History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: November, 1950 Vancouver Medical Association Nov 30, 1950

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The Vancouver   tedical Association
dr. j. h. MacDermot
Publisher and Advertising Manager
OFFICERS  1950-51
Dr. Henry Scott Dr. J. C. Grimson Dr. W. J. Dorrance
President Vice-President Past President
Dr. Gordon Burke Dr. E. C. McCoy
Hon. Treasurer Hon. Secretary
Additional Members of Executive:
Dr. J. H. Black Dr. D. S. Munroe
Dr. G. H. Clement
Dr. A. C. Frost Dr. Murray Blair
Messrs. Plommer, Whiting & Co.
Eye, Ear, Nose and Throat
Dr. N. J. Blair Chairman Dr. B. W. Tanton -^ Secretary
Dr. C. J. Trefry Chairman Dr. Peter Spohn Secretary
Orthopaedic and Traumatic Surgery
Dr. D. E. Starr Chairman Dr. A. S. McConkey Secretary
Neurology and Psychiatry
Dr. F. E. McNaib- Chairman Dr. R. Whitman Secretary
Dr. Andrew Turnbull Chairman Dr. W. D. Sloan Secretary
Dr. E. France Word, Chairman; Dr. A. F. Hardyment, Secretary;
Dr. F. S. Hobbs, Dr. J. L. Parnell, Dr. S. E. C. Turvey, Dr. J. E. Walker
Co-ordination of Medical Meetings Committee:
Dr. R. A. Stanley Chairman Dr. W. E. Austin Secretary
Summer School:
Dr. E. A. Campbell, Chairman; Dr. Gordon C. Large, Secretary;
Dr. A. C. Gardner Frost; Dr. Peter Lehmann; Dr. J. H. Black;
Dr. B. T. H. Marteinsson.
Medical Economics:
Dr. F. L. Skinner, Chairman; Dr. E. C* McCoy, Dr. T. R. Sarjeant,
Dr. W. L. Sloan, Dr. J. A. Ganshorn, Dr. E. A. Jones, Dr. G. Clement.
Dr. G. A. Davidson, Dr. Gordon C. Johnston, Dr. W. J. Dorrance
Special Committee—Public Relations:
Dr. Gordon C. Johnston, Chairman; Dr. J. L. Parnell, Dr. JT. L. Skinner
Representative to B. C. Medical Association: Dr. W. J. Dorrance
Representative to V.O.N. Advisory Board: Dr. Isabel Day
Representative to Greater Vancouver Health League: Dr. L. A. Patterson VANCOUVER MEDICAL ASSOCIATION
Founded 1898; Incorporated 1906.
(Spring Sesjsion)
JANUARY 2nd—GENERAL MEETING—Speaker: Dr. R. B.  Kerr, Professor and
Head of the Department of Medicine, University of British Columbia.
FEBRUARY 6th—GENERAL MEETING—Devoted to Medical Economics.
MARCH 6th—OSLER DINNER—Dr. H. A. DesBrisay, Osier Lecturer.
APRIL 3rd—GENERAL MEETING   (Speaker to be announced).
MAY 28th to JUNE 1st (inclusive)—ANNUAL SUMMER SCHOOL.
FIRST TUESDAY—GENERAL MEETING—Vancouver Medical Association—T. B.
Clinical Meetings, which members of the Vancouver Medical Association are invited
to attend, will be held each month as follows:
Notice and programmme of all meetings will be circularized by the Executive Office
of the Vancouver Medical Association.
Dates of Refresher Courses and Weekly fixed meetings in the various hospitals.
WShy Refresher Courses for the General Practitioner
NEUROLOGY, NEUROSURGERY and PSYCHIATRY—January 15th, 16th, 17th,
SURGERY—February 12th', 13th, 14th, 1951.
EYE, EAR, NOSE and THROAT—March 5th, 6th, 7th, 1951.
OBSTETRICS and GYNAECOLOGY—April 9th, 10th, 11th, 1951.
Regular Weekly Fixtures in the Lecture Hall
Monday, 12:15 p.m.—Surgical Clinic.
Tuesday—9:00 a.m.—Obstetrics and Gynaecology Conference.
Wednesday, 9:00 a.m.—Clinicopathological Conference.
Thursday, 9:00 a.m.—Medical Clinic.
12:00 noon—Clinicopathological Conference on Newborns.
Friday, 9:00 a.m.—Paediatric Clinic.
Saturday, 9:00 a.m.—Neurosurgery Clinic,
edition, 1950.
Regular Weekly Fixtures
Tuesday, 9:15 a.m.—Paediatric Ward Rounds.
Wednesday, 9:00 a.m.—Medical Ward Rounds.
Second and Fourth Wednesday's in month—Obstetrical Clinics.
Friday, 8:00 a.m.—Surgical Clinic   (and alternate weeks)   Clinical Pathological Conference.
Tuesday, 9:00 a.m. to 10:00 a.m. (weekly)—Clinical Meeting.
B. C. Surgical Society meeting dates:
Spring meeting—March 3 0th-31st—Vancouver Hotel (open to all members of the
Regular Weekly Fixtures
Tuesday, 8:30 a.m.—Dermatology.
Wednesday, 10:45 a.m.—General Medicine.
Wednesday, 12:30 p.m.—Pathology. ji|p
Thursday, 10:30 a.m.—Psychiatry.
Friday, 8:30 a.m.—Chest Conference.
Friday, 1:15 p.m.—Surgery.
Publishing and Business Office — 17-675 Davie Street, Vancouver, B.C.
Editorial Office — 203 Medical-Dental Building, Vancouver, B.C.
The Bulletin of the Vancouver Medical Association is published on the first of
each month.
Closing Date for articles is the 10th of the month preceding date of issue.
Manuscripts must be typewritten, double spaced and the original copy.
Reprints must be ordered within 15 days after the appearance of the article in question, direct from the Publisher. Quotations on request.
Closing Date for advertisements is the  10th of the month preceding date of issue.
Advertising Rates on Request. =p|||
Page 26 m Vasoconstriction
combined with
antibiotic therapy in
(brand of phenylephrine}
In upper respiratory tract infections,
topical application of penicillin to the nasal cavity has a decided bacteriostatic action against
typical respiratory pathogenic microorganisms.
To provide clear passage for such therapy,
Neo-Synephrine is combined with penicillin—
shrinking engorged mucous membranes and
allowing free access of the antibiotic.
Neo-Synephrine—a potent vasoconstrictor—
does not lose its effectiveness on repeated application ... is notable for relative freedom from
sting and absence of compensatory congestion.
Stable • Full Potency
Supplied in combination package for preparing 10 cc. ot
afresh buffered solution containing Neo-Synephrine hydrochloride 0.25% and Penicillin 5000 units per cc.
New York 13, N. Y.    Windsor. Ont.
Neo-Synephrine, trademark reg. U.S.& Canada
Total   Population—Estimated     385,500
Chinese   Population—Estimated       6,877
Hindu  Population—Estimated h    133
Rate per
Number 1000 Pop.
Total deaths   (by occurrence)     340 10.6
Chinese deaths 1 •        15 26.2
Deaths,   residents   only «     313 9.7
(Includes late registrations)
September,  1950
Male .     3 74
Female .       357
INFANT MORTALITY—Residents  only:
September,  1950
Deaths under 1  year of age       7
Death rate per 1000 live births |       9.6
Stillbirths   (not included in above item)       9
Scarlet  Fever	
Diphtheria Carriers	
Chicken Pox .	
Rubella «.
Whooping Cough	
Typhoid  Fever  I	
Typhoid Fever Carriers	
Undulant Fever	
Infectious Jaundice	
Salmonellosis Carriers	
Dysentery  Carriers	
Cancer  (Reportable):
September, 1950     September, 1949
Page 27 A new form . . .
Since the advent of crystalline sodium and potassium penicillins, the search for
new salts of penicillin which exhibit unusual and useful properties has been intensively
carried on. A number of such salts has been developed in the Connaught Medical
Research Laboratories. Of these Ethyl Tyrosine Penicillin G has been selected by the
Laboratories for distribution. This salt is a crystalline compound of penicillin G and
the ethyl ester of the naturally occurring amino-acid tyrosine. Ethyl tyrosine penicillin
G is exceptionally non-toxic, is stable and is but slightly soluble in water. It exhibits
prolonged penicillin activity when suspensions are administered parenterally.
This new product of the Laboratories, Ethyl Tyrosine Penicillin G, is presently
available for oral administration in the form of conveniently small tablets as follows:—
Tube of    15 Tablets, each of    50,000 International Units
Tube of    15 Tablets, each of 100,000 International Units
Vial of 100 Tablets, each of    50,000 International Units
Vial of 100 Tablets, each of 100,000 International Units
University of Toronto Toronto 4, Canada
The question of hospital accommodation for the sick of British Columbia, and
more especially of Vancouver, has rapidly become one of the most urgent and serious
of the problems confronting the people of this province. We do not think that the
public as a whole fully realises how very serious this problem really is.
The population of Greater Vancouver has practically doubled in the past twenty
years. The number of hospital beds available has hardly risen at all in that time: and
certainly has not risen commensurately with the growth of population.
Further, the use of hospitals for the care of the sick has become, during those years,
more and more a matter of common practice. Twenty or thirty years ago, many confinements were carried out in homes, many minor operations, such as tonsillectomies,
haemorrhoids and so on, were done at home. Today this is out of the question. With
the increasing perfection in anaesthesia, and the national demand for better and safer
anaesthetics, no physician would dare take the risks we more readily assumed in those
A couple of years ago the Province of British Columbia, through its government,
assumed responsibility under the Hospital Insurance Act, for hospitalization. The
medical profession, which was not consulted, warned them at that time that there were
not enough hospital beds available, even for things as they were then: and warned
them that they must expect an increase in demand under the new Act. A hospital
survey by James Hamilton & Associates was made but beyond this no steps were taken
to meet the needs that then existed, nor does there seem to be any plan to meet the
logical and inevitable increase in these needs that Was bound to follow.
Lately a charge has been made that the average hospital days' stay has risen from
10 to 11 days. If this is all, then someone, and we believe it is the medical profession,
deserves considerable credit for the fact that it is no worse. Some years ago, under
"free enterprise," the average days' stay was 14 or more.
The Government finds itself in a position where the operations of the Act shew
a deficit. Very naturally, two things follow: first, the authorities try to lay the responsibility on hospital administration, which they say is costing more than it should, and
they demand further economy. In this year of grace, with all costs of living at a
rather low estimate of 170% over the 1939 standard—with the increases in equipment
and so on, we do not believe that the cost of hospital administration can he lowered
much: and we believe that hospital authorities have done and are doing all they can
to keep costs down.
The other natural corollary of this deficit is that the Government is in no hurry
to build, or authorize the building, of extra beds—since this will increase the difficulty
of financing the scheme.
And so everybody is suffering. First, and most important, sick people are suffering.
To take only one instance. As a profession, we urge early diagnosis and early treatment
for cancer. Yet cases diagnosed, and operable at the time of diagnosis, are unable to
obtain beds, sometimes for many weeks while their cancer goes on growing, and their
chances for recovery dissolve rapidly. And it is not only in the case of cancer that
people suffer. We venture to say that every day of the week, through no fault of the
admitting offices of the hospitals, but through sheer, stark necessity arising from the
fact that there is no room, scores of patients who urgently need hospital care are
turned away, or postponed for days or weeks.
The medical profession, next, is suffering very acutely. We cannot do our work
properly, we cannot get beds to treat our patients. Many of us cannot get a place at
.   Page 28 all on the visiting staffs of the hospitals. This is bad, not only for us, but again for
the sick people to whom we are supposed to give modern medical care.
Lastly, the whole economy of the Province is suffering. The reluctance of people
to pay their hospital tax is, we verily believe, in large part due to a sense that they
are not getting what they are paying for. They must be nearly dead before they can
get into the hospital, or in imminent danger of death:  and this is not good enough.
Nor are the hospitals to be blamed for this. Daily the big hospitals perform
miracles of legerdemain and manipulation, in their efforts to meet the demands that
swamp them. With unfailing patience and good temper they listen daily to bitter
complaints, to urgent demands, to the grimmest tales of woe—and they do the best
they can. When every bed is filled, and every ward has extra beds, and there is not
one bed left in the entire institution, what are they to do?
What is the answer to all this? It is that the Government must in some way
provide more beds: and if this costs us, as a province, more money, we must find the
money. Otherwise, the Government is breaking faith with the people to whom they
promised hospitalization under their Hospital Insurance Act.
There does not appear to be any policy of hospital building, such as one would
expect. The Water Commission, for instance, builds according to plans covering a
period of twenty or more years ahead—the Workmen's Compensation Commission plans
similarly according to their estimate of future needs. If the Hospital Insurance Commission is working to any plan, we have no knowledge of the fact. Their policy, so
far at least, is a purely ad hoc one.
The plans that one would expect to take form, should take due cognizance of
density of population, ease of transport to and from hospital, medical staffs available,
etc, and in these days of uncertainty and peril, of military necessities. Centralization
should be avoided as far as possible
We understand, on good authority, that several of the hospitals now in existence,
and other bodies, are willing and anxious to put in more hospital beds—the figures we
have heard quoted, amount to some 500 beds—and we understand that they cannot
do so because the Hospital Insurance Commission will not allow them to do so. Why?
And again, why? These beds would not cost the Province anything to build—but yet
we hear of nine million dollars that are to be spent on erecting 500 beds.
And while we are bickering and arguing about who is to build, and where buildings are to be put, no hospital beds are being built. We believe that it is the duty of
the Government to tackle this problem honestly and boldly: to deal squarely with the
public and to meet their own obligations, assumed by themselves, and so far not
We need as many beds as possible, as soon as possible, to be built as cheaply as
possible. This should be the only consideration.
Page 29 I
Library Hours:
Monday, Wednesday and Friday :  9:00 a.m. - 5:00 p.m.
Tuesday and Thursday 9:00 o.m. - 5:00 p.m.
Saturday  9:00 a.m. - 1:00 p.m.
Recent Accessions
Bancroft, F. W. and Pilcher, C. Surgical Treatment of  the Nervous System,   1946
(second printing).
Barsky, A. J. Principles and Practice of Plastic Surgery 1950.
Baruch, S., An Epitome of Hydrotherapy, 1920 (reprinted 1950). Gift of the Baruch
Committee on Physical Medicine.
Best, C. H. and Taylor, N. B., The Physiological Basis of Medical Practice, 5 th edition,
Feldman, M., Clinical Roentgenology of the Digestive Tract, 1938   (Gift of Dr. A.
Foote, R. R., Varicose Veins, 1949.
Hewitt, Richard M. et al (editors)—Collected Papers of the Mayo Clinic and the Mayo
Foundation, 1950.
Kemp, W. N., The Value of Hormones in General Practice, 1949  (Gift).
Medical Clinics of North America—Symposium on Specific Methods of  Treatment,
Boston Number,  1950.
Mote,  J.  R.   (editor)—Proceedings of  the First  Clinical ACTH  Conference,   1950
(Historical and Ultra-Scientific Fund).
Nelson, W. E., Mitchell-Nelson Textbook of Pediatrics, 5th edition, 1950.
Simmons, J. S., Whyne, T. F. et al., Global Epidemiology—A Geography of Disease
and Sanitation, 1944.
Surgical Clinics of North America—Symposium on Clinical Surgery, St. Louis Number,
Ungerleider, H. E. and Gubner, R., Roentgenology of the Heart and Great Vessels,
1950 (Gift of the Equitable Life Assurance Soc.)
The following was published in The Lancet in their issue of March 11th, 1950
(p.463) and we publish it here in the hope that our readers will get some idea of the
librarian's lot! We hope that it will spur those who are about to prepare papers to
give the librarian ample time to look up those exotic and obscure references!
When a doctor's not engaged on his dissections and injections,
Or in chasing little microbes up a sewer,
He will delve into the mysteries of recondite case-histories
With reference exotic and obscure;
A symposium in Spanish about mumps in Machrihanish
With footnote from Guadeloupe on glands,
Page 30 A report on sudden death by a lady called Macbeth,
With the title "Don't forget to wash your hands."
Through labyrinths of literature on frailties of the flesh
I search from crack of dawn till set of sun.
Ah, who would be a handmaid of the medical profesh?
The librarian's lot is not a happy one.
"An infection found in beavers was transmitted to retrievers,
And carelessly contracted by a vet,
While the organism, injected in a toad in Timbuktu,
Was recovered from a tadpole in Tibet.
Now, was it in the Lancet in 1892?
or the B. M. J. in 1923?
Or maybe Path & Bact.? No. I can't be more exact,
And I think the name was Smit, or Smut, or Smee."
Good sons of sage Hippocrates and Galen's gallant heirs,
May your battle with the bugs be timely won,
But spare a pang of pity for the writer of this ditty,
The librarian's lot is not a happy one.
This little manual is offered as a guide in the training of undergraduate students
of Dietetics, Nursing and Medicine, though it should also prove of great practical value
to graduates, particularly the practicing physician. It offers a brief discussion of the
general principles of diet therapy and contains tables of dietary standards approved
by the Canadian Council on Nutrition for 1948. All the common therapeutic diets
are shown in some detail. With each diet section there is a preliminary discussion stating
most briefly the main objectives of the diet, and this is followed by the necessary food
lists and a suggested meal plan. The diabetic diet still conforms to the marked restriction
of fat in vogue at the Montreal General Hospital for nearly 25 years, but this still
has many advocates elsewhere. There is no attempt in the manual to make any provision for highly specialized or rarely used diets. The manual is not written or intended
for patients but office diets could be taken from it quite easily. There is an informatirve
summary of the main principles in the feeding of healthy infants and children. The
manual is attractively bound and printed. R.A.P.
(Canadian Medical Association, British Columbia Division)
203 Medical-Dental Building,
Vancouver, B.C.
Dr. J. H. MacDermot, August 15, 1950.
Editor, The Bulletin,
Vancouver Medical Association.
Dear Doctor MacDermot:
Enclosed please find a "thank you" letter from the Canadian Red Cross Society.
The Executive Committee of The British Columbia Medical Association would
appreciate having you place a notice in the Bulletin, similar to that of last year, in
respect to this matter.
Yours very truly,
Honorary Secretary-Treasurer.
Dr. J. C. Thomas,
President, B. C. Medical Association,
Raam 203 - 925 West Georgia, Vancouver, B.C.
Dear Dr. Thomas:
We have been advised that the following resolution was unanimously passed at
the recent Annual Meeting of Central Council:
"This Central Council of the Canadian Red Cross Society hereby
expresses its thanks to the medical, dental, nursing and teaching
professions for their continued assistance and advice in the work
of the Society in its peacetime programme through the year."
We shall be grateful for your assistance in conveying the above message to the
members of your Association.
Yours sincerely,
July 5, 1950.
the opening of
2665 Point Grey Road
Vancouver, B. C.
Specializing in the care of medical
and convalescent patients.
Not just another nursing home, but a quiet hospital on the shore of
English Bay, with an unsurpassed view of the mountains and water,
where your patients will receive excellent nursing care in pleasant surroundings.
Special diets carefully adhered to
Telephone—BAyview 4213
CHerry    9667
By A. L. Chute, M.A., M.D., F.R.C.P.(C)
Toronto, Ontario
Hypoglycemia is only the overt manifestation of some more basic metabolic disorder. It is frequently the signpost which directs us to the correct management of a
number of pathological  conditions  arising in  childhood.
Before embarking on a discussion of the clinical aspects of hypoglycemia, it will
probably be to our advantage to review for a moment the various factors responsible
for the maintenance of the normal blood sugar values. As in any dynamic system, these
values will depend on the one hand upon the supply and on the other hand on the
rate of utilization or demand for the substance in question. The utilization of glucose
occurs in the brain, heart and other tissues but the chief consumer is the large mass of
voluntary muscle. The latter also acts as a store house for carbohydrate in the form
of glycogen. It should be noted, in passing, however, that this glycogen unlike that
of the liver can never, become directly available for conversion to blood glucose.
The constant demand for carbohydrate by tissues can be met in 3 ways:
1. By the ingestion and assimilation of carbohydrate into the blood stream.
2. By the conversion of glycogen stored in the liver to glucose.
3. By the conversion   of other foodstuffs especially protein to carbohydrate.
The latter mechanism becomes of the- greatest importance during periods of fasting,
since certain organs such as the brain are incapable of proper functioning in the absence
of adequate amounts of glucose.
Claude Bernard was the first to demonstrate the fact that the glucose content
of the blood from the hepatic veins was greater than that in the portal circulation of
fasting animals; from which he rightly concluded that the liver contributed to the
maintenance of normal blood sugar values in the fasting state. Mann's classical experiment in which the portal circulation was successfully short-circuited and the liver
removed demonstrated the indispensability of the liver in the maintenance of normal
blood sugar levels. Even in diabetic animals hypoglycemia rapidly develops when the
liver is removed from the body.
The action of the pituitary, the adrenal cortex and the thyroid, indeed the action
of insulin itself must be regarded as secondary mechanisms which merely serve to
regulate the release of sugar from the liver to the blood or the removal of sugar from
the blood by the tissues. &jm 0m
Having established the liver and the tissues as the primary factors in the main-
tenace of the blood sugar level, let us examine the effects of the various regulator's
which we have just mentioned.
Of all the regulators insulin alone is capable of lowering the blood sugar. In the
normal animal insulin causes an increased deposit of glucose in muscle, but apparently
not in the liver. It increases the rate of oxidation of glucose and inhibits gluconeogenesis.
In the diabetic it also causes the glycogen deposition in the liver. The action of insulin in
lowering the blood sugar is antagonized by the effect of the anterior pituitary, the
adrenal cortex and the thyroid.
Thus, we have three main mechanisms whereby the blood sugar may be abnormally lowered.
1. Inability of the liver"—through disease—to maintain the blood sugar in face
of the constant utilization going on in the tissues.
2. An excess production of insulin.
3. There may be deficient activity on the part of the insulin antagonists, pituitary,
adrenal and thyroid.
Page 33 To return to the clinical aspect of the problem, let us deal first with the disease
of the liver, as a cause of hypoglycemia.
First, I shall list the causes of liver diseases which bring about hypoglycemia and
then discuss each one briefly as it related to our problem.
1. Acute Yellow Atrophy.
2. Toxic Hepatitis.
3. Diffuse Carcinomatosis.
4. Fatty Infiltration or Fatty Metamorphosis.
5. Glycogenesis or Von Gierke's Disease.
Acute Yellow Atrophy is usually a sequel to a severe virus infection such as
infectious hepatitis, or homologous serum jaundice, or it may be due in a few cases
to a severe chemical chemical toxemia. These patients are usually critically ill and
gastro-intestinal symptoms associated with jaundice are the prominent features. In the
early stages, the liver may be large, but if they survive for a short time there may
be so much liver destruction that it becomes very small and shrunken. It is usually
not until this latter stage that the ability of the liver to maintain the blood sugar level
is sufficiently diminished that hypoglycemia results. This hypoglycemia may contribute
in part to the early demise of the patient.
Toxic Hepatitis is usually the result of a severe bacterial infection or due to
some chemical poisoning such as chloroform, carbon tetrachloride or phosphorus. The
clinical symptoms and findings here are very similar to those already described for
acute yellow atrophy; the resultant hypoglycemia is brought about in the same fashion.
Diffuse Carcinomatosis of the liver is not particulaly common in children but
may be seen as a result of neuroblastoma in the abdomen. In this condition, there is
so much replacement of liver tissue with malignant new growth that the liver is
unable to function adequately and hypoglycemia may develop as a result.
Fatty Infiltration—The preceding conditions all have obvious clinical signs pointing to the liver as a cause of the disturbance producing hypoglycemia. In those cases
of hypoglycemia due to fatty infiltration of the liver, however, there are not so many
evident signs pointing to the liver. Fatty infiltration of the liver may result from a
number of conditions; obesity, diabetes, familial hypercholesterolemia and some poisonings. This condition may also be produced experimentally in animals which are fed
on a high fat diet from which choline and methionine have been omitted. It is interesting to recall that when Banting & Best first made their discovery of insulin they soon
learnt that their diabetic depancreatized dogs on a diet of meat and sugar alone appeared
to require less and less insulin and finally no insulin at all. These animals were far from
well, however, and soon died. At autopsy the animals' livers were exceedingly large.
and fatty. The natural conclusion was that there was some essential factor present in
the pancreas which had been removed by pancreatectomy which was necessary for
the normal functioning of the liver. Consequently, the animals were fed raw pancreas
as well as their diet of meat and sugar. On this diet the diabetic dogs remained permanently hyperglycemic and their livers remained a normal size and failed to become
fatty. The next step, of course, was to determine what substance in the raw pancreas
was responsible for the prevention of these fatty livers. Subsequent work has shown
that choline or the amino acid methionine is capable of preventing this type of fatty
accumulation in the liver. In patients suffering from this condition physical examination usually reveals the presence of an enlarged soft liver. These patients are best
treated by marked restriction in .the fat intake and by increasing the protein content
of the diet. Such measures are usually sufficient to control most cases. Some workers,
however, report benefits from the use of choline or methionine in conjunction with
the above treatment.
Glycogen Disease or Glycogen Storage Disease first described by Von Gierke is
a defect in the metabolism of glycogen. Although the condition is undoubtedly
present from birth it often goes unrecognized until the child is a year or more of age.
Page 34 At this time attention is usually called to their lack of growth and retarded development and to the presence of a protuberant abdomen; the child frequently has disturbing
symptoms as well. There may be bouts of nausea or vomiting in the morning and
in a number of cases frank convulsions may be seen at this time. Similar symptoms
may arise at any time that food is withheld for long periods of time. Physical examination o«f these children reveals a grossly enlarged liver, which in some cases may be
right down into the pelvis; an important characteristic of these cases is that there is
no splenomegaly. Glycogen disease may not be confined to the liver alone; in some
cases the heart is also involved and may be enlarged as a result. A few cases have been
described in which glycogen storage was manifest in a great many organs of the body
including the skeletal muscles and the tongue. The characteristic feature of this disease
is the ability of the liver to store glycogen but its inability to release it for bodily
needs. This is well demonstrated by the adrenalin tolerance test. Normally, on administering 3 to 4 mms. adrenalin subcutaneously, to an infant, the blood sugar will rise
rapidly by as much as 50 to 75% mgms. percent above the fasting level. In children
with glycogen disease there may be no response at all or only a 5 or 10 mgms. elevation
of the blood sugar level. The glycogen content of the blood may also be elevated.
The normal glycogen content is from about 5 to 10% mgms. In these patients suffering from glycogen disease, however, the glycogen content of the blood may be as
high as 50 to 100 mgms. %. Probably the only certain way of making a diagnosis
is to do a liver biopsy. If the biopsy material is analyzed for glycogen, it will be found
to contain a very high concentration, usually more than 10% of glycogen. The nqrmal
glycogen in the liver rarely exceeds'this value. The chief characteristic of glycogen
in this disease is that when the liver is left at room temperature for 24 hours, very
little glycogen is removed so that at the end of this period there is the same amount
of glycogen present in the liver as there was 24 hours previously; whereas glycogen
in normal liver is very rapidly removed by the enzymes present to form lactic acid;
so that at the end of 24 hours at room temperature no residual glycogen is present in
normal liver tissue. If normal liver tissue is mixed with that from a case of glycogen
disease the enzymes present in the normal tissue will cause hydrolysis of the glycogen
in the liver from the patient suffering from glycogen storage.
There is no specific treatment for this condition. It is possible that the biochemist
may some day discover some specific enzyme which is deficient in these patients and
if this substance is administered to them they may be able to break down their
glycogen. At the present, however, we are confined to symptomatic treatment. There
has been a suggestion that the glycogen built up from lactose is different and more
difficult to break down than that built up from glucose. Consequently, milk has been
eliminated from the diet of these children. From my own experience I have found
comparatively little benefit from this procedure. Because of the inability of the liver
to form glucose from it's own glycogen, these children should not be allowed to go
for long periods of time without food. Frequent small feedings are indicated and in
the more severe cases which are apt to have convulsions in the morning, it is probably
wise to wake them around midnight in order to give them a small snack of food at
that time. Unlike the patients suffering from hyperinsulinism, which we will discuss
in the next section, there is probably little rationale for treating these patients with
low carbohydrate, high protein feedings. These children contract infections very readily
and if this interferes with appetite they may develop an acidosis exceedingly rapidly
and die as a result. Chemotherapy should be used at the first opportunity and if food
intake is inadequate intravenous glucose administration should be started at once.
In the past, most cases died of infections at an early age. Proper dietary management and the use of antibiotics has improved the prognosis and a number of these
children have survived to puberty and beyond. The prognosis has improved and Van
Creveld who has been interested in this group of cases states that following puberty,
these children appear to have less difficulty with hypoglycemic attacks and that the
liver becomes definitely smaller.
Page 35 The second main cause of hypoglycemia is an increased production of insulin.
Following the discovery of insulin in 1922, Sele Harris postulated that there undoubtedly iWOuld be cases found in which over-activity of this hormone was present leading
to a condition of hypoglycemia. Subsequently, Wilder described such a case resulting
from adenoma of the islet cells of the pancreas. The first successful treatment of such
a condition, however, was performed by Dr. Roscoe Graham in Toronto. The case
was that of a middle-aged woman who had severe hypoglycemic attacks and at operation was found to have small adenoma of islet tissue, Removal led to a complete
subsidence of all symptoms. These adenomata may be single, more often they are
multiple, and at operation may be exceedingly difficult to discover. In place of adenomata,
the islet cells may be greatly increased in number throughout the whole of the gland
or in certain regions leading to areas of hyperplasia rather than to definite tumour
formation. Hyperplasia rather than tumour formation is common in children. These
cases appear to arise chiefly in infants and usually become manifest around the fifth
and sixth month. The children are nearly always seen first by the neurologist, because
they suffer from attacks of unconsciousness or staring spells in which they seem to
be oblivious of their surroundings. Careful questioning usually reveals that these spells
are relieved following the taking of food, and are most commonly seen in the morning
or after periods of rest when food has been withheld for some time. Unless the
condition is suspected, it may be missed completely, and the convulsions attributed
to epilepsy, to some form of birth injury, or as symptomatic convulsions due to infection.
It is important, therefore, in all cases of convulsions in small children to take a fasting
blood sugar. Many of these children will have fasting blood sugars as low as 20 mgms. %
before they begin to have any obvious symptoms. Blood sugars consistently below 50
mgms. % on a fasting sample merit further investigation.
A glucose tolerance test usually reveals a very slow or insignificant rise or if
the blood sugar rises to normal levels, it usually quickly falls to markedly sub-normal
levels as a result of the stimulation of an excess amount of insulin from the pancreas.
It pays, therefore, to carry on the glucose tolerance test for 5 or 6 hours after the
administration of glucose to demonstrate this marked hypoglycemic effect. Glycogen
disease can be ruled out by an adrenalin tolerance test since this causes a normal
mobilization of glucose in these children, unlike glycogen disease where no glucose
is liberated. A number of forms of treatment have been devised for this condition.
Medical treatment consists in giving a high protein diet containing little or no readily
available carbohydrate. By this means, it is hoped to avoid stimulation of the pancreas
by a sudden rise in blood sugar, but to provide for the needs of the body by the
gradual conversion of protein to glucose without excessive rise in the blood sugar level.
In some of the milder cases this may prove successful; but in the more severe ones
medical treatment is not adequate. These patients usually require a pancreatectomy
and a very large portion of the pancreas has to be removed in those cases wherie
hyperplasia is the cause of the increased insulin production. At least 8/10ths of the
gland must be removed in order to prevent recurrence of symptoms. If a definite
adenoma is found this may be removed and the pancrease left intact.
One should emphasize, however, that the incidence of multiple adenoma is
very high and that the whole gland should be thoroughly searched to ensure the
removal of other adenomata, if present. Since these ate frequently within the body
of the gland they are readily missed, with the result that the patient has continuing symptoms and a second operation has to be performed. Unfortunately, even
after 8/10 th of the pancreas has been removed some children continue to have
symptoms. This is possibly due to the fact that some cases have aberrant pancreatic
islet tissue; one such case which came to post-mortem at the H.S.C. revealed the
presence of aberrant tissue containing islet cells right within the wall of the duodenum.
One may ask, is one justified in carrying out such a radical surgical procedure in
children simply because they suffer from hypoglycemia. The answer is very definitely
in the affirmative. Most cases left untreated develop marked degrees of cerebral atrophy
Page 36 by virtue of their constantly low blood sugar level and in a number of cases they
become permanently mentally defective. A number of patients also die suddenly in
a hypoglycemic attack. One might also wonder regarding the availability of digestive
ferments and the likelihood of producing a severe steatorrhea. In none of the cases
which we have operated on in the Children's Hospital have we seen this complication.
Apparently there is sufficient enzyme production by the succus entericus together with
the small amount of pancreas which remains to carry out adequate fat and protein
digestion. Recently two other forms of medical therapy have been tried. A substance
known as alloxan was shown by Dunn, Sheehand and McLetchie, to cause selective
destruction of the islet cells of the pancreas in animals. Unfortunately, this substance
has a severe toxic effect on both liver and kidney cells as well, and there is little leeway
between the lethal dose and that necessary to cause destruction of the beta cells ctf
the islet. However, it has been tried in a number of cases of carcinoma of islet cells
with varying results. Baily, in Boston, was the first to use it in the treatment of
hypoglycemia in an infant. Employing a technique of repeated small injections he
was able to bring about a marked improvement in the child's condition. This drug,
however, is exceedingly toxic and the difficulties in its administration make it not
suitable for treatment of  this condition in most cases.
With the discovery of ACTH which stimulates the adrenal gluco-corticoids and
causes a rise in blood sugar, another means of attacking this problem has been presented. At a recent meeting of the Paediatric Association, Dr. McQuarrie-of Minneapolis,
reported that he has been able to carry a number of children on small doses of ACTH
and keep their blood sugars sufficiently high to prevent them from having reactions.
Unfortunately, this drug is so difficult to obtain that it is not a practical
form of therapy at the present time. Furthermore, beneficial effects are evident only
during continual administration of the drug. It is interesting to note that in a number
of these cases even following radical removal of a large part of the pancreas, symptoms
have persisted. Furthermore, examination of the pancreas failed to reveal any increase
in insulin content or hyperplasia of the islet cells. It has been suggested, therefore,
that there may be a lack in the normal insulin antagonists, pituitary, adrenal cortex,
and possibly thyroid in some of these cases. Nevertheless, a number of them have been
studied from this standpoint and no evidence of pituitary deficiency has been found;
The growth and development has been normal; likewise adrenal function has been
measured and in most cases appears to be within normal limits. A recent suggestion
has brought the possibility to light that the pancreas itself may again be at fault,
though not as a result of an increased insulin production, but because of decreased
production of a hyperglycemic factor. It has been known for some time that insulin
injected intravenously causes over the first 15 minutes or ^4-hour a rise in blood
sugar levels. Thanks to the work of some Danish experimenters, it has been shown that
this hyperglycemic factor can be separated from the insulin and when injected intravenously causes a rise in blood sugar. It has been suggested that this hyperglycemic
factor arises from the alpha cells of the Islets of Langerhans whereas insmlin is known
to arise from the beta cells. Some further experimental proof that a hyperglycemic
factor is produced by the pancreas is brought forward by the knowledge that following alloxan diabetic rats require considerable more insulin than they do following
pancreatectomy, indeed if an alloxan diabetic rat has its pancreas removed the insulin
requirements of that animal decrease. Alloxan destroys the beta but not the alpha cells.
The alpha cells are, of course, removed at the time of pancreatectomy. One or two
observers have recently reported that in a pancreas removed in patients suffering with
hypoglycemia in which no increase in insulin production was found, a marked dimuni-
tion in the alpha cells has been noted. It is suggested, therefore, that there may be
a further antagonist of insulin produced by the alpha cells of the pancreas itself. It
is the author's opinion that for the present the most satisfactory treatment in these
cases, especially those who have marked hypoglycemia, is sub-total pancreatectomy
combined if necessary with a high protein diet. il||
Page 37 Turning now to the third group of diseases which may be responsible for hypoglycemia, namely, the insulin antagonists, one occasionally sees severe pituitary disease
in children associated with cranio-pharyngioma. In this condition there is usually a
marked cystic degeneration and overgrowth of cells from the pharyngeal pouch which
united with the outgrowth from the lower portion of the brain to form the pituitary
gland. Very frequently there is a marked degree of calcification in this tumour tissue
and a flat plate of the skull will show these various calcifications usually just above
or in the neighbourhood of the sella turcica. The pressure and destruction caused by
this tumour tissue and cyst formation lead to destruction of the pituitary which in
turn leads to a type of cachexia. Owing to the destruction of the anterior pituitary there
is marked lack in the formation of adrenal corticotropic hormone, also a decrease in
growth hormone and a decrease in thyrotropic hormone. This leads to hypoactivity
of these other organs; the sum total effect being a marked decrease in blood sugar levels
with the result that the normal antagonism of insulin is absent. The treatment of
these cases is surgical; sometimes evacuation of the cyst has led to remarkable improvement for considerable periods of time. As a rule, however, the condition is progressive
and terminates fatally. In the case of the hypopituitary dwarf, while there is obviously
some diminution in the tropic hormones to the adrenals, sex glands, etc., one never
encounters hypoglycemia to such a degree as to cause symptoms. Acute adrenal
insufficiency may arise in childhood as a result of a severe bacteriema or septicaemia
destroying the adrenal glands. This may lead to marked hypoglycemia, but the toxic
effect of the infection and the severe effects on electrolyte metabolism are of much
greater significance. Occasionally, tuberculosis, or atrophy of the adrenal gland may
occur leading to a true Addisonian condition which is accompanied by marked hypoglycemia as well as inadequate regulation of the electrolyte balance of the body. Substitution therapy with adrenal cortical hormone or by implants of desoxycorticosterone
are the methods of controlling this condition. Hypothyroidism as a cause of hypoglycemia is not of any clinical importance.
Finally, one should include a miscellaneous group of causes for hypoglycemia.
Occassionally this is seen as a result of hypothalamic brain tumors. In a few cases of
extremely strenuous exercise, or in the exceedingly over-active child the. utilization
of glucose by its musculature may exceed the supply of glycogen in the liver. Some
children who are chronically tired late in the afternoon are benefited by having a mid-
afternoon snack or by having extra rest at this time. If one takes blood sugar values
these are rarely low enough to indicate a pathological hypoglycemia though they are
usually at the lower limits of normal. Finally, severe convulsions by virtue of the
strenuous muscular effort may exhaust glycogen reserves and if a blood sugar is done
immediately after this, one may be led to the erroneous diagnosis of hypearinsulinism.
Further tests should be carried out on the child after he has recovered from his seizure
to ensure the fact that hypoglycemia was not indeed the cause of his seizure.
To summarize, therefore, the blood sugar level is maintained as a balance between
sugar ingestion and the mobilization of the sugar by liver; on the one hand and the
utilization of sugar by the tissues on the other. Insulin is the only regulator which
tends to lower the blood sugar. Opposing its action we have the effect of the pituitary,
adrenal cortex, the thyroid and possibly a hormone from the alpha cells of the pancreas
jf|P \By J. E. Gregory, M.D.
To uiderstand this subject it is essential to review some of the endocrine experiments made on animals having the milk factor present.
In the first of these experiments, two groups of female mice were used. One
group had the milk factor present and the other did not. Each received the same
amounts of estrogenic hormone. In the group with the milk factor present, 90%
thereupon developed cancer of the breast, while in the other group none developed
cancer; instead, 10% developed benign tumors of the breast. The important point
in this experiment is that the one group, with the milk factor present, developed nine
times more tumors than the other group. This means that the cancer virus sensitizes
cells to react to their growth hormone, or to become nine times more sensitive to
the growth stimulant. Consequently, a physician must take a great deal more care,
in the use of hormones, when treating patients with cancer than he would when treating the average patient without cancer. A doctor must understand hormonal physiology
extremely well if hormones are to take an important place in the treatment of cancer.
Practically every tissue in the body is affected in its growth by the hormones.
For instance, when animals are castrated changes take place, not only in the secondary
sex characteristics but also in such tissues as the mucous membrane of the mouth,
salivary glands, and the intestinal glands. The epithelial cells of the salivary glands,
for example, change from columnar to cuboidal.   (10,11,12).
If animals are hypophysectomized (5), cancer of the breast cannot develop, even
though the milk factor is present and estrogenic hormone is given in large quantities.
The pituitary hormone stimulates breast tissue to grow, and tremendously so, when
the tissue is further sensitized by estrogenic hormone.
If mice are given stilbesterol, 20% will develop pituitary tumors(5) of the gland
cells; and these pituitary tumors will put out quantities of pituitary hormone.
Also, if male mice with the milk factor present are injected with stilbesterol, 20%
will develop cancer of the testicle. The first change is an atrophy of the cells of Leydig
and then a rapid growth back to normal, but in 20% of the cases the growth continues
on into a typical malignancy. In the cancer-resistant animals no cancer developed.
A cancer strain of female mice were injected with estrone, and cancer of the
cervix consequently developed. The same experiment done on guinea pigs developed
only benign fibroma of the cervix.
Mice, with the milk factor present, were castrated at from 1 to 3 days of age,
and cancer of the adrenals developed in every case( 10,11,12), but when the experiment was done on cancer-resistant mice, only hyperplasia or benign tumors of the
adrenals occured. This shows that, when as early as the first three days of life, the
testicles are removed it causes a marked increased activity of the pituitary and as
a result the adrenals are stimulated to grow.
Also, if animals are fed on a high-protein or high-salt diet, the adrenal glands will
develop an increased activity and in some animals,  cortical tumors.
In mice, with the cancer virus present, the ovaries jsvere transplanted into the
spleen. Normally the liver destroys all the ovarian hormone, and so in this experiment
all the ovarian hormone, instead of going into the general circulation, will go through
the liver and thereupon be destroyed. Consequently, the pituitary ovarian physiology
will be changed thus: the pituitary hormone will stimulate the ovary to function but
no ovarian hormone will get to the pituitary to depress its activity. Theoretically this
should develop an ovarian malignancy, and that is what happened. When this experiment was done on cancer-resistant animals, no cancer developed; instead, only cystic
disease of the ovary(l).
This experiment was repeated by leaving one ovary in normal position and transplanting the other into the spleen. The pituitary ovarian physiology was not disturbed,
here, and the transplanted ovary merely atrophied.
Page 39 In work done by me on virus studies in cancer tissues, and not yet published,
it was noticeable that the concentration of virus present in malignant tissues was in
direct proportion to the degree of malignancy (6,7,8). A case of cancer of the breast,
grade IV., was treated with testosterone, and after one month became grade III.; after
another month it became grade II. The concentration of virus in the grade IV. cancer
was high, in grade III. it was diminished, and in grade II. was markedly diminished.
This shows that the same pituitary hormone which stimulates the malignant cell to
grow stimulates the virus to grow also.
As a result of this observation pituitary hormone (especially prepared) was used
on the agar when culturing cancer virus, and this particular technique has given the
best cultures of cancer virus.
In 1940, when Doctor Huggins first showed encouraging results in treating cancer
of the prostate with female hormone, I started treating cancer of the breast with male
hormone. The first case, which was a large inoperable cancer of the breast, is still
doing Well after 10 years.
The physiological result aimed at was the destruction of as. much estrogenic hormone as possible, as well as the depression of the pituitary hormone. It has been well
established that the liver destroys estrogenic hormone when functioning properly, but
if the level of vitamin Bx is low, the liver will fail to do this. Consequently, the case
mentioned above (a female) was given vitamin Bx. Testosterone was also given in
small quantities, just enough to keep the breast tumor regressing.
Another important teaching case was that of an elderly lady with a" large recurrent carcinoma of the breast in the glands of the axilla. She was treated with 25 mgms.
of testosterone on Monday and Wednesday. On Friday the patient complained of a
very dry mouth. This meant that we had reversed her physiology, as was noted in
the castration experiment already mentioned. In other words, we had given more male
hormone than was necessary. The dose was then cut down to 5 mgm. twice a week
for one month. At that time -the tumor had regressed to half the size but then it
began to grow. Consequently, female hormone was used in 2000 unit doses twice a
week, and one month later, the tumor had regressed to a third the size. It then started
to grow again, which showed that we had depressed the pituitary as much as necessary,
and the hormone itself that was being given was making the tumor grow. Thereupon
all treatment was stopped except that of vitamin Bx. The tumor regressed entirely
and hasn't recurred.
Some specialists have felt that in treating cancer of the breast with metastases
to bone, male hormone should be used, and for soft tissue metastases, female hormone
is the best. Actually, I do not feel that there is any difference in the use of either
hormone except for the fact that male hormone forces mineral in the bone faster
than female hormone, which in itself is a healing effect.
Another important phase of physiology is the metabolism of testosterone. If 100
normal women are all given 100 mgm. of testosterone, the next day 50% of the
testosterone will have been lost from the system; of that retained, about 25% will
have changed to female hormone and 25% will have remained as male hormone. But,
if one will check those who are extremely masculine, he will find that very little has
been changed to female hormone; whereas, of those who are excessively feminine, all
will have changed to female hormone. Frequently, girls in this latter group will menstruate following a large dose of male hormone.
For the more excess hormone in the system, the more will be metabolized to
the other hormone. In other words, the more that physiological doses of the hormone,
or only slightly in excess, are used in treating patients, the less will be the change
complications arising from the change to the opposite hormone.
Another important fact in steroid metablism is that adrenocorticosterone, which
is the adrenal hormone that controls salt metabolism, cannot be changed easily to
female hormone, and yet this hormone will depress the pituitary in a manner very
similar to that of the sex hormones.
Page 40 In a case of carcinoma of the ovary, which filled the entire abdomen and which
had been treated with both male and female hormone, adrenocorticosterone in 5 mgm.
doses was given daily for 3 months; at the end of that time the abdominal tumor had
entirely disappeared. With this type of therapy the blood pressure must be checked
To understand the physiology of the male sex hormone it is worthwhile to review
the subject of underdevelopment in children and the results of treatment. If a boy
with undescended testicles is given pituitary hormone the testicles may develop slightly,
and if Antuitrin "S" is added an increase in stimulation, of about six times, is obtained.
This is still hardly enough to notice, but if testosterone is given, the testicles will
descend with great rapidity and enlarge rapidly the same as the penis and prostate.
This shows that the testosterone acts as a much stronger growth stimulant to the
prostate than does the pituitary.
Consequently, when cancer of the prostate develops it is probably true that the
testicular function has decreased and that of the pituitary has increased, which in turn
increased the adrenal activity causing it to form more testosterone. However, it may
also be that the testicles have increased their activity, or the patient is taking testosterone, or the liver has lost the power to destroy the hormone.
In treating these cases the condition of the liver should be improved with diet
and vitamins. Male hormone should also be eliminated from the patient's treatment,
if he is taking it. Now, to balance the endocrine system, the patient may bte castrated,
and if the testicles were making considerable hormone, a noticeable improvement may
be noticed for a few months. The cancer will most likely recur, because with the
sudden elimination of male hormone from the testicles, the pituitary will increase its
function and stimulate the adrenals to make more testosterone, which in turn, will,
with the pituitary hormone, stimulate the prostate to grow again.
To prevent this secondary problem of the increased pituitary activity, stilbesterol
can be given and this will keep the pituitary from increasing its activity.
A sugar tolejrance test is frequently of value in checking for an increase in
pituitary activity. This test can be repeated every two months to see that progress
is being made in the hormonal balance. The best results are obtained if the sugar tolerance curve can be kept below the normal curve.
Another important point in the treatment is to protect the adrenals against a
tendency to overfunction. This is done by stopping all foods with cholesterol .or
high protein as well as meat or salt. The use of vitamin C and fruit in the diet should
also be increased. This sounds simple, but now another problem, mentioned in the
experiments, arises.
In 20% of the cases given stilbesterol, pituitary tumors develop. This is almost
impossible to cope with, for this gland will continue to over-function whether more
or less stilbesterol is given. The best way to prevent the occurrence of this tuanor
is to give small amounts of stilbesterol.
In 1940, treatment of a far-advanced cancer of the prostate, with metastases to
the pelvis, spine, lung and liver was started on this programme. The patient, a man, was
castrated and given 1 mgm. of stilbesterol daily for one year. At the end of that time
there was no evidence of the disease present and treatment was stopped. Thrtee years
later the cancer recurred and treatment was started and continued for three more
months. By that time, there was no evidence of disease and it has never recurred. At
the present time, 10 years after starting treatment, he is in excellent health. He is
85 years old, weighs 200 pounds, and one would judge him to be only about 65 years
of age.
When one examines the statistics pertaining to cancer of the prostate in any
clinic one fact stands out. Although different treatment may be employed, primarily
in the amount of stilbesterol given (from 1 to 300 mgms. daily, for life), the statistics
will differ but little from clinic to clinic. Each will show: 10% of the resuls are good,
Page 41 15% are fair and the rest of the results are poor. This is significant, for if everyone
treated diabetes in this same way, the statistics would likewise be the same.
The reason that we have a satisfactory program for diabetes is because Doctor
Best, and all those that followed him, insisted on carefully regulated doses of insulin.
In controlling any endocrine disease, the secret of success is not so much in the
hormone used, as it is both in the amount used as well as the degree of balance maintained hi the endocrine system, plus the normalization of abnormal physiology. This
is essential both in preventing most organic disease as well as in treating any organic
The question arises, in cases of pernicious anemia, with cancer of the stomach,
as to whether the cancer might not be stimulated to develop by the use of excess liver
extract in treatment. Most pernicious anemia patients, after the anemia is cleared up,
are kept on the same amount of liver extract used in the process of the cure.
Cancer of the stomach in pernicious anemia patients, with treatment, is higher
than in any other group. Of course, the fact that they live longer than th®se not
treated is a factor, but apparently not the only one.
The primary function of cortisone is to stop allergy. Acute leukemia patients
are more allergic to the virus than chronic leukemia patients. Therefore, cortisone
should be more effective in treating acute leukemia than chronic leukemia. Cortisone
also increases a person's resistance to infection in general, probably in the same way,
and therefore would be an extra help in treating acute leukemia where every little
infection overcomes the patint.
Theoretically, eosinophilic granuloma should respond to cortisone.
After all of the above statements, one might wonder whether hormone therapy
is safe in normal people. It is not only safe but also very important in preventing cancer.
If cancer of the. breast, for instance, was due to an excess of female hormone, it
would not occur at the times actually observed in life. The body has the greatest
amount of estrogenic hormone in the system during the years from 18 to 25 as well
as during pregnancy, and yet, at those times cancer of the breast is at its lowest tendency.
Cancer occurs most commonly when the female hormone level goes low.
When the female hormone level goes low the pituitary increases. If the level
goes low rapidly, many symptoms of the change of life occur. This should be treated
with small amounts of female hormone to prevent these symptoms, and in so doing,
cancer of the breast will be prevented also.
Cancer of the cervix is similar. Here, is found an atrophic cervicitis which tries
to heal itself, and before long, the cells are growing at such a rate that a cancer can
With normal hormonal treatment the atrophic cervicitis might have been prevented
and even cured, once it developed.
1. Biskind, M. S. and Biskind, G. R. Development of Tumors in the Rat Ovary after Transplantation
into the Spleen. Proc. Soc. Exper. Biol, and Med., 55:176-179.  1944.
2. Bittner,  J.  J.   Further  Studies  on Active Milk  in  Breast  Cancer  Production  in  Mice.   Proc.  Sod.
Exper. Biol, and Med. 45:805.
3. Bittner, J. J. Breast Cancer in Mice as Influenced by Nursing. Jour. Nat'l. Cancer Inst. 1:155.  1940.
4. Bittner, J. J. Mammary Cancer in Fostered and Unfostered C^H Breeding Females and Their Hybrids.
Cancer Research 2:170.   1942.
5. Gardner, W. U. Steroid Hormones. Presented in a paper to the A.A.A.S. Gibson Island Conference.
Cancer Conference Program.  1946.
6. Gregory, John E.  Electron Microscopic Findings in Malignant Tissue, Exp.  Med.  and Surg.  6:390-
405. 1948.
7. Gregory, John E. A Review of Cancer Research. Exp. Med.  and Surg.  7:289-298.   1949.
8. Gregory,   John   E,   Virus   as   a  Cause  of   Human   and   Animal   Malignancies.   Southern   Med.   Jour.
43:124-128.  Feb.   1950.
9. Heiman, J. The Effect of Progesterone and Testosterone Proprionate on the Incidence of Mammary
Cancer in Mice.   Cancer Research, 5:426-430.   1945.
Page 42 10.   Woolley, G. W. and Little, C. C. The Incidence of Adrenal Cortical Carcinoma in Gonadectomized
Female Mice of the Extreme Dilation Strain.  Cancer  Research   5:321-327.   1945.
11   Woolley, G. W. and Little, C. C. The Incidence of Adrenal Cortical Carcinoma in Male Mice of
the Extreme Dilation Strain Over Ohe Year of Age. Cancer Research, 5:506-509.   1945.
12.   Woolley, G. W. and Little, C. C. The Incidence of Adrenal Cortical Carcinoma in Gonadectamized
Male Mice of the Extreme Dilation  Series. Cancer Research  5:211-219.   1945.
By Dr. Maurice Young
1. Rheumatic fever is a systemic and not primarily a cardiac disease.
2. One third of the cases are not diagnosed at first examination.
3. The severity of an attack of rheumatic fever bears no relation to the cardiac
4. Various murmurs may occur in the course of the disease and these must be
differentiated for accurate diagnosis.
a. A systolic murmur may indicate:
i. Functional origin: soft, musical or groaning, inconstant and variable,
usually over the base or medial to the apex. It is unaccompanied by
other signs of heart disease.
ii. Mitral Incompetence: soft and blowing at the apex, conducted toward
the axilla and accentuated by exercise. Accentuated pulmonary second
sound denoting pulmonary congestion. One school maintains that
presence of  this lesion is presumptive of mitral  stenosis.
iii. Aortic Stenosis: harsh and rasping over the aortic area conducted into
the neck and arms and accompanied by a thrill. Low blood pressure
and diminished aortic second sound.
Aids in the diagnosis are the pulse rate, particularly during sleep, the character
of the heart sounds, and the presence of gallop rhythm.
b. A presystolic murmur: harsh and rumbling and leading up to a loud first
sound at the apex, or a mid-diastolic murmur indicates mitral stenosis,
the characteristic signs may take months or even years to develop.
c. A diastolic murmur: soft and blowing over the aortic area and conducted
down the sternum. Often missed without a diaphragm. Indicates aortic
incompetence. Accompanied by collapsing pulse, visible pulsation in the
neck and nail-beds, and a low diastolic pressure.
5. Laboratory Aids: a. A raised sedimentation rate is an indication of rheumatic
activity but is of no help in the diagnosis of cardiac disease; a persistently
high sedimentation rate calls for caution in management.
b. Prolongation of the P-R interval in the electrocardiogram is frequent in
rheumatic carditis, but may occur both in the active and the chronic stages.
c. Fluoroscopy provides confirmation of the clinical findings and by means
of a barium swallow the left auricular enlargement of mitral stenosis may
be visualized in the RAO view.
6. Pericarditis: is characterized by pain over the praecordium and a friction rub
synchronous with the heart beat. Effusion may develop later. Prognosis serious.
7. Management of Rheumatic  Carditis  resolves itself  into:
i. Treatment of the acute attack of rheumatic fever,
ii. Treatment of cardiac failure.
Page 43 iii. Management of convalescence.
iv. Subsequent management and prevention of recurrences.
8. Treatment of the Acute Attacks:
i. Absolute rest in bed.
ii. Salicylates: gr.  1 per lb. per day; reduce by 10% after 2-3  days and at
1-2 week intervals.
Sodium bicarbonate in similar dosage with salicylates at first and then in
half the salicylate dosage if signs of salicylate intolerance,
iii. Pyramidon: for use in acute fulminating cases or where differential diagnosis
from appendicitis or acute abdomen.
Six times the potency of aspirin;
Patient should always be in hospital;
Never use more than 1 gram total dose per day.
9. Treatment of Cardiac Failure:
i. Sedation:  Luminal given regularly.
Morphine in a dose of mgm. per  10 lbs. body weight for pain or acute
failure; change to codeine when acute phase is diminishing.
Paraldehyde 3 ii - iv per rectum in oil p.r.n.
Syrup of chloral x/z-\ dr. p.r.n.
ii. Oxygen: preferably in a tent.
iii. Diuretics when oedema and large liver are present.
Theocalcin 1-2 tablets  (0.5-1.0 gram)  4 times daily.
Mercurial diuretics (mercupurin, salyrgan etc.)   x/z c.c. initially and 1 c.c.
-. weekly, diluted and given slowly by intravenous route,
iv. Digitalis: indicated in stage of chronic passive congestion.
May be dangerous in active stage.
Dose for 40-100 lb. child is 0.1 gram per 10 lbs. divided into equal doses
over 24-48 hours; maintenance dose of 0.1 gram b.i.d. or even t.i.d.
Dose for standard trade products according to digitalis leaf equivalent of
preparation. bg|
10. Management of Convalescence: Salicylate dosage should be steadily decreased
by 10-20 grains each fortnight till down to 15 grains daily. Thereafter salicylates are stopped provided no symptoms. Patient allowed up only when
sedimentation rate is normal both two weeks and one month after cessation
of salicylates. Allow up %-% hour daily increasing by % hour each week
provided no recurrence, till up 8 hours daily. May return to school after this
for l/z day for 1-4 months, then full day. v
But every patient should be treated individually.
If cardiac involvement, competitive sports inadvisable.
11. Subsequent Management: ||j^|
a. Avoidance of colds and sore throat, etc., whenever possible.
b. Prophylactic sulfa:
0.75 Gm. daily for child of 85-125 lbs.
0.5 Gm. daily for child of 35-85 lbs.
0.25 Gm. daily for child of under 3 5 lbs.
c. Prophylactic sulfa in a dosage of 2-3 grams daily or penicillin for 2 days
before and three days following any minor operation such as dental extraction or tonsilectomy.
d. "Routine" tonsillectomy of little value.
e. Continue maintenance dose of digitalis in patients with chronic passive
f. Regular follow-up every 3-12 months.
Address by DR. HOWARD LEWIS,
Dean of University of Oregon Medical School, Portland, Ore.
Delivered to the Summer School of the Vancouver Medical Association
in Vancouver, B.C., May 30th, 1950.
My subject this morning is one that I have been particularly interested in for a
long time and I think, at the same time, is a subject that is not too well understood
by many practitioners of medicine for several reasons. One is that not very much is
written about it; and second, not enough cases come into the experience of the individual
practitioner to enable him to form conclusions on his own account.
But tuberculous pleural effusion is a lesion every bit as important as a parenchymal
lesion. All of us have a very proper respect for a pulmonary infiltrate due to tuberculosis, and we all have very definite and proper ideas of what to do about such things.
But, on the other hand, when it comes to dealing with an effusion, because of the fact
that there is not, in many cases, a visible pulmonary infiltrate at that time, we are apt
to believe that the lesion is not serious, does not carry a poor prognosis, and therefore
can be a lesion that can be dealt with relatively lightly. But I can tell you this, that a
tuberculous effusion carries with it exactly the same prognostic probabilities and possibilities as does a small pulmonary infiltrate, and, as a matter of fact, requires and
demands exactly the same kind of treatment, as far as convalescent care as does a
pulmonary infiltrate.
The statistics show very clearly the relatively high incidence of active pulmonary
tuberculosis following a tuberculous effusion, particularly in those individuals who have
not been properly cared for following the effusion.
Now there are a number of causes of pleural effusion, all of them well known
to all of us. We are all familiar with the effusions that follow pneumonia, but I think
we make a mistake in one direction, of attributing too many effusions to pneumonia,
particularly massive effusions. Large pleural effusions are unusual with any kind of
pneumonia, with the possible exception of an occasional case of virus pneumonia, but
small or moderately large effusions can follow pneumococcus or other bacterial types of
pneumonia, or, as I said, virus pneumonia. The diagnosis of pneumonia as a case is
relatively easy. There is this to remember, however, that some cases of pulmonary
tuberculosis already have a well-established pulmonary infiltrate which has all the
characteristics from a radiological standpoint, and many times from a clinical standpoint,
of the infiltrate seen in virus pneumonia, and it has been my experience that more
mistakes have been made in the direction of calling a tuberculous effusion with a
pulmonary infiltrate——calling it a virus pneumonia—than any other mistake that I have
been able to notice. The effusions that occur with heart failure, or with an acute
glomerulo-nephritis or nephrosis, or in any of the other hyper-albuminemic states are
relatively easy to recognize and the fact that they are a transudate very clearly establishes
their etiology. We do not have such an easy time with the effusions with carcinoma.
Carcinoma of the lung, as you know, may begin peripherally. Its initial manifestations
may be those of a pleural effusion. If the effusion is bloody that is a big help to us
because most bloody effusions are due to malignant change in the pleura; but where
the effusion is a simple exudate that is not bloody and where the carcinomatous process
is not readily visible, being masked by the fluid, it is sometimes very difficult to tell
the difference between the two. However, there is this to say, that carcinoma is,
as you may know, more frequently present in the older age groups, but we do see carcinoma of the lung with increasing frequency now in younger people, so that we cannot
entirely depend upon the age factors. We must remember, too, that the peripheral types
of carcimona are very frequently unaccompanied by cough. Of course, they do not
produce main-stem bronchial occlusion, they do not cauuse atalectasis and therefore
they may be relatively difficult sometimes to decide upon.  Injuries to the lung, particu-
Page 45 larly to the chest wall, are frequently followed by small effusions and these are readily
recognized; the same may be said of certain types of fundamental diseases of the ribs,
such as sarcomas and so forth, but here again these do not give us much difficulty.
Tuberculous pleural effusion is probably the cause of the great majority of the
so-called idiopathic effusions, that is, those that appear without discernible cause,
and, when we see the patient and examine him we find no evidence of heart failure or
tumour or of the other causes that I have already mentioned.
Now how is a tuberculous pleural effusion caused? There are a number of ways in
which they can be produced, but our knowledge about this is still not entirely complete.
One thing we know quite surely is that probably the most common cause is a sub-pleural
tubercle. Very frequently this is a part of the primary complex, the initial infection;
a tubercle forms directly beneath the pleura or at some distance, or may even form in a
lymphatic gland around the heart or the lung, and then by lymphatic extension the
tubercle bacilli are brought to the pleural surface, and the reaction of the pleura to this
invasion is somewhat in the form of an allergic or a sensitivity type of reaction in the
person who is already tuberculin positive; in the person who is not tuberculin positive
it is more likely collateral oedema we see around a deep-seated infection.   In other
words, the effusion represents more, you might say, an oedematous reaction of the pleura
to an adjacent inflammation, but in this situation actual live tubercle bacilli do not get
into the fluid as far as we know, or, if they do, they get into the fluid in very small
amounts.    Autopsy  examination will  frequently show  no definite evidence of  true
tuberculosis of the pleura itself, but we see only a pleuritis overlying an underlying
disease of the lung.  This, of course, explains so many cases of pleural effusion in which
we are totally unable to demonstrate tubercle bacilli.   Another method by which this
condition can be produced is by tuberculosis of the underlying lung with direct extension
to the pleura in the formation of a true tuberculous pleuritis.  This condition frequently
gives rise to effusions that are positive for tubercle bacilli. This condition can also lead
to tuberculous empyema.   The reason this does not occur more frequently is probably due to the fact that whenever there is an active caseous tuberculosis underneath
the surface of the lung, that is caseous tuberculosis of an adult type generally, the
fibrous reaction of the pleura is so strong that adherence of the two pleural membranes
takes place, and this pleural synthesis prevents the accumulation of fluid, so that it is
somewhat fortuitous that certain cases do have tuberculosis of the pleura and a pleural
effusion at the same time.    Now another route by which infection can take place is by
the hematogenous route, a direct spread by the circulation. This is probably the less
common route by which this condition is caused, but nevertheless, it forms a considerable
proportion, or a considerable number of the cases we encounter.   Here we see multiple
tubercles of the pleura and we can see them either by thoracoscopy or an autopsy
examination as little tuberculous nodules here and there on the pleura.   This condition
is very frequently bilateral—we may see effusions appear on both sides, as I have seen in
a number of instances, and occasionally we see simultaneous occurrence of tuberculous
pericarditis, and sometimes tuberculous peritonitis al^, appearing with an explosive type
of onset which indicates that dissemination could only have taken place probably by
way of circulation.
Now the diagnosis of this condition, the manner of onset, must be considered.
Tuberculous pleural effusion can come on in a number of ways, probably one of the
most common ways is for it to appear out of a clear sky. Many times the onset has
been preceded by a little period of ill-health, f atigueability and perhaps loss of appetite,
or decrease in appetite and a fall in weight. But otherwise there are no respiratory
symptoms and the first thing that calls the trouble to the patient's attention may be
very mild pain in the chest and then the distress from the compression of the pleural
exudate; when the patient presents himself for examination you find by that time a
well-established pleural effusion. How very frequently these individuals do not present
very serious elevations of temperature, they do not appear under-nourished, they may
not appear particularly ill, except illness from the effects of an actual compression of the
Page 46 lung or distortion of the cardiac structures. Another relatively common onset is rather an
acute one, in which the patient develops malaise, fever of moderate degree, pain in the
chest of the typical pleural type, and then within a very few days the effusion is well
established and rapidly progresses. This is the most easily recognized type because the
patient's own systemic manifestations bring him to the doctor early enough for the condition to be noted. The third type that I have seen more than once—a very puzzling
type at onset—is one in which one seriously suspects a hematogenous cause behind the
whole clinical picture. In this one the patient develops a violent and acute illness, very
frequently ushered in by chills; he develops a high fever which may go up to 104 or 105;
he remains extremely ill sometimes for many days, without there being any answerable
cause for Ms illness. He does not exhibit any significant changes in his white blood cell
count. Usually his sedimentation rate is elevated, but there is nothing else to find. He
is just a sick person with a fever. I have seen them run this type of high fever for as
long as two weeks before any evidence of any trouble appears. Then, out of a clear sky,
in the midst of this fever comes acute chest pain and in very rapidly oncoming pleural
effusion. Now in this type of person, who more frequently has bilateral pleural effusions
—I think in these people, it has been my assumption, my belief, that we are dealing probably with a hematogenous dissemination of the organisms and that the hematogenous
phase accounts for this acute rather septicemic typhoid type. Of course that we see initially.   This can be most puzzling for long periods of time.
Now there is no need to detail to you the signs of pleural effusions because they are
well known to you all. It is well to keep this in mind, that from statistical studies by and
large, tuberculous effusions tend to be relatively large effusions. Very small pleural
effusions are less often tuberculous, as we would gauge from the incidence of active pulmonary disease later on. Dry pleurisy has about the same connotation as does the small
pleural exudate; that is, probably the smallest percentage of the dry pleurisies do indeed
represent tuberculous infection, but I think there is this to say, that we always rriust
remember, and that is, that any pleural effusion or any case of dry pleurisy, without
another demonstrable cause such as pneumonia and so forth, must always be regarded
with suspicion, and no patient who has such a disorder should be lost from our sight
until a period of five years are past, when he can be reasonably safe; but in any person
who has an idiopathic large effusion, the odds are preponderantly in favour of its being
tuberculous in origin and, as a matter of fact, we can say, rather dogmatically, I think,
that any large idiopathic effusion is tuberculous till you can furnish incontrovertible
proof to the contrary.
Now what does the laboratory do to help this? The laboratory can give us a
great deaLof aid. In the first place, one of the first things we have to find out is
whether or not we are dealing with an exudate or a transudate. All tuberculous
effusions, as of course you know, are exudates with a specific gravity above 1015, with
a large content of protein in them. Some men have done studies, and we have done
some too, that indicate there is a sharp fall in the total sugar content of the effusion.
That is, if one measures the sugar content as a quantitative estimation in the fluid,
the total pleural fluid sugar will be at a very low level in the tuberculosis type of
effusion. We also see, always and invariably, an increase in the cell count in the fluid.
Now this cell count is usually preponderantly lymphocytic but there is this to remember,
that early in this game, particularly during the first one or two weeks, I have seen
more than one case in which the cells were preponderantly polymorpholeukoctyes; I
have seen them where polymorpholeukocytes were 90 per cent or more of the total
cells of the fluid. Naturally, seeing such a cell count one would immediately be suspicious
that he was dealing with an ordinary pyogenic type of empyema in its incipiency, but
I have seen this cell count reverse itself within a week from a high "poly" count over
into an exactly opposite high lymphocyte count, so that all things being equal, the mere
presence of a temporary high "poly" count by no means rules out this condition.
Now next we do smears and cultures which we do on 'all fluids and wherever
Page 47 suspicious we look for malignant cells. Now here is where we make our greatest error
in that we use too small an amount of fluid as a general rule. As you know, the incidence of positive examinations of pleural fluid for tubercle bacilli run at a very low
level. Probably the best statistics indicate that 50 per cent of the tuberculous effusions
will be positive. That is not unexpected in view of the nature of the causation of this
condition. But in many instances the incidence of positives is at a very very low point,
and I think due to the fact that many times we do not use proper technique. No less
than 300 c.c. should be taken for examination. That 300 c.c. of fluid should be
examined grossly and microscopically in its own right, and then the whole batch should
be centrifugated down and then the centrifugate from the whole 300 c.c. should be
used for direct smear examination, should be used for guinea pig inoculation, and should
be used for culture. Now we cannot consider our examination of this fluid complete
without that procedure, and that procedure invariably must include wherever possible
guinea pig inoculation, culture and smear. I have seen more than one case in which
the guinea pig inoculation is positive, the culture and the smear negative. I have
seen others in which the culture was positive, the guinea pig inoculation negative and
the smear negative. I have seen others in which the culture was positive the guinea
pig inoculation negative and the smear negative. I have seen them where the inoculation
of the guinea pig and the culture are negative and the smear is positive. So that only
by using a combination of all three can we bring the percentage of our hits up to a level
closely approaching what we could ideally expect. Under these procedures you will find
that the degree of positive hits runs up between 3 5 and 5 0 per cent. But always take a
large amount, 300 c.c. of fluid centrifugated and study the centrifugate bacterio-
logically.   That also applies to bacteriological study for other organisms as well.
Now another thing; we must study the sputum and we must study the gastric
washings. I know for a long time I had believed that there was little point, in the
average idiopathic pleural effusion case in studying the sputum, because these people
have very little sputum, so frequently had little pulmonary infiltrate, and therefore
could hardly be expected to have much in the sputum. Certainly my own experience
has shown me this, that more than one case in whom you totally unsuspect, or in whom
you are totally unsuspecting of an active parenchymal disease, will have a positive
sputum or will have positive gastric washings, and I have seen this demonstrated often
enough to convince me of the great usefulness of the co-existent careful examination of
the sputum and of the gastric washings. I remember so well one patient whom we'
had about decided did not have a pleural effusion due to tuberculosis, we did the routine
gastric washings and the sputum studies, and to our great amazement, in spite of the
fact after the fluid had been removed there was still no pulmonary infiltration, this
patient still had a positive sputum. Subsequent bronchoscopic examination revealed in
unsuspected tuberculous bronchitis which apparently was the nidus for the occurrence
of the effusion.
Now here again, techniques can improve or can increase the number of positive
reactions. It has been our policy to examine not less than three sputums, and many
more when the occasion indicates, and not less than three gastric washings, or more if
necessary. We examine each one in turn separately by concentration methods; then
we take three days' sputum or three days' gastric washings and combine them and pool
them; we then concentrate those and pool three days' accumulation, concentrated and
certifugated and take the pooled accumulation, and it is from these pooled sputum or
pooled gastric washings that I have seen the greatest number of positives. The single
specimen examinations have a far poorer average than does the pool group of specimens.
So I would certainly commend that to you wherever you have this problem before you,
and I am sure that you will find'—if you do not do this already—that it will greatly
enhance the diagnostic accuracy of these cases.
I think the sedimentation rate is a lot of help. Not every case of tuberculous
pleural effusion has an increased sedimentation rate, but practically every one does.   In
Page 48 my experience, I have seen two whose sedimentation rate remained within normal limits.
The reason I know they were tuberculous is that we recovered the organism so that
there could be little doubt; but they must be counted as being definitely unusual.
The sedimentation rate usually rises to considerable heights, and, as a matter of fact, it
has been my observation that the heights it reaches are quite disproportionate to any
parenchymal disease we see, but that is not illogical in view of the large pleural surface
that is involved in the infection. The same thing can be said of the tuberculin reaction.
All tuberculous pleurisies sooner or later will have positive tuberculin reactions, with,
again as usual in medicine, the few exceptions, and I have again seen several exceptions
to this rule; persons with proven tuberculous effusion from whom the tubercle bacilli
were recovered, grown, cultured, demonstrated in guinea pigs, and at home the tuberculin test remained consistently negative. Now the tuberculin test remained negative
far beyond the time necessary for the tuberculin allergy to develop. This negativity of
the tuberculin reaction was not the result of an overwhelming type of tuberculous
disease because these patients recovered and were not critically ill at any time, so that
occasionally tuberculin reaction, helpful as it is, fails us and we should not let a negative
tuberculin test necessarily overthrow our clinical judgment if the signs are pretty clear
Now what should we do about treatment? In the first place these patients demand
bed rest, they demand sanitarium care, they demand the same kind of care you would
give anyone with active tuberculosis of the lung. The question of what to do with the
fluid has been a point of great contention. We usually find many many opinions about
this. One of my old Chiefs in the Army, who was a great tuberculosis'man for many
many years, was horrified at the thought of removing fluid for anything else but
pressure. I know of other people equally eminent who feel exactly the opposite way
—you can read literature and get a^l sorts of opinions on the subject, but I have formed
definite opinions of my own, based on my own experience and study of these cases, and
I think the indications are relatively clear as far as I am concerned. I don't think we
should do anything about the fluid at the acute stage of the disease, except to take
fluid away to the point necessary to relieve distressing compression symptoms; that is,
those persons who have a marked mediastinal shift, dypnea, cyanosis, interference
with the cardiac filling and so forth need to be relieved of that—700 c.c. or 1000 c.c.
of fluid in the average case will ordinarily do the trick. Sometimes repetitious taps
' may be necessary in order to give them comfort, but we ordinarily, outside of the fluid
we take for diagnosis or relief of compression, leave the fluid strictly alone during the
acute stage. It has been found—we have found that removing the fluid too early in
the game—except for the certain reasons I have mentioned—often seems to causd
somewhat of an exacerbation of the disease, but that may be only a fallacious opinion.
If, after four weeks the fluid and the patient's temperature has gone to normal, and
he is obviously in the convalescent phase of the condition, that is, the fluid is not
accumulating, it has reached a static level, if, after four weeks—some men say sixi
weeks, I believe better four weeks—'there is no sign of absorption of the fluid, then
I think it should be removed. Now the reasons I think it should be removed are these:
All old tuberculous exudates accumulate protein in them, accumulate fibrin in them,
and you will begin to see fibrin precipitation in the average effusion at the end of about
three weeks, this fibrin precipitates in larger and larger amounts and quite soon will
establish a real interlacing fibrinous web throughout the effusion. So that after that
time, if you try to evacuate it you find that you are up against a loculated effusion
that you can do nothing about—loculated effusions resolve very slowly, often result in
great pleural scarring, and lead to prolonged disability. Another thing that I have seen
happen is for the fluid to coagulate spontaneously. I remember so well one case, the
first one that really called this to my attention; the patient had some fluid removed
for diagnosis one day, the fluid was perfectly fluid, came out easily, it coagulated spontaneously a few minutes after it was put in the test tube. The next day attempts to
withdraw the fluid from that chest were completely without success, in spite of the
Page 49 fact that the X-ray showed what apparently was a large effusion extending clear from
the apex to the base. Multiple punctures throughout the chest failed to get a single c.c.
of fluid. That coagulum stayed in that patient's chest for many, many, many months,
and we have since been able to get follow-up studies of some of these patients who have
had such coagulums to prove in fact that they are fibrinous coagulums, and furthermore
prove that tubercle can be cultured from these coagulums, and furthermore that tuberculosis of the pleura has been demonstrated in cases with such coagulums. If you have
an opportunity to see the disability, the deformity of the chest, the tremendous chronicity
of the convalescent period that complicates such coagulations of this exudate, I think
you would have a wholesome regard for removal of fluid, particularly any fluid that
shows a tendency to want to coagulate spontaneously. I believe that all fluids that want
to coagulate spontaneously should be removed promptly, other conditions permitting.
Now, if you remove fluid, how much should you take off? I believe you should
take it all off. You may have to take it off in stages, that is, if the effusion is very
large. We ordinarily do not like to take off over 1000 to 1500 c.c.'s at a single sitting,
but the fluid can be taken off, and the pleural space should be kept dry, because here
again, the longer the fluid accumulates, the greater will be the fibrinous coagulum,
and the greater will be the fibrosis of the pleura, and therefore there will be the greater
restriction of pulmonary ventilation that will eventually result.
Now with the patient who has no obvious pumonary infiltrate at the time you
remove the fluid one can go ahead and take out the fluid and let the two pleural surfaces
unite. Where there is a doubtful area in the lung field one had best then establish a
hydropneumo-thorax, a small one, so that you can keep the pleural surfaces apart until
you have a chance to observe this further. It may be that the pulmonary infiltrate is
so well established that a therapeutic pneumo-thorax may well be established at that
time. You run a little risk—I don't think it is great—of some thickening of the pleura
which may make subsequent expansion of the lung difficult, but I do not think this is
materially greater than that encountered in ordinary pneumo-thorax therapy.
Now how long should we keep these patients down? It goes without saying that
the usual care for a tuberculous person, bed rest, good nutrition and so forth, go along
in the treatment of this condition. I think these patients should be kept in bed a
minimum of three months. If they have had a particularly stormy course, better six
months, but we know that in any minimal pulmonary infiltrate which we believe is
tuberculous we ordinarily believe a bed rest period of the shortest length of time is
three months. During this time we should demand that the patient has no fever, that
his sedimentation rate returns to normal, that he feels well and that he gains weight.
If none of these qualifications are fulfilled, or only part of them fulfilled, there is still
a strong probability that the disease is still active and further bed rest is definitely
indicated. Should he progress favourably—and many of them do—as a matter of fact,
the majority of them do—then his return to activity should be begun very gradually.
At that time his temperature must be followed carefully, his sedimentation rate must be
followed carefully, and we must have frequent serial X-ray films made of his chest.
Should his sedimentation rate start up again, should he start again to have a little fever,
or should he begin to show fatigueability, back to bed he should go. I have seen too
many patients in whom just one of these things would indicate the trouble they have
had, but letting them go ahead resulted in a relapse, either with a pulmonary infiltration,
or with a new massive effusion. On the opposite side, I can remember two patients
particularly who made a spectacular recovery, whose effusions resolved beautifully
without removal, who gained weight, whose sedimentation rates came to normal; we let
them out, they felt well, they were well-nourished. Their sedimentation rate rose a
little, the rise was not too much and we were inclined to scout the rise in both of them
and to consider it not significant. But, in both instances, within a few weeks, out came
a new effusion on the opposite side. So that we have to take these people just as seriously
as we do any parenchymal disease if we are to prevent complications of active parenchymal tuberculosis that will appear later on.
Page 50 Now the figures in that regard vary a great deal from place to place. They are
given variously from 15% up to the most optimistic ones of 85% of all patients with
tuberculosis. I think the truth lies closer to around 25% or 30% of the patients who
have tuberculous pleural effusion can be expected to have active parenchymal tuberculosis within five years unless they have had adequate sanitarial type of care and follow-
up during and after the effusion. I think that every person who has had a tuberculous
effusion, or every person in whom you suspect such a thing as having been present, that
you should keep them under your finger for a minimum of five years. They should have
serial X-ray films every two months during the first year, serial X-ray films every three
months during the second year, and serial films every six months during the remaining
years of their five-year period. Statistically, after the five-year period has passed the
incidence of active parenchymal disease drops down to a very much lower level than
it does during the first five years, so that getting by this period gives them some
reasonable degree of safety.
But I do want, in closing, just to again impress you with the fact that, certainly
from my own personal experience in tuberculous pleural effusion, the so-called idiopathic
pleural effusion—you may not be able to demonstrate tubercle bacilli—is a serious
condition which carries a prognosis of active pulmonary tuberculosis of 25 to 30 per
cent, it is something that can't be treated lightly, must be given the most careful type of
sanitarial care and must be subjected to long periods of follow-up.
Obiit  (November 5th)
Another of the older generation of medical men passed away recently in
the person of Dr. H. L. Turnbull. He had practised in Vancouver for some
thirty-five years, and was in practice almost till the day of his death.
Dr. Turnbull was a quiet, rather shy man, who went his way and did
his work without fuss or ostentation. As a physician, he was able and competent, and had a large practice. He had many other interests in life, and took
part in various community activities.
In his early days he was M.H.O. of South Vancouver, a post he filled,
if we remember rightly, until its amalgamation with the City of Vancouver.
To his family we extend our condolences, in their loss.
The death occurred in Toronto on October 24th of Dr. Howard Coulthard,
age 70.
Born in Picton, Ontario, he "graduated in medicine from the University
of Toronto in 1905. In 1907 he was appointed ship's surgeon on the S.S. Empress
of Japan between Vancouver and Hong Kong.
At the outbreak of World War I, he left his Vancouver practice and
served with the R.C.A.M.C. and later transferred to the Imperial Army.
Following war service, Dr. Coulthard engaged in private practise in London,
England, and on retirement in 1944 spent some time in Vancouver before
moving to Toronto where he died.
M.D., F.R.C.S.(Can)., F.A.C.S., O.B.E.
Obiit   (November 1st)
The passing of Dr. A. B. Schinbein of Vancouver marks the loss of one
of our finest surgeons, and of a man who served selflessly and well, not only
as a physician, but as a citizen. He had the habit of complete devotion to the
task he had in hand.
His primary work in life was, of course, surgery—and for nearly forty
years he practised this art with distinction—rising steadily in the esteem of
his colleagues and of the community, to a level where his opinion was regarded
as among the best and highest obtainable. He reached this eminence through
sheer hard work. He was a glutton for work, and scrupulously meticulous in
his methods. He took nobody's word as final—but investigated each of his
cases himself, thoroughly and carefully: then reached his own decision.
Schinbein regarded his patients as his friends, and gave to their service
a devotion and interest which never failed. Their troubles were his—and he
really suffered with them, which is the true meaning of the word "sympathy."
When he had a hopeless case, and faced the fact that no skill of his could
do more than merely palliate the patient's suffering, he was woebegone and
unhappy, and many of us can testify to the grief which he evidently felt over
some case he was attending, which was hopeless, and before which he was
himself helpless. This was especially true of cancer cases, of whom Jie had more
than his fair share.
Behind a blunt and abrupt manner, he was a most tender-hearted man,
and shewed many kindnesses to many people. The hold that he had on the
affection of those who came in contact with him, was shewn in the enormous
attendance at his funeral, to which came people from every walk in fife,
and was evidenced by the many tributes paid to him by the Press and by those
in high places.
He served his country in the First World War, being mentioned in dispatches for his work; he was member of the Senate of the University of
British Columbia; he was president of the Vancouver Medical Association,
and filled many other high positions. His honesty and integrity and his sincerity
of purpose, evoked confidence and respect, and made him a valued counsellor
and colleague.
,His end was the one he would himself have eagerly welcomed. His one
dread was that he might become helpless and unable to work-—and he died,
as he once said to the writer that he wanted to die, with his boots on, and
working to the last. To him, retirement and inaction would have been a fate
worse than death.
To his family, who mourn the loss of a devoted husband and father,
we extend our sincerest sympathy.
Page 52 we
(cortisone Acetate Merck)
Now Fully Available
Cortone is Manufactured in Canada
at Our Valleyfield, Quebec, Plant.
Montreal       Toronto        Valleyfield
'Registered trade-mark of Merck & Co. Limited
for its brand of cortisone.
Now available through your usual source of
medicinal supplies without restriction.
Another significant reduction in the price
of cortone* (Cortisone Acetate Merck),
effective October 16th, 1950, makes this
remarkable drug available to an even greater number of patients suffering from conditions for which cortisone therapy is
Key to a New Bra in Medical Science
(cortisone Acetate Merck)
(11 -Dehy dro-l 7-hydr oxy corticosterone-


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