History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: November, 1941 Vancouver Medical Association Nov 30, 1941

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 Vol. XIII.
No. 2M
of the
|      f/ANCOUVER
With Which Is Incorporated
Transactions of the
Victoria Medical Society
Vancouver General Hospital
tst Paul's Hospital
In This Issue:
NEWS AND NOTES %   ^^^^^^^^^W B ||-: 29
CONSIDERATIONS - l§jjj ■    ^ffW&m''    fllP ^^^^^B 46
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E. B. S.
{4-4 Dihydroxy?a-b Diethyl
Stiiboestrol Di-propionate)
Shuttleworth's   Orestol   is
available in tablets of three
sizes, put up in bottles of
100 sum 500, as follows:
C.C.T. No. 530 % mg
-CC.T. No. 531 lmg
C.C.T. No. 532 5 mg
Descriptive booklet on Orestol
will shortly be mailed to all
TM& Answer...
to  repeated  demands  for a
substance with oestrogenic
activity |jwhen administered
One milligram Orestol by mouth, is equivalent
to one milligram of natural hormone by
injection; and Orestol may be regarded as an
effective substitute for the natural follicular
hormone of the ovary.
INDICATIONS: In the treatment of ovarian hypo-function, Orestol
is of therapeutic value only in the first half of the menstrual cycle,
while in the treatment of menopausal conditions, its use may be
more or less continuous.
Amenorrhea... due to malnutrition or temporary ovarian deficiency responds to ORESTOL as its use in this condition has
produced oestrin withdraw! bleeding and epithelial growth of
vagina, uterus and breast tissue.
Dysmenorrhea... may be treated with ORESTOL E.B.S. plus
adequate water, iron and vitamin intake, for according to
*M. C. Watson, fluid is important as the oestrogens act by altering the local circulation and water metabolism in the tissues.
ORESTOL can also be used for relief of menstrual pain.
The Menopausal Syndrome & Atrophic Vaginitis: ORESTOL
E.B.S. provides excellent symptomatic relief of hot flushes, lassitude, etc. and promotes great improvement in the local ulcerative
condition of the vagina.
Inhibition of Lactation: By its effect on the lactogenic hormone
of the anterior lobe of the pituitary, ORESTOL inhibits lactation.
Sterility: Where uterine hypoplasia is the cause, ORESTOL may
be administered during the first half of the cycle. It increases
circulation in uterus and vagina... stimulates epithelial growth.
Amenorrhea—One-half to 1 mgm     Menopausal[Conditions—One-half
Specify E.B.S.
one to three times daily for two weeks,
followed by a treatment-free period of
two 'weeks. This treatment should be
followed for at least three such
courses when the cycle is not known,
in an endeavour to establish a cycle.
If the cycle is known, then Orestol
should be given only during the first
Dysmenorrhea—One-half to 1 mgm
daily for the first half of the cycle.
Adjunctive treatment... Ferrochlor
E.B.S. with Vitamin Bl; liquid or
to 1 mgm daily. In severe or resistant
cases,  1 mgm twice, or even three
times daily. Dosage should be reduced
as soon as possible to gradually adjust
the   patient   to   the   new  level of
endocrine activity.
Inhibition of Lactation—One mgm
three or four times daily, until flow
has ceased.
Sterility—One mgm once or twice
daily during the first half of the cycle.
*Watson M. C Academy &Medicme
Bulletin, Toronto, March, 1940, p. 1*7'
"S§| /us* 'o
be sure!
Published Monthly under the Auspices of the Vancouver Medical Association
in the interests of the Medical Profession.
Offices: 203 Medical- Dental Building, Georgia Street, Vancouver, B. G.
Db. J. H. MacDermot
Db. G. A. Davidson Db. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
Vol. XVin
No. 2
OFFICERS, 1941-1942
Dr. C. McDiabmid Dr. J. R. Neilson Dr. D. F. Busteed
President Vice-President Past President
Dr. W. T. Lockhabt Dr. R. A. Palmer
Hon. Treasurer Hon. Secretary
Additional Members of Executive: Dr. Gordon Burke, Dr. Frank Turnbull
Dr. F. Brodie Db. J. A. Gillespie Db. W. L. Pedlow
Auditors: Messbs. Plommeb, Whiting & Co.
Clinical Section
Db.  Ross  Davidson Chairman
Eye, Ear, Nose and Throat
Dr. J. A. McLean Chairman Dr. A. R. Anthony.
Pwdiatric Section
Dr. G. O. Matthews Chairman
Dr. F. J. Buller. Dr. D. E. H. Cleveland, Dr. J. R. Davies,
Dr. A. Bagnall, Dr. A. B. Manson, Dr. B. J. Harrison
Dr. J. H. MacDermot, Dr. D. E. H. Cleveland, Dr. G. A. Davidson.
Summer School: >&*&
Dr. H. H. Caple, Db. J. E. Habbison, Db. H. H. Hatfield,
Dr. Howard Spohn, Dr. W. L. Graham, Dr. J. C. Thomas
Dr. A. W. Hunter, Dr. W. L. Pedlow, Dr. A. T. Henry
V. O. N. Advisory Board:
Dr. W. C. Walsh, Dr. R. E. McKechnie II., Dr. L. W. McNutt.
Metropolitan Health Board Advisory Committee:
Dr. W. D. Patton, Dr. W. D. Kennedy, Db. G. A. Lamont.
Greater Vancouver Health League Representatives:
Db. R. A. Wilson, Dr. Wallace Coburn.
Representative to B. C. Medical Association: Dr. D. F. Busteed.
Sickness and Benevolent Fund: The President—The Trustees.
'& *A
It is well recognized that a frank
deficiency of a single nutritional
factor is rare. Since most vitamin
deficiencies are multiple in nature,
the following Squihb Vitamin Products will find a wide field of usefulness in your practice. They supply
several important vitamins.
Supplies Vitamins A, D and Bj and the
other B-Complex factors in the proportions
found in yeast. For routine use as an
economical diet supplement. These chocolate-coated tablets are easy to swallow,
cause no flatulence, have no oily taste.
Supplied in bottles of 80, 250 and 1,000
tablets. Sig: 3 or more daily.
So potent that one capsule supplies the
estimated daily requirement in Vitamins
A, B, C, and D and other B-Complex
factors from a Special High Potency Yeast.
Especially useful to prevent avitaminosis,
particularly after surgical procedures or
severe infections. Supplied in bottles of
25, 100 and 250 capsules.
♦Strauss, M. B., J. A.M. A. 110:953, 1938.
Aii Syphilis 	
Phone MA. 4027
Total Population—estimated   272,352
Japanese Population—estimated
Chinese Population—estimated
Hindu Population—estimated
Total deaths 248
Japanese deaths 4
Chinese deaths 6
Deaths—residents only 222
Male, 233; Female, 228
Deaths under one year of age 13
Death rate—per 1,000 births 28.2
Stillbirths (not included in above) 6
Scarlet Fever	
Chicken Pox	
Measles '-I	
Whooping Cough 4
Typhoid Fever      1
Undulant  Fever 0
Poliomyelitis ' 1
Tuberculosis 22
Erysipelas 0
Meningococcus Meningitis 1
Paratyphoid Fever —     0
West North
Burnaby   Vancr.  Richmond   Vancr.
Another Product of the Bioglan Laboratories, Hertford, England
Stanley N. Bayne, Representative
Descriptive Literature on Request
7- 'V
' ■   !
Sample on request
In affections of the upper
respiratory tract, Antiphlogistine is
an ideal adjuvant to the general
treatment. Its medication and
sedative warmth are an aid
to decongestion and  repair.
Made in Canada
Founded 1898 .. . Incorporated 1906
Programme of the Forty-fourth Annual Session
Dr. W. D. Keith: "Safety in the Operation for Toxic Thyroid.
Dr. E. J. Curtis: "Meningococcus Meningitis."
December    2—GENERAL MEETING.
Dr. F. E. Saunders: "Sterility in the Female."
"after a debilitating illness...
Guinness often supplies just the necessary fillip to nudge the patient out of
the rut of lour health.'*
M. B.
Literally by the thousands, doctors in Britain have reported in this way.    As
yon know, the tonic properties of Guinness Stout are famous.
In addition, Guinness has proved invaluable in
treating insomnia. It obviates the depressing after
effects 'which most hypnotics produce. Guinness is
a stimulating, appetizing food for middle-aged
and  elderly  people.
All of its natural  goodness is  retained.  Nutritional elements   are  not filtered out  for  the  sake
Total solids 	
Etbyl  alcohol   (73%  by volume).
Total carbohydrates   	
Reducing   sugars  as  glucose	
Protein s	
Total  nitrogen   	
Calcium    _
fuel value .
Vitamin B\.
Vitamin   G..
      5.87 gm.
      6.25  gm.
     3.86  gm.
      0.66 gm.
 : _"   None
 0.10  gm.
     0.28 gm.
  38.50  mg.
     7.00 mg.
     0.072 mg.
 0.049 mg.
  61  col.
  6 Int. Units
of sparkle. And because it is not pasteurized,
Guinness in bottle continues to mature, contains
active yeast—a source of Vitamins B and G. Only
four ingredients are used: barley malt, hops,
Guinness yeast and water. Brewed in Dublin
since 1759. Foreign Extra Guinness is obtainable
through   all   legal   outlets.   Write   for   file   card
giving complete analysis and indications; address
R e p r e sentative, A.
Guinness, Son & Co.,
Limited, 501 Fifth
Avenue, N. Y. C.
-33   Sherman  Bourquin Units
SON & CO.,
DUBLIN   and
Page 27
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The contents of an apple read like a medical prescription
Levulose, Sucrose and Dextrose sugars; pectin and hemi-
cellulose—good  sources of  Uronic  acid;   iron, calcium  and
phosphorus; vitamins A, B and C with a trace of G; Tannic,
Malic and Citric acids, and water.
In Europe, apples have been used therapeutically for over
two centuries. More recent research in Canada and the United
States has confirmed many of the European findings and has,
in addition, shown many new uses and values in the apple.
The physical and nervous strains of these war years make
national health even more a matter of supreme importance,
and medicinally and therapeutically, the Canadian apple has
the elements necessary for playing a major role in the maintenance of Canada's war-time health.
From an economic viewpoint, the use of the Canadian
apple takes on an added importance in that no foreign exchange need be spent for it that could be spent for essential,
imported armaments.
The twenty-six hundred apple growers in the interior
valleys of British Columbia, by whom this advertisement is
published, are interested in the further nutritional and medical
knowledge and use of the Canadian apple.
Your comments on this would be much appreciated.
Address your letters to—
KELOWNA B. C. Within the past few months, we have seen arising in Vancouver a number of quasi-
! insurance organisations, known by various names.   They undertake the sale to the public
of policies, purporting to insure the beneficiary against the costs of sickness—chiefly, it
may be noted, the costs of operative conditions.
The sale of these policies is being very energetically pushed—and many people are
buying them. When the patient has had an operation, the bill is given to the company
involved, and a cheque is sent to the surgeon.
There is no doubt that the rapid increase in this sort of insurance has been brought
about by the success of such mutual health insurance associations as the B. C. Telephone,
the B. C. Electric, the Vancouver School Teachers and the Medical Services Association.
All these organizations, as our readers know, have made contracts with the medical profession of British Columbia through its organised B. C. Medical Association. A 25%
cut in scheduled fees is accepted on certain well-defined terms.
There is no contract or agreement between the B. C. Medical Association and any of
these other organisations to which we refer. Therefore, when they send in a cheque in
full settlement, subject to a 25% reduction, we should not accept it. Our contract is
with the patient—not with any insurance company—and we should make it clear to
our patient that he or she is liable for the full amount of the bill.
There are several reasons why this should be so; we take leave to mention a few:
. (1)  As stated, we have made no contract with any of these people and they have
no right to dictate to us what our charges shall be.
(2) They make an agreement with the patient, based on our ordinary schedule.
Then they cut the bill, and pocket the difference. This is why there is such a rapid
increase in this sort of thing—it is becoming very profitable.
(3 They do not pay for all medical services, as do the Telephone, B. C. Electric,
M-S-A, etc.   They only pay for operative work.
(4) A very serious point for us to consider is that by accepting these people and
their terms we are allowing a very dangerous principle to be introduced into the practice
of medicine: this is, third-party gain. It is a dangerous principle, that a third party
should make money out of the sick and squeeze out of both the sick and the doctors
attending them, profit which they have not earned. Our Medical Services Association
exists, and we should urge people to join this. It gives infinitely more value for their
money, and is under close supervision and control.
The modus operandi of these gentry is to send a curtailed cheque, and if the doctor
protests, to utter all sorts of threats of blacklisting, etc., as well as to assure the doctor
that everyone else is accepting the cut. We think that the only answer to this sort of
blackmail is to insist firmly upon payment of our bill, and ignore completely their
threats. If we tell our patients the facts and shew them where they can get equitable,
honest, and complete medical service on a health-insurance basis, we shall have done
them a service, and helped to protect- them, as well as ourselves, against what is fast
becoming a racket.
We hope to publish a brief account of the result of a court case where a doctor here
sued for his bill, and where the presiding judge handed down a decision which is of great
importance to us all. It is by way of being a test case. If we all take the same stand
as did this doctor, we shall soon force these companies either to act fairly and honestly,
or to go out of business.
Page 28
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In the passing, on Octover 7th, 1941, of Dr. D. J. Bell of Vancouver, the profession
has lost a very loyal member.
Dr. G. E. Kidd of Vancouver has the sympathy of his colleagues in the loss of his
wife on October 26th.
Sympathy is extended to Dr. R. B. Robertson of Victoria in the loss of his mother
on October 28th.
Capt. A. W. Bagnall, who is now serving with a Field Ambulance, was made a Fellow
of the Royal College of Physicians of Canada by examination. Capt. Bagnall is the son
of Dr. A. W. Bagnall of Vancouver.
Dr. and Mrs. A. B. Schinbein of Vancouver were visitors in Toronto.
Dr. and Mrs. A. M. Agnew of Vancouver are visiting in Toronto.
*t *-t **. *JL
•S* »? *T "tT
Dr. .W Harold Brown of Vancouver travelled by air to the meeting of the American
Academy of Ophthalmogy and Otolaryngology. Dr. Brown will receive life membership in the Academy.
*       *       *       *
Surgeon-Lieut. H. G. Farish, son of Dr. J. C. Farish of Vancouver, and Dr. Hazel
W. Krause of Montreal were married on October 18th.  They have our best wishes.
Dr. D. E. H. Cleveland will leave on''November 11th to do post-graduate study in
New York. While in the East he will attend the American Academy of Dermatology
and Syphilology, returning to Vancouver on December 22nd.
Flying Officer H. B. McGregor, Medical Officer with the R.C.A.F., returned to
Penticton for a short visit before leaving for Toronto.
Penticton's contribution to His Majesty's Forces includes: Capt. R. P. Borden, Capt.
W. Roy Walker of the R.C.A.M.C, and Flying-Officer H. B. McGregor of the R.C.A.F.
It is reported that Dr. W. M. Toone of Nelson is planning to enter War Service, and
Dr. R. B. Brummitt of Smithers will carry on in a holding capacity during Dr. Toone's
lit 11
Nelson has already lost Dr. B. Dunham, who is now serving with the R.C.A.M.C.,
and Dr. W. McC. McCallum, who was associated with Drs. Borden and Morrison.
Dr. J. J. Gibson, formerly of Tulsequah, is now associated with Dr. R. Geddes Large
of Prince Rupert.
Dr. W. T. Kergin, formerly of Premir, is now at Ocean Falls.
Dr. W. T. Kergin and Dr. C. A. Armstrong are carrying on the practice at Ocean
Falls, both Dr. R. D. Coddington and Dr. G. D. Saxton having entered the Forces. By
arrangement the latter are on extended leave from their positions at Ocean Falls.
Page 29
4 liv
Dr. T. J. Agnew, who has been at Courtenay associated with Drs. P. L. Straith and
H. A. L. Mooney, is now located at Campbell River, holding the practice of Dr. N. B.
Hall, who is now serving with the R.C.A.M.C.
Dr. J. A. Murison of Powell River has been away on vacation. Dr. W. B. Clarke
has been with Dr. O. O. Lyons during Dr. Murison's absence.
Dr. G. E. Darby of Bella Bella is having a vacation.
Dr. B. J. Hallowes, who has been at Alexis Greek, is now located at Port Renfrew.
Dr. W. Sutherland Groves has left Port Renfrew and is now at Chemainus, holding
the practice of Dr. R. N. Dick.     *      *      *      *
Dr. R. N. Dick of Chemainus is now serving as Medical Officer with the Royal
Canadian Air Force. *       *       *       *
Dr. T. C. Harold, formerly of Ladysmith, is now serving as a Medical Officer with i
His Majesty's Forces. *      *      *      *
Dr. J. H. Rivers is assisting Dr. Gordon James at Britannia.
Dr. R. B. Brummitt, formerly of Smithers, has taken over the practice of Dr. W.
M. Toone of Nelson. *      *      *      *
Dr. L. F. Brogden of Penticton called at the office when in Vancouver on vacation.
Dr. J. P. Ellis of Lytton was in Vancouver over the week-end.
Dr. H. Cantor of Atlin, who has been relieved by Dr. G. W. Meyer of Telegraph
Creek, has returned to Vancouver to join the Medical Services with the Forces.
We are glad to report that Dr. V. B. Latimer, formerly of Penticton, and latterly
of Port Alberni, is making a good recovery following his recent illness, and will spend
the winter months in Vancouver.
Medical Clinics of North America, Symposium on Specific Methods of Treatment, Boston
Number, September, 1941.
Arthritis and Allied Conditions, 2nd ed., 1941, by Bernard I. Comroe.
Abdominal Surgery of Infancy and Childhood, 1941, by William E. Ladd and Robert
E. Gross.
Dietetics for the Clinician, 4th ed., 1941, by the late Milton Arlanden Bridges.
William Henry Welch, and The Heroic Age of American Medicine,  1941, by Simon
Flexner and James Thomas Flexner.
Some interesting symposia appear in the current issues of several periodicals.
Annals of Surgery presents two subjects—
I. Peptic ulcer: Surgery of its complications and differentiation from cancer.
II. Cancer of the body and of the ducts of the pancreas.
The American Journal of Surgery devotes its entire number to Thoracic Surgery.
The Practitioner publishes Part I of a Special Number on Advances in Treatment,
this issue including Medicine, Surgery, Gastro-Enterology, Dietetics, Diseases of Children, Endocrinology, Neurology and Rheumatic Diseases.
The September issue of Medical Clinics of North America (Boston Number) is
devoted to Specific Methods of Treatment, and covers a wide range of material.
Page 30
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OBIIT OCT.  18, 1941.
The medical profession of British Columbia has lost one of its outstanding figures
in the passing of Doctor Thorn.
Doctor Thom arrived in Trail in 1908, shortly after graduating in medicine from
the University of Manitoba: and in the ensuing years filled a large place as a professional man and a citizen of the community.
In his professional career he served in many capacities in local and provincial
circles. His inspiration and leadership made a large contribution to the organization
of the Trail-Rossland Clinic, later known as the C. S. Williams Clinic, in honour of
one of is early members, and now one of the finest organizations of its kind in Western
Doctor Thom also served as Coroner and Provincial Medical Officer of Health for
the district, and was regarded as the dean of the profession in the area.
He took a prominent part in organized medicine in the Province: serving for
several years on the Council of the College of Physicians and Surgeons, of -which he
was Vice-President. He kept himself well-informed, and made a contribution to the
study of economic and social changes as they related themselves to the medical profession. His professional attainments secured him a Fellowship in the American College of Surgeons.
As a citizen, Doctor Thom was the friend and supporter of every good cause. He
served one term as Mayor of Trail. He served at one time as President of the Trail
Curling Club, and was a member of the Trail Board of Trade. He served, too, as Past
Master of Fidelity Lodge A.F. and A.M. The unusual distinction of being made an
honorary member of the local branch of the Canadian Legion bore testimony to the
esteem in which he was held.
Doctor Thom was versatile in his talents. An able organizer, executive and
administrator; he was equally guide, counsellor and friend to untold numbers of
people in every walk of life. In discussion, his thought went straight to essentials,
and his subtle humour or kindly sarcasm often relieved a tense moment. Doctor
Thorn had steadfastness of purpose and was capable of carrying through a programme
with inflexible determination when necessary.
Doctor Thom was a man of sterling character and deep religious convictions—not
with ostentation, but as the dominating force in a personality that was widely respected and beloved. He was a member of the original Session of Knox United Church
in Trail and also served on its Trustee Board. He was the friend and confidant of
ministers; and, in thinking of his life, one calls to mind the requirements of the ancient
Hebrew prophet—"What doth God require of thee but to do justly, love mercy, and
walk humbly with thy God?"    Doctor Thom measured up to that standard.
It was characteristic of the man that nearly a year ago he left directions for his
own funeral service—there was to be no laudatory address: he desired that his life
tell its own story. He chose the hymns he wanted—one being the universally beloved
"Easter Hymn"—and they -were to be sung by a full choir, in joyful tempo, and
triumphant strains.
As one so beloved passes from pur ken into the Unknown, we, his confreres, bid
him adieu, "till the day break, and the shadows flee away."
. F. M. A.
OBIIT OCT. 7, 1941.
In the passing of Dr. J. Bell of Vancouver, at the age of 79, our profession has
lost one of its oldest and most beloved members.
Some few years ago, almost the entire population of Vancouver Heights and
vicinity turned out to honour him at a reception held by his patients and friends, to
celebrate his long and faithful service to them as their family doctor and friend.
Few men evoke such warm affection and esteem.
Dr. Bell graduated in 1888 in Maine, and later went to McGill where he obtained
the degree of M.D.CM. He practised in the Yukon for some time, then moved to
Vancouver, where for many years he conducted a very large practice in Vancouver
Heights and Grandview.
Kindly and gentle, he was a man of high professional attainment ,and his personal
character was above reproach. He belonged to an old school of doctors, who did their
best -work perhaps through the confidence and sense of security that they were able to
inspire, as well as through their ability and medical skill: and his reward was the
love and trust of a large host of people.
Page 31 British  Columbia  Medical   Association
President. : : Dr. C. H. Hankinson, Prince Rupert
First Vice-President— Dr. A. H. Spohn, Vancouver
Second Vice-President Dr. P. A. C. Cousland, Victoria
Honorary Secretary-Treasurer Dr. A. Y. McNair, Vancouver
Immediate Past President Dr. Murray Blair, Vancouver
Executive Secretary Dr. M. W. Thomas, Vancouver
1941 - 1942
President: Dr. C. H. Hankinson, Prince Rupert.
1st Vice-President and Chairman of the Board of Directors and Executive Committee:
Dr. A. H. Spohn, Vancouver.
2nd Vice-President: Dr. P. A. C. Cousland, Victoria.
Honorary Secretary-Treasurer: Dr. A. Y. McNair, Vancouver.
Immediate Past President: Dr. A. Y. McNair, Vancouver.
Executive Secretary: Dr. M. W. Thomas.
Representatives from the Council qf the College of Physicians
and Surgeons of B. C.
Dr. Wallace Wilson, Vancouver.
Dr. F. M. Auld, Nelson.
Directors at large (elected at Annual Meeting)
Dr. G. F. Amyot, Victoria.
Dr. P. S. McCaffrey, Agassiz.
Dr. H. McGregor, Penticton.
Dr. A. H. Meneely, Nanaimo.
Dr. G. F. Strong, Vancouver.
Representatives of District Associations
Dr. D. F. Busteed, Vancouver Vancouver Medical Association
Dr. F. M. Bryant, Victoria Victoria Medical Society
Dr. G. T. Wilson, New Westminster \ Fraser Valley Medical Association
Dr. R. W. Garner, Port Alberni i Upper Island Medical Association
Dr. Arnold Francis, New Denver West Kootenay Medical Association
Dr. W. O. Green, Cranbrook East Kootenay Medical Association
Dr. H. L. Burris, Kamloops No. 4 District Medical Association
Dr. W. G. Saunders, North Vancouver North Shore Medical Society
Dr. E. J. Lyon, Prince George Central Inetrior Medical Association
Dr. C. H. Hankinson, Prince Ruperts Prince Rupert Medical Association
Chairmen of Standing Committees
Dr. H. H. Milburn, Vancouver Constitution and By-laws
Dr. G. F. Strong, Vancouver . Programme and Finance
Dr. Thomas McPherson, Victoria Legislation
Dr. K. D. Panton, Vancouver Medical Education
Dr. D. E. H. Cleveland Archives
Page 32 !fr
H  -
Dr. C. T. Hilton, Port Alberni 1 Maternal Welfare
Dr. G. O. Matthews, Vancouver | Public Health
Dr. Stanley Paulin, Vancouver   1 Ethics and Credentials
Dr. W. A. Clarke, New Westminster Economics
Dr. C. H. Vrooman, Vancouver Pharmacy
Dr. R. A. Seymour, Vancouver Hospital Service
Dr. Ethlyn Trapp, Vancouver -Cancer
Dr. J. H. MacDermot, Vancouver Editorial Board
We publish herewith a letter that speaks for itself, from Capt. W. M. G. Wilson,
the Adjutant of No. 13 Field Ambulance, R.C.A.M.C. The Bulletin, while regretting its failure to note these facts publicly, assures No. 13 Field Ambulance that it was
through no slightest lack of interest in the doings of our friends and colleagues. Military movements are conducted, as they should be, silently and without tuck of drum,
and so are often missed by the onlooker. We are grateful to Capt. Wilson for his letter,
and wish all the best of good luck to him and all in his unit. Ed.
No. 13 Light Field Ambulance, R.C.A.M.C, C.A.(A.)
Camp Borden, Ontario,
8 th September, 1941.
Dr. J. H. MacDermot,
Editor, Vancouver Medical Assn. Journal,
203 Medical Dental Building,
Vancouver, B. C.
Dear Sir: .
I am directed by the Officer Commanding to write to you.
We have noted with some regret that there has been no mention in your journal of
the fact that this unit left B. C. early in July. Since this is the first medical unit to
leave B. C. in the present war, it is felt that this fact would be of definite interest to
the medical profession in the province.   All of the officers formerly practiced in B. C.
Below follows our slate of medical officers.
Lieut.-Col. Roy Mustard, M.C., Officer Commanding, Vancouver; Major C. A.
Watson, Victoria; Capt. J. S. McCannel, Victoria; Capt. G. L. Stoker, Vancouver; Capt.
W. M. G. Wilson, Kamloops; Lieut. G. C. Johnston, Vancouver; Lieut. T. K. MacLean,
This unit is one of three Light Field Ambulances attached to the 5 th Ganadian
(Armoured) Division, at Camp Borden, Ontario. The other Ambulances are from
Other B. C. medical officers with the Division are Capt. A. J. Stewart and Capt. H.
E. Gislason, with the B. C. Dragoons and the Westminster Regiments, respectively.
Your admirable journal is welcomed each month by our officers, and we hope it will
continue to reach us. We also hope you will afford space in a forthcoming issue for
some of the above mentioned facts.
Yours very truly,
W. M. G. Wilson, Capt. and A.-Adj.,
No. 13 Light Field Ambulance, R.C.A.M.C, CA.(A.)
Doctor J. H. MacDermot,
Vancouver, B. C
184 College Street, Toronto 2,
October 28th,  1941.
Dear Doctor MacDermot,
Your esteemed favour of October 21st enclosing a cheque in the sum of $1147.50
for the War Relief Fund of Great Britain is hereby acknowledged.    A copy of your
Page 33 letter together with the cheque is going immediately to our Honorary Treasurer who,
I am sure, will be glad to transfer the money to England.
You folks in British Columbia are doing a great job for this fund and I think you
are to be highly congratulated on the result of your efforts.
Yours sincerely,
T. C Routley, General Secretary.
as requested by the
is  being  made  by  the  Office,
203  Medical Dental Building.
A cheque for $1147.50 was sent to Dr. T. C. Routley, General Secretary of the
Canadian Medical Association, in October, for transfer to the British Medical Association's Relief Fund.   A further list of contributors is attached. Ed.
Bagnall, A. W.,  Vancouver $
Ball, Norbert J., Oliver	
Barrett, G. R., Nelson .	
Beevor-Potts, C. H., Cowicnan Lake	
Bowles, A. W., New Westminster	
Cannon,  Bruce,  New  Westminster	
Buckell,  Edward, Salmon  Arm	
Chipperfield,  L.   S.,   Coquitlam	
Eaton, C. M., Vancouver	
Fiddes, R. G., Port Simpson	
Felton, Richard,  Victoria	
Graham, H. C, North Vancouver	
Haugen,  R.,  Armstrong	
Herstein,  A., Victoria.
Janowsky, A., Victoria	
King, Donald  M., Bralorne	
Large, R. Geddes, Prince Rupert	
Lawson, J. T., New Westminster	
McCaffrey, R.,  Chilliwack	
MacDonald, H. A., Surf Inlet:	
15.00 McHaffie,  D.   S.,  Duncan  5.00
5.00 McLaughlin, G., North Vancouver  5.00
5.00 McK.,   M.D.  5.00
5.00 MacPherson,  T.,  Victoria  50.00
15.00 Miller, D. J., North Vancouver  2.00
10.00 More,   George,   Duncan !  10.00
10.00 Phillips, Paul,  Princeton  10.00
10.00 Purvis, George, New Westminster  10.00
15.00 Ridewood, H. E., Victoria  50.00
2.00 Robertson, Wm. A., New Westminster  10.00
25.00 Rose, A. O., Langley Prairie  10.00
2.00 Ross, A. C, New Westminster  10.00
10.00 Saunders, W. G., North Vancouver  2.00
10.00 Stanier, Francis T., Cobble Hill  5.00
10.00 Trites, A.  E., Vancouver  25.00
25.00 Vosburgh, J. W., Princeton  10.00
10.00 Wall, J. T., Vancouver  5.00
10.00 Watson, H. N.,  Duncan  5.00
25.00 C. S. Williams Clinic, Trail  200.00
3.00 Wride, G. E., Hedley  10.00
—Please get in touch with Librarian, 203 Medical Dental
Building, MA. 4622.
I H« ..
Page 34 8 Si
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H Hi
The Annual Meeting of the Upper Island Medical Association was held on Wednesday, October 29th.
In the afternoon, the members played golf at Qualicum. At 7:30 that evening,
they foregathered at the Island Inn, Parksville, and made ready for their Annual
Dinner. Following an excellent Dinner, the business meeting was held, which was presided over by Dr. R. W. Garner, President.
The elections placed the following in office: Dr. T. L. Briggs of Courtenay as President; Dr. E. N. East of Qualicum as Vice-President; Dr. G. K. MacNaughton of Cumberland as Honorary Secretary; Representative to the Board of Directors of the British
Columbia Medical Association—Dr. R. W. Garner of Port Alberni; Reporter—Dr. A.
H. Meneely of Nanaimo.
The retiring officers, Dr. R. W. Garner, President, and the Honorary Secretary, Dr.
G. B. Helem, were complimented and thanked for their splendid programme which had
been prepared for the two meetings held during the year.
During the business session, Dr. M. W. Thomas, Executive Secretary of the College
of Physicians and Surgeons, addressed the members.
The clinical programme was provided by Drs. Lee Smith and J. R. Neilson of Vancouver. The subject of Dr. Neilson's paper was, "Biliary Tract Disease, Medical and
Surgical," and Dr. Lee Smith dealt with "Genito-Urinary Conditions in General Practice." Both speakers used lantern slides and radiological films. The interest shown by
the members strongly supported the vote of thanks passed by the meeting.
Those present at the dinner inluded: Surg.-Lieut. Ross of the R.C.N., Lieut.-Col.
F. W. Lees, Major S. A. Wallace, Capt. J. A. Ganshorn, Capt. J. E. Walker, Lieut. K. J.
Haig, Capt. H. N. C. Begg, Capt. Ira S. White, Doctors R. W. Garner, G. B. Helem,
W. C. Pitts, A. P. Miller, of Port Alberni; C. C. Browne, A. H. Meneely, W. F. Drysdale, S. L. Williams, E. D. Emery of Nanaimo; W. R. S. Groves of Chemainus; E. N.
East of Qualicum, T. L. Briggs of Courtenay, E. R. Hicks of Cumberland, T. J. Agnew
of Campbell River, H. N. Watson and C. H. Beevor-Potts of Duncan, J. R. Neilson,
Lee Smith and M. W. Thomas of Vancouver.
The physician is often faced by the problem of a lesion that is seemingly benign,
but possibly might be an early malignancy. Is the lesion to be observed carefully over
a period of time, during which time metastases may occur, or is a biopsy to be taken
early—thinking of the slogan, "Biopsy early and save a life"?
If he decides to biopsy, what is the best method of go about the procedure? Oftentimes the patient cannot afford any extensive procedure necessitating loss of time or
even moderate financial outlay unless the procedure is necessary. Also the doctor
cannot afford to gain the reputation of operating indiscriminately on suspicion. If the
biopsy could be made a simple office procedure that could be carried out frequently
without great physical or economic distress to the patient, then more biopsies would be
taken and more lives saved.
The biopsy of a lesion on the surface of the body can readily be done in the office
in many cases. Some novocaine, a sharp scalpel and perhaps a stitch, plus a drachm or so
of 5 % formalin from the nearest pharmacy is all the equipment needed. A wedge-
shaped piece of firm tissue, the size of a grain of wheat or larger, taken at the edge of
the lesion to include normal and abnormal tissue for comparative purposes is the ideal j
small specimen. Infected or degenerating areas should be avoided, or, if unavoidable,
larger portions should be removed.    The specimen should immediately be placed in the
Page 35
■)■ formalin and accompanied by a notation of the patient's age, sex, site of biopsy and a
brief history, sent to the nearest pathologist.
This type of biopsy usually does not discommode the patient greatly as the wound
is small and painless and will heal readily with little care. The taking of the biopsy in
this manner is recognized as not tending to spread the disease unduly in epidermoid
There are many instruments devised for biopsy work. Of these the punch—a small
inexpensive instrument for taking a biopsy of skin lesions—is about the best and should
be standard equipment in all doctors' offices. This instrument is pencil shaped, one
end having a circular hollow knife. The instrument is placed over the selected, anaesthetized site and twirled in the fingers with slight pressure. A core is cut out quickly
and this is separated off at the base easily with a scalpel or scissors and little damage is
Biopsies of lesions situated in the deeper structures of the body need special consideration. These problems will be dealt with in discussing malignancies in various parts
of the body.
(Part H)
Active movement in bed with muscles stretching and tensing is encouraged early.
When breasts permit, face-down lying is advocated. From sixth to eighth day, patient
begins abdominal muscle strengthening. Clasping the hands behind neck, the head, and
shoulders, are raised to look down at the toes and this position is held for increasing
periods of time. As strength improves, this is supplemented with leg-raising exercises
such as "scissors" and "bicycle." The hands are placed palms down under the buttocks
for support, the heels are held six inches off the floor during all exercises and counts up
to 20 and 30 of each are done. These are probably the most important exercises a
woman can do, for they not only restore the tone of abdominal musculature for future
labours (not to mention cosmetic effect) but in the low back pain of forward lumbosacral strain (sway back) which occurs in a very high percentage of post-partum
women, they shorten the anterior abdominal wall and take the strain off the anterior
aspect of the lumbo-sacral joint.
Most patients nowadays insist on getting up tenth day and home by twelfth. This
is all right if they stay in bed most of the day during the following week at home,
while involution becomes more complete. During this period, they should increase
their exercises and may supplement them with knee-chest position (separating vulva to
allow air to enter the vagina), and the monkey walk.
Another exercise should now be started, which is hardly less important than the
abdominal ones. Its purpose is to restore pelvic floor muscle tone. It consists of a
tightening of the sphincter muscles of rectum, vagina and bladder, and a "drawing up"
or contraction of the levator ani muscles. This is done in one effort, is maintained as
long as possible and is followed by_ relaxation, then repetition. Patients should be
encouraged to do this several times ~ a day. Anyone who has watched the marked
strengthening effect of this exercise on the whole pelvic muscle structure will advocate it.
The day of the patient's discharge from hospital, pelvic examination should be done.
The condition of the episiotomy and vaginal walls, the state of parametria and position
of uterus may be noted, and it also gives one a chance to stress the treatments or exercises most needed.
At about six weeks, patient should return to the doctor's office, for a complete
physical examination, and the points which should be particularly noted are: General
Page 36
Up condition, weight, blood count, haemoglobin, condition of teeth, breasts and abdominal
muscles. The perineum, vagina and cervix are inspected and bi-manual palpation of
uterus determines its position, size, shape and mobility, as well as the state of the parametria and adnexa. If retroversion is not congenital, with short anterior vaginal wall,
a pessary may be introduced for two or three months to hold fundus forward,—lying
on face, knee-chest postures, and pelvic floor exercises to be stressed the while.
Cervix erosions may be treated with strong silver nitrate solutions but preferably
with cautery. All exercises should again be encouraged and patient should be brought
back again in one month, if any treatment has been given, for final check-up.
The breasts should not be neglected during the post-natal period. Heavy breasts
must be supported, and all patients should be given exercises to strengthen the fascial
attachments of the breasts to the underlying pectoral muscles. This is particularly
important during weaning, and will do much to restore the breasts to former tone and
o   ege o
f Ph
ysicians a
nd Su
President Dr. Wallace Wilson, Vancouver
Vice-President ! Dr. W. A. Clarke, New Westminster
Treasurer Dr. F. M. Bryant, Victoria
Members of Council—Dr. F. M. Aulo, Nelson; Dr. F. M. Bryant, Victoria; Dr. W. A.
Clarke, New Westminster; Dr. Thomas McPherson, Victoria; Dr. H. H. Milburn,
Vancouver; Dr. Osborne Morris, Vernon; Dr. Wallace Wilson, Vancouver.
Registrar ' Dr. A. J. McLachlan, Vancouver
Executive Secretary Dr. M. W. Thomas, Vancouver
The conditions necessary for the surgeon are four: first, he should be learned; second,
he should be expert; third, he must be ingenious, and fourth, he should be able to adapt
himself. It is required for the first that the surgeon should know not only the principles
of surgery, but also those of medicine in theory and practice; for the second, that he
should have seen others operate; for the third, that he should be ingenious, of good
judgment and memory to recognize conditions; and for the fourth, that he be adaptable
and able to accommodate himself to circumstances. Let the surgeon be bold in all sure
things, and fearful in dangerous things; let him avoid all faulty treatments and practices. He ought to be gracious to the sick, considerate to his associates, cautious in his
prognostications. Let him be modest, dignified, gentle, pitiful ,and merciful; not
covetous nor an extortionist of money; but rather let his reward be according to his
work, to the means of the patient, to the quality of the issue, and to his own dignity.
(From the Introduction to the General Chapter, Ars Chirurgica.)
The above is copied from a translation of the Ars Chirurgica published in Venice in
1546 and translated by William A. Brennan of Chicago in 1923. It was originally
written by Chauliac and completed in 1363.  An English edition was published in 1541. I
(The last sentence as regards fees is just as appropriate at the present time.)
Page 37
The Registrar has received a communication from the Commissioner,
British Columbia Provincial Police, informing him that when making investigations of thefts from doctors' cars it is found in a large percentage of cases
narcotics are included.
It is suggested, since this is the main reason for such theft and rummaging
in doctors' cars, that narcotics and hypodermic syringes be carried on the person
of the doctor rather than in his professional bag. If this practice were followed, it would eventually become known that narcotics cannot be found in
doctors' cars and such plunderings would be discouraged.
It is necessary to lay special emphasis on certain points in connection with
the prescribing of narcotics. These are constantly being overlooked by doctors,
and are absolutely vital.
1. All narcotic prescriptions must be written in ink.
2. They must be dated.
3. They must be signed bi full by the doctor.   Initials alone must not be
Medical men must recognize the fact that these rules are mandatory, and
there is no exception. Druggists who fill a prescription improperly -written are
breaking the law, and render themselves liable to fine or other penalty: and
we ourselves are similarly liable to penalties for breach of this Act.
Do not forget. A properly written, dated and signed prescription must be
in the hands of the druggist before he can fill it. There is no exception to this
(Signed)     A. J. MACLACHLAN, Registrar,
B. C. College of Physicians and Surgeons.
D. E. H. Cleveland, M.D.,
The Bulletin of the Vancouver Medical Association,
Vancouver, B. C.
Dear Doctor:
The principal object of the American Urological Association is "to encourage the study, improve the
practice, elevate the standards and advance the cause of Urology." The simplest way to impress upon
neophytes the value of true scientific work is by means of a material award. Hence, we would like to
have each year an outstanding medical paper that would warrant a $500.00 check, but if such is not
forthcoming we can make several smaller prizes. We are not interested in stereotyped theses for an advanced
degree unless they represent original work of potential value. The competition is open to all properly
trained urologists, and for that reason we would like to have this chance of a young man obtaining some
money at a period when it is badly needed, widely publicized, so that all may have an equal opportunity.
Please publish in your magazine the following notice: SHI
"Urology Award:—The American Urological Association offers an annual award 'not to
exceed $5 00.00' for an essay (or essays)- on the result of some specific clinical or laboratory
research in Urology. The amount of the prize is based on the merits of the work presented, and
if the Committee on Scientific Research deem none of the offerings worthy, no award -will be
made. Competitors shall be limited to residents in urology in recognized hospitals and to
urologists who have been in such specific practice for not more than five years.
"Essays shall be in the hands of the Secretary, Dr. Clyde L. Deming, 789 Howard Avenue,
New Haven, Conn., on or before April 1, 1941."
Yours very truly,
Chairman, Committee on Scientific Research.
Page 38
■s: mf
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Report presented to Annual Meeting by Dr.' Murray Blair, Chairman.
It is probably known to most medical men that at the outbreak of war the Canadian
Medical Association offered its services to the Department of National Defence. Its
object was two-fold:
First—To aid and advise in supplying competent medical care for the armed forces.
Second—To see that the civilian population did not seriously suffer because of medical enlistments.
Provincial Advisory Committees were set up in the various Divisions of the Canadian
Medical Association, and the Advisory Committee for this Division has been, I believe,
of some use to the District Medical Officer of this Medical Division No. 11. Certainly
we have had a harmonious relationship with that office at all times.
Your Ck>mmittee has met regularly during the past year, has been in constant touch
with the Central Advisory Committee, and has a contact member in Victoria who has
kept us in touch with the D.M.O.
Your Committee has entertained the D.M.O. as its guest some three times. It has
also entertained the Chief Surgeon Commander of the Navy, and the Principal Medical
Officer of the Air Force in this area. At each of these meetings we have placed the
facilities of our Committee before these men and have made plain our desire to be fo
assistance to all branches of the Armed Forces.
We have made it clear that we are an advisory body, not an enlistment committee.
It is not our function or aim to urge medical men to join the army. It is our duty,
however, I take it, to advise medical men of the need—and there is a need, a very grave
At a meeting of the Canadian Medical Association central committee in Winnipeg
in June of this year a statement was received, signed by the medical heads of the three
Armed Services.   I quote in part:
"1. The requirements in medical officers for the balance of the current year will be
approximately 350.   These officers are divided into two classes:
(a) For service in Canada—Approximately 140.
(b) For service overseas—Approximately 210.
The officers for service in Canada may be in categories "A", "B" or "C" and up to 55
years of age, or, in special circumstances, over. The officers required for service overseas must be in category "A" and should be preferably under 40 years of age.
"2.   It is becoming increasingly difficult to obtain medical officers and it is anticipated that during the next year it will be still more difficult.    There is approximately j
12% of all the doctors registered in Canada now in the services."
In view of the latter figure it might be of interest to review the enlistment figures j
for our own province. Much has been said and written about general enlistments— j
what about voluntary medical enlistments in this province? There are in Canada, in
round figures, 12,000 doctors. About 12%, or about 1400, have enlisted and are
engaged, full time, in one of the armed services. In this province there are some 750
on the active colls of the College—of these there are 130 enlistments among medical
men in this province, to date, or some 17% of our total enrollment. It is on the whole,
perhaps, a fair record, neither good nor bad.
Your committee will continue to function during the coming year.   It will, I hope,
continue to serve a purpose.    Again we emphasize the need—350 medical enlistments j
are needed in the armed forces in the next few months.    Medical men may contact j
either the office of the D.M.O. at Victoria or our Executive Secretary, Dr. Thomas, at I
Vancouver, for information.
Page 39
By Dr. W. D. Keith.
(Delivered before the Vancouver Medical Association October 7th, 1941)
Sub-total thyroidectomy properly performed is, in the opinion of the majority of the
medical profession, the best therapeutic measure yet known to overcome hyperthyroidism.
However, in considering this operation it is important as physicians and surgeons
that we have as thorough a knowledge as possible of the histo-pathological changes which
take place in other organs than the thyroid gland in this disease.
A generation ago Sir James Barry, the leading thyroid surgeon of his day in London,
considered that the thymus gland was really a lymph gland draining the thyroid gland.
Berry stressed the fact that all cases coming to post-mortem after an operation for
exophthalmic goitre had a much enlarged thymus gland.
Whartin of Ann Harbour believed from his study that there existed a thymico-
lymphatic type or condition which forms the soil from which, under certain conditions,
toxic goitre springs, and that this constitution is congenital and can be recognized
Quite a number of studies of the changes in the thymus gland in hyperthyroidism
have appeared from time to time. Margolis in the Mayo Clinic 1930 volume reports a
study of the thymus gland in toxic goitre in 8 5 cases which came to post-mortem after
operation in that clinic. Fifty-five of the cases were exophthalmic goitre, forty-seven
of which showed varying degrees of hyperplasia of the thymus gland. Thirty cases were
associated with toxic adenoma and fourteen of these showed thymic hyperplasia.
In a general sort of way the more acute and recent the disease the more active and
widespread the hyperplasia of the thymus.
Of the eight cases of exophthalmic goitre which failed to show any hyperplasia of
the thymus, four had a thymus gland much larger than normal; one of these weighed
62 grammes, the greatest weight of any of the glands in this series. This greatly enlarged
gland contained practically no glandular tissue, merely areolar, fatty and fibrous tissues.
Thus it is important to bear in mind that because a thymus gland is enlarged is no
indication that it is hyperplastic.
The hyperplasia of the thymus in cases of toxic adenoma of the thyroid was not so
extensive or complete as that found to be associated with exophthalmic goitre. This
finding seemed to be consistent with the longer, slower toxic history of hyperthyroidism
in toxic adenomatous goitre.
Thus from the above study and from similar findings in other reports one must
conclude that there is a very close relationship between the thyroid and thymus glands.
The other organ besides the thymus gland which shows histo-pathological changes in
this disease is the liver.
In an article in the Annals of Internal Medicine, vol. 7, 1933-4, D. C. Beaver and
J. dej. Pemberton report a study of 107 cases of exophthalmic goitre which came to
post-mortem during a period of ten years. The changes found in the liver were divided
into: Acute—fatty; necrotic—central or focal; Chronic—simple atrophy; toxic
cirrhosis; subacute toxic atrophy.
The authors state the lesions in the liver are due to thyroid intoxication, as they are
intimately related in their severity to the intensity and duration of the disease.
In all cases in which there was a crisis or near crisis, acute hepatic lesions were found.
Very often the liver exhibited both acute degenerative and chronic atrophic changes
side by side or at least in the same liver.
In November, 1933, Annals of Internal Medicine, p. 543, C. V. Weller reports a
study of hepatic pathology in exophthalmic goitre.    Changes in the liver from a slight
Page 40
« degree of chronic hepatitis to a widespread necrotizing and degenerative process—glis-
sons islands enlarged; lymphocytic infiltration; patchy interlobar fibrosis—were found,
the main lesion being patchy chronic parenchymatous interlobular fibrosis.
In this study of forty-four cases, the liver was normal in only six, hepatic changes
were moderate in sixteen and marked in twenty-two.
In view of these observations the condition of liver function should be a most
important consideration in the success of the operation for hyperthyroidism.
Lahey even suggests that liver failure is the main cause of thyroid crisis which is
one of the most serious complications following thyroidectomy for hyperthyroidism.
A liver function test which is considered fairly satisfactory was described by Battels
in 1938. It is known as the hippuric acid test. Six gm. of benzoic acid are given and
in four hours three gm. of hippuric acid should be excreted by the kidneys. Battels
reported results in 148 cases of hyperthyroidism. Only eight cases were normal by this
test on admission.
The absence of weight loss or the adrninistration of iodine for some tune prior to
admission was associated with normal liver function.
Another organ of the body which is directly affected by hyperthyroidism is the
heart. Tachycardia, usually with an increased pulse pressure, is one of the most constant symptoms of hyperthyroidism. The cause of the increased heart rate is probably
the result of the direct stimulation of the heart muscle by a very much increased output
of normal or altered thyroid secretion.
If the hyperthyroidism is not diagnosed and continues for months and years, besides
tachycardia, a slight enlargement of the heart not infrequently occurs, cardiac arrhythmias may develop, particularly auricular fibrillation, and finally congestive heart failure
may result.
Pathologists have found no specific pathological changes in the heart tissues due to
this disease. Many pathologists have described segmentation and fragmentation of
muscle fibres, increase of fibrous tissues, fatty degeneration and lymphocytic infiltration
as being found in the heart in hyperthyroidism, but these changes have also been
described as occurring in other diseases.
It seems to be generally agreed that great enlargement of the heart rarely or never
occurs as the result of uncomplicated hyperthyroidism. Parkinson and Cookson found
by orthodiagrams and teleroentgenograms that cardiac enlargement—usually slight or
moderate—occurred in 45% of uncomplicated hyperthyroidism.
Kepler and Barnes state: "In 89 cases of fatal hyperthyroidism without evidence of
hypertension or complicating heart disease, the weight of the heart in 49% exceeded
maximum standard values calculated on the basis of the patients prior to illness.'*
Physiological research has shown that the heart muscle in hyperthyroidism contains
very little glycogen, nad this may have a weakening effect on the heart muscle itself.
Ingenious experiments by various investigators have shown that the tachycardia of
hyperthyroid animals persisted after the heart had been isolated from the peripheral
vascular tree and from all neural pathways.
Cecile, Markowitz and Yates further showed that thyroxine causes tachycardia to
occur in fragments of the heart muscle removed from two-day-old chick embryos,
before any nerve cells within the heart or neural pathways have been formed.
Now, with this mental picture of the pathological changes in the thymus gland and]
the liver, and the physiological and metabolic changes which occur in the heart, we are
in a better position to evaluate clinical conditions properly as they present themselves inj
In 1922 Plummer found that iodine given in large doses daily lowered the B.M.R
and the pulse rate within a period of from 7 to 10 days after beginning its administration, in cases suffering from hyperthyroidism.    It was then widely accepted that in
Page 41
4 1925-9—Lahey Clinic,    .72%.
1902—Kocher Clinic, 6.5%.
1915—Kocher Clinic, 1%.
deaths—0.3 3%.
this way sub-total thyroidectomy could in almost all cases be done as a one-stage operation, on or about the tenth day after the start of the administration of iodine. It was
felt also that a great deal of the danger of the operation had been overcome.
Let us now consider the mortality rates reported from various surgical clinics where
diseases of the thyroid receive special consideration.
During the last forty years the mortality rate for thyroidectomy in toxic goitre has
gradually declined, as the following reports will show:
1894-1907—Over 10% in 20 hospital reports.
1908-1917—Over    5% in 7 out of 28 hospital reports.
1907-1920—2-5% Mayo Clinic.
1921—3.39%Mayo Clinic.
After the introduction of iodine by Plummer in 1922:
1922—Mayo Clinic, 1.74%. 1929—Crile Clinic,    .6%.
1924—Mayo Clinic,    .84%.
1925—Mayo Clinic, 1.1%.
1926—Mayo Clinic,    .83%.
1939—Richter, H. M.—900 cases with 3
1939—Young reports from two general hospitals in Duluth—St. Mary's and St.
Luke's—2569 thyroidectomies for Hyperthyroidism with 54 deaths—a mortality rate of 2.1%.
In spite of iodine Von Eiselberg reported 6% mortality in 1930. And Dunhill of
London 2.7% in 1930. Joll states that the mortality for sub-total thyroidectomy for
toxic goitre should not be more than 1%. Bevan states that he believes that the average
mortality in the U.S.A. is between 3 and 5%, but he recognizes that to a large extent
two or more stage operations have been done away with and cases which were formerly
considered inoperable are now in the operable class.
From the above statistics one realizes that there were measures of great value in the
safe conduct of thyroidectomies practised before the introduction of iodine in the
preparation for this operation.
Let us now pursue the problems which here and there occur in the preparation of
patients with toxic goitre for thyroidectomy by the administration of iodine. Certain
cases of hyperthyroidism are refractory to iodine—by that is meant that even with the
administration of iodine in adequate dosage the symptoms become more pronounced and
the metabolism rises—a general increase in the tempo of the disease results. It is uncertain whether the refractoriness of the disease is due to iodine or to the general progress
of the disease.
Thompson states that the administration of even 100 min. of Lugols solution is
of no more value in the refractory period than the use of smaller doses.
Many hold to this belief now, though I understand that at the Mayo Clinic large
doses of iodine are still found of help in some of these cases.
However, it has been shown by a number of observers that if the iodine be discontinued for 4-6 weeks and then given, the metabolism and pulse rate respond satisfactorily.
Thyroidectomy is not an emergency operation and therefore should be made to fit
in with a satisfactory condition of the patient.
The 10 days or so of pre-operative administration of iodine has practically no effect
on the thymus gland or the liver.
Lahey has remarked that "it is distinctly possible to have such an apparent improvement following the use of Lugol's solution that one is tempted to do a complete operation only to have the patient die in extreme hyperthyroidism."
Lahey and Clute reported cases which died in crisis before operation could be taken,
in spite of active measures, including iodine in large doses.
Page 42
f*J< VW%
'.. w,
Therefore we must realize that there is more to the treatment of toxic goitre than
the administration of iodine and the performance of sub-total thyrodiectomy.
In regard to the dosage of iodine given preoperatively, it has been shown by Thompson et al that large doses must be given from the beginning, that doses smaller than
6 mg. a day are ineffective.
Probably no article in recent years, on account of its clarifying candour, has done
more to reduce the mortality in thyroidectomy in the average general hospital than that
by "w% O. Thompson et al—{Arch. Intl. Medicine, Dec. 1938, p. 217), and I cannot
do better than quote freely from this article.
Cook County Hospital in Chicago has 3200 beds and its patients are the poorest in
the city. Disease is seen in its most advanced stage as a rule and in the case of toxic
goitre a large number of severe cases of long standing in markedly undernourished individuals had to be treated.
During 1931 there were 16 deaths in 159 thyroidectomies for toxic goitre—i.e.
1% mortality.
The factors responsible were inadequate pre- and post-operative care and operators
without special training in this procedure.
The usual ward diet for seven to ten days, with iodine, regardless of other conditions,
was given.   The B.M.R. tests were inadequately carried out.
In the latter part of 1932 the authors took charge of half of the toxic thyroid
cases in the hospital. Each case was treated as an individual problem. Surgery was
withheld till the condition of the patient justified operation, no matter how long this
took.    The surgeon who operated was specially trained in this field.
It is our contention that the battle is practically won or lost before the operation is
begun, and that in most cases a post-operative crisis means inadequate pre-operati^
During 1932-7 there were 54 deaths following 572 thyroidectomies—a mortality of
9.4%, and during the same time 9 deaths followed 317 thyroidectomies for toxic goitre
in patients under their care—a mortality of 2.8%.
In 1935-7 there were 19 deaths in 249 operations on patients not under their care—
a mortality of 7.6%. During the same time in cases under their care there were 188
thyroidectomies with 3 deaths—mortality 1.6%.
Of the nine deaths which occurred in this series eight had exophthalmic goitre and
one toxic adenoma.
The causes of death were: Thyroid crisis, 2; pneumonia, 3; heart disease, 1; sudden
respiratory failure, 3.
In two of the cases of sudden respiratory failure there was bi-lateral vocal cord
paralysis. The other death from this cause was due to a hasmatoma pressing on a collapsible trachea.
These three deaths were purely surgical complications and could have been prevented
by early tracheotomy in two of the cases and the third by early recognition of the
seriousness and nature of the condition by a nurse experienced in the possible serious
complications that may follow thyroidectomy.
A more careful search for upper respiratory infection prior to the operation might
have prevented the two deaths from pneumonia.
I might add that Thompson considers it most inadvisable to do a thyroidectomy till
at least two weeks have elapsed since the occurrence of an upper respiratory infection,
otherwise one is courting a possible pneumonia.
The two cases dying from thyroid crisis would probably have been saved by more
careful preparation.
The rather sudden death of a man of sixty years of age ten days after operation was
probably unavoidable.
In St. Paul's Hospital, from 1935-9 inclusive, 263 operations were performed on the
thyroid gland by 35  different surgeons;  216  of these were for hyperthyroidism, all
Page 43 having microscopical evidence of an over-active thyroid. Some, of course, were of a
very severe grade; others presented moderate or even slight degrees of hyperplasia.
Of the 216 cases with hyperthyroidism, 207 had the usually performed sub-total
thyroidectomy and 9 had a lobectomy or partial resection of the gland.
I might add that of the remaining 47 of the 263 cases operated on for thyroid disease during the above mentioned period, 17 had a partial removal of the gland. Three
cases proved to be carcinoma of the gland, one tuberculosis of the thyroid, and one the
so-called woody thyroid. The microscopic study of the 42 remaining cases showed them
to be either colloid goitres or simple adenomatous thyroids or goitres of an adenomatous
type undergoing degenerative changes—cystic, calcareous, or fibrous.
Of the 216 thyroid operations for toxic goitre there were seven deaths—a mortality
rate of 3.2%.
It is well for us to consider the deaths in this series, seven in all:
(1) Female, aet 44, was admitted one day and operated on the following day and
died a few hours after the operation.
This patient had a severe grade of hyperthyroidism and, as post-mortem revealed, a
myocarditis, chronic pleuritis, and an enlarged thymus gland.
(2) Female, aet 59, was in the hospital 13 days and then operated on. The patient
died the day following a sub-total thyroidectomy.
The post-mortem showed general arterio-sclerosis and myocardial degeneration.
According to the records of this case cardiac enlargement was noted in the history and
an electrocardiogram was done four days before operation: this report read myocardial
changes probably coronary sclerosis, auricular extrasystoles—urinary report, albumin
plus 2.
(3) Male, aet 37. Immediately after the operation there seemed to be a great deal
of thick mucus in the larynx. The pulse was very rapid though Lugol's solution was
given in large doses per rectum, death occurred about twenty-four hours after the
operation. A trachetoomy was performed a few hours before death without any
apparent improvement.
Post-mortem—Lungs airless, thymus gland 72 gms., spleen three times normal size.
Considerable thick mucus in. the larynx and trachea—one small branch of the left recurrent laryngeal nerve was included in a suture. Mediastinal emphysema and collapse
of the lungs.
(4) Female, aet 46. Died two days after the operation. This was a death which
followed a complication in the actual technique of the procedure. In the removal of a
substernal projection of the gland, the thyroidea ima artery was seized close to the aorta
and as the artery was pulled on in some way by a movement of the forceps before being
tied, it was torn off at its point of origin from the aorta and could not be secured again.
The wound had to be packed, mediastinitis ensued and death occurred in a day or two.
(5) Female, aet 48.    Died within a few hours of the operation.
The patient was admitted to the hospital with a fractured right femur. The pulse
was 136 on admission and continued around 120. A diagnosis of hyperthyroidism was
made and eight days after admission a thyroidectomy was performed. No post-mortem
was obtained.
(6) Female, aet 43. Died six days after the operation. There was a certain amount
of oozing on her return to the ward.    Six days before the operation the N.P.N, was 47.
Laboratory report—occasional areas of hyperplasia; extensive cystic degeneration.
(7) Female, aet 56. Died a few days after the operation. Death was considered
due to sudden cardiac failure. This patient had quite a severe grade of hyperthyroidism
over a period of years.
The operation was a difficult one as there was a large substernal portion of the gland.
Considering the seven deaths in retrospect as if they had occurred in one's own
practice, one would feel that some of the deaths might have been avoided.
Page 44
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Thee cases where myocardial degeneration is known to be present should not be
operated on simply because the patient elects to take the chance.
In my opinion careful meticulous physical examination should be made by a physician
as well as the surgeon so that a combined opinion should decide for or against the
advisability of such a severe undertaking.
The method not infrequently followed in Vancouver is for a patient suffering from
thyroid disease to be referred by an out-of-town or local physician to a surgeon who
has an excellent reputation for his skill in thyroid surgery. Or the patient may go to a
surgeon whose reputation is known to him. Or thefamily physician who makes the
diagnosis in the first place may feel himself competent to undertake the operation himself. The operator then takes full charge and when he things the patient is ready, having
been prepared usually in the hospital, the operation is performed. The reports from the
metabolic and where thought necessary from the electrocardiographic departments,
are considered as sufficient guides. Very seldom is the opinion of a physician as to the
advisability of the operation been sought.
In recent years, owing to a wider knowledge amongst the medical profession of the
signs and symptoms of hyperthyroidism and the freer use of the basal metabolism
apparatus, many more patients of over 60 years are recognized as suffering from this
Angina pectoris, hypertensive heart disease, arterio-sclerosis, chronic nephritic, prostatic hypertrophy and diabetes may be complicating factors. Kepler and Barnes, in a
study of a series of cases of fatal heart failure associated with hyperthyroidism, found
that one-third of the cases had no other disease than hyperthyroidism, one-third had mild
hypertension or minimal independent cardiac disease, and another third had marked
hypertension or severe valvular lesion or coronary disease.
Therefore in two-thirds of the cases of congestive heart failure associated with hyperthyroidism the patients will be greatly improved by the removal of the burden of the
diseased gland.
In the preparation of the thyrocardiac for possible operation Pemberton states that'
digitalis is very seldom indicated and should be given with caution to elderly patients.
Rest, partial or complete, high caloric diet and Lugol's solution for two or three weeks
are usually sufficient to prepare these patients for operation. Where congestive failure
is present a moderately restricted intake of fluids, with salt restriction and the use of
mercurial diuretics where necessary, will often result satisfactorily enough to permit
operation. Where auricular flutter is present quinidine, given cautiously at first in order
to avoid an idiosyncrasy, should be tried.
Barnes sums up his ideas on the operability for thyroidectomy as follows: "It seems
to me that the operability of such patients can be determined on a rather simple basis,
namely, that any patient with cardiac failure and hyperthyroidism may become an
acceptable risk for thyroid surgery, provided compensation can be restored by rest and
therapeutic measures, and provided further that this compensation can be maintained for
at least a few days with the patient on a moderate ambulatory programme."
St. Paul's Hospital, around which this paper particularly is built, possesses an operating department equipped with every essential necessity for the successful conduct of
thyroid operations. The anaesthetic department is under skilled and specially trained
physicians, the hospital laboratory department has supervision of all solutions for intravenous therapy and is equipped with an up-to-date metabolism apparatus and also an
electracardiographic apparatus.
The only other task which the hospital might include in its responsibilities is to see
that a nurse conversant with the complications and emergencies liable to follow a thyroidectomy is in charge of the patient for the first 24 hours subsequent to operation.
This is important, since there are certain immediate complications, e.g., haemorrhage,
difficulty in breathing from damaged recurrent laryngeal nerves or pressure from a
Page 45 a
blood clot on a soft trachea or tracheitis with thick mucus in addition to partial cord
paralysis—these conditions as well as the early symptoms of thyroid crisis should command instant recognition and treatment if lives are to be saved.
In conclusion, there are certain general guiding points which should be carefully
considered in undertaking the operation of sub-total thyroidectomy for toxic goitre:
(1) Thyroidectomy is never an emergency operation. Do not be in a hurry to
operate. The preparation for this operation should have no set time. It may take a
week or several weeks. Iodine has not altogether done away with two or more stage
operations—a procedure which may be life-saving here and there.
(2) The signs and symptoms necessary to permit operation are: A definitely lowered
metabolism; a pulse rate not too rapid; a gain in weight; a lessening of the nervous
symptoms; an absence of upper respiratory infection. Follow Thompson's advice to wait
two weeks after the subsidence of an upper-respiratory infection before operating.
(3) Each case should be meticulously examined by an internist conversant with the
prolbems of thyroid disease before operation is decided upon. Close co-operation should
exist between the surgeon and internist during the pre- and post-operative care of the
(4) Nurses specially trained in the post-operative complications which may arise
after a thyroid operation should be in charge for the first 24 hours after the operation.
By G. E. Trueman, M.D.,
In this paper the approach of the radiologist to the problem of biliary disease will
be outlined, and an attempt will be made to indicate what interpretation may be put on
the radiological findings, both as regards diagnosis and choice of treatment.
The principle of visualization of the gall-bladder is simple. The dye is given orally,
is absorbed in the small bowel, and excreted exclusively by the liver. The dye passes
into the gall-bladder where it is concentrated in the same manner as bile until it is of
sufficient density to cast a shadow on the X-ray film. Following a fatty meal, the gallbladder empties, and bile and dye pass through the duct system into the duodenum.
This process can be studied radiologic ally.
The commonly recognized contra-indications to the use of dye are advanced cardiac
disease, asthma, cachexia, acute infections of the liver and gall-bladder, and hepatic
The question is often asked, "Is jaundice a contra-indication to cholecystography?"
The answer would seem to be that jaundice itself is not a contra-indication unless it be
accompanied by hepatic insufficiency of a degree which can be detected by the more
reliable liver-function tests. In the presence of jaundice, cholecystography may be of
value in differentiating between obstructive and hepatogenous jaundice. In three series
of cases1, tested in the presence of jaundice, the total number of cases of fcatarrhal
jaundice or hepatitis was thirty-two; of obstructive jaundice, fifteen. Of the thirty-
two "medical" cases, the gall-bladder was visualized in twenty-five. In the fifteen
obstructive cases, the gall-bladder was visualized only once, and in this case revealed a
gall-bladder containing a great number of non-opaque stones. Later work2 has shown
that in "medical" jaundice where the gall-bladder is visualized, it emptied normally
Page 46
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under the stimulus of the fatty meal, but. in small number of cases of obstructive
jaundice, the gall-bladder failed to empty after the fatty meal and the shadow disappeared gradually, presumably by absorption of the dye through the gall-bladder wall.
Successful visualization, then, followed by normal emptying, points to hepatitis or
catarrhal jaundice as the cause of the jaundice. Successful filling with failure to empty
suggests obstructive jaundice. However, failure of the gall-bladder to visualize in the
presence of jaundice cannot be used for diagnosis at all because one does not know
whether the dye reached the gall-bladder.
In addition to the above considerations, the problem involves the differentiation of
stone, cholecystitis, dyskinesia, and, less commonly, other diseases from each other and
from a normal gall-bladder. Radiological opinion is built on four types of evidence,
namely, stone, concentration of the dye, rate of emptying, and changes in the size and
shape of the gall-bladder and changes in the size of the ducts.
A stone may be diagnosed directly or indirectly. The demonstration of a stone by
direct means is dependent upon the presence in the stone of radiopaque substances,
usually calcium, and the dye is of value in these cases only insofar as it enables one to
distinguish between intra-cholecystic and extra-cholecystic opacities. The common
extra-cholecystic opacities are calcified glands and renal calculi.
Gall-stones may be demonstrated indirectly only by the use of the dye method and
only in cases in which the dye is concentrated to a degree sufficient to throw a shadow
on the X-ray film. In such cases, the evidence of the stone is to be found in a negative
shadow produced by a radiotranslucent stone occupying a space which would otherwise
be occupied by the radiopaque dye. Table I3 exhibits two series of cases in which the
presence of stone was verified at operation, and in which a previous gall-bladder visualization had been attempted. The table shows with accuracy which may be expected
in a particular type of case, namely, that type of case which the surgeon deems it
advisable to treat surgically. These percentages will be influenced by the care and skill
of the radiologist and by the surgeon's selection of cases.
The absence of a shadow outlining the gall-bladder is presumed to indicate loss of"
the gall-bladder's physiological function of concentration and may be considered presumptive evidence of cholecystitis. There are several alternative explanations which;
must be ruled out before the diagnosis of chronic cholecystitis can be made with certainty. The patient may have failed to take the dye, or having taken it may vomit, or
be purged of it, or it may not be absorbed. If bis liver function is depressed he may
excrete it not through the liver but through the kidneys. The duct system may be
blocked so that the dye does not reach the gall-bladder or the gall-bladder may be
obliterated by non-inflammatory disease. The dye may pass into the bowel through an
inconstant sphincter of Odd! or cholecysto-colic fistula. Table II presents a comparison of the X-ray diagnosis and the clinical diagnosis in twenty-seven cases. Bearing
in mind the pitfalls numerated above, the cases in which a presumptive diagnosis of
chronic cholecystitis was made incorrectly were investigated to determine the source
of error.
Normal concentration is presumptive evidence of a normal gall-bladder. Table III
is an analysis of thirty-six cases in which cholecystitis was eliminated radiologically.
The subsequent clinical course indicated that the cholecystographic conclusion was cor-
rest in twenty-five cases and clinically incorrect in eleven cases. The basis of the
inaccuracy of the test was the persistence of biliary dyspepsia which, as we shall see,
in many cases is not relieved by cholecystectomy, so that in these eleven cases there is
included a number in which the negative diagnosis may have been correct.
The diagnosis of stone is one matter; the expression of an opinion regarding the
probability of existing disease apart from stone is another. The radiological diagnosis
of chronic cholecystitis is frequently reported as heing inaccurate in upwards of 95%
of cases. This accuracy is of value in distinguishing between those cases which must
be considered normal and those which have chronic cholecystitis.    Beyond this, it is of
Page 47 little value. It does not indicate the severity of the disease, whether treatment should
be medical or surgical, or what results may be expected from either form of treatment.
Hodges and Lampe3 report a series of cases as outlined in Table IV, where the radiological and the pathological finding was not the all-inclusive term "chronic cholecystitis"
but "major inflammatory disease readily recognized in the gross or microscopic findings
beyond question of dispute." By these standards the test is less accurate (than 95%)
but it lends itself to more direct clinical interpretation.
Kunath3 reports an analysis in which a series of one hundred cases of stone-less
gall-bladder was compared with a similar series of cases in which stones were present
at operation. The stone-less cases showed a greater morbidity, a higher post-operative
mortality, and only about half as many cures. The stone-less cases were analyzed carefully from the standpoint of cholecystography evidence and also pathological changes
present in the gall-bladder wall, but little help was offered from either of these sources
in regard to the prognosis following cholecystectomy. In general, the end result seemed
to be better as the pathological changes became more marked. From this the radiologist
must conclude that the demonstration of stone is all important and that the syndrome
of "biliary dyspepsia" is related not so much to pathological change in the gall-bladder
as to disturbed function of that organ together with the rest of the extra-hepatic biliary
tract and every endeavour should be made to increase the radiological and clinical
accuracy of this diagnosis. Radvin3 writes in a similar vein: "The end results of
cholecystectomy in the absence of stone are so bad that surgeons now realize that regardless of the roentgenological evidence and the pathological findings that in over one-half
the cases -operatod upon the cause of the patient's symptoms was not to be found in the
Let us refer again to the eleven cases in the Vancouver General Hospital series which
showed normal concentration and in which biliary dyspepsia persisted. The clinical and
radiological diagnosis which should be made in this type of case is not well understood.
Until recently infection has been considered to have played a major, if not indispensible,
role in the production of biliary disease. In the last decade a considerable amount of
new work has been done in an attempt to show that the major role is played by stasis
rather than by infection. These workers contend that stasis is the end result of a disturbance of motor function or dyskinesia of the gall-bladder of which three types have
been described: (1) hypotonic, (2) hypertonic, and (3) reflex hypertonic. These
dyskinesias have definite clinical signs and symptoms when they occur in their pure form.
Radiologically, they present the features shown in Table V. The diagnosis of these
conditions is being studied at the Outpatient Department Gall-Bladder Clinic. Our
department has been co-operating in this study. An attempt to correlate the clinical
findings and radiological findings has so far met with only a moderate degree of success.
In summing up, it may be said that the hypothesis of dyskinesia seems to be a rational
one, there is considerable clinical, radiological, and therapeutic evidence to support it,
and it provides, so far as one can determine, the only explanation for a large number of
cases which radiologically and pathologically do not have cholecystitis but who do have
persistent biliary dyspepsia. Workers4 supporting this hypothesis report an evidence of
1 to 15% of all biliary disease.  The treatment of this type of case is medical.
The hypothesis of biliary dyskinesia can be carried one step further. If the biliary
dyspepsia can be explained on the basis of malfunction of the extra-hepatic biliary tract
which is organically normal, may not the biliary dyspepsia which accompanies a case of
known chronic cholecystitis be duetto the biliary dyskinesia which preceded and may
still accompany the chronic cholecystitis. The removal of the gall-bladder would not,
then, remove the cause of the patient's symptoms. In other words, a clinical and
radiological diagnosis of chronic cholecystitis may be correct and yet the cause of the
patient's symptoms is a derangement of the motor function of the whole of the extra-
hepatic biliary tract.
The diagnosis of cholesterosis5 of the gall-bladder is not commonly made. Clinically
and radiologically, it may be confused with the diagnosis of biliary dyskinesia and must
Page 48
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be differentiated. Most cases complain of indigestion, gas and distress after meals.
Jaundice and colicky pains are absent. The condition is almost entirely confined to
women and is frequently seen in relation to a recent pregnancy. The cholecystogram
shows a good gall-bladder shadow. The gall-bladder is seen to be much more active
than normal, particularly if cholesterol stones are present. The emptying may be
extremely rapid.
The interpretation of a "faint gall-bladder shadow" is very difficult. In fact, it is
difficult sometimes to determine what is a faint shadow and what is a normal shadow,
even for an experienced radiologist. According to Hodges and Lampe's3 figures, 60%
of gall-bladders having a faint shadow show major inflammatory change. On the other
hand, some authorities6 feel that if the oral administration is used and a faint gallbladder shadow is obtained, the gall-bladder should be checked by the intravenous
method and that a faint shadow obtained in this way warrants the radiological diagnosis
of a pathological gall-bladder. The contra-indications to the intravenous method are
more rigid. The dye solution must be freshly prepared, diluted in at least 200 c.c. of
fluid, given over a period of twenty minutes, and followed by another 100 c.c. of fluid.
Kirkland suggests the following plan for reporting the cholecystographic findings:
(1) Normal visualization without stone.
(2) Normal visualization with stone.
(3) Faint visualization without stone.
(4) Faint visualization with stone.
(5) Non-visualization without stone.
(6) Non-visualization with stone.
It is further suggested that the gall-bladder be described as large, medium or small,
hypertonic or hypotonic, and that an estimation of the amount of emptying at one and
a half hours and, if necessary, at three hours after the adrninistration of the fatty meal
be made.
In concluding, I would like to express my appreciation to Dr. B. J. Harrison for his,
personal interest and for the use of his library.    I wish to thank Dr. Perry, with whom
I reviewed the Outpatient charts.    I am indebted also to Mr.  Fish of  the Records
Department, to Miss Roberge for the preparation of the slides and to Miss Ross for her
valuable assistance in the preparation of the manuscript.
Table I.
No Dye Shadow  88
Dye   Shadow ;  33
Total  121
Stone Falsely Reported  2
Table II.
Cholecystitis  diagnosed  correctly 16 cases
Cholecystitis   diagnosed  incorrectly j 11  cases
Source of Error:
dges & Lampe
. G. H.
Gall-bladder removed	
Portal  cirrhosis	
Catarrhal jaundice	
Carcinoma  of  glall-bladder..
Widespread  tuberculosis  I
Senility .J 1  case
Duodenal  ulcer 2
Renal calculus 1
Steatorrhcea 1
Dyskinesia 1
Table III.
1. Cholecystitis   eliminated   correctly 25
2. Cholecystitis   eliminated   incorrectly 1 11
The basis of Group 2  is  the persistence of biliary  dyspepsia,  which  may be  due to
cholecystitis or dyskinesia.
Page 49 >m
Table IV.
Cases      Major Disease %
No Dye Shadow —. 131                 104 8 0
Poor Dye Shadow 23                   14 61
Normal  Dye   Shadow '.       44                     7 16
Table V.
Roentgenological   Characteristics Hypertonic Type Atonic Type
1. Concentration    Normal. Poor.
2. Size Normal. Long and thin.
3. Emptying after fatty meal    Delayed. May be delayed.
4. Ducts dilated Reported in some cases. Probable, though none reported.
5. Stomach H~rperesthenic  and  empties   rapidly      Hypoesthenic and empties
unless   there   is   associated   pyloro-       slowly,
[ Rudsil: Gall-bladder Visualization in Jaundiced Patients.   Jour. Amer. Med. Assoc.,  1930, 95:1425.
1. \ Foley: Cholecystography in Jaundice.   Med. Clinics of North America, 1933, 17:467-472.
[jacobi: Glucose Tolerance as a Diagnostic Aid in Jaundice. Surg., Gyn. & Obst., 1936, 63:293-297.
2. Foote and Carr: Differential Diagnosis by Roentgen Ray.    Surg., Gyn. & Obst., 1936, 63:570-575.
3. Hodges and Lampe:  A Comparison of Oral  Cystographic Findings  and  Proved Evidence  of  Gall
bladder Disease.   Amer. Jour. Roentgenology & Radium Therapy, 1937, 37:145.
4. Hill: Functional Disorders of the Extra-Hepatic Biliary System, Biliary Dyssynergia or Dyskinesia.
Radiology, 1937, 29:261-275.
5. Levene, Lowman and "Wissing: Roentgen Disgnosis of the Strawberry Gail-Bladder.   Radiology, 1940,
[ Scott and Moore:  Consideration of Faint  Gail-Bladder  Shadows  in Intravenous  Cholecystography.
6. \ Amer. Jour, of Surgery, 1938, 40:157-161.
1 Newcomber: The Twenty-four Hour Gall Bladder.    Radiology, 1940, 3 5:575-583.
Department of Radiology, Vancouver General Hospital.
Golf is a form of work made expensive enough for business men and doctors to
enjoy. It is what letter-carrying, ditch-digging and carpet-beating would be if they
all had to be performed on the same hot afternoon.
The game is played on carefully manicured grass with little white balls and as many
clubs as the players can afford. A golf-course is 18 holes, 17 of which are unnecessary
and are put in to make the game harder. A hole is a tin cup in the centre of the green.
A green is a small parcel of grass costing about $1.65 a blade and usually located
between a brook and a couple of apple trees or a lot of unfinished excavation.
The game is to get the ball from a given point into each of the tin cups with the
fewest number of strokes and the greatest number of words. The ball must not be
thrown, pushed or carried. It must be propelled by about $200 worth of curious looking
implements, especially designed to provoke the owner. After the final or 18 th hole the
golfer adds up the score and stops when he reaches 87. He then has a shower, a pint
of rye, sings Sweet Adeline with six or eight other liars and calls it a perfect day.
Page 50
Dr    F    W.  Boak
Dr.   1R_   Rt  Howertson
Honorary Secretary
Dr.  T.. W-  Bassktt
Hnnnrarv   TreasUrpr
Dr.   P.   A.  C.   ConsTAMn
R. Y. Staneer
Hopkins Marine Station, Pacific Grove, Calif.
Delivered before Victoria Medical Society at their regular monthly meeting on Monday, Sept. 8, 1941.
I should like to start this evening by posing a seemingly very simple question which
I am sure every member of this audience would feel ready and able to answer—namely,
what are vitamins? Actually, during the forty-odd years which have elapsed since the
first recognition of the role of vitamins in health and disease, the answers given by
experts in the field would have shown remarkable differences from time to time.
During the earliest and longest stage the answer would have been that they were
mysterious and probably rather complex substances chemically, the omission of which
from the diet of animals produced pathological symptoms of various descriptions. In
Other words, vitamins were recognized solely by the symptoms resulting from their
deficiency in the diets of higher vertebrates.
The second stage, beginning about ten years ago, was ushered in by intensive work
on the chemical constitution and synthesis of the various vitamins. In an extremely
short space of time it has been shown that the vitamins are comparatively simple chemical substances, many of which can be synthesized without difficulty by the organic
chemist. An interesting and significant point which has emerged from these studies is
that the vitamins do not fall into any one chemical class; in fact, from the chemical
standpoint they comprise an extremely heterogeneous group of compounds.
The vitamin chemist of this second period could have given a chemical formula
representing, say, Vitamin Bl5 thus providing a valuable supplement to the previous
picture. However, he would have been completely unable to explain why the absence of
this simple organic chemical from the diet should have provoked the well-marked and
profound symptoms characterizing Bi deficiency in. the rat or in man.
Another great extension of our knowledge of the vitamins which took place about
the same time as the chemical work was the outgrowth of a new field—comparative
biochemistry. Comparative biochemistry is what its name implies: the analogue of
comparative anatomy. Just as the comparative anatomical concept strengthened and
unified our knowledge of zoology by directing attention to the underlying similarities of
structure in the various forms of animal life, so has comparative biochemistry illuminated and clasified the basic identity of function in living organisms. The statement
that the fundamental biochemical activities of man, of a flowering plant and of a bacterium are essentially similar will probably come as a shock to most of you, yet this is
a statement which few biochemists today would care to contest. The study of vitamins
provided at first a challenge, and later an important support for the concepts of comparative biochemistry. When the great Dutch biochemist Kluyver put forward his
ideas on comparative biochemistry in 1926, vitamins were only known to be of importance in a few of the vertebrates; yet it is obvious that if these ideas were correct, the
vitamins might be expected to play an equally important part in other forms of life.
The work of the last six years has shown that this is a fact.
Page 51 Let us first consider the case of the higher plants. It has long been known that
one can grow plants in a solution containing various inorganic substances alone. The
nitrogen requirements are met by nitrates or ammonia and in addition simple compounds
of P, Ca, Fe, S, K, and Mg, as well as traces of other elements, are needed. The carbon
requirements are met by CO2 of the atmosphere and energy is obtained by the utilization
of light through photosynthesis. From these, all the complex organic substances composing the structure of the living plant are produced. Can we then conclude that the
plant does not need vitamins? The evidence might be thought to. point to this, but
there is another possibility: namely, that the plant requires and uses vitamins just as do
animals, but is able to synthesize them itself. As a support for this view, there is the
fact that green plants are the major sources of many vitamins. Actually, it has been
definitely proven that some vitamins are necessary for the growth of plants. A few
years ago, biologists began studying the growth of plant roots in the absence of stem
and leaves. It was soon found (1) that under sterile conditions excised roots were
unable to grow in a simple salt solution such as supported the whole plant, even when
this was supplemented with glucose to compensate for the carbon and energy no longer
supplied by photosynthesis. However, the further addition of traces of vitamin Bj
provoked a prompt and rapid growth. This can only be explained by assuming that
the root did indeed require Bl5 but that under ordinary conditions the total needs of
this vitamin were synthesized by the stem and leaves.
The study of micro-organisms, particularly bacteria, has provided ample additional
evidence of the universal importance of vitamins. The work of the past twenty years
has demonstrated that the bacteria are a sort of vast biochemical melting-pot in which
can be found parallels to all the individual biochemical processes of higher forms of life,
as well as many reactions which are peculiar to bacteria alone. This is nowhere better
brought out than in the field of vitamins. Bacteria range from organisms with as
simple nutrient requirements as the higher plants to forms whose requirements are almost
as complex as those of man. Furthermore, it is often the case that one can find within
a single closely-interrelated group of bacteria a graduated series of increasingly complex
vitamin requirements. Interestingly enough, it is nearly always the parasitic or pathogenic forms in such a series which have the most complex requirements; rare indeed is
the parasite which will grow well on a simple medium. This has led to a new and fruitful concept of the nature of parasitism and other forms of organic interdependence, as
being conditioned by the loss of ability to synthesize vitamins and other needed nutrients.
For example, a bacterium which has lost the ability to synthesize vitamin Bi will be
forced into a closer relationship with other organisms which are able to produce this
substance themselves {e.g., higher plants) or else have access to external supplies {e.g.,
higher animals) and may thus become parasitic on them. Once an association of this
type has developed the abundant presence of other vitamins produced by the host
organism makes their synthesis by the parasite superfluous, so that a gradual functional
degeneration or simplification sets in, the bacterium sloughing off one part of its biochemical apparatus after the other, much as parasitic invertebrates throw off those
organs which are only of use in a free-living existence. This thesis was first put forward
by the French protozoologist Lwoff, and has been brilliantly developed in his "Etude
sur les fonctions perdues"4.
A striking experimental demonstration of the biochemical causation of symbiosis
has been provided by the Swiss plant physiologist Schopfer6. He made an intensive
study of vitamin Bi requirements among the yeasts and fungi, for many of which this
is the only vitamin which must be supplied preformed. Chemically, Bi consists of two
different ring compounds, pyrimidine and tbiazole, which are linked together. Schopfer
found that certain fungi did not require the whole molecule, but could synthesize it provided that they were given a fraction. Thus the organisms he studied could be graded
into a series as follows:
1. Can synthesize the entire Bi molecule.
2. Can synthesize Bi if given the pyrimidine half.
Page 52
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;?; «■■
3. Can synthesize B^ if given the thiazole half.
4. Can synthesize B^ if given both halves separately.
5. Must be provided with the whole molecule.
It occurred to Schopfer that organisms of groups 2 and 3 might be able to grow in
a medium completely devoid of Bi or its fractions by supplying each other with the
complementary, unsynthesizable half of the molecule. Consequently, he inoculated a
simple medium containing only glucose and the necessary inorganic salts with a representative of each group. The two organisms not only grew luxuriantly, but even lost
to a considerable extent their morphological identity, becoming so closely intermingled
as to resemble a single organism. It is an interesting fact that there exists in nature a
large group of plants, the lichens, which consists of a symbiotic association between an
alga and a fungus, both of which have lost to some extent their individual morphology.
It seems quite likely that the lichen association is a biochemically conditioned one similar
to that produced artificially by Schopfer.
One aspect of the studies on the vitamin requirements of bacteria has already
assumed great practical importance: namely, the development of vitamin assay methods
which use bacteria as the test organisms instead of the higher animals. Already recognized assay methods for several of the B group are based on this. The advantages are
great; one can obtain in a few days with the use of inexpensive equipment data which
would require weeks of laborious work with animals (see, e.g., Woolley9).
From the foregoing it is clear that we can regard the need for vitamins as an index
of the loss of synthetic function in any given organism. How does the necessity for
vitamins differ from other needs based on the loss of synthetic function? As an example
of other needs we might consider the nitrogen requirements. Many micro-organisms
and all the higher plants are able to build up the complete array of necessary amino-
acids—and hence proteins—from nitrates or ammonia alone. However, the higher
animals and a number of micro-organisms cannot synthesize certain amino-acids and
nave to be supplied with these in a preformed state, although the remaining non-essential
amino-acids can be synthesized from ammonia and the intermediary products of carbohydrate metabolism. In a certain respect these unsynthesizable amino-acids might be
regarded as "vitamins" if we base the definition of vitamins solely on the loss of synthetic ability. However, there is one significant difference between the amino-acid
requirements and the vitamin requirements proper of an organism. Relatively enormous
amounts of the amino-acids are needed, but only a minute quantity of the vitamins.
This has long been regarded, and rightly so, as an indication that the vitamins must have
a specific function in metabolism, since if they were used, like the necessary amino-
acids, for a non-specific purpose such as the building up of body proteins are requirements would be very much greater.
The unravelling of this great scientific problem—the specific function of vitamins—
has only just begun, but the facts already obtained (almost entirely in the past four
years) form one. of the most revolutionary advances in all biochemistry. So far the
specific roles of three vitamins—Bi, B2 and nicotinic acid—have been elucidated. As
it happens, they are all involved in the metabolism of carbohydrates, or, to put it more
generally, carbon compounds. This must not be taken to mean that all vitamins function in carbohydrate metabolism; probable the fat-soluble ones at least have entirely
different activities. Carbohydrate metabolism has received a disproportionate amount
of attention from biochemists, and it is not surprising that the vitamins involved in it
should first have been tracked down.
In order to make what follows intelligible I must turn for a moment to a seemingly
entirely irrelevant topic, the mechanism of biological oxidation.
According to the classical theories of oxidation, this phenomenon is due to the
addition of oxygen to the substance being attacked. Thus, the complete oxidation of
one molecule of glucose is expressed as:
C6H12Oe + 6 02 -> 6 C02 + 6 H20
Page 53 ii
Another example is the oxidation of ethyl alcohol to acetic acid, a process carried out
by certain bacteria:
CH3CH2OH + 02 -*- CH3COOH + H20
After Lavoisier's discovery of oxygen at the end of the 18 th century, these equations
were the accepted way of describing oxidations for well over a hundred years. At the
beginning of this century the German chemist Wieland put forward an entirely different picture of oxidation: namely, as the removal of hydrogen atoms from the molecule to be oxidized rather than as the addition of oxygen. According to the Wielandian
concept 8, the above-mentioned oxidation of ethyl alcohol was pictured as:
CH3CH2OH + H20 -> CH3COOH -f 4 H.
or, broken down into three steps,, as:
CH;jCH2OH — 2 H -> CH3CHO
CH3CHO + H20 ->- CH3CH3O2
CH3CH3O2 — H -»- CH3COOH 	
Wieland postulated that in order for this process to occur, there had to be present
a hydrogen acceptor to take up the hydrogen atoms removed. He showed that a large
number of substances, both organic and inorganic, were capable of acting in this
manner. His theory was backed by much convincing experimental evidence which it
would take too long to describe here. However, one of the great difficulties was that
it did not appear to accord with the known facts of biological oxidation. For this
reason, considerable opposition to Wieland's theory arose, headed by Warburg, another
German chemist who had done much work on biological oxidations and had considerable
evidence to show that oxygen itself, when activated by catalysts, could carry out oxidations7. It was not until 1925 that the solution of this controversy was reached, and
as it turned out both Wieland and Warburg had been partially correct. Biological
oxidation is a process which involves both hydrogen transfer and the activation of
oxygen; these men men had all the time been studying the opposite ends of the same
chain of events. As Wieland postulated, the first step in oxidation is the removal of
hydrogen atoms from the sugar or whatever other substrate is being oxidized. These
atoms are taken up by a substance A acting as a hydrogen acceptor:
A + 2 H -> AH2
and then passed on to a second hydrogen acceptor B:
AH2 -h B j| BH2 + A,
A then being ready to accept two more hydrogen atoms from the substrate. Substances
capable of undergoing this periodic oxidation and reduction are known as hydrogen
carriers. In this way the hydrogen atoms torn off the substrate are passed along a
chemical chain of intermediary substances acting as hydrogen carriers until, at the far
end of the chain, they come in contact with actviated oxygen and unite with it to form
H2O2, which is immediately broken down into water and oxygen. In this way, the
classical picture of biological oxidation can be fulfilled. The sugar molecule, after the
removal of sufficient hydrogen atoms, will fall apart forming CO2, while the oxygen
is used up uniting with the removed hydrogen atoms to form water.*
Once this interpretation became generally accepted, biochemists turned their attention to discovering the nature of the links in this chain which act as hydrogen carriers.
As a result, we have today a fairly good picture of the entire chemical sequence between
the substrate and the oxygen; what is more, this chemical sequence appears to be
almost the same in all living organisms which carry on an aerobic type of metabolism.
The links in this chain have received the name of oxidative enzymes, a name designed
to stress the differences between them and the enzymes of digestion. It is particularly
the first two enzymes in the chain which deserve attention. Ironically enough, the
study of these two substances, which show so clearly the essential correctness of the
* This is, of course, a highly simplified account; for a detailed chemical presentation see Oppen-
heimer and Stern-5.
Page 54
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Wielandian concept of oxidation as a hydrogen transfer, has been carried out chiefly by
Warburg and his colleagues8.
What are enzymes? Ten years ago this question could not have been answered, but
since then a considerable number have been isolated and purified, so that today we can
say with fair confidence that all enzymes are proteins. In itself, this statement tells us
nothing about the mechanism of enzyme action; however, the further study of the
oxidative enzymes in particular has shed much light on the way in which enzymic
catalysis is brought about.
The oxidative enzymes belong to a special class of proteins known as conjugated
proteins; that is, ones which have linked to them some other different chemical substance. In the first two members of the oxidative chain the linked substances are vitamins or vitamin derivatives. In one the linked substance is a somewhat complex derivative of nicotinic acid amide known as codehydrogenase, while in the other it is simply
vitamin B2 or riboflavin. In both these cases the vitamin fractions are the active portions of the enzyme since they are the hydrogen carriers and by their successive oxidation and reduction the hydrogen torn off the substrate is transferred. The role of the
protein is, however, in neither case negligible. The riboflavin and codehydrogenase can
only act when linked to them; in their free states these two substances are biochemically
inert. Furthermore, the protein linked to the codehydrogenase has another important
function; it determines the specificity of the oxidation to be carried out. Thus there
are a large number of different protein molecules which can link to codehydrogenase
and each one will activate it for the oxidation of a different substance.
Protein 1  -j- codehydrogenase will oxidize glucose
Protein 2 -j- codehydrogenase will oxidize ethyl alcohol
Protein 3  -f- codehydrogenase will oxidize lactic acid
and so on.
The third vitamin whose specific function has been elucidated—Bi—is not a link
in the chain between foodstuff and oxygen, but it has an equally vital part in oxidation;
the release of CO2 from the carbon skeleton of the foodstuff after the removal of
hydrogen. In order to understand this, it is necessary to examine first a little more
closely the fate of a sugar molecule undergoing oxidation. Generally such a molecule
does not, as I have previously indicated for the sake of simplicity, undergo an oxidation
as such, but is first split into two equal halves with 3 carbon atoms each:
C6H1206 -> 2 C3H603 I
Each of these C3 molecules is then oxidized by the removal of two hydrogen atoms:
C3HC03 — 2 H -> C3H4O3
resulting in the production of a keto acid, pyruvic acid (CH3COCOOH). Pyruvic
acid is the keystone of intermediary metabolism, since it can easily be built up into fatty
acids and thence fats or amino-acids and thence proteins. However, it may simply be
destroyed to furnish energy, in which case it next undergoes a decarboxylation {i.e., a
removal of CO2 from the molecule). It is in this way, by the decarboxylation of keto
acids, that all the CO2 resulting from oxidation is released. Phosphorylated vitamin Bi,
linked to a specific protein, is the enzyme which carries out this decarboxylation.
In summing up, I should like to give you a general definition of vitamins. An
organic substances is a vitamin for any given organism if it performs the function of
an active group in some enzyme system and cannot be synthesized by that organism.
Its deficiency will then result in a definite metabolic deficiency which may or may not
(depending largely on the structural complexity of the organism in question) result in
the development of pathological symptoms. Thus the important thing about a Bi
deficiency is not that it produces nerve degeneration in man, but that in all Hying
organisms it results in incomplete carbohydrate metabolism due to weak decarboxylation.
The neurological symptoms of Bi deficiency in the higher vertebrates are essentially
secondary and superficial.   This is one reason why, since the general acceptance of the
Page 55 tenets of comparative biochemistry, scientists have devoted so much greater attention
to micro-organisrns in their studies of general biochemical problems. In bacteria, all
biochemical processes are reduced as it were to their lowest common denominator, and
an avitaminosis can usually be recognized by its primary symptoms. A very striking
example of this is provided by some recent studies on the importance of nicotinic acid
for the dysentery bacterium. It has been shown that nicotinic acid is not a vitamin if
the bacterium in question is grown on a proteinaceous medium. However, as soon as
the medium is supplemented by a fermentable carbohydrate, nicotinic acid becomes
necessary for proper growth and development; in its absence the carbohydrate is only
superficially attacked. As it happens, this particular discovery merely confirms what
we already know about the function of nicotinic acid, but had it been made ten years
ago it would certainly have led to a more rapid appreciation of the function of this
substance. I venture to predict that it will be through similar studies on the lowlier
forms of life rather than through investigations made on animals that most future discoveries concerning the biochemical function of vitamins will be made.
1. Bonner, J.—1937—Vitamin Bi a growth factor for higher plants.    Science, 85:183-184.
2. Kligler, I. J., and  Grossowicz, N.—1941—The function of nicotinic acid in bacterial metabolism.
/. Bad., 42:173-192.
3. Kluyver, A.  J., and Donker, H.  J.  L.—1926.—Die Einheit in  der Biochemie.    Chem.  d.  Zelle u.
Gewebe, 13:134-190.
4. LwofF, A.—1936—Etude sur les fonctions perdues.    Ann. des Fermentations, 2:419-427.
5. Oppenheimer, C, and Stern, K. G.—1939—Biological Oxidation.   Nordemann Publishing Co., New
6. Schopfer, W. H.—193 8—Symboise et facteurs de croissance.    Premier Congres  des microbiologistes
de langue francaise.  Paris.
7. Warburg, O.—1928—Ueber die  katalytischen Wirkungen  der lebendigen Substanz.   Verlag von J.
Springer, Berlin.
8. Warburg,   O.—1938—Chemische   Konstitution   von   Fermenten.    Ergebn.   d.   Enzymforschung,   7:
9. Wieland, H.—1933—Ueber den Verlauf der Oxudationsvorgange.   F. Enke Verlag, Stuttgart.
10.   Woolley, D. W.—1941—Studies on nutrient requirements of bacteria.   J. Bad., 42:155-163.
The simplest yet one of the best sources of information on this subject is "On oxidation, fermentation, vitamins, health and disease" by A. von Szent-Gyorgi (Abram Flexner lectures, series No. 6, Williams and Wilkins Co., Baltimore, 1939). An excellent, but more technical, recent monograph covering
much of the work on the biochemical functions of vitamins is "Mechanisms of biological oxidations" by
D. E. Green (Cambridge University Press, 1940).
In the October, 1941, issue, on page 12, the dosage of Argyrol to be instilled into
the bladder following catheterization was mistakenly given as an ounce. It has been
called to our attention that such an amount used routinely after catheterization or
frequent irrigation, is much too large—a drachm should be quite enough. Therefore
for "one ounce" read "one drachm."
Page 56
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William Magner
Synopsis of Lecture given at the Summer School of the Vancouver Medical Association,
Vancouver, June, 1940.
Formation and Excretion of Bilirubin:
Bilirubin, the chief pigment of human bile, is identical with the iron-free pigment,
haematoidin, which is found in old blood extravasations. It is formed by the reticuloendothelial cells of the body from haematoglobin liberated from disintegrating erythrocytes. It is then transferred to the liver in the blood stream and excreted through the
liver cells into the bile passages.
In man the bone marrow and the spleen are the chief depots of the reticulo-endo-
"thelial cells, and it is in these organs that the greater part of the bilirubin is manufactured. A small amount of bilirubin is produced in the human liver by the reticuloendothelial cells (Kupffer cells) which form an interrupted lining for the sinusoids.
The parenchymatous cells of the liver excrete bilirubin but play no part in its formation.
In its passage through the livel cells the bilirubin is altered from a form which yields
only an indirect van den Bergh reaction (Bilirubin I of Aschoff; "Direct negative" bilirubin of Elton) to a form which yields a direct van den Bergh reaction (Bilirubin II of
Aschoff; "Direct positive" bilirubin of Elton). The nature of this change is uncertain
l>ut there is evidence that it is one from a colloid to a crystalloid state.
Formation and Excretion of Urobilinogen:
In the intestines bilirubin is transformed into urobilinogen by bacterial action. Some
of the urobilinogen is passed in the faeces (as stercobilin), the remainder is absorbed,
carried to the liver in the portal blood and again excreted into the intestines. Normally
only very little urobilinogen escapes through the liver into the general circulation and
is excreted by the kidneys. The presence of an excess of urobilinogen in the urine (positive reaction with paradimetheylaminobenzaldehyde in urine dilutions of 1 in 20 or
greater) indicates either damage to the liver cells (impaired excretion of urobilinogen)
or excessive destruction of red cells (excessive production of bilirubin and urobilinogen).
Normal Bilirubin Content of the Blood:
Normally the blood contains a small amount of bilirubin. This is the bilirubin which
has been formed by the cells of the reticulc—endothelial system and is on its way to the
liver to be excreted. It is the bilirubin I of Aschoff or the "direct negative" bilirubin
of Elton. Opinions vary as to the bilirubin content of the blood in health. Greene,
Snell and Walters found it to lie between 0.5 and 2 mg. per 100 cc. Vaughan reports
that 93 per cent of 100 normal people showed values between 0.2 and 0.8 mg. per 100
c.c, and that in the other 7 per cent values up to 1.7 mg. per 100 c.c. were obtained.
She concludes that figures up to 1.3 mg. per 100 c.c. should be considered as probably
normal, and figures between 1.3 mg. and 1.7 mg. as probably but not necessarily
Hyperbiltrubincemia {Jaundice):
Theoretically, an excess of bilirubin in the blood, leading to jaundice or pigmentation of the tissues, may be due to the following causes:
(a) Overproduction of bilirubin I by the cells of the reticuloendothelial system.
(This is the "hyperfunctional jaundice" of Aschoff. It is caused by haemolysis or in-
■creased destruction of red cells.)
(b) Impaired excretion of bilirubin I by the liver. (This is the "retentional jaun-
•dice" of Aschoff.   It is caused by damage to the liver cells.)
(c) Escape of bilirubin II from the liver cells or bile capillaries into the blood. (This
is the "resorptional jaundice" of Aschoff. It may be caused by disintegration of liver
cells or by obstruction in the bile ducts.)
(d) A combination of two or more of these factors.
Page 57 Hyper functional {Hemolytic) Jaundice:
The belief that jaundice may be purely hyperfunctional or haemolytic in origin
(that is, that it may be due to excessive destruction of red cells and consequent excessive formation of bilirubin) is not universally accepted. In haemolytic diseases, such as;
familial haemolytic icterus, pernicious anaemia, sickle-cell anaemia and paroxysmal haemo-
globinuria, the blood bilirubin is increased in amount, the van den Bergh reaction is
indirect, the stools are rich in pigment and the urine contains an excess of urbilinogen
but no bile. It is difficult to explain these findings except upon the basis of overproduction of bilirubin I by the reticuloendothelial cells and excretion of large amounts
of bilirubin II by the liver. Those who deny the occurrence of purely haemolytic jaundice (Rich and others) argue that the reserve excretory power of the liver is so great
that hyperbilirubinaernia cannot be due solely to overproduction of bilirubin. They
believe, therefore, that there must be a hepatic factor in so-called haemolytic jaundice.
To my mind this argument is fallacious. The jaundice of haemolytic diseases is usually
of slight degree and it may be latent (that is, there may be hyperbilirubinaernia without
obvious pigmentation of the tissues). I find no difficulty in believing that the mild
jaundice of these conditions is due entirely to overproduction of pigment. It seems
obvious that the discharge of an increased amount of bilirubin from the reticuloendothelial cells into the blood stream must cause an increase in the amount of bilirubin in
the blood even in the presence of a perfectly normal liver.
Retentional Jaundice:
Following removal of the liver in dogs, deep jaundice develops and the icteric serum
yields an indirect van den Bergh reaction (Mann). This is retentional jaundice. Bilirubin I is produced in normal amount by the cells of the reticuloendothelial system,
but owing to the absence of the liver it cannot be excreted. As no bile reaches the
intestines, no urobilinogen is formed.   It is probable that deficient excretion of bilirubin
I is a factor in many cases of clinical jaundice, and it is possible that) the mild jaundice
of such conditions as lobar pneumonia and cardiac failure, in which the serum may
yield an indirect van den Bergh reaction, is purely retentional. It seems justifiable to
believe that slight damage to the liver may lead to depression of its excretory function,,
with retention of bilirubin I in the blood and the appearance of mild jaundice with an
indirect van den Bergh reaction, whereas more severe injury to the liver causes jaundice
with a direct van den Bergh reaction because not only is the excretion of bilirubin I
impaired but, owing to disintegration of liver cells, disruption of bile capillaries and,
possibly, blocking of bile capillaries, "direct-reacting" bilirubin II is resorbed into the
Rcsorptional Jaundice:
Jaundice following obstruction of the common bile duct is primarily resorptional
in type.   That is, it is due to resorption (Aschoff) or regurgitation (Rich) of bilirubin
II from the liver cells and bile capillaries into the blood. The serum yields a direct
van den Bergh reaction. If obstruction is complete, bile pigment is absent from the
stools and the urine contains large quantities of bilirubin but no urobilin. With incomplete obstruction, varying amounts of bile pigment reach the intestines and the urine
contains both bilirubin and urobilin. Obstruction of the common bile duct is soon followed by degenerative and inflammatory changes in the bile-engorged liver, so that in
jaundice which is primarily resorptional (due to mechanical obstruction of the outflow
of bile and resorption of bilirubin II) the factor of retention or failure in excretion
of bilirubin I comes to play a part.
Macrocytic, hyperchromic Amemias.
It will be remembered that the "liver principle" or "anti-pernicious-anaemia factor"
is formed in the stomach by the interaction of an intrinsic factor secreted by the gastric
mucosa and an extrinsic factor present in the food, and that it is stored in the liver and,
to a less extent, in the kidneys and pancreas.    Deficiency of this substance causes a
Page 58"
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profound disturbance in the maturation of the red cells and the appearance of a macro-
cystic, hyperchromic anaemia. Such deficiency may be due to: (1) failure in the
secretion of the intrinsic factor, (2) failure in the supply of the extrinsic factor, (3)
failure in the absorption from the intestinal tract of the substance formed in the
stomach by the interaction of the intrinsic and extrinsic factors or, possibly, to (4)
failure in the utilization of this substance by the bone marrow.
(1) Castle's work leaves no doubt that failure in secretion of the intrinsic factor
is the cause of true (Addisonian) pernicious anaemia. In this disease the red cell count
is usually below three million when the patient seeks advice, and it may be as low as one
million. As the red cells are larger than normal the volume index is above unity (1.2
to 1.8), and as these large cells are fully charged with haemoglobin the colour index
is also high (1.2 to 1.8). The leucocyte count is usually below 5,000, and a differential
leucocyte count shows neutropaenia with relative lymphocytosis. The Arneth count or
polynuclear count shows a shift to the right. The platelet count is reduced. In stained
films the majority of the red cells are seen to measure 12 or 13 microns in diameter and
many of these large cells (magrocytes or megalocytes) are oval in shape. Red cells of
normal and reduced size are also to be seen and poikilocytosis is well marked. Nucleated
red cells (normoblasts and megaloblasts) are usually to be found and there may be a
considerable number of stippled red cells. In severe cases the serum or plasma shows an
excessive bilirubin content (3 to 6 mg. per 100 c.c.) with an indirect van den Bergh
reaction, and the urine and faeces contain an excess of urobilinogen. The gastric contents show absence of hydrochloric acid and, as has been mentioned, absence of the
intrinsic factor of Castle. Postmortem examination shows generalized megaloblastic
hyperplasia of the bone marrow, an accumulation of iron-containing pigment (haemo-
siderin) in the liver, fatty degeneration of the myocardium and slight enlargement of
the spleen. There may also be glossitis, atrophy of the gastric mucosa and degenerative
changes in the postero-lateral columns of the spinal chord.
Anaemia which is indistinguishable from Addisonian pernicious anaemia, and which,
presumably, is also due to a deficiency of the intrinsic factor, appears in a small percentage of patients with carcinoma of the stomach and in a small percentage of patients
who have undergone partial or complete gastrectomy. The rare pernicious or macrocytic anaemia of pregnancy is probably due to a temporary, unexplained, suppression of
the secretion of the intrinsic factor, but there is some evidence that it may be caused
by deficiency of the vitamin B complex (? extrinsic factor) in the diet.
(2) Case reports, describing the successful treatment of pernicious anaemia by the
oral administration of yeast or of liver residue devoid of the active "liver principle,"
sugest that, very rarely, this disease may be due, not to absence of the intrinsic factor
from the gastric juice but to absence of the extrinsic factor from the food.
Tropical macrocytic anaemia, which differs from pernicious anaemia in that severe
untreated cases do not show evidence of active haemolysis (hyperbilirubinaernia and
excess of urobilinogen in urine and faeces) seemls to be due to a dietary deficiency, but
it appears unlikely that this deficiency is of the nature of a lack of the extrinsic factor
of Castle. This disease can be cured by the administration of an autolyzed yeast or by
the injection of crude liver extracts, but not by the injection of the purified and concentrated extracts which are so efficacious in the treatment of pernicious anaemia.
(3) Failure in the absorption of the liver principle or anti-pernicious-anaemia factor
{which is produced in the stomach by the interaction of the intrinsic and extrinsic factors) may be the cause of the macrocytic anaemia of tropical and non-tropical sprue
(idiopathic steatorrhcea) and of the macrocytic anaemia found in patients who have had
partial resection of the small bowel or intestinal anastomoses. Some years ago I saw a
girl, 16, who had had several abdominal operations and who was left with an ileo-
colostomy and a caecal fistula. This patient had achlorhydria and a severe anaemia
which Was indistinguishable from pernicious anaemia and which responded promptly and
satisfactorily to liver extract therapy.
Page 59
mm (4) There is a group of macrocytic hyperchromic anaemias which respond unsatisfactorily or not at all to liver therapy. Some of these are clinically similar to pernicious
anaemia and run a more or less chronic course; perhaps improving temporarily on treatment with liver extract. In others the clinical course is that of an aplastic anaemia, as
the red cell count falls progressively in spite of all treatment and death occurs in a few
weeks or a few months. It has been suggested that such anaemias are due to non-
utilization of the liver principle by the bone marrow (achrestic anaemias) but there is
no evidence to support this theory. It would seem more likely that macrocytic anaemia
may be due to some other cause or causes than deficiency of the liver principle. In
leukaemia the anaemia is often of macrocytic type, and there is a form of haemolytic
anaemias which resembles falilial haemolytic icterus in showing increased fragility of the
red cells but which differs from it in showing macrocytosis instead of microspherocytosis.
This disease is not benefited by liver therapy, but it is often cured by splenectomy.
Macrocytic Hypochromic Anamia.
Macrocytic hypochromic anaemia occurs when there is a deficiency of both the liver
principle and iron. Such deficiencies are often present in idiopathic steatorrhea a (sprue)
and the patient shows a macrocytic anaemia with a colour index about 1. In stained
films many of the large cells are seen to be deficient in haemoglobin (large unstained
centres) but, strangely enough, others show a normal haemoglobin content. This variation in the haemoglobin content of the red cells is stressed by Vaughan as being highly
suggestive of a diagnosis of steatorrhcea.
Not rarely in pernicious anaemia there may be an associated deficiency of iron and
films show hypochromasia as well as macrocytosis. This picture is seen most often in
the second or third week of liver therapy, when the iron reserves of the body may become
temporarily depleted as a result of the rapid outpouring of young red cells from the
In cirrhosis of the liver the blood often shows macrocytosis with hypochromasia. It
is uncertain whether the macrocytosis is due to failure on the part of a diseased liver to
store the active "liver principle" or whether it is explained by swelling of the red cells
owing to physico-chemical changes in the blood plasma.
Microcytic Hypochromic Ancemia.
In pernicious anaemia, which is due to a deficiency of the "liver principle," the
maturation of the red cells is retarded at the megaloblastic level, the marrow's store of
normoblasts is rapidly depleted and the production of normal erythrocytes is almost
completely suppressed. The normal deposits of red marrow become crowded with proliferating megaloblasts and the yellow marrow of the long bones is particully or completely replaced by similar megaloblastic red marrow. There is no interference with
the formation of haemoglobin and many of the megaloblasts undergo a pathological
type of ripening and enter the blood as large haemoglobin-rich corpuscles which are
known as megalocytes. These changes in the marrow lead to the appearance of a severe
macrocytic (megalocytic) hyperchromic anaemia.
Just as the liver principle is essential for the transformation of megaloblasts into
normoblasts, so iron is essential for the transformation of normoblasts into erythrocytes.
If the supply of iron to the marrow is deficient, the maturation of the red cells is
retarded at the normoblastic level-, the marrow becomes crowded with normoblasts
which fail to mature, the output of red cells is reduced and those erythrocytes which
do reach the blood stream are poor in haemoglobin and smaller than normal. This type
of marrow disturbance leads to the development of a microcytic, hypochromic anaemia.
A deficient supply of iron to the marrow may be due to: (1) a diet" poor in iron-
containing foods, (2) a need for iron which is greater than can be supplied from a
normal diet, (3) failure in the absorption of the iron in the food, (4) loss of iron from
the body or (5) a combination of two or more of these factors.
Page 60
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(1) A deficient intake of iron is the cause of the ordinary hypochromic anaemia of
infancy. A normal infant possesses at birth three times as much iron in proportion to
its weight as a child over one year of age (Sherman). This iron is stored, chiefly in the
liver, and is utilized by the bone marrow in the production of haemoglobin. Theoretically
it should be sufficient to supply the need of the baby until the birth weight is tripled
and, therefore, hypochromic anaemia should not appear during this period, even though
the child is on a milk diet which is poor in iron. If the iron-poor (milk) diet is continued after the prenatal store of iron is exhausted, anaemia is likely to develop. In full-
term infants, hypochromic or dietary anaemia rarely appears until at least one year after
birth. Children who are born with an insufficient supply of iron, owing to the presence
of iron deficiency and hypochromic anaemia in the mother, may show anaemia as early as
the sixth month of extrauterine existence.
A deficient intake of iron-containing foods may also cause microcytic, hypochromic
anaemia in adults. This is seen most often in women of the poorer classes. There is
usually an associated lack of animal protein in the diet, and unless both these deficiencies
are supplied, anaemia persists.
(2) The hypochromic anaemia of pregnancy may develop in women whose diet is in
all respects adequate for the ordinary needs of the body. It is probably caused by a
relative deficiency of iron due to a drain of iron from the material of the foetal tissues.
(3) Microcytic hypochromic anaemia due to failure in absorption or utilization of
the iron in the food is exemplified by the condition known as the idiopathic hypochromic
anaemia, chronic microcytic anaemia or simple achlorhydric anaemia. This is common in
middle-aged women. It resembles pernicious anaemia in the frequent presence of gastrointestinal symptoms, achlorhydria, glossitis and splenomegaly. It differs from pernicious
anaemia in the frequent presence of trophic changes in the na'.ls (koilonychia) and
dysphagia (anaemia -j- glossitis -j- dysphagia = Plummer-Vinson syndrome), in the
changes -which occur in the marrow and in the blood and, of course, in its failure to
respond to liver therapy. In this disease the red cell count is usually between three and.
four million when the patient seeks advice, but it may be much lower. As the disease
is essentially a haemoglobin deficiency, the colour index is always reduced and it may be
0.5 or even lower. The height of the volume index depends upon the degree of micro-
cytosis; it may be within normal limits but usually it is reduced. As a rule the leucocyte
and platelet counts are normal. In stained films the majority of the red cells are smaller
than normal with large unstained centres. The bilirubin content of the blood is low.
In at least 80 per cent of cases there is achlorhydria. The marrow shows normoblastic
It is important to remember that the changes in the blood in idiopathic hypochromic
anaemia are similar to those in other types of anaemia due to deficiency of iron A diagnosis of idiopathic hypochromic anaemia should not be made until known causes of iron
deficiency anaemia, such as chronic haemorrhage and organic lesions of the gastro-intestinal tract, have been excluded.
(4) Microcytic hypochromic anaemia due to loss of iron is exemplified by the anaemia
of chronic haemorrhage. The differences in the blood pictures of chronic post-haemorr-
hagic and chronic haemolytic anaemias are due to the fact that profuse or repeated
haemorrhages leads to exhaustion of the body's store of iron and other red-cell building
materials, and resulting inactivity of the marrow, whereas when red cells are destroyed
within the body the products of their disintegration are available for the formation of
new erythrocytes, and the regenerative response of the marrow is active and continuous.
Hyperbilirubinaernia, urobilinuria, reticulocytosis, haemosiderosis and normoblastic hyperplasia of the marrow are features which are common to all types of haemolytic anaemia.
In chronic post-haemorrhagic anaemia, on the other hand, the blood picture is identical
with that of other forms of iron deficiency anaemia. It is to be noted, however, that
when profuse haemorrhage occurs into the tissues or body cavities the disintegration
products of the extravasated erythrocytes are available for the formation of new red
Page 61 .i
cells and the picture may resemble that of haemolytic anaemia in showing re iculocytosis,
hyperbilirubinaemia with an indirect van den Bergh reaction and an excess of urobilinogen in the urine and faeces.
Normocytic Hypochromic Ancemia.
In the early stages of an iron-deficiency anaemia, while the red cells show a reduction
in their haemoglobin content there may be little or no reduction in their size. The picture is then that of a normocytic hypochromic anaemia. The anaemias of vitamin C
deficiency (scurvy) and of chronic infections are usually of similar type but they may
be microcytic.
Normocytic Normochromic Ancemia.
Anaemias due to deficiency of haemopoietic substances (liver principle, iron, vitamin
B, vitamin C, animal protein) are characterized by changes in the size and haemoglobin
content of the red cells. In anaemias due to injury to the marrow such changes are
commonly absent and the red cell picture is normocytic and normochromic. Thus in
true aplastic anaemia, that is, anaemia characterized by marked hypocellularity of the
marrow, whether it is of so-calle idiopathic type or due to the action of known toxic
agents (benzol, arsenic), there is a rapid reduction in the numbers of erythrocytes,
leucocytes and platelets in the blood but the red cells in stained films show no abnormality other than slight anisocytosis and poikilocytosis. In many cases which simulate
true aplastic anaemia in showing a progressive fall in the numbers of all the cellular
elements of the blood, the marrow is hyperplastic and blood films may show macrocytosis with variable numbers of immature red and white cells. Cases of this type
should be classified under the heading of progressive hypocythaemia, rather than of
aplastic anaemia (Krumbharr); many of them are examples of aleukaemic leukaemia.
The anaemia of renal insufficiency is, as a rule, monocytic and normo chronic, but
colour indices above 1.1 have been reported in this condition.
Other Types of Amemia.
Two haemolytic anaemias which are classified according to the shape of the red cells-
are the microspherocytic anaemia of familial haemolytic icterus and the sickle-cell anaemia
which is common in negroes.
The anaemia which is due to progressive mechanical destruction of the bone marrow
by tumour growths (secondary carcinoma, multiple myeloma) or by osteosclerotic
processes is known as myelophthisic anaemia. In it, while owing to reduction in the
total amount of red marrow the output of red cells is greatly reduced, overactivity of
the remaining red marrow leads to the appearance of many reticulocytes, nucleated red
cells and immature leucocytes in the blood.
Magner, W~.—A Textbook of Hematology.    P. Blakiston's Son & Go., Philadelphia. ;
:   i
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Page 62
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.       ;„s A and D decreases o ^ |hc
«« Vitamins a »  . . . m order
them increases. .»--- montns ^
huitt op dorin9 ! • «hle to begin ad-
stores buin    p u aavlsable to
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W*in,S^    nt^he  need far them  I g
to wart  u"*1 we   |    .oseS  in time  may
i——• es$:^:-ch.«9«^,o,e'on-
Concentrate of defatted cod liver oil,
biologically standardized to contain
10,000 International Units Vitamin A and
1,750 International Units Vitamin D in each
soft gelatin capsule. Boxes of 25,50,100,500.
The original "bottled sunlight"
brand, biologically standardized to
contain 3,000 International Units Vitamin
A and 400 International Units Vitamin D
per gram. Bottles of 4 and 16 ounces.
Biological and Pharmaceutical Chemists


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