History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: July, 1948 Vancouver Medical Association Jul 31, 1948

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Published By
The Vancouver Medical Association
j. h. macdermot
Editorial and Business Office
203 Medical-Dental Building
Vancouver, B. C.
Publisher and Advertising Manager
JULY, 1948
No. 10
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OFFICERS,  1948-49
Db. Gordon C. Johnston
Db. Gordon Bubke
Hon. Treasurer
Db. W. J. Doebance        Db. G. A. Davidson
Vice-President Past President
Db. Heney Scott
Hon. Secretary
Additional Members of Executive:
Db. A. S. McConkey, Db. Rocke Robeetson
De. A. M. Agnew
Db. A. C. Fbost
Auditors: Messbs. Plommeb, Whiting & Co.
Db. E. B. Tbowbbidge Chairman Db. J. A. Ganshobn Secretary
Eye, Ear, Nose and Throat
De. G. H. Fbancis Chairman Db. J. F. Minnes Secretary
De. G. O. Mathews— Chairman        . Db. A. F. Habdyment Secretary
Orthopaedic and Traumatic Surgery
Db. H. H. Boucher- Chairman Db. Bruce Reed : Secretary
Neurology and Psychiatry
Db. A. E. Davidson Chairman Dr. G. H. Gundby Secretary
Dr. Andrew Turnbull Chairman Dr. Marvin R. Diokey Secretary
Dr. J. E. Walker, Chairman; Dr. F. S. Hobbs, Dr. R. P. Kinsman,
Dr. R. A. Palmer, Dr. S. E. C. Tubvey, Dr. E. F. Word.
Summer School:
Dr. A. B. Manson, Chairman; Dr. E. A. Campbell, Dr. J. A. Ganshorn,
Db. D. S. Munboe, Db. D A. Steele, Db. G. C. Labge.
Db. H. A. DesBbisay, Db. Frank Turnbull, Dr. G. A. Davidson.
Representative to B. C. Medical Association: Dr. G. A. Davidson.
• Representative to V. 0. N.: Dr. Isabel Day.
Representative to Greater Vancouver Health League: Dr. J. W. Shier.
iKS? 1
<***   ?.». ts.5 t« & ^f <ww
Each gram of "Tomectin"
(No. 951) provides:
Nickel pectinate 150 mg.
Sodium chloride 50 mg.
Dried tomato pulp.. .800 mg*
In bottles of 50 grams
riickel pectinate has proved
to be unusually effective in treating simple
diarrheal conditions. Early improvement with;
disappearance of acute symptoms, tenesmus
and diarrhea is reported to follow its use.
In "Tomectin" nickel pectinate is combined with
another antidiarrheal substance — dried tomato pulp.
"Tomectin" is readily dispersed in water.
Its prompt action, ease of administration
and palatability make it a useful
preparation to treat diarrhea
in infants, children and adults.
Descriptive literature will he sent on request.
Biological and
Founded 1898; Incorporated 1906
(Fall Session)
iptember 7—SPECIAL GENERAL MEETING—Discussion of Economics and Health
Insurance—Auditorium—Shaughnessy Hospital.
ctober   5—GENERAL MEETING—"Cardiac Arrhythmias, Significance and Treatment"—Dr. G. R. Brow, Professor of Medicine, McGill University.
ctober 19—CLINICAL MEETING—Vancouver General Hospital.
bvember   2—GENERAL MEETING—"The Role of Radiotherapy in the Treatment
of Malignant Disease"—Dr. A. Maxwell Evans—B.C. Cancer Institute.
[ovember 16—CLINICAL MEETING—St. Paul's Hospital.
Response of the Adrenal Cortex to Disease and Injury"—Dr. J. S. L.
Browne, Professor of Medicine, McGill University.
jecember 21—CLINICAL MEETING—Shaughnessy Hospital.
Breaks the vicious circle of perverted
menstrual function in cases of amenorrhea,
tardy periods (non-physiological) and dysmenorrhea. Affords remarkable symptomatic
relief by stimulating the innervation of the-
uterus and stabilizing the tone of its
musculature. Controls the utero-ovarian
circulation and thereby encourages a    i
normal menstrual cycle.
Full formula and descriptive
literature on request
Dosage: l to 2 capsules
3 or 4 times daily. Supplied
in packages of 20.
Ethical protective mark MHS
embossed on inside of each
capsule, visible only when capsule is cut in half at seam.
Page 307
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A significant advance
in penicillin therapy..|
• NO   OIL—avoids danger of oil embolism and oil sensitivity.
• NO  WAX—no pain at site of injection—no danger of tissue damage.
• STABLE—WYCILLIN is supplied in dry form. It is the first penicillin
preparation for aqueous injection winch, when reconstituted with
water, does not require refrigeration.
without drying needle or syringe—any method of sterilization
may be used.
• THERAPEUTIC^EFFECTIVENESS —a single injection of 1 cc
(300,000 units) maintains effective 24 hour blood levels in
nearly all cases.
• R ETA INS   P OTE N CY—after reconstitution with water for seven days
without refrigeration.
Each vial of WycUUn contains sufficient crystalline
procaine penicillin-G in powder form to permit
withdrawal and administration of five 1 cc. doses
(300,000 units each).
Ready for aqueous reconstitution.
cityjM       lb?
■Total Population—Estimated   *  .54 «4g
I Chinese  Population—Estimated     7 o7o
I Hindu Population—Estmated   275
Number Rate Per 1,000 Population
Total deaths   „_•_     373 12.9
Chinese  deaths *       15 153
Deaths, residents only 325 11.2
Male •- i 421
Female , 432
853 29.4
Deaths under 1 year of age \       17
Death rate per 1000 live births 27.0
Stillbirths  (not included above) 18
scarlet Fever
Diphtheria  Carrier   	
Chicken  Pox 	
Whooping  Cough
Typhoid  Fever   _
Undulant Fever _
Meningococcus   (Meningitis)
infectious   Jaundice   	
pysentery  (Carriers) 0
Tetanus .	
syphilis  (not available)   I ! ! ~ 1	
gonorrhoea   (not   available)	
Mncer (Reportable)
Resident ,~
Number    Rate
Per 1,000 Population
,   294
'   2
i    0
rM ■ «
■,.■•■:-■„<>: ■
Page 308
A New Development in the Use of Penicillin
The introduction of prolonged-acting penicillin accomplished
through the suspension of penicillin in peanut oil containing beeswax has been followed by the development in the United States
of an improved preparation in which the penicillin is rendered less
soluble by the addition of procaine.
Clinical observations with this new preparation,
Procaine Penicillin G in Oil, indicate that an important advance has been made and that the objections
to the use of beeswax have been removed.
1-cc. cartridges, each containing 300,000 International Units of Procaine Penicillin G in Oil, for use with B-D* disposable plastic syringes or as replacements for
B-D* metal cartridge syringes.
10-cc vials, each containing 3,000,000 International Units.
*T.M. Reg. Becton, Dickinson & Go.
University of Toronto Toronto 4, Canada
We hear a great deal nowadays about medical economics—it has, indeed, become the
most important single issue in the deliberations of medical associations everywhere—
dominion, provincial and local assocations all have strong and active committees devoting a great deal of time to this subject.
It is a far cry to the old days, when the attitude of the medical man to money was
almost one of repugnance—the doctor accepted an honorarium for his services—the
patient left a fee on the doctor's desk as he went out—the doctor coughed politely and
looked the other way. Gradually the payment of a doctor for his work became a legal
ebligation on the patient—fee lists came into being, vague and chaotic, and doctors even
began pressing patients for payment, legally or otherwise. But not yet have we a clear
business-like system of payment, uniform and measured, so that a definite amount of
service is regarded as calling for a definite amount of money—as is the case when we
buy shoes or groceries or real estate; and we feel that this indefiniteness and lack of
system has perhaps something to do with the difficulties which confront us economically.
The public never knows where it stands — nor do we. Fee lists appear from time to
time, and are helpful but rarely final—except in the matter of surgical fees, and
certain recognised procedures. One way or another, we get the system to work—but
not according to any known law of business.
Perhaps we should have gone on indefinitely in this blissful fog if it had not been
that of late years a steadily increasing volume of demand for better distribution of
medical services has been forcing us to take stock and make up our minds as to our
economic necessities. The consumers of our product, and that includes the whole community, are demanding more of it, and insisting that it must be provided at a price,
and according to methods, that they can afford, and that will provide all they need.
And we know they are right in this demand. We know, too, that we have our own rights
in the case and that we must assert these rights and protect ourselves, or we shall be
running grave risks, not only to ourselves personally, but to the standards of our profession, and most important of all, to the value of our services to the community.
We should, perhaps, be grateful that we have been forced to study this whole
question of economics. In the long run it will be best both for ourselves and for the
public who are our customers, that we should be adequately equipped to discuss economic
matters and to speak with knowledge and authority. We may as well face the fact that
changes in medical practice are bound to come, and in many particulars, are long overdue. But we have a right to demand that these changes be made gradually and with
due respect to our rights. This is a matter of concern to every medical man, not merely
te those who work on the various committees on economics. This point is emphasized in
the announcement printed in this issue of the Bulletin, of the formation of such a
committee by the Vancouver Medical Association.
This committee, we take it, will work in an advisory and consultative capacity
with the committee on economics of the B.C. Medical Association. Whenever the need
for expression arises, the profession must, of course, speak with one voice, and this
must represent all of us, and not merely one section, no matter how large. But such a
committee as this of the VJM.A. can do valuable and useful work and greatly assist
the major effort. A most important thing it could do would be to bring home to each
member of the Association that all these matters are his personal business and that he
must take a personal and active interest in them.
Page 309
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Monday to Friday, 9.00 a.m. to. 5 p.m.
Saturday, 9.00 a.m. to 1 p.m.
A Clinical Atlas of Sternal Bone Marrow, 1946, by Carl Reich (Gift of Abbott
A History of Scientific English, 1947, by E. Andrews.
Chemical Methods in Clinical Medicine 3rd edition, 1947, by G. A. Harrison.
Diseases of the Skin, 7th edition (revised), 1948, by Ormsby, O. S. and Montgomery, H.
Hodgkin's Disease and Allied Disorders, 1947, Jackson, H.  (Jr.)  and Parker, F.
Hospital Organization and Management, 2nd edition, 1947, by M. T. MacEachern.
Love Against Hate, 1942, by K. Menninger.
Medical Clinics of North America,  Symposium on Neurology  and Psychiatry,
New York Number, May, 1948.
Medical Research in War  1939-1945—Report of  the  British Medical Research
Recent Advances in Pathology, 5th edition, 1947, by Hatfield, G. and Garrod,
L. P.
Surgical Disorders of the Chest, 2nd edition (revised), 1947, by J. K. Donaldson.
The American Language—Supplement Two, 1948, by H. L. Mencken.
The Anatomy of the Nervous System,  8th edition,  1947, by S. W. Ranson—
revised by S. L. Clark.
The Development of Modern Medicine, revised edition, 1947, by R. H. Shyrock.
The Effect of Bombing on Health and Medical Care in Germany,   1945, U.S.
Strategic Bombing Service.
The Foot and Ankle, 3rd edition, 1947, by P. Lewin.
The Neurotic Personality of Our Time, 1937, by K. Horney.
Virus as Organism, 1946, by F. M. Burnet.
The following will be of interest to us all. We have not received reports from the
rest of the Province, but are sure that the response elsewhere to this appeal has been
equally satisfactory.—Editor.
Dr. G. C. Johnston, President,
Vancouver Medical Association,
203 Medical Dental Building,
Vancouver, B.C.
Dear Doctor Johnston:
Your Committee on the B.C. Flood Emergency Fund carried out its duties. A
personal canvass of the profession in the City was made. More than 90% of the men
were contacted and as a result I herewith report that the sum of $11,312.50 was contributed by the doctors of this City.
Yours very truly,
Committee B.C. Flood Emergency
A directive issued by the Department of National Revenue, Taxation Division,
is reproduced in full herewith:
Subject: ASSESSMENTS—Convention Expenses of Medical Profession
Effective 1st January, 1948, the reasonable expenses incurred by members
of the medical profession in attending the following Medical Conventions will
be admitted for Income Tax purposes against income from professional fees:
1. One Convention per year of the Canadian Medical Association.
2. One Convention per year of either Provincial Medical Association or
a Provincial Division of the Canadian Medical Association.
3. One Convention per year of a Medical Society or Association of SpeciaU
ists in Canada or the United States of America.
The expenses to be allowed must be reasonable and must be properly
substantiated; e.g., the taxpayer to show (1) dates of the Convention, (2) the
number of days present, with proof of claim supported by a certificate of
attendance issued by the organizations sponsoring the meetings, (3 ) the expenses
incurred, segregating between (a) transportation expense, (b) meals and (c)
hotel expenses, for which vouchers should be obtained and kept available for
None of the above expenses will be allowed against income received by
way of salary since such deductions are expressly disallowed by statute.
(Signed)  D. SCULLY,
Deputy Minister (Taxation).
Appropriate certificates are being prepared and will be available upon application
to the office of The British Columbia Medical Association, Room 203, Medical-Dental
Building, Vancouver. These certificates will also be at the Registration Desk for the
Annual Meeting of the Association this year.
The Executive of the Vancouver Medical Association, acting on the recommendations made at a general meeting of the Association has appointed a Committee of Economics to consist of five members, of which four have already accepted appointment.
(Chairman, Dr. J. A. Ganshorn, Members—Drs. J. W. Shier, E. C. McCoy and W. A.
The Committee has an opportunity to do a great deal of work. It is a time in
medical affairs when Economics exerts a tremendous influence and stands to mould the
future of medical care. It is a time when each of the profession should know the "winds
that blow" and a time when the profession together must know its aim; must know
its destined port and together set its sails.
The Committee would hope to be able in various ways to present to the Association
information on economic matters and to present also recommendations and resolutions
on economic problems. This can be done at open meetings with free discussion. It can
be done through the "Bulletin."
The Committee wants to serve the profession and.would welcome the presentation
of ideas and problems to it. It would urge that all members of the profession in Vancouver become members of the Association so that its efforts and their efforts can be more
effective. A change in the whole of medical practice is inevitable and imminent. Your
local medical organization is your means of giving direction to that change.
Page 311 Iff.'i
Vancouver  Medical   Association
President Dr. G. A. Davidson
Vice-President : '. Dr.  Gordon  C.  Johnstone
Honorary Treasurer j Dr. Gordon Burke
Honorary Secretary j ! Dr. W. J. Dorrance
Editor i Dr. J. H. MacDermot
; V ■ •'
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Vancouver, B.C.
For many years physiologists and clinicians have been interested in the problem of
the measurement of cardiac output in man. Direct methods are not applicable to patients, and workers have been obliged to use some such methods as the ethyl iodide procedure of Starr, or the acetylene procedure of Gollman. It was with a view to making
possible the application of the Fick principle to man that the cardiac catheter was
introduced a few years ago. This instrument allows the recovery of a sample of mixed
venous blood from the right side of the heart and permits the application of Fick's
formula, which is:
Oxygen intake
Cardiac Output=	
Arterial oxygen saturation minus  mixed venous oxygen saturation
With the re-awakening of interest in congenital heart disease, which was stimulated
by the invention of operative procedures by Gross and by Blalock, it became evident that
the cardiac catheter could play a useful role in both the diagnosis of congenital heart
disease, and the elucidation of the physiology of disturbed circulation in these diseases.
An increasingly large number of investigators are now constantly adding to our knowledge of this subject, among whom are Cournand and his associates in New York, and
Bing and his associates at Johns Hopkins.
The catheter in general use is a modified ureteral catheter, with a small hole at the
tip, and a beak about 2 inches in length, making an angle of about 30 degrees with the
body of the catheter. In infants and children a catheter of size No. 6 is used, and in
adults one of size No. 8 or No. 9. The larger the catheter, the easier it is to obtain pressure
readings. A small incision is made over one of the arm veins emptying into the brachial
vein on either side. The left side is usually the more satisfactory because the catheter can
then describe a single sweeping curve in proceeding into the pulmonary artery. The
catheter is connected to a drip apparatus and is then introduced into the vein and
pushed along until it enters the right side of the heart. This is always controlled under
the fluoroscope.
jSometimes difficulties are encountered, such as passage of the tip into the internal
jugular vein, or obstruction by a tortuous innominate vein. A little manipulation will
usually succeed in bringing the tip into the right heart. It is then pushed through the
tricuspid valve into the right ventricle and thence through the pulmonary valve into
the pumonary artery and out into either lung field. In the presence of congenital anomalies, the catheter may take an aberrant course into the aorta and very rarely into the
left ventricle. It frequently passes spontaneously from the right auricle into the inferior
vena cava, and experimental use of this has been made to secure blood coming directly
from the kidneys. The catheter having been introduced, pressure determinations in the
variqjus chambers of the heart are made, using one or another of the available mano-
Page312 .1$
meters. The simplest and easiest to operate is a saline manometer, such as is used to
make venous pressure readings in the arm. The difficulty is that on account of its inertia it gives only the mean pressure. The Hamilton manometer, which has an optical
recording device which registers changes in the contour of a tense membrane, is more
accurate and gives readings of both diastolic and systolic pressure, but it is difficult to
operate and requires an expert technician. Recently a strain gauge has been adapted for
this purpose and has given satisfactory results. It utilizes the principles that changes in
tension on a wire will produce a current which can be recorded on a galvanometer, such
as an electrocardiograph.
Oxygen determinations are carried out on samples of blood taken from various
points along the course of the catheter. Some technical difficulties are involved here in
collecting blood uncontaminated by air. It requires a meticulous technique and the use
of oil to prevent the escape of gas.
Arterial oxygen determinations are done on blood collected from the peripheral arteries, usually either the brachial or the femoral. When serial determinations are required, multiple punctures may be done or a needle may be inserted which is equipped
with a stylet and left w situ.
Measurement of oxygen consumption is done either with a Douglas bag or with a
Benedict-Roth machine.
Difficulties and complications encountered during this procedure include failure to
pass the catheter. This may be due to small veins, unusual and tortuous course of the
veins, presence of a mediastinal mass, etc. Occasionally the tip of the catheter seems to
become entangled in the: trabecular or chordae of the left ventricle and it refuses to pass
into the pulmonary artery. Spasm of the veins may temporarily prevent the passage of
the catheter along the arm, but this can be overcome by merely waiting for a short
time, or, if necessary, by the injection of novocaine along the course of the vein. It is
necessary to tie off the vein that is being used to catheterize, and this of course destroys
its further usefulness. Local thrombophlebitis is not uncommon but serious sequelas have
not been reported. The patient frequently complains of extrasystoles when the catheter
is impinging on the endocardium. One patient with whom I had experience was surprisingly able to localize the tip of the catheter. No fatalities from the procedure have so
far been reported. Brennon, Weens and Warren have done 420 without serious trouble.
Cournand et al have done 260 in which they have left the catheter in place up to as
much as 24 hours without serious complications other than mural thrombosis of the
vein. The applications of this technique to the study of congenital heart disease are in
general four:
1. One observes the course of the catheter. It may go into the left auricle,
in cases of interauricular septal defect; into the aorta, in cases of dextro position; and rarely into the left ventricle in cases of left interventricular septal defect or degrees of cor triloculare biatriatum. In cases of suspected tetralogy of
Fallot, its failure to pass into the pulmonary artery is not of significance, but
should it do so one can be confident that the opening is at least large enough to
admit the catheter and that pulmonary stenosis is not extensive, if present.
2. Deviation ef pressures from what experience has shown to be normal
are often significant, for example, increased ventricular pressure in the tetralogy
and Eisenmenger's complex, or a normal right ventricular pressure with elevated
pumonary arterial pressure in cases of patent ductus arteriosus.
3. Changes in the oxygen saturation of various chambers are of importance.
That of the right ventricle exceeds that of the right auricle in cases of interventricular septal defect, including the tetralogy. When the oxygen saturation of the
right auricle exceeds that of the mean saturation of superior and inferior venas
cavae, it is indicative of interauricular septal defect. When the saturation in the
pulmonary artery is greater than that in the right ventricle, patent ductus arteriosus is present.
Page 313
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,4. Finally, a number of formulae have been adduced by Bing and his associates which allow at least an approximation of such factors as cardiac output, I
oxygen content of blod in the pulmonary vein, pulmonary arterial flow, systemic !
flow, pulmonary capillary flow,  collateral flow into the lung,  and intercardiac 1
From these observations we may conclude that the use of the cardiac catheter is
not a dangerous procedure. It is, however, an exacting technique which demands team- j
work of a high degree from the physician, the radiologist, the laboratory, and the pa-1
tient. Its use for the determination of cardiac output alone is at present purely a research procedure. Its use in the diagnosis of congenital heart disease is not necessary in
many cases, probably in the majority, but it is of great value in the elucidation of
atypical cases which cannot be definitely diagnosed on the basis of the usual methods l
of investigation.
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M.D., Columbia University Press, 1937.
This volume, of slightly less than two hundred pages, presents a terse, clear formu-
latio nof the subject embraced by the title. Of especial interest to the specialist in
neuropsychiatry, it commends itself to all professionally concerned with "mind-healing."
It is not a treatise on method, and does not aim at giving instruction in the specific
ways and means of psychotherapy. Maybe herein lies its chief value, because it tolerantly discusses the main concepts of the major disciplines of scientific psychotherapy,
and provides data on which an individual can build his own concepts to apply with his
own unique personal qualifications. "To learn to use oneself most effectively is the im-
postant challenge of psychotherapy" for all assuming such responsibilities.
In his Foreword, the author states, "The purpose of this book is to indicate the
general conceptions that prevail with respect to the structure and function of the
mind, and to show, as well as possible, what influences these conceptions have had
upon the problems of psychotherapy." At this time in the progress of medicine, with
the ever increasing emphasis on psychological factors in the aetiology of disease, any
serious effort to clarify the techniques of providing support for mentally ill people is
worthy of perusal. When the effort, as here, is well planned and understandably expressed, more careful study is advised.
The contents are divided into six chapters. The first is an introduction, and states
that the whole volume is "a preface to psychotherapy," and describes the course along
which this branch of healing has come. The author points out that at the beginning of
this century there were several important concepts, and that of these, two have continued to grow conspicuously, and to become more and more integrated into medical
usage. These are the psychoanalysis of Freud, and the psychobiological attitudes of
Meyer. The disciplines of Alder and Jung, though useful at times in the practice of most
therapists, and though particularly useful in the hands of some at most times, have not
received a comparable place in medical usage. He points out the values of all psychological
methods and techniques that help sick people get well.
The second chapter is devoted to the psychoanalysis of Freud, and indicates that
this method is of primary use in the understanding and treatment of the psychoneuroses.
He gives several brief clinical sequences, supporting such statements as "Fears are like
physical* pains that give warnings of deep lying pathology. Patients know only that they
have pains. . . ." The author draws a vivid analogy, "When the novitiate first attempts
to look into a microscope he may see nothing more than the eye-piece. He has to practice looking. He must usually be taught to see the field by means of a, lens of low
Page 314 power. Microscopy is a special type of examination requiring much training and experience. By analogy, when one first glances into the realm of the unconscious, little
or nothing may be seen, but eventually, with training and practice, the previously unrecognizable features stand out with clearness."
Analogies, in fact, are freely and tellingly used throughout the book. Quoting
Freud, the author refers to the emotional "stream," with its origin, flow, with variations in surface-area and depth, pooling of the stream, damming back, etc.
The important concepts of "regression," of "projection," and of "rationalization"
are neatly sketched. Critical comments on the data of other observers are included.
Chapter three is devoted to the psychobiology of Meyer. Earlier the author has
stated that Meyer's forte is the "psychotic" individual, as Freud's is the "neurotic."
The psychobiological approach gives careful evaluation of the background, and the
growth phenomena, to point the interaction of the human individual with the various
environments in which he moves. Dr. Hinsie notes the heartening trend towards fusion
of interest and method of the "psychoanalyst" and the "psychobiologist.
Chapter four reviews the "individual psychology of Adler" and the analytical psychology of Jung," and describes some of the situations where these formuations are particularly supporting in psychotherapy.
The fifth chapter is a statistical evaluation of psychotherapeutic methods by Carney
Landis, Ph.D., and includes some tables regarding recovery-and-improvement rates, as
reported from various clinics.
The last chapter is "conclusions." The author makes a plea for the statistical
evaluation of results of psychotherapy, and points out the foibles of general appraisal on
the basis of "personal experience."
The author concedes the enormous difficulty of evaluating therapy because of the
many variables that enter into it, and because of the many causal factors that provide
the morbid process, to counteract which the therapy is applied.
The bibliography is extensive, and the index is useful.
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"THEIR MOTHERS' SONS," by Edward A. Strecker.
This is an angry book, and an accusing book. Dr. Strecker's target is "Momism"
and the book is mostly a collection of anecdotes illustrating the very harmful effects of
*Mom' on her children. "Mom" as used in this book is not a very well defined term and
may mean anything from a mother who dislikes wars to a bottle of whiskey. Her prototype, however, is the possessive mother who makes development towards maturity
impossible in her children. That an infant should experience an emotionally secure, safe,
dependent relationship to his mother first, and that the main task in "helping to grow
up" consists in gradual, well timed encouragement towards independence, is a well-
accepted concept in psychiatry. But the author does not deal with 'development.' Flis
ideal in this book is the brave soldier and his profound anger is stirred at the thought
that Mom's sons do not make good soldiers.
The author recognizes that Fathers, or school teachers, or the Army may be ,a
"Mom," Le. the factor restraining a person's development towards independence, but
he holds that the most decisive influence is that of the Mother, and he lays all the blame
for any failure of her children on her. There are just two sentences in the book which
state that "Mom is not of her own making," and that "Mom's actions are motivated by
the unconscious" but these findings do not alter the accusing and condemning approach. Dr. Strecker has one central idea which he states in the first few pages, but the
rest of the book merely serves to illustrate it, without adding anything to it. It might
have been a very fertile idea, if the author had written a little more searchingly and less
accusingly. He could have' investigated the present American Mother-ideal, the moral,
educational and economic upbringing which results in the undesirable attitudes which
he stresses. He might also have investigated the moral, sexual and economic male atti-
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tude towards the mother as a cause rather than only a result. There is not much sug-
gestion of treatment or remedy beyond the exhortation to the Mom that she be a Mom j
no more. Surely this is psychiatry at its most primitive. Altogether this is a superficial ]
book; it generalizes sweepingly, it accuses indiscriminately; and it points at well-known
faults without helpful suggestions of how they might be removed.
Division of V.D. Control
It is important that the diagnosis of syphilis be established and treatment begun
early in pregnancy.
We recommend that all cases of syphilis in pregnancy, irrespective of previous
treatment, be hospitalized for penicillin therapy, i.e. intramuscular injections of 50,000
units every 2 hours for 90 doses. This treatment is then followed by regular weekly injections of alternating courses of mapharsen and bismuth. The courses of bismuth after
the fifth month of pregnancy should not exceed four consecutive injections and the last
six or eight injections before term should be arsenicals. Blood pressure and urinalysis
are recommended weekly while the patient is receiving arsenotherapy and haemoglobin
taken every three months. The serology should be followed monthly, and if there is
any evidence of a rising titre we would recommend that consultative service be requested
with the view to possibly repeating the penicillin course.
If the cerebrospinal fluid has never been taken, and if it is indicated in the routine
follow-up of these patients, the Division recommends that advantage be taken of the
woman's hospitalization (at delivery) and the spinal tap be performed during this postpartum period rather than in the prenatal period.
It is recommended that a routine Cord Kahn be taken at birth. If this is negative
the infant's blood test should be repeated at six weeks and three months of age.
If the Cord Kahn is positive, treatment should not be given unless there are confirmatory clinical or x-ray evidences of infection. In many cases the positive Cord Kahn
is due to carry over of reagin from the mother. These patients should have repeated
quantitative Kahn tests. If the titre is rising the diagnosis is confirmed and treatment
should be started. If the titre falls the child should be kept under observation until
freedom from infection is established.
(For details of management of Prenatal syphilis refer to Symposium dated June
1947, and distributed to all members of the medical profession in B.C.)
Penicillin is used routinely in the initial treatment of gonorrhoea. Exceptions are
made when indicated-r—e.g. when a concomitant spyhilitic infection is suspected, sulphathiazole therapy is given.
A.    Penicillin Therapy of Proven and Suspected Infections:
1.   Institute therapy immediately in all instances where clinical evidence exists or
where there has been contact with known infection.
Page 316 b.
2. Take specimens for smear examination but do not withhold treatment pending
return of laboratory reports.
3. Take a blood Kahn before therapy is instituted.
4. Treatment for both male and female patients is suggested as follows:
a.   Penicillin 2 injections of 100,000 units each dissolved in 2 to 4 c.c. of
diluent, administered 3 to 4 hours apart in the upper outer quadrant of the
gluteal muscle.
Instruct patients carefully—See Appendix "A"—N.B.
Observe for recurrence. If bacteriological response is unsatisfactory after 517
days repeat above course or give smaller amounts at more frequent intervals
over a longer period of time. Do not repeat penicillin without bacteriological confirmation and in staining assure yourself smear is not over decolorized and that gram negative cocci seen are not in reality gram positive cocci.
In the majority of instances discharge following penicillin is nongonococcal and will not respond to penicillin. If discharge has perisisted after
5-7 days and it is bacteriologically negative use sulphathiazole as indicated
d. Take smears once a week for three weeks as test of cure.
e. Take a blood Kahn in 3 and 4 months to check for concomitantly acquired
Note: If reaction observed following penicillin, i.e. chill or fever, suspect concomitant syphilis. Do repeated blood tests and observe carefully for four
B.    Sulphathiazole Therapy (Used only when specifically indicated)
Sulphathiazole—45 grs. stat., then grs. 15 Q.I.D. for first week.
In the second week give grs. 7Y/z Q.I.D.
This treatment is also recommended for cases of chancroid.
N.B.—It is felt that many of the patients who show discharge following penicillin
for gonorrhoea are non gonococcal. Information available from large centres in
U.SJV. and Canada show that 95%-98% of all V.D.G. is cured by 200,000 units
of penicillin. The discharge still present in many instances is due to poor patient
co-operation and it is thus most important that Appendix "A" be brought to
their attention.
yA. '■>■ * .'
1. You have just had one injection of Penicillin. To complete this treatment you
must have a second injection at the specified time. The worker has given you
instructions for your second injection and when to return for tests to determine
if you are cured.
2. If you take all your treatments as prescribed you may not need any further
treatment but the only sure way to tell if you are cured is to have further tests
made. The absence of a discharge does not necessarily mean you are free from
infection, so be sure to return to the clinic until the doctor says you are cured.
3. Avoid all sexual excitement and especially intercourse for 2-3 months.
4. Avoid all alcohol for 2-3 months.
5. Drink lots of water as this will help wash out the infection.
6. Keep your body warm. Avoid unnecessary exercise. Do not wear tight-fitting
7. Do not repeatedly examine yourself.
8. When you got this disease, you may have caught syphilis at the same time.
Penicillin may hide or delay the appearance of syphilis in your body, therefore
Page 317
, - mm
it is absolutely essential that you have a blood test either here or from your
private doctor in 3 and 4 months. This is the only way you can know for sure
that you haven't syphilis. Dottt forget. A Blood test is your only way to be
9. Watch your body carefully during the next four months and if you notice any
sore on your genitals, or. should a skin rash appear, see your doctor, or go to
your clinic IMMEDIATELY.
• •• • .■
' ■'■''.    '
April 26th, 1948
It is a prevalent belief among many that the children born of tuberculous patients
are likely to be under par physically and mentally. Though our numbers are comparatively small, it was felt that we should make an endeavor to see whether this rule applies
to the Province of British Columbia.
Children of six months to eight years were examined. A fair percentage of our
cases were presented for examination, being about 50% of the tuberculous maternity
cases that were cared for through the Tuberculosis Division. Height and weight estimation were made and compared with averages. General appearance with estimation of
virility and general development were considered. The age of dentition, walking, talking,
and a rough estimation of intelligence were made. Relative age of training and feeding
and toilet habits were considered also. The frequency of infectious disease and non-
communicable conditions, the incidence of positive skin tests and general nervous
In general it was noted they seemed of fair weight and stature for their age. One
definite impression was that there was a greater degree of nervous tension present than
in the average. A higher percentage appeared to have enlarged tonsils. Clinically, the
children seemed to be in good health and to have good resistance to disease. The average
age of dentition, walking, talking, were normal as closely as could be judged, only one
case of unerupted incisor teeth at age 6l/2 years was noted.
It would seem, therefore, that the children of tuberculous parents were possibly
somewhat more highly strung than the average, otherwise, they were in a very good
state of development, and it would seem that their solicitous parents gave them better
care than is usual.
Doctor, 29, married, veteran, seeks opportunity for assistantship to
recognized general surgeon, preferably in Vancouver. Two and one-
half years post-graduate work in Montreal, twelve months Shaughnessy. Available in six months. For information please contact Dr.
F. L. Whitehead, Executive Secretary, 203 Medical-Dental Building,
MArine 3657.
Page 318 '"I-
Vancouver, B.C.
This is the testimony of one who has suffered from many physicians for many
years—through curbstone and cloak-room advice.
At last, however, after my wife had reached the limit of her endurance, and after
my daughter had decided to write a book entitled "The Ulcerated Marriage," I found
myself in the hands of the Philistines and under close arrest.
Trial was by jury, but with two surgeons to one medical man. I was advised to
put .my affairs in order. I was asked if I had anything to say. Knowing vaguely of the
recent trend in stomach surgery, I timidly enquired as to the effects of vagotomy on
some 30 feet of intestine and other organs. I was told that no one knew, but here was a
God-given opportunity for a medical man to make scientific observations on his own
gastro-intestinal tract. Thus I was inveigled into keeping a diary.
I shall not bore you with a detailed play by play recital of my woes and, reactions
following a vagotomy and gastroenterostomy (on the 30th day of November, 1946,
A.D.) There are, however, a few memories that linger and some symptoms that perhaps bear analysis. I know now that patients may experience very considerable postoperative discomfort.
Early ambulation is a great experience, and the patient having regained his confidence to move and walk within twenty-four hours after an operation, feels that he
is taking part in a great advance in the annals of surgery. He is conscious of a slight
heroic glow in his wobbling knees. He may even feel the urge to express the event in
My Doctors agreed with George Dock,
That surgical cases be told
To disregard pain—to get up and walk,
Likke Spartans, in tough days of old.
So the patient, the brave little fellow,
Not showing quite all his fears,
And not wishing to appear quite so yellow,
As he felt—with a great buzz in his ears,
And suspended above by his sutures,
Half fell and half slid through the air,
And when further urged on by his butchers,
He zig-zagged, and collapsed in a chair.
At this point I should just mention in passing that I received 800 mgm. of Dicou-
marol—because of a pain in my right calf on the 10 th post-operative day.
A stomach tube kept in place for four long days is a nasty feature. This item (in
a patient) never before gave me any great concern. (I would make a plea for as small
a tube as possible).
I realized how a sick person feels when, the Doctor's patience worn thin, as he
tries to re-insert the stomach tube, with the patient gagging and puking in his face,
he says rather gruffly, "Come on now, you can take it."
To have one's own arm veins thoroughly and methodically punctured for any
remaining patent venule (for about an hour) before the intravenous fluid will run, is a
recommended experience for any doctor. In my case I was greatly comforted by remembering about certain alexins,' nebulous protective substances, which the body is
said to develop as a result of trauma. These are the factors that bring out the manly
qualities in boys playing football, when bruised and kicked in the shins.
(Read before the North Pacific Society of Internal Medicine at Tacoma, Washington,
April 5, 1947.)
! Page 319
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It is riot given to many persons to experience a bang-up reaction to intravenous
ami no-acids (according to the manufacturer's folder). Perhaps it was something else,
the sedative, or the multiple vitamins which were added with loving solicitude, that
caused me to float off into a dim, hot, parched, trackless Sahara, where the only hope of
reprieve was to be found in an oasis, bubbling over with cold beer. As my mind cleared
I began to dutifully observe reactions, and to enter in my diary such items as—
Food eaten—Steak and chops by the fifth day.
Appetite—Present and fairly good from the fifth day—stimulated by the sight
and smell of food. My eyes, however, were often bigger than my stomach. Once I
began to take food, I tended more as time went on, to keep on eating like a decerebrated
frog, until sensations of acute fullness supervened. These were associated with some
palpitation and "hot flushes." The palpitation did not come on immediately after eating, but in 10 to 20 minutes. This feature has persisted to some extent, but gradually
became less noticeable.
Pyrosis—Heartburn evident from the first and marked when the stomach tube
was still in place, and most evident when stomach seemed to be sucked almost dry. It
was felt that this was due to mild spasm of the lower end of the oesophagus from the
presence of the tube and from operative trauma. It is usually stated that pyrosis is due
to acid stomach contents in the oesophagus, but after vagotomy there should be little
or no acid.
Dull pain—Substernal, associated with, but not always present with the pyrosis—
produced, it seemed, when the lower oesophageal spasm was of sufficient degree. This
pain may have been aggravated by tobacco, for I soon smoked a little, for obvious
scientific reasons.
Regurgitation of bitter stomach contents—which it was realized occurs for a
time after a simple gastroenterostomy.
Belching—of considerable degree—Good Lord, a belcher, a cribber, I had become.
Nausea—almost entirely absent—except with an acute dilation of the stomach on
the third day, and at times when too much food and fluid was taken aboard. Only
three times did vomiting occur, after leaving the hospital, once after a large intake of
milk. There is no great desire for milk.
Abdominal pains—The old ulcer type pain—associated in my mind with pylorospasm and intense nausea—for many years past, entirely absent from the first postoperative day. Dull, niggling, halfhearted, colicky pains, chiefly lower abdominal, left
side—as if an argument were going on in one or two knuckles of gut, with the ancient
primitive intrinsic action, attempting to, but not always delivering the goods in
smooth manner, and not infrequently for a tume, the undisturbed sacral parasympathetic taking over with a rush.
Number and description of bowel movement—carefully recorded for a time (with
natural distaste). However, I soon realized that as a result of such written analysis, I
might easily be branded by some uncharitable person as a psychopath. On the 12 th day
I recorded:—"I feel like a stool gazer. Unless especially interesting specimen is observed,
I shall cease recording data on colonic casts."
For the first few weeks I must confess that it seemed that I had but traded in
the old ulcer symptoms for those associated with a stagnant stomach and a growling
I tried to recall my fading knowledge of physiology. I secured a text book, and
read, and I quote:-
"If both vagus nerves in a dog are divided at the diaphragm, a large amount of
food may remain in the stomach in an undigested condition. The secretion is deficient,
and the opening of the pylorus is not easily carried out. Such dogs tend to die of
sapramia, being poisoned by the absorption of products of putrefaction from the
gastrict contents."
Page 320 Well—the poor dogs; I felt rather ill myself — probably sapraemic! — until I
realized that Starling had written this 35 years previously in his book published in 1912.
Searching into more recent works on physiology, it was noted :-
That section of the vagi tends to depress motility of the stomach—even to the
ponit of atony, to cause spastic contraction of the sphincter, especially of the cardiac
end, and to decrease gastric secretion. The cephalic phase of gastric secretion is abolished,
The production of atony and retention would seem to be a disadvantage (but nowhere
did I find further reference to death from sapraemia!) The manner of integration of
the vagus and sympathetic fibres is not entirely clear. It is known that the vagus is
concerned with the secretion of ferments, water, salts and hydrochloric acid through
cholinergic action on the end-plates. It is known that the sympathetic nerves evoke
by adrenergic action a slight production of mucus, but have no effect on the chief cells,
which produces pepsin and rennin. Therefore, after vagotomy there should be only a very
slight production of acid—with full secretion of mucin by sympathetic action, but
complete abolition of ferments ... all factors conductive to ulcer healing.
NOTE: Variation in the effect of vagotomy on pepsin production has been reported, however the influence of the sympathetic on the peptic cells is not definitely
known. According to some, the effect is inhibitory (Best & Taylor).
Some experiments indicate that there are other efferent routes than through the
vagus, for the production of inhibition or excitation. Also, although the efferent pathway from the stomach is by way of the vagus, yet strong irritations in the stomach
and gastro intestinal tract will still induse vomiting after vagotomy. Therefore, the
sympathetic must be concerned; and possibly when necessity arises, as after vagotomy,
some cholinergic fibres in the sympathetic may attempt to carry on, or even more, may
be developed. This would xplain the return of almost normal secretion in dogs, 2 to
3 years after vagotomy. Nature always has a reserve—a margin of safety—"Probably
all fibres of nerve trunks do not participate in normal reflexes, as they do experimentally and only those fibres are used which are necessary to produce a proper response.
Stimulation and section of nerves does not induce a simple effect, but evokes a whole
series of reactions, with mechanical, hormonal and vascular reactions playing subsidary
roles." (Wiggers.)
In all animal life, as Wiggers points out, those reactions which are brought about
by the intermediation of the nervous system play such a preponderant part that we
have almost forgotten the possibility of other means of co-adaptation among the
various organs of the body. Foods alone, may produce a variable secretion of hormones,
capable of affecting contractions (as the enterograstrone of Ivy). Some central coordination of antagonistic innervations also no doubt exists. Faradic stimulation of the
forntal and premotor areas causes inhibitions of movements of the full stomach.
Hypoglycemia stimulates the vagus centre, and increases gastric sections if vagus
fibres to the stomach remain. Theoretically, a heightened blood sugar, as following a
meal, could depress the centre, and allow unchecked play of the sympathetic—to produce effects like increased heart rate and further relaxation of the stomach musculature
in a vagotomized animal or person.
Mental depression is associated with decrease in gastric motility and secretion (as
shown by Wolf & Wolff's Experiments on a human subject). May it not be then, that
in an ulcer patient feelings of depression are part of a protective mechanism, to cut
down acid secretion and hypermotility. Peptic ulcer may thus be thought of as not so
much a psycho-somatic disease, but a somato-psychic condition, with emphasis on the
A gastroenterostomy in association with vagotomy appears to be logical. It
contributes to the lowering of the acidity through regurgitation of bile and pancreatic
juices, and by decreasing the emptying time of the stomach.
Gastric digestion, moreover, is not considered to be so important as formerly
thought, for the small intestine is the chief organ of digestion.
Page 321
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What of the effect of vagotomy on the intestinal tract below the stomach, and on
the gall blader, liver and pancreas? (The original question.)
In the small intestine vagus action is'the same as in the stomach—secretomotor to
the glands, and motor to the muscular coats, but inhibitory to the ileo-colic sphincter.
The response to stimulation of nerves here is not always consistent, and may be
reversible, possibly due to a mixture of cholinergic and adrenergic fibres in both nerves.
Mechanical and chemical stimulants applied to an isolated small intestinal loop
may provoke a greater secretory response, if the loop has been denervated, than if the
nerves are intact.
It would seem then that the diarrhoea which may follow vagotomy is due to
several factors.
The anatomy and physiology of the vagus innervation to the right side of the
colon is nowhere clearly defined. The distribution probably varies in different individuals. Wiggers states that evidence indicates that the ascending and transverse
colon are supplied by the vagus.
However, the whole gastro-intestinal tract can function even with the abolition
of all extrinsic nerves—for all smooth muscle has an intrinsic rhythm of its own.
(Smooth muscle does not show the "Reaction of Degeneration," as does voluntary
muscle, after the nerve supply is sectioned.)
After vagus section there still remains the sacral parasympathetic (from 2nd, 3rd
and 4th sacral nerves) which appears, along with the inherent rhythm of the intestine, capable of producing satisfactory evacuation, after a period of re-adjustment.
Some looseness of bowel movements and often disappearance of former constipation is
usual after vagotomy.
The gall bladder is supplied by the right vagus nerve chiefly, and by splanchnic
nerves. (Sympathetic from D VI to L I.)
The vagus action is said to be the same essentially as in the stomach—motor to
the organ itself and inhibitory to the sphincter of Oddi. (This sphincter consists of
three different sphincters capable of functioning independently, or all together.) Section of the vagus in cats is said to cause gall bladder stasis. The sympathetic is considered to be mainly inhibitory. Most physiologists favour a dual mechanism for each
set of nerves. It was thought by Howell that the vagus normally carries afferent im«*
pulses to the brain and that the splanchnic fibres provide the efferent pathways; and
yet pain sensation is lost by section of the right splanchnic nerves, and vomiting is
prevented by cutting of the vagus—all of which is somewhat confusing.
The reciprocal innervation of the gall bladder somehow works effectively, but
just how it works has not yet been clearly explained. Physiologists state (Wiggers)
that the bulk of evidence indicates that gall bladder contraction and evacuation are
chiefly due to the fact that fats and dilute acids in the duodenum cause the formation
of a hormone—cholecystokinin. (Secretion—also produced the same way—augments
secretion of bile by the liver cells.) Lack of hydrochloric acid—after vagotomy—may
perhaps disturb this mechanism. The liver is not disturbed to any extent by vagus
section, it seems.
The pancreas has secretory fibres from both sympathetic and vagus nerves. Vagus
stimulation apparently increases the concentartion of pancreatic ferments more than
the volume of secretion. Sympathetic stimulation calls forth a smaller secretion of a
juice not greatly dissimilar to the vagal juice. As this action is abolished by atropine, the
sympathetic appears to carry cholinergic fibres. The pancreas appears to be the only
gland in the body in which the same type of secreting cells are activated by two nerve
supplies, each with the same action. However, chemical humoral effects play the chief
roles, as shown by a pancreatic transplant, severed from all nerve supplies, which secretes a juice essentially the same as that from a "pancreatic fistula animal." Vagotomy
then would not be expected to greatly disturb pancreatic function. Practically this
appears to be true.
Page 322 Internal secretion: Some evidence suggests that insulin secretion is under vagal
control, but this is not thought to be important. Denervation of the pancreas does ont
affect sugar tolerance to any significant extent. (Wiggers.)
After vagotomy then, we must visualize an altered autonomic nervous system,
with altered mechanics and altered chemical balance—all this in a patient who has had
long standing disability, who has become conditioned to certain foods and fancies,
habits, and a way of life. It would not seem reasonable to expect a complete change
Surgeons may be too prone to say, as they did three or four decades ago—after
"curing" an ulcer by ample gastroenterostomy "now you can eat anything, smoke
and drink whiskey." My own experience would suggest that the patient go a bit easy
on certain foods—especially fats. (Fats theoretically should further increase relaxation
of the stomach.) Perhaps the absence of rennin accounts for a lack of desire for milk—
which condition apparently is common. As coffee stimulates gastric secretion directly,
and alcohol, through the production of histamine, these substances may even aid diges-
-after the ulcer has healed. Possibly some patients will feel better to take dilute
Hydrochloric Acid, or enzymes, such as rennin.
Tobacco. Ivy states that if smoking has any effect, it is to depress gastric secretion
and retard evacuation. Therefore, it may aggravate the feeling of fullness following vagotomy. Wolff and Wolf showed that in their human subject with a gastrostomy, when
smoking was pleasurable, no evident effect was produced, but when used to the point
where the mucous membrane paled and motility lessened—nausea occurred. Smoking,
which may aggravate feelings of fullness following vagotomy is then best avoided, at
least soon after a heavy meal.
While my vagus nerves were still intact, the reports on vagotomy were very
encouraging. Excellent results were reported by Draegstedt, the pioneer in the field,
and by others. Lately considerable criticism of this operation has been voiced. There
are many skeptics who point out that while the immediate results may be brilliant, yet
they fear the long-term effects. Many surgeons no appear to feel that they prefer to
await th passage of time for vagotomy to find its level, and that in the meantime they
intend to use it only when other tried procedures fail. They ask "Will megalocolon
develop, sphincter spasms persist, even degeneration of the vagus center occur?"
What are my reactions at this time to my vagotomy and to my skeptical, mostly
surgical friends, to those who shake their heads (and figuratively tap their foreheads) as they tell me that I have lost weight, and ask me when I last vomited? At my
age I am too cautious to make rash statements. I realize that a further period of readjustment is necessary. Apart from some sense of post-prandial fullness with attendant
symptoms, I can report that now, four months after operation, the old ulcer pain and
associated nausea have never recurred. My sour disposition has changed for the better.
Life is much brighter. (My Psyche depends upon my soma). Not for years has food
tasted so good, and been so varied. I am very glad that I had a vagotomy done.
When I look before and after,
And muse on what's been cut,
I find in life there's laughter,
Through the soothing of the gut;
For the colon does not grumble,
Gives now no noisy rumble;
There is no pain—no spasm;
Food scarce fills the empty chasm;
Gone is that sense of tension;
But—I fear I'll lose my pension,
For to take it, I would be a sort of twirp,
Now that my only symptom is—
A gentlemanly burp.
Page 323
m BNfc'
Vvwcouvel Qe+ieicd <Jlo4fu£cd Section
Associate  Resident  in Medicine,
Vancouver General Hospital
The renal lesions commonly seen in diabetes mellitus fall into two broad groups,
viz. the vascular degenerative lesions and the inflammatory lesions.
The first of the vascular lesions to be considered is arteriosclerosis of the atheromatous type. It is generally agred that arteriosclerosis is more common and more severe
in diabetics of all age groups than in non-diabetics (1, 2, 3, 4 , 5.). It would be expected that the kidneys of diabetics would show an increased incidence of senile arteriosclerotic changes. The medical literature fails to reveal this because most reports do not
distinguish between arterial and arteriolar changes but instead often group them under
a heading of renal arteriosclerosis or vascular nephritis. In any case arteriosclerosis of
the larger renal vessels, i.e. senile arteriosclerotic nephrosclerosis rarely if ever causes
functional incapacity of the kidneys and need not be considered further.
The second vascular lesion to be discussed is arteriolar nephrosclerosis, the lesion
associated with hypertension. It is controversial whether or not hypertension and its
concomitant arteriolar lesions are more common in diabetics than in non-diabetics.
In statistical surveys of hypertension in diabetics and non-diabetics a few pitfalls
are found. First, in reporting only systolic readings of any group which includes a
large proportion of older people one will include many cases of systolic hypertension
which may be due to senile arteriosclerosis and is not true hypertension (6). The second
pitfall is that there is a distinct difference in the incidence of hypertension in the two
sexes and unless a series is separated into the two sexes it may los its significance or be
misleading  (7).
In Bell's series (8) systolic hypertension was more common in diabetics over 50
years of age than in the Wetherby control group.
Major in 1929 (as quoted in 1.) showed that after 35 years of age the systolic
blood pressure was slightly higher in diabetics than in routine clinic patients and that
it was considerably higher than in normal people of the same age group. However,
Wilder (9) states that neither systolic or diastolic blood pressure were significantly
elevated in 200 diabetic patients as compared with 200 non-diabetic patients of the
same age. Wilder also quotes studies by Wollaeger and Wagener and also by Waite and
Beetham showing that hypertensive retinal lesions are no more frequent in diabetics
than in non-diabetics.
When studies are made of the incidence of arteriolar nephrosclerosis among diabetics there is also some difference of opinion. Bell (8) finds that although arteriolar
lesions are infrequent in young diabetics they are 5 times as common in diabetics over
50 years of age as in non-diabetics. He also shows that arteriolar lesions are more
frequent and more severe in diabetic females than in diabetic males. The series of
Warren (quoted in 1.) and of Lisa et al (2) would substantiate this although the difference of incidence is not so marked in their series. On the other hand, the experience
of Wilder (9) is that arteriolar lesions are no more common in diabetics than in non-
Staff Clinical Meeting, Vancouver General Hospital, March 23, 1948.
Page 324 It would seem that although the evidence for an increased incidence of hypertension among diabetics is perhaps equivocal, the evidence from post-mortem examination
of the kidneys fairly definitely shows that arteiolar nephrosclerosis is more common
and more severe among diabetics than among non-diabetics.
The third and most interesting vascular lesion to be discussed is so-called "Inter-
capillary Glomerulosclerosis."
In 1936 Kimmelstiel and Wilson (10) reported 8 cases all of which showed distinctive lesions in the renal glomeruli characterized by focal round or oval masses of
hyaline material in the center of a glomerulus or in the center of a glomerular lobule.
Seven of these eight cases were diabetics and the eighth died before history could be
obtained. Since they believed that th hyaline masses represented a broadening of the
connective tissue between the glomrular capillaries they gave to this lesion the name
Intercapillary glomerulosclerosis. Allen (11) has shown that the hyaline material comes
not from intercapillary connective tissue but from the walls of the capillaries. Bell
(8) agrees with Allen in this view.
The hyaline masses are easily recognizable as round or oval nodules of 20 to 100
microns in diameter with a concentric layer of flattened capillaries at their periphery.
The degree of involvment of glomeruli varies from case to case.
Laipply et al (12) recognize an earlier form in which all glomeruli show uniform
focal fibrosis without hyaline masses and they have observed in some cases transitions
from areas of focal fibrosis to the typical circumscribed hyaline masses.
The clinical picture of this condition has been described by many observers (12,
13, 14, 15, 16, 17.). It usually consists of a history of diabetes mellitus, the presence
of hypertension, gross oedema of renal origin, marked albuminuria, retinal changes
of diabetes, and sometimes renal insufficiency. Of these the history of diabetes is by far
the most constant. Albuminuria is present in about 80 to 90% of cases hypertension in
about 60 to 70% of cases and oedema in about 50% of cases. Retinal lesions have been
present in about two-thirds of the cases where ophthalmoscopic examinations were
reported. The complete nephrotic syndrome of pronounced albuminuria, extensive
oedema and low plasma proteins is present in only 6 to 8% of cases and when it is
present the retinal and glomerular lesions are severe. Significant elevation of nonprotein nitrogen in the blod is present in less than 20% of cases and death has been due
to uremia in a few instances.
The youngest case reported was in a girl of 16 years (12) and a few cases have
been reported in the 20's and 30's. However most of the cases reported have been in patients over 40 with the highest incidence in the seventh decade. The lesions are found
more commonly in females than in males.
The incidence of intercapillary glomerulosclerosis among diabetics has varied in
different reports from 18 to 63% (17, 12.). The average appears to be that about 30%
of diabetics coming to autopsy show these lesions.
The incidence of intercapillary glomerulosclerosis among • non-diabetics has been
extremely low. Diegal and Allen (16) found only one case among 200 non-diabetics,
100 of whom were hypertensives. Laipply et al (12) found only one case among 124
non-diabetic hypertensives. Various reports have indicated that about 8% of chornic
glomerulonephritis show hyaline masses similar in appearance but Allen (11) and Bell
(8) indicate that the hyaline masses in glomerulo-nephritis are not identical with those
of intercapillary glomerulosclerosis.
This it is evident that intercapillary glomerulosclerosis is highly specific for diabetes mellitus and it has been stated by Siegal and Allen (16) and by Laipply et al (12)
that intercapillary glomerulosclerosis is the most reliable criterion of the post-mortem
diagnosis of diabetes mellitus.
What is the cause of intercapillary glomerulosclerosis?  A high incidence among
diabetics suggests a causal relation but the occurence of this condition in a few cases
of non-diabtics indicates that diabetes is not the sole cause of the renal lesions. Further-
Page 325
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more there is no close correlation between severity or duration of diabetes and the
presence of intercapillary glomerulosclerosis (12). As a matter of fact it is the mild
diabetic who is more prone to develop these lesions.
All patients with intercapillary glomerulosclerosis have renal arterial or arteriolar
sclerosis of some degree. There is fairly good correlation between the severity of the
arteriolar sclerosis and the degree of intercapillary glomerulosclerosis. Newburger and
Peters (14) state that, "the pathogenesis of this condition appears to depend on severe
and extensive arterial and arteriolar degeneration associated with and perhaps resulting
in diabetes mellitus hypertension and renal damage." However, some cases of intercapillary glomerulosclerosis have only minimal arteriolar sclerosis and it is noted that
severe ateriolar sclerosis of non-diabetics is not accompanied by the lesions of intercapillary glomerulosclerosis. These two observations minimize greatly the etiologic role
of arteriolar sclerosis in the production of these lesions.
One is left with the impression that diabetes mellitus, renal arteriolar sclerosis and
renal capillary sclerosis are inter-related although one does not know which is cause
and which is effect; nor does one know what other factors may be involved.
How can we diagnose this condition? The occurrence of a full blown nephrotic
syndrome in a mild diabetic past middle life who has hypertension, retinal changes and
some renal failure is almost certainly due to intercapillary glomerulosclerosis. When
various components of this picture are missing we can only suspect the presence of
these renal lesions.
Siegal and Allen (16) state that the nephrotic syndrome in a young diabetic is
more likely to be due to chronic glomerulonephritis than to intercapillary glomerulosclerosis. Joslin's text (1) states, "Chronic glomerulonephritis is most commonly seen
among young diabetics with oedema and often in a nephrotic phase." Although one
might infer from both the above statements that chronic glomerulonephritis is relatively common in young diabetics this is not evident in various reports in the literature.
Adams (18) recently reported four young diabetics who died in uremia and whose
kidneys showed mixed vascular and inflammatory changes but no lesions of intercapillary glomerulosclerosis. The significance of this apparent difference of the juvenile
and adult diabetic in relation to the development of degenerative vascular changes
must await further elucidation.
The second group of renal lesions seen in diabetics is the group of inflammatory
It has been stated (19) that 4% of all autopsies reveal upper urinary tract infections which may or may not have been a cause of death. In autopsies on diabetics the
incidence of upper urinary tract infections has been shown to be approximately 20%
(20, 21). Various writers (20, 23) draw attention not only to the frequency of
.renal infections among diabetics but also to their chronicity and to the fact that the
majority of them appeared to be asymptomatic since they were not diagnosed during
life in two-thirds of cases.
Bow en and Kutzmann (23) carried out complete uro logic examinations on 84
unselected diabetic women between the ages of 36 and 79 without regard for complaints that would suggest trouble in the upper urinary tract. Some degree of involvement in the upper urinary tract was found in 60% of the 84 cases. Abnormal findings
in the lower urinary tract were found in 31% of cases and only about 9% of these
84 women had what was regarded as a completely normal urinary tract. Many of
these patients were asymptomatic or else their symptoms could not be differentiated
from diabetic symptoms.
Harrison and Bailey (22) compared the urine of 50 diabetics with that of 50
non-diabetics. They found bacilli in the urine 6 times as frequent and pus in the urine
5 times as frequent in diabetics as in non-diabetics.
It would therefore appear well established that the incidence of upper urinary
tract infections is higher in diabetics particularly in female diabetics and that it is
Page 326 and
often symptom-free. The route of infection is chiefly either hematogenous of uro-
genous. From various reports it is difficult to decided which route is the more common
in diabetic renal infections but Weiss and Parker (24) pointed out that, "in the
majority of instances even the combined clinical bacteriologic and histologic evidence
fails to reveal in any degree of certainty whether we are dealing with pyelonephritis
of hematogenous—urogenous—or lymphatic origin. In general it can be stated that
the two most common organisms encountered are B. Coli in the urogenous group and
Staph, aureus in the hematogenous group.
The effects of pyelonephritis on the diabetic patient are many: 1. It may cause
marked fluctuations in the control of the diabetes.
2. It may be a precipitating cause of diabetic coma.
3. In some cases it undoubtedly gives rise to hypertension and its sequelas.
4. In a few cases it cases death by uraemia or toxaemia.
The types of pyelonephritis seen are either acute or chronic with exacerbations
Since pyelonephritis is one of the few renal complications of diabetes that can be
treated effectively in its incipient stage it is of great importance that one should suspect its presence not only in cases who show unexplained fever and urinary symptoms
but in unexplained difficulty of control, etc., in patients who may hove no urinary
There is one form of acute pyelonephritis which deserves special mention. It is
a fulminating, usually fatal process which is characterized by necrosis of the renal
pyramids, especially of the papillae. This has been described since 1877 but only in
1937 was it stressed by Gunther that it is much more common among diabetics. Various names have been given to this lesion and I shall refer to it as necrotizing renal
papillitis (25). It is more common in females and is rare under the age of 40. ]£i
diabetics it may occur in either hematogenous or urogenous infection whereas in non-
diabetics it is practically limited to patients with urinary obstruction.
As a result of the necrosis the papillae may slough out and he free in the renal
pelves. Thus hematuria and renal colic may be present.
The pathogenesis is not fully understood but it is felt that the diabetic state, renal
vascular disease and the inherently poor blood supply of the renal papillae may be
contributing factors (25, 26).
It may appear as a fulminating generalized systemic infection in a person who has
been well or it may appear as a rapidly progressive fatal exacerbation of an acute pyelonephritis which has existed for some weeks and which may even have undergone
remissions. Urinary symptoms are not necessarily present but pyuria and oliguria with
azotaemia are usually present. Death is due to uraemia or septicaemia in most cases.
The incidence of necrotizing renal papillitis among diabetics is about 4.5% (25,
26); in other words about 1 in every 4 cases of pyelonephritis in diabetics coming to
autopsy show this lesions. In most cases where pyelonephritis has been losted as the
immediate cause of death in diabetics necrotizing renal papillitis has been present (25).
An analysis was attempted of diabetic autopsies in the Vancouver General Hospital for the five year period 1942 to 1946 inclusive in order to assess causes of death
and renal lesions. After excluding some cases due to lack of a positive diagnosis of
diabetes a group of 77 cases remained. Of these, 41 were male and 36 female. Their
ages ranged from 1 to 83 with the majority between 50 and 80 and the greatest incidence in the 7th decade. There were 10 cases under the age of 40.
Of the cases in which blood pressure was recorded about 40% had systolic and
diastolic hypertension taking 150/90 as the upper limit of normal. When heart
weights and/or blood pressure are taken into account approximately 63% had hypertension.
Page 327
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The clinical features of these cases is shown in Table 1. The frequency of significant urinary findings is apparent while only 5 out of 32 showed a markedly elevated
Cases Tested Present Absent
Oedema  22 13 9
Albuminuria (plus 3 or more)  65 24 31
W.B.C. in Urine (plus 2 or more)  65 30 35
Gran. Casts (plus 2 or more)  65 12 53
N.P.N. Over 60  32 13 19
N.P.N. Over 100  32 5 27
The causes of death are shown in Table 2, and compared with two other autopsied
series. The first column is a series of 429 diabetic deaths at the Baker Clinic from 1923-
1945 (1). The second column is a series of 307 diabetic deaths autopsied at the Mallory
Institute of Pathology in the years 1932-1942 inclusive (27).
Baker      Robbins      V.G.H.
||      (429) (307) (77)
1. Coma     3.0 7.2 22.0
2. Vascular
A. Cardiac Decomp. :  4.2 11.4 10.4
B. Coronary Disease    21.7 10. 16.9
C. Cerebral (Hem. or Thromb.)  4.7 4.9 6.5
D. Peripheral  12.3 4.2 6.5
E. Embolic   (Pulmonary)    \  3.5 2.3 1.3
3. Infections
A. Pulmonary     7.1 23.8 10.4
B. Others     11.7 13.7 5.2
4. Renal Dis.
A. Ac. Pyelonephritis    3.5 6.8 2.6
B. Glomerulonephritis    .  3.5 0.7 1.3
C. Others  1.5 0.7 2.6
5. Cancer  11.2 7.8 1.3
6. All Others and Unknown  12.1 6.5 13.0
It is immediately evident that a large proportion of the diabetic deaths in this
hospital are due to coma. Coma was present in 33 cases and in 17 of these it was felt
death was primarily due to coma.
It is difficult from charts and autopsy reports to be certain that a death was or
was not due to coma, and it is possible that in spite of a considerable degree of care in
analysing these cases of coma some of them should be classified under other causes of
death such as infections, either pulmonary, renal or other. Nevertheless it is apparent
that deaths from diabetic coma are unduly high in this hospital.
Of the 13 deaths due to coronary disease 11 were acute myocardial infarctions.
Three of these were male and eight female. It should be noted that arteriosclerosis
accounted for over 40% of the deaths in our group.
Of the two deaths due to acute pyelonephritis necrotizing papillitis was present in
The rest of the table needs no comment.
Of the 77 cases microscopic sections of the kidneys were availble in 23.
Page 328 *fc<
Benign   Arteriolar   Nephrosclerosis     12
Inter Capillary Glomerulosclerosis  6
Acute (or acute and chronic)  4
Necrotizing   Papillitis  3
Chronic | _  2
Chronic  Glomerulonephritis  1
Other j  3
No Significant Disease Process  4
Table 3 gives the renal lesions found in these 23 cases. Since there had been some
method of selection in having saved only 23 of the 77 sets of slides there are no conclusions to be drawn from the group.
If, .-,
Cause of Death
pi. 2
Ac. Cholecystitis
marked legs
Cong,   heart   failure
Cong, heart failure
Lobar pneum.
Cerebral Infarct.
Table four shows the clinical features o fthe six cases of intercapillary glomerulosclerosis.
Summary and Conclusions
1. Although it is agreed that arteriosclerotic vascular changes are more common
in diabetics no conclusions are made regarding senile arteriosclerotic nephrosclerosis.
2. Hypertension and the renal lesions associated with it, i.e. arteriolar nephrosclerosis are more common in diabetics than in non-diabetics.
3. The Kimmelstiel-Wilson lesion is a degenerative vascular lesion highly specific
for diabetes. It is usually associated with hypertension, oedema and albuminuria but
these are not all invariably present. Its cause is unknown. If forces our attention to the
fact that the vascular lesions associated with diabetes, be they arterial, arteriolar or
capillary, constitute the greatest problem with which we are faced in the management
of this disease. It is only in the solution of this problem that the nature of diabetes
will be understood.
4. Until the above problem is solved the complications which we can and
should prevent from taking such a toll of death are coma and infections, including
renal infections.
1. Joslin, E. P., and others. The Treatment of Diabetes Mellitus, 8th ed., Philadelphia,
Lea & Febiger.
2. Lisa, J. R., Magiday, M., Galloway, I., and Hart, J. F.: Arteriosclerosis with diabetes Mellitus; study of pathologic findings in 193 Diabetic and 2250 non-
diabetic patients, J.A.M.A., 120: 192, 1942.
3. Eisele, H. E., Juvenile Diabetic Patient Surviving 20 years. J.A.M., 120:188, 1942.
4. Root, H. F., Bland, E. F., Godron, W. H., and White, P. D., Coronary atherosclerosis in diabetes mellitus; post-mortem study. J.A.M.A., 113,27, 1939.
\ Page 329
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5. Hart, J. F., and Lisa, J. R., Diabetes Mellitus and Arteriosclerosis—The effect
of Duration and Severity on the arterial changes. New York State J. Med. 44:
2479, 1944.
6. Russek, H. I., Blood Pressure in the aged; Study of 1000 elderly male subjects.
Amer. Heart Jour. 26:11, 1943.
7. Hanssen, P., Diabetes Mellitus in Bergen Acta Med. Scandinav. Supp. 178.
Accompanying Vol. 125, 1946.
8. Bell, E, T., Renal Diseases. Philadelphia, Lea & Bebiger, 1946.
9. Wilder, R. M., Clinical Diabetes Mellitus and Hyperinsulinism, Philadelphia,
W. B. Saunders Company, 1941.
10. Kimmelstiel, P., and Wilson, C, Intercapillary Lesions in the Glomeruli of the
Kidney. Am. J. Path. 12:83, 1936.
11. Allen, A. C, So-Called Intercapillary Glomerulosclerosis, a lesion associated with
Diabetes Mellitus. Arch. Path. 32:33, 1941.
12. Laipply, T. C, Eitzen, O. and Dutra, F. R., Intercapillary Glomerulosclerosis,
Arch. Int. Med., 74:354 1944.
lh Derow, H. A., Altschule, M. D., and Schlesinger, M. J., Syndrome of Diabetes
Mellitus Hypertension and Nephrosis: Clinical and Pathological Study of Case.
New England J. Med., 221:1012, 1939.
14. Nerburger, R. A. and Peters, J. P., Intercapillary Glomerulosclerosis: Syndrome of
Diabetes Hypertension and Albuminura; Arch. Int. Med., 64:1252, 1939.
15. Porter, W. B. and Walker, H., Clinical Syndrome Associated with Intercapillary
Glomerulosclerosis, J.A.M.A., 116:459, 1941.
16. Siegal, S., and Allen, A. C, Intercapillary Glomerulosclerosis (Kimmelstiel-Wilson)
and the Nephrotic Syndrome in Diabetes Mellitus, A.J.M. Sc., 201:516, 1941.
17. Henderson, L. L., Sprane, R. G., and Wagener, H. P., Intercapillary Glomerulosclerosis, Am. J. Med,, 3:131, 1947.
18. Adams, L. J., Renal Complications in Young Diabetics, Canad. M.A.J., 57:540,
19. Ophuls, William, Statistical Survey of 3000 autopsies: From the Department of
Pathology of the Stanford University Medical School, Stanford Univ. Publ., Univ.
Series, M.Sc. 1:127, 1926.
20. Sharkey, T. P., and Root, H. F., Infection of the Urinary Tract in Diabetes,
J.A.M.A. 104:2231, 1935.
21. Baldwin, A. D. and Root, H. F., Infections of the Upper Urinary Tract in the
Diabetic Patient, New England J. Med. 223:244, 1940.
22. Harrison, J. H. and Bailey, O. T., The Significance of Necrotizing Pyelonephritis
in Diabetes Mellitus, J.A.M.A., 118:15, 1942.
23. Bowen, B. D. and Kutzman, N., The Urinary Tract in Diabetic Women; Its Contribution to the Incidence of Hypertension. Am. Int. Med., 17:427, 1942.
24. Weiss, Soma and Parker, F., Pyelonephritis: Its Relation to Vascular Lesions and
to Arterial Hypertension, Medicine 18:221, 1939.
25. Robbins, S. L., ^fallory, G. K. and Kinney, T. B., Necrotizing Renal Papillitis: A
form of Acute Pyelonephritis. New England J. Med., 235:885, 1946.
26. Edmondson, H. A., Martin, H. E., and Evans, N., Necrosis of Renal Papillae and
Acute Pyelonephritis in Diabetes Mellitus. Arch. Int. Med., 79:148, 1947.
27. Robbins, S. L., and Tucker, A. W., Jr., The Cause of Death in Diabetes, a Report"
of 307 Autopsied Cases. New England J. Med., 231:865, 1944.
Vancouver, B.C., Canada
(Publications of St. Paul's Hospital)
The choice of methods of treatment in haemangiomata of the skin depends on (1)
the present condition of the lesion, size, depth, location, amount of pigmentation, presence of ulceration, and other factors; (2) the previous history, with special reference to
other forms of treatment employed (for example, many cases have recurred after surgery, when first seen, and large scars may be present, which are difficult to treat; (3)
the pathological histology of the lesion. The present report is concerned with the management of the uncomplicated cavernous hemangioma, which is the type most susceptible
to irradiation.
This lesion is noticed at t>irth or shortly afterward. It usually enlarges rapidly in the
early months, and then becomes stationary or continues to grow slowly. At any time
it may take on more rapid growth, the cause of which is unknown, but at times this
enlargement may be associated with slight trauma. Malignant degeneration is rare in
the cavernous haemangioma and there were no cases in our series.
Superficial ulceration may be observed in larger lesion, with or without trauma, and
is probably related to the blood supply of the skin, which is in rather unstable balance.
Scarring is seen more often in these cases, and is more extensive when trauma has
occurred. This spontaneous ulceration was not a serious factor in the management of
the present series. No hard, fixed scars, and no tendency to keloid were seen in these
cases. Most cases observed occur on the face and other exposed parts of the body, but
in young children—largest group—the parents are often concerned about recent growth
of the lesion and possible serious consequences, as well as the child's appearance. A good
cosmetic result is especially desirable in facial naevi, and with the cavernous type complete disappearance, with little or no trace of permanent change in the overlying skin,
can be expected.
Cases that have been previously treated by other means and are complicated by
scar tissue will show some residual increase in fibrous tissue elements. In some locations,
regional atrophy of the surrounding tissues may be seen. This should be remembered in
the young child, in locations like the lip or tongue, where asymmetry from this cause
might result. This susceptibility of adjacent tissues to irradiation is a factor in the choice
of heavily filtered radium rather than x-rays. Distortion of the soft parts of the lesion
itself, particularly about the mouth and eyelids, is rapidly corrected as the haemangioma
resolves. In lesions involving the scalp, hair loss has been temporary. Even in large
growths, the site was found to be completely covered by hair within a few months.
Radio-sensitivity is the rule in scalp lesions, but on the hands they may be found to be
quite resistant. This is particularly true on the extensor surfaces where the skin is thin,
and the blood supply vulnerable; and should infection complicate the treatment, slow
healing with moderate scar tissue is almost inevitable.
Each patient is individualized as much as possible, and it is not possible to give
detailed dosage for all, as this depends on many factors, e.g., age, size, depth of lesion,
previous treatment, etc. Severe generalized tissue reactions were not observed. Occasionally a mild toxic condition may develop in a patient with a large lesion, and a mild
Page 331
- v.:-JV..!.
l&tfL *
• "•
generalized erythema or a patchy eczema may be seen. This clears rapidly in a few days,
as a rule. Local erythema is not usual with our technique, but occasional slight burning
or itching may be experienced during the second week following treatment. The mother
is warned to prevent the child from rubbing or scratching the area at this time. Slight
superficial ulceration occurred in a few cases, but with healing the amount of scar tissue
was minimal, and the end result not unfavourably affected. Evenness of application and
uniform dosage to the lesion is aimed at in all cases.
In cases where there is considerable tumour mass, maximum dosage of about 2/3
E.D. is sought for the deeper layers, and in these cases the radium needles are implanted
5 and 10 mg. strength, platinum 0.5 mg. filtration. Radon seeds were not employed in
any case, owing to the undesirability of leaving a foreign body in a mass of this character.
The best general rule is to avoid over-dosage. Repeated treatments are employed where
the initial application falls short of the ideal. Sufficient time—four to six months—
should pass, however, before the initial result is judged insufficient. At the angle of the
jaw, due consideration is given to the underlying parotid gland, and a residual mass in the
deeper layers may have to be accepted.
Before employing radium interstitially, Luminal, gr. l*/2, is given the young child,
and small holes made through the uninvolved skin around the lesion, with a sharp trocar. The needle is immediately inserted, and no bleeding occurs, either at this time or
later when the needle is removed. As in the case of contact radium, the mother remains
with the child, which usually sleeps through the period of treatment, under close repeated observation.
A few case reports are appended, illustrating the main types of lesions encountered,
and some details of their therapeutic management:
CASE 1. Miss J.G., aged 17. Lesion 5 cm. in diameter, posteromedial left thigh.
Present since birth, and gradually increasing in depth, with slight surface ulceration in
some areas that intermittently bleed and heal. July 4, 1944, fourteen 10 mg. radium element incerts in peripheral area and six 5 mg. inserts centrally, all platinum 0.5 mm.
filtration. Time 4 hours. Total dosage, 700 mg.-hours, Biopsy confirmed diagnosis of
thin-walled venous type of congenital nxvus.
Follow-up examination showed progressive healing following complete desquamation. Observation February 25, 1945, showed complete disappearance of the mass, with
smooth thin resolving scar.
This case illustrates the use of interstitial radium in a large deep lesion in an adult,
in a non-exposed area. Single treatment was effective, and thin superficial scar resulted,
without any disfigurement or tendency to keloid.
CASE 2. Baby A.F., aged 9 months. Cavernous type of congenital naevus, with
some superficial vessel dilatation, and pigmentation as well. The lesion covers the volar
surface of the distal forearm, extending to the wrist. Measurments, 4 cm. by 7 cm.
Treatment, April 3, 1944: eleven 10 mg. needles, platinum .5 plus three 10 mg.,
platinum, 1.0 mm. filtration, distance 4 mm. Time 5 hours. Total dosage 70 mg.-
No reaction was observed, and repeated observations showed considerable resolution on the periphery—but the central area on January 3, 1945, was noted as showing
residual thickening and pigmentation. Further treatment was given.' Six 10 mg. platinum 0.5 m., with the addition of Pb to 1.5 mg., was applied, contact method, for
4% hours, 255 mg.-hours.
Follow-up observations showed marked improvement, and on May 1, 1946, the
resolution was practically complete, only very faint pigment increase in superficial skin
This is a typical excellent result, following the use of heavily filtered radium, contact method. Two treatments, nine months apart, were required before final resolution
of the large mass. A smaller dose would have to be accepted had the lesion been on an
extensor surface.
Page 3 32 CASE III. Baby F.R. A raised and slightly pigmented naevus, left malar region,
measuring 3.5x3.0 cm. The lesion had received several treatments with carbon dioxide
snow, without result. Dilatation of the deeper vessels was observed, and radium was
advised. April 3, 1943, five 10 mg. and one 5 mg. radium inserts were used. Time 2
hours, 20 minutes. Total dosage 130 mg.-hours. Repeated examinations showed complete resolution and blanching of the overlying skin by December, 1943—after eight
months. On examination two years later, the area approximated normal.
In this case inserts were employed, and proved ideal. A scar was feared, as other
methods of treatment had been employed previously, but resolution was complete, with
no residual scar.
CASE IV. Baby GN., aged five months. Small lesion, measuring 0.8 cm. in diameter,
lower lip, mucous surface, to the left of the midline, present since birth. Again inserts
were employed. Three 10 mg., platinum 0.5 mm. needles for 3 hours, 15 minutes. Total
dose 10 mg.-hours, November 3, 1944. On April 2, 1946, following repeated observations of progressive resolution, the lesion had entirely disappeared. Follow-up examination was still advised, but atrophy of the left lower lip area not anticipated, due to
heavy filtration employed. ,
CASE V. Baby J.M., aged 7l/z months. Naevus, measuring 2.0x1.7 cm., in the
scalp, region of the anterior fontanelle. Rate of growth was in proportion to growth of
child's head. Deeper layers were dilated, with slight pigmentation in the cengral area.
Six 10 mg. radium needles, platinum 1.0 mg. filtration, were applied by contact
method for 2 hours, 40 minutes. Dosage 160 mg.-hours, April 29, 1944. Repeated observations showed recession without erythema. The hair came out temporarily, but soon
grew in again, and one year after treatment, resolution was complete—pigmentation or
mass observed. The hair over the treated area remained somewhat thinner in texture.
This case illustrates the usual good response of scalp lesions, which are relatively
radiosensitive. ,
CASE VI. Baby L. McN., aged 6 months. This child was first seen in November,
1940 with cavernous naevi, episternal region, 5x6 cm., and right cheek, buccal surface,
6 cm. in diameter. The anterior chest area received 1950 mg.-hours, with a radium pack,
comprising 170 mg., platinum 1.0 filtration at 2.5 cm. distance, and the right cheek
50 mg., platinum 0.5 mg. inserts, total 135 mg.-hours. After follow-up examination, it
was decided to treat the chest area again on April, 1941, 5 months later. The episternal
area received 60 mg. contact radium. Platinum 1.5 filtration for 2 hours, total 120 mg.-
hours. Subsequent observations confirmed complete resolution and on April 8, 1946,
5^4 years after the first treatment, the condition in both areas was quite normal. One
noted the long period of observation with no recurrence or residual atrophy.
CASE VII. Baby A.B. Cavernous naevus involving entire upper left eyelid, present
since birth, and not growing. Radium 10 mg., platinum 10 mg., platinum 1.0 mm.
inserts were used. Time 3 1/3 hours. Dosage 133 mg.-hours. Slight erythema with superficial ulceration was observed, but healed rapidly. The lesion showed marked resolution,
without complication.
These cases are presented to show the variety of problems persented by these
patients, and the necessity for individualizing treatment in each case.
Problems in the management of the common haemangioma are discussed and a few
case histories given to illustrate uncomplicated cases.
St. Paul's Hospital.
Read at the 1948 meeting of the Pacific North West Radiology Society in Vancouver, B.C.
Page 3 3 3 1&OT
We regret to record the sudden and tragic death of Dr. W. A. Finlayson of
Vernon. Born in Edinburgh, Dr. Finlayson came to B.C. with his family at an early age.
He won the Governor-General's matriculation award on his graduation from High
School, and returned to Edinburgh for medical training, graduating in 1938. He joined
the Canadian Army Medical Corps in the first week of war and served until the end of
action. After two years post-graduate work he commenced practise in Vernon. We
extend our sincere sympathy to Mrs. Finlayson and family.
Dr. J. W. Laing is now the Senior Pensions Medical Examiner for British Columbia.
He replaced Dr. B. F. Keillor who has retired.
Dr. W. Roy Walker formerly of Premier is now practising in Penticton.
We regret to record the passing of Dr. A. S. Simpson. He graduated from McGill
in 1901 and has practised in this Province since 1928. Sincere sympathy is extended to
Mrs. Simpson and family.
Dr. J. B. Gendron has left Vancouver to take up practice at Beattie Anchorage.
Dr. P. W. Jaron of Cranbrook is now residing in Premier.
Dr. J. G. McPhee formerly of Penticton has accepted a post with The Mason Clinic
in Seattle, Washington.
Deepest sympathy is extended to Dr. W. B. McKechnie on the death of his wife,
and to Dr. J. F. Minnes on the death of his mother.
We note the appointment of Dr. H. Bruce McEwen as the first Medical Director
of the Royal Columbia Hospital.
Congratulations are extended to the following doctors and their wives on their
recent good fortune:
Dr. and Mrs. J. F. Arthur—a son.
Dr. and Mrs. H. C. Caple—a son.
Dr. and Mrs. H. Dumont—a son.
Dr. and Mrs. H. Emanuele—a son.
Dr. and Mrs. J. W. Frost—a son.
Dr. and Mrs. A. F. Hardyment—a daughter.
Dr. and Mrs. R. H. Irish—a son.
Dr. and Mrs. M. D. Wall—a son.
Sir William Fletcher Shaw of Manchester, who was one of the guest speakers at the
Annual Summer School this year, has forwarded a donation to the B.C. Flood Emergency
Fund. Sir William was here when the floods were at their height and his thoughtful gesture is much appreciated.
Miss E. J. ELY
Members of Canadian "Physiotherapy Association
CEdar 6644
Chartered Physiotherapists (B.C.)
1470 West 12th Ave., Vancouver, B.C.
Page 334


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