History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: April, 1950 Vancouver Medical Association Apr 30, 1950

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Published By
The Vancouver Medical Association
Publisher and Advertising Manager
APRIL, 1950
OFFICERS, 1949-50
Dr. W. J. Dorbance       Dr. Henry Scott
President Vice-President
Dr. Gordon Burke
Hon. Treasurer
Dr. Gordon C. Johnston
Past President
Dr. W. G. Gunn
Hon. .Secretary
Additional Members of Executive:
Dr. J. C. Grimson Dr. E. C. McCoy
Dr. G. H. Clement Dr. A. C. Frost Dr. Murray Blair
Auditors: Messrs. Plommer, Whiting & Co.
Dr. M. M. MAcPHERsoN-Chairman Dr. W. H. S. Stockton Secretary
Eye, Ear, Nose and Throat
Dr. J. F. Minnes Chairman Dr. N. J. Blair Secretary
Dr. J. R. Davies Chairman Dr. C. J. Treffry Secretary
Orthopaedic and Traumatic Surgery
Dr. R. H. B. Reed Chairman, Dr. D. E. Starr Secretary
Neurology and Psychiatry
Dr. G. H. Gundry Chairman Dr. G. M. Kirkpatrick—Secretary
Dr. W. L. Sloan Secretary Dr. Andrew Turnbull Chairman
Dr. R. A. Palmer, Chairman; Dr. E. F. Word, Secretary; Dr. J. E. Walker;
Dr. S. E. C. Turvey; Dr. A. F. Hardyment; Dr. J. L. Parnell.
Summer School:
Dr. E. A. Campbell, Chairman; Dr. Gordon C. Large, Secretary;
Dr. A. C. Gardner Frost; Dr. Peter Lehmann; Dr. J. H. Black;
Dr. B. T. H. Martensson.
Medical Economics:
Dr. J. A. Ganshorn, Chairman; Dr. Paul Jackson ; Dr. W. L. Sloan ;
Dr. E. C. McCoy; Dr. J. W. Shier; Dr. T. R. Sarjeant; Dr. John Frost.
Credentials: jjg||
Dr. H. A. DesBrisay ; Dr. G. A. Davidson ; Dr. Gordon C. Johnston.
Representative to B. C. Medical Association: Dr. Gordon C. Johnston.
Representative to V.O.N. Advisory Board: Dr. Isabel Day.
Representative to Greater Vancouver Health League: Dr. L. A. Patterson.
Representative to the Board of Trustees for the Medical Care of
Social J*sistance Cases: Dr. J. A. Ganshorn
'■<   9 Vasoconstriction
combined with
antibiotic therapy in
(brand of phenylephrine)
In upper respiratory tract infections,
topical application of penicillin to the nasal cavity has a decided bacteriostatic action against
typical respiratory pathogenic microorganisms.
To provide clear passage for such therapy,
Neo:Synephrine is combined with penicillin—
shrinking engorged mucous membranes and
allowing free access of the antibiotic.
Neo-Synephrine—a potent vasoconstrictor—
does not lose its effectiveness on repeated application ... is notable for relative freedom from
sting and absence of compensatory congestion.
Stable • Full Potency
Supplied in. combination package for preparing 10 cc. ot
a fresh buffered solution containing Neo-Synephrine hydrochloride 0.25% and Penicillin 5000 units per cc.
New York 13, N. Y.    Windsor, Ont.
Neo-Synephrine, trademark reg. U.S. & Canada
Founded 1898; Incorporated 1906
(Spring Season)
MARCH 2nd—SPECIAL MEETING Speaker—Professor F. H. Bentley, Department
of Surgery, University of Durham Medical School, England.
MARCH  6th—SPECIAL MEETING, Lecture by Sir Reginald Watson-Jones,  title:
"The New World of Orthopaedic Surgery."
A. DAVIDSON, HOTEL VANCOUVER Title: "Men of Osier's Time."
MARCH 28 th—SPECIAL MEETING—"Lecture by Dr. Cecil Watson, Professor of
Medicine, University of Minnesota, Title: "Some Fundamental and Clinical Aspects
of the Problem of Hepatic Cirrhosis." |p§
APRIL 4th—GENERAL MEETING—"The Problem of the Prostate", Dr.  L. G.
It has been the practice in the past to hold a meeting of the Clinical Section of
the Vancouver Medical Association on the third Tuesday in each month. These meetings
were held at alternate hospitals and owing to this fact, often two Clinical meetings were
held at a hospital in one month. To overcome this situation a plan has been worked
out whereby the members of the Vancouver Medical Association are invited by the
various hospital Directors to attend their Clinical Staff meetings. These meetings will
be held as follows:
Second Tuesday—Shaughnessy Hospital
Third Tuesday—St. Paul's Hospital
Fourth Tuesday—Vancouver General Hospital
Notice and programme of these meetings will be circularized by the Executive
Office of the Vancouver Medical Association.
All special and general meetings will be held in the Tuberculosis Institute Auditorium.
Publishing and Business Office — 17 - 675 Davie Street, Vancouver, B.C.
Editorial Office — 203 Medical-Dental  Building, Vancouver,  B.C.
The Bulletin of the Vancouver Medical Association is published on the first of
each month.
Closing Date for articles is the 10th of the month preceding date of issue.
Manuscripts must be typewritten, double spaced and the original copy.
Reprints must be ordered within 15 days after the appearance of the article in question, direct from the Publisher. Quotations on request.
Closing Date for advertisements is the  10th of the month preceding date of issue.
Advertising Rates on Request.
Page 126 Amphojel-
double action
with a
WALKERVILLE - ONTARIO An extensive bibliography
testifies to the outstanding
advantages of treating menopausal
symptoms with "Premarin".
Prompt symptomatic improvement
is usually experienced following
"Premarin" therapy.
at the menopause
Although "Premarin" is highly ;
potent, it is exceptionally well
tolerated and untoward side effects
are seldom noted.
The sense of well-being which
almost invariably follows the use of
"Premarin", helps to restore the
patient's confidence and
normal efficiency.
Ninety-five and eight-tenths per
cent. . . obtained complete relief of
symptoms . . . General tonic
effects were noteworthy."
PerlpfF, W. H.: Am. J. Obst. &
Gynec. 58:684 (Oct.) 1949.
Supplied in tablets of 0.3. 0.625 (with or
without XA grain phenobarbital). 1.25 and 2.5 mg
conjugated estrogenic substances {equine),
or as liquid containing 0.625 mg. per teaspoonful.
Biological & Pharmaceutical Chemists
Montreal, Canada
Total Population—Estimated  385 500
Chinese Population—Estimated  6 877
Hindu Population—Estimated ,  133
Rate per
Number 1000 Pop.
Deaths, residents only- 389 12.1
Total deaths (by occurrence)     419 13,0
Chinese deaths >       15 26.2
(includes late registrations)
January, 1950    ^
Male     372
Female .     368
740 23.0
INFANT MORTALITY—Residents only:
ggpE January,  1950.
Deaths under 1 year of age  H
Death rate per 1000 live birth  21 2
Stillbirths  (not included in above item)  15
January,  1950
Cases      Deaths
Scarlet Fever t.  12            0
Diphtherit I  0             0
Diphtheria Carriers -. g | L s 1  0             0
Chicken Pox • cMui J 154            0
Measles  117            q
Rubella  sa . 1 r_  6             0
Mumps— !    284             0
Whooping Cough _'_ tjal |P|  14             0
Typhoid Fever J__n__. 1    -Sfi£ 0             0
Typhoid Fever  Carriers ^^vf?^' ^^jfe^frrg 0             0
Undulant Fever I : _.  0             0
'Poliomyelitis ^—Sllr: "?fe _'-!_•— -._...   1             0
Tuberculosis -r--^-  - -  49             7
Erysipelas . . | -_  5             q
. Meningitis ....._ -3H--   1             0
. Infectious Jaundice _
Salmonellosis Carriers
Dysentery Carriers __
Syphilis  —
Cancer (Reportable)
For over 10 years heparin has been extensively employed in
vascular surgery and for other purposes where it is necessary or desirable
to prolong the clotting time of blood.
Its rapidity of action and freedom from toxicity enhance its
therapeutic value as an anticoagulant.
A. Solution of Heparin—Distributed in 10-cc. rubber-stoppered vials containing neutral
solution of the sodium salt of heparin and supplied in the following strengths:
1,000 Units per cc. £0&.
5,000 Units per cc.
10,000 Units per cc.
B. Dry, amorphous sodium salt — Dispensed in 100-mg. and 1-gm. phials, containing
95 units per mg., for the preparation of solutions for laboratory use.
University of Toronto Toronto 4, Canada
MEDICAL-DENTAL BUILDING, VANCOUVER, B. C. In a recent issue of the Vancouver Daily Province, we noted an advertisement which
read as follows: Physicians' Office Assistants.
Night School Classes in Receptionist Duties, Office Routine and
Medical Laboratory Technique.   Apply, etc.
To our mind, this brings up a very disturbing chain of possibilities. We would
ask some questions. Who gives the course in laboratory technique? How accurate is
it?  What sort of diploma do the graduates receive?   What is it worth?
There are three persons concerned here. First, the doctor who may employ one
of these technicians; second, the patient who is the subject of the tests; thirdly, the
person who receives the training.
To our mind, it would seem obvious that each of these people should have some
sort of guarantee that the training given conforms to rigid standards of competence and
accuracy—standards that would be recognized by some competent authority, such as
the University of British Columbia, through its Preventive Diseases and Public Health
Department, or the Provincial Health Department of the Province of British Columbia.
Otherwise, the doctor cannot rely on the tests made—serious injury and damage may be
done to the patient through inaccurate diagnostic tests—and the person who spends his
or her money to take the course has been swindled.
In British Columbia, so far as we know, the standard of medical laboratory work is
very good. The big hospitals and the Provincial Health Department give adequate courses
to those that they train, the time devoted to the course is adequate, and the training is
such as to make reliable technicians. But there is, as far as we know, no standard laid
down by the governmental authorities which must be reached before any aspirant can
practise as a fully-qualified technician—though we understand that the Provincial
Department of Education has some responsibility in the matter.
This is a very serious problem, and not one that can be regarded lightly. There is a
very comprehensive article (appearing in the April number of the Women's Home
Companion) dealing with this question. It is entitled "Menace in the Medical Labs,"
and it contains some very disturbing statements. Cases of faulty diagnosis, due to
incorrect laboratory tests, are quoted freely. The article states that "every year from
2% to 3 million illnesses are wrongly diagnosed because of faulty laboratory tests" (out
of some 300,000,000 tests made in the United States).
The Pennsylvania Society of Clinical Pathologists "discovered that the leading
cause is poorly trained technicians. . . . Unfortunately, thousands of technicians . . .
are too often hastily taught by slipshod methods." "A number of Lab. technicians . . .
are turned out by profit-making private diploma mills." (Such as we imagine is the one
whose advertisement appears above.) fc|^
These quotations apply, of course, to the United States—but we cannot doubc that
a survey of Canadian conditions would reveal that there is the same danger threatening
us in Canada. The remedies suggested in this article include "proper supervisory control
(by the States) over medical Labs." California, for instance, has laws requiring that
Lab. technicians and technicologists must pass licensing examinations. In Seattle, we
understand, there is a training school, recognized by the King County Medical Society,
reauiring nine months' training as a minimum, and proper examinations.
We would suggest that it would be well worth the while of our medical authorities
to look into this matter, and make recommendations, possibly through the Provincial
Health Department, that legislation be instituted which will control the training and
licensing of all who wish to do medical laboratory work, with a view to protecting the
public at large, the medical profession, and the technical workers themselves.
Page 156
it Vancouver Medical   Association
Honorary Treasurer-
Honorary Secretary-
 Dr. W. J. Dorrance
 Dr. Henry Scott
 Dr. Gordon Burke
 I Dr. W*. G. Gunn
 -_Dr. J. H. MacDermot
Monday, Wednesday and Friday - 9:00 a.m. to 9:30 p.m.
Tuesday  and Thursday 8:00 a.m. to 5.00 p.m.
Saturday  9:00'a.m. to 1:00 p.m.
A Guide to the Diagnosis of Occupational Diseases, Industrial Health Division, Department of National Health and Welfare, 1949.    (Gift.)
American Cancer Society and National Cancer Institute of the U. S. Public Health
Service—Proceedings of the First National Cancer Conference, 1949.   (Gift.)
An Introduction to Essential Hypertension, by R. F. Herndon, 1946.
Association of American Physicians—Transactions of the 62nd Session, 1949.   (Gift.)
Canadian Ophthalmological  Society—Transactions of the Eleventh Annual Meeting,
1948.   (Gift.)
Handbook of Medical Emergencies, by T. B. Fitzpatrick, 1949.
Medical Clinics of North America—Symposium on Pediatrics, January, 1949.
Medical Etymology, by O. H. Perry Pepper, 1949 (Historical and Ultra-Scientific Fund).
Medical Research Council Memorandum No. 23—Nomenclature of Fungi Pathogenic
to Man and Animals—Names recommended for use in Great Britain by the Medical-
Mycology Committee.   London: H.M.S.O. 1949.
Medical Research Council Report for the Years 1945-1948.  London: H.M.S.O. 1949.
Medical Research Council Report No. 266—Infection and Sepsis in Industrial Wounds
of the Hand: A Bacteriological Study of Aetiology and Prophylaxis, by Rl E. O.
Williams and A. A. Miles.   London: H.M.S.O. 1949. g|
Modern Surgical Technic, by M Thorek, 1938.    (Gift from Dr. Watson Dykes.)
Ophthalmological Society of the United Kingdom—Transactions, 1948.
Surgical Clinics of North America—Symposium on Recent Advances in Surgical Physiology, December, 1949.
Surgical Clinics of North America—Symposium on Urology; Obstetrics and Gynecology,
February, 1950.
The following is a further list of some of the specialized journals taken in the
American Journal of Syphilis, Gonorrhea and Venereal Diseases.
Archives of Dermatology and Syphilology.
British Journal of Dermatology and Syphilis.
Excerpta Medica—Section XII—Dermatology and Venereology.
Journal of Venereal Disease Information.
Medical Economics Acta Radiologica.
Public Health Economics. American Journal of Roentgenology
British Journal of Radiology.
Page 157
American Review of Tuberculosis.
British Journal of Tuberculosis.
Communicable Disease Center Bulletin
(U.S. Public Health Service).
Journal of the History of Medicine.
AUTHORITY AND THE INDIVIDUAL—The Reith Lectures for 1948-49, by
Bertrand Russell. London: George Allen and Unwin Ltd. pp. 125 (portrait
The Reith Lectures, established- by the B.B.C. in 1947, are an annual series of
broadcast lectures given each year by an acknowledged authority in a particular field,
sociology, literature, history, public affairs or economics, who has been invited to undertake some study or original research on a given subject, the results to be presented to
B.B.C. listeners.  The lectures are named after Lord Reith, the founder of the B.B.C.
Lord Bertrand Russell is known not only to students of philosophy and mathematics,
but to the general public as well, for his views and activities have been such as to
bring him into conflict with the state on a number of occasions, and his philosophic
doctrines have violently opposed large bodies of popular opinion, sentiment and orthodox
beliefs. His earlier life was devoted to mathematics, and his first important book was
"The Principles of Mathematics", followed later by a joint work with Alfred Whitehead,
who became Professor of Philosophy at Harvard, "Principia Mathematica". Stirred from
time to time by the rise of British Imperialism at the beginning of the century, his
philosophy led him to enter the field of politics. His outspoken opposition to conscription in 1915, and defense of conscientious objectors, won him a fine which cost him
his library. When invited to Harvard to give a course of lectures he was denied a
passport, and in 1918 he served a six-months term inj prison for publishing a pacifistic
He lectured in several universities after coming to the United States in 1938, and
when his right to teach philosophy in the College of the City of New York was questioned
because of his moral beliefs, the legal action which followed was played up on the press
as a cause celelfre, somewhat similar to the Dayton "monkey trial". His claims were
not sustained, and he was then appointed for a five-year term as a lecturer for the Barnes
Foundation. This was later cancelled by the director of the Foundation, again not
without wide publicity.
Orphaned at the age of three, his father's designs to have him raised as an agnostic
were apparently successfully circumvented; nevertheless it would appear that the
paternal desires came to eventual fruition. The fundamental characteristic of Russell's
^philosophic position has been an intensive application to his successively developed views,
of the logical mind. By a series of logical progressions he has concluded that "the ultimate constituents of mind and matter are of the same type, the difference between minds
and bodies lying in their structure and not in the elements of which thy are composed
. . . the difference between physics and psychology lying not in the events which they
seek to establish, physics being concerned with structure and psychology with quality."
Stussell thus identifies sensations and images, which compose a man's mind, with physical
events in his brain. It would appear to follow from this therefore that in his theory
of knowledge Russell has modified his original rationalistic views in the direction of
^pragmatism or behaviourism, which he has demonstrated in his work, "An Outline of
The foregoing sketch of Bertrand Russell's life and philosophy has been given at
some length in the belief that such a background is necessary to a consideration of what
Lord Russell now has to say about the relationships existing between Authority and
the Individual.   The views of an individual who during more than half of his life has
Page 158
lifl frequently been in conflict with what is considered as "duly constituted authority" can
not be lacking in interest.
On the first page of Lecture One, entitled "Social Cohesion and Human Nature",
Russell states brieflfly and clearly the fundamental problem which he proposes to consider
in this and the five lectures which follow: KHow can we combine that degree of individual
initiative which is necessary for progress with the degree of social cohesion that is
necessary for survival?" This is followed by an analysis of the problem in successive
steps, followed by an examination of what can be done towards its solution, and finally
a consideration "as a matter of ethics the whole relations of individual thought and
effort and imagination to the authority of the community".
The subject of social cohesion, its history, the stage at present reached and its
possible future development is first discussed; then the subject of individual initiative
is similarly discussed, and finally, as Russell phrases it, "the conflict which modern
technique has introduced between organization and human nature, or, to put it in
another way, the divorce of the economic motive from the impulses of creation and
possession" is considered.
It appears to the reviewer that with the social and economic problems which face
the medical profession, individually and collectively, everywhere today, the addition
of this small volume to the medical library is most timely. It deserves careful perusal,
and the reader will find that its style lends itself to ready comprehension, instruction
and even entertainment. Whether the conclusions arrived at are accepted or not, it is
stimulating reading, hence profitable. —D. E. H. C.
Dr. Deward O. Ferris,
Mayo Foundation, Rochester, Minnesota.
APRIL 27th and 28th, 1950 §|§
Reservations may be made by applying directly to the Hotel.
A special invitation is extended to members of the following Societies:
North Pacific Surgical Association.
Seattle Surgical Society.
Spokane Surgical Society.
Portland Surgical Society.
Tacoma Surgical Club.
President Dr. Arthur B. Nash, Victoria, B. C.
Vice-President Dr. J. R. Neilson, Vancouver, B.C.
Secretary-Treasurer .-. Dr. R. J. Wride, Victoria, B.C.
Dr. W. D. Marshall, Chairman
Dr. J. D. Stenstrom Dr. W. J. Cochrane
Dr. T. M. Jones
Lecture by Sir Reginald Watson-Jones.
A special meeting of the Vancouver Medical Association at the Chest Clinic Auditorium on March 6 was addressed by Sir Reginald Watson-Jones, F.R.C.S., M.Ch.Orth.,
B.Sc., M.B., Ch.B., L.R.C.P., Orthopedic Surgeon to the Kings' Household.
Sir Reginald is the first Sims Commonwealth Professor of the Royal College of
Surgeons and in this capacity was making his second visit to Canada, his first to
The subject of Sir Reginald's discourse was "The New World of Orthopedic
Surgery," and dealt principally with the physical aspects of this new world as exemplified
in the realm of traumatic surgery. He is a renowned teacher, an accomplished platform
speaker, and nobly carries on the tradition of his illustrious predecessors who have led
the field of orthopedics, Sir Owen Thomas and Sir Robert Jones. He spoke clearly and
with charm, the accents and modulations of St. James and Mayfair triumphing over
a temporary difficulty with phonation owing to laryngitis.
The speaker announced that he brought a special greeting to the medical profession
of British Columbia; this came exclusively to this province, the home of the youngest
medical school, from the centre of the British Commonwealth, where ancient and
honourable institutions of medical teaching of world-wide renown have their seat.
He then briefly reviewed the history of the last fifty years in surgery, and more
specifically traumatic surgery starting with reference to the dictum of Sir Owen
Thomas, "the mechanical shall not trespass upon the physiological". "Surgery," it was
declared, "is the restorer of symmetry; nature if unthwarted, will do the rest." This
was beautifully demonstrated by a splendid series of slides which showed how this has
proved true in very many cases of formidable disorganizations of bone and soft parts
which in by-gone days would have furnished summary indications for amputation. With
these were shown some "horrible examples" of what unwarranted and excessive interference may do. To emphasize the broad philosophy of surgery as opposed to mere
mechanical dexterity, and give point to the concept that no advance can take place in
one branch of science without corresponding advance in others, Arbuthnot Lane's "no
touch" technique was referred to as it applies to bone surgery. The work of W. E. Gallie,
of Toronto, in bone and fascia transplants was also referred to and many illustrations
of successful restorations by such means were shown.
Sir Reginald spoke feelingly and admiringly of the fine work of the late Murray
Meekison, of Vancouver, at R.A.F. "crash stations". Many of the best illustrations
displayed were from the photographs and roentgenographic records of R.A.F. crash
That the Air Force injuries and restorations were a subject near to the speaker's
heart was evident especially in his remarks, and the attention he has given to the rehabilitation of these young men. The incredible skeletal damage they sustained and the even
more incredible restoration which was achieved was elaborately demonstrated in the
illustrations of men restored to active and vigorous life who had apparently been destined
inevitably for total crippling.
Restoration, the speaker showed, must be psychological and physiological. Both
physical and psychological education must be right. This must take place in a succession of four stages: Good surgery, good rehabilitation, good re-education and good
"re-settlement". "The job must be fitted to the man, not the man to the job. Instil
hope, resolve anxiety, remove fears—only then are we physicians to the body and the
soul." In this latter connection a note of admiration was sounded for the conception
and working of the Vancouver Rehabilitation Centre. It was evident that his visit to
this institution had strongly and favourably impressed the speaker.
Sir Reginald's arresting style and eloquence drew his address to its conclusion as
he said: "We do not need better mechanics; we need knowledge that will aid repair-"
Page 160
.i or*
He ended most appropriately with Wordsworth's lines from "The Prelude", apostrophizing the Age of Youth, "the chosen time",
"Bliss was it in that dawn to be alive,
But to be young was very Heaven." ||||
A very large and enthusiastic audience greeted the eminent speaker and heartily
showed its appreciation.
Dr. J. R. Naden, in a few well-chosen words expressed formally the thanks of the
Vancouver Medical Association and the pleasure enjoyed by the audience.
—D. E. H.X.
1949 - 1950
President - Dr. J. C. Thomas, Vancouver
President-Elect Dr. Stewart A. Wallace, Kamloops
Vice-President i Dr. H. A. L. Mooney, Courtenay
Honorary Secretary-Treasurer Dr. J. A. Ganshorn, Vancouver
Immediate Past President— i Dr. F. M. Bryant, Victoria
Delivered before the British Columbia Medical Society's Annual Meeting
at Victoria, B. C, 1949.
What is sinusitis? It is a word for the most fashionable conglomeration of symp-
tims suffered by our generation. Only the layman is sure of the diagnosis. To the
rhinologist, the divers forms it takes are an'endless challenge to his special training.
The past 25 years have seen a swift evolution in our concept of sinusitis. After
the First World War, Austria and Germany were considered the centre and fount of
this knowledge. The ear, nose and throat specialist had been a curiosity in the allied
armies. When the war was ended, hundreds of American doctors flocked £o Berlin and
Vienna. These ambassadors of the new specialty returned each with a case of beautiful
hand-forged instruments, a lifetime of prestige, and a conviction that sinusitis was a
disease of the sinuses which could be cured by surgery. Today we think that sinusitis
is a local symptom complex, often of systemic disease.
The first book about the physiology of the nose was written less than t:n years
ago. Since then there have been tremendous advances in enocrinology, nutrition, psychiatry, biochemistry, bacteriology and allergy. Fitting together knowledge from these
fields rescued rhinology from the abyss of disrepute into which it has been flung by the
purely surgical mind.
For example, in the field of endocrinology are syndromes of sinusitis which are due
solely to the lack of estrogenic hormones, yet which present exactly the same symptoms
as acute or chronic bacterial sinusitis. The differential diagnosis is not so much concerned
with whether sinal symptoms exist, or whether we shall call a syndrome sinusitis, as it
is concerned with the underlying etiology. We can no longer think of etiologies in
terms of strains of bacteria, but must think also of systemic endocrine imbalances and
nutritional deficiencies which may have resulted in vaso-motor swelling of the nasal
mucosa, giving rise to symptoms of sinusitis.
Let us consider a not too hypothetical clinical example of vaso-motor rhinitis:
It is sundown.   (It could be tonight in Victoria).   A gentleman stands with a cigarette
Page 161 /
Ml dangling from his lips in the corner of a drawing room by an open window. He is
wearing silk socks, holds a drink in one hand and a handkerchief in the other. His back
is wracked with sneezes, his eyes are watery, his nose is running. He is hawking and
spitting into his handkerchief. His throat is raw from coughing and his neck muscles
are sore.  He has a headache.
Hersh, of New York, in a recent analysis of 1000 headaches, traced 25% to
vasomotor swelling of the intra-nasal and sinal mucosa, and ascribed another 25% to
reflex cervical muscle spasms, variously termed myositis, fibro-myositis, or the cervico-
somatic syndrom. Muscle changes in the neck, particularly of the trapezius, were
demonstrated by Wolff using myographic electrical tracings.
Patients of this type present themselves to their physicians complaining of "sinusitis". They are literally holding their heads in their hands and say: "But, Doctor,
the headache is worst right back here in the cords of the neck. If you could only do
something about that."
It is the older clinical physician who knew, long before Wolff came along with
his myographical electrical tracings, that the best treatment was a hot poultice, a
Liniment and massage, and local heat. He knew that the swelling inside the nose was
best controlled by bed-rest, stable room temperature and steam inhalations. He knew
there existed a definite relationship between cervical muscle spasm, occipital headache,
and so-called sinusitis. The rationale of traditional heat and massage therapy becomes
more scientific.
A. Infectious (bacterial or viral) I  15%
B. Mechanical or Anatomical . 10%
C. Vasomotor - | I 75%
fl. Allergic   I I 35%
[2. Physical Agents _ 15%
3. Endocrine 10%
4. Nutritional 10%
5. Miscellaneous 5%
Intrinsic factors.
Vasospastic Drugs
*Not necessarily vasomotor.
Weather:   (Temperature, humidity,
light,  barometric  pressure,  fumes,
dust, etc.)
Excess Carbohydrate
Psychological (emotional)
Febrile states*
Debilitating disease*
The term "Sinusitis" itself is unfortunate in that it ascribes the notion of inflammation and infection to a phenomenon which is^ above all, vasomotor. The incidence of
primary bacterial or viral agents in sinusitis is probably less than 15%. What infection
we do see is often secondary to intra-nasal oedema, stasis and obstruction. That
architectural or mechanical defects within the nose contribute to nasal obstruction and
sinal symptoms cannot be denied. The large cystic turbinates, the fracture deformities
and pressure-point spurs of the nasal septum are all too common, but that they constitute a surgical challenge in more than 10% of cases no longer holds.
What has happened to our friend in the drawing room? Concerning him we
might say that vasomotor responses are commonest in the early morning and at nightfall,
when temperature variations and chilling most frequently occur. There are frequently
vasomotor responses to the ingestion of alcohol, the presence of excessive smoke, or
dust, or humidity.   Sinusitis may be complained of when the mucous membrane is
Page 162
& producing either too much or too little moisture. The patient becomes conscious of
discharge in the throat when mucous is either abnormally fluid or excessively viscid,
when it becomes mechanically or chemically irritating, odorous or obstructive. A dry
condition of the nose and throat is often produced by belladonna which reduces humidi-
fication and ciliary activity. The same parasympathetic symptoms can be experienced
by the unaccustomed public speaker. It often times occurs in circumstances of social
stress. We all know the dryness of febrile states, the nasal mucoid stasis in debilitating
disease, the vasomotor isecretory disturbances in cardio-nephritics and in heart failure.
We see the stuffy nose and the accompanying headache that may characterize emotion,
recumbency, or simple chilling.
As human beings, we physicians are personally familiar with the relation of recumbency and simple chilling to a stuffy nose. When we arise in the morning, and our feet
—unslippered—touch the cold floor, there is a reflex vasomotor flooding of the nose.
We frequently sneeze or cough at this time. People like the Finns, for example, who
live in an unfriendly cold climate, have evolved in their culture the habit of steam baths
followed by a plunge into ice water. They have learned through countless years of
previous living the secret of what we modernists call "contrast baths". They now know
that thermal conditioning toughens, as it were, our labile vasomotor responses. We have
learned that histamine is released in vasomotor responses. It appears likely that in this
country we may succeed in substituting for the bath—Benadryl.
These disturbances are not diseases of the nose. They cannot be dismissed as rhinitis
whether it be intumescent rhinitis, allergic rhinitis, simple rhinitis or catarrhal rhinitis.
These complaints are frequently rhino-sinal manifestations of systemic vasomotor phenomena. To repeat, these phenomena may or may not give rise to sinus symptoms, and
this depends upon the degree of oedema, the advent of secondary infection, or the local'
pressures within  the nose,  aggravated by architectural or mechanical  abnormalities.
The nose and sinuses must be thought of as belonging to the respiratory tract.
Bronchiectasis and bronchial asthma illustrate very well this unity. We no longer believe
that sinusitis causes bronchiectasis. They simply co-exist. Nor is bronchial asthma often
seen in the absence of allergic rhinitis. In either case, that the sinusitis should have
become bacterial and suppurative is neither more nor less remarkable than that the
bronchiectatic lung should suppurate.
The sinus mucous membranes are extended portions of the nasal mucosa. Patholgic
changes in the nasal mucous membrane are accompanied by similar changes in the
sinal mucosa. During the growth of the face, from babyhood to maturity, the nasal
mucosa grows into the scaffolding we call the paranasal sinuses. Hence, whatever
happens in the nose can happen also in the sinuses. Vasomotor rhinitis is frequently
vasomotor sinusitis. An antrum that is dark today may transilluminate beautifully
tomorrow, or it may remain dark in the presence of a deviated septum, because of altered
function. It is for precisely these same reasons that X-Rays of the sinuses are so often
negative despite the reality of sinal symptoms.
1. Wet obstructive nose with or without sneezing.
2. Post nasal discharge.
3. Dull frontal—occipital headache
4. Cervical myalgia
5. Mental depression.
1. Cough
2. Sore throat
3. Pain
4. Stuffy ears or deafness
Page 163 What, then, is sinusitis if it is not a disease? Certainly it is a reality. Articles in
the Readers' Digest, paragraphs in Time, pictures in Life all attest to its existence.
Sinusitis is a symptom complex of considerable variability. The basic features are
the wet obstructed nose, the post-nasal drip, the dull frontal or occipital headache, the
cervical myalgia and the mental depression that every man who practices medicine
knows very well indeed. If there should also be present a mechanical or structural
defect within the nose or sinuses and a super-imposed infection, one can usually add
one or more of the following symptoms: Cough, sore throat, ear complaints and facial
These basic symptoms are those that characterize vasomotor rhinitis. They are
secondary to swelling and congestion within the nose. Anyone who has lived through
those endless hours of total nasal obstruction in the early phases of a common cold (and
I think most of us have) are convinced that irritability and mental depression can be
symptoms of intra-nasal oedema and pressure.
Now a word about the accessory symptoms of sinusitis:
1. Pain:
Contrary to lay opinion, severe pain is rarely found as a symptom of sinusitis
except in the acute inflammatory type when suddenly the lining membrane swells.
Occasionally a slowly evolving empyema will give pain and tenderness. Whereas
there is fever in the early inflammatory type, fever is rarely seen in chronic empy-
emata. However, an elevated sedimentation rate is invariably found when pus is
2. Cough:
The drainage openings of the antra are on the top mesial side. This is because the
face grows downward as the jaws and maxilla adapt themselves to adult chewing
needs. The antrum started its growth as a small bud, high in the nose. This bud
becomes the opening of the antrum and remains located high in the nose during
adult life. At night when we lie down, the antrum is turned on its side. The outlet
then becomes dependent, pus runs into the nose, flows back over the ustachian
tubes causing oedema ,of the tubes and deafness. The exudate continues into the
throat causing sore throat; on into the larnyx and trachea causing cough.
3. Sore Throat:
A sore, red throat is sometimes the only symptom and sign of chronic suppurative
4. Chronic Cough:
A chronic cough in the presence of a dark antrum is highly suggestive of suppurative sinusitis.
5. Ear Symptoms:
As a consequence of irritation or oedema at the naso-pharyngeal end of the eustachian
tubes, there may be referred to the middle ear fleeting moments of sharp pain.
There may be popping and crackling sensations in the middle ear. Occasionally,
with persistent tubal oedema, the hearing becomes muffled and dull; episodes of
light-headedness may occur. These symptoms of the ear may accompany suppurative sinusitis, or vasomotor rhinitis, from whatever cause. Indeed, they may be
our only clue to the existence of such traditionally unrelated diagnoses as Sinusitis
—or the menopause.
The significant feature of the classification of sinusitis as shown is that 50%
of sinal symptoms derive from so-called allergic sources. There is not time to enter the
controversial subject of allergic sinusitis. There is not yet an agreement of definition
among rhinologists as to just what allergic rhinitis is. There are few reputable criteria
of diagnosis. Eosinophiles in the nasal secretion are like skin tests for foods and inhalants
—variable and inconclusive. When does a chemical rhinitis, due to the use of Privine,
become an allergy?   Is it because eosinophiles may appear in the exudate?   Eosinophils
Page 164
-S W?.:
may also appear in the early coryza or in the serous rhinitis (to use an outmoded pathologic classification) of chilling and of emotion.
The physical characteristics of the allergic nose, upon inspection, are variable.
The mucosa that is very pale, translucent with oedema, in a nose which appears to be
full of wet, swollen turbinates, is usually an allergic nose. The symptoms may b$
indistinguishable from those of any vasomotor, rhino-pan-sinusitis whether due to
emotion, chilling or the virus. The antra will usually be either very dull or completely
dark upon transillumination. The onset is frequently acute. Vasomotor rhinitis caused
by inhalant allergens is the commonest type and usually presents a pale grey nasal
mucosa. In general, the degree of paleness is directly proportional to one's ability to
make the diagnosis of an allergic nose. In contrast, fumes that are chemically irritating
to the nose cause a congestion, which although wet, is more apt to be red than pale
grey. The questions whether one wishes to include vasomotor rhinitis which is secondary
to physical agents, in the allergic group* is an open queStidn. More important is the
realization that allergic or not, the rhinitis is vasomotor. The treatment of the acute
vasomotor nose is often one of finding the most effective and well-tolerated antihistamine for that particular person. Chlor-Trimeton, 4 mgms. 4 I. D. for adults and
2 mgm 4 I. D. for children, seems to be the drug of current choice. Chlor-Trimeton
has a remarkably low incidence of toxicity and a high incidence of efficicy. However,
all cases of low-grade perennial rhinitis that do not respond to the anti-histaminics
deserve to be skin-tested for the inhalant allergens. Skin tests are about 20% accurate,
as we know, especially for foods. A negative skin reaction for milk does not mean that
milk may not be the cause of post-nasal drip. Again and again, patients ask: "Is milk a
mucus producer?" It seems to be a part of the folklore of rhinology that milk produces
mucus. There is scientific evidence that many people are allergic to milk (milk, eggs
and chocolate are common foods to which people are.allergic). One can be sure only
by eliminating particular articles of food from the diet and noting the effect on the
patient's symptoms. When tests for inhalants fail, many rhinologists empirically give
a course of dust-desensitization. Standard dust extract contains many environmental^
allergens that occur in the home: hair, dander, feathers, lint, molds and bacteria. It is^
a shotgun extract which in the absence of specific allergenic evidence is used with;
surprisingly effective results in many cases of perennial allergic rhinitis—cases that
would otherwise be dismissed as hopeless. Dust is relatively harmless to administer and
certainly can b^ undertaken by the general practitioner. The complications of neglected
childhood simple allergic rhinitis are seen in adult asthma.
There are a number of interesting and specific causes of sinusitis. One of these
comes under the heading of intra-nasal medicaments. In medical literature exists too little
condemnation of nose drops. They are advertised widely as vaso-constrictors. Most of
them are actually vasospastic drugs. This is especially true of the synthetic drops. Those!
in soluble combination with antiseptics and the sulfonamides are particularly harmful.
Napthazoline and a solution of 1.25% sodium sulfathiazole have caused marked fibrosis,
permanent ciliary damage, epithelial metaplasia and fixed vascular dilation in experimental rabbits, in a matter of weeks. One per cent of ephedrine in normal saline is a
harmless and efficient vaso-constrictor, both topically and orally. Its action is mild
and it does not further insult the vasomotor imbalance already present. Many cases of
sever pseudo-allergic rhinitis, better termed chemical rhinitis, have been terminated by
insisting that the patient give up all nose drops. Privine is the most consistent offender
in this category. I have seen dozens of cases—cases representing all the symptoms of
severe pan-sinusitis. If these patients were using Privine, the cure required 48 hours
of complete withdrawal. It was sometimes necessary to hospitalize the patient so that
he might be well sedated, and the withdrawNal of Privine assured. Here, again, Chlor-
Trimeton and steam inhalations were allies. In 48 hours these people were well and
unbelievably grateful. One case had been using Privine every three hours, day and
night, for more than six months following a simple cold!
Page 165 j Penicillin solutions up to 5000 units per cc. have been shown to be quite harmless
experimentally and clinically. The calcium salts are thought to be especially well
tolerated by the nose. This arit-i-biotic, however, has a very limited application, but it
does combat bacterial ethmoiditis effectively when used with 1% ephedrine. Penicillin
powder in the nose seems to be quite effffective in cases of bacterial ethmoiditis. That it
might cure vasomotor rhinitis is preposterous.
Penicillin aerosol for office use is effective and seems to be associated with a lowered
incidence of irritative reactions in the nose as compared with the powder. In cases of
suppurative ethmoiditis, gentle lavage of the nose with warm, normal saline after
shrinkage with one per cent cocaine and ephedrine, followed by penicillan aerosol gives
gratifying results.   (One's nurse can do the treatment.)
'Although endocrine-rhinitis has been touched on previously, the subject merits
reiteration because of its common occurrence among females of the climacteric age group.
These ladies complain of stuffy nose and frequently stuffy ears, and of excessive mucus
in the throat. They frequently also complain of being light-headed and, of course, as we
all know, of being mentally depressed and irritable. Physical examination of the nose
in these cases reveals a pale indolent cyanotic nasal mucosa throughout—a suggestion of
what the textbooks call atrophy. It is amazing how the stuffiness vanishes and the
pale cyanotic indolence gives way to pink healthy mucosa when adequate estrogen
substitution therapy is employed. The same results can be achieved in cases of hypothyroidism. The appearance of vascular atonicity here is not characteristic. These people
are not profound hypo-thyroids and often a very short course of thyroid extract is
adequate to get them over the vasomotor imbalance which brought them to the rhinolo-
gist complaining of a stuffy wet nose. Of these two the menopausal symptom is by far
the more commonly seen.
Among nutritional causes of vasomotor disturbances in the nose, excessive carbohydrate is probably the single greatest offender in children. Sugar, as we all know, has
little body-building value. It has* energy, caloric, value only, and its oxidation takes
place at the expense of essential food elements found in raw vegetables, fruits and meat
products. The huge tonsils and adenoids, the deafness, dental caries, and anaemia found
in malnuitrition have their expression in the nose. Avitaminosis especially of C is
related to tissue oedema. There is growing evidence that the naturally occurring vitamins
are preferable.
Among specific bacteria problems in the nose maxillary sinus empyema is the most
satisfactorily treated. The concomitant use of systemic triple sulfonamides, or penicillin,
with surgical lavage of the antrum renders antral empyemata easily cured without
It is also true that a few suppurating maxillary sinuses harbor penicillin-resistant
organisms. In these, the use of streptomycin systemically and one per cent sulfa-mylon
locally are often effective. In bacterial sinusitis there is usually associated a vaso-motor
disturbance which may have anteceded the bacterial suppuration, or which may have
developed because of the infection. Often it is advisable to use one per cent ephedrine
in normal saline nose drops four times a day, plus chlor-Trimeton by mouth in order
to establish drainage; at the same time combining the systemic use of either penicillin
or streptomycin with surgical lavage of the antrum. Despite this regime, a few cases
will require naso-antral window.  But rare today is the need for radical sinus surgery.
When a general practitioner advises a patient never to let anyone puncture his
sinus, he builds up patient-resistance to proper antral-management. Thereby he does
both his patient and the rhinologist an injustice. This bias is a heritage the specialty
well deserves because the method employed in the past, in which amid great crunching
Page 166
MB of bone and near-shock the deed was done, is anachronistic. Today, using a middle
meatus catheter where there is no bone, antral lavage is a simple procedure whether the
patient is 7 or 70. Using this method there is no bleeding, no pain, no shock. It is the
memory of less felicitous methods that give rise to patient and.doctor resistance.
Suppurative frontal sinusitis usually develops during the course of the common
cold. It is, as we know, an extension of pyogenic secondary invaders into the frontal
sinus. Severe inflammatory oedema of the frontals causes prostrating supra-orbital pain.
Penicillin, the sulfonamides, and local ephedrine in normal saline are usually adequate
therapy. However, when an empyema develops and is retained, the help of a rhinologist
is urgent. Any frontal headache which comes on between two and three hours after
arising in the morning and grows worse during the day, is aggravated by bending or
stooping, which disappears toward evening only to reproduce this pattern day after day,
should be referred to the rhinologist. External trephination for drainage is rarely
required. Fracturing the middle turbinate medialwards toward the septum is a minor
procedure, and will provide drainage in nine out of ten cases. Neglected, the frontal
sinus empyema is potentially the most dangerous of all sinusitis, because the posterior
wall leading to the frontal lobes of the brain is much thinner than the anterior sinal
walls. Penetration into the silent area of the brain is fatally insidious. Any persistent
frontal headache that comes on two to three hours after getting up in the morning,
that pounds and gets worse during the day only to subside at night and recur the next
day is a bombshell.
In conclusion, it is well to re-emphasize the changes that have occurred in our
concept of sinusitis, its etiology and treatment, in the past decade. Otorhinology has
passed from a surgical to a medical specialty ... as the same otolarnygologist has expanded
his surgical talents toward the fields of broncho-esophagology and rhinoplasty.
Six-room house, separate entrance to waiting room and office, one
acre. Landscaped garden. Located in rapidly growing municipality.
Previously owned by Dr. Marr.
For particulars apply:
Phone: Langley 18X1
D. S. MUNROE, M.D., M.R.C.P. (Lond.), F.R.C.P.(C)
Vancouver, B. C.
Read at Meeting of North Pacific Society of Internal Medicine, at Victoria, B.C.
September, 1949.
The subject of fat embolism is one which has occasionally been discussed before
medical groups for many years. It has, however, never become a condition which
readily crosses the mental threshold of the average doctor when he approaches an acutely
ill patient with an apparent chest or brain lesion. Even the presence of a plaster cast
on one or more extremities may not be sufficient to force the diagnosis on one's mind.
Fat embolism remains one of those many conditions in medicine which is comparatively
easy to diagnose if it is considered. It also remains the one non-surgical condition that
the orthopedic surgeon will diagnose before his medical consultant even thinks of it.
Since the war, we have had occasion to see several cases of fat embolism. I do not
propose to present any statistical review of these cases because I do not think that any
new diagnostic or therapeutic point has been brought forward. A brief review of the
subject, however, I thought might be of interest. \
The frequency of fat embolism seems to be almost impossible to estimate. A few
reported figures will serve to exemplify this point. Denman & Gragg (1) in 1948, studied
99 autopsies selected at random. In 32%, fat emboli were present, and 7% died as a
result of fat embolism. Vance (2) in 1931 in a study of 246 routine autopsies found
fat embolism in 44%, and in 5.7% it was considered to be the cause of death.
These two series suggest that in routine autopsy material, fat embolism is the
cause of death in about 6%, and that the condition may be diagnosed as being present
in 35 to 40% of cases.  These are, to me, surprising figures.
Robb-Smith (3) in 1941 reported the presence of gross fat embolism in 33% of
125 autopsies done on patients in which death was due to accident. In another series
of autopsied cases due to injury reported by Mavor (4), 40 cases had a fracture of one
or more long bones. Of these in 7 deaths (17%), the cause of death was due to fat
embolism. On the other hand, Darrach (5) has reported only two cases of fat embolism
among 12,000 fractures in New York.
There are thus big differences in the reported incidence and mortality in fat embolism. Why the discrepancy? Perhaps the greatest factor is the varying index of suspicion
of the man doing the autopsy and the required technique to demonstrate the fat. Perhaps fat embolism occurs very commonly with such few or such mild symptoms that
no additional entity is suspected. Perhaps many mild cases are passed by as a mild
post-operative bronchitis. Many of these would be diagnosed at autopsy by a searching
pathologist or missed by one who was not impressed with the possibility of fat embolism.
On the clinical side, no reliable figures are available as to the incidence of fat
embolism. Many writers insist that it is present much more frequently than suspected.
Robb-Smith (3) may be quoted as saying that "there is little doubt that many of the
complications of injury such as traumatic pneumonia, delirium, delayed shock and blast
are in reality fat embolism." Newman (6) has added concussion to this list.
Precipitating Factors
Injury, and especially injury with a fracture of a long bone, is by far the commonest precipitating cause. Extensive burns are perhaps the next most common cause,
although fat embolism is an uncommon complication of burns. Fat embolism may be
found at autopsy in a multitude of other conditions, but these are usually of no import.
Finally, I must mention one of our cases in which massive fat embolism occurred following resection of a large lipoma on the medial aspect of each thigh.
The pathogenesis of fat embolism has been a source of much argument and considerable investigation.  There is unanimity of opinion on only some of the factors involved
Page 168
»' %»
and much speculative and often contradictory evidence on others. Harris, Perrett and
MacLachlin (7), in 1939, published an interesting paper and listed three things that
were necessary for fat embolism to occur.
(1) An accumulation of fluid fat freed from its cellular envelope by trauma.
(2) Open veins, the ends of which do not collapse.  Veins normally collapse when
they are opened.
(3) The pressure on the accumulation of fat must be greater than the pressure
in the veins.
It will thus be evident that in the case of fractures, all these requirtements may
be met—the fat is freed, the veins are held open in the Haversian canals and the wound
exudate may readily accumulate under tension. These authors did some experimental
work using human fat. Previous investigators had used vegetable or mineral oils. They
were able to establish that hydrolyzed fat (dilute hydrochloric acid added to human
fat) was very much more toxic to experimental animals than neutral fat. The pathological picture of human fat embolism could be reproduced and it was their opinion
tht the serious effect of fat embolism may be due to alteration in the fat, whereby it
becomes much more irritative and toxic. Thus, the chemical as well as the physical
characteristics of fat may be important.   Proof of this is lacking.
The elimination of fat is said to be by four ways.
(1) Passage through the glomeruli into the urine.
(2) Excretion by the liver cells into the bile.
(3) Absorption by phagocytes.
(4) Solution by lipase in the blood stream.
Pathology (8)
Perhaps the most characteristic gross pathological lesion is acute pulmonary oedema.
Petechial haemorrhages may be noted in the brain. Microscopically, fat droplets may
be found in almost every tissue in the small vessels and capillaries. The droplets are of
irregular shape and varying size and in ordinary paraffin sections appear ps vacuoles.
The true nature of these vacuoles is readily demonstrated by appropriate fat stains.
Considerable degree of coronary embolism can be demonstrated. The fat passes through
the alveolar walls into alveoli and may often be recovered in the sputum as early
as 36 hours later. It also passes through the glomerular capillaries to appear in the
Clinical Picture *
The clinical picture of the victim with fat embolism is often fairly characteristic—
often very obscure. The patient is one who has suffered a fracture of one or more bones.
His early symptoms are usually related to his traumatic lesion alone. After an interval
which varies considerably but which averages about 36 hours, the patient becomes
dyspnoeic and begins to cough. The cough is soon productive of watery mucus, which
very frequently is heavily stained with red blood. An attempt to bring forth his history
may be satisfactory, disappearing, or even useless because of his mental state. This
mental state may be quite clear, slightly dulled, or so dulled that the patient superficially would appear to have encephalitis. His memory may be poor, he may be restless,
disorientated, irritable, stuporous, or even comatose.
The symptoms are thus either pulmonary or pulmonary and cerebral.
In the lesser grades of the condition, examination may reveal nothing. Usually,
however, cyanosis is present, the pulse rate is elevated and the temperature ranges to
104 degrees F. The patient coughs almost continuously and at first glance the picture
is one of acute pulmonary oedema or extremely acute bilateral pneumonia. Widespread
rales are present throughout both lungs. Vague unrelated and fleeting neurological signs
may be present. Petachiae should be sought for, and if they are only few in number, they
are most likely to be found in the lower neck, pectoral areas, and in the conjunctivae.
If more numerous they may spread over the trunk and even to the legs. Usually, how-
Page 169
BBS ever, only a few petechiae are to be found and they are easily missed.
Exudate round the macula and following the course of the retinal vessels as well
as small haemorrhages may be seen by opthalmoscopic examination (9).
X-ray of the chest gives the picture of pulmonary oedema, or a more irregular
picture of blotchy infiltrative lesions. There is nothing characteristic from a radiological
point of view. A considerable quantity of fat may be held up in the lungs without
producing radiographic changes, although functional impairment may be present. This
statement is suggested because fat can often be found in the sputum with a negative
radiograph, and also by animal experiments.
Differential Diagnosis: ?MM
Several things must be considered and almost any one of them might be diagnosed
unless one considers fat embolism. These include broncho-pneumonia, acute heart
failure, septicaemia, cerebral concussion or compression, and even alcoholism, if the fat
embolism comes on soon after the accident. Each can usually be excluded in time, if
not immediately. |pp
The diagnosis can often be confirmed by the use of two laboratory aids.
(1) Fat in the sputum: It is said that fat may be obtained in the sputum in normal
individuals and especially in those with pulmonary disease. In these instances, however,
the fat is said to be in the form of fine globules within the phagocytes. Finding of
extra cellular fat globules in a suspected case of fat embolism is strong confirmatory
evidence. The larger the size of the globules, the stronger is the evidence. This usually
does not occur until at least 36 hours after the onset.
(2) Fat in the urine: This occurs later (after 4 to 5 days) but is a more reliable
diagnostic aid. Two technical points should be remembered—fat floats on the surface
of urine and thus is most likely to be present in the last bit voided, and secondly, a
lubricated catheter may be the means of obtaining a false positive result. Some surgical
lubricants are water soluble, but it is best in these cases to use water only as a lubricant.
All the urine for 24 hours should be saved and allowed to stand. The fat rises to the
surface. A capillary tube is then allowed to just touch the surface of the urine and
the drop transferred to a slide and stained with a fat stain. The most important thing
to differentiate from the fat globules is air bubbles.
The course of the disease is one of acute illness for a period of several days. During
this period it is most important to do a daily red blood count and haemoglobin, because
a fairly acute anaemia may develop. Harris et al (7) were the first to point out this
fact and to them it was taken to be a corroborating sign in the diagnosis.
Treatment is usually stated to be of little avail or "symptomatic". I cannot concur
with this feeling of futility and I am confident that much can be done to tide the
patient over.
The following are the most important things:—
(1) Oxygen—this is well worthwhile and often considerable immediate improvement occurs. It is preferably administered by tent, especially in the "cerebral"
cases. pll
(2) Penicillin—this is of distinct prophylactic value.
( 3 ) Blood transfusions—these are not infrequently required to alleviate the anaemia
and should be given if the erythrocyte count falls.
Recovery is not followed by any permanent damage.
As far as prophylaxis is concerned nothing is of much value except early immobilization of fractures.
To summarize, fat embolism is not rare, it is not always or even usually fatal; it
exhibits a reasonably uniform clinical picture and therapy is of avail. The most difficult
thing about the diagnosis is to remember that such an entity exists.
Page 170
du Bibliography:
(1) Denman, F. R., & Gragg, L.—"Fat Embolism," Arch. Surg. 57: 325, 1948.
(2) Vance, B. M.—"Significance of Fat Embolism"—Arch. Surg. 23: 426, 1931.
(3) Robb-Smith, A. H. T.—"Pulmonary Fat-Embolism," Lancet 1: 135, 1941.
(4) Mavor, H. R. R.—Quoted by Newman, P. H.—"Clinical Diagnosis of Fat Em-
balism," J. Bone & Joint Surg. 3OB: 290, 1949.
(5) Darrach, W.,—Discussion of paper by Harris, Perrett — MacLachlin, Ann. Surg.
110:  1095, 1939.
(6) Newman, P. H.—"The Clinical Diagnosis of Fat Embolism," J. Bone & Joint Surg.,
30B: 290, 1948.
(7) Harris, R.  L.  Perett,  T.  S.  & Maclachlin,. A.—"Fat  Embolism"—Ann.   Sur
110: 1095, 1939.
(8) Warren, S— "Fat Embolism," Am. J. Path., 22:69, 1946.
(9) Fritz, Mi H. & Hogen, M. J.—"Fat Embolization Involving the Human Eye,
Am. J. Ophth., 31: 527, 1948.
F. W. GRAUER, M.D.C.M., F.R.C.S. (ED.), F.A.C.S., F.I.C.S.
Perforation of a gall bladder apart from traumatic rupture is usually a complication of pre-existing gall bladder disease. Perforation may occur slowly and quietly
or more commonly be the outcome of an acute or subacute exacerbation in a chronically
diseased gall bladder. Over 90% of patients with perforated gall bladder give a positive
history for previously existing biliary system disease.
Prior to 1924, when Graham and Cole introduced the dye concentration X-Ray
test, the diagnosis of gall bladder disease was made largely on a clinical basis. The commonest sign of cholecystitis in those times was, according to Dr. Terence /Turner, an
appendectomy scar. The discovery of the dye concentration test stimulated much interest
in gall bladder disease and as so often happens, this test, for a while at least, was held as
the ultimate in finality of diagnosis. Today we realize that it provides only another useful
aid in the study of any given patient. By 1934, many surgeons were recommending
early surgery for all patients with acute cholecystitis and prophylactic cholecytectomy
for those with chronic cholecystitis, particularly those with calculi. «|
It is difficult to obtain accurate figures to demonstrate the incidence of gall bladder
perforation. Many case histories show just the word "cholecystitis" and many diagnoses
are in reality clinical impressions. The number of perforations we know, but the number who had acute or chronic cholecystitis we do not know for certain.
To simplify, one uses the term "Total Cases" to include acute, subacute and exacerbations of chronic cholecystitis; in short, all conditions which might lead to perforation.
TABLE I. Incidence of Gall Bladder Perforation
Total Cases        No. Perforated    "   % Perforated
Cowley and Harkins. * 12,915 433 2.8
BachhubereftfJ I     1.699 90 5.3
Vancouver General Hospital     2,493 19 .8
O—Acute, subacute, and chronic cholecystitis.
X—1932 to 1947 inclusive.
TABLE II. Incidence of Gall Bladder Perforation in Post Mortem Room*
No. of Consecutive     No. of Gall Bladder
Autopsies Perforations i°
Johnstone & Ostendorph I 12,000 32 .26
X Vancouver General Hospital  10,941 7 .065
X—1932 to 1947 inclusive.
Page 171 Since perforation must be the end result of pathological process, be it acute, subacute or chronic, in point of time, the pathology of these processes may be of interest.
Niemeier's classification appears widely quoted in the literature. He recognizes three
clinical types:
Type I. Acute, free perforation into the abdominal cavity with generalized peritonitis. This may be a suppurative or biliary peritonitis depending upon the patency of the
cystic dust and presence of infection.
Type II. Pericholecystic abscess with gall bladder perforation and localized peritonitis.   The abscess may be in the adjacent liver substance.
Type HI. Biliary fistula. This may be external or internal. The external type
results from an abscess bursting through the abdominal wall or more commonly following
surgery. The internal type applies to perforation of an adherent gall bladder into a
neighboring hollow viscus such as the duodenum, stomach or transverse colon.
It will be noted that this classification depends largely on whether adhesions have
formed prior to perforation and on whether the gall bladder adhesion has involved
another viscus.
In Cowley and Harkins series the pathological laboratory diagnosis in perforated
gall bladders was as follows:
Acute exacerbation of chronic cholecystitis  33.6% i    .
Chronic  cholecystitis  i  28.6% J    62-2%
Gangrene  1 1 24.0% "J    tg *<y
Acute cholecystitis  .  14.3% J
Carcinoma   I Rarely
Johnstone and Ostendorph show an incidence of calculi associated with perforation
in 85% in a combined series of 265 cases of gall bladder perforation. It would seem
fair to assume then that chronic gall bladder disease, particularly with cholelithiasis, is
the commonest pathological background leading to perforation.
From an etiological point of view the diseases leading to gali bladder perforation
may be listed as follows:
1. Non-specific Inflammations
(a) With or without calculi;
(b) With or without cystic duct obstruction.
2. Traumatic rupture of the gall bladder.
*3.   Specific inflammations, such, as tuberculosis, typhoid and syphilis.
4.   Carcinoma of the gall bladder.
Gangrene of the gall bladder is included under non-specific inflammations because
it is doubtful whether it occurs primarily. It may, however, occur along with perforation following torsion of the gall bladder.
Pursuing the calculus further, we find several methods of mischief. A stone by
direct mechanical attrition and ulceration on a softened, inflammed wall or gangrenous
wall, or one with intramural abscess, may eventually work its way through to perforation. Since 90% of 433 patients with perforated gall bladders gave a history of previous
gall bladder attacks, it would seem reasonable to assume that the majority of calculi
required more than exacerbation to complete the penetration.
Another method of penetration is by the nature of the calculus, wherein a small,
hard, pointed stone, acting as an arrowhead, finally punctures the gall bladder and leads
to free perforation into the abdominal cavity and generalized peritonitis. The opening
may be only pin hole in size. yp|
A calculus may lodge at the mouth of or in the cystic duct and give rise to
empyema or mucocele, depending upon the presence of obsence of infection. Either
of these may result in perforation. The shrivelled up gall bladder containing stones may
well have gone through an obstructive phase with final absorption and contraction, or,
Page 172
* more directly, such a gall bladder may reach its contracted, thickened state through
repeated inflammation with resulting scar tissue contracture in the absence of
Cases have been described in which perforation with stone extrusion into surrounding adhesions has occurred, creating a false diverticulum or sac communicating with the
gall bladder and assuming a reservoir function. If there should be an infection in this
cavity a localized abscess will form, but suppuration does not necessarily follow upon
the perforation of a gall bladder. Stones may be found in adherent masses of omentum
with no obvious signs of inflammatory exudate.
All of us are familiar with gall stone ileus wherein usually a large stone lodges
in the terminal ileum, having entered the small bowel through either a cholecystoduo-
denal or other fistula. Patients have been known to vomit biliary calculi as well as pass
them per anum. Some indeed rare internal fistulae have been reported. Communication
between gall bladder and right kidney pelvis with the passage of many biliary calculi
into the urinary bladder, as well as bile stained urine, has occurred. Communication
between gall bladder and uterus with subsequent passage of calculi pet vaginam has
been reported. Fistula between gall bladder and inferior vena cava with extrusion of
calculi into the latter has been described at the post mortem. Communication between
gall bladder and bronchus through the intermediary of a subphrenic abscess resulting
from gall bladder perforation, the abscess having ruptured spontaneously into the
bronchus, has also occurred. A less rare type of fistula is described wherein the gall
bladder has perforated into the liver substance. This may result in intrahepatic abscess
or in fistula formation with the right intrahepatic biliary tree. Free calculi have l>een
found extruded from the gall bladder into a cavity in the liver substance. The gall
bladder may form a fistula with the common duct.
In Cowley and Harkins series of gall bladder perforations the following signs and
symptoms were described:
Persisting R.U.Q. pain with nausea and vomiting was usual. 40% had pain radiation to the back. 20% had jaundice. 96% were tender or rigid. 28 % had generalized
abdominal tenderness. 24% had a palpable mass in the R.U.Q. The white blood cell
count varied from normal to 20,000. The temperature varied from subnormal to marked
elevation.  The diagnosis was correct in 12% of cases.
Johnstone and Ostendorph state that 49% of 32 instances of perforated gall bladder
coming to autopsy were undiagnosed clinically. tW^
The mortality rate in gall bladder perforation is strikingly high and may be
attributed, in part, to difficulty in diagnosis, resulting delay in surgical treatment and
the peak incidence being in the past 50 age group. The following figures speak for
TABLE III. Mortality in Perforated Gall Bladder.
No.  of Cases No. of Deaths %
Heuer   (1937)    j  500                 225 45.0
Cowley & Harkins  (1943) | S 443                   92 20.8
Bachhuber (1945)   (operated on)_     54                     7 12.9
(Not operated on)     36                   36 100.0
Vancouver General Hospital 19                     7 36.8
At this point I would like to present briefly 5 cases of perforated gall bladder I
have been party to during the past 3 years.
Case I. A white male, aged 45 years, was in a medical ward with deepening jaundice
for 10 days. When seen in consultation he was practically moribund, with fever, somnolence, general abdominal resistance and moderate distension. On opening the abdomen
there was generalized dark green staining of all serous surfaces. There were no adhesions
about the moderately thickened,  half-shrivelled   gall  bladder,  and  a  careful  search
Page 173 revealed no microscopic perforation of the biliary system or bowel. No stones were
palpable. The abdomen was closed with a drain in the R.U.Q. The patient died. Post
mortem revealed a pinhole perforation of the fundus in the grooved reflection between
liver and gall bladder. There was a single, small, pointed stone with its tip in the pinhole.
The gall bladder showed evidence of chronic cholecystitis and cholelithiasis.
I recall an article describing primary biliary peritonitis in which several cases were
operated upon. No perforations were found in the presence of marked greenish soiling
of the peritoneum. There were many theories mentioned, including oozing of bile through
microscopic openings in the gall bladder wall, and these are of developmental origin and
something akin to the Thebesian foramina in the auricles. One wonders if in reality
these might have been pathologically similar to Case I.  •
Case II. A white female, aged 44 years, was admitted to hospital on December 31, 1947,
with a diagnosis of acute appendicitis. Her symptoms began at 3:00 a.m. on the date
of admission, with sudden onset of lower abdominal pain, then vomiting and settling
of constant pain in the R.L.Q. The W.B.C. was 13,510 with 82% polys. There was
a history of previous occasional gaseous indigestion associated with constipation. The
diagnosis was not clear and gynaecological consultation was sought. More tenderness
was reported in the right adnexal than in the appendiceal area. The sedimentation rate
showed moderate activity. Intravenous pyelograms on January 5 th, 1948, were normal.
The patient was discharged on January 22nd, 1948, having been treated for non-specific
The patient went to bed at home and a day later began to have pains in the R.U.Q.
with nausea and vomiting. The pain persisted, but the nausea stopped. She was readmitted on January 27th, 1948, with a diagnosis of acute cholecystitis. There was
no jaundice. The gall bladder area was very tender for the first time, with slight
abdominal distension, moderate rigidity in the R.U.Q. She was treated conservatively
and a gall bladder X-Ray series on February 6th, 1948, showed a non-functioning gall
bladder without radio-opaque stones. On February 13 th, 1948, the abdomen was opened
and a thickening gray colored gall bladder was stripped from surrounding adhesions and
viscera. In Hartman's pouch area a small facetted stone was encountered lying outside
the gall bladder. On completion of cholecystectomy, no perforation could be found in
the gall bladder wall, which incidentally contained other calculi.   Recovery followed.
This was a case in which perforation must have occurred at first admission, with
escape of one stone and fluid enough to run down the right paracolic gutter to the pelvis
to cause inflammation there. Subsequent sealing off of the perforation took place, and
in the absence of infection, no abscess was formed.
Case III. A white male, aged 68 years, was admitted to hospital on May 29th, 1948,
with severe, colicky pain in the R.U.Q. radiating to the right shoulder. The pain began
on May 23rd, and by May 27th had moved to the R.L.Q. There was a previous history
of gall bladder colic on many occasions since 1930. It was sometimes followed by
jaundice. On examination, there was tenderness and rigidity over the right half of the
abdomen, with restricted movement. The sclerae were faintly icteroid. The W.B.C.
was 14,350 with 81% polys. The pulse was 92 and temperature 98.8° F. The urine
showed albumen and W.B.C, there being a degree of prostatism.
The abdomen was opened and clear, slightly bile stained, mucoid fluid was encountered. There were no omental adhesions. A thick walled semi-friable, pearly gray gall
bladder was removed which contained stones and exhibited a perforation. The common
duct appeared dilated. It was opened, and two large stones were removed. The patient
made an uneventful recovery. The pathological diagnosis was acute cholecystitis and
This case demonstrates the importance of common duct inspection for other
calculi. I believe that there are three main causes of jaundice associated with gall bladder
perforation which may exist independently or in combination.  First, absorption from a
Page 174 free biliary peritonitis; second, hepatitis from contiguous abscess or inflammation and,
third, stones in the common duct.
Case IV. A white male, aged 62 years, was admitted to hospital on April 9th, 1948,
with a history of epigastric pain of increasing severity for three days, and vomiting for
two days. There was a previous history of gaseous indigestion and fat intolerance of
some years standing. The patient had considerable weight loss and mild jaundice for
three months prior to admission. On examination, the patient showed emaciation and
all the signs of a perforated ulcer, except for the jaundice. The pulse rate was 140, the
blood pressure 90/55 and the temperature 102. The pre-operative diagnosis was perforated carcinoma of the stomach though no mass was felt.
At operation a cholecysto-duodenal fistula was found with free perforation into
the abdominal cavity at the adhesion line between gall bladder and duodenum. The gall
bladder containing calculi was removed and the duodenal perforation was repaired. The
common duct contained palpable stones and these were removed. The pathological
diagnosis was tuberculosis of the gall bladder. The patient subsequently developed
a chronic sinus at the site of the drain. After X-Ray therapy and intra-muscular
streptomycin had failed, the sinus healed by daily instillations of streptomycin
solution into its opening. The patient is now robust, has a good colour, has gained weight
and has shown no evidence of tuberculosis elsewhere in his body.
^Case V. A white male, aged 72 years, was admitted to hospital on December 11th, 1948,
with severe epigastric pain following a large meal the same day. The pain persisted and
radiated to the right shoulder and R.L.Q. and he soon became nauseated and vomited.
There was. no history of previous attacks of pain, indigestion, flatulence, fat intolerance
or jaundice. Examination revealed obesity, tenderness and rigidity in the right half of
the abdomen most marked in the R.U.Q. Rebound pain phenomenon was present.
There was no evidence of icterus. The pulse rate was 100, the temperature 100.8° and
the blood pressure 145/80. The W.B.C. was 17,900 with 11% staffs. The preoperative diagnosis lay between acute cholecystitis and acute appendicitis. A The urine
showed sugar.
The abdomen was opened alongside the umbilicus and the appendix was found to
be normal. The incision was enlarged upwards and a large pericholecystic abscess was
encountered. The pus was suctioned off and the gall bladder was found to be very dark
in color and oedematous with surrounding adhesions. The gall bladder was too friable to
remove, so a cholecystostomy was done. No stones were seen. A separate drain was
placed in Morrison's pouch. The patient was then treated for diabetes meflitus and made
an uneventful recovery.
This case demonstrates perforation through a necrotic patch in the gall bladder wall
occasioned by either intramural abscess or gangrene, which, literally translated, means
ischaemic necrosis. Certainly infection was an essential part of this case and, as with
infection elsewhere in the presence of uncontrolled, diabetes, the course of events was
All of us have had the experience of incidentally finding gall stones in the course
of investigating a patient perhaps for some other complaint. Very often, such a patient
will give an entirely negative symptomatic history for gall bladder disease. The question
of the innocuous gall stone has not infrequently been the subject of papers in the medical
literature. As early as 1911 W. J. Mayo gave a paper entitled "Innocent Gall Stones A
Myth." |j|
By and large physicians take a conservative view regarding silent gall stones, while
surgeons take a more positive view. Lahey, for instance, stat'd in 1938 "There are no
harmless gall stones"—and that cholecystectomy should be advised unless special contraindications exist when the diagnosis is made.
As surgeons, we are aware of the association of gall stones with gall bladder carcinoma in over 95% of instances of the latter; and of the association of gall stones with
Page 175 perforation of the gall bladder in about 85% of instances. By comparison, we are also
aware of the havoc urinary calculi and salivary calculi may cause and the diligence with
which they are sought and extricated.
I should like to close with the thought that it might be better surgical practice
to remove calculi with their diseased gall bladders prophylictically, rather than wait
until some complication arises. Elective cholecystectomy is said to bear a mortality rate
of .5%. A compromise could be reached with the conservative point of view, if cholecystectomy were advised in known cases of asymptomatic cholelithiasis only after
the onset of early vague symptomatology.
Dr. J. S. Madul has moved from the North Vancouver General to the Royal
Columbian in New Westminster, as associate radiologist.
Dr. C. G. McNeill, president, and Dr. R. B. Townsley, secretary-treasurer, are new
officers of the North Vancouver Shore Medical Society.
Dr. J. T. Hugill, formerly of Vancouver, is now on the anesthetic staff' of the West
Coast Hospital at Port Alberni.
Dr. (B. F. Green of Vancouver has joined the staff of the Elizabeth Hospital in
Prairie Grove, Arkansas.
Apprentice help during the summer months may be obtained by writing the
CAMSI executive at the University of Montreal.
Aortic stenosis has been treated in Philadelphia by sliding a bougie down the aorta
through an incision behind the clavicle.
Dr. G. H. Manchester, of New Westminster, has had to vacate offices he has used
for forty-two years, because of renovations. He still plans to continue as a psychiatric
Dr. R. G. Walton of the Vancouver General Hospital will continue studies in
dermatology at Stanford next year.
Dr. Harold Spiro has begun a private radiology specialty in Vancouver.
Dr. L. C. Kindree of Squamish made a 20-mile mercy trip on jeep and skis, to an
injured man on Mount Garibaldi last month.
Dr. David B. Boyd recently arrived in Victoria from Toronto, where for the past
two years he has been studying at the Hospital for Sick Children. He has opened a
Pediatric office in the city.
Dr. Ernest A. Frejd, formerly of Prince Albert, Sask., is now established in general
practice in Victoria.
Drs. D. Murphy, L.- T. Maxwell, L. B. MacLaren and A. L. Chambers of Priince
George attended the recent convention of the Northern Interior District Medical
Dr. and Mrs. L. W. Warcup of Vancouver, a daughter. p|||
Dr. and Mrs. J. H. Lindsay of Britannia Beach, a daughter.
Dr. and Mrs. B. T. Marteinsson of Vancouver, a son.
Dr. and Mrs. R. S. Clarke of Vancouver, a son.
Dr. and Mrs. /. A. Porter of Vancouver, a daughter.
Dr. and Mrs. F. J. Marshall of Vancouver, a daughter.
Dr. and Mrs. M. C. Hay of Vancouver, a son.
Dr. and Mrs. A. C. Lang of Vancouver, a daughter.
Dr. and Mrs. F. H. Mills of Ashcrof t, a daughter.
Dr. and Mrs. J. T. Cruise of Victoria, a son.
Dr. and Mrs. C. A. Matthews of Vancouver, a son.
Dr. and Mrs. F. L. Skinner of Vancouver, twins.
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• . . when   iron   alone   is  not  enough
 |any of the common iron deficiency anemias
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In certain microcytic and macrocytic anemias,
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three IBEROL tablets,
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Thiamine Hydrochloride .. .6 mg. (6 xMDR*)
Riboflavin 6 mg. (3 x MDR*)
Nicotinamide 30 mg. (2 x RDAf)
Ascorbic Acid 150 mg. (5 x MDR*)
Pyridoxine Hydrochloride 3 mg.
Ponthothenic Acid 6 mg.
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Folic Acid 5.1 mg.
Liver Concentrate 1.5 Gm.
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Niacinamide (Nicotinamide) 5 mg.
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(5years later)
Kenneth Clark Gorman
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Current Clinical
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An investigation of the sleeping habits of infants six to
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This study is part of an
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In Swift's original test feedings, Kenny
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foods. Contrast this with the general practice five years ago. Before the development
of specially prepared Swift's Meats for
Babies, the customary age to start meat was
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He's big and husky now
Kenny's mother will verify the fact that he's
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Swift's appetizing variety includes: beef,
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When Hypersensitivity To
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It has been observed generally that Vitamin B12 has not given
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Anacobin is, therefore, recommended especially for the
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Anacobin is issued in 1 ml.
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Issued in boxes of 6, 25 and 100 ampoules
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NOTE: To date there is no evidence of toxic reactions with Gravol. However, some individuals may
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1. Carliner, P.E., Radman, H.M., and Gay, L.H.:
Science, 110: 215 (Aug. 26, 1949). 2. Gay, L. H.,
and Carliner, P.E.: The Prevention and Treatment
of Motion Sickness. Bull, Johns Hopkins Hosp.,
May, 1949. 3. Beeler, J. W., Tillisch, J. H., and
Popp, W. C.: Proc. Staff Meet. Mayo Clinic (Sept.
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Vitamin A...jH| £;Mz;..........    1,000 I.U.
Vitamin D '..^ :$m 'Q.     - 500 I.U.
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The average dosage is 2 drops daily.
T/ie average daily dose of 10 drops  {0.6  cc.) provides
Vitamin Al   -      5,000 I.U.
Vitamin D"     I7OOO I.U.
Ascorbic Acld...M^^^^^^^i^.^L^.A      50.0 mg.
Thiamine ^..^plg.,.:;^!^.' **•'*      1-5 mg.
Riboflavin....aljre^ii^iL.^^i..  1.0 mg.
Niacinamide        20.0 mg.
Pyridoxine....t.^;.„.^..-^^.-.;^i.;  1.0 mg.
Calcium d-Pantothenate 4,3^;*^^.;      5.0 mg.
Mixed Natural Tocopherols (as Antioxidant)        2.0 mg.
In bottles of 8, 15 and 30 cc. with dropper.
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15 minims of Creosote.     5 minims  of Creosote.
Contain the bitter principles of Quassia (alpha
and beta picrasmin) along with Quinine Sulphate.
Each Suppository represents:
Chloral Hydrate  1*4 grains
Potassium Bromide  l*/4 grains
Presented in 3% grains and 7% grains strengths.
Each Suppository represents:
Antipyrine 1 grain     Camphor % grain
Ext. Belladonna 1/20 grain   Po. Ipecac % grain
Creosote 5 minims
Each Suppository represents:
Chloral Hydrate	
.5 grains
_ II |i_
especially prepared brand of
calcium gluconate available
in tablet, granule and ampoule form for therapeutic
use. Vitamin D is added for its
value in promoting the absorption and utilization of
advantages   of CALGLUCOL
Readily absorbed
Non-irritating when used parenterally
Less upsetting to digestive system than other
calcium salts when taken orally
C.T. No. 149A (Pink) Aromatic
Calcium Gluconate U.S.P. 10 grains
combined with 500 international units of
Vitamin D in each tablet
Indicated in calcium deficiency, dental
caries, malnutrition, neurasthenia, osteo
malacia, lactation and pregnancy
DOSE—One tablet tour times a day
before meals and at bedtime.
Control        u t ^ t)   \  S
calcium deficiencies
intractable pain
lead poisoning
muscular cramps
CALGLUCOL D E.B.S. C.T. No.  149A,  10 gr.  calcium gluconate and 500
I.U. Vitamin D per tablet, in bottles of 100, 500 and 1,000.
CALGLUCOL E.B.S. C.T. No. 149, 10 gr. calcium gluconate per tablet, in
bottles of 100, 500 and 1,000.
CALGLUCOL D GRANULES  E.B.S.,  each  ounce contains 330 gr.  calcium
gluconate and T,600 I.U. Vitamin D per oz. in 5-oz. bottles.
CALGLUCOL AMPOULES E.B.S.  No.  A-31,   10 gr. calcium gluconate per
10 cc. ampoule.
SINCE 1879
Representatives: Mr. V. Garnham, 3228 West 34th Avenue, Vancouver, B.C.
Mr. F. R. Clayden, 3937 West 34th Avenue, Vancouver, B.C, the answer to seasonal allergies
all allergies
Hay fever
Spasmodic coryza
Allergic asthma
Zona, pruritus
Vomiting in pregnancy
25-50-100 mg
nasal drops
Hhe bedtime antibistaminic"
nocturnal or persistent allergies
Nocturnal pruritus
_            tablets
10-25 mg.
"pioneers in the
amine field."
FAir. 0080
When prescribing Ergoapiol
(Smith) for your gynecologic patients,
you have the assurance that it can be obtained only
on a written prescription, since this is the only manner
in which this ethical preparation can be legally
dispensed by the pharmacist. The dispensing of this
uterine tonic, time-tested ERGOAPIOL (Smith) —only
on your prescription — serves the best interests
of physician and patient.
INDICATIONS: Amenorrhea, Dysmenorrhea, Menorrhagia,
Metrorrhagia, and to aid involution of the postpartum uterus.
GENERAL DOSAGE: One to two capsules, three to four
limes daily—as indications warrant.
In ethical packages of 20 capsules each, bearing no directions.
Literature Available to Physicians Only.
Ethical protective mark,
M.H.S., visible only   ■
when capsule if cat la
half at seam.
NEW   YORK  19i NiYi


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