chief mechanisms: If a nerve trunk, accustomed to carry sensations from
an area of skin, is stimulated along its course at a point where it is not accustomed to receive
stimuli, the sensation will be referred; to the skin normally served. This is, of course, the
mechanism by which pain is felt in the toes of an amputated leg or tingling is felt in the
little finger from a sharp blow on the ulnar nerve.
It is responsible for the reference of pain to the abdomen from spinal arthritis or tumour.
The other mechanism involves the central nervous system and is dependent on misinterpretation by the brain of the path by which the painful stimulus reached it. If a
nerve unaccustomed to carry pain at all be strongly stimulated and this nerve reach the
cord in close relation to another nerve which is accustomed to carry pain, the brain may
interpret the sensation as coming by way of this second nerve. Thus the nerves supplying
the pleura and peritoneum of the diaphragm1 are not accustomed to carry sensation of any
kind. If they are strongly stimulated, the pain produced is likely to be interpreted as
corning along peripheral nerves entering the cord in their immediate neighborhood and is
referred then to the areas which these peripheral nerves serve.
Joseph Capps1 at the Cook County Hospital has investigated the reference of pain from
the diaphragm by the simple method of stimulating it with a wire passed through a thoracentesis or paracentesis trochar and has placed our understanding of the paths of this pain
reference on a sound basis.
The nerve supply of both pleural and peritoneal surfaces of the diaphragm is the same.
A peripheral zone from one to four inches wide (narrower in front than behind) is supplied
by the lower six intercostal nerves. The large central zone is supplied by the phrenic nerve.
Stimuli from the pleura near the periphery of the diaphragm are carried to the spinal
cord by fibres going with the intercostal nerves, but since the brain is unaccustomed to
receive painful sensation from the diaphragm they are interpreted as coming by other fibres
in the same intercostal nerves supplying the skin of the flank and abdomen. Since the last
six intercostal nerves supply the skin of the abdomen nearly down to the groin, pain produced on the diaphragm maybe felt over the gall bladder, for instance, or over the appendix.
Stimuli from the central zone of the diaphragm, travelling by the phrenic nerve, enter
the cord at the third and fourth cervical segments. Into these same third and fourth
cervical segments enter nerves supplying the skin of the base of the neck and out toward
the point of the shoulder.  This diaphragmatic pain is likely toi be referred to this region.
Reference of pain to the shoulder is, of course, likely to put us on our guard against a
wrong diagnosis rather than lead us astray. It is reference by way of the intercostal nerves
that presents abdominal localization of pain and so leads to confusion.
Unlike the diaphragmatic pleura and peritoneum, visceral peritoneum has a definite
pain sense and a fair sense of localization.   Pain produced in the appendix or in the gall
[87] bladder is usually felt quite directly over the diseased viscus. Careful attention may distinguish differences between the two kinds of pain. Most important of these is the fact that
true visceral pain is produced by tension within a hollow organ distended with fluid, within
a smooth muscle tube in spasm over a stone or in tissue swollen by inflammation. Pain
referred along intercostal nerves is superficial and not dependent upon tension. So that,
while there is Well-marked tenderness in either case, referred pain will be accompanied by
skin tenderness to pinching, pricking or scratching while the tenderness of visceral disease
will be demonstrated by slow, steady, deep pressure.
Well-marked muscle spasm over the painful area is likely to be present with either
local or referred pain, but the cutaneous reflexes are usually more active with referred pain.
If the diaphragmatic pleurisy is due to lung infection, evidences of respiratory disease
are likely to be present even if physical signs from the chest fail—cough, expectoration,
rapid respiration, herpes of the lips. A very important point is that referred pain is likely
to be induced or aggravated by movements of the diaphragm incident to cough or deep
inspiration. If any of these signs suggest doubt of diagnosis, an x-ray may show the consolidation of a central pneumonia.
Finally, if a sufficient surface of the diaphragm is involved to include the central area
supplied by the phrenic nerve, reference of pain by it to the neck or shoulder also may put
us on the right track.
*      *      «•      *
Whether by these mechanisms or otherwise, acute abdominal pain is produced by a great
variety of extra-abdominal conditions. The first and most important safeguard against
error in diagnosis is to have the possibilities in mind.
A very useful classification of diseases to be considered in differential diagnosis—both
those within and those without the abdomen—-may be made on the basis of the presence
or absence of accompanying signs of inflammation (see Table).
SURGICAL
NON-SURGICAL
With signs of inflammation
Group I
Acute appendicitis
Acute diverticulitis
Acute pancreatitis
Perforated ulcer
Cyst with twisted pedicle
Haemorrhage
Acute  cholecystitis
Group IV
Pneumonia
Coronary thrombosis
Renal  stone  and  pyelitis
Acute tonsillitis
Arachnoidism
Henoch's purpura
Without signs of inflammation
/
i
\
Group II
Intestinal obstruction
Group III
Lead poisoning
Gastric crises
Angina   (without thrombosis)
Renal crisis
Spinal arthritis or tumour
Herpes
Uraemia
Diabetes
Allergy
Erythema multiforme
Angioneurotic oedema
Hysteria
The first group consists of the true abdominal emergencies—acute appendicitis, cholecystitis, pancreatitis, perforated ulcer, mtra-abdominal haemorrhage, twisted pedicle cyst,
etc. It may not always be possible to distinguish these one from another, but we are not
likely to miss the fact that one or other is present for the important reason that they are
all characterized, not only by pain, but by signs of inflammation of the peritoneum—fever,
nausea, elevation of pulse-rate, leucocytosis, muscle spasm, local tenderness. But there is one abdominal disorder of urgent importance (Group II) which does not,
until late at least, give rise to any signs of inflammation—intestinal obstruction. The
profound chemical disturbances of fluid and salt loss and even blood loss occur long before
actual gangrene of bowel wall, and it is only when secondary infection occurs in tissues
with lost blood supply that leucocytosis and fever or even elevation of pulse rate appear.
Fortunately the pain of obstruction is usually characterized by its periodic recurrence
and there are available to us the signs of visible or audible peristaltic rushes, obstipation,
perhaps even beginning distension, even before nausea and vomiting come on. And our
rapidly increasing knowledge of the x-ray appearances in obstruction promises to be of
the greatest help.
Confronted, then, with acute abdominal pain without signs of inflammation, and
having satisfied himself that no bowel obstruction exists, the surgeon considers next and
systematically examines for a group of disorders, non-surgical in their indications (Group
III). The classical examples are lead poisoning and the gastric crises of tabes. Usually it is
only necessary that they be thought of when simple tests confirm the diagnosis.
Finally we come to the group (group IV) which offers most difficulty—conditions
outside the abdomen yet presenting both acute abdominal pain and also signs of acute
inflammation.
Pneumonia, especially in children, stands at the top of the list. Adams and Berger2
reported that, of 145 patients with lobar pneumonia admitted to the Boston City Hospital,
25 were sent in with a diagnosis of acute appendicitis. The sudden onset, the fever, leuco-
cystosis and even the presence of muscle spasm and tenderness, point to fulminating abdominal inflammation.
But if one keeps in mind the possibility, some lead may set him right. Something about
the picture may not fit. The fever may be too high, the leucocytosis too great, the temperature-pulse-respiration ratios wrong, onset with too severe and genuine chill, face the
slightest bit cyanotic, a little cough, herpes of the lips, the whole patient too sick. Careful
examination may show the tenderness superficial rather than deep. Jarring over the diaphragm may produce pain.  The astute surgeon will have a chest film before operating.
Coronary thrombosis (like angina but with fever and leucocytosis) is a frequent source
of confusion. I have explored one case on the diagnosis of perforated ulcer and was just
saved from doing the same in another case by the discovery of a pleuro-pericardial friction-
sound just before the patient was to go to the operating room. It is astonishing that
coronary disease should produce absolutely board-like abdominal rigidity.
Twice I have operated for acute appendicitis when the cause of pain was a stone
impacted in the kidney pelvis. With the ureter plugged, no urine came through and blood
and pus were missing. Looking back on these two cases, I realize that the tenderness
extended around into the flank more than one should expect, even with a retrocecal
appendix, and I have been on my guard ever since when a supposed appendicitis presents
this atypical distribution of tenderness. But I think it highly likely that I shall make the
same mistake again some time. I shall be afraid to leave unopened an abdomen so characteristic of acute fulminating appendicitis. Even the finding of blood cells and leucocytes in
the urine does not prove that appendicitis is not present. We have all seen these go together.
Perhaps this is an appropriate place to remark that disorders outside the abdomen may
be present coincident with true abdominal emergencies. I shall not soon forget the patient
on whom I almost refused to operate because of the presence of a well-marked lead line
and numerous stippled cells in the blood smear, but who did actually have a perforated
duodenal ulcer as well.
Several authors have stated that acute tonsillitis may be responsible for typical signs
and symptoms of acute appendicitis, the appendix itself being innocent. One is inclined
to doubt this because there is no reasonably probable path of pain reference. On the other
hand, we have seen real acute appendicitis develop during the course of1 acute tonsillitis
and in one case (my own daughter) during an attack of otitisi media. We do not yet feel
that we have positive proof but it is our distinct impression that the incidence of acute
appendicitis goes up in the wake of the usual winter epidemic of acute respiratory infections.
[89] Althausen and his associates3 at the University of California Hospital have recently
drawn attention to Henoch's purpura as a cause of symptoms simulating acute abdominal
emergency. This is a disease on an allergic basis presenting spasm of smooth muscle with
visceral haemorrhage and urticaria, angioneurotic oedema and other allergic stigmata.
They reported eight cases of this remarkable condition, all presenting acute, sudden,
violent abdominal pain, commonly with muscle spasm and tenderness, fever and leucocytosis. Four of these patients had been operated upon from one to three times each and
one barely escaped splenectomy only because his brother had had it done without relief.
One patient later died after a cholecystectomy and gastro-enterostomy at another hospital.
The operations had been done following varying diagnoses from acute appendicitis to acute
pancreatitis and perforated ulcer.
Althausen points out that a diagnosis was possible in the cases reported and that it was
usually possible to find the allergic stimulus (food of one kind or another) by attention to
a history of previous attacks, a family and personal history of allergy, an eosinophilia with
a polynuclear count not increased in proportion to the total white count and by shifting
pain and the finding of purpuric spots or of urticaria on the skin.
Finally, we in California have to be on our guard against the most bizarre of confusing
pictures—that following the bite of the "black widow" spider, the female latrodectus
mactans. The disease has been aptly named arachnoidism and has been very completely
described by Bogen4, chiefly from his own experience at the Los Angeles County Hospital.
Formerly thought to inhabit only the outdoor privy in rural districts, about half the
Los Angeles cases arose from bites in city garages and even in bedrooms.
Symptoms, usually following the bite within an hour, include pain in most of the large
muscles but most intense in the abdominal muscles—sq much so that complaint is limited
to this region. The abdomen present board-like rigidity, fever and leucocytosis are usually
present, and vomiting may occur, thus completing the picture of acute perforated ulcer.
I am quite sure that I operated in one case through this mistake in diagnosis.
Bogen points out some helpful points in diagnosis:
1. History of a bite or of exposure to bites within an hour of onset of symptoms. In
many cases, however, the patient is unaware of having been bitten.
2. Pain and rigidity in other regions! than the abdomen.
3. Restlessness instead of the immobility of peritonitis.
4. True local tenderness is usually absent or disproportionately slight.
5. A definite increase in blood-pressure and, curiously, an increase of spinal fluid
pressure.  Bogen states that rather striking relief follows lumbar puncture.
Gilbert and Stewart5 state that intravenous calcium gluconate (10 to 2 0 cc. of 10 %
solution) produces the same spectacular relief in arachnoidism that it does for the colic
of lead poisoning.
Summary: Without attempting to present any original research, I have tried to point
out the wide variety of extra-abdominal disorders which can produce acute abdominal
crises and to offer a classification which has been helpful in a systematic differential
diagnosis.
In the groups not giving rise to fever and leucocytosis (signs of active inflammation)
we should make few errors if we rule out obstruction before deciding against surgery.
In the group which does produce the signs of infection simulating very closely indeed
real abdominal emergencies, we shall not always be right. In spite of every care we shall
sometimes operate upon abdomens only to find nothing wrong. But we shall make this
mistake less often if the other possibilities are kept always in mind.
REFERENCES:
1. Capps, Jos. A.: Pain in the Pleura, Pericardium and Peritoneum.  New York, 1932.
2. Adams, F. J., and Berger, B. S.: Differential Diagnosis or Lobar Pneumonia and Appendicitis in Children.
J. A. M. A., 79:1922, 1809.
3. Althausen, T. L., Deamer, W. C, and Kerr, W. J.: "False Acute Abdomen": Henoch's Purpura and
Abdominal Allergy.   Annals Surg., 106:1937, 242.
4. Bogen, Emil: Poisonous Spider Bites.   Annals Int. Med., 6:1932, 375.
5. Gilbert, E. W., and Stewart, C. M.: Effective Treatment of Arachnoidism by Calcium Salts.  Amer. Jour.
M. S., 189:1935, 532.
[90] INDICATIONS FOR THE PROPER USE OF
THYROID SUBSTANCE
»       By Dr. Hans Lisser.
It is the impression of many of us that it would be highly desirable if there was more
widespread appreciation of the indications for the use of this material with resulting benefit
to many people who, unfortunately, are not treated by that substance nowadays. I think
perhaps some thirty years ago Sir William Osier coined the epigram, "Know ye syphilis in
all its ramifications and all other things will be added unto you." That epigram had its
effect and riveted attention on that disease and probably as the result of it came the routine
Wasserman test. I should like to paraphrase that remark and say, "Know ye well all the
hidden hints and vagaries of myxcedema and hyperthyroidism and much satisfaction will
accrue unto you," and if as a result of that there is a greater recourse to basal metabolism
estimation, that will be helpful.
I hasten to say, of course, that any good observant clinician does not need a basal
metabolic rate to diagnose hyperthyroidism or thyrotoxicosis or Graves' Disease, but even
the experienced endocrinologist will admit that the basal metabolism is quite helpful in
uncovering or substantiating hypothyroidism where it might otherwise be missed clinically.
I also hasten to add that even a remarkably low basal metabolic rate does not constitute a
diagnosis of thyroid condition. For example, the basal rate is low in Simon's Disease or
cachexia, and yet no amount of thyroid substance would be of any help in that condition.
So that in the final analysis it may be said that the final test of a diagnosis of thyroid
deficiency is the response of the patient to the administration of thyroid substance. And
with that preface we will turn to the slides and show you the sort of clinical conditions for
which a thyroid deficiency is responsible.   (Slides were shown here.)
Now this picture, not one of my own patients, is childhood cretinism as seen in Switzerland and the Himalaya Mountains. Sir William Osier, in one of his early papers, got together
something like sixty cases of what used to be called, and still is frequently called, sporadic
cretinism, in the United States and Canada and about 1922 Gordon amplified that and got
together out of the literature about 250 cases of childhood myxcedema, a much better term.
The conditions are not alike nor do they respond in the same way to thyroid treatment. In
cretinism the response is not nearly so good.
You see here this huge goitre. We have a lot of goitre in North America and yet this
particular type of condition, viz., severe childhood thyroid deficiency, is very, very rarely
found in association with goitre. What we see is a different condition due to the lack of
development of the thyroid gland. Now, here is an extraordinary example of childhood
myxcedema. You will read there that this child is twelve years old and you see the pot belly
and the umbilical hernia and the abundant coarse straight dry hair, the bracelet padding.
Here is another view, showing the saddle-nose. If you can exclude a fracture of the nose,
or syphilis, you can look for myxcedema when you have a saddle-nose.
Now, this is the most profound osseous retardation that I have come into contact with.
The utilization of bone age determination is most important in the diagnosis of thyroid
deficiency prior to puberty and is quite reliable, and, of course, very easy to perform. A
basal metabolism test on that child would be utterly impossible. The child was more or
less of an idiot and unable to co-operate in a basal metabolism test. Usually, you will find
that the osseous age is several years behind the chronological age in childhood hypothyroidism, this one, of course, being extreme. You see this child here with a younger brother, the
brother being 10 years old, and you see the older brother here. Twenty-seven months later,
after the administration of thyroid substance, still the most valuable endocrine product
that we have to administer, we see this picture. I wonder how far endocrinology would
have gone if this thyroid substance had not been so valuable. The child is now quite transformed and has grown with remarkable rapidity.
There are those who hint at primary anterior pituitary for almost anything endocrinological these days and would even suggest that myxcedema is primarily of pituitary origin
and, therefore, that all retardation of growth must involve the anterior pituitary. Well,
possibly it does, but I venture to predict that even when we have available a highly potent
pituitary growth hormone, nothing comparable to this will be accomplished in childhood
[91] myxcedema. Here you see what happened to the bone age in a period of two years of treatment. The bone age advanced from one-half year to a period of nine years in twenty-seven
months of treatment.
Now, this graph is quite valuable and points out a lesson to us. This child, in her fifth
year, came to a clinic and the diagnosis was correctly made of thyroid deficiency. May I
emphasize this. You are not through when you have made a diagnosis and given the patient
a prescription. You have then assumed a responsibility and that responsibility is to see that
that patient takes thyroid and gets it in the proper dose and continues it steadily and faithfully, and that, therefore, means that you must keep such patients under observation, at
first probably once a week, then once in two weeks, and, later on, once a month, and then
two or three times a year. The problem of thyroid dosage is an individual one. You cannot consult any textbook as to how much thyroid to give a person such an age. You might
think that the dosage can be gauged by the depth of the basal metabolism rate. Quite the
contrary. The more severe the degree of thyroid deficiency, the less dosage they can tolerate.
As regards the desiccated substance—I always like to be sure that the physicians I speak
to are aware of the fact that the dosage of this is quite different from almost all other forms.
That is, if you read the label on the bottle, it states very definitely that the tablet represents
1 grain of the fresh substance, whereas others are described as 1 grain of the desiccated
substance. One grain of the desiccated substance is equivalent to 4 or 5 grains of the fresh
substance.
To return to the graph—the patient did not come back to the clinic for quite some
time, until someone who was interested in the case got in touch with the child and had her
return to us. Here you see the sharp rise in growth under the administration of thyroid
substance. Here is another example. You might think you were looking at a Chinese girl,
but she is a white girl from California. You see the saddle-nose, the coarse, straight, dry
hair, etc., and here you see her after treatment.
In this slide you will see this girl of sixteen. There seems to be nothing wrong with the
picture. She began to menstruate at 11 l/z years of age. Her periods were irregular in interval, but when they occurred, they certainly occurred. She flowed heavily and for a long
period of time. This indicates that more or less she was menstruating from November to
April. At this point we saw her. With that story, and having found nothing in the pelvis
responsible for such bleeding, then most certainly have in mind the possibility of thyroid
deficiency as the cause. That applies to the adult woman as well. Just as formerly one made
a therapeutic test where the diagnosis was in doubt, so here, also, you are justified in a
therapeutic control test with thyroid substance. Irrespective of what the basal metabolism
would have been in this patient, I would have administered thyroid substance. There was
nothing myxcedematous at all in her external appearance, so I might say that there is apparently what one might call an internal myxcedema. So menorrhagia is one of the presenting symptoms in thyroid deficiency.
This women was 3 5 years old, came from Texas. Any physician passing her on the
street could have diagnosed childhood myxcedema. The main thing is: Why did she come
to the clinic? Seemingly, a very minor complaint—recently she had noticed some stiffness
of the knees and an ache. That was her sole complaint. So, there again, may I suggest that
if rheumatism or arthritis are present in a patient, have in mind the possibility of a thyroid
condition. Ask them: "Do you prefer hot or cold weather?" And you will find that these
patients prefer hot weather. They wear more clothing than the average individual. They
need more bed clothing than the average individual. The first symptom they appreciate as
a sign of having been relieved is a warming-up of their bodies. Also ask them: "Are you
drowsy? Do you want to sleep in the daytime?" You will find that they usually do. In
this picture we see quite an improvement in this woman.
This patient's voice also underwent quite a change under treatment, from a hoarse,
raspy one to a natural voice. Her personality also changed and in time she married and had
a very nice baby. When any woman with thyroid deficiency becomes pregnant, it is just
as important to treat her properly through her pregnancy as it is to treat a syphilitic pregnant woman before her confinement. Here is a woman who came in complaining of heart
palpitation. We were a little suspicious of her on account of puffiness. Here is her electrocardiogram during one of these attacks and again during an interval. When she admitted
that she was cold in very hot weather, somewhat drowsy, it occurred to us to get a basal
[92] metabolism rate, which was about 3 5 % below. We managed along with her and here you
see an improvement in her electrocardiogram after treatment.
This patient came in feeling weak and tired. Examination showed she had a marked
anaemia. She also had manifestations of hypothyroidism and you will find on record a pernicious anasmia type of blood picture in myxcedema. In this patient, thyroid therapy alone
restored the blood to normal. Here is another one. This woman had severe menorrhagia.
Her basal metabolism was 40% minus and under thyroid therapy she improved
considerably.
Here is another case, rather a rare symptom, of marked distension of the abdomen with
ascites. No other symptom. She had a peculiar story, that eight years before she had had
a large abdomen and some dyspepsia, and some fluid had been removed, and she had improved. There are several such cases on record of fluid due to myxcedema. This was her
heart—a heart distended in all its chambers—called a myxcedema heart, enlarged in all
diameters. Here is her colon before and after thyroid treatment. So. that constipation is
suggestive of probable thyroid deficiency. Here is the Bright's Disease type of thyroid
deficiency. This man shows one of the things we have been talking about. He always felt
cold, even in warm weather. Thyroid therapy gave him much improvement. This man
came to the clinic on account of achiness in the back and shoulders, which cleared up
nicely on thyroid therapy.
In hypothyroidism there is sometimes a patchy loss of hair on the extremities, and
thyroid substance will grow the hair back. In these pictures we see this patient at different
ages. You see the gradual onset of symptoms. Under thyroid therapy we see a remarkable
change for the good. He is now more like the boy he was at 21.
I wish to deplore the frightening attitude that the medical profession has taken to the
use of thyroid substance in these conditions. There should be no excuse for over-dosage
of this substance.
CANCER OF THE COLON AND RECTUM
Dr. A. T. Bazin
When I submitted the topics on which I would speak on this trip, amongst them was
"Carcinoma of the Rectum," but somehow or other it became enlarged to "Carcinoma of
the Colon and Rectum." I am going to concentrate on cancer of the rectum because it is
much more accessible than cancer of the colon. Cancer of the rectum is accessible. You
can actually see and feel it, and, also, carcinoma of recto-sigmoid. Of all carcinomas of
the large intestine, cancer of the rectum constitutes about 51%. Carcinoma of the rectosigmoid takes care of 48% of the others. It is customary to consider that accessible carcinoma should be detected early, diagnosed early, and, therefore, treated promptly. Eighty
per cent of cancers of the rectum can be felt with the finger. The remaining 20% can be
detected by an office procedure of proctoscopic examination.
Why is it that so many patients reach us in such an advanced stage? I don't believe
that it is ignorance on the part of the physician. It must, therefore, be negligence on the
part of the patient. Examination of the rectum can be very distasteful, but with the
proper equipment this should not be so. I always carry a pair of rubber gloves and a jar
of vaseline for that specific purpose. If this were adopted by all physicians, many more
cancers would be detected in the early stage. Digital examination of the rectum would
discover all of these cases at an early stage. I remember one case that was worked up and
diagnosed as duodenal ulcer, but these duodenal symptoms were really reflex symptoms of
a carcinoma of the rectum. There was no digital examination done and the true condition
was missed. These instructions do not apply to you, to you medical men who attend
meetings. You men are alert. The question is, how to reach the men who don't attend
the meetings. If they are negligent in that respect, then they are liable to be negligent in
all matters. The only thing is to educate the people so that they will demand a proper
examination of their case.
The early signs of cancer of the rectum are discomfort, bleeding and occasionally
obstruction.  Much more frequently we find diarrhoea.  The discomfort is usually a sense
[93] of fullness after defecation: the defecation is not a satisfying one. This sense of fullness
is not due entirely to the growth, but is more due to the congestion, oedema of the wall,
associated with the ulceration and inflammation superimposed on that ulceration and a
surrounding area of proctitis. A sense of fullness and the desire to stool frequently, very
often with straining, results in the development of haemorrhoids, and haemorrhoids will
frequently bleed as a result of the straining efforts, and so the patient ascribes his discomfort to the piles and ascribes the bleeding to the piles. Don't let us have doctors making the
mistake of taking the patient's interpretation. The bleeding from; haemorrhoids is always
clear-cut. The bleeding from cancer of the rectum is almost invariably associated with
the discharge of mucus; and it is essential or desirable, when a patient complains of bleeding
from the rectum, that the character of the bleeding should be gone into in detail. Then
the examination should be such as will explain the type of bleeding. If you find from that
patient that the bleeding has been associated with a mucous discharge, it is not enough to
diagnose haemorrhoids. Diarrhoea is much more common than constipation. This is due
largely to the proctitis and the excessive mucus. The patient will have a desire for stool but
will pass mostly bloody mucus, sometimes associated with stool, sometimes nothing but
bloody mucus.
There is a type of carcinoma of the rectum that causes definite stricture of the canal.
That type is the small round-cell type of tumour, commonly called the Krukenberg type
of tumour. It grows rapidly, does not ulcerate, infiltrates and causes obstruction. I had
one such case in a school teacher, twenty-four years of age, who, in the course of a few
months, became so strictured that she could not get any bowel movement without an
enema. The finger could not enter the canal. Biopsy made the diagnosis. It was very
malignant and she was dead of general carcinomatosis in two years.
Carcinoma of the rectum, compared to carcinoma of any other site, occurs very frequently in the young. Now, one could go further into details of symptoms and signs, and
analyze all these symptoms and signs in order to make a diagnosis, but there is no use
speculating. When a patient complains of any rectal discomfort, the part is so easy of
examination and you can go straight to this examination—first a digital one, then proctoscopic. Proctoscopic examination is an office procedure. Sigmoidoscopy often requires
more equipment than the ordinary office has. For the proctoscopic examination,, have the
patient on a tilted table—any table which will give a good Trendelenberg position is
satisfactory for this examination. The danger is that you don't know just what kind of
a lesion you have in the sigmoid until you have reached it and seen it and you can't reach
it until you have induced a certain amount of inflation. The knee-chest position is
unsatisfactory, because you can't, in the majority of instances, especially in males, get
around the loop of the sigmoid without exerting a good deal of pressure on the coccyx,
which is painful. An x-ray examination of the rectum and lower sigmoid is very unsatisfactory and unreliable. It will show up gross lesions, but it will not show up minor lesions,
and if you place any dependence upon it you are going to be bitterly disappointed.
Now comes the question of biopsy. When, on clinical examination, you have diagnosed
a stricture, how much can you depend on biopsy if the lesion is high up? The clinical
picture is so typical that a negative biopsy would have very little weight unless the tissue
removed by the biopsy forceps had been a very satisfactory piece of tissue. So often, when
one attempts to get a biopsy, just as soon as the window of the proctoscopy is opened there
is a deflation, and the biopsy forceps removes, not a portion of the lesion, but a portion of
the mucosa which overlies the lesion. Therefore, a negative biopsy is only a negative biopsy,
and, all other things being taken into consideration, the clinical picture that is seen through
the proctoscope is much more reliable than the evidence from a negative biopsy.
Cancer of the anal orifice must be considered when you are discussing cancer of the
rectum. It is a very different kind of growth from cancer of the rectum. It is always a
squamous epithelioma. The other cancer above the white line is adenocarcinoma. You
can have adenocarcinoma of the mucosa of the rectum proper and you can have an adenocarcinoma which arises just outside the musculature of the rectum. The cancer of the
anal orifice is an epithelioma. It is usually detected very early because the patient has pain
and seeks advice very early.  The early carcinoma, being indurated and inelastic, becomes
[94] fissured very early and is painful. Any ulcer which shows induration of its edges should
be removed and subjected to histological examination. Another point to remember is
that the drainage path from carcinoma of the rectum is up in the wall of the rectum, in
the mesentery of the rectum and mesentery of the sigmoid, occasionally laterally out to
the lateral pelvic glands along the path parallel to the middle haemorrhoidal artery and vein.
The lymphatic drainage path from the anal orifice is up to the glands of the groin, so that
the first findings may be a hard gland in either of these regions. Any operative treatment
of carcinoma of the anal orifice would necessarily require removal of the sphincter. It is
not necessary to go very high. Fortunately these epitheliomata of the anal orifice are radiosensitive, so that radiation is a better form of treatment than operative procedure. Radiation of the local lesion with radium implants, radiation with x-ray—thorough radiation—
and then, after the lapse of five or six or seven weeks, a block dissection of the glands of
both groins with the lymph structures round about. If this anal orifice carcinoma is
detected early, that treatment can be carried out without destruction of the sphincter, but
it is much better to have a temporary colostomy during the time of treatment.
Now, what are the signs and symptoms of early cancer of the colon? If the colon
were divided by a line drawn from the left splenic region down to the right iliac fossa, one
could say that bleeding carcinomas are to the right and obstructing carcinomas to the left
of that line. Why does carcinoma obstruct? Seldom because of a growth that projects
into the lumen, but because, in the arrangement of the lymphatics, the carcinoma spreads
in an annular fashion. As soon as it becomes completely annular it obstructs. The sym-
toms and signs of early carcinoma of the colon would be bleeding or obstruction, or both.
The bleeding—especially because most commonly the type of ulcerating carcinoma is of
the right side of the abdomen where the faeces is liquid—is commonly mixed with the faeces
and is not observed by most pateints; so it will go on to secondary anaemia before the
patient becomes cognizant of his condition. Sometimes one will get an incomplete obstruction. In an x-ray film in which examination has been carried out and it looks as if there
were a partial obstruction or a lesion at one point, the mere fact that there is no distension
of the bowel immediately proximal to the sigmoid does not preclude the possibility of an
obstructing lesion. The muscle of the bowel wall will hypertrophy to overcome the
resistance of the increasing obstruction and there will be no distension as long as that
hypertrophy compensates for the increasing load. The muscle of the bowel acts just as
the muscle of the heart acts. There will be cramps because of the obstruction but not
distension in the early stages.  Later on you will get distension of the proximal sigmoid.
Now, because the caecum is much thinner-walled than the remainder of the colon, the
caecum will distend more readily, and that is why patients frequently keep, complaining of
discomfort in the right lower quadrant when the obstruction is in the recto-sigmoid. I
won't go into the details of making a diagnosis of incomplete obstruction.
I have mentioned cramps, and you may or may not get visible or palpable peristalsis.
If you get palpable peristalsis you will get it in no condition but that of chronic incomplete
obstruction. You will not get it in the complete obstruction due to, say, a strangulated
hernia. You may get visible peristalsis but you will not get palpable peristalsis. That incomplete obstruction may go on to a complete obstruction in one of two ways: active and
passive. Suppose you have an incomplete obstruction and you have hypertrophy of the
wall. All of a sudden that narrow orifice is completely obstructed by the skin of a vegetable or fruit, more frequently by inflammatory oedema; you then have a stormy scene
and you get the active method of a.n incomplete obstruction passing on to a complete
obstruction. Now, in the passive type, this hypertrophied muscle gradually gets tired out
and lies down on the job. The lack of contractibility in that muscle means that the cramps
get less severe. It is not a stormy scene and it is the passive method of incomplete obstruction going on to complete obstruction.
The bleeding from a scirrhous carcinoma is very hard to detect. Bleeding from the
papillary carcinoma is pretty abundant. Now, of course, of available methods of examination, one is the x-ray, and I think it is wise to stress this point: Whenever you are suspicious that there is obstruction in the large bowel, always use a barium enema first but
see if the large bowel is clear.  If the barium meal is given in the presence of an almost
[95] complete obstruction in the colon, the barium is held proximal to the obstruction, the
function of the colon carries on and takes the moisture out of that barium and it becomes
inspissated and causes complete obstruction, and then you have an emergency on your
hands. Free fluid in the peritoneal cavity does not always mean that there is carcinoma of
the peritoneal cavity, because in the presence of an obstruction which is at all complete
there is always such distension in the abdominal wall that there is no value in a differential
diagnosis in finding free fluid in the peritoneal cavity. If that free fluid is drained off, it
may show the presence of cancer cells, and that, of course, is a positive finding. Loss of
weight is not the sign of early cancer in the colon or anywhere.
There are certain complications and certain conditions which may complicate carcinoma of the rectum. Take the caecum. You may have an anaemia develop from the
bleeding, but very frequently there is abscess formation by infection passing along the
lymph channels. This may simulate an acute appendiceal abscess. In the lower rectum,
especially in females, the presence of a lymphogranuloma inguinale must be kept in mind
as a differential diagnosis when carcinoma is suspected. And here is another possibility:
A woman who was spending her winter on the Pacific Coast and had prolapsing haemorrhoids was treated under local anaesthesia and was relieved of her haemorrhoids except for
one small haemorrhoid. Within a year she was complaining of stricture, and that stricture
got worse and worse. She was referred to me as carcinoma of the rectum, but it did not
look exactly like a carcinoma of the rectum. It proved to be paraffinoma of the rectum,
from the insertion of paraffin for the treatment of haemorrhoids.
The primary purpose of this paper is to advise early diagnosis and treatment. The
surgical treatment of cancer of the colon or rectum demands the same surgical procedure
as carcinoma of the breast. It means removal of the original lesion with removal of the
involved glands as well. Never attempt an anastomosis in the presence of an obstructing
bowel. Resort to two or even three-stage operations in patients of low vitality from any
cause. Resort to two or three-stage operations when you are not sure of your own ability
to do as well as some master surgeon that you have watched. I myself do the Ernest Myles
type of operation for carcinoma of the rectum in three stages. I am quite satisfied with this
procedure. Consider your own individual ability and experience and never be ashamed
of doing an operation in as many stages as necessary for the absolute safety of the patient.
What about radiation in carcinoma of the rectum? Well, if I saw a case of papilloma
which looked benign and I removed that papilloma, and the pathologist said "beginning
malignancy at the base," then I should be tempted to use radiation by just surface radiation. Radiation of an established carcinoma of the rectum is, in my opinion, not only
valueless but is harmful. Introduction of radium from the mucous surface simply infects
the tissues. I myself do not think radiation by any method is of any value in carcinoma
of the rectum except in advanced cases for the relief of pain.
PRACTICAL CONSIDERATIONS IN THE HANDLING OF
>   ACUTE APPENDICITIS AND ITS COMPLICATIONS
Dr. A. R. Kilgore.
Patients do not die of appendicitis. They die of peritonitis with its train of abscesses,
general abdominal sepsis, ileus, obstruction.
Infection reaches the peritoneum both by perforation and by extension through the
appendix wall without perforation. Either we prevent peritoneal infection by removing
the appendix early, or treat it, once established, if we must.
In the selection of operative and post-operative procedures an appreciation of the
behaviour of the peritoneum toward infection is of first importance. Four facts must be
in mind constantly:
(1) The peritoneum tolerates infection remarkably well under two conditions—(a)
that it be uninjured; (b) that it be not long subject to continuing contamination from a
source of infection. We need only call on common experience to verify both statements.
The injury of rough and extended operative handling of the peritoneum quite obviously
[96] reduces its resistance. And we have all seen the peritoneum take care of gross, extensive
soiling from perforation of ulcers or from penetrating or gun-shot wounds if the wounds
are promptly repaired and the source of continued contamination shut off.
Of the two insults, continued contamination is, of course, more important than the
injury of necessary operation. Faced with an appendix, perforated and leaking into the
open peritoneum, no one questions the necessity of appendectomy, but we can at least
carry out the surgery with the least possible peritoneal injury.
(2) The peritoneum is very easily injured. Contact with any foreign body—gauze,
instruments, even gloves—especially if there be forcible pushing or pulling, abrades the
delicate surface. After a gauze pack has been in place even several minutes it has actually
to be pulled off the already adherent peritoneum. How much of the thin, tender endothelium can remain? Drying and overheating offer very real injury. The less handling,
the less contact with gauze, the less area' of peritoneum exposed in the wound, the better
able will it be to resist whatever infection may be present.
(3) Infection is readily spread to new areas on gloves, sponges or instruments.
(4) Any foreign body, left in contact with peritoneum for even a short time, is
promptly surrounded by adhesions and, once walled off, is no longer really in the peritoneal
cavity at all.  It is absolutely impossible to "drain" the open peritoneal cavity.
In the light of these characteristics of the peritoneum certain extremely important
decisions about operative procedure may be made:
(1) Selection of incision. The right rectus and even more the mid-line incision require
that the appendix be reached across several coils of small bowel and usually the intestine
has to be forcibly held away by sponges and retractors. Extensive injury from handling
and the wiping of infection on gloves, gauze and instruments across new areas of peritoneum
are inevitable. Through the muscle-splitting "McBurney" incision, on the other hand, the
appendix is usually removed without even exposing, much less handling, any bowel but
the end of the caecum and the last inch or so of ileum. One would expect the surrounding
uninjured peritoneum to handle infection better and it certainly does. The mortality of
acute appendicitis operated on by the McBurney incision is half or less that following
the rectus or mid-line incisions.
Many surgeons are afraid of a retrocaecal appendix or one lower or higher than usual.
If one finds he must have more space it is a simple matter to carry the incision into the
rectus sheath, retract the muscle toward the mid-line and go up or down as far as necessary.
I believe the only reasons for selecting rectus or mid-line incisions for acute appendicitis
are: (1) serious doubt of the diagnosis; (2) known gross malposition of the appendix.
(2) Drainage. Dr. George Rhodes and his associates2 have made an outstanding contribution toward the reduction of mortality and morbidity on appendicitis in their study
of drainage. The pathology seen at operation allows classification into four groups: (a)
Simple acute appendicitis without gangrene or perforation. Probably no one would drain
such cases, (b) Appendicitis with localized, walled-off abscess. Here a collection of pus
is contained in a cavity of its own, no longer lined by peritoneum but by granulation tissue.
It is really extraperitoneal and to be treated like any other abscess. Everyone doubtless
would drain such cases, (c) Appendicitis with gangrene and (d) appendicitis with gangrene and perforation. It is in these types, and particularly in the latter—the appendix
which has perforated into the open peritoneal cavity, not into a walled-off abscess—'that
drains are still commonly used by many surgeons.
Now, as pointed out above, a drain is a foreign body and so a source of injury. And
because of this very fact it is promptly walled off by adhesions, so that within an hour or
two it is no longer in the peritoneal cavity at all but in its own pocket. It is astonishing to
see what harm can be done by useless drains. Table I (from the article quoted) shows the
incidence of post-operative complications and the mortality in gangrenous and gangrenous
perforated appendicitis according to the use or non-use of drains. The figures speak louder
than any comment could.
Those of us who have seen this work developed at the San Francisco Hospital under
the leadership of Dr. Harold Brunn, Chief of Staff, no longer use drainage under any
[97] TABLE I.
Complications
Drained	
Not Drained.
(rost-operati
haemon
ve ab
■hage
scesses, ileus,
, etc.)
Mortality
Gangrenous
imperforated
Gangrenous
perforated
Gangrenous
unperforated
Gangrenous
perforated
19%
37.7%
9.3%
10%
2.7%
8.9%
0.0%
2.4%
circumstances other than the presence of a localized, walled-off abscess, not even when
there is actual free pus in the peritonal cavity with spreading or generalized peritonitis.
(3) Drainage of abscess without appendectomy. It requires conviction and strength
of will for a surgeon, once in the abdomen, to close without removing an acute appendix.
Yet when the appendix is in the wall of a definitely established abscess I believe it is a
life-saving procedure to do just that—drain the abscess and leave the appendix. The injury
of handling and the spread of infection by manipulation are often enough to disarm the
peritoneum with death the result.
Table II is the result of a study of 440 operations for acute appendicitis at the San
Francisco Hospital made by Dr. Bret Smart and myself. Appendectomy plus drainage
carried a mortality of 12%, nearly five times as great as that following drainage only,
leaving the appendix to be removed at a later time.
TABLE II.
Drainage plus appendectomy	
Drainage only:
1. Intraperitoneal (through open abdomen)	
2. Extraperitoneal (through adhesions in flank or by rectum)
Number of Cases
51
Mortality
6 =  12%
\ 1  =    2.6%
J
(4) Table II suggests another question, that of delayed operation in late cases. There
has been in recent literature a considerable swing of opinion back toward the so-called
Ochsner treatment. Our conviction is that an exact diagnosis of the stage of the disease
at any moment is extremely difficult and often impossible. We believe it is hazardous to
attempt to select cases for delayed operation and we do so for only two groups: (1) those
in which the diagnosis of general peritonitis is clinically perfectly apparent—patients who
would probably not tolerate any operative procedure, and (2) a small group in which we
can determine that a local mass is forming. In these some delay may be wise to allow more
complete walling off and a final approach from the flank, or even the rectum or vagina,
into the abscess entirely through adhesions and without opening the general abdominal
cavity at all.
Of course this should be an ideal procedure, but we have been surprised to find how
relatively safe it is to drain through the open peritoneum if the appendix is not searched for
and removed. From Table II it will be seen that of a total of 89 cases with abscess formation only 14 were drained extraperitoneally (through the flank or rectum). In the
others the abscess was found only at laparotomy and drains were necessarily placed through
the open peritoneum. Yet, of 24 thus drained none died. The only1 f atality in the group
drained without appendectomy occurred in a case drained extraperitoneally.
(5) Minimal use of gauze packs and sponges. Gauze, even wet with salt solution,
pressed against or rubbed over the delicate peritoneal surface, cannot fail to injure it.
One is led to gravely doubt the effectiveness of gauze in preventing spread of infection,
remembering that, after all, wet gauze is really a very porous wick. We use sponges as
little as possible and for "walling off" the field only when it becomes apparent that we
must open an abscess with consequent gross soiling.
Complications.
In spite of education of patients to avoid, cathartics and be operated on early we shall
still have neglected cases, and be obliged to deal with post-operative complications.   By
[98] far the most common of these is distension. Usually causing only suffering, it may actually
be responsible for death. Added to peritonitis which a patient might otherwise surmount,
marked distension may certainly turn the balance against him.
An attempt to deal with all or even many of the post-operative complications of appendicitis would expand this paper beyond reasonable length and discussion will be confined
therefore, to the problem of distension.
Prevention. In addition to atraumatic operating, avoidance of drainage, etc., two
things we can do to minimize the incidence of distension:
(1) Avoidance of pre-operative bowel disturbance. Doubtless the fact that appendectomy is usually done as an emergency procedure without bowel disturbance explains
why the convalescence for so many patients is as smooth as it is. Enemas we believe to
be almost as vicious as laxatives.
(2) Avoidance of ether anaesthesia. Table III shows the incidence of distension
according to method of anaesthesia used—approximately the same (30%) when gas and
oxygen or spinal anaesthesia was used, it was 50% greater after ether. We have come more
and more to depend on spinal anaesthesia.
TABLE III.
Anaesthetic
Total
Cases
Cases
with No
Distension
Slight or
Moderate
Distension
Marked
or Severe
Distension
Total
with
Distension
4
80%
1
20%
0
1
20%
197
70%o
35
12%
48
18%o
83
30%
80
70 %
17
14%
18
16%
35
30%
23
56%
8
20%
10
24%o
18
44 %
Local   5
Spinal    280
Gas and Oxygen  115
Ether  41
Treatment. In the great majority of cases distension is readily controlled by hot stupes,
rectal tube and colon flushes or enemas. It is important to insist that in giving enemas or
flushes only a small amount of water or solution be used at one time and at low pressure
to avoid the danger of perforating a weak caecum or appendix stump. This accident has
occurred.
Pitressin and related drugs are theoretically contra-indicated in peritonitis. We would
like to have the inflamed bowel at rest rather than active. But distension and ileus constitute a vicious circle. The more the bowel is dilated, the less ability it has to contract.
And a degree of dilatation is reached at which the very stretching of the bowel wall
interferes with its blood supply, and this, in turn, robs the peritoneum of its ability to
fight infection.
Choice must sometimes be made between rest and progressive distension or maintenance
of tone and blood supply at expense of stimulating intestinal activity. The latter must be
chosen. Pitressin is dependable, rapid in action—a highly useful drug. Its action is so
prompt that its use prophylactically, before even slight distension appears, or even before
operation, seems unnecessary. We use it at once when it becomes apparent that early
distension is not yielding to stupes, flushing or enemata, and continue small doses at regular
intervals until peristalsis is definitely established.
Nasal gastric or duodenal tube drainage. Even with bowel more or less completely
inactive it is possible to greatly minimize distension by keeping the stomach and duodenum
empty. About 70 per cent of the gas in distended bowel is swallowed air. Saliva, gastric
and duodenal secretions, bile and pancreatic secretion amounting altogether to several
liters are poured daily into the upper intestine. If this fluid and air is withdrawn certainly
there will be less to distend the bowel.
An inlying tube makes it possible for the patient to drink fluid almost at will and
this contributes much to comfort.
It is essential that constant suction (by the Connell or similar apparatus) be maintained.  Intermittent suction by syringe is relatively ineffective.
Maintenance of water and salt balance. Intestinal muscle will not regain or maintain
its tone and activity in the presence of dehydration or deprivation of salt.  How much is
[99] lost? How much to give? One finds no clear agreement in the literature nor any accurate
method of estimation for an individual case—for certainly individuals vary in their
requirements according to their state before operation, the duration of operation, method
of anaesthesia—all factors not readily lending themselves to accurate measurement. In
general, two to three liters daily will be required to restore fluid lost in urine, perspiration
and respiration evaporation—more if additional fluids are lost by vomiting or gastric tube
suction. Since the chloride excretion averages 12 to 15 grams daily, 2000 cc. of normal
salt solution will be adequate to make this loss good. In all but early cases (when we expect
fluids to be taken promptly by mouth) it is our practice to give one or two liters of normal
salt solution (with or without glucose) during the first twenty-four hours and give enough
thereafter to maintain urine output at 1000 to 1500 cc. daily.
Hypertonic salt solution. In an occasional case when other measures have failed, the
results of intravenous administration of hypertonic salt solution are little short of miraculous. Whether the prompt establishment of peistalsis is due to restoration of last chlorides
or to direct stimulation of bowel muscle one may not always say. But the fact is that a
patient whose distension is increasing, not responding to pitressin, enemas or flushes, who
has reached the stage of cold, clammy sweating and rapid thready pulse, will sometimes
empty his bowel and present an entirely changed picture within a few minutes.
Again one cannot lay down rigid rules about the amount and concentration to use.
Too much may produce oedema. We have given as much as a liter of 10 % solution without
ill effect! Such heroic doses are usually unnecessary, however; 100 to 250 or even 500 cc.
of 5 % solution will usually serve tl0 purpose.
We are convinced that this is a life-saving procedure not used as generally or as often
as it should be.
REFERENCES:
1. Reid, Mont R.: Some Remarks on the Operative Procedures for Appendicitis.   Surg., Gyn. and Obst.,
59:1934, 529.
2. Rhodes, Geo. K., Birnbaum, Walter, and Brown, Maurice J.: Acute Appendicitis.   Cal. and West. Med.,
45:1936, 458.
SULPHANILAMIDE THERAPY
Dr. E. G. Bannick.
This is still a very controversial subject. Let us consider the indidcations and contraindications for the use of this drug. These should be subdivided into these distinct groups:
(1) The use in those infections in which sulphanilamide has proven to be of therapeutic
value; (2) the use in those diseases where the drug seems to be of some value; (3) the use
in those infections where the drug has been little used but a trial is justifiable.
Slides were then shown of the conditions for which sulphanilamide is used by way of
treatment:
First group—Drug gives benefit: Haemolytic streptococcic infections; gonococcal
infections; pneumococci, especially Type III; meningococcal infections; infections
of the urinary tract.
Second group—Drug worth trying: Chronic ulcerative colitis; undulant fever; mononucleosis.
Third Group—Where a trial is justifiable.
The trouble with the present use of this drug is that too many people are using it
where it has no effect at all. I think it is justifiable to use it in diseases or infections where
it has not been used previously. However, the drug should not be used to treat headaches,
backaches, etc.
Now, as to the contra-indications. The drug should not be used in patients with gross
renal insufficiency.  It should not be used in patients with very marked anaemia or leuko-
[ ioo] penia, nor with gross hepatic insufficiency. Nor should it be used in patients with marked
inanition or cachexia. Sometimes we use it in these conditions because the possibility of
doing good with the drug overshadows the dangers that we are facing. In streptococcus
viridans infections and chronic rheumatic arthritis the drug has proved to be of little value.
The dosage of this drug is as yet unsettled. I believe that it depends on the severity of
the infection, but the fact remains that the dosage is still a very controversial matter. I
have followed the middle road: I have never used as high a dosage as Long,, nor as low a
dosage as Osgood. Over a year ago I made the following slide and outlined the dosage to
be used in different types of cases and different individuals. Sometimes these very sick
persons are vomiting and cannot tolerate the drug, so then we dissolve 1 % sulphanilamide
in normal saline and it is injected. In the mild infections and in patients who are underweight we use smaller doses. At the present time I still think that this chart is not very far
off but I would make some changes. I think there is some value in keeping the dose regular.
When we give the smaller doses, because the drug is so rapidly eHminated in the urine, it is
important to give the drug at shorter intervals, five or even six times a' day.
Now, concerning toxicity. It is true that sulphanilamide has a relatively low toxicity,
but it is, nevertheless, a very potent medicine and we must regard it as such. The idiosyncrasy to this drug is rare, but when present it is very severe. That is why I don't like to
give a huge initial dose. This slide shows the toxic effects of the drug. Mild toxic effects
are malaise, headache, vertigo, nausea. Moderate effects are the above with fever, increased
cyanosis, abdominal pain, acidosis, dermatitis, mild jundice. If any of these signs appear,
stop the use of the drug. Severe effects are: (1) picture of a very severe toxaemia; (2) very
significant jaundice; (3) leukopenia or agranulocytosis; (4) haemolytic anaemia.
There is a distinct advantage in the oral administration of Prontosil. I think that in
the vast majority of infections sulphanilamide is the most effective drug, but neoprontosil
is effective and, in some cases, was adequate. It was also much better tolerated than the
sulphanilamide. Therefore, we see that in cases where prontosil is adequate and better
tolerated than sulphanilamide, then that is the drug to use.
Treatment of some cases of chronic ulcerative colitis with sulphanilamide: I had a
patient a little over a year ago, a young woman who had had chronic ulcerative colitis for
six years. She had tried one treatment after the other and came to the Mayo Clinic two
years ago and showed definite proctoscopic evidence of chronic ulcerative colitis, which
was confirmed by x-ray. She was given vaccine treatment, serum treatment, etc., without
much benefit. She went home and then came back to Rochester for four months, during
which time she was getting regular treatment of one kind or another. She did not get the
slightest benefit. She continued to pass eight to ten to twelve bloody pussy passages from
day to day and she was very much discouraged, so she came in to see me. I reasoned in
this way: If sulphanilamide is good in gonococcal infections and pneumococcal infections,
and if chronic ulcerative colitis is due to a diplococcal infection, then there might be some
advantage in trying this drug for this condition. So we gave her some sulphanilamide and
the girl got a very severe reaction. We had to stop the drug then and she made a prompt
recovery. About one week later she came into the office and stated that this was the only
thing which had done her bowels any good. This was a very interesting thing and this
improvement continued for about two weeks. Her condition became worse again, however, and we gave her smaller doses of the drug. She became quite! ill again, so then I tried
her on neoprontosil. She took 60 grs. a day for two weeks and the improvement that was
obtained by the sulphanilamide was obtained by the neoprontosil. Her improvement has
continued and she has had no recurrence of symptoms up to the present time. We have
tried it on a number of cases. Thirteen cases were tried and in nine of them there has been
some striking improvement. In some of the cases the proctoscopic condition has cleared up.
I am not offering this drug as a cure for chronic ulcerative colitis but I am merely submitting preliminary data in which this drug has been used for this condition. This is still
in its infancy and I don't know what is going to happen to these patients. I do believe that
this drug is beneficial to certain selective cases of chronic ulcerative colitis. I am afraid to
use it on very ill patients.  These selective ones were all ambulatory cases.
[101] CLINICAL OBSERVATIONS OF THE PRESENT STATUS OF
GONADOTROPIC AND SEX HORMONE THERAPY     i
By Dr. Hans Lisser.
If I was at all confusing in my first talk, I am certain that I shall be most disappointing.
in this second talk.  It is an extremely complicated subject and those of us who have been
especially interested in it for a long period of time will know what I mean.
I think you are all entitled to treat the following conditions, and should do so, and can
do so effectually.
1. Cryptorchidism, which has been taken away from the surgeon, and which can be
handled by the proper use of anterior pituitary hormones obtained from human pregnant
urines or from human placenta. Given in adequate amounts and persisted with in boys
who have undescended testes, it will, in a gratifying percentage of cases, aid in the descent
of the testes. Occasionally, a case will be found which wjll not react because of some
mechanical obstruction, but you will have helped the surgeon and made his job easier, and
the testicle will be easier to replace in the scrotum and will have a better chance to develop
later.
2. You also have a right to, and should, treat menorrhagia or metrorrhagia with the
following precautions. It is assumed that you will have examined the patient carefully
enough to exclude such pathological lesions as fibroid, carcinoma and other lesions which
can cause bleeding; that you will have obtained a careful hisitory and made a careful
examination and obtained a basal metabolic rate to exclude hypothyroidism or myxcedema,
which can cause menorrhagia and will respond well to thyroid substance. If this has been
done and these conditions excluded, then you are certainly entitled to use these gonadotropic hormones; but, just as our original high hopes with regard to any of these things
tends to vanish into thin air, so the original enthusiasm for Prolan has somewhat subsided.
It is helpful in many ways and, when successful, it acts promptly. So if you have a
functional menorrhagia and you use this hormone and you get no response in a few days,
then further treatment will most likely be of no value and curettement will be necessary.
Finally, you should be aware of a somewhat unusual condition; namely, a granulosa cell
tumour of the ovary. That condition is common in little girls. It is easy to suspect it in
a woman in the late 50's who bleeds from the uterus, but in the normal menstrual span
one is not so likely to think of this as a cause for1,protracted and copious menstruation.
The diagnosis is not so easy because these tumours can be quite small. Fortunately, they
do not usually become malignant.
3. When it comes to female sex hormones, you have a right and an indication to treat
the menopause. With every wish to be conservative in the field of endocrinology, I nevertheless believe very strongly that the symptoms of the menopause are quite real and can
be properly treated if they are adequately treated. For example, a woman about a year ago
came into my office and, although our staff has been there for many years and are reasonable, efficient, and so on, all of us were prepared to throw her out of the office. She was
so unreasonable and impossible to deal with that it was quite a problem. It was soon
apparent that her condition was not her fault and that it was an aggrevated case of menopausal symptoms. She had been treated. When you are dealing with patients with 20 or
30 hot flashes a day, or awakening with a drenched nightgown, that is not imaginary.
When that patient was given estrin, 2000 units twice a day, she came under control in
about two weeks. For the first month we gave her this dose and it utterly transformed
her. That was an unmistakable benefit to her. Not only was she appreciative, but so was
her husband. The adequate treatment of the menopause is something you should do and
are entitled to do.
4. Senile vaginitis is likewise helped by estrin therapy. Likewise, involutional melancholy can be helped by adequate amounts of this same hormone. But when we come to
many of the functional disturbances of menstruation, such as the various amenorrheas
with no definite cause, then treatment is extremely complicated and difficult.
I trust you will not take offence if I make this suggestion in the interests of our
patients—I take it that if any of you had a patient in whom you were suspecting a' brain
tumour, you would hardly hazard operating but would very probably refer her to a neuro-
[102] surgeon, even though the neuro-surgeon might not be able to remove the tumour but
might, in so doing, kill the patient. Nevertheless, you would refer the case to him. Now,
merely because there is little risk in injecting hormone, certainly no risk to life and no
risk in producing carcinoma either, yet that is hardly an excuse for wasting the patient's
money and time. I rather think that it is not fair to go on puttering when there is a capable
endocrinologist in the neighborhood. He is ready to admit that he is not very successful
and just plods along, but at least he knows a little of what he is doing. As to the matter
of expense—this is not the fault of the manufacturers. The cases are always chronic and
I think one should hesitate before fiddling with expensive therapy. If you will read over
the literature of some of these successful cases, you will usually find a footnote of thanks
to this or that therapeutic house which has very generously supplied this or that hormone.
When you read of eunuchoidism which is treated, and cases where the growth of infantile genitalia is improved with doses of hormone, have you ever thought of the expense
that it would have been to the patient if those hormones had been bought by the patient
and not supplied by the manufacturers? Addison's Disease is a disease which is very expensive to treat and sometimes a patient with this disease will die because no one can afford
the expense that goes with the treatment of the disease.
(Slides were then shown, giving some of the trade names of these sex hormones and
showing just what they are.)
Here we see a girl with acromegaly who stopped menstruating at twenty. It would be
of no use to treat her with a hormone. Here we see a case of Simon's Disease—no value
in treating her with hormone. It is very, very confusing. Many of them die, some of them
get better. It is very hard to form an opinion. Here we see something else. Here are two
girls, both 24 years of age. There is no mammary development; small amount of pubic
hair; masculine pelves; no axillary hair; neither of them has ever menstruated. But they
are not the same condition. This one is a little under 5 feet; this one is reasonably tall.
The first is hypophyseal infantilism; this one is preadolescent eunuchoidism. The first one
needs gonadotropic hormone in the form of anterior pituitary therapy in large amounts
for a very long time. This one needs female sex hormone in large amounts for a very long
time. Here we see the same two conditions in males. The matter is in the process of
development. We are still feeling our way and five years from now I hope that treatment
will be much more precise.
[103]  

Cite

Citation Scheme:

        

Citations by CSL (citeproc-js)

Usage Statistics

Share

Embed

Customize your widget with the following options, then copy and paste the code below into the HTML of your page to embed this item in your website.
                        
                            <div id="ubcOpenCollectionsWidgetDisplay">
                            <script id="ubcOpenCollectionsWidget"
                            src="{[{embed.src}]}"
                            data-item="{[{embed.item}]}"
                            data-collection="{[{embed.collection}]}"
                            data-metadata="{[{embed.showMetadata}]}"
                            data-width="{[{embed.width}]}"
                            async >
                            </script>
                            </div>
                        
                    
IIIF logo Our image viewer uses the IIIF 2.0 standard. To load this item in other compatible viewers, use this url:
http://iiif.library.ubc.ca/presentation/cdm.vma.1-0214360/manifest

Comment

Related Items