History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: August, 1943 Vancouver Medical Association Aug 31, 1943

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 rife Btiwfltei
of the
l  ^NdKuvaR-
Vol. XIX.
With Which ^ Incorporated
Transactions of the
Victoria Medical So$ietM
In This Issue:
NEWS^ND gjp^pB    ^y^^^^^M
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EVALUi^Kw|j^|LEKI^^ FUNG||o*i||
Make Y9uwM^s^kvatioM:NOW fICCOLAM
Trade Mark
Desiccant paste for exudatory and other dermatoses
Though p&mari lyi^tendeG^^^the adsorption of ?^pdfe;and aMevfi|jj|ojj^
accompanied b|§£rofuse exudaf^^^i^§|^^;Jhas been^^^^iisef^
pm^numero^ be absef^f
=^^ilC^|juseMas sh<a^r^hat Slcco\art^^;_^^^^^^$^^^oa^^$.: anc|;
Jer^onlg^forrhs of e^^tha^0^ki\r)g Besnier's pr^tgdiMp^c dermal
titis, both urticarial and'erythematous types,.the seborrho3ic-ldiathesi|,ll
N|*anfhemafa^pa^^^ dermatjt^. herpejP^>rrjr>^
Ifera^ejpis Jpg^.cases?^hic^|had proved '||sisf|n^|ta othe^f<>r:fl^^^i
:jfreatmenr^^^^^^side.^>le peiaf^H|§|||yas fo^pd ^a|^^^|^e d|g|
Toronto Canada
-Sicc/Can/438; jrl\i
Published Monthly under the Auspices of the Vancouver Medical Asociation
in the interests of the Medical Profession.
Offices: 203 Medical-Dental Building, Georgia Street, Vancouver, B.C.
Db. J. H. MacDermot
Dr. G. A. Davidson Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
Vol. XLX. AUGUST, 1943 No. 11
OFFICERS, 1943-1944
Dr. A. E. Trites Dr. H. H. Pitts Dr. J. R. Neilson
President Vice-President Past President
Dr. Gordon Burke Dr. J. A. McLean
Hon. Treasurer Hon. Secretary
Additional Members of Executive: Dr. J. R. Davies, Dr. Frank Turnbull
Dr. F. Bbodie Dr. J. A. Gillespie Dr. W. T. Lockhart
Auditors: Messrs. Plommeb, Whiting & Co.
Clinical Section
Dr. J. W. Miller Chairman Dr. Keith Burwell Secretary
Eye, Ear, Nose and Throat
Dr. C. E. Davies Chairman Dr. Letth Webster Secretary
Pediatric Section
Dr. J. H. B. Grant Chairman Dr. John Piters Secretary
Dr. A. Bagnall, Chairman; Dr. F. J. Buller, Dr. D. E. H. Cleveland,
Dr. J. R. Davies, Dr. J. R. Neilson, Dr. S. E. C. Turvey
Dr. J. H. MacDermot, Chairman; Dr. D. E. H. Cleveland,
Dr. G. A. Davidson
Summer School:
Dr. J. C. Thomas, Chairman; Dr. J. E. Harrison, Dr. G. A. Davidson,
Dr. R. A. Gilchrist, Dr. Howard Spohn, Dr. W. L. Graham
Dr. D. E. H. Cleveland, Chairman; Dr. E. A. Campbell, Dr. D. D. Freeze
V. O. N. Advisory Board:
Dr. L. W. MacNutt, Dr. G. E. Seldon, Dr. Isabel Day
Metropolitan Health Board Advisory Committee:
Dr. W. D. Patton, Dr. W. D. Kennedy, Dr. G. A. Lamont
Representative to B. C. Medical Association: Dr. J. R. Neilson
Sickness and Benevolent Fund: The President—The Trustees • IRON ALONE
SlRON w« B,
* IRON with B-Com pi ex
Obviously, the selection of a hematinic for the
treatment of secondary anemia depends to a large
extent upon the needs of the individual patient.
Some patients do well with iron alone; others
require Bi in additon to iron; still others should
have the benefit of iron with the B Complex.
Tablets Ferrous Sulphate Exsiccated
Squibb—where iron alone is indicated. Supplies
iron in ferrous form—shown in numerous clinical
studies to be more effective in smaller dosage than
other forms of iron and to have fewer undesirable
side-effects. Supplied in 3-grain enteric-coated
tablets in bottles of 100 and 1000. Three grains is
the U.S.P. dose for exsiccated ferrous sulphate
as compared to 5 grains of the hydrated salt.
Squibb has always used the exsiccated form.
Capsules Ferrous Sulphate with Bi
Squibb—Designed for prevention anti treatment
of secondary anemia, especially in patients with
anorexia or other manifestation of vitamin Bi
deficiency. Each capsule contains 3 grains of
ferrous sulphate exsiccated and 1 mg. of thiamine
hydrochloride (333 U.S.P. units of vitamin Bi).
Supplied in bottles of 100 and 1000 capsules.
Hebulon,* because of its content of iron,
liver extract and vitamin B Complex, provides
factors often simultaneously required by the
patient with secondary anemia. Each easy-to-
swallow gelatin capsule contains 2 grains
exsiccated ferrous sulphate (approx. 40 mg. iron);
50 U.S.P. units of vitamin Bi; and liver extract
(derived from 16 Gm. fresh liver) containing
appreciable amounts of certain B Complex factors
including riboflavin and filtrate factors. Supplied
in bottles of 100, 500 and 1000 capsules.
*"Hebulon" is a trade-mark of E. R. Squibb & Sons.
For literature address
36 Caledonia Rd., Toronto, Ont.
of Canada, Ltd.
MANUFACTURING chemists to thb
Total Population—Estimated      288,541
Japanese Population—Estimated  Evacuaetd
Chinese Population—Estimated i i 5,541
Hindu Population—Estimated  i :  301
Rate per 1,000
Number       Population
Total deaths  1    315 13.3
Japanese deaths           Population evacuated
Chinese deaths  I      20 43.9
Deaths—residents only    282 11.9
Male, 360: Female, 342    742 29.6
INFANTILE MORTALITY— June. 1943 June, 1942
Deaths under one year of age      16 24
Death rate—per 1,000 births - __     22.8 44.9
Stillbirths (not included above) •      15 18
May, 1943 June, 1943     July 1 to 15,1943
Cases Deaths Cases  Deaths Cases Dteaths
Scarlet Fever j    41 0 31 0 8 0
Diptheria _4    0 0 0 _ 0
Diptheria Carrier j      0 0               0 __. 0
Chicken Pox 200 0 211 0 14 0
Measles 691 0 167 0 17 0
RubeUa 1 S 14 0 11 0 3 0
Mumps 138 0 64 0 10 0
Whooping Cough 64 0 36 2 5 2
Typhoid Fever 0 0 0   0
Undulant Fever \      0 0               0   0
Poliomyelitis      0 0               0 —. 0
Tuberculosis j 36 0 65 13 15
Erysipelas      4 0 5 _ 1 0
Meningococcus Meningitis      10 3   1
West North       Vane.   Hospitals &
Burnaby    Vane.   Richmond   Vane.      Clinic   Private Drs.   Totals
Syphilis, Gonorrhoea—Figures not yet available.
Another Product of the Bioglan Laboratories, Hertford, England
Phone MA. 4027
Stanley N. Bayne, Representative
Descriptive Literature on Request
Vancouver, B. C.
Page 294 Control diet tests show KELLOGG'S
ALL-BRAN reliable in producing
desirable laxative action
To test whether theoretically equalized
amounts of crude fibre from different sources
would produce equal results, a group of medical students in a leading university were put on
a control diet from which crude fibre had been
removed. The "equalized" amounts, measured according to crude fibre tables in nutrition textbooks, were then added, and laxative
effects compared.
Fully expected were slight variations from
individual to individual, since no two people
are exactly alike. But wide variations appeared
also in the relative digestibility of crude fibre
from the various natural sources studied.
The fibre sources found to be most consistent in their action were cabbage and
KELLOGG'S ALL-BRAN. These showed pronounced "bulk"-forming properties and satisfactory laxadve action. Fruits and other vege-.
tables gave variable and less pronounced effects.
To be noted, however, is the fact that even
cabbage, because of different methods of preparation in the home, would vary in its effectiveness. But KELLOGG'S ALL-BRAN, a uniformly prepared cereal, has a ■;. practically
constant crude fibre content and is therefore
reliable in its desirable laxative effect.
Reprints of published research on laxation are
available to physicians and others interested.
Just write to:
effective treatment suggests the use of
agents to correct mineral deficiency,
increase cellular activity, and secure
adequate elimination of toxic waste.
orally given, supplies calcium, sulphur,
iodine, and lysidln bitartrate — an
effective solvent. Amelioration of
symptoms and general functional improvement  may  be  expected.
Since the best evidence is clinical
evidence, write for literature and
Canadian Distributors
350  Le Moyne   Street,   Montreal
Colonic and
Physiotherapy Centre
Up-to-date Scientific Treatments
Medical and Swedish Massage
Physical Culture Exercises
Post Graduate Mayo Bros.
1119 Vancouver Block
MArine 3723      Vancouver, B.C. LIVER EXTRACT
The value of liver or liver extract for the specific treatment of pernicious
anaemia has been clearly proven. The use of fresh liver or liver broth is
undoubtedly useful but for those who cannot tolerate large amounts of fresh
liver, liver extract powder has obvious advantages. While oral treatment is
much less economical than the parenteral supply of liver extract (injectable),
its use is frequently advisable.
The Connaught Laboratories distribute LIVER EXTRACT for
Oral Use in powdered form in packages which contain ten
vials; each vial contains extract derived from approximately
one-half pound of liver.
LIVER EXTRACT INJECTABLE is supplied as a purified and
concentrated solution in 4-cc. rubber-stoppered vials, and in
12-cc. vials for hospital use.
Note: A change has been made in the packaging of these products.
Formerly supplied in packages with yellow or brown wrappers, they are now
distributed in blue and white packages. The extract contained in each
package is identical with that formerly supplied.
University of Toronto    Toronto, Canada
•*V> 0<*e * V>0*e*
VC^" —*«0»0<*
->e con*0
y ten It
.t.cM.^ The coming month will be a very important one for the medical profession in Vancouver particularly and British Columbia generally: for two reasons. The first is the
Annual Meeting of the British Columbia Medical Association, which will be held in the
Hotel Vancouver on Sept. 8th, 9th, and 10th. The programme is published here and in
a previous number of the Bulletin, and there will be no doubt in our readers' minds
that it will be a meeting of a greatest value, and not to be missed.
One of the most important features will be the Annual Meeting itself, on Sept. 8th.
We shall have with us Dr. J. Sclater Lewis, president of the Canadian Medical Association, and the ever-welcome Dr. T. C. Routley, our General Secretary. There will be
a discussion of Medical Economics in the form of a Round-Table—with specially fitted
speakers to lead the various phases of the discussion.
Another very important meeting is the Public Meetings to be held in the Banquet
Room of the Hotel, where Dr. Howard Spohn, president of the B.C.M.A., will be in
the chair. It is hoped that Lt.-Col. D. H. Williams will be there, but in any case there
will be a full presentation to the public of the question of Cancer and Venereal Disease.
Everyone should try and attend all the meetings he or she can. There are no fees,
and we are all members of the B. C. Medical Association.
The second matter, of great consequence to us all, is the Community Chest Campaign, which opens in September. This campaign is part of a nation-wide eflforj, made
annually, as we all know. In Vancouver, it is known as the Vancouver Welfare Federation. It is one of the great projects of the year. No cause is more worthy of our attention, and more, of our active support. We should support it by word and deed. We
should urge it on people, and contribute to it as much as we can. It is not any longer
merely a charitable organisation: nor do we discharge our duty to it when we contribute
a nominal sum, just to salve our consciences, and get rid of the worker who calls on us.
It is a great national effort, which contributes immeasurably to the good of the community, and is accepted by all authorities on social service as an indispensable part of
our social structure.
The Community Chest needs no justification or vindication. It is an actual necessity: it is a scientific, coherent, and admirably managed method of dealing with a whole
series of problems that arise from various social maladjustments. The fact that the
best business, professional and scientific men of the community endorse it, and eagerly
give their services, unpaid, to the work of the campaign, is a proof, if any were needed,
of the fact that it is accepted as a necessary part of our life as a community. And,
from a strictly selfish point of view, it is of immense service to us as medical men.
Merely read the list of agencies included: the Victorian Order, the Children's Aid, the
Family Welfare Bureau, the Crippled Children's Hospital—and many others: and we
realise that our work is aided and made far more efficient, by this organisation. From a
business point of view, the economy of collection and administration are a sound reason
for our support. Of every dollar contributed, ninety-four cents or over are actually
applied to the work of the Welfare Federation.
The Community Chest Campaign is not confined to Vancouver. It will be held in
every important centre in British Columbia, and we urge our members everywhere to
give their strongest support to their local effort.
Page 295 ■ NEWS    AND    NOTES
A son was born to Capt. Gordon McL. Wilson, R.C.A.M.C, and Mrs. Wilson at
Kamloops Hospital on July 19th.
Congratulations are extended to Dr. and Mrs. Hubert Dumont of Vancouver on the
birth of a daughter, July 20th.
# *       #       *
Dr. and Mrs. Howard Mallek of Vancouver are receiving congratulations on the
birth of a son, August 16th.
# *       |       *
Sympathy is extended to Dr. Gerald Burke of Vancouver in his bereavement in the
loss of his wife.
The whole profession in British Columbia will extend to Dr. Thomas McPherson its
sincere sympathy.    Mrs. McPherson died on Saturday, August 14th.
A A *** A
We regret to announce that the son of Dr. George H. Wilson of Burnaby, an officer
with the Canadian Forces, was listed among the fatal casualties in Sicily.
A number of doctors in Victoria, officers of the 13 th Reserve Field Ambulance
Corps, attended Army camp from July 11th to 25th. These included: Capt. A. B.
Nash, Officer Commanding; W. H. Moore, G. B. B. Buff am, P. A. C. Cousland, W. A.
Trenholm, L. W. Cromwell and V. L. Annett.
In tjie Bulletin of the British Columbia Board of Health, August, 1943, we{l wishes
were passed to Dr. R. J. Macdonald, formerly Director of the Prince Rupert and District Health Unit. Capt. Macdonald is now serving with the R.C.A.M.C. Dr. Roger
G. Knipe, who has recently completed a course at the University of Toronto and received
his diploma of Public Health, is quoted in the Bulletin as having taken over the "cuties"
of Director of this Unit. The mention of this amusing item, which was brought to
our attention by an out-of-town member, does not lessen our good wishes which go with
Doctor Knipe to his new field of endeavour.
Dr. B. T. H. Marteinsson has proceeded to Toronto and is taking a special course
in R.C.A.F. training.
Sfc *\ A •&.
"F *S* «S* fl?
Capt. N. H. Jones, R.C.A.M.C, formerly of Port Alberni, we understand, is now
stationed at Prince Rupert.
While Dr. Wilfrid L. Graham and family were vacationing at Mirror Lake in the
West Kootenay, the Nelson Doctors held a meeting which was attended by Doctor
Dr. George Young, who at one time practised at Salmo, visited his friends at Nelson
recently.    Doctor Young is now with the D. P. & N. H. at Calgary.
Doctor Shillington of the D. P. & N. H. at Calgary spent a holiday at Kaslo.
Dr. A. W. Bagnall of Vancouver was holidaying at Kaslo and on the Kootenay Lake
during several weeks.
Page 296 Dr. and Mrs. E. S. Hoare of Trail had a two weeks' vacation at Willow Creek near
Dr. Wilfrid Laishley of Nelson has just returned from a fishing trip on the What-
shan Lakes near the Kootenay end of the Monashee Pass road.
Flight-Lieut. A. S. Underbill, R.C.A.F., now stationed in Alberta, has been on furlough and visiting in Kelowna.
**• A A A
Dr. S. B. Walker, formerly of Manitoba, has entered practice in West Summerland.
Since Flight-Lieut. A. W. Vanderburgh, R.C.A.F., entered the Service, Dr. F. W.
Andrew has been very much overworked and will welcome the relief afforded by Doctor
Walker's arrival.
•e" •«• 3^ S^
Dr. L. Giovando of Nanaimo has a new boat—a 34-foot express cruiser called
•{. A A A
Dr. A. H. Meneely of Nanaimo is spending his vacation at Qualicum Beach.
*fr "P 5^ 9^
Capt. S. L. Williams, R.C.A.M.C., formerly of Nanaimo, we hear, is in charge of
the Venereal Disease programme in the Manitoba District.
Dr. W. F. Drysdale of Nanaimo has been ill in Nanaimo Hospital. We are glad to
say he is reported to be up and about again.
* *       *       *
Dr. C. C. Browne will spend his vacation with his family on his yacht the "Ann."
* *       *       *
Dr. D. J. Millar has returned from his annual trip of exploration in the rivers and
lakes of Lillooet.   We have no report on the size of the big one that got away.
Dr. R. V. McCarley is holidaying in Eastern Canada.
»t A A A
.    Both Dr. A. C. Nash and Dr. Claire M. Onhauser of West Vancouver have managed
a vacation.
* *       *       *
We are glad to report that Dr. A. T. Johnston of West Vancouver recovered from
his operation when he lost a troublesome appendix.   He is back in practice again.
Dr. L. A. Patterson, who has been serving as doctor in the logging area on Moresby
Island, is entering the R.C.A.M.C.
* *       *       *
Major J. Ross Davidson is at Prince George donig Surgery at the Prince George
Military Hospital.
*t A *t *t
*r *r nr ^r .
Dr. K. K. Pump of Williams Lake called at the office. He is extremely busy covering the needs of a wide area.
•tL. A A A
#6* *T *s" *F
Dr. D. M. King, who has been at Bralorne for some years, is entering the R.C.A.M.C.
Dr. John Brown, formerly of Shaughnessy Hospital and more recently at Sooke Harbour
on Vancouver Island, is now at Bralorne.
Dr. Allan Beech, after considerable period of service with the R.C.A.M.C., has
returned to civil life and has accepted an appointment as medical officer in the Industrial
Medical Service in the North Vancouver shipyards.
*Page 297 Dr. Earle Hall of Vancouver also spent a short vacation in the Kootenay country.
Dr. E. H. Cooke is also doing Industrial Medicine at the West Coast shipbuilding
plant. Other doctors involved in the shipbuilding programme of Wartime Merchant
Shipping Limited, of which Dr. W. G. Saunders is the Director, are: Doctors J. Scovil
Murray, formerly of Calgary, and W. Sager, formerly Health Officer in Burnaby.
Since Dr. R. H. Fraser has become a Medical Officer, R.C.A.M.C, Dr. Agnes Black
is Medical Officer of Health in Burnaby.
Major W. M. Carr, since leaving the Service, has been serving with Wartime Merchant Shipping in the Industrial Hygiene programme, and has now returned to Victoria
and will serve the shipyards there.
Dr. J. M. Burnett of Greenwood visited Vancouver recently. Greenwood is quite a
busy spot with the augmented population due to Japanese evacuees.
Dr. C. T. Hilton of Port Alberni called at the office when last in Vancouver. He
reports that the doctors are very busy in that area.
Dr. Murray Blair and family have been having a well-earned rest at Okanagan
Landing near Vernon.
Dr. Howard Spohn has been rusticating on a ranch near Cranbrook.
Dr. K. D. Panton has not yet reported on the fishing at Buccaneer Bay.
Dr. F. J. Buller has been at his summer cottage at Roberts Creek. ,
Dr. Anson Frost has returned refreshed after a few weeks spent at Hope.
Recent Accessions to Library—
Surgical Clinics of North America.    1. Symposium on Surgery of the Biliary Tract.
2. Symposium on Surgical Diagnosis.
Diseases of the Nose, Throat and Ear, 8th ed., 1943, Ballenger & Ballenger.
Collected Papers of the Mayo Clinic, v. 34, 1942.
Chemotherapy of Malaria, by James H. Williams.
(Donated by Lederle Laboratories, Inc.)
The following books and journals are missing from the Library, no record having
been made by the borrowers:
Obstetrics and Gynaecology, 6th ed., DeLee.
Vaginal Hysterectomy, Kennedy and Campbell.
American Journal of Obstetrics and Gynaecology, vol. 43, 1942.
Bulletin of the New York Academy of Medicine, April, 1943.
It is urgently requested that they be returned to the Library at once.
Page 298 IS,
gti rl
i*f gjflt J $ »it«i' 11
- ^«**JM«SSSSSSS!N«««SJW'™
British Columbia
111 DAL
Sept. 8,9,10
with Headquarters at
Hotel Vancouver
Dr. William Boyd, Professor of Pathology, University of Toronto, requires no introduction. Dr. Boyd will give two lectures, address the Public Meeting and be the Guest
Speaker at the Annual Dinner. He is Chief of the Department of Cancer Control of
the Canadian Medical Association.
His lecture subjects are:
1. Recent Advances in Cancer Research.
2. Tumours of the Neck.
Dr. R. F. Farquharson, Assistant Professor of Medicine, and Head of the Department
of Therapeutics, Faculty of Medicine, the University of Toronto. Doctor Farquharson
(or "Ray" as some of his Toronto contemps call him) was here as Summer School
Speaker in 193 8, and is well remembered and his return as Lecturer at the September
Meeting is welcome.
His subjects will be:
1. Pituitary Syndrome.
2. Physical Manifestation of Emotional Disorders.
3. Anaemia.
Dr. D. Sclater Lewis of Montreal is President of the Canadian Medical Association
and Professor of Therapeutics, Medical Faculty, McGill University. Doctor Lewis will
be accompanied by Dr. T. C Routley, General Secretary of the Canadian Medical Association, and is travelling throughout Western Canada and will be in attendance at the
Annual Meetings of the four Western Divisions, all of which are held in September,
British Columbia Division at Vancouver, commencing September 8 th, 9th, 10th, and
then to Calgary, to Regina, and'finally at Winnipeg.
Dr. Lewis and Dr. Routley will address the Official Luncheon on the first day and
will attend the Annual Meeting on the first evening; will attend a meeting of the Board
Page 299 of Directors; will address the Public Meeting; will participate in the Round Table Conference on Medical Economics and Health Insurance on the second evening; will be
present at the Annual Dinner on the final day of the Meeting. On the lecture programme
Dr. Lewis' subject will be "Idiosyncrasies to Drugs."
Dr. G. Gavin Miller of Montreal is Associate Professor of Surgery, Faculty of Medicine, McGill University.
Doctor Miller is the Surgeon in the Canadian Medical Association party which comprises Doctors Sclater Lewis, R. F. Farquharson, William Boyd, Gavin Miller and Clarence Routley.
Doctor Miller's subjects for the Lecture Programme are:
1. Personal Experiences and Conclusions in Gastric Surgery.
2. Recent Experiences in Burn Therapy.
3. Useful Methods for the Diagnosis and Treatment of Ano-rectal Conditions.
Dr. T. C Routley, the General Secretary of the Canadian Medical Association, brings
much helpful information to the Divisions. The British Columbia Division is glad to
welcome him once again. The tremendous' amount of work which war and post-war
planning brings finds him ever willing.
Both Doctor Routley and Dr. Sclater Lewis will address the Official Luncheon on the
first day of the Annual Meeting.
Doctor Routley will attend the Annual Business Session on the first evening; will
participate in the programme of the Economic Session; will attend the Annual Dinner;
will attend the meeting of the Board of Directors and several other meetings.
Doctor Struthers of Montreal is Professor of Pediatrics, Medical Faculty, McGill
University. To find that Doctor Struthers was willing to travel to Vancouver was
welcome news. He has held a warm place in British Columbia since he came to Vancouver as speaker at the Summer School in 1941.
Doctor Struthers has had an excellent opportunity to study the results to be achieved
by the timely use of the Nurse Kenney method of treatment in cases of Acute Poliomyelitis.    He will lecture on that subject.
His second lecture will be of widespread interest.
His subjects for Lecture Programme are:
1. Poliomyelitis.
2. The Obese Child.
Doctor Struthers will give a clinic at St. Paul's Hospital on Friday, September 10th,
and will deal also with the subject: "A Classification of Diarrhceal Diseases."
Col. W. P. Warner, R.CA.M.C, by consent of Brigadier J. C Meakins, Ottawa, and
through arrangement with Col. Wallace Wilson, C.M.O., Pacific Command, will be in
Vancouver and participate in the Lecture Programme.
Col. Warner is Consultant in Medicine to the Canadian Army. In pre-war years he
was widely known as Associate Professor of Medicine at the University of Toronto.
Colonel Williams will be present at the Annual Meeting and will address the Public
Meeting to be held on the second evening. He will also present a paper on the lecture
programme on Friday morning.
"Don" not only deservedly holds a warm place in the hearts of the profession in
British Columbia but has found an opportunity to make a fine contribution in the service of Canada.
A Public Meeting will be held on Thursday, September 9, which will be addressed by:
Dr. Howard Spohn, President of the British Columbia Medical Association, who will
be the Chairman.
Dr. Sclater Lewis, President'of the Canadian Medical Association.
Dr. William Boyd, Head of the Department of Cancer Control of the Canadian
Medical Association.
Dr. W. H. Hatfield, Director of the Division of Tuberculosis Control.
Dr. C. E. Dolman, Head of the Department of Preventive Medicine and Bacteriology at the University of British Columbia and Director of Provincial Laboratories.
Lieut.-Col. D. H. Williams, R.C.A.M.C, who has been during several years the
Director of the Division of Venereal Disease Control in the Provincial Department of
Dr. G. F. Amyot, Provincial Health Officer, will close the meeting.
The Provincial Department of Health is deeply appreciative of this feature of the
Annual Meeting.
Dr. Ethlyn Trapp is in charge of arrangements.
At the Vancouver General Hospital on the first day, Wednesday, September 8th.
At St. Paul's Hospital,, on Friday, September 10th, Dr. Struthers will hold his Clinic.
On Thursday afternoon those who are not playing golf will find a warm welcome
at the Open-house Sessions at:
1. 2.30 o'clock—The Tuberculosis Division, Chest Hospital, 2647 Willow Street.
Dr. W. H. Hatfield, Director.
2. 3.30 o'clock—The British Columbia  Cancer Institute,   685—11th Avenue  West.
Dr. Ethlyn Trapp, Medical Superintendent.
These three splendid institutions would be glad to have large numbers attend this
feature of the Annual Meeting.
At the British Columbia Cancer Institute the British Columbia Medical Association
has arranged that tea will be served. Dr. Ethlyn Trapp and the staff at the Institute
have kindly agreed to provide this closing refreshment to the afternoon sessions.
Annual Business Meetings of the College x>f Physicians and Surgeons of British Columbia which comprises every registered doctor in this Province and of the British Columbia
Medical Association.   These meetings should be largely attended.
Thursday evening will be devoted to this important subject.
This meeting will take the form of a Round Table Conference. Questions are
invited and should be submitted by the members on the card which has been sent to you.
Such a conference should attract a large attendance.    Such a session is timely.
The Committee on the Study of Economics is busily engaged in arranging this Conference. Both Doctors Sclater Lewis and Routley will be available and join the group
on the platform.
Golf will be played on Thursday afternoon. The Association Trophy and other
prizes will be played for.    Dr. D. Fraser Murray is in charge of arrangements.
The Annual Dinner will be outstandingly good. It will be held on Friday, September
10th. Dr. William Boyd will be the guest speaker and this should not only guarantee
a good attendance but assure a very worthwhile address.
LADIES        It M
Mrs. Howard Spohn, the wife of the President, will be supported by a local com-
mitee which will provide a very inviting programme of entertainment for the ladies, who
it is hoped will join in this feature of the Annual Meeting.
Mrs. Wallace Wilson has agreed to be General Convener of the Ladies' Local Committees. At this date all arrangements have been made for two large functions in which
all the ladies are urged to participate.
On Thursday afternoon at 3 o'clock the ladies will be the guests of the British
Columbia Medical Association at a Reception and Tea at the Vancouver Art Gallery.
This should be largely attended.    It promises to be an affair which all ladies will enjoy.
The Ladies' Dinner will be as well done as usual, and they always have a good time.
The Social Suite provides most suitably for such a happy affair.
Mrs. Wilson has kindly arranged a tea at her home on the Wednesday for the wives
of Members of Council and of the Board of Directors of the British Columbia Medical
The only request the Ladies' Committees make is that the doctors' wives accompany
their husbands to Vancouver and attend these delightful parties.
Dr. Alan Y. McNair, Chairman of the Conunittee on Programme, and the members
of his committee have arranged an excellent programme and your attendance will help
to repay them for their efforts.
The 1943 Annual Meeting promises to be the best ever.
We should attend.
It would be well to post at your home and office the phone number of the Registration
Desk: MArine 4184.
"Dear Dr. Thomas:
"On instructions of the Council of the Pharmaceutical Association of the Province
of British Columbia, I have been asked to bring to the attention of your office a matter
that is causing considerable concern amongst the druggists of the Province and would
ask your co-operation in this matter.
"Recently benzedrine inhalers were added to the list of restricted drugs under Order
in Council 8443 and can no longer be purchased, as you know, other than through a
doctor's prescription due to the abuse of this drug. The Council's attention was drawn
to this fact that doctors were prescribing benzedrine inhalers or similar products in
indiscriminate quantities and to persons who were using them not for their legitimate
"It was felt that in bringing this to your attention you may be able to advise the
doctors of this Province in this regard and to ask their co-operation that this type of
drug be not prescribed indiscriminately but only as is required by the patient. You
undoubtedly know that this drug is being used by persons who can no longer obtain
norcotics and phenobarbiturates, and is being used by such persons as a substitute.
"In bringing this matter to your attention I feel sure that the medical profession of
the Province of British Columbia is only too willing to co-operate and that possibly
they do not fully realize to what extent the abuse of this particular drug has been put.
"Thanking you in this matter."
The Committee on Nutrition of the British Columbia Medical Association recommended to the Ration Officer of Wartime Prices and Trade Board that conditions in
which extra meat rations may be required would include the following:—
1. Diabetes Mellitus
2. Malnutrition—
Nutritional Anaemia
Nutritional Oedema
3. Pregnancy and Lactation.
4. Cceliac Disease—
(Non-tropical sprue)
Tropical sprue
5. Certain Food Allergies.
The following extracts from letters received from the Wartime Prices and Trade
Board contain certain information regarding meat rations and procedures to be followed
in prescribing extra rations of other commodities:—
"At the present time, diabetic and cceliac diseases are the only ones for which
extra meat is granted on medical grounds."
Authorizations should contain the following information and be addressed .to the
Wartime Prices and Trade Board in the district in which the doctor resided.  Branches
are located in Vancouver, Victoria, Prince Rupert and Kelowna:—
"1.   Name and address of patient.
2. Disease from which the patient is suffering.
3. Quantity of extra rationed commodities the patient requires. (The doctor can bear in mind that each patient has a Ration Book, and consequently can procure from this Ration Book one half pound of butter per
week; one ounce of tea per week; one half pound of sugar per week; and
two coupons of meat per week.)
4. Length of time for which the patient will require such extra rationed
Extract from letter from Dr. Routley.
"I checked on the situation this morning and I find that there are three classifications set up for car repairs:
(1) The Armed Services;
(2) Essential services such as Doctors;
(3) All others.
"It would appear, therefore, that a Doctor should not have to wait for repairs unless
the time of the garage is completely occupied on military cars."
The Bulletin gladly publishes a communication received from Dr. D. E. H. Cleveland, Acting Director Venereal Disease Control of the Provincial Department of Health.
The article, which Dr. Cleveland has abstracted, is indeed well worth our careful reading and consideration.
Editor, Bulletin of the Vancouver Medical Association.
Dear Sir:
In the Journal of Social Hygiene (Vol. 29, April, 1943, page 225) an article appeared by a Mr. Alan Johnstone, General Counsel, Federal Works Agency, Washington,
D.C., entitled "The Law and Social Hygiene." This was an address given at the Southeastern Conference on Social Hygiene Day, Atlanta, Georgia, February 3, 1943.
Page 303 I considered this article, which was quite brief, very well done, and it presented most
forcibly and picturesquely many viewpoints which the Provincial Health Department
holds. I therefore excerpted from this article those which I considered were most valuable and applied most closely to our British Columbia viewpoint, and suggested to Dr.
G. F. Amyot, to whom I sent my excerpts, that if the permission of the Editors of the
Journal of Social Hygiene and the permission of the author could be obtained, it might
be published in the Bulletin.
Dr. Amyot thought this was an excellent idea and I have now obtained the desired
permission from the American Social Hygiene Association, Inc., asking that proper credit
be given to the Journal of Social Hygiene, and I have also obtained the permission from
the author.
D. E. H. Cleveland, M.D.,
Acting Director, Venereal Disease Control.
Alan Johnstone
General Counsel, Federal Works Agency, Washington, D.C.
As I came to your great city of Atlanta today to take part in this meeting I thought
back twenty-five years. Just that long ago I was sent here by the Government to
attack the same problem that we consider now. We were at war then as we are today.
Then, as now, the venereal diseases were the greatest cause of disability in the armed
This plague came to the army from civil life. The army cured its soldiers. It taught
them the truth about these scourges. It combatted false standards of conduct and
health. Men learned to respect their bodies and to think of their future wives and
children. I heard a great Commander of that day—Leonard Wood—say, "Do not think
of these men in-uniform as anything less than the best you have got, and they will rise
to the level of your opinion." Under the leadership of two great War Ministers, Baker
and Daniels, America organized the cleanest, fittest Army and Navy the world had ever
known. And after peace the services kept up their fight for fitness so that in 15139 the
venereal rate of the Army reached the all time low of 30 per thousand per year or 3
per hundred per annum. The military authorities made great strides. And so did the
civil population—but not so great. When the war clouds gathered again and men came
to the army from civil life the rate increased by more than 25 per cent to 42.5 per
thousand per year. Since then it has declined and is still declining as military and civil
action has quickened.
I speak „ of the role of the law in the eradication of these plagues. The law is the
expression of the public opinion and conscience of the people. For a hundred years and
until well after the turn of the present century we derived our opinion and schooled our
conscience on sex morality and hygiene from two great characters in modern history.
They were Napoleon Bonaparte and Queen Victoria.
Napoleon was a great commander and a great lawyer. He conquered Europe and
dictated the Code Napoleon—the finest re-statement of the Roman or Civil law. But
in sex he took counsel of his lust.^ And on the hygiene of sex he surrendered his great
mind to a complete fallacy. He said that there was a sex necessity in men which made
promiscuity inevitable and he formalized the double standard of sex morality. He
established a system of public toleration and regulation of prostitution with medical
inspection and certification of prostitutes. The first doctrine demoralized modern
France. The second poisoned its blood stream. When Abraham Flexner and Raymond
Fosdick published their scientific studies on "Prostitution and Police Systems in Europe,"
they showed what havoc the Napoleonic system had wrought on the police, the courts
and the public health. And ajh the second battle of the Marne, when France nearly fell
in the first world war, she had. more soldiers* in hospital from ..venereal infection than
from battle wounds.
3    •
Page 304 Victoria was a woman of great strength of character. She established a great commonwealth of nations in which the humanities played an important if not the dominant
role. She respected order and enforced it. So great was her respect for order and for
decency that when disorder appeared which she could not conveniently correct she
ignored it. When indecency occurred that baffled her administration she convinced herself that it did not exist. Influenced by these attitudes we established a public silence
on these great scourges and spoke their names only in whispers.
Napoleon's system was seductive. It was thought to be smart to believe in it. Victoria's attitude was smug and comfortable. Under it we cleansed ourselves by simply
ignoring the dirt.
We in the United- States embraced both systems. We passed laws to satisfy our
Victorian ideas. We failed to enforce them to satisfy our Napoleonic complex. And so
when Lord Bryce examined our institutions and wrote his critique on municipal government he exposed the rot at the core of our great cities. Organized vice was so entrenched that it was big business. Public officials who had the courage to expose it and
to suppress it had to run the gauntlet. They were blamed by good people for stirring
up scandal. They were attacked by the underworld in the political forum. Some of
them were actually indicted in the courts for doing their plain duty.
*       *       *       *
Let me be emphatic if not dogmatic.
The venereal diseases are first rate threats to our safety.
They can be controlled.
They are spread by prostitution and promiscuity.
Men and women who exploit the weakness of their fellows and profit from this filthy
business are common outlaws and ought to be stopped in their tracks.
Toleration and attempts at regulation have uniformly failed.
However pitiful the victims of this traffic, they should be apprehended, treated and
We quarantine for smallpox. How foolish to allow carriers of the big pox to roam
at large.
The human rights and public safety involved in the enforcement of these laws
demand the attention of the best minds in the legal profession and among our public
Our police and our courts need the support of an informed and active public opinion.
A soldier and a sailor are precious fighting units. They must not be disabled from
community neglect.
We are getting ahead with the war.   But we need all our strength to win it.
In the issue lies all that we have.
Our men are dying on land, on sea and in the air. But, God rest their souls, freedom
is living!
We shall need all our sagacity and force to secure the peace.
The well springs of the race must not be polluted.
Our liberties are. dear to us.   Our destiny in the world is great.
The President has said that this generation has a rendezvous with destiny-.-
We must not fail that rendezvous. ',
Page 3OS c
ollege o
f Ph
ysicians a
nd Su
President : Dr. F. M. Bryant, victoria
Vice-President Dr. H. H. Milburn, Vancouver
Treasurer ?L Dr. G. S. Purvis, New Westminster
Members of Council Dr. F. M. Bryant, Dr. Thomas McPherson, Victoria (District No. 1);
Dr.   G.  S.  Purvis, New Westminster   (District  No.   2);   Dr.  H.  H.
Milburn,   Col.   Wallace   Wilson,   Vancouver   (District   No.   3);   Dr.
Osborne Morris, Vernon  (District No. 4); Dr. F. M. Auld, Nelson,
(District No. 5).
Registrar Dr. A. J. MacLachlan, Vancouver
Executive Secretary i Dr. M. W. Thomas, Vancouver
The employees of the following firms are now enrolled as members of the Medical
Services Association. The M-S-A has had a number of inquiries regarding the groups
covered and the list below is published for the information of doctors. It is interesting
to note the widespread and increasing growth of this service which means that it satisfactorily fills a need.
Allard Machine Works Ltd.
Burrard Rivet & Forgings Ltd.
Clarke Bros. Timber Co.
G. H. Cottrell Ltd.
Dominion Bridge Co. Ltd.—
Burnaby Bridge Plant
Dominion Rustproofing Co. Ltd.
Dominion Steelweld Co. Ltd.
Crossman Machinery Co. Ltd.
Electric Power Equipment Ltd.
Graham Electric Co. Ltd.
Hayes Manufacturing Co. Ltd.
M. B. King Lumber Co.  (North Shore)  Ltd.
Kootenay Engineering Co. Ltd.
Morrison Steel & Wire Co. Ltd.
Pacific Coast Terminals Ltd.
Rat Potage Wood & Coal Yards Ltd.
Arrow Transfer Co. Ltd.
Westminster Canners Ltd.
Heaps Engineering (1940) Ltd.
Ash Temple Co. Ltd.
Henry Birks & Sons (B.C.) Ltd.
Canadian General Electric Co. Ltd.
Fleck Bros. Ltd.
Associated Dairies Ltd.
Fraser Valley Milk Producers' Assn.
Lawrence Manufacturing Co. Ltd.
Langley Manufacturing Co. Ltd.
Letson & Burpee Ltd.
Mohawk Handle Co. Ltd.
Mohawk Lumber Co. Ltd.
Pacific Pine Co. Ltd.
Pacific Veneer Co. Ltd.
Patterson Boiler Works Ltd.
Prefabricated Buildings Ltd.
Shell Oil Co. of B. C. Ltd.
Stewart Sheet Metal Works Ltd.
Vancouver Breweries Ltd.
Wartime Metals  Corporation—Emerald
Tungsten Project
Westminster Hog Fuels Ltd.
Tyee Machinery Co. Ltd.
Coates Ltd.
McKay & Flanagan Bros. Lumber Mill Ltd.
Wartime Metals Corporation—
Kootenay Florence Project.
Blane, Fuller ton & White Ltd.
Confederation Life Association
General Accident Assurance Co. of Canada
Great West Life Assurance Co.
Montreal Life Insurance Co.
Crehan, Meredith & Co.
Cowichan School Teachers' Assn.
Creston Valley United School District.
Canadian Association of Social Workers—
B. C Mainland Branch
Agriculture, Food & Drug Division Employees
Campbell & Smith Ltd.
Dominion Income Tax Employees
Income Tax Specialists Ltd.
News-Herald Ltd.
Page 306
Galbraith & Sulley Ltd.
International Business Machines Co. Ltd.
Fred C. Myers Ltd.
Powell River Co. Ltd.
Seaboard Lumber Sales Co. Ltd.
George Straith Ltd.
Victor X-ray Corporation of Canada Ltd.
H. A. Roberts Ltd.
Travelers Insurance Co.
Sun Life Assurance Co. of Canada
Retail Credit Co.
Yorkshire & Pacific Securities Ltd.
Marsh & McLennan Ltd.
MacKenzie and Son Ltd.
Metropolitan Health Conunittee
North Vancouver General Hospital.
Port Coquitlam School Board.
Robertson, Douglas & Symes.
Vancouver Board of Trade
Victoria City Hall Employees.
Roy Wrigley Printing & Publishing Co. Ltd.
Western Sales Book Co. Ltd.
Young Women's Christian Association. ancouver
Lieut. H. G. Weaver, R.C.A.M.C.
(Formerly Senior Resident in Medicine, The Vancouver General Hospital)
Mr. G. S., at the age of 27 years, was in good health in July, 1940. He was working
hard and keeping late hours. In August, 1940, while working one morning, he had a
twinge of pain in the lower left axillary region. He paid no attention to it, as he had
had such pain before. After lunch he experienced a peculiar sensation described as a
lump forming in his upper abdomen. He says he actually felt as if he might die. A
short time after this he suddenly had excruciating pain in both elbows; it was accompanied by a similar but not so severe pain in both knees. His memory of this attack is
not too clear, but he had pain in his chest as well. That afternoon he was admitted to
a small country hospital, still complaining of substernal pain and pain in most of his
joints. The temperature and pulse rate were normal, but they gradually and steadily rose
to a temperature of 103° and a pulse rate of 120 in five days. He had a troublesome,
mildly productive cough and was dyspnceic. No diagnosis was made so after five days
he was sent to a hospital in a nearby city. On admission his temperature was 101.6°
by rectum, he was markedly short of breath, and his heart was enlarged, a gallop rhythm
being present. No pericardial friction rub was heard. An eltctro-cardiograph was
taken in which the T wave of the first lead was inverted with a slightly high take-off,
the QRS complex in lead 3 was inverted, and the T wave in the fourth lead was inverted with a high take-off. This suggested the presence of an acute anterior myocardial
infarction of recent occurrence, with left axis deviation. A radiograph was taken which
showed fairly marked general enlargement of the cardiac shadow, especially in relation
to the left ventricle, with increased pulmonary markings. The next day, on the
seventh day of his illness, his temperature dropped to normal, and stayed- there except
for an occasional spike to 99°. The dyspnoea was not present after the seventh day of
illness. A white blood count on the sixth day was 22,500 and it remained elevated at
13,000 to 14,000 throughout his six to seven weeks in hospital. History revealed that he
had never had joint pains before. He had suffered from frequent colds for many years,
during which he would have a mild productive cough. He had measles and mumps
when a child. His father, aged sixty-sixx, had a "leaking heart valve." There was an
indefinite history of tuberculosis on the maternal side of the family.
After discharge from hospital the patient stayed in bed at home for another six
weeks, after which he got up and around by degrees. Since that time he has considered
himself a semi-invalid. He moved to Vancouver in July, 1941, and reported to the
Out Patients Department of the Vancouver General Hospital. Electro-cardiographs
were taken which confirmed the previous impression of anterior myocardial infarction,
but there was still a high take-off in lead four and a deeply inverted T wave, which is
an unusual finding one year after an attack.
In March, 1942, the electro-cardiograph showed left axis deviation with inversion of
the T wave in leads one and four, but the ST segment in lead four had become flattened
and this was interpreted as a healing infarction. A radiograph showed, marked diminution in the size of the cardiac shadow as compared with previous radio-graphs and the
pulmonary markings had returned nearly to normal.
In July, 1942, he was working as a hotel clerk but complained frequently of palpitations and some dyspnoea after exertion. During that month he had an attack of
diarrhoea which lasted about one and one-half weeks and he complained of some lower
back pain.
Page 307 On August 10, 1942, almost exactly two years after the first heart attack, he was
suddenly stricken with an acute pain in his left anterior chest. It was not similar to
the previous attack in 1940. The pain did not radiate and was much worse on the
slightest movement. He was admitted to hospital at which time his temperature was
101°, pulse 110 and regular. Examination revealed a heart clinically enlarged, a definite pericardial friction rub was heard over the precordium, which was enhanced
when the patient held his breath. The blood pressure was 120/74. The white blood
cell count was 21,500 and the sedimentation rate was 3 mm. in three-quarters of an
hour; the urine was normal specific gravity, plus 2 albumin, and a few white blood cells.
A portable radiograph showed very, marked general enlargement of the cardiac shadow
and suggested the possibility of pericardial effusion. The pulmonary markings were
not increased as in the previous examination in August, 1940. The pain diminished on
the second day, the friction rub disappeared after the third day and the pain was entirely
absent after five days. The temperature went as high as 102.2° on the fourth day, but
dropped to normal on the seventh day and stayed there. The white blooud cell count
came down to 8,500 in one week, at which time the sedimentation rate was 41 mm. in
three-quarters of an hour. A tuberculin test using 1/1000 old tuberculin was negative.
The sedimentation rate was down to 6* mm. in one and one-half months, and the patient
was allowed up after a little over two months. A radiograph two months after the
attack showed definite decrease in the size of the cardiac shadow and it was quite similar
to the one taken in August, 1940, and August, 1942. The electro-cardiograph was interpreted as being a healed anterior infarction. jtSi
Since discharge from hospital, the patient has been up and around at home. He
feels quite well and has gained weight. He has not yet gone back to work but can
walk eight blocks without being dyspnoeic. However, when the patient over-exerts
himself he feels quite fatigued the next day.
A radiograph taken in April, 1943, shows no essential changes from the previous
one. An electro-cardiograph taken in April, 1943, shows some change since 1942. Previously the T wave on the second lead has varied, being upright on several occasions
and inverted, on at least one occasion. T 1, 2 and 4 are now inverted, the left axis
deviation is still present and there appears to be some evidence of possible left ventricular
While this case is hot the youngest case of myocardial infarction on record, it is
important to keep in mind that such conditions can occur in the younger age group,
before arteriosclerosis usually appears. There has been some discussion as to the actual
etiology of this particular case. Two suggestions have been offered: (1) That it was
due to hardening of the coronary arteries. The patient has had albuminuria and this
might indicate some arteriosclerotic change but the radial arteries are soft. (2) That it
was due to inflammation of the same arteries. However, at this time it is difficult to
elaborate further on these two possible factors.
In summary, the patient, aged twenty-seven years, had an acute heart attack in
August, 1940, which "was diagnosed as an acute anterior myocardial infarction. The
fever was somewhat higher and more prolonged than is customary in such an attack.
He complained of substernal pain, pain in his elbows, and in addition had pain in othet
joints. Two years later, in August, 1942, he had an acute heart attack definitely diagnosed as acute pericarditis.   He appears to be recovering from this attack.
A discussion of physiological applications in the assessment
of kidney damage.
By Max M. Cantor, B.Sc, M.D., F.A.C.P.
Assistant Professor of Biochemistry, University of Alberta.
(Read to the Summer School Session of the Vancouver Medical Association, Vancouver,
June 23rd, 1943.)
Effective therapy depends upon early diagnosis. Tests which show impaired function of an organ before clinical symptoms appear are thus of great value. While mlany
tests for the evaluation of the function of many organs have been described, those of
great clinical importance concern the kidney, the liver and the endocrine glands. Tests
of function do not always differentiate between organic and functional disease but they
do provide a numerical expression of the amount of functioning tissue. No one function test can indicate that alterations have taken place in other functions of the same
organ to the same degree—one does expect, however, that good tests of the same function, should show reasonable agreement and their value is based on such confirmation.
No discussion of renal function tests is complete without a few preliminary notes
■on the modern theories of renal physiology which provide the bases for function tests.
The modern theory of renal function evolves from the work of Richards, Marshall, Smith, Shannon and others. It is the theory originally proposed by Heidenhain,
modified by Cushny and proven by these observers. The function of the kidney suggests that we are dealing with an extremely complex organ. In reality this is not so.
The kidney is composed of about one million units—nephrons—which consist of a capillary tuft or glomerulus attached to an unbranched tubule which may be divided
structurally into three distinct parts. These tubules drain into collecting ducts which
find exit into the renal pelvis.
Formation of urine begins in the glomerulus and passes into Bowman's capsule and
thence along the tubule into the pelvis of the kidney. When the tubule leaves Bowman's capsule it forms a series of convolutions (proximal convoluted tubule) and then
descends in a straight line to the pelvis of the kidney (proximal tubule). Here it reverses its direction (Loop of Henle) and returns as the distal tubule to the region of the
glomerulus where it forms another series of convolutions (distal convoluted tubule).
From this region is joins a collecting duct. Both convoluted tubules form a network
about the glomerulus which gave them origin. The organization of the nephrons in
pyramidal lobes has no physiological function. The cortex is composed of the glomeruli
and convoluted tubules and the medulla represents the proximal and distal tubules and
the loops of Henle. From the point of view of function, there is no difference between
the convoluted tubules and the partes rectae.
The tubular portion of the nephron is divisible histologically into three parts, the
proximal tubule, the thin segment of Henle's Loop and the distal tubule. A complete
discussion of the histological differences is beyond the scope of this paper—suffice it to
say. however, that each segment has specific functions, the total of the whole being the
basis of the modern conception of renal physiology.
In this theory,, as the blood courses through the glomerular capillaries, part of the
plasma water is filtered out into the capsular spaces of the glomeruli. Along with water,
which represents about 20% of that of the plasma, come glucose, salt, urea, uric acid,
creatinine and other crystalloids which are present in the plasma. The fluid, however,
contains no protein and no colloidal material. These filtered substances are present in
the capsular fluid in about the same concentration as they are in the plasma and the pH
of the fluid, like the plasma, is about pH 7.4. The blood pressure, 55 mm. Hg. in the
glomerular capillaries, is high enough to produce filtration against the osmotic pressure
(25 mm. hg.) of the blood and it is generally agreed that the capsular material is a
protein-free fluid produced by mechanical physical filtration from the blood by filtration
Page 309 pressure (30 mm. hg.).   The rate of glomeular filtration is about 6 L. per hour or 150
L. in 24 hours.
The capsular filtrate contains in it not only waste products such as urea and uric
acid but substances such as glucose, and bicarbonate which the body needs. Furthermore, the water in which these are dissolved and salt are excreted in larger amounts
than the body can afford to lose. In order to get rid of waste products yet conserve the
essential materials, the cells lining the tubules exert a selective action in reabsorption
depending upon the body's requirements.
The re-absorption of water, which is the most important constituent of the filtrate,
probably occurs along with the reabsorption of glucose and essential electrolytes and is
made possible by the reabsorption of these. Marked absorption of water occurs in the
thin segment and some further absorption is effected in the distal tubule. This obligatory reabsorption of water is enhanced by a facultative reabsorption under the stimulus
of the antidiuretic hormone. The antidiuretic hormone is responsible for about one-fifth
of the water reabsorbed while four-fifths of the glomerular filtrate are reabsobed isos-
inotically. The effect of the antidiuretic hormone is physiologically and anatomically
independent of the obligatory reabsorption mechanism, and when it is deficient, gives
rise to diabetes insipidus.
The reabsorption of chloride with its attendant sodium and other inorganic constituents occurs along the whole length of the distal tubule. Glucose is reabsorbed in
the proximal tubule, the concentration diminishing rapidly as it moves down the tubule,
and it is almost completely absorbed from the filtrate when it is only half way down.
The distal half of the proximal tubule can, however, still absorb glucose* but none is
absorbed from the distal tubule itself. Glucose is reabsorbed at a constant rate of about
200 mgm. per minute. Raising the concentration in the plasma and increasing as a
consequence the amount in the glomerular filtrate, exceeds the capacity of the reabsorp-
tive process and gives rise to glycosuria. This is the basis for the term renal threshold
for glucose.
Phosphate is usually concentrated and excreted in the urine. Under certain, conditions it may be required by the body, and in those circumstances it is reabsorbed in the
proximal tubule in much the same way as glucose.
Urea in mammals is excreted entirely by glomerular filtration. It is, however, reabsorbed to a considerable extent by the tubules.
Apart from the power of selective absorption, the tubules have a reserve function of
excretion. While this function is of no special importance and remains inactive in the
excretion of natural urinary substances in humans, it is used to handle certain foreign
substances which do not pass the glomerular filter. Thus phenolsulfonphthalein is
excreted by this mechanism and it forms the basis of some function tests.
The pH of the glomerular filtrate is the same as that of the plasma. Freshly excreted
urine has a pH of between 4.8 and 7.4 with an average of about 6. When the pH is
lower than 7.4 the kidneys must be excreting acid products which if retained would
lower the pH level of the blood. Even at the lowest pH of the urine strong acids are
not present. Olf the acid products excrete, acid phosphate H(BHP04) is the most
important. The relative quantity of acid phosphate and basic phosphate B(BHP04)
among others, determines the reaction of the urine. This adjustment, a process of acidification, takes place exclusively in the distal portion of the tubule, and in a segment
nearer its distal end measuring no more than one-fifth of its extent. This segment does
not show any outstanding histological features except a widening of the lumen but it
can alter the reaction of a buffer from 7.5 to 6.8 in one minute.
From what has been said, it will be seen that the function of the kidney is threefold:
(1)   The excretion of:
(a) Waste products of metabolism.
(b) Chemical and bacterial poisons which have been rendered innoxious by the
(c) Foreign substances.
Page 310 (2) The regulation of osmotic pressure of the blood by the excretion or reabsorption of electrolytes, especially chlorides.
(3) Regulation of the hydrogen ion concentration (the reaction of the blood).
These functions are the basis of more than sixty tests, but only a few of these have
been widely accepted. Of these, th Mosenthal test, Volhard and Fahr's concentration
and dilution tests, the. P.S.P dye test, Van Slyke's urea clearance test, changes in the
N.P.N, components of the blood and tests for pathological constituents of the urine.
These tests may be divided into two groups:
(1) Those which measure glomerular function and which include the urea clearance and the blood N.P.N. components, and
(2) Those which measure tubular absorption such as the concentration test or tubular excretion as does the P.S.P. dye test.
Before dealing with these tests it should be emphasized that the performance of
renal function tests in the certain absence of proteinuria is a complete waste of time.
A routine urinalysis in full detail should be performed in all patients before attempting
to assess kidney function.
A.     Evaluation of Glomerular Function
1.   Tests of non-protein nitrogen retention (N.P.N.).
These tests are dealt with first not because they are of primary importance but rather
since they are commonly performed early in the investigation of renal failure. Actually
they have only corroborative value with regard to renal function.
By non-protein nitrogen we mean nitrogen of the blood, tissues, urine or excreta
which is not thrown down by the usual protein precipitants. Specifically we refer to the
nitrogen in the protein-free filtrate of blood. This amounts to from 15 to 25 mg. %
in the post absorptive state and represents ^4% of all the nitrogen in the blood. The
N.P.N, is composed of a mixture of heterogeneous substances including urea, ammonia,
creatine and creatinine, amino acids, uric acid and several others. Expressed as nitrogen,
urea accounts for nearly 50% of the N.P.N., the remainder being divided among all
the others in amounts ranging from one to four per cent. The estimations most frequently called for are urea, creatinine and uric acid.
Creatinine.—The concentration of creatinine in health and in disease not involving
renal function is remarkably constant. Blood retention occurs with gross kidney damage. Most of the extra-renal conditions which alter urea and uric acid have very little
influence on creatinine. The chief value of creatinine determinations lies in the differentiation of urologic from medical-nephritic conditions. In nephritis there is a parallelism between the concentrations of creatinine and urea. In purely urologic conditions,
such as obstructive lesaons of the lower urinary tract, no such parallelism exists.
Uric Acid.—Uric acid is a substance which has a peculiar fascination for the lay
mind and patients often seek to impart information concerning it. There is something
about uric acid as there is about alcohol which seems to turn the mildest man into the
most heated partisan. Most authorities now regard uric acid and other purines as byproducts of metabolism which are harmless in the majority of cases. It has special historical significance in being the subject of the first blood analysis ever attempted (Gar-
rod, 1848). Uric acid in the urine is derived from two sources, exogenous from purine
bases in the food and endogenous possibly from the breakdown of dell nuclei. Only
part of the uric acid broken down is excreted by the urine, the remainder being destroyed
elsewhere in the body. Birds and reptiles excrete uric acid as such. Mammals, with the
exception of man and the chimpanzee, convert uric acid to allantoin for excretion. Man
occupies an intermediate position: like mammals he forms uric acid from purines, but
like birds, much of it must be excreted in the urines. In the process of evolution he
has lost the ability to oxidize all the uric acid. This may explain man's peculiar liability
to gout and urate calculi in the kidney.
Some physicians lay so much stress on the level of uric acid in the blood that it seems
pertinent to spend a few moments on discussion.
Page 311 Proteins and carbohydrates accelerate the excretion of uric acid while fats produce
retention, due possibly to ketosis.
The normal level of uric acid in the blood varies from 2-4 mg. %. It is increased
in starvation, exercise, in the last stages of pregnancy and delivery. The blood uric acid
content at birth is the same in the maternal blood. It rises during the first three or four
days of life, then falls gradually to reach the adult level at about the 8 th day. These
changes are probably associated with normoblast destruction. High values are also found
in leukaemias.
The estimation of uric acid is performed most frequently in gout or suspected gout.
Here values rarely exceed 10 mg. %. In advanced chronic interstitial nephritis, the
level may rise as high as 20 or 25 mg %. In the lesser grades of nitrogen retention,
values of the order of those found in gout are common. It should be recalled that
chronic nephritis may co-exist with gout or with other arthritic disease, especially in
elderly pateints. Pneumonia also produces a rise in blood uric acid and in susceptible
individuals may precipitate an attack of gout.
In nephritis with impaired renal function the uric acid in the blood is at a higher
than normal level but the rise shows no consistent relationship to the degree or progress
of renal impairment. Because of this failure in consistency, many investigators have
abandoned uric acid estimation as an aid in diagnosis of the nephritides. Thus in anuria
following bichloride poisoning, there is no increase in uric acid, while in arteriosclerosis
and cardiac decompensation without evidence of renal failure it is increased to an extent
entirely out of proportion to the retention of other non-proteinnitrogenous substances.
Urea.—Urea ccupies a unique place in the development of human thought. Its
synthesis by Wohler in 1828 was the first demonstration of the possibility of preparing
artificially a substance elaborated by the living organism. In the philosophy of the last
century it had an effect comparable to "Darwin's theory of the origin of the species
and Pasteur's demonstration of the parasitic origin of pestilence." It shattered the
entire vitalistic conception and laid the foundation for the extraordinary developments
in synthetic chemistry—developments which have proven so epoch-making for medicine.
Its importance in the present discussion is threefold:
1. It is the chief end-product of protein metabolism.
2. It is the main metabolite which the kidney must eliminate.
3. It is a natural diuretic—exerting a continual effect on urine flow.
Its high nitrogen content (46.6%), its neutral non-toxic character and ready dif-
fusibility make it peculiarly adapted for the excretion of nitrogen. In normal urine,
urea accounts for nearly 90% of the nitrogen. Lowering the protein intake of the diet
will decrease urea excretion without altering the level of the other nitrogen components.
This illustrates the importance of considering the diet before interpreting the results of
excretion tests. In addition to changes in available protein, urea excretion is modified
in such conditions as acute yellow atrophy, where the ability of the liver to form urea
is diminished, and in ketosis and acidosis where it is converted in part to ammonia for
the neutralization of acid.
The concentration of urea in the blood is not especially influenced by mixed meals,
but it is altered by great reduction in protein intake. Its blood level, in cases of renal
disease on low protein diet, may thus be misleading. In uraemia, it is not unusual to
find a high value for urea reduced to within normal limits by protein restriction. The
same is true in prostatic obstruction with anorexia. For this reason some advocate the
determination of blood urea one hour after administering a 15 -gram test dose by mouth
(under normal conditions of renal function this should double the blood urea).
One of the difficulties in interpreting the meaning of an increase in blood urea is the
exclusion of non-renal factors. Any disease which is complicated by anhydraemia will
show an elevation in urea in the blood. The same is true of low blood pressure, slowed
circulation and severe bleeding into the gastro-intestinal tract.
The estimation of urea in the blood is a measure of the efficiency of nitrogen excretion and nothing else. Normally the level varies from 8-15 mg. %. This represents
about 50% of the N.P.N. Where the N.P.N, is greatly elevated, most of the increase
Page 312 is due to urea, so that in very high values this may represent 80% of the total. Values
below 80 mg. % offer some difficulty in assessment, but there is no doubt about levels
in excess of 100 mg. %. The estimation is of value in watching the progress of a case
and as a guide to therapy. Taken either as part of the urea concentration test or together with a single estimation of urea in the urine, its value is greatly enhanced.
2.  Clearance Tests.
Under this heading it is my purpose to deal with urea clearance only since it yields
all the information usually necessary for the evaluation of glomerular filtration. It is
necessary, however, to say something about the concept of clearance. The term clearance was first used in connection with urea and was defined as "the volume of blood
which one minute's excretion of urine suffices to clear of urea." The volume is virtual
rather than real, because all the blood flowing through is partially cleared but it is
obtained by dividing the quantity of urea excreted per minute by the quantity contained
in each cubic centimeter of blood. If "U" is the concentration of urea in the urine,
"V" the volume of urine formed in one minute, and "B" the concentration of urea in
the blood, then the mathematical expression UV/B describes the capacity of the normal
kidney to excrete urea. It should be noted, too, that clearance by these terms also means
"the minimum volume of blood required to furnish the quantity of a substance excreted
in the urine in one minute's time."
Different substances are cleared at different rates and to different extents. This
depends upon the degree of tubular reabsorption of this material. 'Thus a substance
which is present in the glomerular filtrate but which is completely reabsorbed will have
a clearance of zero. If tubular reabsorption of a substance is decreased, the substance
will appear in the urine until if there is no reabsorption at all, the clearance will equal
the rate of filtration (glomerular clearance). If a substance is excreted by the tubules
as well as the glomeruli then the clearance will be greater than the rate of filtration—
the limit being the amount of a substance which is brought to the kidneys by the blood.
We do not know if the kidney can effect complete clearance.
Actually, the efficiency of the kidney in excreting most substances is not great and
the clearance is much less than the blood flow. A substance suitable for measuring
glomerular filtration should be one which passes through the glomerular filter easily and
it should not be absorbed, excreted or synthesized by the tubules. It should be physiologically inert, and it should be one which is capable of being easily and accurately determined. Inulin has been used extensively in such determinations, but for clinical purposes, the facility with which urea is estimated makes its use preferable, although it
does not quite meet all the criteria set out.
The excretion of urea in the normal adult is such that 75 cc. of blood are cleared
in one minute. The actual amount cleared depends upon the urine flow. Below a certain level which is critical and which is called the augmentation limit (about 1.5 cc. of
urine per minute), the urea excretion is related to the blood level in proportion of the
square root of the rate of urine flow and UV/B becomes (UV/B) sqjuare toot of
l/V or U square root of V/B. This is called the "standard clearance" as opposed to
the "maximum clearance" where the urine flow is abundant. The mean normal value
of the standard clearance is 54 cc. per minute. Expression of results is in terms of
% of normal maximum or normal standard clearance, the values 75 and 54 respectively
being taken as 100%.
It should be noted that the volume of blood cleared is the same irrespective of the
level of the blood urea and regardless of the rate of urea formation. A clearance of 75
does not indicate complete removal of urea from that amount of blood in one minute.
Actually this does not happen, but the theoretical conception is a useful measure of
renal efficiency—the larger the volume of blood which could in theory be cleared, the
more efficient the kidney. It is very much like removing eggs from baskets on an
endless chain—the same result can be expected if 100 eggs are removed from one basket
in a minute or 10 from each of 10 baskets in the same time.
Interpretation of Urea Clearance.—The urea clearance test is in reality a fractional
retention test.    Since it includes the determination of the ratio of the urea blood level
Page 313 -
1  1
to the urea excreted by the kidney per unit of time it actually measures what has been
called "the functional elasticity of the filtering mechanism" and gives a reliable picture
of glomerular reserve. This ratio varies directly with the volume of blood flow and
inversely as the infra glomerular pressure. Any alteration in the rate of flow such as
might occur in shock, haemorrhage, dehydration and cardiac failure, or any change in
intra glomerular pressure as might occur in pyelonephritis and ureteral or bladder neck
obstruction, will affect the clearance.
In partial destruction of the kidney parenchyma, the total filtration does not vary
over long periods of time. This is evident from studies of blood non-protein nitrogen
components which remain normal. This is so because the remaining glomeruli compensate by hypertrophy or overactivity. The urea clearance will, however, be diminished
because the same amount of blood cannot be cleared per unit of time since there is no
glomerular reserve.
The usual range of clearance in man is taken as between 70% and 130% of the
average normal. With decreasing clearance in nephritis the variation is net so great.
The lower limit of normal is generally taken at 70% although values as low as 30 to
40% of normal urea clearance may be consistent with fair health. There is always a
danger in using mathematical terms in interpreting biologic tests since these are nearly
always plus (or minus) 20%.   The following values are, however, widely accepted:
Over 70 per cent | normal
70-40 per cent mild deficit
40-20 per cent r moderate deficit
Below 20 per cent . j .-severe deficit
Below 5 per cent uraemic coma imminent or present
It is difficult to interpret accurately the urea clearance in nephritis in terms of
glomerular damage. The proportion of destruction to urea clearance is not direct. The
urea clearance falls quite slowly, about 20%, until there is about 50% glomerular destruction.    After this the rate is increased rapidly.
B.    Evaluation of Tubular Function
Although the tubules in humans are concerned predominantly with absorption of
water and essential substances in the glomerular filtrate they have the reserve function
of excreting foreign substances.   Tests of tubular function are, then, of two types.
1.   Evaluation of tubular absorption.
The logical test for this function -is-the ability of the tubules to concentrate the
glomerular filtrate by the absorption of water under conditions of stress (water deprivation) . The result as indicated by the specific gravity of the urine provides a test of this
In order to concentrate, the kidney performs thermodynamic work. It has* been
calculated that the urea, for example, which is present in 50 L. of blood (12 mg. %)
can be concentrated by the normal kidneys in one litre of urine (600 mgm. %). This
takes as much work as the compression of 6 litres of gas at atmospheric pressure into 1
litre at 6 atmospheres. Damage to the kidney interferes with this thermodynamic
function. Glomerular filtration does not entail such a load (30 mm. Hg.) and it is
for this reason that diniinished ability to concentrate is often the earliest evidence of
damage. For this reason, too, after recovery, persistent low specific gravity may be
evidence of residual damage long after the urea clearance and N.P.N, have returned to
normal. Thus failure to concentrate is evidence of kidney damage even in the face of
normal urea clearance.
Decreased power of concentration, however, in the absence of diminished urea clearance is not as serious as when both are decreased. There are cases in everyone's experience of patients with persistently low fixed specific gravities who have carried on for
years because glomerular function was able to compensate for the deficiency in concentration (polycystic kidney). Such individuals, however, are very susceptible to extrarenal influences which may affect their over-compensating glomerular function.
Normally at least one of the samples in the concentration test should have a specific
gravity of 1.030 (or at least over 1.025).   Values below this indicate failure of tubular
function, 1.010 being taken as a uraemic level.
Page 314 In interpreting concentration tests it should be recalled that the absorptive function
is influenced by endocrine, nervous and metabolic changes. The excretion of oedema
fluids may lower the specific gravity without indicating renal damage. Diabetes inspidus
and an anaemia may also produce a low fixed specific gravity. The presence of protein
in the urine will elevate the readings and corrections should be made to the extent of
0.003 for each gram of protein present in 100 cc. of urine.
2.   Evaluation of Tubular Excretion.
This is generally measured by the excretion rate of phenolsulfonphthalein (P.S.P.)
after intravenous or subcutaneout injection. Given intravenously and estimated in the
urine at 15-minute intervals, it is said to be as sensitive as the urea clearance. By the
subcutaneous route with hourly estimation in the-urine it is definitely less sensitive than
the urea clearance.
P.S.P. is excreted entirely by the tubules and measures their excretory ability as
applied to a substance foreign to the organism. While tubular excretion probably
parallels absorption it may not be so under stress. Estimations of the color are open to
error and the method is not applicable when hematuria is present. So, also, in advanced
nephritis the output of dye is so low that the test fails to indicate further change. The
chief value is in following the progress of a case. Normally about 40-50% of the dye
is eliminated in one hour and 60-80% in two hours. Values below 60 are considered
From what has been said it seems clear that the urea clearance and concentration
tests should be the criteria for evaluating kidney function, the tests of nitrogen retention serving as corroborative evidence.
In acute nephritis a rise towards normal in urea clearance nearly always occurs within
four months and is a good prognostic sign. Where no rise occurs, chronicity may be
assumed. The return of clearance to normal, however, is no assurance of escape from
chronicity so long as the concentration test shows a low specific gravity, and other
abnormalities such as hematuria, casts and so forth are present.
In other words, a normal renal function test is not a clear indication of absent renal
Diminished renal function shown by these tests should not be interpreted as evidence
of renal damage until extra-renal factors such as traumatic shock, gastro-intestinal
obstruction and acute infection are eliminated. Reflex anuria following surgery also
fits into this list of exceptions as do cases of obstructive uropathy (ureteral, prostatic
or urethral).
A special note of caution should be added. Damaged kidneys are very susceptible
to sudden changes in factors which control glomerular activity. In the presence of
renal damage, operative procedures and anaesthesia should be chosen with that point in
view. Vomiting dehydration following surgery and anaesthesia in a nephritic may
cause renal failure and premature uraemic death.
In conclusion I would emphasize that the kidneys possess a great reserve for compensation and recovery. It has been estimated that nearly two-thirds to three-quarters
of the kidneys must be functionless before there is evidence of renal failure by the best
function tests. However, while our tests may not be absolute, they have great diagnostic and prognostic value.    Used as criteria of therapy they are of equal importance.
Mild Moderate Severe Uraemic Coma
Test Deficit Deficit Deficit Imminent Normal
N.P.N.  mg.   %..-,  30-50 35-75 45-150 100-450 20-30
Urea N. mg.  %  15-30 20-50 30-110 60-350 10-15
Cretinine  mg.   %  1-2 2-3 3-8 6-35                 1-2
Uric Acid mg. %  2-4 3-6 5-15 10-25                  2-4
Urea  Clearance  %  40-70 20-40 10-20 0-5 70-130
P.S.P.  % in 2  hours  45-75 25-60 5-45 0-25 60-80
Sp. G. in Cone Tests 2  1.015-1.027 1.009-1.020 1.008-1.015 1.008-1.010    1.025-1.035
By Max M. Cantor, B.Sc, M.D., F.A.C.P.
Assistant Professor of Biochemistry, University of Alberta.
Paper read to the Summer School Session of the Vancouver Medical Association, Vancouver,
June 25th, 1943.
For more than twenty-five years attempts have been made to elaborate tests which
would measure the functional capacity of the liver. The earlier difficulties concerning
the nature of hepatic function have been dissipated by careful investigations on the
effects following experimental, partial and total hepatectomy. As a result, tests became
more accurate, but it is still necessary to warn that the status of one function provides
no indication of the degree of effectiveness of any other function, and that the function
tests singly or combined provide no evidence of abnormality until most of the organ is
destroyed. This is so because the reserve function of the liver is very great and its
recuperative power extensive.
The tests generally used measur only one function and indicate the degree of
derangement in that regard only. For purposes of classification these are listed on the
basis of what is known concerning liver function.
1. Bile pigment metabolism and execretion:
(Van den Bergh, bilirubin, icterus index and urobilinogen in serum.    Bilirubin
and urobilin in urine).   Bilirubin tolerance test.
2. Eunction with respect to metabolism of:
(a) Proteins and deamination:
(variations in plasma and excretion of amino acids proteins.)
(b) Carbohydrates:
(Laevulose and Galactose Tolerance Initial insulin hyper-glycaemia test.)
(c) Eat and cholesterol and Eat soluble vitamins:
Hemokonia test, cholesterol and cholesterol esters in plasma.
3. Metabolism and excretion of bile acids:
(Bile acids in duodenal contens and in urine.)
4. Excretory Function with respect to dyes:
(Rose bengal and bromsulfalein.)
5. Function with respect to Coagulation Factors:
(Coagulation time, prothrombin time.)
6. Function with respect to detoxification:
(Synthesis of hippuric acid.)
7. Hematopoietic function.
8. Miscellaneous tests:
(Takata-ara, Weltmann reaction, colloidal gold test, appearance of erythrocytes.)
From this classification it will be noted that the liver has at least seven distinct
functions and tests have been described for their measurement. From the nature of
these it is unlikely that any test of one function can provide sufficient information about
another function to be significant. By combining several of these tests we are provided
with a somewhat clearer picture and such a procedure does assist in diagnosis and in
1.   Bile Figment Metabolism and Excretion.
Haemoglobin fro msenile erythrocytes is converted in the resticulo-endothelial system
to haemobilirubin. The chemical nature of this pigment complex has not been determined but it is probably associated with the lipoid globulin fraction of the plasma. It
circulates in the blood and is responsible for the indirect Van den Bergh test. This
pigment is taken up by the liver cells and is excreted into the bile capillaries as chole-
bilirubin. The chemical change which is effected is such that it now gives a direct Van
den Bergh reaction. It is secreted into and concentrated by the gall bladder, whence it
passes into the intestine. .Here cholebilirubin is reduced by bacterial action to the
chromogen stercobilinogen.    Most of the stercobilinogen is excreted in the feces in the
Page 316 oxidized form stercobilin. This material gives feces their characteristic color. The
small amount which is not excreted is absorbed into the circulation. Much of this is
returned to the liver and re-oxidized to bilirubin. Small traces.remain in the blood and
are excreted in the urine as urobilinogen. This is converted to- urobilin on exposure to
air and accounts for some of the color of urine. Normally then, the urine cantains
traces of urobilin but no bilirubin. The feces contain large quntities of urobilin (stercobilin) but no bilirubin. The presence of bilirubin in the feces or urine or the presence
of blirubin in the feces or urine or the presence of large quantities of urobilin in the
urine and the absence of stercobilin in the feces signify a derangement in the bile pigment mtabolism.
Haemolytic jaundice is associated with the formation of excessive amounts of haemo-
bilirubin. To compensate for this the liver excretes larger amounts of bilirubin. Tim
increases the quantity of stercobilinogen formed and absorbed and results in increased
renal excretion of urobilinogen. The feces are darkly colored. The blood serum gives
an indirect Van den Bergh test.
The determination of serum bilirubin gives as useful information regarding liver
function as does the estimation of urea in renal function. Generally speaking the Van
den Bergh reaction by which the estimation is carried out differentiates between haemolytic and obstructive jaundice. The presence of increased serum bilirubin depends on
excess production and on the decreased excretory function of the liver cells. Actually
pure forms of one or the other types of jaundice must be very rare. There is never
gross obstruction to the bile passage without some evidence of injury to the hepatic
parenchyma, conversely there is never pure hepatogenous jaundice without injury to or
obstruction of the finer bile passages. It is more accurate to say that jaundice is preponderantly haemolytic hepatogenous or obstructive depending upon whether one is
dealing with a blood disorder, a parenchymatous lesion of the liver or an obstruction
in the extra hepatic bile duct system. The differentiation is useful, however, for purposes of clinical distinction.
A direct reacting bilirubin is conclusive proof of injury of the liver and rupture of
the bile capillaries. Its presence has a quantitative relation to the function of the liver,
since its appearance indicates the point at which the derangement is so great that the
liver cells cannot handle the pigment and must return it to the circulation. For this
reason high indirect values nearly always give way to direct-reacting bilirubin.
It should be recalled that all sera giving direct reactions contain varying amounts
of indirect-reacting bilirubin and better correlations with function are obtained by deter-
mining both rather than assuming that all the pigment is of the direct-reacting type.
Normal values for serum bilirubin vary from 0.1 to 0.25 mgm.%. The highest
values 30-50 mg. are found in severe hepatogenous jaundice and in neoplastic biliary
obstruction. Milder forms of parenchymatous damage and intermittent or partial
obstruction are associated with values between 10 and 30 mg. Lower grades, 2-10 mg.,
are usually associated with subsidence of acute intrahepatic forms of jaundice and with
the chronic forms of hepatitis which follow biliary obstruction, intrabiliary infection,
portal cirrhosis and infectious forms of cholecystitis without gross obstruction.
The level of serum bilirubin is not static from day to day and frequent determinations should be made and plotted on a curve. This procedure may be carried out using
the icterus index and provides data of diagnostic and prognostic significance. A rapidly
rising curve is the rule, in neoplastic biliary obstruction, especially if the gall bladder
has been removed or is not functioning. A functioning gall bladder converts this into
a slow gradual rise.
Where obstructive biliary cirrhosis complicates stricture or stone in the common
duct, a low plateau curve is the rule. Where the liver is. not involved extensively
(recent neoplastic obstruction) the plateau is a high one. Acute intrahepatic forms of
jaundice produce a rapid rise and a rapid fall. Chronic parenchymatous hepatitis gives
a low irregular curve, as does also long standing biliary obstruction. If rapid degeneration supervenes this will be marked by sustained rises.    Falling curves indicate restora-
.    Page 317 tion of bils passage potency and liver repair, the one exception being the very chronic
type of biliary obstruction.
The bilirubin tolerance test measures the excretory function of the liver for that
substance. Retention of more than 5 % of the injected dose (1 mg. per kg. body
weight) at the end of 4 hours is considered as evidence of hepatic injury. The test has
a high degree of sensitivity where the serum bilirubin level does not exceed 1 mg.%.
The test has some serious drawbacks from the technical point of view and on the basis
of cost.
Estimation of urobilinogen in the blood is complicated by technical difficulties.
Measurement of urinary excretion of urobilinogen in a roughly quantitative manner is
as valuable as accurate estimation, since the amount formed varies considerably from
day to day. Single examinations have no special diagnostic value. Significance of
urobilinogen excretion has already been discussed as has the excretion of bilirubin.
2.   Function with respect to the metabolism- of'.
(a) Proteins and the process of deamhtation:
Variations in plasma proteins occur with injury to the hepatic parenchyma. Proteins are manufactured in addition in sites other than the liver but there is a reserve of
protein building material, 50% of which is albumin, in the liver. In advanced chronic
hepatic lesions the serum proteins are moderately reduced, diminution occurring especially in the albumin fraction. The albumin-globulin ratio is nearly always disturbed.
The changes in this ratio take place rapidly and are of prognostic significance in that
they indicate failure of the function of the liver to produce protein. The reduction in
serum albumin is related to the production of oedema and ascites and contributes to that
complication along with portal venous stasis and chronic peritoneal irritation.
Tests depending upon the decreased formation of urea in hepatic injury with coincident increase in amino acids are of some value in the diagnosis of acute yellow
strophy. The procedure for the analysis of amino acids is quite involved and analysis
is not commonly performed except for experimental purposes. The excretion of urea
is modified by extra-hepatic considerations and is generally of little significance as a
measure of hepatic function. \
The estimation of amino acids excreted following the administration of gelatin has
the some drawbacks as those noted for amino acids and does not yield any practical
(b) Carbohydrates:
One of the most important functions of the liver is to maintain the level of blood
sugar at normal. For this reason it might be expected that this function would be the
last to be lost. This is the case and also the reason why most tests designed to measure
this function are clinically disappointing. Hypersensitiveness to insulin has been noted
and forms the basis of a little-used test (test of initial insulin hyperglycemia) which
measures the glycogen reserve.
Laevulose and galactose have been used extensively in the study of hepatic function.
The normal liver stores these as glycogen without producing hyperglycaemia or glycosuria.
Tests based on the use of these two sugars have been open to serious objections which
modified procedures tend to overcome.
The laevulose tolerance test depends upon the estimation of blood sugar at intervals
following a test dose. An increase of more than 30 mg.% indicates damage to the
hepatic parenchyma. When laevulose instead of blood sugar is estimated the test is
made more sensitive. It has no value in the diagnosis of hepatic disease—it simply
measures the extent of hepatic damage and is thus useful in prognosis. A serious drawback is that it takes no account of disturbances in absorption of the sugar from the
gastro-intestinal tract.
Galactose tolerance has had wider application. This test is based on the observation
that a normal person can assimilate 4 gm. of galactose, losing no more than 2.5 to 3.0
gm. in the urine within five hours of the time of administration.    Where hepatic injury
Page 318 is present, glycosuria above this level occurs and the amount of sugar lost is a measure
of the degree of injury. Originally designed to differentiate intrahepatic from obstructive jaundice, it is now used simply as a means of assessing parenchymatous damage since
portal and biliary cirrhosis have been found to give consistently negative results and
between 25 and 40% of obstructive jaundice give positive results. It may be said,
however, that in the acute development of jaundice a positive test provides strong
grounds for a lesion which is primarily hepatic. The test is of no value where no
jaundice is demonstrated.
It has the same drawbacks as those noted for laevulose tolerance and a recent refinement in technique by which the sugar is administered intravenously and estimated at
intervals in the blood shows promise. This modification is free from theoretical objections and evidence is presented that it distinguishes clearly between jaundice due to
gross obstruction of the biliary tract without liver cell damage and jaundice due to
liver cell damage. It does not detect minor grades of liver damage in the absence of
(c)  Fat and Cholesterol:
In parenchymatous liver disease the individual hepatic cells have an increased fat
content. The relationship of liver function to fat metabolism and transport depends on
a great many factors. The part played by the.liver is difficult to assess in the light of
present knowledge. The hemokonia test which measures the increase of fat globules in
the blood after a mixed meal is an indication of failure of fat absorption and offers very
little of clinical importance.
The estimation of cholesterol and cholesterol esters in the plasma has provided some
information of hepatic function. Cholesterol is excreted with the bile and concentrated
in the gall bladder. In biliary obstruction the concentration of cholesterol rises. Normally the liver cells esterify about two-thirds of the total cholesterol, i.e., there is a
cholesterol to cholesterol ester ratio of 1 : 2. In liver damage the process of esterifica-
tion is impaired and the ratio is reduced although the total cholesterol may be and
usually is increased. When obstructive jaundice is complicated by secondary hepatitis,
the ratio becomes altered in accordance with this thesis. It is clamied by proponents of
the method that the value for cholesterol esters varies with the degree of hepatic injury
and is a guide in prognosis. Independent critical observers are not so optimistic and
point to the possibility of extra hepatic influences on cholesterol metabolism about
which we know very little. Tests based on the rate of absorption of vitamin A are not
well developed.
3. Metbolism and excretion of bile acids.
The salts of cholic acid present in the bile are exclusively hepatic products. Formed
in the liver and excreted in the bile, they pass into the intestine. Small amounts are
excreted with the feces and traces find their way into the urine. The rest are rapidly
absorbed into the portal blood and re-excreted in the bile. In obstructive jaundice the
quantity excreted in the urine is increased but with continued obstruction they disappear
only to reappear again when the obstruction is relieved. The chief value of their estimation in the urine is in jaundice following arsenical therapy or the use of any other
drug which is toxic to the liver. Their appearance in the urine in increased amount
gives early warning of toxicity. The bile salts are technically difficult to estimate. Simplification of the method might provide a very useful means of evaluating liver function.
4. Excretory function with respect to dyes.
Of the numerous dyes used to test hepatic function only two, rose bengal and
bromsulfalein, have had general application. Of the opaque dyes used for gall bladder
visualization, tetraiodophenolphthalein is the commonest.
The requirement for estimation of the rose bengal test and the rigid routine which
must be followed in its performance make this test self limiting. The dye is photo
sensitive and the patient has to be protected from sunlight for several hours, after the
dye is administered.    Normally less than 50% of the dye should remain in the blood
Page 319 eight minutes after it is injected. Greater amounts are associated with varying degrees
of hepatic damage.
The bromsulfalein test- is simple and as satisfactory a procedure as has yet been
described. It measures the ability of the liver to excrete 5 mg. of dye per kg. of body
weight by the end of one hour. Retention of dye occurs in over 90% of the cases in
which there is evidence of parenchymal injury or moderate mechanical obstruction of
the bile ducts of a degree sufficient to produce jaundice. Even retention as low as
10% is considered significant of hepatic disorder. Individual estimations are not of as
great value as tests repeated at intervals to evaluate prognosis. The test has no value
in frank jaundice. When the serum bilirubin does not exceed 3 mg.% dye retention
gives a fairly good estimate of the degree of damage. When the serum bilirubin is normal, the degree of dye retention is most significant. Positive tests are genrally found in
chronic liver atrophy, cirrhosis, hemochromatosis, fatty degeneration and so forth. The
greater the degree of retention the more unfavorable is the prognosis.
Even moderate hepatic involvement as may occur in malignant metastases will produce some retention, as will also toxic or infectious hepatic lesions.
Any opaque dye such as tetraiodophenolphthalein is excreted into the bile but does
not show in the roentgenogram until it is concentrated in the gall bladder. Where the*
liver is damaged, the dye is not excreted (positive Graham-Cole test). This is also the
case in biliary obstruction and damage to the gall bladder mucosa. Jaundice regardless
of origin gives a positive test so that its value apart from gall bladder visualization is
5. Function with respect to coagulation factors (measurement of the tendency to bleed)
The patient with hepatic disease bleeds because vitamin K is not absorbed from the
intestine. This is due to the absence of bile acids. Or it is not stored in the liver
because of hepatic impairment. In both cases there is a prothrombin deficiency.
Administration of vitamin K in jaundice without parenchymatous liver damage is
followed by a rapid and prolonged elevation in the level of prothrombin, in cases where
there is extensive liver damage there is only a slight, unsustained rise since the formation
of prothrombin is interfered with. A falling prothrombin level in the jaundiced patient
with or without associated hemorrhagic diathesis is indicative of severe. secondary
hepatic damage.
6. Function with respect to detoxification.
Under normal conditions the liver removes from the circulation and renders inert a
large variety of noxious substances. The conversion of indole to indican, the conjugation of salicylic acid to form glycuronates, the acetylation of the sulfa drugs are
examples of this action. While many tests have been devised to assess this function only
one seems to have stood the test of time. This test measures the ability of the liver to
synthesize hippuric acid by combining 6 gm. of benzoic acid with glycine (amino acetic
acid). Under the conditions of the test and in the absence of renal damage a normal
individual excretes about 3 gm. hippuric acid, but no less than 2.5 gm., in the four hours
following the administration of 6 gm. benzoic acid by mouth. It is generally agreed
that where the blood urea is normal (or the urea clearance normal) the rate of hippuric
acid formation by the liver is an accurate measurement of hepatic injury. Values less
than 2 gm. are significant. In the surgical types of jaundice values less than 1.5 gm. are
judged as of grave prognosis.
The test is simple and reliable, and in the absence of renal damage, gastric retention,
dehydration and malnutrition, it provides an excellent means of evaluating prognosis and
estimating surgical risks.
7. Haematopoietic function.
It is well known that the liver stores and may be concerned with the formation of a
substance or substances effective in producing maturation of the erythrocyte. It is well
known that liver damage is frequently accompanied by a hypochromic macrocytic
anaemia and that there is an alteration in the fragility of the red cells.    These findings
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are corroborative evidence of liver damage but do not serve as a test of function. The
macrocytes which appear in the blood stream can be explained on the basis of the altered
plasma osmotic pressure associated with the decrease in serum albumin.
8.   Miscellaneous tests.
(a) The alkaline phosphatase test. The enzyme phosphatase splits organic phosphorus compounds, liberating inorganic phosphorus. It is distributed widely in the body
but is found in greatest concentration in the bone, kidney, intestinal mucosa and liver,
where it is intimately concerned with the metabolism of phosphorus compounds.
Whether or not it is formed in the liver is not known but it is excreted in the bile, so
that in disturbances of biliary excretion (extra hepatic obstruction or intrahepatic block)
it is increased in the plasma. In our hands the procedure has not justified the time it
takes to perform.    This has been the experience of other laboratories.
(b) The Takata-Ara Test: The cephalin-cholesterol Flocculation test. These tests are
designed to evaluate the functional relation between the liver and protein metabolism.
The effect on albumin globulin ratio has already been noted. In acute liver damage
there is some alteration in the nature of the globulin and the tes'ts depend on the flocculating reaction which these globulins produce in dilute serial solution of mercuric chloride or in cholesterol cephalin emulsions. A similar effect has been noted in a special
application of the colloidal gold test. It is claimed that the cephalin-cholesterol and
colloidal gold tests are valuable in acute hepatitis and differentiate fibrotic from exudative processes. Judgment in all these tests should be reserved until more knowledge of
the mechanisms involved is available.
Liver function tests are extensions of the physical examination and are not intended
to supplant it. Their purpose is to corroborate the diagnosis and assist in prognosis. A
satisfactory appraisal of liver function entails the testing of as many functions as possible consistent with the comfort of the patient and economy. Most of the dissatisfaction experienced with tests of liver function is due to the tendency to rely on one test.
Any particular liver function test gauges the degree of liver damage only when it is
performed repeatedly on the same patient: the results cannot be related to those of
another patient. It is important to recognize conditions when certain tests should not
be done. Dye tests are valueless in the presence of increasd bilirubin in the serum with
a direct Van den Bergh reaction. This is also true of the bilirubin excretion test. The
intravenous galactose test can be performed under all circumstances. The hippuric acid
test has no value in the presence of renal damage although it may be used together with
the urea clearance test and the result re-calculated.
Generally speaking, the tests adopted should have sound physiological bases and
should combine ease of performance with accuracy of estimation. They should be
planned in such a way that the combination of tests used may provide information of
diagnostic and prognostic significance.
(a) The Van den Bergh reaction and the estimation of serum bilirubin.
(b) Examination of the urine for bile pigments and urobilinogen.
(c) The color of the stools.
(d) The blood count and perhaps erythrocyte fragility.
(a) Serum bilirubin—repeated estimations.
(b) Examination of urine for bile pigments and urobilinogen and stools for urobilinogen.
(c) Intravenous galactose tolerance.
(a) Serum bilirubin repeated estimations, charted graphically.
(b) Examination of urine for bile pigments and stools for stercobilinogen.
(c) Duodenal drainage.
(1) Van den Bergh and serum bilirubin at frequent intervals.
(2) Examination of urine and stools.
(3) Intravenous galactose tolerance.
(4) Hippuric acid test and/or bromsulfalein test.
(5) Plasma proteins.
(6) Prothrombin level.
(1) Rapid rise in serum bilirubin.
(2) Decreased prothrombin during administration of vitamin K.
(3 )   Decreased hippuric acid excretion.
(4)   Decreased intravenous galactose tolerance.
(1) Rise in serum bilirubin.
(2) .Decrease in prothrombin level.
( 3 )   Decrease in plasma proteins.
(4) Increased excretion of amino acids  (decreased excretion of urea).
(5) Cholesterol-cholesterolester ratio less than 1:1.
(6) Decrease in galactose tolerance.
(1) Increased serum bilirubin.
(2) Bilirubin in urine by sensitive tests.
(3) Bromsulfalein reteniton.
(4) Albumin-globulin ratio altered or reversed.
(5) Galactose tolerance test  (intravenous).
Phone MArine 5411
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Page 323 T
flDount pleasant TUnbertaking Co. %tb.
KINGSWAY at 11th AVE. Telephone FAirmont 0058 VANCOUVER, B. C.
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W.   L.  BERTRAND 1930 TisdaI1. F- F- Drake. T. G. H.. and
Brown, A.: A new cereal mixture con-
taining vitamins and mineral elements. Am.
J. Dis. Child. 40:791-799. Oct. 1930.
-iQ-i-1 Tisdall. F." F.: Dietary factors and
*'J1 health. Soc. Tr.. Am. J. Dis. Child.
42:1490. Dec. 1931.
1932 Summerfeldt, P.: The value of an in-
creased supply of vitamin Bi and iron
in the diet of children. Am. J. Dis. Child.
43:284-290. Feb. 1932. - Morse, J. L.: Fads
and fancies in present day pediatrics. Pennsylvania M. J. 35:280-285, Feb. 1932. Hen-
ricke, S. G.: The vitamin B complex: Its role
in infant feeding in the light of our present
knowledge. Northwest Med. 31:165-169,
April 1932. Langhorst, ,H. F.: Vitamins:
Their role in the prevention and treatment of
disease. M. J. & Rec. 135:326-329. April 6,
1932. Crimm. P. D.: Dietary of Childhood
Tuberculosis: Cereal as a source of added
mineral and vitamin elements; preliminary
report. J. Indiana M. A. 25:205-206, May
1932. Troutt, L.: Quality studies of therapeutic diets: I. The ulcer diet; a committee
report. J. Am. Dietet. A. 8:25-32. May 1932.
Summerfeldt, P., Tisdall, F. F., and Brown,
A.: The curative effects of cereals and biscuits on experimental anaemias, Canad.
M.A.J. 26:666-669, June 1932. Sneed, W.:
Ununited and delayed union of fractures,
Kentucky M. J. 30:363-370, July 1932.
Silverman, A. C.: Celiac disease. New York
State J. Med. 32:1055-1061, Sept. 15, 1932.
von Meysenbug, L.: Infant feeding with
especial reference to some of its problems
daring the first year, Texas State J. Med.
28:543-547, Dec 1932.
1933 "Sampler, P- J-. and Forbes. J. C.: Cal-
cium and phosphorus metabolism in a
case of celiac disease. South. M. J. 26:555-
558, June 1933. Brown, A., and Tisdall,
F. F.: The role of minerals and vitamins in
growth and resistance to infection, Brit. M.
J. 1:55-57, Jan. 14, 1933; Effect of vitamins
Orleans M. & S. J. 87:738-743. May 1935.
Tarr. E. M., and McNeile, O.: Relation of
vitamin B deficiency to metabolic disturbances during pregnancy and lactation. Am.
J. Obst. & Gynec. 29:811-818, June 1935.-
Blatt, M. L., and Schapiro, I. E.: Influence
of a special cereal mixture on infant development. Am. J. Dis. Child. 50:324-336. Aug.
1935. Coward, N. B.: Infant feeding.
Nova Scotia M. Bull. 14:525-532. Oct. 1935.
Tisdall, F. F.: Inadequacy of present dietary
standards,-Tr. Sect. Pediat., A.M.A., 1935:
Canad. M. A. J. 33:624-628. Dec. 1935.
Marriott, W. McK.: Infant Nutrition, second
edition. C. V. Mosby Co.. St. Louis. 1935, p.
202. Summerfeldt, P.: Iron and its availability in foods, Tr. Sect. Pediat., A.M.A.
1935, pp. 214-220.
1936 Dafoe> A- Rv Further history of the
care and feeding of the Dionne quintuplets, Canad. M. A. J. 34:26-32, Jan. 1936.
•Conn. L. C, Vant. J. R.. and Malone. M. M.:
Some aspects of maternal nutrition, Surg.,
Gynec. & Obst. 62:377-383, Feb. 15, 1936.
Ross, J. R., and Summerfeldt, P.: Haemoglobin of normal children and certain factors
influencing its formation, Canad. M. A. J.
34:155-15S, Feb. 1936. Smyth. F. S.: Allergic diseases. J.  Pediat. 8:500-515.   April
1936. Lemmon, J. R.: Problems of the crying infant. Southwestern Med. 20:2455-250,
July 1936. Rice, C. V.: The success of treating
celiac disease from a standpoint of vitamin
deficiency. Arch. Pediat. 53:626-629, Sept.
1936. Smith, C. H.: Management of nutritional anemia in infancy, M. Clin. North
America 20:933-950. Nov. 1936. Strong,
R. A., editor: Nutritional anemia of infants,
Orleans Parish M. Soc. Bull., pp. 6-9, Nov.
9, 1936. Jeans, P. C: Specific factors in
nutrition. Round Table discussion, J. Pediat.
9:693-698, Nov. 1936. Young. J. G.:
Meeting the requirements for proper nutrition in infancy. Texas State J. Med. 32:531-
533, Dec 1936.
1 Q37 Stearns. G., and Stinger, D.: Iron re-
tention in infancy, J. Nutrition 13:127-
ner. B.. and Gruehl. H. L.: Anaphylactogenic
.properties of certain cereal foods and bread-
stuffs: Am. J. Dis. Child. 57:739-758. April
1939. Monypenny, D.: Early introduction
of solid foods in the infant diet, Soc. Tr., Am.
J. Dis. Child. 58:1144-1145, Nov. 1939. Brown,
A., and Tisdall, F. F. Common Procedures in
the practice of paediatrics, third edition, McClelland & Stewart. Ltd., Toronto. 1939. pp.
1940 McI?ougal. L. L.. Jr.: Feeding a nor-
mal infant, Mississippi Doctor 17:437-
442. Jan. 1940. Monypenny, D.: The early
introduction of solid foods in the infant diet,
Canad. M. A. J. 42:137-140, Feb. 1940.
Robinson, E. C.: A study of two hundred and
forty breast-fed and artificially fed infants in
the St. Louis area. Am. J. Dis. Child. 58:816-
827, April 1940. Ratner, B.: Round Table
discussion On food allergy, J. Pediat. 16:653-
672. May 1940. Rosenbaum, I., Jr.: The
management of the allergic child, Kentucky
M. J. 38:199-203. May 1940. Barondes, R.
de R: Report of a case of pellagroid, M. Rec
151:376-380. June 5. 1940. Brown, A.:
The fourth Blackader lecture on a decade of
paediatric progress, Canad. M. A. J. 43:305-
313. Oct. 1940. Drueck, C. J., Vitamin
therapy in colon and rectal disease, Illinois
M. J. 78:337-341, Oct. 1940. Swift. F. L.:
Infant feeding, Lackawanna Co. M. Soc
Reporter, 33:16-18, Nov. 1940. Bogert.
L. J., and Porter, M. T.: Dietetics Simplified.-'
ed. 2, Macmillan Co., New York, 1940, p.
181. Davison, W. C: The Compleat Pediatrician, third edition, Duke University Press,
Durham, N. C, 1940. No. 216. Hawley,
E. E., and Maurer-Mast. E. E.: The Fundamentals of Nutrition. C. C. Thomas, Springfield. III.. 1940, pp. 296, 456. Kugel-
mass, I.N.: The Newer Nutrition in Pediatric
Practice. J. B. Lippincott Co., Philadelphia.
1940. p. 372. Leaman, W. G.. Jr.: Management of the Cardiac Patient, J. B. Lippincott Co.. Phila., 1940. p. 549. Paterson.
D., in Index of Treatment, edited by R.
Hutchison, ed. 12,revised, Williams & Wilkins
Co.. Baltimore. 1940, p. 491.     Thomas, G.
Mead's Cereal was introduced in 1930, and Pablum in 1932, by
Mead Johnson & Company. Since then, the growing literature
indicates early recognition and continued acceptance of these
products and the important pioneer principles they represent.
and the inorganic elements on growth and
resistance to disease in children, Ann. Int.
Med. 7:342-3527 Sept. 1933. Crimm, P. D..
Raphael, I. J., and Schnute, L. F.: Diet of
tuberculous and non-tuberculous children:
Effect of increased supply of vitamin B concentrate and minerals. Am. J. Dis. Child.
46:751-756. Oct. 1933. Smith, A. D.: Consideration of various infants' foods. Pacific
Coast J. Homeop. 44:463-465. Sept.-Dec 1933.
1Q34 Somers, R., Rotton, G. C, and Rown-
tree, J. I.: Possibilities of improving
dental structures, Soc. Tr., Bull. King Co. M.
Soc 13.-6, Jan. 15. 1934. Blatt, M. L.:
Development of infants on a diet of a special
cereal mixture, Soc Tr., Am. J. Dis. Child.
47:918, April 1934. Rice. C. V.: Anemia of
infancy and early childhood, J. Oklahoma
M. A. 27:125-129. April 1934. Hawk. W.
A.: A few of the commoner feeding problems
in infancy, Univ. Toronto M. J. 11:218-229,
May 1934. Ross. J. R., and Burrill.L. M.:
The effect of cooking on the digestibility of
cereals, J. Pediat. 4:654-659, May 1934.
Rice, C. V.: Sauerkraut juice.for the acidification of evaporated milk in infant feeding.
Arch. Pediat. 51:390-395. June 1934. Eder.
H. L.: Iron therapy: A routine procedure
during infancy. Arch. Pediat. 51:701-713,
Nov. 1934. Lynch, H. D.: Fundamentals
of infant feeding, J. Indiana M. A. 27:571-
574. Dec 1934. Chaney, M. S., and Ahl-
born, M.: Nutrition, Houghton Mifflin Co.,
Boston, 1934, p. 323.
1Q35 Bailey, C. W.: Anemia in infants and
young children, J. South Carolina M.
A. 31:54-58, March 1935. Kugelmass, I.
N.: The recent advances in treatment of
nutritional disturbances in infancy and "childhood, M. Comment 17:5-13, March 1, 1935.
Ross, J. R., and Summerfeldt, P.: Value of
increased supply of vitamin Bi and iron in
the diet of children: Paper II, Am. J. Dis.
Child. 49:1185-1188. May 1935. von Meysenbug, L.: Breast feeding with especial
reference  to  some  of  its  problems.   New
• 141, Feb. 1937. Strong, R. A.: Nutritional
anemia, Mississippi Doctor 15:13-16. Aug.
1937. Smith, C. H.: Prevention and treatment of nutritional anemia in infancy. Preventive Med. 7:115-124. Aug. 1937. Saxl.
N. T.: Pediatrics, in Dietetics for the Clinician, edited by M. A. Bridges, third edition,
Lfea & Febiger, Philadelphia. 1937. pp. 637-
639. Boyd, J. D.: Nutrition of the Infant
and Child. National Medical Book Co., Inc.,
New York, 1937, p. 110. Brennemann, J.:
Practice of Pediatrics, W. F. Prior Co.. Inc.,
Hagerstown. Md., 1937, Vol. 1. Ch. 25. p. 19.
Griffith, J. P. C„ and Mitchell, A. G: The
Diseases of Infants and Children, second,
edition, TV. B. Saunders Co., Philadelphia,
1937, pp. 106, 111. Saxl. N. T.: Pediatric
Dietetics, Lea & Febiger, Philadelphia, 1937,
pp. 131-133.
1938 Hoffman, S. J., GreenhiU, J. P., and
Lundeen, E. C: A premature infant
weighing 735 grams and surviving, J.A.M.A.
110:283-285, Jan. 22, 1938. Krasnow, F.:
Nutritional influence on teeth. Am. J. Pub.
Health 28:325-333, March 1938. Ratner, B.:
Round Table discussion on asthma and hay
fever in children, J. Pediat. 12:399-413,
March 1938. Ratner, B.: Panel discussion
on the role of allergy in pediatric practice,
J. Pediat. 13:582-604, Oct. 1938. Snelling.
C. E.: Nutritional anaemia. Bull. Acad. Med.
Toronto 12:710, Oct. 1938. _ Dauphinee.
J. A.: The iron requirement in normal nutrition,   Canad.   M.AJ.   39:483-486.   Nov.
1938. Summerfeldt, P.. and Ross, J. R.:
Value of an increased supply of vitamin Bi
and iron in the diet of children, Paper III,
Am. J. Dis. Child. 56:985-988, Nov. 1938.
Tisdall, F. F.. and Drake, T. G. H.: The
'utilization of calcium, J. Nutrition 16:613-
620. Dec. 1938. Drake. T. G. H.: Introduction of solid foods into the diets of children, Canad. M. A. J. 39:578-580, Dec. 1938.
1 Q'kO Strong,  R. A.: The most frequent
-'-'7 causes of vomiting in infancy, Texas
State J. Med. 34:665-676, Feb. 1939.     Rat-
I.: Dietary of Health and Disease, ed. 3, revised. Lea & Febiger. Phila., 1940, pp. 171.
JQAl Gipson, A. C: The role of allergy in
pediatric practice, J. M. A. Alabama
10:272-274, Feb. 1941. Ross. J. R.. Monypenny, D., and Jackson, S. H.: II. The effect
of cooking on the digestibility of cereals, J.
Pediat. 18:395-398, March 1941. Kennedy,
A. S., Snider, O., Hazen, J. S., and McLean.
C: The dietary management of intestinal
tuberculosis. Canad. M. A. J. 44:380-385.
April 1941. McAlpine, K. L.: Management of the nutritional anaemia of infancy,
Canad. M. A. J. 44:386-390. April 1941.
Patek, A. J.. Jr., and Post, J.: Treatment of
cirrhosis of the liver by a nutritious diet and
supplements rich in vitamin B complex, J.
Clin. Investigation 20:481-505, Sept. 1941.
Bercovitz, Z., and Johnson, H. J.: Ulcerative
Colitis, in Dietetics for the Clinician, by M.
A. Bridges, fourth edition, revised. Lea &
Febiger, Phila., 1941, p. 295. Bridges. M.
A.: Dietetics for the Clinician, fourth edition,
•revised. Lea & Febiger, Phila., 1941, pp. 727,
751. 809. Griffith, J. P. C. and Mitchell.
A. G.: Textbook of Pediatrics, ed. 3, revised.
W. B. Saunders Co., Phila., 1941, pp. 87, 91.
Rowe, A. H.: Elimination Diets and the
Patient's Allergies,  Lea &  Febiger,   Phila.,
1941. p. 230. Twiss. J. R.: Gall-bladder
Disease, in Dietetics for the Clinician, by
M. A. Bridges, fourth edition, revised. Lea &
Febiger, Phila.. 1941, p. 401.
1QA7. Gleich, M.: The premature infant.
i:^    Part II. Arch. Pediat.59:99-135. Feb.
1942. Part IV, Arch. Pediat. 59:241-263.
April  1942.       Brown,  A.,  and   Robertson.
E. C: Factors to be considered in the construction of the diet of the older child, J.
Kansas M. Soc 43:237-244, June 1942. Porter, L.. and Carter, W. E.: Management of the
Sick Infant and Child, ed. 6, C. V. Mosby Co.,
St. Louis. 1942. p. 125. Proudfit, F. T.:
Nutrition and Diet Therapy, ed. 8, Macmillan
Co., New York, .1942. p. 515. Willard. J.
H.: Digestive Diseases in General Practice.
F. A. Davis Co.. Phila.. 1942. p. 147. n
HEMROYDINE E.B.S. is an astringent,
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Hemroydine E.B.S. contains:
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Hemroydine E.B.S. is antiseptic, antipruritic and sedative in action, for
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reports have testified to the efficacy of "Emmenin".
This naturally-occurring oestrogen has been proved to
be essentially safe even when taken over long periods
of time. "Emmenin" Liquid is supplied in bottles of
4 ounces;   "Emmenin" Tablets in bottles of 42.
AYERST, MdCENNA & HARRISON LIMITED • Biological and Pharmaceutical Chemists • MONTREAL, CANADA ^J
f   Breaks the vicious circle of perverted
menstrual function in cases of amenorrhea,
tardy periods (non-physiological) and dysmenorrhea. Affords remarkable symptomatic
relief by stimulating the innervation of the
uterus and stabilizing the tone of its
musculature. Controls the utero-ovarian
l    circulation and thereby encourages a    \
\    normal menstrual cycle.
Full formula and descriptive
literature on request
Dosage:   l to 2 capsules
3 or 4 times'daily.   Supplied
in packages of 20.
Ethical protective mark MHS
embossed on inside of each
capsule, visible only when capsule is cut in half at seam.
: .:•./':: .;-:.:.:.v: ::>>>*; .-.■
Jleai GoldU Checked
(1:1000 solution of 2-(naphthyl—l~methyl)—imidazoline hydrochloride)
Clinical investigations on Privine Nasal Drops have proved that
they are excellently suited for the treatment of all forms of nasopharyngeal affections. In head colds, a few moments after the
instillation of 3 drops of Privine in each nostril, the headache and
sensation of heaviness in the head disappear, while the nasal respiration becomes easier, the watering of the eyes stops, the voice regains
its normal tone and the sense of smell is restored.
In bottles of Vi ounce with dropper, and bottles of 4 ounces.
Brand of Benzyl -Tridlkonium Chloride
a low toxicity index is realized in Zephiran
Chloride, cationic detergent and germicide; a mixture of high molecular alkyl-
dimethyl-benzyl-ammonium chlorides.
In an evaluation of germicides for clinical
use by Hirsch and Novak,* using the phagocytosis inhibiting technic for determining
toxicity, Zephiran Chloride was found to be
germicidal in a 1:3970 concentration sterilizing infected blood completely, whereas
the phagocytosis inhibiting concentration
was shown to be 1:3370. The toxicity index
of Zephiran Chloride thus is 0.85 as against
an average of 5.2 for 70 per cent and 95 per
cent alcohol and 900 for tincture of green
♦Hirsch, M. M., and Novak, M. V.: Evaluation of
Germicides with Relation to Tissue Toxicity. Proc.
Soc. Exper. Biol, and Med., June, 1942.
ZEPHIRAN  CHLORIDE  . . . Germicide for Surgery, Obstetrics and  Gynecology,
Urology, Dermatology, Eye, Ear, Nose and Throat, Sterile Storage of Instruments.
NEwJjpRK, NJlte? Successor WINDSOR, P^B
Detergent Properties .
A Wetting-. Agent'
High Tissue* Tolerance'
Penetration Ability
Rapicf Action^
Emollient Effect
; Wide Application
II ciinTiFiiiiiiitiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiitiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiriiiiiiiiiiiiiiiiiiiiiiiiiiniiiiiiiiiiiiiiiiiiiiiiiiif [iiiiiiiiiiiiiiiiiiiiiiiiiiiiiitiiiiiiiiiiiiiifiiiine
"come back strong
. In the infant dietary, Carnation Evaporated
Milk is especially valued as a dependable
source of calcium and phosphorus, with
vitamin D increased by irradiation, for
normal tooth formation and calcification.
After weaning, Carnation Milk continues
to assist in the development and protection
of sound, fully formed teeth. This is one
of the many nutritional reasons — there
seem to be none to the contrary—for
recommending Carnation as a suitable
"eating" and drinking milk for older
ifhysicians are invited to
write for "Continuing After
Weaning With Irradiated
Carnation Evaporated
Milk" Address Carnation
Co. Limited, Toronto, Ont.
'FROM CONTENTED COWS"      ^s^z?%g^    A Canadian Product
niiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiitiiiiiiiiiiiiiiiiiiiiiiiiiiiitiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiifiiiiiiiiHiiiiiiiiiiiiilllIllilllilflilliiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiifiiiinx wXrSi^hHBI
MArine 416
there^^J^^^jsome few unobtainabfe
medl^ials^—but ever^precauttorQhras
been takei§|by Georgia Pharmacy to re-
gjfckejlhe possibility o^these^pfe^ing
ouBser^^^tojape medt^f profession.
iJ&u&M* ~&. Jc&n&'lten \
-i- r«4 .t\j:- d
North Vancouver! B. C.
Powell River, Bv&; ^IfflS
New Westminster, B, |||
NE uibP^^pA T$1C
Reference-^-B. C.Wedic&Association
fori^fefrmation appty'00


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