History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: August, 1938 Vancouver Medical Association Aug 31, 1938

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Vol. XIV.
AUGUST, 1938
No. 11
In This Issue:
(With Cascara and Bile Salts)
. . FOR . .
Chronic Habitual
Western Wholesale Drug
(1928) Limited
(Or at all Vancouver Drag Co. Stores) THE    VANCOUVER    MEDICAL   ASSOCIATION
Published Monthly under the Auspices of the Vancouver Medical Association
in the interests of the Medical Profession.
203 Medical-Dental Building, Georgia Street, Vancouver, B. C.
Editorial Board:
Db. J. H. MacDermot
Dr. M. McC. Baird Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
Vol. XIV
AUGUST, 1938
No. 11
OFFICERS  193 8-1939
Dr. Lavell H. Leeson Dr. A. M. Agnew
President Vice-President
Dr. W. T. Lockhart
Hon. Treasurer
Dr. G. H. Clement
Past President
Dr. D. F. Busteed
Hon. Secretary
Additional Members of Executive: Dr. J. P. Bllodeau, Dr. J. W. Arbuckle.
Dr. F. Brodie
Dr. Neil McDougall
Dr. J. A. Gillespie
Historian: Dr. W. D. Keith
Auditors: Messrs. Shaw, Salter & Plommer.
Clinical Section
Dr. R. Palmer Chairman     Dr. W. W. Simpson Secretary
Eye, Ear, Nose and Throat
Dr. S. G. Elliott Chairman     Dr. W. M. Paton Secretary
Pediatric Section
Dr. G. A. Lamont Chairman     Dr. J. R. Davies Secretary
Cancer Section
Dr. B. J. Harrison Chairman     Dr. Roy Huggard Secretary
Dr. A. W. Bagnall, Dr. H. A. Rawlings, Dr. D. E. H. Cleveland,
Dr. R. Palmer, Dr. F. J. Buller, Dr. J. R Davies.
Dr. J. H. MacDermot, Dr. D. E. H. Cleveland, Dr. Murray Baird.
Summer School:
Dr. J. R. Naden, Dr. A. C. Frost, Dr. A. B. Schinbein, Dr. A. Y. McNair,
Dr. T. H. Lennie, Dr. Frank Turnbull.
Dr. A. B. Schinbein, Dr. D. M. Meekison, Dr. F. J. Buller.
V. 0. N. Advisory Board:
Dr. I. Day, Dr. G. A. Lamont, Dr. Keith Burwell.
Metropolitan Health Board Advisory Committee:
Dr. W. T. Ewing, Dr. H. A. Spohn, Dr. F. J. Buller.
Greater Vancouver Health League Representatives:
Dr. W. W. Simpson, Dr. W. N. Paton.
Representative to B. C. Medical Association: Dr. G. H. Clement. .
Sickness and Benevolent Fund: The President—The Trustees. Protection Against Typhoid
Typhoid and Typhoid-Paratyphoid Vaccines
Although not epidemic in Canada, typhoid and paratyphoid infections remain a serious menace—particularly
in rural and unorganized areas. This is borne out by the
fact that during the years 1931-1935 there were reported,
in the Dominion, 12,073 cases and 1,616 deaths due to
these infections.
The preventive values of typhoid vaccine and typhoid-
paratyphoid vaccine have been well established by military and civil experience. In order to ensure that these
values be maximum, it is essential that the vaccines be
prepared in accordance with the findings of recent laboratory studies concerning strains, cultural conditions and
dosage. This essential is observed in production of the
vaccines which are available from the Connaught
Residents of areas where danger of typhoid exists and
any one planning vacations or travel should have their
attention directed to the protection afforded by vaccination.
Information and -prices relating to Typhoid Vaccine and to
Typhoid-Paratyphoid Vaccine -will be supplied
gladly upon request.
Toronto 5
Depot for British Columbia
Macdonald's Prescriptions Limited
Total Population—estimated	
Japanese Population—estimatecL
Chinese Population—estimated —
Hindu Population—estimated —-
Total deaths  219
Japanese deaths      8
Chinese deaths    12
Deaths—residents only  195
Male, 202; Female, 139_
Deaths under one year of age    10
Death rate—per 1,000 births    29.3
Stillbirths (not included in above)      3
Rate per 1,000
June, 1937
July 1st
to 15th, 1938
Cases Deaths
May, 1938
Cases Deaths
June, 1938
Cases Deaths
Scarlet Fever  32 0 20           0 14          0
Diphtheria    0 0 0           0 0           0
Chicken Pox  167 0 180           0 22           0
Measles   10 0 10 10
Rubella   2 0 0           0 10
Mumps -  12 0 22           0 10
Whooping Cough  34 0 55           1 7           0
Typhoid Fever  5 0 10 10
Undulant Fever  4 0 2           0 0           0
Poliomyelitis    0 0 10 10
Tuberculosis  37 13 35           9 27
Erysipelas  2 1 0           0 0           0
Ep. Cerebrospinal Meningitis 0 0 11 0           0
Vancouver      Hospitals and
Clinic        private doctors      Totals
Syphilis      55 38 93
Gonorrhoea       68 23 91
Conducted in accord with the ethics of the Medical
Profession and maintained to the standard suggested by
our slogan:
Pharmaceutical Excellence
AACG'II 6 Ormc,
L-l MiTED V-«'
FORT STREET (opp. Times)      Phone Garden 1196      VICTORIA, B. C.
Page 2^6 Literature and samples from:
In dealing with the question of cancer, and in considering the best- method
of attacking this ruthless and cruel enemy of ours, one finds two schools of
thought mutually antagonistic. There is the school which wants to go all out,
which believes that "attack, always attack," is the best, nay the only, defense
we can employ. This school wants to engage at once with all the forces at
our' disposal—propaganda, public education, etc.—to warn people as fully
and as freely as possible of the danger that they themselves, not merely their
friends, may have cancer, or may be in danger of getting it, to urge them to
seek advice and examination, and, if necessary, treatment.
This school believes that it is better to frighten people a bit than to let
them die of cancer, in more or less blissful ignorance of the fact that if they
had sought help sooner they might have escaped. It believes that it is better
to swamp our existing hospital accommodation with the cases that require
diagnosis and treatment, than to go on allowing patients to reach a hopeless
stage of the disease because there is not at present sufficient room for them.
After all, they submit, all these cases become hospital cases eventually in any
case—and besides, not until the public realizes the extent and urgency of the
problem will it bring the necessary pressure to bear on its various governmental bodies to provide the necessary accommodation and equipment.
The other school is very much more logical and sensible. It argues that
we must not run the risk of precipitating a public panic in this matter—we
must not do anything which will overload, dangerously if not fatally, our
present machinery for coping with cancer. It argues that if people apply for
diagnosis and treatment before we have had time to get these ready, they will
suffer intensely and uselessly. They are for a more gradual approach; they
would tackle it by gentler and more leisurely means, by education from above
This school argued this way about tuberculosis, till some rebellious and
dissatisfied souls refused to listen, and went ahead and got something done.
They evoked the same bogey about venereal disease, but again there were
those who refused to believe in the imminence of disaster, and today we are
immeasurably ahead of our former position in both these fields. They are
saying the same things about the pasteurization of milk today. "Let sleeping
dogs lie" would seem to be their motto. They are very probably right,
theoretically, in all they say—but we can never meet any crisis successfully
in this spirit of defeatism. Every step forward in human affairs carries the
risk of stepping on someone's toes, and is a shock to this type of thinker; he
and his kind have "always stoned the prophets." It is this inertia, which is
an inherent and often a most valuable trait in our human nature, which
always stands in the way of the more reckless, but perhaps more far-sighted
souls whose attitude is that attributed to Beatty of the British Navy: "Full
speed ahead, and damn the torpedoes."
So we confess that we rejoice to see, springing up all over British Columbia, a series of groups of men and women who intend, come what may, to do
what they can to awaken the people of this Province to the deadly nature
of this problem, its huge extent, and its vital urgency. If this knowledge
leads to temporary dismay and consternation, so much the better, and so
much the sooner shall we get results—legislatures will always respond to a
sufficiently vocal and widespread demand for action. In the long run it will
be infinitely the quickest and most effective course for us to pursue. The
demand will come, not from a few experts and informed people, but from the
great mass of people, who must be interested in this matter, and all of whom
must be enlisted in the fight, if we are to obtain speedy and lasting results.
Anything else is merely palliative, a treating of symptoms only—and actually
dangerous, in that it "cries peace when there is no peace," and creates a false
sense of security. We cannot bribe or coax cancer to stay its hand, and our
only hope of success is to go out boldly and take it by the throat.
Dr. R. A. Perkins, of the Research Staff of Parke Davis & Company,
Detroit, will be in Vancouver early in August, and will address a meeting of
the Vancouver Medical Association in the Auditorium of the Medical-Dental
Building on August 2nd. His subject will be "Treatment of Venereal Disease."
The Association extends its hearties congratulations to two of its members
who were married in July. Dr. K. P. Groves was married on July 2nd to Miss
M. Clugston, and Dr. W. W. Simpson was married on July 7th to Miss K. Sol-
loway. Both Dr. Groves and Dr. Simpson are in practice in Vancouver and
will make their homes here. We offer our best wishes to Dr. and Mrs. Groves
and Dr. and Mrs. Simpson.
* *     *     *
The congratulations of the Association are extended to Dr. and Mrs. A.
M. Gee of Essondale, B. C, on the birth of a daughter on June 27th.
3f£ 3{C 3|C ]|C
We also offer congratulations to Dr. and Mrs. H. S. Stalker upon the
birth of a daughter on June 23rd.
"t* "P 1* H"
Dr. Lyon Appleby is very happy this year over the success of his beautiful
little two-year-old, Vade Retra, which has been winning races very easily.
The best wishes of the Association are extended to Dr. and Mrs. J. W.
Shier upon the birth of a daughter on July 4th.
9; * 5p V
We also congratulate Dr. and Mrs. J. A. McLean upon the birth of a
daughter on July 6th.
* * % V
Military manoeuvres have engaged the attention of a number of members
of the Association during the past month. The 12th Field Ambulance,
R.C.A.M.C, were in camp at Sidney, B. C, with Lt.-Col. L. H. Leeson, O.C.,
and Major H. R. Mustard, Major H. H. Pitts, Capt. H. A. DesBrisay, Capt.
F. H. Bonnell, Capt. R. Huggard, Lt. S. A. McFetridge and Lt. F. Turnbull
all attending.
V *F V f
Dr. R. Irving is in Vancouver to attend the races. Dr. Irving has a very
promising two-year-old, which lived up to his name and made an excellent
showing in his first "out."
* *     *     *
We offer best wishes to Dr. and Mrs. A. R. Anthony upon the birth of a
daughter on June 29th, and to Dr. and Mrs. K. F. Brandon upon the birth
of a daughter on the same day.
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We also offer good wishes to Dr. and Mrs. Frank Emmons upon the birth
of a son on July 5th.
3|C SfC 9|C 3(C
Dr. E. B. Trowbridge has opened offices in the Medical-Dental Building
and will confine his practice to Obstetrics and Gynaecology.
]K #j% rj% «K
Dr. W. H. White, until recently Surgical Interne at the Vancouver General Hospital, has now established himself in practice in Penticton and will
be associated with his father, Dr. R. B. White, and Dr. J. R. Parmley. "Bill"
has the goodwill and wishes of the profession.
* *      *      *
Dr. W. O. Green is now associated with his father, Dr. F. W. Green, and
Dr. G. E. L. MacKinnon in the practice at Cranbrook.
Page 248 Dr. J. A. Taylor and Dr. J. L. M. Anderson have returned to the Province,
having completed the course at Toronto leading to D.P.H. qualification. Dr.
Taylor will have charge of the Unit at Abbotsford under the Department of
Public Health. Dr. Anderson has been Medical Schools Inspector in Victoria
and is returning to resume his work.
* ♦      *      *
Dr. and Mrs. W. Leonard of Trail have returned from a three-months'
trip abroad, during which time Dr. Leonard did post-graduate work in
London in Obstetrics and Gynaecology.
* *      *      *
Dr. Frank L. Wilson and Dr. J. Bain Thorn were in Vancouver in June
and attended the Summer School sessions.
•p f 1* *p
Dr. W. Laishley, the Eye, Ear, Nose and Throat specialist of Nelson, has
just returned from Chicago, where he did post-graduate work. Incidentally,
there was a big baseball game on that Sunday.
* *     *     *
Dr. E. E. Topliff of Rossland will spend the month of August at Loon Lake.
* *      *     *
Work on the new $115,000.00 wing on the Hospital at Rossland is pro*
gressing.   It will house the Operating Rooms, Maternity Section and the
X-Ray Department.
* *     *     *
Dr. L. N. Beckwith of Trail and Miss B. McGauley of Castlegar were
married recently at Castlegar.  Our sincere good wishes.
* *     *     *
Dr. F. P. Sparks, M.H.O. at Nelson, and Miss Mai Norris of Nelson were
married recently. They have our best wishes.
jp «p 9* V
Dr. and Mrs. C. M. Bennett of Nelson are receiving congratulations on
the birth of a son.
*»* *t* f* ^»
Dr. J. A. Ireland of Kamloops spent a week at the Military Camp at
Sidney. He is the Medical Officer to the Rocky Mountain Rangers, the regiment with the illustrious band.
* *     *     *
Dr. Stewart A. Wallace of Kamloops arrived back from Halifax. Apparently he had to help the engine-driver to dodge a bear on the track. Dr.
Cheeseman of Field has a wonderful new Buick and he detours passengers
at that point to the Great Divide, where one meets one's own train again.
* *     *      *
Dr. Alan Hall of Nanaimo is having a great summer with his new cruiser,
the Rathgail.
* *      *      *
Dr. and Mrs. C. C. Browne of Nanaimo have been away in their sea-going
craft and visited Maple Bay and Montague Harbour.
* *     *     *
Dr. A. H. Meneely of Nanaimo was in Vancouver last week.
* *      *     *
Dr. C. T. Hilton of Port Alberni happened into Vancouver and attended
the Dr. Leland luncheon.
* *      *     *
Dr. and Mrs. R. W. Garner of Port Alberni are away on vacation this
* *      *      *
Dr. and Mrs. E. D. Emery and baby leave for Edmonton and Jasper
during August.
Page 249 Dr. and Mrs. H. H. Boucher of Vancouver and the infant daughter are
visiting Dr. and Mrs. Knox in Kelowna.
♦ ♦      #      $
Dr. J. Vernon Murray of Creston, who is spending a vacation at the Coast,
called at the office en route to Vancouver Island.
# ♦      #      #
Dr. D. H. Williams of Vancouver, Director of the Division of Venereal
Disease Control, Provincial Board of Health, recently visited Victoria and
Nanaimo in connection with the work of the Department.
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Dr. W. F. Anderson, who has been associated with Drs. Green and MacKinnon in Cranbrook, is now in practice with Dr. A. S. Underhill at Kelowna.
* *      *      *
Dr. Peter L. Straith of Courtenay called at the office while in Vancouver
in July. He is looking and feeling well, and we hope he maintains his present
standard of good health.
On August 11th, Dr. O. S. Lowsley, of New York City, will
address the members of the Vancouver Medical Association. Dr.
Lowsley is a specialist in Urology and was a lecturer at the Summer
School in 1929. Notices, giving details of time and place and Dr.
Lowsley's subject, will be sent out later.
The Dean Lewis System of Surgery has now been brought up to date, and
all new pages have been inserted. The Library is also receiving the International Abstract of Surgery, which is issued monthly.
New articles for the Nelson Loose-Leaf System of Medicine include the
"The Common Cold," by A. R. Dochez and Y. Kneeland.
"Cerebrospinal Fever; Recent Progress," by W. Herrick.
"Anatomy and Physiology of the Pituitary Gland," by P. E. Smith.
"Diseases of the Pituitary Gland," by L. M. Davidoff.
"Coronary Artery Disease and Coronary Occlusion," by H. B. Sprague.
"Coronary Insufficienty (Angina Pectoris)," by P. D. White.
"Diseases of the Kidney," by R. F. Loeb.
Recent revisions in the Oxford System of Medicine include the following:
"Diseases of the Pleura," by Dr. J. A. Capps and Dr. R. B. Capps.
"Irregular Action of the Heart," by Dr. J. Hay.
"Essential and Orthostatic Hypotension," by Dr. F. R. Taylor.
"Sulfanilamide in the Treatment of Infections," by Dr. M. A. Schnitker
and Dr. M. Pijoan.
"Malaria," by Col. C. F. Craig.
Commencing with next month's issue, a list of books added to the library
since the beginning of the year will be published in the Library Notes. As far
as possible the books will be listed according to the subject of the book, so
that the list may be kept for reference.
Radiation Therapy : Its use in the treatment of benign and malignant conditions. By Ira I. Kaplan, B.Sc, M.D., Clinical Professor of Surgery, New
York University Medical College; Director, Radiation Therapy Department, Bellevue Hospital, New York. New York: Oxford Press,. 1937.
As the author states in his preface, "the book aims to give the student,
the general practitioner, as well as the specialist, an understanding of the
The increasing death rate from Cancer is a definite challenge to Medicine.
Page 250 fundamentals of irradiation, and enumerates the conditions for which this
form of therapy is of value." Dr. Kaplan is well qualified to write such a
book, both by his position in the Bellevue Hospital and by his connection
with the Year Book of Radiology, the therapeutic section of which he has
edited since its inception in 1932.
An insurmountable difficulty for the writer of any text book on radiation
therapy is the rapid development of this new branch of medical science. Old
methods of treatment are being so quickly replaced by new that by the time
a book is published it must of necessity be partly out of date and the radiation
therapist himself must depend on current articles and visits to the larger
centres for the more recent developments. However, the book does give an
excellent idea of the scope and possibilities of both x-ray and radium therapy,
and for this reason should be of particular value to the general practitioner.
X-ray doses are given in "r" units without backscatter, but no attempt is
made to calculate tumour dosage, a method so useful in the treatment of
many types of cancer. Radium doses are still expressed in milligramme
hours or millicuries destroyed, a method almost entirely abandoned in
English and Continental clinics.
The illustrations are excellent and show what a wide variety of conditions
passes through Dr. Kaplan's hands. Unfortunately some old ones have been
included which show radial arrangement of interstitial radium, a method
universally condemned, since physical measurements have shown that it
gives unequal distribution of radiant energy. The chapter on x-ray physics
by Carl B. Braestrup is unusually clearly writen and repays even a casual
reading. A controversial point in the treatment of sterility by stimulating
doses of x-ray delivered to the ovaries. Kaplan himself has had surprising
success by those method, but more conservative radiologists feel that treatment of the very radiosensitive germplasm is fraught with too much danger
to be undertaken before more cerain knowledge of the subject is available.
There is a useful chapter on the nursing care of patients and the book ends
with a suggested plan for the construction of a unit radiation department in
a municipal hospital. —E. T.
SEPTEMBER  15,  16,  17,   1938
VICTORIA IS READY and invites you and the ladies to attend th©
Annual Meeting.
Five lectures each morning for three days. At this date there are no
changes in the programme and list of speakers published in the July
Already we have received numerous requests for accommodation at the
Empress Hotel.
The Annual Meeting of the College of Physicians and Surgeons, of which
all are members, will be followed by the Annual Meeting of the British
Columbia Medical Association. These meetings will be held on Friday
evening, September 16th, and should be attended by every member of the
profession in this Province.
These will be held on Thursday afternoon, September 15th, at the Jubilee
There will be some things to see.
Thetre will be a conference on Public Health to which all are invited.
This will be held on Friday afternoon, September 16th. Leadership will be
provided under the direction of Dr. Frederic Kincaid of Victoria.
This session on Friday afternoon, September 16th, will be under the
leadership of the Committee on Economics of the College of Physicians and
Surgeons. There should be a large attendance as this study affects the
structure of Medicine in the Province, Standards of Practice, Working and
Living Conditions, and Economic Security.
Thursday—First day, September 15th.
Speakers: Doctors Spohn and Dolman. "Milk Situation" (Medical Supervision).
Friday—Second day, September 16th.
Speakers: Doctors MacKenzie and Routley. "Canadian Medicine."
The Annual Dinner on Saturday, September 17th, always possesses
quality.   Outstanding guests—short address and Golf prizes.
Royal Colwood Golf Club
Saturday, September 17th, all will play. Many
prizes. Dr. Keys has lined up Doctors George
Hall, Frank Bryant, Ronnie Scott-Moncrieff and
Joe Bilodeau (as mainland whip) to help put
this over. It is rumoured that Johnny Walker
will be on the Committee.
Golf Trophy and Many Other Prizes
The British Columbia Trophy will be in annual
competition. The winner also receives a token
Dr. Joe Lennox states that all members of his Commitee will work harder
than he does. He will ask you to attend the two Luncheons, the Annual
Dinner, the Danee on Thursday night, go to Butchart's Gardens on Friday
(late afternoon) and we hope he will provide medical comforts and cheer
us up on the Golf Course.
You will be welcomed and asked to register—this is necessary,
attend the sessions should register at once.
All who
The demand for space for Commercial Exhibits makes it appear that
our friends who offer us Pharmaceuticals, Instruments, X-Ray machines
and Electrical gadgets wish to support the Annual Meeting.
The Committee in charge will help the Ladies to convey everyone to the
Gardens of Mr. and Mrs. Butchart on Friday afternoon. There will be
cars going to the Royal Colwood Golf Club on Saturday early afternoon.
Please notify the Registration Desk.
You will be notified later if you are to purchase one way fare going to
Victoria on certificate plan. We shall try to arrange fare and third rates
for all.
The programme for Ladies will be a very happy one. The Committees in
Victoria should be warned that there has been much favourable comment
on last year's meeting in Vancouver. Well, they have advertised the ladies'
programme and more wives are bringing more husbands this year.
There is the Dance on Thursday, (first night), September 15th. Then
the Tea Party on Friday, September 16th, in the gardens at "Benvenuto"
through the kindness of Mr. and Mrs. Butchart—and finally the Ladies'
Dinner on Saturday, September 17th.
On July 8th, a Luncheon Meeting was held in the Hotel Georgia when
Dr. R. G. Leland, Director of the Bureau of Economics of the American
Medical Association, was the guest speaker. Those who were able to
attend profited largely by the wealth of knowledge which Doctor Leland
has acquired in his study of conditions in practice.
The above Committee has been very much occupied in its task of preparing the changes necessary in the Constitution and By-Laws so that they
may be presented to the Annual Meeting on September 16th.
Certain alterations are needed to place British Columbia's organization
in tune with the Canadian Medical Association. These must be ready for
entry in Federation. Dr. H. H. Milburn as> Chairman and Dr. G. F. Strong
were appointed a Sub-Committee to draft the new set-up. This was further dealt with at a meeting on July 26th. They will be vised by the Board
of Directors at the regular meeting on August 4th. Two weeks notice of
motion will be posted to all members of the British Columbia Medical
Cancer is the most challenging problem confronting our profession today, and the
lay public is rightfully looking to us to assume! leadership in this field.
Progress in the organization of the British Columbia Branch of the
Canadian Society for the Control of Cancer has been more than gratifying
despite hot weather, vacations and the numerous other distracting factors
that obtain during the summer season.
The response of the members of our Association, who were delegated
to organize units throughout the province, to say the least, has been excellent.
More than one hundred have already very willingly accepted the task
in their respective communities.
Twenty units have selected executives and are definitely on the map.
Forty-nine are in the process of organization and in the very near
future should be completed—truly a wonderful showing and bodes well for
the success of the whole undertaking.
The central executive is more than gratified that the medical profession
throughout British Columbia has accepted leadership in this most important field.
Things are moving rapidly. The next two months should show an
enrolment of 20,000 members in this Society in British Columbia.
[Read by Dr. A. Gardiner Frost before the Fraser Valley
Medical Association.]
It is not the toxaemias of pregnancy in the ordinary sense of the term
that I wish to discuss this evening, but rather toxaemias from the viewpoint
of whether the hypertension is causing, or will cause if allowed to continue,
permanent and irreparable damage to the mother.
When a patient comes to us for prenatal care, and begins to show signs
of hypertension or toxaemia, the first thought that comes to our minds is:
Is she likely to develop into an eclamptic, or can we carry her safely through
her pregnancy and obtain a living child? This latter is our objective, and
rightly so. But when we have carried this patient through her toxaemia, and
a successful delivery, we feel our job is done.
Six weeks later she comes to the office for final checking, which usually
consists of only a pelvic examination. Little do we realize, if the blood pressure is not taken at this time, that this toxaemia, however mild, may have
caused this mother permanent renal or cardiovascular damage, and that her
expectancy of life is materially shortened.
Only in the recent past have we begun to realize what serious effects these
toxaemias of pregnancy have in later years of the mother's life, how essential
it is to follow every case of toxaemia, however mild, for a least a year, in
order to arrive at the conclusion of just how much damage has been done.
It is in this light that I wish to discuss these cases of hypertension tonight.
First of all I wish to briefly classify the various types of toxaemia. The
classification I am using is that formulated by Stander at the Johns Hopkins
Clinic in 1926. A patient is at once classed as a toxaemia if during the antepartum, intra-partum or post-partum period she shows a rise of blood pressure
on two or more occasions, a systolic pressure of 140 or more, or a diastolic
of 90 or more.
These toxaemias fall into four groups:
1. The Low Reserve Kidney;
2. Pre-eclampsia;
Page 254 3. Eclampsia, and
4. Chronic Nephritis complicating pregnancy.
Taking the Low Reserve Kidney group, it is well known that in a healthy
person, all of the glomeruli are not functioning to capacity at any one time,
and it has been estimated that there is usually a margin of safety which
approaches 50%—in other words, there is a decided kidney reserve which
may be called into play. Thus it is that the kidney reserve in this group of
cases is too low to meet the extra demands of pregnancy. This type of
toxaemia is the most common, and constitutes about 44% of all toxaemias
of pregnancy. It usually appears during the last trimester and may or may
not be accompanied by subjective symptoms. In many cases the patient
notices oedema of the ankles and legs, complains of headache and general
malaise, but does not feel seriously ill. Occasionally all subjective symptoms
are lacking, so that the condition would escape observation were the blood
pressure not taken and the urine examined, as part of the routine medical
care. The blood pressure is always elevated, and albuminuria is usually
present along with a few casts. The characteristic feature of this condition
is that the blood pressure does not attain great height, the systolic pressure
rarely exceeding 160 and the diastolic 90 milimeters, and that the albumen
content does not exceed 2 grams per litre, and frequently only a fraction of
one gram. Sometimes excessive gain in. weight occurs, and its cause is
evident when oedema is pronounced and the urinary output decreased. The
blood chemistry is always normal.
The treatment is simple, as a few days' rest in bed along with a low
protein and salt free diet is usually followed by the disappearance of the
oedema, a considerable loss in weight, the return of the blood pressure to
normal, and the disappearance of albumen from the urine. The induction
of premature laboc is rarely if ever necessary. If the patient has been in
bed for one or two weeks under a proper dietary regimen and no improvement is noted, one is probably dealing not with a case of low reserve kidney
but with a chronic nephritis or a pre-eclampsia.
The important feature of this type of toxoemia is that the blood pressure
returns to normal soon after delivery and remains so, and in future pregnancies a similar picture may appear, but the kidney are not left in a damaged state, as is shown by the follow-up findings as regards blood-pressure
and kidneys.
The second group of toxaemias is classified as Pre-eclampsia. It is the
least common form of the toxaemias of pregnancy, those affected constituting
about 5% to 8% of all toxemic patients. By the term pre-eclampsia we mean
the same disease entity as eclampsia except that it is not accompanied by
It occurs more frequently in women pregnant for the first time and
usually develops in the last trimester of pregnancy. In general it pursues
a more acute course than the Low Reserve Kidney. The blood pressure is
always higher than in Low Reserve Kidney and frequently systolic readings
approach 200 millimeters while the diastolic pressure is proportionately
high. There is more albumen in the urine than in Low Reserve Kidney, and
the amount varies from several to 10 or more grams per litre. The urinary
excretion may be greatly diminished and in severe cases may be entirely
suppressed. The urine contains casts of all kinds and occasionally blood.
The chemical examination of the blood shows changes analogous to those
occurring in eclampsia, but usually to a slighter degree—thus the uric acid is
definitely increased while the carbon dioxide combining power is sometimes
diminished. Ordinarily there is no nitrogen retention in the blood. Visual
disturbances are common and ophthalmoscopic examination may show
haemorrhage into the retina and a spastic condition of the arterioles, but
never albuminuric retenitis, and in many cases the findings may be negative.
Page 255 Oedema is frequently very marked and usually involves the face and
neck as well as the extremities. Its development is associated with a rapid
increase in weight and frequently an abnormally large weekly gain constitutes the first sign in the development of this condition.
It should always be borne in mind that pre-eclampsia is the toxaemia of
pregnancy par excellence and that one of the essential aims of routine prenatal care is to detect it in its incipiency and to institute prophylactic meas
ures to prevent an outbreak of eclampsia. Accordingly, the treatment to
be pursued will depend upon the seriousness of the condition. As soon as it
is recognized the patient should be put to bed and placed on a low protein,
salt-free diet. If marked oedema is present Epsom salts should be given each
morning, allowing four to five fluid bowel movements per day. If improvement follows, the treatment should be continued.
If the pre-eclampsia is fairly severe we place these patients on a modified Strogonoff treatment, which I shall describe later on. If improvement
does not follow this sedative treatment it is our practice to terminate pregnancy. Fortunately the number of patients requiring such interruption is
relatively small. Labour may be induced by castor oil, quinine and carefully
regulated doses of Pitocin, beginning with 3 minims and increasing one
minim every half hour until a maximum of 7 minims is given. If the presenting part is engaged, artificial rupture of the membranes is done.
If, however, the symptoms become more urgent, as indicated by the sudden development of intense headache, epigastric pain and stupor, the only
hope of preventing an eclamptic outbreak lies in the prompt termination of
pregnancy by Caesarian section.
The third group of toxaemias are classed as eclamptics.
Because of the many hypotheses that have been offered concerning the
etiology of eclampsia, it has been called the "disease of theories."
The incidence of this condition is in about 1% of women entering lying-in
hospitals, and is one of the most important causes of maternal deaths.
It is much more frequent in primparae than multiparae, and occurs almost
exclusively in the last trimester of pregnancy.
In about 20% of cases the convulsion does not occur until after labor
has been completed.
An eclamptic convulsion sometimes occurs without warning, like a bolt
from a clear sky, in women who were apparently in perfect health.
However, in 85% of 2000 cases, analyzed by Eden of England, the patients
had signs and symptoms indicative of pre-eclampsia several days or even
weeks beforehand.
In most cases the blood pressure is markedly increased—sometimes well
over 200 systolic. Very exceptionally no rise is noted whatsoever, and we are
ignorant of any trouble until an actual convulsion occurs.
Albuminuria is almost constantly present, and the uring during the
eclamptic seizure usually gives evidence of marked renal insufficiency. It is
invariably diminished in amount and occasionally entirely suppressed. In
the majority of cases there is at least 10 grams of albumen per litre of urine.
The ocular changes may show a haemorrhagic retinitis, but never albuminuric retinitis.
Within the past few years a great amount of chemical work has been
done on the blood of eclamptic women in the hope that alterations in its
constitution might throw light upon the nature of the toxaemic process, but
as yet little helpful information has been obtained.
The outstanding features consist of an increase in the uric acid content
of the blood and a decrease in the carbon dioxide combining power.
There is rarely any nitrogenous retention, and when the N.P.N, is increased it is probably due to kidney damage incident to the eclamptic attack.
The prognosis is grave—the maternal mortality being about 25%, while
that of the child approaches 50%.
Page 256 However, if we calculated the mortality on a ten-year basis, the death
rate would be much higher, as 20% of eclamptics eventually end up with a
chronic nephritis.
Treatmen t: Once the patient has had a convulsion, treatment should be
conservative. At the Hopkins Clinic the Strogonoff treatment was used. Prior
to this conservative form of therapy the mortality rate was 23% ; since then
it has dropped to 13%.
I shall first describe the method used in Baltimore, and then briefly
enumerate other forms of treatment.
The patient is placed in a darkened room and every effort made to secure
the greatest possible quiet.
Immediately upon admission % grain morphine is given, the patient
catheterized and examined medically and obstetrically. If laboratory facilities are available, blood may be withdrawn for chemical investigation. At
this time there should be no thought of delivery unless the cervix is fully
Let us suppose our patient is admitted at 6 a.m. with eclampsia. At this
tmie morphine % grain is given. At 7 a.m. 30 grains of chloral hydrate is
given per rectum if patient is unconscious or by mouth if not.
At 9 a.m. she is again given % grain of morphine. At 1 p.m. chloral
hydrate is repeated. This is again repeated at 7 p.m. and 3 a.m.
If the patient is conscious she should drink water freely. If the coma
lasts for one or two hours, 500 cc. of 20% glucose-is given. If improvement
is noted, labour should be induced, because after a few days the blood pressure
again begins to rise and the eclampsia is likely to recur.
On the other hand, if the patient is admitted in labour or if pains begin
during the course of the attack, labour may go on without serious disturbance.
As soon as the cervix has been completely dilated, delivery should be
effected by forceps under gas anaesthesia.
Unfortunately, in more severe cases, irrespective of whether the patient
is in labour or not, the convulsions become more frequent in spite of treatment, the coma deepens and the general condition becomes more alarming.
In such circumstances Caesarean section under local or spinal anaesthetic
should be done. Such interference, however, should be regarded as exceptional, and should be considered only as a last resort. General anaesthesia
for such cases should never be used, for it has been shown that degenerative
changes occur in an already damaged liver.
Other modes of treatment consist of venesection, and intravenous administration of magnesium sulphate 20 cc. of a 10% solution every hour until
convulsions cease.
The lowest mortality rate reported in the British Isles is by the use of
the Dublin treatment, which consists of: (1) Starvation; (2) gastric and
colonic lavage, and (3) submammary infusion of sodium bicarbonate solution.
I, personally, have never seen this method used.
However, it is now a well established fact that the results following all
types of conservative treatment are much better than those following the
radical methods.
Now, the three types of toxaemias that I have just mentioned, namely,
Low Reserve Kidney, Pre-eclampsia and Eclampsia, do not permanently
injure the renar nor cardiovascular system. In other words, she may safely
have more children. Because a woman has once had eclampsia is no indication that she should be advised against future child bearing. Her chance
of having a recurrence of eclampsia is only 5%. However, it must be proven
beyond a doubt that she has not suffered permanent renal or cardiovascular
damage, and if this damage has occurred then she should be advised against
further pregnancies.
And so we come to our fourth group of so-called toxaemias. This group
we as obstetricians classify as chronic nephritis.  Internists subdivide this
Page 257 group into those of a true chronic nephritis and those of a true cardiovascular hypertensive disease. Whether one case is a chronic nephritis or
is a hypertensive varcular disease, it makes no difference when a woman is
pregnant or contemplates pregnancy—for the prognosis and treatment are
essentially the same:
Unlike the patient in actual eclampsia, this is the type of toxaemia that
kills, not immediately, but in a few years to come.
In our annual maternal mortality statistics it is usually stated that:
first, infection; second, haemorrhage, and third, toxaemias, are the main contributing factors, while eclampsia is given as the most serious type of
toxaemia concerned, due to its high accompanying maternal and foetal mortality.
However, if the annual statistics would include a ten-year mortality
figure, nephritis would be the second greatest factor in this death rate, being
surpassed only by infection.
Let us look into the mortality figures of chronic nephritis associated with
pregnancy. Peckham and Stander at the Johns Hopkins Clinic found that
in patients who are pregnant and in whom a diagnosis of chronic nephritis
can be made while in this pregnant state, 42% of such patients are dead
within a period of ten years.
These men also found that, excluding cases of vomiting of pregnancy
and eclampsia, 40% of all toxaemias show up as a chronic nephritis, not
necessarily during the pregnancy but within a year or two afterwards.
Herrick of the Presbyterian Hospital in New York found that of 500 cases
of mild toxaemias of pregnancy that were thought to be Low Reserve Kidney
during their pregnancy, 15% were dead at the end of six years due to renal
or cardiovascular damage.
With the result of these almost unbelievable findings, it was felt that we
had been far too conservative in the treatment of chronic nephritis associated
with pregnancy—that we must diagnose these cases much earlier and terminate pregnancy before the foetus does irreparable damage to the mother.
How are we to differentiate between a chronic nephritis on the one hand
—and by this term I include the cases of so-called hypertensive cardioV
vascular disease—and those cases of low reserve kidney and pre-eclampsia\
on the other?
Gentlemen, the most important single sign we have is the blood pressure.
First of all may I briefly enumerate the main points in which a diagnosis
of chronic nephritis is relatively easy to make. Let us first take the kidney
function tests. It was felt at the Baltimore Clinic that the two most satis-
factor tests were the phenolsulphthalein excretion test and the urea clearance test. A single renal function test is of no value. It is often necessary to
do several tests and repeat them several times. However, it was felt that
with a repeatedly low phenolsulphthalein test there is some evidence of
damaged kidneys.
Any urea clearance test that gives values below 50% is very strong proof
of the existence of a chronic nephritis.
The ocular charges also enable us to differentiate this condition. When
albuminuric retinitis is present we may safely diagnose a chronic nephritis.
When there is definite nitrogenous retention in the blood one may conclude
that the kidneys are permanently damaged.
When a case of chronic nephritis complicating pregnancy can be so easily
diagnosed by the aforementioned findings, the pregnancy should be immediately terminated, no matter what period of gestation, and future pregnancies
prohibited. We all know too well that the further we allow this mother to
proceed with her pregnancy the more are her kidneys and cardiovascular
system going to be permanently damaged. These women fall into the group
who have a 42% mortality in ten years hence.
Page 258 It is our problem, then, to diagnose these cases much earlier, before they
reveal such permanent kidney and cardiovascular damage, and only in this
way can we hope to prolong a mother's life by not allowing her to become
, pregnant, or if she does, to terminate this pregnancy as soon as the diagnosis
is made.
How are we to differentiate, then, these early cases of chronic nephritis,
and by this term, I again repeat, also those cases of cardiovascular disease,
from the other types of toxaemia?
More and more are we beginning to realize that the blood pressure is
probably the most miportant sign we have in enabling us to differentiate the
toxaemias which are relatively harmless to the mother and those which are
causing her irreparable damage the longer she is allowed to carry on her
First, let us take the patient who comes to us within the first three months
of pregnancy. If during this time her blood pressure is constantly around
150 or more systolic and 90 or more diastolic, the chances "are very great
that this is the type of toxaemia in which cardio-vascular or renal system
will become permanently damaged. The urine may be perfectly free from
albumen, all kidney function tests may be normal, and the blood chemistry
not altered, but as we follow this patient along in her pregnancy we will
almost invariably find the blood pressure gradually becoming more elevated.
The odds are very much in favor of this patient not being classed as a preeclamptic or becoming an eclamptic, because pre-eclampsia and eclampsia is
a true form of toxaemia which makes its appearance in the last trimester of
pregnancy. We may deliver her of a living child and the mother then be free
of all toxic signs and symptoms. But it is after delivery that with the blood
pressure readings taken every two months for at least a year we can really
evaluate what damage has been done. If the blood pressure remains elevated
—even so much as 150/95—six months or more after delivery, we know that
she should not be allowed to become a mother again. For if she does, each
following pregnancy will only increase the damage already done, and she
will then fall into the group of true chronic nephritis whose mortality rate
is so appallingly high. Her case is now relatively easy to classify—the hypertension is excessive, the kidney function tests are lowered, there may be
retention of nitrogenous products in the blood, and so on. She is then beyond
our help.
Let us next take the case whom we see in the second trimester of the
gestation period. In some clinics it is an axiom that patients with a hypertension, even a slight one of 150/95 before the seventh month, that she must
be regarded as an eventual candidate for chronic nephritis or hypertensive
cardiovascular disease.
The fund in such cases help us a great deal. Some authorities say that
the arterioles in the retina are spastic in 70% of all toxaemias. As long as
these lesions are spastic one may temporize. However, if exudates form and
cotton-wool appearance develops, this gives us warning of a near approach
of permanent organic damage of the arteriolar system. If these lesions
increase in number from day to day pregnancy must be interrupted, for the
presence of lesions in the retinal arterioles is an indication of the involvement of systemic and renal arterioles. This is important for the future of
the mother, as hypertension will probably persist in the presence of a generalized arteriosclerosis.
Again, this patient who comes to us at her seventh month with a hypertension may show normal kidney function tests, no oedema, no albumin in
the urine, no visual disturbances and no disturbances of her blood chemistry,
and yet it is only the slight rise in blood pressure that puts us on the look-out
for further vascular or renal damage as pregnancy advances.
Now let us take the patient who either comes to us in the eighth month
of pregnancy or one where blood pressure has been normal up until this time.
Page 259 This is the period that the low reserve kidney type of toxaemia, the preeclamptic and eclamptic forms make their appearance. In the great majority
of these cases at this period of gestation it is impossible to differentiate
them from a beginning chronic nephritis or cardiovascular disease. Our first
aim at this stage is to carry the mother and child safely through to delivery.
But it is after delivery that we can estimate what form of toxaemia she had
and how much, if any, damage her renal and cardiovascular system have
suffered. And again I emphasize the importance of blood pressure readings
taken once every two months for at least a year. The fact that the blood
presure falls to normal two weeks post-partum is no indication whatsoever
that we are not dealing with a chronic nephritic, for it has been found that
a good percentage of eventual chronic nephritics had normal blood pressure
when they left hospital two weeks after delivery.
If we do find the blood pressure elevated six months and more after
delivery we can safely say that the pregnancy has caused permanent renal
or cardiovascular damage.
True, all the known tests for kidney function may be normal at this time,
but when we see her again in her next pregnancy the blood pressure will
become elevated earlier, the kidneys and cardiovascular system will become
more damaged, until finally, maybe not this pregnancy but certainly the
next, she will reveal herself as a full-blown chronic nephritic or hypertensive
cardiovascular disease.
And in conclusion, may I say that if we are to cut down the appalling
high mortality rates that follow several years after pregnancy, we must do
so by diagnosing the relatively mild cases of chronic nephritis or cardiovascular disease early, and when once diagnosed we can advise against further pregnancies, and that the taking of the patient's blood pressure every
two months after delivery is one of our most reliable signs of whether the
toxaemia has, or has not, left a permanent scar.
Dr. G. A. McCurdy
Victoria, B. C.
During the last five years there have been definite advances made in
haematology, especially with respect to the anaemias, and within the last ten
years the entire subject has been revolutionized. One.hears less and less of
that old-fashioned entity, "secondary anaemia." It is not so very long ago
that anaemias were grouped into two classes, viz: promary and secondary,
with possibly a third—haemolytic anaemia. Now the trend is to regard all
anaemias as due to one of the following causes: (1) Lack of one of the essential principles for normal erythropoiesis; (2) increased haemolysis; (3)
In the past the anaemia has received the greater amount of attention and
very little was definitely known concerning its etiology. We must remember
that anaemia is only a symptom, just as jaundice is a symptom. When a
patient is jaundiced the usual procedure is to try to locate the underlying
condition causing the jaundice, and when this is done treatment is commenced. Likewise with regard to anaemia the same procedure should be followed. Boycott has suggested the term erythron as the name for the erythropoietic organ, which includes the circulating erythrocytes and the cells from
which they are derived. To give you an idea of the size of this organ, I will
quote the following figures: The volume of the marrow cavity is estimated
at 1400 cc, the total volume of circulating blood at 4000 to 8000, and so disregarding the plasma (which is really the stroma of the erythron), we arrive
at a figure arout 2500 to 3000 ccs. as the volume of the erythron; looked at
in this fashion we have an organ which is as large as the liver and brain
taken together. So when we think of anaemia we should have in mind this
Page 260 large organ, some part of which is not functioning as it should. Let us also
keep in mind that the erythron is an organ which may underfio the same
changes as any other organ; for example, atrophy, hypertrophy, degeneration, etc.
During this presentation I wish to say a few words first upon the mechanism of normal erythropoiesis, then I shall discuss the anaemias which are
due to a lack of one of the essential principles, then a short account of the
important haemolytic anaemias, and finally I shall take up the laboratory
investigation necessary for the diagnosis of the different types of anaemia.
Normal Erythropoiesis
The most primitive cell in the erythron is the retico-endothelial cell which
lines the haemopoietic capillaries. This is the so-called stem cell. Under some
unknown stimulus this cell develops into a megaloblast which multiplies, and
under the influence of the erythrocyte maturing factor (also called the pernicious anaemia factor, and the haemopoietic factor) develops into the normoblast. This cell in turn multiplies and under the influence of the following
principles, Fe, Cu, vit. C and thyroxin, develops into the mature erythrocyte.
All these changes take place in the haemopoietic capillaries which are joined
to the peripheral capillaries. At first there is no communication between the
two sets of capillaries, for the immature cells are very sticky and are embedded in a reticular network. When the cells mature the reticulum dis-
appars, the cells lose their adhesive properties, plasma filters through and
the cells are washed into the circulation.
The Haemopoietic Principles
Now let us discuss as far as we are able the different factors responsible
for enabling the primitive reticulo-endothelial cell to differentiate into mature
erythrocytes. I have already stated that the principle necessary causing the
reticulo-endothelial cell to differentiate into the megaloblast is still unknown.
The next factor which goes under so many names is the one responsible
for the development of the megaloblast into the normoblast. I will use the
term introduced by Haden, viz: the erythrocyte maturing factor (EMF), as
this term is the only one which appears adequate and free from ambiguity.
Castle and others have shown that the EMF is synthesized by the interaction
of two substances, which have been named the intrinsic and the extrinsic
Not a great deal is known about the extrinsic factor. It is found in lean
beef and foods rich in vitamin B2. The vital fraction does not appear to be
due to this vitamin but to one of its break-down products. It is interesting
to note that marmite is very rich in this substance.
The intrinsic factor likewise has not been isolated in the pure state, and
actual facts concerning it are scarce. To summarize the present knowledge
we find that: (1) It is normally secreted with the gastric juice; (2) it is
thermolabile and is destroyed at 70° C.; (3) it is destroyed by peptic activity;
(4) according to Klien and Wilkinson, this substance is in the nature of an
enzyme. Before passing on to the remaining factors, I would like to mention
that Greenspon of Montreal has put forward experimental proof, which to
him is decisive evidence, that the intrinsic factor as secreted by the stomach
has the same biological properties as the EMF which is supposed to result
from the interaction of extrinsic and intrinsic factors. However, five independent groups of workers have failed to substantiate his claims.
The other essential principles are all well known and all I will do is to
mention them: vitamin C, Fe, Cu and thyroxin. These factors are the ones
responsible for the development of the mature erythrocytes from normoblasts.
Finally, according to work carried out by Whipple, there is apparently a
factor which is stored in the liver, other than the EMF of iron, which plays
a role in the etiology of certain hypochromic anaemias. Clinical results, however, have been very disappointing.
Now that we have in mind the different principles for normal erythropoiesis, I should like to try to interpret the mechanism of the various anaemias.
Page 261 For this purpose I will use Vaughan's classification, which divides the anaemias into three groups: (1) The dyshaemopoietic anaemias, which are due to
failure or abnormality in blood production; (2) the haemolytic anaemias;
(3) the post-haemorrhagic anaemias.
The Dyshaemopoietic Anaemias
The first anaemia of this type that I will take up is pernicious anaemia or
Addison's anaemia. The pioneer work of Castle, Minot, Whipple and others
has put this anaemia on a rational basis. The anaemia is now known to be due
to a depletion of the intrinsic factor and a consequent diminution of the EMF.
It was first thought that there was a complete absence of the intrinsic factor,
but lately it has been shown hat even in severe relapses the intrinsic factor
can be shown in the gastric juice, though it is greatly diminished in amount.
This can be shown by drawing off the gastric juice of a patient with a severe
pernicious anaemia, concentrating this juice, allowing it to interact' with
minced feed, then feeding another patient with this material. An immediate
reticulocyte response signifies the presence of the EMF. Thus, because of
the absence of the EMF (which in turn is due to the absence of the intrinsic
factor), the megaloblasts of the erythron are unable to develop into normoblasts, and so into normal erythrocytes. Instead of this the bone marrow
undergoes hyperplasia which stops at the melagoblast stage, and though the
bone marrow is the seat of great activity, very few erythrocytes are formed.
The majority of those formed are larger than normal and abnormal in shape.
When the proper treatment is commenced and the EMF is supplied, the
megaloblasts rapidly develop into normoblasts and from these cells normal
erythrocytes are formed.
Up to this point everything appears very straightforward, but there are a
few features of pernicious anaemia which are difficult to explain, namely,
why are cord changes so common in pernicious anaemia and so rare in other
macrocytic anaemias? Also why do patients develop glossitis and stomatitis?
And then on the other hand, why is it possible for a person to remain in good
health for years after a total or sub-total gastrectomy, and finally, in such
cases, if an anaemia develops it is nearly always a hypochromic anaemia? I
mention these points to emphasize that a deficiency of the EMF does not
necessarily explain the entire pernicious anaemia syndrome.
Other Macrocytic Anaemias
There have been a great variety of types described during the last few\
years and they are the result of a variety of causes. First, there is the anaemia
due to the deficiency of the extrinsic factor. This type is seen in tropical
nutritional anaemia, and the anaemia is relieved by feeding marmite and
yeasts rich in vitamin B. The effect of the absence of the extrinsic factor on
the erythron is the same as the absence of the intrinsic, for it results in the
EMF not being elaborated.
Another type is that due to faulty absorption or to the destruction of the
EMF in the intestinal tract before it has a chance of being absorbed. Both
the intrinsic and extrinsic principles have been shown to be present in these
cases, but as I have just said, the EMF is not able to reach the bone marrow.
In these cases the anaemia is not the dominant symptom. Usually there is
diarrhoea present with bulky foul-smelling stools, and decalcification of the
bones. Conditions of this type associated with a macrocytic anaemia are
chylous diarrhoea, cceliac disease, fatty diarrhoea or idiopathic steatorrhea,
and dibothriocephalus anaemia. All these anaemias respond well to liver treatment.
Another group of macrocytic anaemia is due to a faulty storage of the
EMF in the liver; the reason for the inadequate storage being some disease
of the liver which replaces the greater part of liver parenchyma. Such diseases are carcinoma of the liver, cirrhosis, amyloid, in fact any chronic disease of the liver which results in diminishing the functional liver tissue. If
liver extract is supplied to these cases a prompt reticulocyte response is the
Page 262 A fourth type of macrocytic anaemia is that described by Wilkinson and
Israels last year. In this anaemia the intrinsic factor has been shown to be
present and, what is more of interest, the EMF has been demonstrated in the
liver in normal amounts. The rationale of this anaemia apparently is that for
some reason the bone marrow cannot utilize the EMF and for this reason the
anaemia has been called achrestic anaemia. No form of treatment has yet been
proven to be of avail, and the prognosis is practically hopeless. The discoverers of this anaemia point out that it is just possible that there may be
another essential factor still unknown, which is lacking in the so-called
achrestic anaemia.
A fifth type of maycrocytic anaemia is that associated with pregnancy. It
is not known whether the intrinsic factor is present or not. There is usually
free HC1 in the gastric juice. In this anaemia it is quite probable that the
foetal demands for the EMF are so great that the patient's own supply is
depleted. It is the rule for these cases to clear up spontaneously after delivery.
Treatment is of course by giving liver extract, and it has been found that
these cases require much larger doses than the ordinary case of pernicious
A sixth type is seen when that part of the stomach which secretes the
intrinsic factor is destroyed by disease, usually carcinoma, or when it is
removed by operation. The resulting anaemia, of course, is due to diminished
or lack of formation of the EMF. The anaemia is treated by administering
liver extract.
Before leaving the macrocytic anaemias I should like to mention a few
points which differentiate pernicious anaemia from the other macrocytic
anaemias: (1) In pernicious anaemia the megaloblasts have a more primitive
character; (2) high degree of hyperbilirubinaemia, increased bilirubin secretion, and haemosiderosis; (3) hypersegmentation of the polymorphs; (4) the
clinical features will very often serve to differentiate pernicious anaemia from
one of the other macrocytic anaemias.
The next type of anaemias I shall discuss are those due to a deficiency of
iron. There appear to be two main types of Fe deficiency anaemias. First
those due to an absolute deficiency of Fe in the diet, and secondly, those associated with diets containing a normal amount of Fe.
The first type is seen in young infants on a diet poor in Fe, and when the
normal supply of Fe in the liver is depleted, a macrocytic anaemia develops.
Another example of this type occurs during pregnancy, when the intake of
Fe is insufficient to meet both maternal and foetal demands. In both these
cases response to iron is prompt.
In the second type of Fe deficiency anaemia, the diet contains a normal
amount of Fe but the amount of iron available for the bone marrow is insufficient for normal erythropoiesis.
Before we go any further I should like to say a few words on the Fe
exchange in the body.
The total iron in the body amounts to 4 to 4.5 gms. Half of this is in the
circulating haemoglobin. The average diet contains from 10 to 20 mgm., of
which 7 to 9 mgm. are available for erythropoiesis or other body needs. The
iron in the faeces amounts to 5 to 20 mgm. daily, so in the normal diet there is
not much Fe absorbed. There is very little iron loss due to haemolysis of effete
red cells, for practically all of this iron is used over, but if a diet is poor in
iron a small negative balance will slowly produce a severe anaemia. Also
chronic loss of blood (menstruation in females and very often haemorrhoids
in males) rapidly results in loss of Fe, and thus causes iron deficiency
In those cases where the diet contains a normal amount of iron, the anaemia
must be treated by very large doses of iron; as much as 6 gms. a day of Fe
ammonium citrate is used in order to get a satisfactory response. Of course
only a very small percentage of this iron is retained. But in order to have even
a small amount of iron retained massive doses are usually required, until
Page 268 the body is more or less saturated with iron. The reason for the poor assimilation of iron is not well understood. The hypochlorhydria which often
accompanies these anaemias is often blamed, but most workers agree that
there must be some other factors. This feature is still being actively investigated. According to Broch, who has published one of the most recent papers
on this subject, large quantities of iron in the intestine must change conditions there very considerably. It alters the intestinal flora and interferes
with the absorption of other minerals. With this evidence he concludes that
it is conceivable that the presence of large quantities of iron in the intestine
by altering the chemical environment increases the absorption of some undetected haemopoietic factor.
The following is a useful classification of the iron deficiency anaemias:
Hypochromic anaemia of infants; hyperchromic anaemia of infants (Cooley's
anaemia) ; chlorosis; idiopathic hypochromic anaemia; hypochromic anaemia
of pregnancy (defective intake, poor digestion, increased demands) ; hypochromic anaemia associated with idiopathic steatorrhoea; erythroblastic
anaemia associated with idiopathic steatorrhoea; hypochromic anaemia associated with organic lesions of G. I. tract: (a) gastric carcinoma, (b) gastrointestinal operations, (c) intestinal obstruction.
The Haemolytio Anaemias
There still remains to be discussed that obscure and rather rare group of
anaemias which are termed the haemolytic anaemias, and which result from
an increased destruction of red blood cells.
The most important group are those associated with a congenital or
familial origin, viz, haemolytic jaundice, sickle cell anaemia, erythroblastic
anaemia of infants and icterus gravis neonatorum. In the first two conditions
a red cell is produced which is abnormal and when it enters the circulation
it undergoes haemolysis. The reason for the defect is not known. In icterus
gravis neonatorum there appears to be a physiological compensatory phenomenon driven to excess, for in normal intrauterine life the red cell count
is high because the foetal blood is poor in oxygen. This state changes at birth
and the newborn infant has more red cells than it needs, so in order to overcome this the superfluous cells are haemolysed. In icterus gravis neonatorum
this physiological haemolysis continues until normal serum is injected, otherwise the process is not stopped and the patient dies.
Characteristics of the Haemolytic Anaemias
Before discussing the remaining haemolytic anaemias, I should like to
mention briefly the characteristics of these anaemias. Witts divides them into
two groups:  (1) the chronic acquired haemolytic anaemias;  (2)  the acute\
haemolytic anaemias.
The anaemias may develop very rapidly and terminate just as rapidly, or
they may run a long protracted course. If the rate or blood destruction is
high, the patient will develop haemoglobinuria, jaundice, and a high reticulocyte count, and we may get normoblasts or megaloblasts in the peripheral
blood. The fragility test frequently is normal, though it may vary in individual cases. In the etiology of these anaemias we can distinguish three kinds
of factors: (1) a hereditary dystrophy of the erythron; (2) destruction of red
cells by bacterial or chemical toxins; (3) haemolysis of red blood cells from
marked changes in body fluids or due to overactivity of the reticulo-endothelial system. ~ Tx .
** Chronic Haemolytic Anaemia
The irs.1 type I shall take up are the chronic acquired haemolytic anaemias.
This form may occur at any age, most often in young adults. The patient
suddenly develops a haemolytic anaemia which continues over a long period
of time, usually accompanied by reticulocytosis severe anaemia, and with
periodic exacerbations of haemoglobinuria. It may terminate in death after a
few years or the patient may recover spontaneously. It is a very rare anaemia.
Acute Haemolytic Anaemia
In this disease the onset is abrupt and is heralded by fever, sore throat
and biliousness. Haemoglobinuria and jaundice may or may not occur. Severe
Page 264 anaemia sets in and is often accompanied by leucocytosis, with many immature forms. The liver, spleen and glands are enlarged. If blood transfusions
are not given, over 50%'of cases terminate fatally. Usually the response
after blood transfusion is dramatic. The haemolytic anaemias of pregnancy
are of this type.
Laboratory Investigation of Anaemia
In order to understand any anaemia it is necessary to know what is
happening in the erythron. The first thing to do is to determine the severity
of the anaemia. This is found by determining the percentage of haemoglobin
and enumerating the red cells. Next we should determine the rate of blood
formation. The degree of reticulocytosis gives us this information. Then we
should try to learn the rate of blood destruction. This is not as easy as it is
made out to be. Haden, as late as January of this year, advises the use of
the icterus index as an index of blood destruction, but all authorities do not
agree that this gives us a true picture, for they point out that normally bilirubin does not accumulate in the blood above 4 to 6 degrees, because it is
used in the manufacture of new erythrocytes; when it does accumulate, as in
pernicious anaemia, it is not due to increased blood destruction but to failure
of utilization. In the case of the haemolytic anaemias it is of greater value,
however we must be careful how we interpret a raised index.
When all I have just referred to is learned, the next step is to find out
the morphological group of the anaemia. There are ten possible groups, but
Wintrobe has shown that all anaemias fall into one of four groups. These
groups are: (1) macrocytic anaemia; (2) normocytic anaemia; (3) simple
microcytic anaemia; (4) microcytic hypochromic anaemia.
1. Macrocytic anwmia: In this type of anaemia the volume index and the
colour index are greater than 1.1. All anaemias due to lack of the EMF are
of this type.
2. Normocytic anwmia: In these, the volume index and colour index are
equal to 1, there being only a simple reduction in cell count. This type of
anaemia is seen in malaria, aplasia, and semi-aplasia of the bone marrow.
3. Simple microcytic: Here the volume and colour indices are less than
0.9 and the volume index is less than the colour index. In other words, the
cell count is relatively greater than the haemoglobin content. This type of
anaemia is often seen in chronic infection, malignancy uncomplicated by
haemorrhage, or bone marrow involvement. The only satisfactory treatment
here is the removal of the cause. This is the hardest group to treat.
4. Microcytic hypochromic anwmia: In this last type the volume index
and colour index are less than 0.9 but the colour index is less than the volume
index. In other words, the haemoglobin is decreased relatively more than the
red cell count. The anaemias falling in this group are caused by a deficiency
of one or more of the following: iron, copper, vitamin C or thyroxin.
Finally, any unusual features of the anaemia will require additional
methods of examination, such as: Gastric analysis; fragility test; bleeding
time; coagulation time; clot retraction time; study of the bone marrow.
Always Maintain the
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430 Birks Bldgf.        Phone Sey. 9000
Vancouver, Canada.
Page 265 T»JBB
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36-48 Caledonia Road, Toronto ANAHAEMIN   3. D. H
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Westminster 288


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