History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: February, 1932 Vancouver Medical Association Feb 29, 1932

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 The Bulletin
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OF THE
Vancouver Medical Association
Contents
Clinical Aspects of Some Blood Diseases
Additions to the Library
Meetings
General Meeting February 2nd
Cancer Meeting February 15th
Clinical Meeting February 16th
Vol.  VIII.
FEBRUARY,  1932
No.  5
Published monthly at Vancouver, B. C, By
McBeath-Campbell Ltd.,  326 Pender  Street "West
Subscription,  $1.50 per year. 19 H
B^H-!
L
SJ3»»M©^HEATa^©tiD©.
57
ANDERS' §
ALL GLASS NEBULIZERS
Sprays the finest nebula of any on the market
-will spray oils, dextrose solutions,
heavy glycerine, mixtures such
as iodine pigments, etc.
BK§ Sells to patient for $1.50
CHAS. H. ANDERS, Chemist
GORDON M. CLAY, Associate Chemist
u THE     VANCOUVER     MEDICAL     ASSOCIATION
BULLEsTIN
Published  Monthly  under   the  Auspices  of  the  Vancouver  Medical  Association  in  the
Interests of the Medical Profession.
Offices:
203 Medical Dental Building, Georgia Street, Vancouver, B. C.
Editorial Board:
Dr. J. M. Pearson
Dr. J. H. MacDermot Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
Vol. VIII.  FEBRUARY, 1932 No. 5
OFFICERS 1929-30
Dr. C. "W. Prowd Dr. E. Murray Blair Dr. G. F. Strong
President Vice-President Past President
Dr. L. H. Appleby Dr. W. T. Lockhart
Hon.  Secretary Hon.  Treasurer
Additional Members of Executive:—Dr. A. C. Frost; Dr. "W. L. Pedlow
TRUSTEES
Dr. W. D. Brydone-Jack Dr. J. A. Gillespie Dr. J. M. Pearson
Auditors: Messrs. Shaw, Salter & Plommer
SECTIONS
Clinical Section
Dr. J. E. Harrison Chairman
Dr.  A.  M. Agnew Secretary
Eye, Ear, Nose and Throat
Dr. J. A. Smith i Chairman
Dr. A. O. Brown  Secretary
Pediatric Section
Dr.  C. A. Eggert Chairman
Dr. S. S. Murray Secretary
STANDING COMMITTEES
Library Orchestra Summer School
Dr. D. M. Meekison Dr. J. R. Davies Dr- c- e- Brown
Dr. W. H. Hatfield Dr. F. N. Robertson Dr- T- l- Butters
Dr. C. H. Bastin Dr. J. A. Smith Dr- c- h- Vrooman
Dr. C H. Vrooman Dr.  J. E. Harrison Dr- J- w- Arbuckxe
Dr.  C. E. Brown Dr- H- A- Spohn
Dr. H. A. Spohn ,, Dr- H- R- Mustard
Publications rT    ... ,
Hospitals
Dinner Dr- J- M-- Pearson Dr.  w.  C. Walsh
Dr. J. H. MacDermot Dr  F  W  Lees
SR- h \,HlRRISON DR- D. E. H. Cleveland      Dr. a. ^. Bagnall
Dr. N. McNeill j
Credentials V.O.N. Advisory Board
_  ,    .    „   _   ,,  ,    . Dr. A.  T. MacLachlan        Dr. Isabel Day
Rep. to B. C. Meet. Assn.     „      .    i-   ,, -.T _     „   „; i,
* Dr. A. Y. McNair Dr. H. H. Caple
Dr. H. H. Milburn Dr. T. L. Butters Dr. G. O. Matthews
Sickness and Benevolent Fund — The President — The Trustees VANCOUVER HEALTH DEPARTMENT
STATISTICS, DECEMBER, 1931
Total Population—Census,   1931 ;	
Asiatic   Population   (Estimated)    	
         246,579
  15,000
Rate per 1,000 of Population
Total   Deaths   .          211 10.1
Asiatic    Deaths     :  22 17.3
Deaths—Residents   only      187 8.9
Birth   Registrations     310 14.8
Male      166
Female 144
INFANTILE MORTALITY—
Deaths under one year of age   13
Death   Rate—Per   1000   births     41.9   .
Stillbirths   (not  included   in  above)     10
CASES OF CONTAGIOUS DISEASES REPORTED IN CITY
January 1st
November,  1931
Cases    Deaths
December,  1931
Cases    Deaths
Smallpox    	
Scarlet   Fever
2
24
Diphtheria              15
Chicken    Pox     	
Measles       	
Mumps     	
Whooping-cough     	
Typhoid Fever 	
Paratyphoid    _ 	
Tuberculosis      	
Poliomyelitis    	
Meningitis    (Epidemic)
Erysipelas   	
Encephalitis   Lethargica   ..
55
68
24
17
4
0
97
1
0
5
0
0
0
0
0
0
0
1
0
0
10
0
0
0
0
0
20
7
38
285
24
21
1
0
56
0
0
3
0
0
0
1
0
0
0
1
1
0
21
0
0
0
0
to 15th, 1932
Cases    Deaths
2 0
6
2
36
1277
54
9
0
0
6
0
1
4
0
0
0
0
1
0
1
0
0
0
1
0
0
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Regular Bacteriological Control requiring several tests
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Plant equipment and methods designed to approval
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Certified Milk is the only milk permitted to be sold
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Seymour 3838 VANCOUVER MEDICAL ASSOCIATION
Founded 1898 Incorporated 1906
PROGRAMME OF THE 34th ANNUAL SESSION
GENERAL MEETINGS  will be held on the  first Tuesday of the
month at 8 p.m.
CLINICAL MEETINGS will be held on the third Tuesday of the
month at 8 p.m.
Place of meetings will appear on Agenda.
General Meetings will conform to the following order:
8:00 p.m.—Business as per Agenda.
9:00 p.m.—Paper of Evening.
1931.
November 3rd—GENERAL MEETING.
Papers:
Dr. H. A. DesBrisay: "Syphilis in Medical Practice."
Dr. W. T. Lockhart: "Treatment of Syphilis."
D.  A.  L.  CREASE of  Essondale will  discuss  the treatment  of
Degenerative Types of Neurosyphilis.
Discussion: Dr. J. E. Campbell; Dr. W. L. C. Middleton.
November 17th—CLINICAL MEETING.
December 1st—GENERAL MEETING.
Papers:
Symposium on Fractures to be arranged by Dr. A. B. Schinbein
and Dr. D. M. Meekison.
Discussion: Dr. F. P. Patterson; Dr. J. A. West.
December 15th—CLINICAL MEETING.
1932.
January 5th—GENERAL MEETING.
Papers:
Dr. C. S. McKee: "The Interpretation of Blood Pictures."
Dr.  Murray  McC.  Baird:  "The  Clinical Aspect of  Some  Blood
Diseases."
Discussion: Dr. W. H. Hatfield; Dr. A. Y. McNair.
January 19th—CLINICAL MEETING.
February 2nd—GENERAL MEETING.
Papers:
Dr. H. Dyer: "Tracheotomy in Children."
Dr.  C.  Graham:  "Inflammation of- the Accessory  Nasal  Sinuses
in Children."
Dr. E. E. Day: "Indications for Endoscopy."
Discussion: Dr. J. A. Smith; Dr. H. R. Mustard.
February 16th—CLINICAL MEETING.
March 1st—GENERAL MEETING.
The Osier Lecture: Dr. F. P. Patterson.
March 15th—CLINICAL MEETING.
April 5th—GENERAL MEETING
Papers:
Dr. J. W. Thomson: "Emergencies in Abdominal Surgery."
Dr. A. W. Hunter: "Diagnosis and Treatment of Some Urological
Emergencies."
Discussion: Dr. G. E. Gillies; Dr. Lee Smith.
April 19th—CLINICAL MEETING.
April 26th—ANNUAL MEETING.
Page  84 EDITOR'S PAGE
Readers of Kipling's "The Day's Work" will remember one story in
this collection called "The Ship that Found Herself". To those who have
not read the story, or who, having read, have forgotten it, we commend
its perusal. It has a moral for us. The last word in marine architecture,
fitted and equipped with all the latest and most expensive gadgets, this
ship was yet, at the outset of its first trip, laden, to sea, a mere collection
of beams and planks, bolts and rivets—it was not a "ship", with the
soul of its own that every lover of ships, or every man who lives and
works with them, ascribes to the almost living creature of steel and
wood and hemp, that he calls a ship.
And you will remember that its first trip was in midwinter and
through howling gales and mountainous seas—and it was all quite new
and very distressing to the various disjecta membra of the ship, the
rivets, and the deckbeams, and the garboard strakes and the capstan
and so on—and at first, each one growled at and complained of all the
others, for letting the whole load fall on the complainant. Even some
of the rivets, finding themselves blamed for all the others' ills, decided
they might as well pull out, and give up the battle—but the steam persuaded them to stay. And gradually, and here is the moral, each individual unit found to his pride and exceeding joy, that as long as he did
his share loyally, and both supported and trusted the other individual
units, everything went beautifully, and the ship rode out the storm and
arrived , somewhat dishevelled perhaps, but quite sound, in port. And
then the soul of the ship awoke and she was no longer a collection of
parts, but a living, breathing whole, one of the community of ships, an
entity and a personality, and not merely a machine shop.
Perhaps it needed all the trials and afflictions that have beset us for
some time past to awaken us all to the feeling that we are not yet a
unit, and that something must be done to make us a single and united
body. There is an evident feeling amongst medical men today, that by
some means or another, we must in the near future, formulate a plan
by which we shall speak with one voice when we meet with our enemy
in the gates. There have been too many voices, each one sincere and
honest, each one saying what it believes to be true but each with the
weakness that comes from a divided allegiance. There has been no
authoritative body which could really represent the profession, which
could command its undivided loyalty, and speak for it in the full confidence that it really spoke for every one.
And so each part has tended to throw the blame on the other parts.
This is not fair, but it is very human. The truth is, that there has been
lack of mutual understanding, lack of methods by which we could work
smoothly together—overlapping and confusion. Each part has done its
best—but was handicapped in the doing. Attempts have been made
to work together—but the system is rigid and inelastic and needs recasting .
Page 85 There is no need for -blame. If mistakes have been made they have
been honest mistakes, and we all share the responsibility for them. But
it is time to reconsider the whole position, and "look to our fences".
To this end, much hard work has been done in the past two or
three months, and much more must and will be done. To our readers we
would urge that they hold up the hands of those who are working at
this, and that they give them their confidence and moral support. So
shall we acquire corporate unity, and become a ship that has found herself, and really is a ship.  For, to quote the immortal Rudyard once more,
"The game is more than the players of the game
And the ship is more than the crew."
As many of our readers know, Mr. W. G. Hunt, Associate Secretary
of the Alberta Medical Association, and Assistant to the Registrar of the
Alberta Medical Council visited Vancouver during the week of January
9th—16th.
His visit was made at the invitation of the Constitution Committee
of the B. C. Medical Association and while here, he addressed the Executive of that body as well at the Council of the College of Physicians
and Surgeons and the members of the Vancouver Medical Association
Executive who were connected with the work that has been done with
a view to amalgamation of the B. C. Medical Association and Vancouver
Medical Association.
For some time it has been felt that as far as this last-named plan
was concerned, we had about reached an impasse. No plan agreeable to
all could be formulated and decision was postponed again and again—
the real cause being that no decision could be reached.
For some time, too, it has b«en felt that our methods of handling
medical matters in B. C, are not satisfactory—that our relations with
the Government are not as amicable and mutually pleasant as they
should be—and that our standing with the public is not at all what it
ought to be. There are several factors involved and it is possible perhaps
to indicate the main ones.
The administration and enforcement of the Medical Act are vested
in the Council of the College of Physicians and Surgeons. Violation of
the Medical Act must be dealt with by them.
This puts the Council, and indirectly the medical profession, in a
most invidious and uncomfortable position. Why, one feels like asking,
should violations of the law be dealt with by different people for different Acts? All Acts are Acts of Parliament, whose law officer, the Attorney-General and his department, are empowered to see that they are
obeyed and violations of them punished. Why should the Medical Act be
an exception.
Page   86 Inevitably, and we must confess we cannot see how it can be otherwise, the public has come to regard the Medical Act as a fence placed
around the medical profession to protect this body. Violations are prosecuted by the Council. Of a certainty, the public, not understanding
our position at all, sees in this an endeavor on the part of the profession
to maintain for itself a special position of privilege. It need hardly be
said that the real purpose of a Medical Act is the protection of the public
against ill-trained, incompetent practitioners.
Again, as medical men, we have assumed the position of watchdog
of the health of the people. We fight the licensing of "cults" of the
half-educated—because we feel so strongly that they are a menace to
the health of the community. But is this, again one asks, our business?
Is it not the business of the legislature to protect the people's health?
Most of us are beginning to think it is. When we oppose these people,
our motives are misunderstood, we are thought to be afraid of the inroads
they may make on our own livelihood, and we are given no credit for
our real motive, which is the one set forth above.
The B. C. Medical Council has been unjustly blamed by some for
these happenings. It is quite unfair to attach blame to this body. The
members have done their honest best for the profession, and if we now
feel that the plan was a mistaken one, the mistake is ours as much as
theirs. As a matter of fact, they have gone out of their way to consult
with the two Associations, and for the past two or three years there has
been as close contact as possible.
Again, there is too much cost attached to organized medicine in
this province. This makes it very difficult for many who would like to
belong to all the bodies concerned—but cannot afford it. Too, it throws
an unfair burden of cost on those who do belong. It has been felt for
some time that measures should be devised, whereby, in the first place,
every man should pay his fair share towards the expense of the necesary
work done on behalf of all—and in the second place, this share should
be set at a figure- which all could afford.
Lastly, it has been appparent for some time that there has been too
much duplication of effort—too much overlapping' of various bodies
—and coincident with these, unnecessary expense—not only unnecessary
but useless and inefficient. The effort has been useless, because not possessed of sufficient authority and force. One single voice, speaking for
the whole, would impress the hearer—but there are too many voices,
none of them backed by the whole strength of the profession.
In Alberta they are, it would appear, in a fair way to solve these
problems. They have done it in what would seem an eminently sensible
and fair way. Except for local associations, there is only one taxing
body, the Council of the College of Physicians and Surgeons.
This body collects, compulsorily, a fee adequate to carry on the
work of  the profession and allots to the Alberta Medical Association
Page 87 the money necessary for its work. The work of the province is divided
between the Council and the Alberta Medical Association and the Council has representation on the Executive of the latter. There is direct and
continuous contact between the Council and the rest of the profession.
The Medical Act is still nominally under the control of the Council—
but practically they have shifted the administration, as far as violations
are concerned, to the shoulders that should bear it—those of the Attorney-General. Lobbying in the halls of the legislature, war against cults,
etc., are things of the past. But the Council is the body with authority—
and it has teeth and can use them.
The Council of the College of Physicians and Surgeons in B. C. is
studying this whole matter closely, as are the Executives of the B. C.
Medical Association and the Vancouver Medical Association. Our readers
will be kept informed of developments. Meanwhile, it will behoove all
of us to consider these matters and acquire all the information possible.
MEETINGS
The General meeting of the Association was held in the Medical-
Dental Building Auditorium on January 5 th, with an attendance of
ninety-seven members. Dr. C. W. Prowd, the President, was in the
chair. There were two elections to membership—Dr. E. L. Garner,
formerly of Duncan, and Dr. G. F. Amyot, of North Vancouver, both
of whom were unanimously elected. A resolution was carried that the
Vancouver Medical Association does not endorse the Canadian Medical
Indemnity and Health Association and that a letter be sent to every
member notifying them of this resolution.
The Cancer Committee presented a synopsis of a communication
from Dr. J. S. McEachern of Calgary, outlining a plan of development
in Cancer Research under the British Empire Cancer Campaign.
The question of the early closing of gas stations was discussed and
protests were voiced against any such move unless adequate provision
were made for emergency service.
The papers of the evening were presented by Drs. C. S. McKee and
Murray Baird. Dr. McKee spoke on "The Interpretation of the Blood
Picture" and Dr. Baird spoke on "The Clinical Aspects of Some Blood
Diseases". Drs. Hatfield and McNair opened the discussion.
The monthly meeting of the Cancer Investigation Committee was
held in the Auditorium of the Vancouver General Hospital on Monday,
January 18th. Dr. D. F. Busteed gave a summary of the cancer cases
reported in 1931 in the City of Vancouver and a number of interesting
clinical cases were presented. The attendance was good. Dr. J. J. Mason
presided.
The Clinical Section of the Association held its monthly meeting
in the Auditorium, Tenth and Willow, on Tuesday, January 19th,
through the courtesy of Dr. A. K. Haywood.   An excellent programme
Page was presented, those showing cases being Drs. Frost, Strong, Hatfield,
Leeson and Schinbein.   75 members were present.
ADDITIONS TO THE LIBRARY
Surgical Clinics of North America, June, August, October, December,
1931.
Deafness and Its Alleviation.    V. Nesfield, 1930.
History of the War.    Closing Volume, 1931.
Medical Clinics of North America, July, September, November,  1931.
Proctoscopic Examination.    Buie,  1931
Renal Lesions in Bright's Disease.    Addis & Oliver, 1931
Insanity as a Criminal Defence.    Meredith, 1931.
System of Bacteriology.    Vol. 9.    Technique-Methods, 1931.
Transactions American Proctological Society, 1931.
Cancer of the Rectum.    Ernest Miles, 1931.
Home Care of Infant and Child.    F. Tisdall, 1931.
Harvey Lectures.     Volume for 1930.
Quantitative Clinical Chemistry.    Van Slyke & Peters, 1931.
Textbook of Surgery.    John Homan, 1931.
Poisons & Poisoners.    Thompson,  1931.
Recent Advances in Medicine.    Beaumont & Dodds, 1931.
Recent Advances in Pulmonary Tuberculosis.    Burrell, 1931.
Diagnosis & Treatment of Brain Tumours.    Sachs, 1931.
Injuries to Joints.    Sir Robert Jones.
Transactions American Association of G. U. Surgeons.     1931.
Intracranial Pyogenic Dieseases.    Logan Turner & Reynolds.     1931.
Fractures and Their Complications.    G. E. Wilson, 1930.
THE CLINICAL ASPECTS OF SOME BLOOD
DISEASES
By Dr. Murray McC. Baird
I wish to speak to you for a short time about the clinical side of
certain conditions mainly affecting the blood, and shall confine my remarks entirely to anaemia because relative frequency gives it a position
of major importance. We may for our purposes define anaemia as a
condition in which there is a reduction in the number of red cells or in
haemoglobin per unit volume of blood, or both, or a reduction in the
total volume of blood. I wish first to mention a few general considerations with regard to the recognition of anaemia, and then to consider
some of the main clinical types of the disease, going on to a brief review
of recent work on the subject and the modern ideas in treatment.
Delivered at a meeting of the Vancouver Medical Association, January, 1932
Page 89
i—~; It is obvious that upon us as clinicians rests the responsibility of
recognising anaemia when it exists and in these days of free use of cosmetics by all classes of society, the task is more difficult than ever before.
I have known patients to tint even their ears to avoid the pallor which
is so often one of the striking symptoms. We must admit too that many
pale patients are not anaemic, and the appearance of the patient is not
of great help except when the anaemia is extreme. Anybody can recognise the severe type of case, when the patient walks in complaining of
general weakness, dyspnoea, palpitation, and indigestion,and shows on
examination pallor, oedema of the ankles and functional heart murmurs.
There are many milder cases, however, where the patient comes complaining of one prominent sympton to the exclusion of all others. Such
symptoms are varied in the extreme, but the common ones are fatigue,
indigestion, headache, giddiness, tinnitus, constipation, or attacks of
diarrhoea. In such cases the attention is directed elsewhere, and the
diagnosis may be missed because we do not think of the blood as a primary cause. Since the appearance of the patient is often of little help, it
is necessary for us all, having thought of anaemia, to have some instrument of precision for estimating haemoglobin at least. Many use the
Tallqvist Scale and find it satisfactory. Personally, I do not find it
sufficiently accurate. Others use a haemoglobinometer of the acid hae-
matin type. The user should be sure that he is not colour-blind, and that
his instrument has been standardised. I was sold a haemoglobinometer in
Vancouver which gave for my own blood a reading of 120%, which I
knew to be false. So one has to beware of standards that fade. In cases
of doubt it is obviously best both for doctor and patient to seek the help
of the haematologist.
A clinical fact, which we all realise without giving much thought
to it, is that anaemia in general is preponderantly a disease of women.
This is so true that if we see a young adult male suffering from any
considerable degree of anaemia, it is wise to begin at once a search for
some serious cause, such as concealed bleeding ,tuberculosis, or malignant
endocarditis. This does not apply to young women, however, who are
often anaemic without any very patent reason. We should use this fact
in our practice to the extent of thinking of the blood always when we
have a female patient, particularly a middle-aged woman whose symptoms appear to be a vague, irrevelant and incoherent jumble. A routine
haemoglobin estimation in such cases may often be normal, but now and
again it will save us the ignominy of a missed diagnosis and the boredom
of listening to an oft-repeated tale. Incidentally, it may save the patient
years of ill-health and considerable expense.
Clinical Types
For clinical purposes there are still many excellent reasons for dividing anaemias into two main groups, the primary and the secondary.
These terms refer to the blood picture only and not to the etiology. The
terms primary, macrocytic, megalocytic, hyperchromic, Addisonian, and
pernicious anaemia, are used rather indiscriminately to describe a blood
picture where the cells are large and contain more haemoglobin individually than normal,  (hence the colour index is high)   and where megalo-
Page 90 cytes or foetal red cells are found in the bone marrow and sometimes in
the blood. The terms secondary, microcytic, hypochromic, and chlorotic
are used to describe a blood picture where the cells and haemoglobin are
reduced but the haemoglobin is reduced more in proportion than the cells,
(hence the colour index is low) and where there is no foetal response on
the part of the bone marrow.
Primary or pernicious anaemia is not a disease so much as it is a
peculiar kind of blood picture. It is found arising by itself or in association with other ostensibly very far removed conditions, such as:-
1. Carcinoma of the stomach.
2. Sprue,
3. Infestation with intestinal parasites.
4. Syphilis.
5. Surgery of the stomach, notably partial gastrectomy and gastro
jejunostomy.
6. Pregnancy.
The anaemia may be profound with red cells numbering as low as
one million, before the patient comes for advice. The symptoms may be
merely those of anaemia but there are certain special symptoms and signs
which, if present, help greatly to differentiate this type of anaemia
from all others.  These are as follows:-
1. History of recovery from a similar previous attack.
2. Lemon yellow colour.
3. Symptoms and signs of subacute combined degeneration of the
cord.
The first point merely emphasises the strong tendency to remissions
and relapses and will not help much if we are seeing the patient in the
first attack. The characteristic colour is by no means always present; the
patient may be merely waxy pale or show brownish pigmentation of the
skin, but if it is present it is a sign of great usefulness, provided we are
fairly sure of a normal biliary tract. Definite signs of subacute combined
degeneration in a patient of from 40 to 60 may be taken as fairly conclusive evidence of actual or potential pernicious anaemia, at any rate in
this country. The common early symptom of this condition is numbness
and tingling in the hands and feet, but there is a great variety of symptoms. If the posterior columns are first chiefly affected we may have
lightning pains and gastric crises, as in tabes, with Rhombergism and
alteration of sensation. Damage to the pyramidal fibres on the other
hand may give rise to spasticity and increased jerks. Complicated pictures may arise such as absent knee jerks with extensor plantar responses.
The most useful instrument for detecting this degneration is the tuning
fork, because vibration sense is usually affected early. Testing joint
sense in the big toe joint will also help one to avoid missing the early
case. It is almost unnessary to mention that subacute combined degeneration may arise and be well developed before any signs of anaemia are
present, as in the following case.
Page 91 Woman, age 64, sixteen years ago began to fall down without any
apparent reason; fell down stairs several times; if kept talking very long
on the telephone, was apt to fall. Complained of "rheumatic" pains
in the feet. Ten years ago developed indigestion, and would vomit
without cause. Suacute combined degeneration was diagnosed. About
six years ago definite pernicious anaemia appeared.
This case also illustrates the fact that gastric or gastro-intestinal
symptoms may ante-date the anaemia by several years. Indigestion or
diarrhoea are particularly common as symptoms of pernicious as opposed
to other kinds of anaemia, but of course are not absolutely characteristic.
Paraesthesiae of the extremities may occur in secondary anaemia, but
the presence of signs of subacute combined degeneration is probably
the best single clinical evidence we have that any case of anaemia is of
the pernicious type. (Post mortem evidence of degeneration is found
in about 80% of cases.) This applies no matter what the blood picture
may be as in true pernicious anaemia it may be of the secondary type
at times, particularly during the early stages, during remissions and
erythroblastic crises.
Another point often mentioned in the diagnosis of pernicious
anaemia is achlorhydria (absence of free HCL) or achylia gastrica
(absence of any HCL and ferments in gastric juice) There is certainly
a connection between achlorhydria and pernicious anaemia. Wilkinson
and Brockbank in a review of the literature find that there have been
reported 139 families with two or more members suffering from pernicious anaemia with or without subacute combined degeneration; 59
families in which pernicious anaemia and achlorhydria occurred in
different members; 17 families in which achlorhydria occurred without
pernicious anaemia. Of 291 relatives of patients suffering from pernicious anaemia 70, or 24.1%, had achlorhydria; about half of these had
true achylia. This is vastly more than the normal, which is about 1%
to 2%. Several times on routine examination relatives were found to
have full-blown pernicious anaemia of which they were unaware. We
know however that achlorhydria occurs in normal healthy people; also
in people with secondary anaemia. Witts estimates that out of 100
people with achlorhydria, 10 will have pernicious anaemia; 20 will have
secondary anaemia, and the rest will be normal. So we must disabuse
our minds of the idea that there is anything specific about achlorhydria
in pernicious anaemia; also we know now that persons may have an apparently normal acid and pepsin secretion with typical pernicious
anaemia.
Let us now consider for a short time some types of secondary
anaemia. Haemorrhage, either acute and massive, or chronic and slight,
may cause profound anaemia. There are a certain number of cases of
chronic anaemia which seem to date from a single large haemorrhage.
It must be remembered too that a patient may bleed because of anaemia
or because of some other blood condition which is producing the anaemia,
such as leukaemia. In these cases a complete blood examination is the
only thing to do. Chronic post-haemorrhagic anaemia is most commonly
associated with gastric and duodenal ulcers, bleeding haemorrhoids, and
Page 92 menorrhagia, all of which must be looked for in any case as soon as
anaemia is diagnosed. Patients with chronic anaemia and gastro-intestinal symptoms are relatively common, and it may be very difficult to
determine the primary factor clinically. In this case the test for occult
blood in the stool is of great value, particularly if it gives negative
results.   This test is probably not sufficiently used.
All acute infections are inclined to produce an anaemia of some
degree, the most notable example of course being frank septicaemia.
In acute cases, sometimes called acute septic anaemia, there may be increased bilirubin in the blood with mild clinical jaundice and also, of
course, fever. Chronic infections or foci of infection are a much more
doubtful cause. We are beginning to realise that in anaemia just as
in rheumatoid arthritis, we have in the past under-emphasized the fact
that secondary infective complications may be due to the primary condition. Thus pyorrhoea or infected tonsils may be due to chronic
anaemia, and it is improbable that any infection which gives no other
signs or symptoms is causing anaemia.
The conditions associated with secondary anaemia being too numerous to specify in detail, let us pass on to consider more obscure cases
which are often labelled "Idiopathic." Witts has recently described a
form, occurring chiefly in women between 40 and 50, which he calls
chronic microcytic anaemia. The colour index is low and the Van den
Bergh reaction negative. Patients often complain of dysphagia, and
about 50% of his series had glossitis. Achlorhydria was present in 81%,
and one-third had enlarged spleen. Witts considers this type of anaemia
to be allied to the Plummer-Vinson syndrome in which we have a secondary anaemia associated with glossitis, dysphagia and enlarged spleen.
Glossitis as a symptom was first popularised in connection with pernicious anaemia by William Hunter. Clinically there may be complaint of
sore tongue with nothing to see through all the stages of fissure and
superficial ulceration up to a smooth, bald tongue originally described.
Sore tongue in the absence of local causes should lead to blood examination, but is not at all pathognomonic of pernicious anaemia any more
than is enlarged spleen. Witts emphasises the fact that this type of
anaemia occurs in middle-aged females who are often full of complaints,
chiefly abdominal, who often go undiagnosed through years of ill-health,
but who can be restored to usefulness by adequate diagnosis and treatment. Mills describes idiopathic hypochromaemia occurring in females
aged 30 to 40, with low gastric acid or achlorhydria, low colour index,
chronic course, and sometimes glossitis and paraesthesiae of the extremities. Dameshek describes what he considers a new syndrome called
primary hypochromic anaemia, occurring mostly in middle-aged women
who have all the symptoms of pernicious anaemia except jaundice and
subacute combined degeneration. The similarity of these descriptions
is striking, as is also the fact that there are included many symptoms
and signs which we are rather inclined to regard as typical of pernicious
anaemia. The fact is that, clinically, there is no very hard and fast
distinction in some cases. The colour index is not always reliable. As
before stated, the best clinical evidence that an anaemia is primary is
the presence of subacute combined degeneration. If this is absent, we
may have recourse to the best haematological  evidence,  which  is  the
Page 93 average diameter of the red cells. In England Price-Jones has plotted
the diameters of the red cells on a curve called the Price-Jones curve.
Five hundred cells are actually measured, and the results plotted with
numbers of cells as ordinates and the abscissae marked out in microns.
In pernicious anaemia the curve is shifted to the right and the base
usually broadened.
Murphy has recently evolved another method which he thinks is
even better both diagnostically and as a guide in treatment. It is called
the iron index. It is a figure given by dividing the Fe in milligrams
per 100 cc. of blood by the red cells in millions.
Normal figures would be 42/5 == 8.4. In pernicious anaemia this
index is increased; in secondary types it is diminished. It may also be
used as a measure of effectiveness in treatment.
Another type of secondary anaemia which we must consider here
is splenic anaemia. The original description of this form included any
kind of chronic anaemia with enlarged spleen, from which clear entities
such as familial acholuric jaundice, primary splenic tuberculosis, thrombosis of the splenic vein and neoplasms have been split off. There
remains a group of cases consisting of young adults who suffer from a
secondary anaemia, enlarged spleen and leucopenia with relative lymphocytosis. The white cells usually number less than 4000. The anaemia
is subject to febrile exacerbations, and haematemesis is an early symptom.
The spleen may gradually enlarge to an enormous size. It is generally
believed that Banti's Disease is a late stage of splenic anaemia. After
a period of years the liver enlarges, then shrinks again and becomes
cirrhotic, with consequent ascites, jaundice and haematemesis from
oesophageal varices. It is not known whether this is a primary disease
of the spleen or, as some argue, merely a stage of cirrhosis of the liver.
At any rate it is a form of anaemia which should be recognised early
if possible. There are several good grounds for separating this type from
other secondary anaemias:—
1. The incidence in young adults of both sexes.
2. The marked leucopenia, which does not occur, for example, in
Witts' chronic microcytic anaemia.
3. Late development of hepatic cirrhosis.
4. Ordinary treatment for secondary anaemia ineffective.
5. It is one of three blood conditions in which splenectomy has
been shown to be effective treatment, the other two being
chronic thrombocytopenic purpura and familial acholuric
jaundice.
One should refer here to another rare type of anaemia which occurs
almost exclusively in young adults. It is called aplastic anaemia, and
the picture is that which we should expect to find if we were to imagine
that all the blood-forming elements had become senile and ceased to
function. Thus there is a progressive decrease in red cells, white cells
and platelets.   The duration of the disease is usually a matter of months.
Page 94 NEURITIS and
FIBROSITIS
The beneficial effects of physical therapy in the rheumatic
group of diseases are due mainly to influence on circulation,
particularly on the capillary beds.
dressings are very valuable in the treatment of neuritis and
fibrositis in the neighborhood of the brachial and cervical
plexuses. They have the great advantage of supplying continuous moist heat, and they can be easily molded to the
affected part. Intensive hyperaemia can thus be produced
at any particular spot with all its beneficial effects.
EXOSMOTIC
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Medical-Dental Building Vancouver It may follow poisoning with benzol, particularly novarsenobenzol; it
occurs sometimes in phthisis, in the course of pernicious anaemia, or following excessive doses of radium or X-rays. These patients tend to
bleed in a very persistent way from the mucous membranes, a phenomenon possibly associated with the low platelet count. The diagnosis
is made by the exclusion of other types of anaemia, by the blood picture
and finally by examination of the bone-marrow at post-mortem.
There is nothing known at present which will. stimulate the formation of blood cells in these cases. Liver, liver extract, stomach, iron
and arsenic have all been tried and found wanting. Transfusion is the
only measure which is of any value and its effects are only temporary.
In a case recently described by Stewart Harrison 109 blood transfusions
of a full pint had been employed over a period of four years without
any signs of blood regeneration.
Recent Work
Modern ideas on anaemia originated in the experiments of Whipple
and others on the post-haemorrhagic anaemia of dogs, in .which it was
found that liver by mouth was very effective treatment. Minot and
Murphy, applying this to man, discovered that large amounts of liver
would produce a reticulocyte response and a remission in cases of pernicious anaemia. It was subsequently found that kidney and whole stomach
given by mouth had the same power. These organs, then, evidently
contain some factor which, on absorption by the patient, enables his
haematopoietic organs to function normally. Castle and his co-workers,
investigating further, found that there is absent in the gastric secretion
of patients with pernicious anaemia something which interacts with
ordinary food stuffs to produce an anti-anaemia substance. The evidence for this can be condensed as follows:—
Shredded beef muscle given in large quantity to a pernicious
anaemia patient will not produce a remission.
Normal gastric juice, given by stomach tube to a pernicious
anaemia patient will not produce a remission.
Shredded beef muscle and normal gastric juice, incubated together and then fed by tube to a pernicious anaemia patient,
will produce a typical reticulocyte response and a remission.
Shredded beef muscle, incubated with gastric juice from a
pernicious anaemia patient, and then fed to another pernicious
anaemia patient, will not produce a remission.
The conclusion follows that there is, in normal gastric secretion,
an "intrinsic" factor, and in food an "extrinsic" factor, probably of
protein nature, which react together to form a "Substance X," which
on absorption brings about normal blood formation. Castle, Heath and
Strauss, in a recent paper, show that the intrinsic factor was absent in
the otherwise normal gastric juice of two patients with pernicious
anaemia who afterwards reacted to liver, and was present in the achylic
gastric contents of one patient with no anaemia, and three patients with hypochromic anaemia. , Possession of this intrinsic factor seems then to
prevent the development of the pernicious anaemia picture while its
absence is a sinqua non. Pernicious anaemia thus becomes a nutritionly
disease in that it is intimately associated with an inadequate digestion
of food-stuffs probably of a protein nature. The part played by liver
in producing a remission in its relation to this gastric deficiency has not
yet been worked out.
Secondary anaemia is often associated as we have seen with achlorhydria and gastro-intestinal disorders. There is a good deal of evidence
that many of these cases are related to a poorly balanced diet, or to
faulty digestion and assimilation. The practical disappearance of
chlorosis is evidence that better hygienic conditions and a higher standard of living amongst the submerged tenth has a good influence in preventing secondary anaemia. The diets usually recommended as containing most anti-anaemic factor are based on the work of Whipple
on anaemia due to haemorrhage in dogs, where liver is very effective.
This work cannot be applied in its entirety to man under similar conditions. We seem at the present moment to have more information
about the factors concerned in the production of pernicious anaemia
than in the case of the more obscure forms of secondary anaemia.
Treatment
In general it may be said that in the treatment of any severe
anaemia the importance of bed rest cannot be over-estimated. This
was emphasised by many of the older physicians, who found that in
pernicious anaemia rest in bed was often effective after other treatment
had failed. Since the oxygen-carrying power of the blood is reduced
the heart must send out an increased minute-volume in order to supply
the needs of the tissues. This is the reason for the increased pulse rate
so often seen, and rest has a large part in reducing this effect on the
cardiovascular system. All patients with severe anaemia then should be
put to bed and kept there until they are able to be up and about with
a normal pulse rate.
There is now a good deal of evidence that in all kinds of anaemia
diet is also of very great importance, and this applies particularly to
anaemia of the pernicious type. Here we should probably follow the
principles laid down by Minot and Murphy. The main outlines of their
diet for pernicious anaemia are as follows:
1. At least half pound of liver per day.
2. About 100 grammes beef or mutton in addition.
3. Fruits such as peaches,  apricots,  prunes,  strawberries,  oranges
and grapefruit.
4. Enough butter and cream to make the diet palatable.
5. Enough carbohydrate to make  the  diet up  to 2000  or  3 000
calories.
For those who cannot eat so much liver there are potent extracts
such  as  that made by the  Connaught Laboratories  or whole  stomach
Page 96 i
in
preparations such as Ventriculin. There are now available also liver
extracts which can be injected intramuscularly or intravenously. The
effect of these is little short of dramatic, and they are especially useful
in very ill patients who would otherwise require transfusion. The maintenance dosage is that required to keep the blood count normal in the
particular case, and as far as we know these patients should continue
the liver diet indefinitely in order to avoid relapse. It should be remembered that some cases may not react to liver or liver extract, and in
these stomach preparations may be effective. Another point is that in
the presence of infection the dose of liver must be increased. For
example, I am now treating a patient whose effective maintenance dose
was three vials of Connaught liver extract a day. Two months ago
she caught influenza and developed pneumonia at the right base. Her
dosage of liver was not increased at that time, with the result that now
she is suffering from a relapse of her anaemia with the typical clinical
picture. Adequate liver diet at once controls such symptoms as sore
tongue, vomiting and diarrhoea. Appetite comes back, and the patient
is able to eat a proper diet. The return of strength and a feeling of
well-being is very rapid. As far as the nerve involvement is concerned,
cases have been reported showing marked improvement after liver
therapy. This seems to be particularly common in early cases where
the nerve symptoms are of recent onset. It is probable that, as in
pellagra, pernicious anaemia patients often have an associated peripheral
neuritis, and it is the symptoms and signs of this condition which clear
up. There is no good evidence that cases of long standing with well-
marked degeneration show any improvement even after massive doses
of liver. In early cases, even in the absence of anaemia, liver treatment
should be pushed in the hope of preventing extension of the process.
In secondary anaemia, an adequate good mixed diet is undoubtedly
of importance, but it is doubtful as yet whether there is any more
specific factor involved as in the case of pernicious anaemia. Whipple
has worked out a table showing the comparative values of different
foods in producing haemoglobin formation in dogs, and has recently
isolated an anti-secondary-anaemia substance from liver. This substance has not yet been shown to be effective in man. There are of
course many cases of mild secondary anaemia which react quite favourably to quite small doses of iron, but we have learned recently that in
many chronic cases we must push the dosage. Witts regards 90 grains
a day of a scale preparation as a minimum dose for cases such as he
describes under the title chronic microcytic anaemia, and states that,
with improvement in the blood, symptoms such as sore tongue, dysphagia, dyspepsia and enlarged spleen disappear. The medication must
be kept up for a long time, and both Witts and Dameshek stress the fact
that these patients are difficult to cure and very liable to relapse. Mills
has recently published evidence that small doses of copper are very effective in such cases. Out of 22 patients, 19 improved at once and remained well on Blaud's gr. xxx with copper carbonate gr. 1/48 t.i.d.
Some of these patients were previously resistant to large doses of iron alone.
There is other evidence that copper may be of use, based on experimental
work and also on the fact that stores of copper in the livers of infants
on milk diet become depleted just as do the stores of iron.    Lewis has
Page 97 recently published evidence that in anaemia in infants small doses of
copper with iron are very effectual. I should say that at present copper
therapy does not rest on any known scientific foundation, but it is
certainly worth trying in a case of chronic secondary anaemia resistant
to large doses of iron.
In conclusion, we have seen that anaemia is a condition which when
well advanced presents obvious symptoms and is easily recognized. On
the other hand there are many milder cases in which the symptoms are
vague and referred to other parts of the body, and in these the diagnosis
may easily be missed because the blood is not thought of.
Pernicious anaemia is a nutritional disorder associated with a constant defect in gastric secretion. It has certain clinical characteristics
which mark it out from other kinds of anaemia, of which the most
conclusive is subacute combined degeneration. As a result of recent
observations it can be treated effectively over long periods.
Secondary anaemia is predominantly a disease of women, and may
be due to many causes, but there are many chronic cases of which we
do not know the cause. The most important point in the diagnosis is
to think of anaemia as a cause of the symptoms, which often appear
irrevelevant, and the next is to have some instrument of precision to
check the diagnosis in the suspicious case. Energetic and persistent
treatment will result in marked benefit to many of these patients.
There are clinical varieties of anaemia known as splenic and aplastic
anaemia, the causes of which are unknown and which are more difficult
to treat.
In spite of much progress in the last five or six years we still know
very little about the gastro-intestinal tract, the liver, spleen and bone-
marrow in their relations to blood formation, and it is to be hoped that
continued combined study by clinician, haematologist and biochemist
will gradually elucidate these mysteries, and so place more and more of
the obscure cases within the reach of practical therapeutics.
"DISEASED" BUILDINGS
Several articles have appeared recently in medical journals calling
attention to inaccuracies often noted in scientific terminology, or nomenclature, not only in secular periodicals and newspapers but in technical
bulletins as well.
A well-known tuberculosis laboratory has issued a circular announcing that a "Tubercular Building" for children was to be erected. This is
a misnomer commonly used even among medical workers. Those who
know have repeatedly pointed out that a diseased organ may be "tubercular," but the patient is "tuberculous." It is to be hoped that the
building in question will not suffer from this type of organic disorder,
at any rate not for some years to come.
Page 91 In the field of mental hygiene it has been necessary to explain to the
uninitiated the difference between "mental defect" and "mental disease."
But we too have been careless with our psychiatric vocabulary. Why the
"Psychopathic Hospital"? There may be "psychopathic social workers"
but the state hospitals and mental hygiene clinics try as far as possible
to employ safe and sane "psychiatric" social workers. Facetiously, and
for the sake of brevity, professional workers have referred to students
of mental deficiency as the "feebleminded group."
"Insane" is a good old fashioned word, try as we might to discard
it as a medical term, but why announce, as does a current bulletin that
the foundations have been completed for two "disturbed buildings" and
two "epileptic buildings" for the blank "insane hospital"? Have you ever
seen a "nervous hospital"? But even the purist is stumped at "mental
institutions," the phrase has come into such general use. The technologists have given us the televox, the electric man and the robot, but it
takes a psychiatrist to endow a hospital for the insane with mind.
{Mental Hygiene Bulletin)
THE MODERN MANAGEMENT OF SOME COMMON
FRACTURES—Continued
Dr. Murray Meekison
Spine Fractures.
A few high lights in  the management of certain spine fractures.
1. Those of the body of a vertebra. Here one should always have
a lateral radiograph made where the spine has been injured. Indeed
compression fracture of a body is usually missed and the importance
of diagnosis and adequate treatment will be realized when you have
seen such cases a year or so after injury, and have tried to do something for the disorganized mechanics of the unfortunate victim's back.
One can almost positively state that in early, uncomplicated cases adequate non-operative methods may be expected to restore full wage-
earning capacity. The ideals of treatment are simple. 1. To reduce the
fracture and 2. adequate protection until the injured area can take the
strain of weight-bearing. I would like to describe to you the device first
reported by Rogers in Surgery, Gynaecology and Obstetrics Vol. 50,
p. 101, 1930, which has met with widespread apporoval. He devised a
frame, essentially a Bradford frame with flexible sides and a cross-bar
capable of being elevated which can be moved to any point under the
frame. The patient lies in the dorsal decubitus on the tight canvas
cover and the spine is gradually hyperextended by cranking up the
crosspiece, correction of the fracture being gained by means of the action
of gravity on the spine above and below. Maximum correction is usually
obtained in about ten days. The patient is then placed on a Whitman
or bent Bradford frame and kept there for an additional eight weeks. He
then wears an ambulatory plaster jacket for several months. There is
grave doubt as to the value of forcible reduction of these fractures but
I can speak for the efficiency of this conservative method. Let me again,
before leaving this type of fracture, urge prolonged treatment. In frac-
Page 99 tures of the transverse processes, particularly lumbar, which are by no
means uncommon, I am beginning to think that the disability is mainly
mental. The most important part of the whole treatment is to refrain
from telling the patient that he has a broken back. I have stopped using
body casts on these patients, and now simply put them to bed for a month
of physiotherapy and exercises. The majority of the patients should be
back at work well within three months and those disabilities lasting
longer than six months are very much out of the ordinary. The continuance of symptoms is due to the associated sprain or contusion
resulting in scarring, and not to the fracture itself. The most important
factor in treatment, I reiterate, is to impress upon the patient how
negligible the injury is. Tell him he has a broken back and he may be
a cripple for life purely by alteration of his mental point of view.
Fractures of the Pelvis.
There is nothing new to report. The treatment of complications
would require a long paper in itself, while the usual uncomplicated
fractured pelvis is easily handled and if properly reduced and held for
three or four weeks there is no residual disability. Extension, as usual,
with counter-traction is probably the best method in displaced fractures
while some men prefer manipulation under anaesthesia followed by
plaster. In those where there is no displacement, a stout binder, adhesive
plaster or a pair of plaster tights may be used.
Fractures of the Neck of the Femur.
Let us now dogmatize for a moment on fracture of the neck of
the femur. This is a condition about which much has been written.
There is an old and established treatment that yields a high percentage
of excellent results and, moreover, is fairly simple to carry out. It is
most satisfactory for the handling of any fracture in the region of the
head of the femur, and if it fails to accomplish the purpose, one would
be wise to try and pass the case on to someone else. Briefly outlined, it
is as follows. Use the Hawley Table if it is available and prepare to apply
a double hip spica with the plaster extending well up on the chest. Short
anaesthesia is necessary, preferably gas in the aged, or spinal if one is so
inclined. With counter traction by the use of the post and applied to
the sound leg in medium position, the surgeon lifts the injured hip forward, rotates it inward, extends it with a good steady pull and carries
it outward to an abducted position of about 45 degrees. Here it is held
while a plaster spica is applied around the pelvis and down to the toes
on the affected side with the knee slightly flexed and the foot at right
angles. I believe it is sound practice to include the opposite thigh down
to the knee. The plaster is carried up to about the level of the nipples
and is generously cut out in front to aid respiration and eating. One is
usually gratified to find that the hip is in good position and may be
left to unite. The cast is left on for three months and frequent changes
of the patient's position are strongly indicated. At the end of this time,
the plaster is removed and for another month the patient is kept in bed
during which period massage and exercises are carried out. X-rays, of
course, are taken from time to time to determine the stage of union.
Page 100 When they indicate bony union, the patient is allowed up on crutches
or a walking caliper, preferably the latter, but in no case is he allowed
to bear weight until six months have elapsed from the time of injury.
Then it is assumed gradually. After another six months, the average
case has recovered to an approximately normal state. Let me quote a
few reviews before I pass from this fracture. Using the Whitman method Campbell reports 95 per cent good results in 70 cases; Anderson 95
per cent in 200 cases; 93 per cent in 16 cases. Even discounting these
figures, I think we have the answer to the question of how to treat a
fractured hip.
Fractures of the Femur-shaft. i
I will now briefly review the treatment of fractures of the shaft
of the femur. For this purpose they may be conveniently grouped into
three  classes which we  will  take  in  order.
1. Up to age 5. I believe in these, the best and easiest treatment
is overhead suspension to a gallows frame of both legs using Buck's extension. The usual 3 inch wide strips of adhesive plaster are applied to
the inner and outer sides of both legs from high in the thigh to the
malleoli and bound in position with bias-cut flannelette bandages. The
cord from each spreader is passed through its own pulley fixed to the
frame and then they join. On the connecting cord rides another pulley
to which are added sufficient weights to keep the buttocks free of the
bed. The child is quite happy in this position, strange to say, and the
extensions are adjusted from time to time. In five or six weeks union
is sound, in most cases in excellent position, and the child may walk
after another week or so in bed.
2. Age 5 to 15 or later. Again Buck's extension applied as before
but this time in conjunction with a Thomas splint. The extension is
fastened to the splint and the splint fastened to the end of the bed.
The foot of the bed is then elevated on blocks for counter-traction, and
the fracture just naturally reduces itself. Both this and the fracture
in younger children can be reduced without anaesthesia. A grain of
codeia by hypo or an eighth of morphia is useful as a preliminary. With
the usual atention to keep the apparatus tidy, the extension is left on for
four weeks. Then the patient is taken up to the O. R. where a single short
hip spica is applied without anaesthesia from the level of the crests of the
ilia down to and including the foot. This is left on for four or five weeks
and after another week in bed the patient is allowed to walk. This, I may
say, was the routine treatment at the Children's Hospital in Toronto,
for fracture of the shaft of the femur, and a common fracture it was.
3. After age 15 Here the controversy starts, and here the multiplicity of treatment commences. I belive that many can be treated
successfully by means of the Buck's extension and Thomas splint with the
addition of overhead suspension and counter-traction by means of pulleys
and weights. I have not found manipulation and plaster an adequate
treatment, although in the hands of some men it yields excellent results.
Page 101 I believe that, taking results all around, (and this fracture is almost as
much written about as that of the neck of the femur) the best and most
accepted form of treatment at the present time is direct skeletal extension combined with the Thomas splint and overhead suspension. Extreme
care must be used in employing skeletal, as the fear of infection is
always with us. The surest preventive of infection is to leave the dressing
alone, once the traction is applied. Fiddling around with the dressings
is almost bound to lead to trouble. There are several devices for obtaining
skeletal traction, and they all have their advocates, Pearson's icecaliper
tongs or some modification, Steinman pins or nails. They are used above
the condyles of the femur, above the malleoli of the lower leg or above
the os calcis. I prefer a modified Pearson tong used just above the condyles of the femur. The knee is flexed and the pull is arranged in the
direction of the upper fragment. I will omit the details of fixing the
tongs as these are readily available. Less weights are required than when
using skin traction, and when measurements show that the leg is out to
length, the weights may be cut down to the point where they are just
sufficient to hold the fractured ends in position. The calipers may be
left in for five or six weeks, if they are left alone, and following their
removal the leg may be left in the bent Thomas splint until X-ray indicates sufficient solid callus to allow it to be removed. The patient is
then kept in bed for a further two weeks, while movements are encouraged and massage is carried out. Special attention should be paid to the
knee throughout the treatment, and it may be moved from time to time
while the calipers are in position. Finally when the patient is allowed
up, a good walking caliper is an excellent device to use for a month.
Many a good result has been ruined by allowing weight bearing too
early.
Fractures of Both Bones of the Leg.
My paper is beginning to assume untoward proportions so I will
hurriedly run through one or two ideas or devices that I have found
of value in the treatment of fractures of both bones of the lower third
of the leg and ankle. Firstly in speaking of those of the lower third of
the leg we all know how difficult it is to reduce, and hold reduced
the fracture of the tibia, without anterior angulation. In George Wilson's
book, he makes a suggestion that is contrary to all accepted teaching
flexion. Along with this idea he uses the two stage plaster, and puts the
knee at the angle something between 45 and 90 degrees. First of all
the upper portion of the cast is applied from well up on the thigh down
to within 3 inches of the fracture. Then the foot is encased to the
toes and up to within 3 inches of the fracture line on its distal side).
The fracture is then reduced by extension and hyperangulation if necessary, and the gap is bridged. One finds in most cases excellent reduction. This plaster is left in position for about three weeks or a little
longer. At the end of this period, it is removed and the knee extended
to a slightly flexed position and the foot gently brought to a right
angle and slightly inverted position. This is left on for a further six or
eight weeks when it is bivalved and physiotherapy commenced. I am
rather in favor of gentle attempts at active movement and gentle massage
as early as seven weeks from the time of the injury and in some cases
Page 102 even six weeks. At all events it is important to start it early. I have
used this method of reduction and retention exclusively for the past
year and have been extremely gratified with the results. I might add
that I believe it is good surgery to keep the foot strapped in inversion,
for at least three months after weight-bearing is commenced. Further,
the patient should never be allowed to commence weight-bearing in a
slipper.    Nothing less than a boot is adequate support.
Just one point in connection with Pott's fracture before I pass on.
This is a trick in its reduction. I do not know who told me about it
or where I saw it, but wherever it was it has stuck in my mind and) I
have always used it. The patient lies, of course, on his back anaesthetized,
with the injured leg slightly flexed at the knee over a sandbag and the
lower half of the leg extending beyond the end of the table. A loop
made of factory cotton bandage is hung over the leg above the ankle
and it is made long enough to allow the surgeon to place his right foot in
its lower end. With the right hand grasping the ball and the left holding the anterior part of the foot, you will find that you can hold the
leg immobile with counter traction by shoving down with your right
foot, and can place the patient's foot in the properly reduced position
with the greatest of ease.    Try it sometime.
Fractures of the Os Calcis.
I was going to speak about fractures of the os calcis, but the subject
is much too controversial and certainly there has not yet been a sound
and universally successful treatment devised. The continuous traction
method is not without danger. The method of reduction by remodelling
either with thumb and forefinger, or a wrench is uncertain. I have never
been able to understand the wisdom of pounding the os calcis with a
mallet. It seems to me that it adds insult to injury. Reconstruction
operations seem to be of doubtful value. Subastragalar arthrodesis is not
always indicated, but I feel that in old cases with persistent pain this
is the only treatment that, so far, is worth considering. I think that it
is best to leave the treatment of this particularly obnoxious fracture to
the dictates of your own minds or hearts until something really good is
produced. All our results are for the most part bad, and I am sure that
I have nothing startling to offer.
Fractures Not Dealt With.
In this mad gallop through fracture treatment I have omitted several.
Fractures of the carpals are controversial as regards treatment and are
unsatisfactory in anyone's hands. Fractures of the skull forms a subject
by itself. There is nothing new in the handling of ribs or sternum
fractures. Some fractures always require open operation and these I will
but enumerate:—
1. Head of the Radius—if the joint surface is injured or whole
fragment is displaced.
2. Olecranon—if any displacement.
Page 103 3. Exeternal condyle or epicondyle of the humerus.
4. Patella.
5. Many joint fractures.
In closing, I would advise you to read an article by Hey-Groves in
the Lancet of Jan. 28 th, 1928. The title of this article was striking
and productive of much food for thought. It was called "Damages to
Bones and Reputations." He summarizes the histories of the last 100
patients seen by him for residual disability following fractures.
Summing up he says:
1. Make a radiological examination of every injury.
2. Secure good reduction.
3. Prove that after reduction, the alignment is satisfactory.
4. Use simple traction, and in case of failure, resort to open operation and impact the fragments.
5. Do not plate unless you can plate efficiently.
6. Never plate an open fracture.
7. Do not comment on another physician's treatment.
Discussion
These papers were followed by a very full discussion in which Dr.
F. P. Patterson took the leading part. He dealt with the matter of time
loss due to fractures and emphasized the fact that this was largely due
to the following causes: (1( Interference with joint motion where
arthritis ensued. This is increasing, especially in the Lower Mainland.
The anatomy of the joints concerned must be borne in mind here and the
limb so placed when reduction is effected that if arthritis should ensue
we shall obtain a favourable position for function. Arthritis must be
guarded against by a suitably long period of immobilisation and avoidance of early weight-bearing. (2) Improper alignment, producing incorrect joint planes and causing strain. Proper alignment Dr. Patterson
considered most essential, angulation giving a particularly bad functional
result. This can be prevented by traction which the speaker considered
was of supreme importance in the treatment of fractures. Another
point Dr. Patterson emphasized was that a fracture is an emergency
case which should be treated at once. We should not wait till the swelling
goes down, and muscle spasm is best overcome by traction. To obtain
correct anatomical position is more important in adults than in children,
with a view to subsequent function.
As regards treatment, Dr. Patterson emphasized the following points:
In industrial fractures we should not be in too great a hurry to get the
Page   104
ill
I patient back to work—too early weight bearing is bad and will produce
arthritis owing to the abnormal strain on the joint structures. Indications of delayed union are (1) excess of callus, (2) tenderness and heat
at the site of fracture and as long as these two conditions are found
we must avoid weight-bearing.
Dr. Patterson dealt with the question of physiotherapy, which he
considered of very doubtful value in the treatment of fractures. Massage
in the later stages may be of value in restoring muscle tissue, but if in
doubt do not massage was the rule he gave. Too early and too rough
movement in fractures around joints will inevitably produce bad results.
The speaker drew attention to two conditions often overlooked in
the treatment of fractures. These conditions cannot be discovered by
X-ray but must be borne in mind if we are to avoid the charge of malpractice: (1) nerve lesions. In every fracture this possibility should be
borne in mind and paralyses or nerve injuries should be looked for at
the time the fracture is first seen and before it is reduced. (2) Vascular
damage. This is frequently overlooked, especially in fractures around
the elbow joint and ischaemias may result which are no fault of the
surgeon but may be attributed to his supposed carelessness. Large
haematomata or interrupted circulation of the extremities give the clue
and must be looked for.
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C.A.M.R.G.
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