History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: August, 1953 Vancouver Medical Association Aug 31, 1953

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 B uIl L_He!t I N
h&# The Vaneovtver Medical Association
EDITOR
dr. "j. h. MacDermot
EDITORIAL BOARD
DR.  D.  E.  H.  CLEVELAND DR.  J.  H.  B.  GRANT
DR. H. A. DesBRISAY DR.  J. L.  McMILLAN
Publisher and Advertising Manager
W. E. G. MACDONALD
OLUME XXIX.
AUGUST, 1953
NUMBER
Dr. D. S. Munroe
President
Dr. George Langley
Hon. Treasurer
OFFICERS 1953-54
Dr. J. H. Black
Vice-President
Dr. E. C. McCoy
Past President
Dr. F. S. Hobbs
Hon. Secretary
Additional Members of Executive:
Dr. R. A. Gilchrist Dr. A. F. Hardyment
TRUSTEES
Dr. G. H. Clement Dr. Murray Blair Dr. W. J. Dorrance
Auditors: R. H. X. Whiting. Chartered Accountant
SECTIONS
Eye, Ear, Nose and Throat
Dr. W. M. G. Wilson Chairman Dr. W. Ronald Taylor Secretary
Dr. J. H. B. Grant
Paediatric
-Chairman Dr. A. F. Hardyment.... Secretary
Orthopaedic and Traitmatic Surgery ^jp
Dr. W. H. Fahrxi   .^2.—-.Chairman Dr. J. W. Sparkes _4$S_-Secretary
Neurology and Psychiatry
Dr, A. J. WARREN-jSM^Chairman Dr. T. G. B. Caunt fe. Secretary
Pr. W. L. Sloan
Radiology
.Chairman Dr. L. W. B. Card Secretary
STANDING COMMITTEES
Library
Dr. D. W. Moffat, Chairman; Dr. R. J. Cowan, Secretary;  Dr. W. F. Bie;
Dr. C. E. G. Gould ; Dr. W. C. Gibson ; Dr. M. D. Young.
Summer School    ' |^
Db. S. L. Williams, Chairman; Db. J.- A. Elliot, Secretary;
Dr. J. A. Ibvine; Db. E. A. Jones; Db. Max Fbost; Db. E. F. Wobd
Medical Economics
i Db. E. A. Jones, Chairman; Db. W. FowleB, Db. F. W. Hublburt, Dr. R. Langston,
mbi-   Db. Robebt Stanley, Db. F. B. Thomson, Db. W. J. Dobbance
Credentials
Db. Henby Scott, Db. J.-C? Gbimson, Db. E. C. McCoy.
V.O.N. Advisory Committee
Db. Isabel Day, Db. D- M. Whitelaw, Db. R. Whitman
Representative to the Vancouver Board of Trade:  Db. J. Howabd Black
Representative to the Greater Vancouver Health League: Dr. W. H. Cockcboft
[WJtthed  monthly  at  Vancouver,   Canada.     Authorized  as   second   class   mail,   Post   Office  Department,
1 ;~**-:- IlitSllNSIf " * Ottawa,- One- - ": 4|plJr;^P^^7   5^^^ ^^
Page 471 ASSISTANT REQUIRED
in northern practice at Terrace, B.C, Salary $600.00 per month with
living accommodation available, busy growing community. Contact
Dr. R. Hicks, Terrace, B.C.
L^anada J   //lost   Ulnique /si
v
>edor<
t
WALLACE   ISLAND
A glorious vacation adventure awaits you . . . An entire privately-owned:
island exclusively your holiday domain.   Miles of enchanting trails, colorful
shoreline, hidden coves and lovely beaches ... all inviting exploration.
Deluxe Cottages—privately located. Perfect for families. Safe, sandy beaches for
children. Excellent fishing. Recreational activities. WRITE TODAY FOR
COLOR FOLDER.
Telephone WALLACE ISLAND now for reservations and information
WALLACE    ISLAND
c/o GANGES, B.C.
David B. Conover, Mgr.
1 x/z hr. scenic drive from Victoria — Princess Elaine from Vancouver
or direct plane service.
PURITAN BABY MEATS
Meat used in ail PURITAN BABY FOOD is finest quality.
All meat is carefully trimmed to remove fat and gristle,
then properly cooked with only salt and broth added.
The texture and consistency of PURITAN strained meats for babies
is as specified by leading pediatricians. It never varies. It is easily
swallowed by very small babies, and quickly digested and assimilated
into their systems. Also the manufacturing process removes none
of the meat's nutritional values.
VITAMIN, PROTEIN AND MINERAL CONTENT
Puritan Baby Meats contain iron, phosphorous and vitamin A and
B complex in full strength so that healthy growth of the baby is
assured.
Your Doctor will tell you when
to start your baby on Puritan Meat
m JUST HEAT AND SERVE '«|      i
Keep unused portion covered in your refrigerator.
SIZE: 3V_ OZS. (approx. 2 servings)
AVAILABLE AT ALL DRUG AND GROCERY STORES
100% B.C. Owned and Operated
Page 472 HOSPITAL CLINICS
VANCOUVER  GENERAL HOSPITAL
Regular Weekly Fixtures in the Lecture Hall
Monday, 8:00 a.m.—Orthopaedic Clinic.
Monday, 12:15 p.m.—Surgical Clinic.
Tuesday—9:00 a.m.—Obstetrics and Gynaecology Conference.
Wednesday, 9:00 a.m.—Clinicopathological Conference.
Thursday, 9:00 a.m.—Medical Clinic.
12:00 noon—Clinicopathological Conference on Newborns.
Friday, 9:00 a.m.—Paediatric Clinic.
Saturday, 9:00 a.m.—Neurosurgery Clinic.
ST. PAUL'S  HOSPITAL
Regular Weekly Fixtures
12nd Monday of each month—2 p.m. Tumour Clinic
Tuesday—9-10 a.m. . I Paediatric Conference
Wednesday—9-10 a.m. Medical Clinic
Wednesday—11-12 a.m Obstetrics and Gynaecology Clinic
Alternate Wednesdays—12 noon Orthopaedic Clinic
Alernate Thursdays—11 a.m Pathological Conference (Specimens and Discussion)
Friday—8 a.m Clinico-Pathological Conference
(Alternating with Surgery)
Alternate Fridays—8 a.m Surgical Conference
Fridays—9 a.m Dr. Appleby's Surgery Clinic
Friday—11 a.m Interesting Films Shown in X-ray Department
SHAUGHNESSY  HOSPITAL
Regular Weekly Fixtures
Tuesday, 8:30 a.m.—Dermatology. Monday, 11:00 a.m.—Psychiatry.
Wednesday, 10:45 a.m.—General Medicine. Friday, 8:30 a.m.—Chest Conference.
Wednesday, 12:30 p.m.—Pathology. Friday, 1:15 p.m.—Surgery.
BRITISH  COLUMBIA  CANCER  INSTITUTE
2656 Heather Street
Vancouver, British Columbia
SCHEDULE OF CLINICS—As at June,  1953
MONDAY: 9 a.m.—10 a.m Nose and Throat Clinic
TUESDAY: 9 a.m.—10 a.m j Clinical Meeting
THURSDAY: 11 a.m.—12 a.m Gynaecological Clinic
(not during summer months)
FRIDAY: 9 a.m.—10 a.m.  j -Skin Clinic
9 a.m.—10 a.m.  Lymphoma Clinic
DAILY: 11:45 a.m.—12:45 a.m.       cfe.v, -W£': Therapy Conference
Page 475 CANADA'S FIRST AND FOREMOST
PROFESSIONAL PHARMACY
icriplions
Medical Dental Building
PA. 4141
^Jree (~*ity JLJelivery and ^Tree f-'rovincial f^o&taeu
Page 476 VANCOUVER HEALTH DEPARTMENT
STATISTICS—APRIL,  1953
|Total population   (estimated) j .._- 390,325
June,
Number
?Total deaths (by occurrence)     338
Deaths,  residents  only 309
1953
Rate per
1000 pop.
10.4
9.5
Birth Registrations—residents and non-residents  (includes late registrations)     403
Male ______ - . H .     3 68
itFemale ! ^ 	
June,   1953
[infant Mortality—residents only
Deaths under 1 year of age	
Death rate per 1000 live births	
Stillbirths   (not included in above item).
771
5
8.6
7
23.7
CASES OF COMMUNICABLE DISEASES REPORTED IN CITY
June, 1953
s Chickenpox	
iDiphtheria	
Diphtheria  Carriers
[Dysentery	
£ Dysentery Carriers .
erysipelas
Cases
144
-Gonnorrhoea	
Infectious Jaundice
Measles	
  1
  80
  15
 J§ 140
Meningitis   (meningococcic)  —
[Mumps g*_' -  222
  1
  8
  10
^Poliomyelitis	
[Rubella 1	
Salmonellosis	
[Salmonellosis Carriers	
[Scarlet  Fever	
■Syphilis	
Tetanus	
Tuberculosis	
Typhoid  Fever   ,    .
Pyphoid Fever Carriers.
Undulant  Fever	
Whooping Cough 	
33
7
29
OTHER REPORTABLE DISEASES
Cancer i	
Deaths
Cases
145
June, 1952
Deaths
1
129
82
98
6
17
101
11
37
1
7
128
61
128
65
iHouttt pirasant Chapel
FUNERAL    SERVICE
Kingsway at Hth Ave. — Telephone EMerald 2161
Vancouver 10,  B.C.
flfot pleasant TOnbertafcina Co. Xtb.
Page 477 -C CONNAUGHT >
—FOR PROLONGED ACTION—
CORTICOTROPHIN (acw
with
PROTAMINE  and  ZINC
Corticotrophin with Protamine and Zinc, for prolonged action and in a
form convenient for use, is now available from the Laboratories. The
product is prepared as a milky suspension in aqueous medium and is ready]
for use after shaking. In clinical investigations, two injections per day!
have been found to replace adequately four daily injections of regular!
Corticotrophin (ACTH). In some cases even greater prolongation of effectj
may be experienced.
Corticotrophin with Protamine and Zinc is prepared with ingredients!
whose properties are of established value in parenteral administration.
The Connaught Medical Research Laboratories now provide Cortico-j
trophin (ACTH) in three forms—a dried powder, a sterile solution, andj
a suspension with prolonged-action properties.
HOW SUPPLIED
Dry Powder —10 International Units per Vial
—25 International Units per Vial
Sterile Solution   —10-cc. vial (20 I.U. per cc.)
Prolonged-acting
Suspension       —10-cc. vial (40 I.U. per cc.)
CONNAUGHT   MEDICAL   RESEARCH   LABORATORIES
University of Toronto Toronto, Canada
Established  in  1914 for Public Service  through  Medical Research and  the  development
of Product* for Prevention or Treatment of Disease.
DEPOT FOR BRITISH COLUMBIA
MACDDNALD'S    PRESCRIPTIONS    LIMITED
MEDICAL-DENTAL BUILDING, VANCOUVER, B.C
Page 478 The other day in the mail we received a letter with regard to the extension of
M.S.A. privileges to those who work in doctors' offices, as receptionists, nurses, technicians and so on. We presume that each of these is entitled to a beneficiary on payment
of a due amount.
This is admirable, and we are all for it. But as we read it, the thought occurred
to us—why can every member of the working classes, amongst which we include ourselves, get prepaid medical care, except the doctors themselves and their families? And
a further thought struck us—why-don't we make provision for the medical care of
ourselves and our families? Why do we, and especially why do our families, have to
ask somebody to give us for nothing a service that costs money, and sometimes much
money, to give—a service for which every other member of the community is expected
to pay, unless he is willing or forced to acecpt charity?
Tradition dies hard, and we so often cling for so long to a tradition which has lost
its meaning, and has become a shackle, rather than a tradition.
It has been a noble tradition in the profession of medicine, for a long time, that
no member of the craft would ever accept payment for the care of another physician
or any of the members of his family. We cannot but honour the spirit behind the tradition but there are several reasons why this tradition has become, to say the least of it,
very shopworn: and why it has even become an unfair and often a burdensome load
on some few men's shoulders and its acceptance a burden to those who receive it.
Till thirty or forty years ago, the practice of medicine was a comparatively simple
thing. The average medical man, even the specialist, of whom there were few, carried
his equipment mainly in his head, under his hat, where he kept his stethoscope, or in
his pockets.   His investment, except in his education, was small.
But to-day it is very different. The range of medical'knowledge has grown very
greatly, and with it has grown the use of technical methods and technical devices. B.P.,
E.K.G., B.M.R., X-rays, C.B.C., S.R., E.E.G., all the letters of the alphabet—are all
parts of the routine examination by the specialist, of nearly every patient that comes
his way: together with many other laboratory and other techniques.
And all this means a very large investment on the part of the specialist. Now,
when we or our folk are sick, we naturally go to a specialist. Our own experience has
always been that such a specialist begins by making one feel that the fact that we
consulted him was the only thing necessary to make his day perfect—he goes on to
load one down with kindness, and the very best he has to give in the way of service.
He lives up to the tradition to the letter, and in the letter, and in the spirit, and
nobody can deny that. After he has saved our life, or removed our gall bladder, or put
us on our feet generally, we are at our wit's end to find some suitable way of acknowledging the debt we owe,—rthe debt of which we are so deeply conscious. The net result
varies from a case of Scotch to a gold watch, or a new four iron.
But is this the right way to do things? As we read past medical history—we read
Ithat in days gone by, no doctor ever charged a fee—he accepted an honorarium, coyly
slipped into his hand as he left the sick room. We have got over all that foolishness,
as regards patients at any rate.   Is it not time that we thought further?
For the trouble is, that the load falls on a few men—as we all know. A few men,
who have high repute, not only with the public, but even more so with us who,
physicians ourselves, know their true worth—tend to carry most of the load: and we
have heard of many cases which we think bear out the point we are trying to make
—no complaint comes from them, you may be sure, but the injustice exists nevertheless.
Page 479 And what of our wives, and our families, who have to consult these men, and want
to consult them—but feel, often, very hesitant about doing so because they feel that
they are taking up time and accepting service for which they are not allowed to pay.
From what we have heard many times, we know that this is the feeling of many who
come into this category.
Why do we not face this fact honestly and squarely, and settle it in the right
way. In old days, there were no prepaid plans, there was no hospital insurance, no
sickness insurance to be obtained. Incidentally, doctors and their families buy hospital
insurance, sickness and accident insurance, automobile insurance and so on. Nobody!
else lets them off any of their obligations.
We feel that this condition should be faced, and studied. There are, even now,
prepaid plans that we could join and surely all the approved plans could be made
available by some means. Personally, we took out such insurance a few years ago.
There have been operations and accidents and sicknesses in our family since then, and
one of the greatest satisfactions we have had is the fact that not only did our hospital
and nursing and drug bills get paid but our surgeons got paid, and our doctors got paid.
They didn't want to take it (dear old tradition) but out of deference to our pleas in
the matter (we had already paid for it)  they took it and everyone was happy.
There is only one way in which this can be done impersonally and without any
unpleasantness. This is through a membership in a prepaid plan. So we hope that some
day, a scheme will be worked out whereby it will be possible for medical men and their
families to be insured against sickness, in such a way that all their bills will be paid.
We feel sure that it will be a great improvement—and everyone concerned will feel
happier about it. We suggest to our already overburdened Comniittee on Economics
that they investigate this further.
NEW REGISTRANTS IN BRITISH COLUMBIA
June 27, 1953
June 29, 1953
July 2, 1953
July 2, 1953
July 8, 1953
July
July
July
July
July
July
July
July
July
July
July
July
July
July
July
July
July
July
July
July
8, 1953
8, 1953
8, 1953
9, 1953
8, 1953
15, 1953
20, 1953
20, 1953
21, 1953
22, 1953
23, 1953
23, 1953
23, 1953
23, 1953
23, 1953
24, 1953
24, 1953
27, 1953
28, 1953
28, 1953
DUTHIE, George Alexander, Invermere, B.C.
ROBINSON, Harold Speers, B. C. Cancer Institute, Vancouver, B.C.
ROBERTSHAW, Arthur Moorehouse, Cassiar Asbestos Corp.,
Watson Lake, Y.T.
ROBERTSON, Gordon Waldron, Bralorne, B.C.
GOULDEN, Leila, c/o Miller Bay, B.C.  Certified Diagnostic Radiology, Royal
College of Physicians & Surgeons of Canada—1949.
REESE, Lionel, c/o K. C. Boyce, 3914 W. 13 th Ave., Vancouver, B.C.
HOLLINGER, Donald Manley, The C. S. Williams Clinic, Trail, B.C.
McKIM, Anson. Temp. 4027 W.  14th Ave., Vancouver, B.C.
RINGWOOD, John Brain, Williams Lake, B.C.
HOWELL, George Rennie, Miller Bay, B.C.
COESTSEE, Ivan Michael, Shaughnessy Hospital, Vancouver, B.C.
DARBY, George Howard, R. W. Large Memorial Hospital, Bella Bella, B.C
ASHBY, Roy Morton, 941 Clent St., Victoria, B.C.
BLOOMFIELD, Joseph Robert, 5798 Victoria Drive, Vancouver, B.C.
CALVERLEY, Milton Oscar, Prov. Mental Hospital, Essondale, B.C.
MOLONEY, Patrick James, Campbell River, B.C.
HUMES, Harry Gordon, Mission, B.C.
ADAMS, Douglas George, 635 Fort St., Victoria, B.C.
LAYNG, John McLean, 8897 Osier St., Vancouver, B.C.
MEDDLETON, Kenneth Robert, Medical-Legal Bldg., White Rock, B.C.
AIKINS, Joseph Anthony, Quesnel, B.C.
WARWICK, William Elmer, 941 Clent St., Victoria, B.C.
CARPENTER, John Calvin, The Medical Associate Clinic, Nelson, B.C.
COLEMAN, Dennis Cleeve, 306 Royal Trust Bldg., Victoria, B.C.
MacDONALD, Donald Arthur, Box 70, Langley Prairie, B.C.
Page 480 THE TREATMENT OF BONE TUMOURS
By SIR STANFORD CADE, k.b.e., c.b., f.r.c.s., m.r.c.p., f.f.r.
Paper given at the Refresher Course on Malignant Disease held at the British Columbia Cancer Institute
October,  1952
Surgeon, Westminster Hospital, London, England
Although there is no single method of treatment which today offers great hope
pi arresting or controlling the course of a primary malignant bone tumour, much has
been learned in recent years about their natural history, their response to surgery and
to radiation and the possibilities of combining both these methods of treatment.
In this talk, I will limit my remarks to one type of bone tumour: the osteogenic
sarcoma. It is, in fact, the commonest sarcoma of bone. The term "osteogenic" was
coined in 1920 by Ewing, and accepted by the registry of bone tumours of the
American College of Surgeons. It means a tumour derived from tissue destined to
become bone; it does not mean a bone forming tumour. The older terms "periosteal
sarcoma" and "endosteal sarcoma" are of anatomical and not clinical or pathological
significance; they indicate only that the tumour has a greater tendency to spread outside
the bone or inside it.
Osteogenic sarcoma is a well known clinical entity; it is essentially a disease of
khe younger age group; the commonest age being 10 to 20 years. It can be said with
truth that in the older age group, above the age of 50 it only occurs as a secondary
development in a pre-existing bone lesion, such as Paget's Disease of bone, or an old
standing benign chondroma. The other types of primary malignant bone tumours show
a somewhat different age incidence.
\Site
As to site, osteogenic sarcoma affects all bones: the long bones of the limbs, the
flat bones of the pelvic or shoulder girdles, the skull bones and the vertebral column.
It shows, however, a great predilection for the long bones, and of these the lower end
of the femur and the upper end of the tibia are the most common sites and account
for 50 per cent o£ all osteogenic sarcoma.
Histology
There is a marked pleomorphism in the histological structure of the tumour; thus
bone, cartilage, osteoid and fibrous tissue and some giant cells are found, but as a rule
these are the matrix or stroma, the tumour itself being composed of spindle cells. I
share the opinion of those pathologists who postulate that an osteogenic sarcoma must
of necessity be a spindle celled tumour, and if a tumour of bone is a round celled
tumour, it is not an osteogenic sarcoma. Of the many cells which account for pleomorphism, cartilage is of interest. The amount of cartilage in a given tumour varies,
some have none, others a little, others again are composed mostly of cartilage. Yet the
terms chondrosarcoma and fibrosarcoma do not denote different tumour entities, merely
a different cell structure. The terms "primary" and "secondary" chondrosarcoma mean
that the tumour containing a large amount of cartilage is derived either from a normal
bone or a pre-existing benign cartilaginous tumour.
Effect of Tumour on the Parent Bone
An osteogenic sarcoma can destroy bone, form bone, alter the parent bone by
sclerosis or osteolysis. In very vascular tumours, there may be complete absorption
of a part of the parent bone. In the sclerosing varieties, the shape of the bone may
remain unaltered, the tumour remaining within the periosteal envelope. Some osteogenic
sarcomata lift the periosteum, spread through it and involve the surrounding soft
tissues. Bone absorption in one part and deposition of bone in another also happen
concurrently.
Page 481 X-Ray Appearances
These variations of the effect of bone sarcoma on the bone are reflected ht the
X-ray appearances. The main radiological features are the sun-ray spicules at nght
angles to the main axis of the bone, Codman's triangle indicating a stripping olthe
periosteum, longitudinal new bone formation (onion peel layers), sclerosis, osteolysis,
calcification in surrounding soft tissue. Any combination of two or more of fcese
changes can be present. There is, in fact, the single X-ray appearance characteristic of
the tumour, but a combination of features which depend on the morbid anatomy of the
tumours.
Plain X-ray films are of great value, but in addition tomographic studies and
arteriograms are helpful. Specially is this the case when the diagnosis is in doubt and
the alternative, such as low grade osteomyelitis, subperiosteal haematoma, or fene
other form of bone dyscrasia such as fibrous dysplasia are possible differential diagnosis.
Spread of the Tumour
It is well known that osteogenic sarcoma gives rise to pulmonary metastases and
this is, in fact, the common cause of death. In addition metastases occur in other
bones, and occasionally in lymph nodes. The disease also spreads along the shaft of the
bone, attacks and destroys both epiphyseal and articular cartilage and the surrounding
soft tissues. The metastases both in the iungs and in the lymph nodes and the extension
into surrounding soft tissue mimic the original type as regards bone or cartilage forming
properties.
Biopsy
There is considerable controversy as regards the safety of biopsy. Biopsy is of value
to establish the nature of the tumour, to differentiate osteogenic sarcoma from other
primary bone tumours and from metastases. Biopsy is an essential when ablation of a
limb is contemplated. It is less essential when conservative treatment, viz. radio-therapy
is decided upon.
Treatment
The time honoured treatment of osteogenic sarcoma is amputation. Yet byMself
amputation has given a very small proportion of five-year survival and does not seem
to affect the subsequent occurrence of pulmonary metastases. It is this dissatisfaction
with the results of amputation as the sole method of treatment which has prompted the
trial of radiotherapy either alone or as a pre-operative measure. A. B. Ferguson (1940)
brought to notice that delay in amputation in cases of osteogenic sarcoma did not
seem to be as harmful as delay in treatment in other forms of cancer. His observations
on 400 cases drove him to the conclusion that amputation should not be done at an
early stage of the disease. In Ferguson's series early amputation resulted in only a 5 per
cent five-year survival, whereas delayed amputation showed 34 per cent of five-year
freedom from symptoms.
These observations encourage the use of radiotherapy. It seems clear that the
delay caused by radiation is not detrimental to the patient and, in fact, may improve
his chances.
Effect of Radiation on Osteogenic Sarcoma
Radiation affects the rate of the growth of the tumour, diminishes or stops mitosis,
promotes healing as seen in the radiological changes in osteolytic and other lesions,
leads to shrinkage of the tumour and relieves pain. To obtain these effects it has been
shown that considerable tissue doses of radiation are required—600Or to 8000r, or
more. Such doses have been given by teleradium and by supervoltage X-rays, with but
minimal damage to the skin and normal tissues. With smaller doses the effects on the
tumour are less marked and not lasting.
In the limbs where amputation is possible, radiotherapy can in all cases be considered as a pre-operative measure and the effect of the treatment observed for several
Page 482 months without harm to the patient. Regression of the tumour and radiological evidence
of repair are indications for delaying amputation for as long as the beneficial effects
last. Lack or response or progress of the tumour in spite of the treatments indicate that
amputation is inevitable.
The level of amputation depends upon the site of the tumour. In the case of the
humerus or the femur, disarticulation at hip or shoulder for tumours at the distal end,
er a forequarter or hindquarter amputation for tumours at the proximal end of the
bone are the operations of choice.
I In the absence of pulmonary metastases, no radiotherapy should be given to the
chest, as prophylactic treatment. It has proved of no value, and should subsequent
metastases develop, handicaps the treatment of the chest.
Summary
\ No extravagant claims for radiotherapy in the treatment of osteogenic sarcoma
are made, but radiation with high tumour doses can in a proportion of patients control
the disease and lead to the arrest of growth and regression of the tumour. In some cases,
the radiological appearance of the affected bone shows a return to near-normal state.
The delay in amputation due to the treatment and subsequent period of observation does
not seem to affect adversely the ultimate prognosis. A combination of pre-operative
radiotherapy and subsequent amputation if the tumour shows activity or no response is
advised.
Discussion following Sir Stanford's paper on Treatment of Bone Tumours
\ Question'. I would like to ask your opinion with respect to biopsy of bone tumours.
Some people, as you know, think that biopsy is dangerous, and should not be done. I
would like to hear your opinion on that view, and also if biopsy is done, whether it
should be an open biopsy, or a needle aspiration biopsy.
Sir Stanford's reply: The first prerequisite of a biopsy is to provide the pathologist
with a sufficient quantity of normal and abnormal bone to express an opinion. He is
no magician. Punch biopsy sometimes comes off in a Ewing's Tumour which is a
round cell tumour, or in an osteoclastoma or a giant cell tumour. But I would not
commit myself on a punch biopsy in an osteogenic sarcoma. So the answer is—if you
are going to do a biopsy, do it widely, put a tourniquet on if possible, make a very big
incision, expose the tumour, cut out the piece with a diathermy needle—a big chunk—
stop the bleeding by electro-diathermy, close the wound. That is the way to do a
biopsy. It is a minor orthopaedic operation. There is no more to it than doing a
cartilage in a knee, but you must provide a big piece for the pathologist, or you will
get no answer. Secondly, you must realize that if you do a biopsy, and you don't
treat the tumour afterwards, it will most likely fungate through the biopsy scar as
you have laid open the periosteum, and deep fascia covering the tumour, without
controlling its growth. Biopsy should be done when amputation is contemplated. If
you are not going to amputate, there is no need for a biopsy. The question: is biopsy
dangerous? and can it disseminate the disease? is one of those articles of surgical faith
to which I do not subscribe. Such a conception implies that cutting into the tumour
with a knife or diathermy endows the cancer cell with a cerebral cortex, that the cancer
cell sits up and says—"Ah, he has cut it and let me loose—I will crawl up the capillaries
—against the bloodstream, instead of being washed out with the blood." There is no
evidence that cutting into a tumour produces a suction action which aspirates these
cells into the capillaries, and so enables them to travel to the lung and there settle in
colonies, multiply and grow and produce metastases. The pros and cons of biopsy have
been discussed, I think, for the last 25 years, and there are as many pathologists in
favour of the idea that a biopsy is beneficial to the patient, by reducing tension inside
the tumour, and thus mmimizing the chance of metastases—as there are contrary
opinions. Personally I am not concerned with such theoretical musings—I am only
concerned with this—am I going to make an awful mistake, and disarticulate the hip
of a child of ten, on the wrong diagnosis?   Not on your life—I will do a biopsy first.
Page 483 TREATMENT OF BONE TUMOURS
By PROFESSOR B. W. WINDEYER, m.d., b.s., f.r.c.s.,  f.f.r., d.m.r.e.
Director, Meyerstein Institute of Radiotherapy,
The Middlesex Hospital, London, England
Paper given at the Refresher Course on Malignant Disease held at the British Columbia Cancer Institute
October,   1952
It is generally accepted that among primary malignant tumours of the bone, there]
are certain ones—for example, Ewing Tumour and Osteoclastoma—which are radiosensitive and in which radiotherapy has an important part to play. Osteogenic sarcoma,
however, has been regarded as one of the chief examples of a radio-resistant tumour in
the treatment of which radiotherapy has little or no place. Sir Stanford Cade has been
advocating the use of radiotherapy in these tumours and I propose to discuss this
question with reference to some patients who have been treated at the Middlesex and
Mount Vernon Hospitals. I am not producing statistical evidence of the value of
radiotherapy in osteogenic sarcoma, as the cases in earlier years were treated mainly
by surgical ablation at as early a stage as possible. Those treated by any method of
radiotherapy were sporadic and unusual cases. In addition, I consider that, with one
or two exceptions, the dose of radiation given in the earlier years was insufficient
according to my present ideas and experience.
From among the records of 150 cases diagnosed histologically as osteogenic sarcoma
I have picked out several patients. There was a man, 24 years old, treated in November
1924 by the insertion of 340 milligrams of radium in needles and tubes for 24 hours.
In January 1925 there was a further insertion of 265 milligrams of radium. He developed a great deal of pain and the leg was amputated. Multiple sections failed to show
active growth.  He is alive and well at the present time.
In 1927 another man, aged 23, with a histologically proven osteogenic sarcoma
in the upper end of the tibia was treated similarly by massive radium insertion and
later amputation. Again no growth was found in the amputated specimen and he
remains well at the present time.
These two cases are mainly of historical interest. They were treated by techniques
which would not be approved today. It may be said that they were treated not by
selective radiotherapy but by massive tissue destruction. They developed necrosis and
had to have amputation on account of this, but they are alive and well 25 years and
nearly 28 years later.
In the second group there are there patients who remain alive and without recurrence having had a preUminary course of X-ray therapy and then amputation.
The first of these was a girl, aged 12, in 1935 who received a dose of 3400
roentgens over one month to a tumour of the right femur and had amputation two
months later.
The second was a girl, aged 11, in 1946 who had 6500 roentgens delivered in 12
days to an osteogenic sarcoma of the right tibia with amputation two days later.
The third was a man, aged 25. In August, 1950, two years ago, he had 4270
roentgens delivered over seven days to a growth of the tibia and amputation one day
later.
These three patients, who were treated in my own era, do not prove anything.
They are part of a small series treated in the hope that preliminary irradiation might
improve the ultimate prognosis. They may link up with some of the later cases which
I will show, although at present my practice is to give a more prolonged course of
radiotherapy with an interval before surgical removal.
That there can be any value in giving pre-operative irradiation and then amputating the limb is by no means widely accepted, as it is argued that this procedure is
Page 484 imlikely to have any effect on the development of metastases which are almost always
Hie cause of death.   I remember one of my radiotherapeutic colleagues, during a discus-
lion on this subject, saying that he thought it would be just as valuable and easier
to amputate first and then irradiate the amputated limb.
There are two patients treated ten and nine years ago in whom there is convincing
evidence of the efficacy of radiotherapy.   They have results of some duration.
In 1942 a man, aged 23, developed a tumour in the upper third of the left femur
through which there was a spontaneous fracture.   It was reported by Professor Scarff
lis a "medullary spindle cell sarcoma of bone."   He was treated by X-rays to a tumour
Hose of 3200 roentgens in 30 days.   He remains well and active at present as the result
of radiotherapy alone.
The second patient is a woman, aged 50, in 1934.   She had a large red swelling
of the left shoulder diagnosed radiologically as an osteolytic sarcoma at the head of the
humerus on the point of pathological fracture.   In June 1934, forequarter amputation
|was performed. The tumour was reported to be composed chiefly of malignant cartilage,
also bone and osteoid tissue—an osteogenic sarcoma.   Within a few weeks a hard mass
appeared at the root of the neck on the same side.   She was given an estimated tumour
dose to the mass of 4800 roentgens over a period of 26 days.   The mass disappeared
|and she remained well for eight years.  In March 1951, she had some haemoptysis and
fwas found  to have an apparently solitary metastasis  in  the  right lung.    This  was
removed   by   lobectomy   but   a   few   months   later   further   intra-thoracic   metastases
developed.
Both these patients had unusual types of tumour. There is some discussion as to
the clasification of the first one.   It is thought now to be a chondroblastoma.
The second one has been reviewed by a group of pathologists.   It is now classified
Us an ossifying chondrosarcoma.   It recurred rapidly after amputation but had a long
latent period before the development of metastases.
There is a further series of more recently treated patients.
A man, aged 22, had a tumour of the neck and trochanteric region of the left
femur with severe pain. In April and May 1950 he was treated by X-rays to a tumour
dose of 6400 roentgens in 41 days. He lost his pain and an X-ray examination the
tumour area became recalcified. A year later there was some return of pain and
|evidence of recurrence on skiagram. Hindquarter amputation was carried out but he
developed intrathoracic metastases.
A girl, aged 19, came in February, 1951, with a tumour of the upper end of the
left femur. Biopsy was taken and found to be osteogenic sarcoma. She had 5100
roentgens to the tumour over 34 days. There has been some discussion about surgical
removal, but she is unwilling for hindquarter amputation and it has been decided to
await events.
A woman, aged 25, came in November, 1951, with a three months' history of
tenderness and swelling of the right hip. Biopsy had shown osteogenic sarcoma. She
was in great pain and her general condition was poor. Traction was applied to the leg
and she was given X-ray therapy from 16th November, 1951 to 2nd February, 1952.
The majority of the treatment was given with a grid, and it is difficult to estimate
accurately the tumour dose. It has varied from 8000 to 10000 roentgens. Her pain
was relieved and she was able to have traction removed during treatment.
A boy, aged 14, came in May of this year. Following an injury playing basketball
he developed a painful shoulder which was fractured playing football. Biopsy showed
osteogenic sarcoma. Arteriogram showed numbers of pathological vessels and displacement of junction of axillary and brachial arteries by the tumour mass. From 12 th
May, 1952 to 16th July, 1952, he received 8200 roentgens by X-ray therapy over 66
days. There is no soft tissue mass to feel and he is quite comfortable with good movement of the shoulder.  A decision will be made in a few months about surgical ablation.
Page 485 A woman, aged 74, with a two months' history came in June, 1951, with a tumour
of the left maxilla which had ulcerated into the mouth. Biopsy showed osteogenic
sarcoma. She was given X-ray therapy to a tumour dose of 8100 roentgens over 52
days. This was followed a month later by partial diathermy excision of the maxilla.
She is well with no sign of recurrence one year later.
A girl, aged 17, came in September, 1951, with a tumour of the right side of her
mandible. It extended into the soft tissues in all directions and was .ungating in the
mouth. She was given treatment by X-rays over a total time of 11 weeks. 6000
Roentgens were given to the tumour to begin with, and then further heavy irradiation
by three grid fields (34,000 -f 44,000 -f- 60,000). It was considered that her only
chance was to give such a dose that necrosis of bone and soft tissues was inevitable
and then to attempt surgical removal. Wide surgical excision was carried out four
months ago and no sign of any neoplasm could be found in the tissues removed at the
operation.   She is now proceeding with plastic reconstruction.
These cases show without doubt that X-ray therapy with the doses that have been
given can produce marked improvement, reduction in size, recalcification and even
complete destruction of osteogenic sarcoma.
This last group of cases which I have detailed were all in sites which were relatively
inaccessible for surgery as a primary measure, and I am convinced that radiotherapy
should be used in this way as a first procedure. We are also using it as a first procedure
in cases in more accessible sites, such as the lower end of the femur and upper end of
the tibia. In view of the evidence we have of the effect on osteogenic sarcoma this
seems a reasonable procedure. There is some evidence that delay in carrying out the
operation is not likely to be detrimental.
A random selection was made of a series of cases, none of them treated during
the last four years, when higher doses of radiation have been used. They were divided
into three groups according to whether surgery alone, radiotherapy alone or a combination of surgery and radiotherapy was used. Surgery alone gave an average survival
of 8.9 months in 11 cases. Radiotherapy alone gave an average survival of 9.4 months
in 19 cases, and a combination of surgery and radiotherapy an average survival of 23
months in 16 cases. One of our cases of intra-medullary fibrosarcoma is of interest as
exemplifying the point made by Sir Stanford Cade that it is dangerous to amputate
through the bone in which the tumour is situated.
There are, of course, some cases in which this has been done which have been
successful but the tumour may spread up the shaft and disarticulation or amputation
above the joint is the safer procedure.
Paget's Sarcoma
Sarcoma supervening on Paget's disease is particularly deadly and radiotherapy
does not appear to be effective. Probably the changes of bone structure in Paget's
disease make the tumour bed less capable of producing any adequate response to irradiation. There is also the fact that sarcoma developing on Paget's disease may be multicentric in origin.
Radiation Induced Sarcoma
The production of osteogenic sarcoma as the result of the ingestion of radium
has received a considerable amount of attention as the result of the excellent reports
on the New Jersey dial painters. I have a case of some interest which occurred in a
dog. He was the pet dog in a radium luminising laboratory during the war. He apparently liked to lick up the floor and obviously protection methods were not very good.
He/ developed an osteogenic sarcoma in the near fore leg and died. I dissected the body
and incinerated the various organs separately. He had 0.78 mgm. of radium in his
bones. Kl!%!
There are also reports of sarcoma of bone induced by external irradiation. Some
of these I consider are suspect and have been asumed to be due to irradiation in cases
Page 486 of osteoclastoma when an equally likely assumption is that they were a malignant type
of tumour from the outset. One patient was treated in May, 1940, by X-rays for
actinomycosis. He developed recurrence and received further X-rays in September,
1941, January, 1942, September, 1942, and November, 1942. He was then treated
with penicillin. In June, 1949, he developed swelling of the jaw and had local excision
of a tumour which proved to be osteogenic sarcoma. In February, 1950, he had wide
excision for further recurrence and in April, 1950, was sent to me for palliation by
teleradium with this condition. He was given in all a dose of approximately 10,000
toentgens to the tumour in three months. He died of sudden haemorrhage three months
later.
The question of whether irradiation is likely to cause malignant change in an
osteoclastoma has caused much discussion. Undoubtedly some of them become malignant and metastasise without any such treatment and it is equally without doubt that
radiotherapy is an efficient method of treating this type of tumour and the only one
possible in many of them.
TREATMENT OF MALIGNANT MELANOMA
J. E. Musgrove, M.D.
The etiology and pathology of malignant melanoma have been greatly clarified
by Allen's 1»2 excellent studies. The treatment of the lesion, however, remains in a
state of confusion. In this article, an attempt will be made to crystallize the present
trends in the therapy of melanoma.
Treatment of melanoma will be considered under two headings: The first is
Prophylaxis and the second, Definitive Therapy, and of these two the first is the more
important.
Prophylaxis
Excise and examine microscopically the following naevi:
1. Known precursor sites;  (a) feet, (b) hands, (c) subungual, (d) genitalia (e)  sites
of irritation.
2. Darkly pigmented naevi of childhood and pregnancy.
3. With alteration in size, color, elevation, ulceration, inflammation, bleeding, crusting,
tenderness or itching.
4. Naevi appearing in the adult.
5. All grey blue, blue black and black naevi.
Definitive Therapy
Electrodesiccation, radiation and surgery are the three methods we have of treating
this lesion at the present time.
Electrodesiccation
This mode of treatment is mentioned only to be strongly condemned. We must
resist the temptation to "burn off" a pigmented skin lesion in our office practice. Amadou3 in 1933 showed the heat of cauterization to cause dilatation of the surrounding
lymphatics and the formation of what he called "tissue-steam," the latter causing
propulsion of live tumor cells through the dilated lymphatics. Numerous cases are
on record, in which the cautery has caused marked activity in what appeared to be a
benign pigmented lesion.
Radiation
Pack4 makes the following statement regarding radiation therapy. "This tumour
possesses such a degree of radio-resistance that X-Ray and radium should never be
Page 487 employed in treatment, as long as the tumour remains in an operable stage. The melanoma is as resistant as the skin which contains it: cauterizing doses of radiation are
necessary to destroy even the primary tumour and for this purpose X-Ray and radium
hold no advantage over any other form of cautery." Raven5, of London, may be
similarly quoted.
This criticism of radiation therapy may be too harsh, particularly when we consider
the possibilities of the "Cobalt Bomb." However, at this time, radiation therapy should
be limited to patients who refuse radical surgery and those in whom the disease has
become inoperable.
Surgery
Prior to any form of surgical intervention, the patient should be thoroughly
examined, including a chest X-Ray, in an attempt to rule out distant metastases, which
would preclude curative surgery.
The basic concepts of surgical treatment are as follows:
1. Wide local excision.
2. Wide local excision plus radical dissection of regional lymph nodes.
3. Wide local excision in continuity with radical dissection of regional lymph nodes.
4. Radical amputation of an extremity.
1. Wide local excision, in itself, is not adequate therapy, for we know that even
when the regional nodes do not show clinical evidence of involvement, the pathologist
will find metastases in the nodes in approximately 50% of cases.4,5
2. Wide local excision plus radical dissection of the regional lymph nodes. This
operation is done when it is impractical to carry out the third type of procedure, namely,
dissection in continuity, owing to the distance between the primary tumour and the
regional nodes, for example, between the foot and the groin. The wide local excision
is done as the first stage of the operation, then after an interval of two to six weeks the
radical gland dissection is done. Pack4 recommends two weeks when the glands are
clinically involved and six weeks when there is no evidence of clinical involvement,
the theory being that in this interval, any tumour emboli present between the primary
site and the nodes will have made their way to the nodes by the time the gland dissection
is performed.
3. Wide local excision in continuity with radical dissection of the regional nodes
fulfils the concepts of cancer surgery, for it removes en bloc the tumour and its lymphatic drainage. This can be employed for most lesions of the arm, thigh, neck or trunk.
4. Radical amputation of an extremity is the most controversial aspect of the
surgical treatment of this lesion. This mode of attack has not been employed long
enough for us to be able to assess its merits at this time. Bowers6, of the U.S. Veterans'
Administration, has done some of the pioneer work in this field. I quote him as follows:
"The prominent factors in more radical surgery demand an operation that will in one
sweep remove the local lesion, all of its lymphatic vessels, and the barrier nodal drainage
without manipulation of the lesion, its tracts, or barrier." He condemns hip and
shoulder disarticulation, which works through instead of above the barrier nodal drainage.
Therefore, if amputation is to be done, Bowers is emphatic that it should be a quarter-
ectomy. He has reported four hind-quarterectomies and more and more of these operations lire being done in some of the larger centers. Janes7, of the Mayo Clinic, states
that he still does not feel justified in doing this radical surgery. Only time will give
us the answer.
I should now like to summarize the methods of surgical therapy I would choose,
at the present time, for treating melanomas depending upon their location.
Page 488 1. Head and Neck
Excision of the lesion in continuity with regional lymph node dissection, when
possible.  The second choice would be local excision with subsequent gland dissection.
2. Trunk
Excision of the lesion in continuity with regional lymph nodes when practical.
If the lesion is so situated that it may drain into two or more regional nodal barriers,
|(eg. mid-line of back or peri-umbilical) then I would favour wide local excision,
ipllowed by careful observation and delayed groin or axillary dissection if nodes' become
clinically involved.
3. Ano-rectal
Exploratory laparotomy, and if the lesion is resectable, do an abdomino-perineal
resection, with subsequent bilateral inguinal node dissection.
4. Genitalia
Radical resection of genitalia and inguinal lymph nodes in continuity.
5. Extremities
For lesions distal to the elbow or knee, a local excision, followed later by a
radical dissection of the axilla or groin.
For lesions proximal to the elbow or knee, a local excision in continuity with
Radical dissection of the axilla or groin.
Subungual melanoma:   Amputation of the digit and subsequent gland dissection.
In conclusion, I would like to make a plea for optimism, rather than pessimism,
prhen considering melanoma. The majority of the medical profession consider the
^diagnosis of melanoma tantamount to a death sentence. This is not so. The average
five-year survival of patients operated upon prior to 1945 was 20 to 25%6, which is
two to three times the survival rate of carcinoma of the stomach or lung during those
years. The year 1945 is significant, for that is when Pack and others began making
a concerted plea for more radical surgery in dealing with this neoplasm. Hogarth
Pringle8, of Glasgow, practised the same surgical principles prior to the turn of the
century and published his work in 1908 and 1937, but very little notice was taken of
his teaching. It is a tragedy that more emphasis was not placed upon his work, but
looking itno the future, radical surgery is almost certain to better the prognosis of
those suffering from "black cancer."
BIBLIOGRAPHY
Allen, Arthur C.   A Reorientation on the Histogenesis  of Cutaneous Nevi and Melanomas.   Cancer
2:28-56, 1949.
2.   Allen, Arthur C, and Spitz, Sophie.   Malignant Melanoma.   Cancer 6:1-45, 1953.
?3.   Amadon, Phillip D. Electrocoagulation of the Melanoma and Its Dangers.   Surg. Gynec. Obst. 56:943-
946, 1933.
14.  Pack, George T.   The Principle of Excision and Dissection in Continuity for Primary and Metastatic
Melanoma of the Skin.   Surgery 17:849-866, 1945.
5. Raven, Ronald W.   The Properties and Surgical Problems of Malignant Melanoma.   Ann. Roy. Coll.
Surg. Eng. 6:28-53, 1950.
6. Bowers,   Ralph   F.    Quarterectomy—Its   Application   in   Malignant   Melanoma.    Surgery   26:523-538,
1949
7. Janes, J. M. Personal Communication.
I.   Pringle, J. Hogarth.  Cutaneous Melanoma.   Lancet 1:508-509, 1937.
Doctors' offices to rent in the Canadian Bank of Commerce Bldg.,
1st and Lonsdale, North Vancouver. Two available immediately, six
offices and waiting room available 1st of October.
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Page 491 Sirtttsfj Columbia fifutBum
Canaittan fftrtttral Assurtatum
1807 West 10th Ave., Vancouver, B.C.      Dr. G. Gordon Ferguson, Exec. Secy
OFflCERS-1952-1953
President—Dr. J. A. Ganshorn	
President-elect—Dr. R. G. Large I	
Vice-President and Chairman of General Assembly—Dr. F. A. Turnbull-
Hon.  Secretary-Treasurer—Dr. W. R. Brewster	
 Vancouver
 Prince Rupert
 Vancouver
.New Westminster
Members of the
Victoria
Dr. G. Chisholm
Dr. E. VV. Boak
Nanaimo
Dr. C. C. Browne
Prince Rupert and Cariboo
Dr. R. G. Large
New Westminster
Dr. J. A. Sinclair
Dr. VV. R. Brewster
Yale
Dr. A. S. Underhill
Dr. C. J. M. Willoughby
Standing Committees
Constitution and By-Laws	
Finance	
Legislation	
Medical Economics	
Medical Education	
Nominations	
Board of Directors
Vancouver
Dr. F. A. Turnbull
Dr. A. W. Bagnall
Dr. F. P. Patterson
Dr. P. O. Lehmann
Dr. G. C. Johnston
Dr. Ross Robertson
Dr. R. A. Gilchrist
Dr. J. Ross Davidson
Dr. R. A. Palmer
Kootenay
Dr. J. McMurchy
Chairmen
 Dr. R. A. Stanley, Vancouver
JDr.  W. R. Brewster, New Westminster
 Dr. J. C  Thomas, Vancouver
 Dr. P. O. Lehman, Vancouver
-Dr. T. R. Sarjeant, Vancouver
Programme and Arrangements	
Public Health	
 Dr. J. A. Ganshorn, Vancouver
 Dr. Harold Taylor, Vancouver
 Dr. G. F. Kincade, Vancouver
Special Committees
Arthritis and Rheumatism-
Cancer	
Civil Defence	
Hospital Service	
Industrial Medicine	
Maternal Welfare	
Membership	
Pharmacy	
Public Relations	
_Dr. F. W. Hurlburt, Vancouver
 Dr. Roger Wilson, Vancouver
 Dr. John Sturdy, Vancouver
_Dr. J. C. Moscovich, Vancouver
 Dr. J. S. Daly, Trail
—Dr. A. M. Agnew, Vancouver
 Dr. E. C. McCoy, Vancouver
-Dr. D. M. Whitelaw, Vancouver
 Dr. G. C. Johnston, Vancouver
ANNUAL MEETING
The Annual Meeting this year promises to be one of the best ever. You will be
receiving a copy of the programme, and I am sure you will find it of great interest in
the scientific field. Great planning has also gone into the making of the business and
social part of the meeting something which will appeal to you all.
On the Monday night, it is expected to have one of our Medical Forums in cooperation with the Vancouver Province, and you will have an opportunity to see your
colleagues in action, and judge for yourself the effect of this angle of Public Relations.
"We think it is a very good project and hope you will attend so that you can give your
opinion at various meetings.
Page 492 The business meetings should be very good.   The Association has quite a record of
iirhich to be proud for this past year, and this is the opportunity to present it to all the
■nembers for approval or criticism.  Your comments in either regard will be of assistance.
We hope you are planning to attend this meeting, and feel that you will be well repaid
for the efforts expended.
While here, be sure to look at the various professional exhibits which is a form
?of Public Relations with those who advertise, and thus helps us.
Now that most of us have finished our holidays for another year and settling down
to the winter's work, we will again meet the usual problems of our practice. "With the
Dominion election over, we have now time to try and estimate what effect this will
pave on the medical profession, and attempt steps along the lines that we feel should
be followed. Your Association will be watching these events for us all, and it is quite
probable they will be calling on you for some assistance in this regard. Remember that
four major Public Relations is the individual relationship between each doctor and his
ipatient, and it is the sum total of these relationships which helps to give the public
^reaction to the medical profession in general.
F.L.S.
ANNOUNCEMENT
MRS. C. T. McCALLUM, widow of the late Dr. C. T. McCallum, radiologist, announces her appointment as a member of the sales staff of the
West Shore Realty Co. Ltd., 1437 Marine Drive, West Vancouver.
Several fine view homes are available now at prices which are reasonable.   These can be shown by appointment.
Fifteen minutes drive from downtown.  Enquiries invited.
Phone: West 848—Days; 2494-L2—Evenings
If MEDICAL  OFFICES   FOR
LEASE
Broadway at Trafalgar
Smart new building on south-east corner with efficient office layouts
—double or single suites. Owner will furnish reception and consulting
rooms.
Now ready
for occupancy.
BOULTBEE, SWEET & CO.
555 Howe St.
LTD.
PAc. 7221   §
Page 493 MEDICAL AND SOCIAL ASPECTS OF CERTAIN
\ WmB HEREDITARY DISORDERS   |§
ANATOLE S. DEKABAN, M.D.
In medicine, as in other sciences, problems and trends change. This change may be
gradual and it may not be easy to perceive the denominator of contemporary times.
Physicians of certain eras may be required to fulfil a particular duty. The fact is now
well appreciated that in the past few decades important contributions were made in
combatting many human illnesses. Following discovery of hemotherapeutics and antibiotics, the majority of the bacterial and infective diseases have lost their former dread.
The lives of many patients suffering from cardiovascular disorders have been prolonged
and made more comfortable. Certain metabolic disorders can also be fairly well controlled. General technical as well as pharmaceutical advances have made surgical
diagnosis easier and treatment more successful. The time seems to have.come for similar
advancement in preventive medicine, particularly in the inheritance of certain disorders
and, perhaps, for consideration of practical applications of some aspects of eugenics.
The purpose of this paper is merely to attract more attention to the importance
of genetics and of inheritance of human disorders, for the wellbeing of future generations and humanity. A few examples of the more common conditions, as they occur in
the practice of medicine, will be given and their hereditary significance discussed.
EPILEPSY:
The term epilepsy denotes a syndrome of periodic impairment of consciousness,
usually associated with an abnormal motor, perceptive, psychic or autonomic activity,
either singly or in combination. Convulsions can be produced by a variety of conditions
and, under certain circumstances, everyone of us is prone to have a "seizure". As Pen-
field (1951) suggests, the term epilepsy should be better reserved for those patients
who suffer from periodically occurring petit mal and/or grand mal attacks without
demonstrable pathological change in the C. N. S. or abnormal constituents in the blood
(uremia, other toxic states, etc.). These persons are usually well between attacks. All
other patients whose attacks are based on demonstrable organic lesions should be classified as those having cerebral seizures. This differentiation would show a clearer
etiological distinction and would also ease the psychological strain for many patients
and their families. For example, a patient who sustained brain injury and is having
focal attacks should not be called epileptic, even if the discharge spreads to become
generalized.
Only thus defined epilepsy or as it is also called idiopathic epilepsy, will now be
considered. Even when so narrowed, epilepsy is still a complex condition. From the
etiological viewpoint, there can be no doubt that certain instances of this disorder are
familial (Thorn and Walker 1922, Brain 1926, Conrad 1936, Lennox 1942, and others).
Here follows a description of an interesting family with inherited cerebral dysrhythmia*
and epilepsy: Family D**: Eight children of this family (Fig. 1) are alive; there were
four abortions, one of which was twins. Father (Mr. D.), 46 years of age, and his progenitors did not have any evidence of epileptic disorder. His E.E.G. (Fig. 2A) is entirely
normal. Mother (Mrs. D.), 46 years of age, does not have clinical epilepsy but has
been subject to migrainous headaches in the past two years; her E.E.G. shows dysrhythmia typical of idiopathic epilepsy (Fig. 2C). Her sister, 39 years of age, has
clinical epilepsy and has an E.E.G. record of the projective epilepsy type. One of
mother's brothers was a heavy drinker and died of unknown cause at the age of 29
years. Mrs. D.'s mother, maternal aunt and grandmother all. suffered from clinical
epilepsy; her maternal uncle was a heavy drinker.
* Cerebral dysrhythmia as used here is an E.E.G. term.
** This family was studied in the O.P.D. of the Royal Victoria Hospital, Montreal.
Page 494 Figure 1
o-
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O
Q
dtD     O    &     D
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4     D    Q
V
@
/rrx Clinical epilepsy with
fill) E.E.G. typical of idiopath-
HLk    jc   cerebral   dysrrythmia.
©No clinical seizures, E.E.-
G. typical of idiopathic
dysrrythmia   epilepsy.
No clinical seizures, E.E.-
G. typical of idiopathic
dysrrythmia epilepsy plus
migraine.
Heavy drinker.
Abortion.
12
S7
"V
^7V
<m>   i   u   Dili   H   q   q   n
Otorg.tt. Cvrftld  ~rCi* Kyvod GlUt* Ch.ri Selen Tolant* Roger
V_-/   Twin abortion.
J- Further history unknown.
Figure 2
ij*5
I *'WV*H^^
^.    E.E.G. record of Mr. D., which shows normal, well regulated alpha rhythm.
B. Georgette's E.E.G. showing bilaterally synchronous wave and spike discharges.
C. E.E.G. record of Mrs. D. showing burst of 3-4 per second slow waves with an occasional spike superimposed.
D. E.E.G. record of Helen.   3-4 per second rhythmic, bilateral synchronous discharges of slow waves with
a very sharp wave component.
Figure 3
d>
o-
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>
6
1  <D
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6
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Mental  defective.
Spina   bifida.
"Queer",  committed suicide.
<tt     6
6
B
O
D
"Queer".
Stillborn.
Further history unknown.
Page 495 Of eight children of the D. family, three (Georgette, 20, Gerald, 18, and Gilles,i
13 years) are having clinical evidence of epilepsy (petit mal and grand mal) and their
E.E.G. is typical of idiopathic projective disorder (Fig. 2B, Georgette's E.E.G.). It is
interesting to note that all of them began to have attacks at puberty (between 11 and
14 years). Three of the remaining five children (Cheri, 10, Helen, 9, and Yolanta, 7
years of age) have E.E.G. showing cerebral dysrhythmia of epileptic type (Fig. 2D,
Helen's E.E.G.). As these three are still between 7 and 10 years of age, it seems possible
that they will develop clinical epilepsy when they arrive at the age of puberty, similar
to their three older siblings. The youngest (Roger) is 3 years of age and his E.E.G. is
considered to be normal for that age. Rymond (17 years of age) is the only one who
passed puberty and did not develop epilepsy. His E.E.G. shows only slight instability,
which may be considered to be within normal limits.
Physical examination revealed that Mr. D. had absent knee reflexes and his ankle
reflexes were obtainable only with reinforcement. Mrs. D.'s tendon reflexes were all
present and equal. All children but one had some impairment of tendon reflexes, particularly of the lower extremities. This impairment consisted either of an absence of
certain reflexes or of depression, so that they were obtainable only with reinforcement,
and then usually they were unequal. The only child who had all reflexes physiological
and equal was Rymond, who also was the only one to pass puberty without having!
epileptic attacks. The significance of this abnormality in tendon reflexes of the D.
family is not clear from either the neurological or genetic point of view.
Besides the general physical and neurological examinations, both parents and all
children had X-rays of skull, blood serology, and E.E.G. There were no abnormal findings with the exception of the E.E.G. records already discussed and the elevation of
Mrs. D.'s blood pressure to 190/95.
It seems certain that cerebral dysrhythmie of the epileptic type in the family is
of genetic origin. It is difficult, however, to be definite about the mode of inheritance
of this disorder. The information about Mrs. D.'s family (which was transmitting this
condition) is not complete. One sister has clinical epilepsy and an abnormal E.E.G.
It was not possible to examine her other siblings. Her parents and grandparents were
dead. From what data is available, however, it seems probable that the inheritance of
the epileptic type of cerebral dysrhythmia in this particular instance was of a dominant
charter; the high incidence of affected children in the D. family signifies high penetration in this particular generation.
It is to be stressed that not all instances of idiopathic epilepsy are thought to bei
hereditary and those that are would not not necessarily follow the above patterns.
Abnormality of different genes or even multiple factor inheritance may well be responsible for transmission of epileptic disorder.  Thus certain pedigrees of familiarly occurring epilepsy may show clearly recessive or other type of inheritance.
DIABETES:
It has been known for a long time that diabetes mellitus may run in families. There
are several reports of large series of cases of this disorder with genetic documentation
(Pinkus and White 1933 and 1934, Lawrence 1951, and others). More recently, Han-
hart (1950) and Steinberg (1952), on the basis of their extensive investigations, expressed the view that the mode of inheritance of familiarly occurring diabetes is of
simple autosomal recessive type. Certainly a majority of pedigrees conform to this,
although there are instances when diabetic inheritance seems to be more complicated.
What kind of implications can be derived from the knowledge of inheritance of
diabetes mellitus? Consideration of an instance will bring out some practical aspects
more clearly. A diabetic man, whose father also suffered from the same disorder, married and desires to have a family. The possibilities of recessively inherited diabetes will
be as follows:
Page 496 (a) His wife is neither diabetic nor carrier: Children will not be diabetics but they
will all be carriers. (If one of these carriers marries another carrier, their offspring will show the following ratios: Diabetic:  carrier: normal as  1:2:1.)
(b) Wife is not a diabetic but is a carrier (heterozygous): Half of children will
be diabetics and half carriers.
(c) Wife is also a diabetic: All their children will be diabetics.
Diabetes may manifest itself early in infancy or late in life. Probably there are a
fair number of diabetics who are not recognized, as well as persons who have abnormal
glucose tolerance curve but no sugar in urine. In ordinary circumstances these factors
make genetic study difficult. It is interesting to note that Miller (1945) and Mass and
Mullholland (1951) recorded the very first physiological changes in newborns of diabetics, consisting of oversized babies, who usually then were potential diabetics.
True, diabetes mellitus can be controlled with insulin and diet quite satisfactorily,
but still, it does not seem fair to endow a child with such a serious handicap even when
not taking social and economical aspects into consideration.
'HARELIP:
Harelip may or may not be associated with cleft palate. Its inheritance is certain,
although its patterns are not agreed upon by all investigators (Test and Falls 1947,
Tiedemann, 1949, Book 1951). The incidence of this deformity in population is estimated as approximately 1:1,000 births. Empirically conducted observations of large
series of cases by Book (1951) revealed that the risk of subsequent children having
harelip if one parent and one child are affected is as 1:7. Fortuntely, this disorder presents a less serious problem and, in many instances, the error can be surgically ameliorated.
MENTAL DEFICIENCY:
Mental deficiency is not an etiological entity, but consists of a great variety of
conditions. A large number of mental defects are the result of noxious environmental
factors acting during intra-uterine life, such as the impairment of exchange of nutrient
and katabolic substances, maternal intoxications, infections, etc. Also birth injury or
infections, intoxications or brain traumas occurring during infancy, childhood or later
life may result in mental defect. There are, however, certain kinds of mental deficiencies
which are inherited. Among these, lipoidoses (amaurotic familial idiocy, gargoylism,
Niemann-Pick disease, and Gaucher's disease), tuberous sclerosis, nevoid amentia, Crou-
zon's disease, phenylpyruvic, oligophrenia, arachnodactyly, hepatolenticular degeneration,
and Huntington's chorea are the most dramatic.
Of considerable practical importance is inheritance of mental degenerative traits.
Certain families show accumulation of an unusual number of epileptics, psychopaths,
| psychotics, mental defectives, and physical anomalies.   Here follows an example  (Fig.
3) of such a family:
The child's parents were first cousins and in both of their families there were
instances of mental or physical abnormalities, which were traceable to their grandparents,
one of whom had a spina bifida (grandmother) and another of whom showed extreme
eccentricity and was described as "queer". Of six children of the grandparents, one had
a spina bifida, one was a certified mental defective, and one was stillborn. Of the
remaining three brothers, who appeared normal, two married and had children. The
youngest one "travelled" and no further information on him is available. There were
two children born to the older brother, both males. One appeared normal, the other
acted "queer". The latter married his first cousin, who appeared to be normal, but one
of her two sister had a spina bifida and the only brother, who showed "extreme eccentricity", committed suicide. The patient to be described was the only child from this
marriage. Following a full-term pregnancy and a normal delivery, a female infant was
born.   Her weight at birth was only 5 lb., 2 oz.   She was breast-fed up to 4 months,
Page 497 being always a poor feeder and weak in suckling. Her development was grossly abnormal;
she always appeared lethargic and did not show any interest. At the age of 13 ^4 months
she was institutionalized, at which time the head appeared small, being only 44.5 cm.
in circumference (normal for this age 46.7 cm.) Some increase of muscle tone in all
extremities was noted, but the tendon reflexes were physiological and plantars were
flexor. She reacted to visual and auditory stimuli in a slow and delayed manner but
made no attempt to speak and did not show any signs of recognition of her mother.
Although spontaneous movements of all extremities were observed, she did not try to
sit up or grasp a toy.  Death occurred at the age of 15 months, from pneumonia.
Postmortem examination revealed presence of bilateral broncho-pneumonia. Internal
organs showed no evidence of congenital abnormality or other pathology. The brain
was small, particularly in the anteroposterior diameter, and weighed 785 gm. (normal
for this age about 920 gm.). Histological examination of the C.N.S. was negative for
presence of lipoid or prelipoid substances. Myelination and glial content of the brain
were normal. The only finding was a questionable irregularity of neuronal patterns of
the cortex, particularly in the temporal and parietal regions.
COMMENT
Hereditary disorders can be traced in every branch of medicine and, if they were
all summed up, the overall incidence would be high enough to warrant consideration of
some measure. According to estimates of Seel (1951), a minimum of 1,000,000 persons
in the United States are affected by disease which has a clear-cut genetic basis. Individuals with inherited diseases in very primitive human populations will be eliminated
in time by natural selection; whereas, in modern societies, many who carry serious
hereditary defects survive and transmit harmful genes to their offspring. Particularly,
mutant genes of a recessive type tend to accumulate to high levels. Steinberg and
Wilder (1952) believe that, among the white population, as many as 20 to 25 percent
are carriers of diabetes mellitus; about 5 percent are potential diabetics (diagnosed and
undiagnosed); and about 1 percent are diagnosed as diabetics.
The inheritance of various disorders of the nervous system, both organic and functional, presents another important problem. This is too extensive and complicated to
be discussed here. However, the two described examples (epilepsy and mental deficiency)
have an eloquence of their own.
Very interesting, though still little understood, is the inheritance of general constitution. Under the term of constitution is meant the total sum of the inborn properties of an individual. Admittedly, it is a loose description and difficult for quantitative measurements. Nevertheless, there is some trend to refer to "hypertensive"
"ulcerous", "asthenic", "endocrine", and other constitutions, both among practising
physicians and in medical literature. Closer appraisal of this particular subject would
have to be left until the distant future.
It is thought that the field of human hereditary disorders is sufficiently important
to warrant more medical attention. The whole problem is very extensive and difficult
but, once the work on this line is started, solutions of some aspects may present themselves in a more obvious way. The management of simpler problems could be effected
by organized co-operation of medical, biological, and social workers, along lines similar
to those already present in some communities. The present-day knowledge of genetics
should also be made more available, not only to physicians but also to the general public.
BIBLIOGRAPHY
1. BOOK, J. A.: The incidence of congenital diseases and defects in a Swedish population. Acta genet.,
Basel 2(4):289-311, 1951.
2. BRAIN, W. R.: The inheritance of epilepsy. Quart. J. Med. 19:300, 1926.
3. CONRAD, K.: Die Bedentung der Erbanlage bei der Epilepsie. Untersuchung an 253 Zwillingspaaren.
Deutsche Ztsch. f. Nervenheilk.  139:76, '36.
4. HANHART, E.: Neue Forschungsergebnisse uber die Vererbung des Diabetes Mellitus so wie An-
haltspunkte fur seine Genese in Stammhirn. Arch. J. Klaus Stif. 25:586-598,  1950.
Page 498 5. LAWRENCE, R. D.: Types of human diabetes. Brit. M.J.  1:373-375,  1951.
6. LENNOX, W. G.: Mental defect in epilepsy and influence of heredity. Am. J. Psychiat. 98:733-739,
1942.
7. MILLER, H. C: The effect of the prediabetic state on the survival of the foetus and the birth weight
of the newborn infant. N.E. J. Med. 233:376-378, 1945.
8. MOSS, J. M. and MULHOLLAND, H. B.:  Diabetes  and pregnancy, with special  reference to the
prediabetic state. Ann. Int. Med. 34:678-691,  1951.
9. NEEL, J. V.: Some applications of the principles of genetics to the practice of medicine. Med. Clin.
N. Amer. 35:519-533, 1951.
10. PENFIELD, W. and KRISTIANSEN, K.: Epileptic seizure patterns; a study of the localizing value
of initial phenomena in focal cortical seizures. C. C. Thomas,  1951, Springfield,, 111.
11. PENKUS, G. and WHITE, P.: On the inheritance of diabetes mellitus. (I) An analysis of 675 family
histories. Am. J. M. Sc. 186:1-14, 1953. (II) Further analysis of family histories. Am. J. M. Sc.
188:159-168, 1934.
12. STEINBERG, A. G. and WILDER, R. M.: A study of the genetics of diabetes mellitus, Amer. J.
Hum. Genetics 4:113-135,  1952.
13. TEST, A. R. and FALLS, H. F.: Dominant inheritance of cleft lip and palate in five generations.
J. Oral Surg. 5:292-297, 1947.
14. THOM, D. A. and WALKER, G. S.: Epilepsy in the offspring of epileptics. Am. J. Psychiat. 1:613,
1922.
15. TEEDEMANN, G.: Primogeniture, maternal age and other invironmental influences in pathogenesis
of hereditary harelip and cleft palat. Ztschr. Meuschl. Vereb. - d. Vionstitutionslehre 29:231-242,
1949.
OBIIT
Dr. Isabel Day — August, 1953
The recent death of Dr. Isabel Day, who had practised medicine in
Vancouver for many years, has removed from our professional roll a very fine
woman, and a very capable doctor.
Dr. Day was a public-spirited woman, who consistently did her duty as
she saw it, in every department of life. She was a brilliant student at college,
a medallist in her final year at Toronto University. She served with the British
Army in France during the First World War as a V.A.D., and was decorated
for her services with the Royal Red Cross by his majesty King George the
Fifth.
She had been practising in Vancouver for many years, and had a large
practice of people who thought most highly of her. She was on the staff of
Grace Hospital, was associated with the Children's Aid, the Greater Vancouver
Health League, and the St. John's Ambulance Society, of which she was assistant provincial surgeon. She was held in the highest esteem by her medical
colleagues. A quiet, rather self-effacing person, she was liked and respected by
all who knew her.   She leaves a great gap in the ranks.
To her husband and family we extend our sincerest condolences.
OPENING FOR MEDICAL MAN
General practitioner required in small town on west coast. Mining,
logging and fishing industry. 25-bed well equipped hospital under
excellent management. Splendid opportunity for young graduate.
Good school and living accommodation.
For further particulars apply to Publisher:
675 Davie Street MArine 7729
Page 499 PUBLIC HEALTH AND MENTAL HEALTH NEWS
G. F. AMYOT, M.D., D.P.H.,
Deputy Minister of Health, Province of British Columbia
A. M. GEE, M.D.,
Director, Mental Health Services, Province of British Columbia
APPROACH TO THE CONTROL OF PARALYTIC
Jl POLIOMYELITIS
We are still so conditioned by past experience that we scarcely realize how striking
has been the success attained in the control of the communicable diseases.
From the standpoint of mortality, only two infectious maladies, tuberculosis and
pneumonia, retain any place among the leading causes of death. So far as morbidity
is concerned, however, the picture is a different one. Here influenza, the common
cold, and other virus infections of the upper respiratory tract continue to be—with
mental and emotional disorders—on the two major causes of disability; while polio-
myeltiis, quantitatively less significant, constitutes an urgent challenge on account of
the dramatic and appealing nature of the suffering which it causes.
The reasons why we have failed, so far, to control these two types of communicable
diseases are obvious. In both instances, measures of isolation and quarantine—so
successful with many infections—are practically useless because of the widespread
dissemination of the germs in the general population without the presence of recognizable disease. As Theobald Smith once said, the successful parasite is one which does
not kill its host—or, we may add, does not in many instances even make its host sick.
In the second place, we have so far failed, in both the upper respiratory diseases and
poliomyelitis, to produce generally effective measures of active immunization. Finally,
we have no "magic bullets" which can destroy these viruses as penicillin and similar
substances will eliminate the causative agents of many bacterial diseases.
Further research along all these lines should, of course, be continued but remembering always that the development of a suitable immunizing agent would be the most
effective and practical method for the control of human paralytic poliomyelitis, it
would appear appropriate at this time to review those past and present accomplishments directed towards this end. Ideally, the logical sequence of events in attempting
to secure the specific (as opposed to the environmental) control of any infectious
disease, comprises (a) the identification of the causal agent, (b) isolation of the latter
in culture, (c) development of an immunizing agent, usually a modified toxin or
microbial agent which has been attenuated or killed (vaccine), and (d) an active
immunization program, aimed at the protection of susceptibles. Thus the description
of the typhoid bacillus by Eberth in 1880, and its isolation by Gaffky in 1884, paved
the way for the development of typhoid vaccine, an active immunizing agent whose
value has been clearly established.
Similarly, the recent progress in poliomyelitis research has been the result of step
by step advances begun in 1908 when Landsteiner and Popper first identified the casual
agent of poliomyelitis as a filterable virus. While Flexner and Noguchi (1913) claimed
to have cultivated the virus on the well-known Noguchi medium, this work was never
wholly substantiated and much of the subsequent work had, of necessity, to be carried
out by the experimental infection of suitable animal hosts—usually monkeys. Unfortunately this consideration, both financially and physically, limited experimental design
in consequence of which all sorts of premature and misleading conclusions were drawn.
The result was a long period of confusion with respect to the immunology and other
aspects of poliomyelitis. This confusion was accentuated by the epidemiologic observa-
Page 500 taon that poliomyelitis antibodies were present at an early age in the blood of individuals
who live in those parts of the world where paralytic poliomyelitis is seldom encountered.
It is little wonder that so critical an observer as Burnet Was tempted to conclude in
1939 that "poliomyelitis antibody is not a result of exposure to, or infection by, the
virus of epidemic poliomyelitis."
In retrospect, it is apparent that much of the confusion originated not only from
inadequately controlled experimentation, but also from the occurrence of multiple
immunologic types of virus. The demonstration that there are three different types of
the virus, each capable of causing paralytic poliomyelitis in human beings, and that
the development of immunity to any one of the virus types did not convey similar
immunity to either of the two remaining types clarified much of the confusion centred
upon the immune response to infection. When further investigative work showed that
significant protection against the paralytic consequences of experimental infection with
the virus was afforded by circulating antibodies, it appeared a logical step to attempt
an evaluation of the protective effect of a human antibody concentrate which had been
prepared earlier under the name of immune serum globulin—better known as gamma
globulin. f$i
As early as 1943, Kramer demonstrated that he could obtain passive protection of
mice against the Lansing strain of poliomyelitis virus by the use of immune serum.
Subsequently, attention was drawn to the possible use of gamma globulin, but it was
not until 1952 that the studies of Hammond et al clearly demonstrated the protective
properties of this substance. In these studies, some 55,000 children were observed in
areas where poliomyelitis epidemics were in progress, half of them being protected by
gamma globulin and half serving as controls. Only 26 cases occurred in the protected
group against 64 cases in the control group, a highly significant result.
These successive advances in scientific knowledge have been most encouraging
and while they indicate that the goal is perhaps in sight, by no means are they an
indication that the goal has. been reached. To temper our enthusiasm with caution and
to allay over-optimistic hopes on the part of the public and our colleagues, are perhaps
the least which we can do in tribute to the many years of patient research which have
brought us thus far.
No one seriously imagines that gamma globulin is the answer to the control of
paralytic poliomyelitis. Since it requires about one pint of whole blood to produce a
single dose of gamma globulin, the chronic shortage of blood limits the supply of
gamma globulin available, while the protection afforded is only a passive immunity and
therefore purely temporary. However, in the above-mentioned field trials it was shown
that naturally occurring paralytic poliomyelitis is preventable by poliomyelitis antibodies which, in turn, suggests that paralytic poliomyelitis could be prevented by
vaccintion, if the vaccine could induce the body to produce each of the three different
antibodies in sufficient amounts.
This brings us back to the fundamental problem mentioned earlier—the development of a method capable of producing active, instead of passive, immunity. Further
considerations would be that the immunizing agent or vaccine must be safe, available
in quantity, easily administered, and capable of producing prolonged immunity.
Attempts to produce a vaccine suitable for human beings, were begun many years ago
—indeed, a vaccine of this type was produced as far back as 1930, but had to be
abandoned as unsafe for administration to human subjects. Basic research, however,
has continued over the years until now, almost a quarter of a century later, we appear
to be upon the threshold of our ultimate goal. During these years we have learned
much—how to obtain the virus in quantity and free of neuro-allergenic substances by
growing it in tissue culture; how to attenuate or inactivate the virus by various biologic
and chemical methods; and how to prolong the immune response obtained by administration in the form of a mineral oil emulsion.
Page 501 SELKIRK HEALTH UNIT OPENS
Dr. H. T. Lowe, having completed the D.P.H. course at the University of Toronto,
has returned to become Director of the new Selkirk Health Unit. This unit, with its?
headquarters at Nelson and sub-offices at New Denver and Nakusp, serves school districts 6, 7, 8 and 10.
STAFF NOTES
Dr. A. F. Balkany, formerly director of the Peace River Health Unit has returned i
from the University of Toronto where he received his D.P.H. Dr. Balkany is now
Director of the West Kootenay Health Unit with headquarters at Trail.
Dr. D. L. Clarke who spent last year at the Harvard School of Public Health has j
returned and will take over as Director of the South Okanagan Health Unit on the
departure of Dr. D. M. Black for post-graduate training.
Dr. P. F. Dubois, formerly director of the Peace River Health Unit has resigned
to take up private practice in Whitehorse.  Dr. Dubois has been appointed a part-time;
Health Officer for that city.
Dr. G. A. Duthie is now practising in Windermere.
Dr. J. I. Horsley of Vancouver has left to take post-graduata surgery in Los
Angeles.
Dr. G. W. Robertson is now practising at Bralorne.
Dr. P. J. Moloney is now practising at Campbell River.
Dr. K. R. Middleton is now practising at White Rock.
Dr. J. C. Carpenter is now practising in Nelson.
Dr. D. K. McElroy is now in orthopedics at Presbyterian Medical Center in New
York.
Dr. C. G. Patten is now at Doctor's Hospital in Coral Gables, Florida.
Dr. Robert Wilson of Shaughnessy Hospital has taken over the Vancouver practice of Russell Marshall who is finishing his specialist surgery training.
Dr. W. Cave is now practising in the Vancouver West Broadway district.
Dr. Lionel Reefe, formerly of Montreal, is practising Urology in the Broadway
West Medical district.
BIRTHS
Born to Dr. and Mrs. Daniel Boyes of Vancouver, a son.
Born to /. E. McDonagh of Vancouver, a daughter.
Born to D. R. Hodgins of Essondale, a daughter.
Page 502

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