History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: October, 1939 Vancouver Medical Association Oct 31, 1939

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of the
Vol. XVI.
No. 1
With Which Is Incorporated
Transactions of the
Victoria Medical Society
Vancouver General Hospital
St Paul's Hospital
In This Issue:
(With Cascara and Bile Salts)
. . FOR . .
Chronic  Habitual
Western Wholesale Drug
(1928) Limited If
(Or at all Vancouver Drug Co. Stores) THE    VANCOUVER    MEDICAL   ASSOCIATION
Published Monthly under the Auspices of the Vancouver Medical Association
in the interests of the Medical Profession.
Offices: 203 Medical-Dental Building, Georgia Street, Vancouver, B. C.
Dr. J. H. MacDebmot
Db. G. A. Davidson Db. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
Vol. XVI.
No. 1
OFFICERS,  1939-1940
Db. A. M. Agnew                  De. D. F- Btjsteed Db. Lavell H. Leeson
President                            Vice-President Past President
Db. W. T. Lockhabt Db. W. M. Paton
Hon. Treasurer Hon. Secretary
Additional Menibers of Executive: Db. M. McC. Baibd, Db. H. A. DesBbisat.
Db. F. Bbodie Db. J. A. Gillespie Dr. F. W. Lees
Historian: Db. W. L. Pedlow
Auditors: Messes. Plommeb, Whiting & Co.
Clinical Section
De. W. W. Simpson Chairman Db. Feank Tubnbull Secretary
Eye, Ear, Nose and Throat
Db. W. M. Paton Chairman De. G. C. Large Secretary
Pediatric Section
Db. J. R. Davies Chairman Db. E. S. James Secretary
Db. F. J. Bullee, De. D. E. H. Cleveland, De. J. R. Davies,
Db. W. A. Bagnall, Db. T. H. Lennie, Db. J. E. Walkeb.
De. J. H. MacDebmot, Dr. D. E. H. Cleveland, Db. G. A. Davidson.
Summer School:
De. A. B. Schinbein, De. H. H. Caple, Db. T. H. Lennie,
Db. Feank Tubnbull, Db. W. W. Simpson, Db. Kabl Haig.
Dr. A. B. Schinbein, Dr. D. M. Meekison, Dr. F. J. Buller.
V. O. N. Advisory Board:
Dr. I. Day, Db. G. A. Lamont, Db. S. Hobbs.
Metropolitan Health Board Advisory Committee:
To be appointed by the Executive Committee.
Greater Vancouver Health League Representatives:
Db. W. W. Simpson, De. W. M. Paton
Representative to B. C. Medical Association: Db. L. H. Leeson.
Sickness and Benevolent Fund: The Pbesident—The Teustees. What are you prescribing for Multiple Vitamin
I'm getting excellent
results with VIGRAN,
the new Squibb five
VIGRAN is economical too when
you consider the
dosage is only
one capsule daily.
There are many conditions in which a deficiency of more than one of
the vitamins may be noted. Such deficiencies may result from peculiar
dietary preferences as well as from the restricted diets imposed because
of illness.
CONVENIENT—VIGRAN, Squibb Vitamin A-B-C-D-G Capsules eliminate the necessity of taking an unpalatable preparation, of eating food
which the individual dislikes, or of taking two or three separate products
in order to provide an adequate supply of these 5 essential food factors.
The capsules are convenient, practical and economical—the dosage
requirement is small. They dissolve readily after being swallowed.
POTENT—Each capsule contains in stable form the full estimated
minimum adult daily requirement of Vitamin A (6300 I.U.), B (222 I.U.),
C (500 I.U.), D (630 I.U.) and probably G (10 gammas). The average
dose is one capsule daily.
VIGRAN capsules are indicated for pregnant and lactating women,
malnourished adults, convalescents, patients on restricted diets or with
prolonged or wasting illnesses requiring supplements of several of the
Average adult minimum daily requirement unknown.
For literature and samples, write
ER:Sojjibb & Sons of Canada. Ltd.
Total population—estimated *  263,974
Japanese population—estimated  8,891
Chinese population:—estimated ?  7,728
Hindu population—estimated  389
Rate per 1,000
Number Population
Total deaths 222 9.9
Japanese deaths        6 7.9
Chinese deaths        8 12.2
Deaths—residents only    194 8.7
Male, 162;  Female, 179    341 15.2
INFANTILE MORTALITY: August, 1939 August, 1938
Deaths under one year of age      10 9
Death rate—per 1,000 births      29.3 25.2
Stillbirths (not included in above)        8 10
September 1st
July, 1939 August, 1939 to 15th, 1939
Cases   Deaths Cases   Deaths Cases   Deaths
Scarlet Fever _     3 0 11 0 3 0
Diphtheria        10 0 0 0 0
Chicken Pox      12 0 10 5 0
Measles        10 0 0 10
Rubella •        2 0 0 0 0 0
Mumps        4 0 2 0 8 0
Whooping Cough I      28 0 10 0 4 1
Typhoid Fever i        0 0 1* 0 0 0
Undulant Fever I        0 0 0 0 0 0
Poliomyelitis        0 0 0 0 0 0
Tuberculosis      28 16 36 16 9
Erysipelas        0 0 0 0 0 0
Ep. Cerebrospinal Meningitis —       0 0 0 0 0 0
* Outside case. |^
West North      Vancr.   Hospitals,
Burnaby   Vancr.   Richmond  Vancr.      Clinic  Private Drs.   Totals
Syphilis      0 0 0 0 45 26 71
Gonorrhoea        0 0 0 0 59 12 71
Descriptive Literature on Request.
A Product of the Bioglan Laboratories, Hertford, England.
Represented by
STANLEY    N.   BAYNE      §
1432 Medical-Dental Bldg.
Phone: SEy. 4239 "Ask the doctor who is using it." Vancouver, B. C. >%.
In the treatment of such conditions, the use of Antiphlogistine,
applied vaginally, as tampons, and abdominally, as poultices,
answers the need for both heat and glycerine medication
for the relief  of  inflammation,  congestion, and pain.
Sample on request
Made in Canada INDEX TO VOLUME XV, V. M. A. BULLETIN, 193 8-1939.
ALCORN, D. E.—Psychiatric aspects of enuresis 1  306
ANTHROPOLOGY—G.  E.  Kidd  159
ARMITAGE—T.  F.  H.—Streptococcic  Meningitis  330
AUTOPSIES—F. J. Fish..._  275
ARMITAGE, T. F. H.—Streptococcic meningitis ."  330
BAILLIE, D. M.—"This Clinic Business'...
BAIRD,  M.  McC.—"Rheumatism"	
BOAK, E. W.—Spinal cord pressure	
Letter from W. H. Malkin	
Activities    :.
Annual   meeting,   1938	
Annual   meeting,   1939	
Annual reports for 193S	
Annual reports for 1939	
Committee on Public Health—"Milk Situation"..
Committee  reports	
Lecture   Team,   1938	
Meeting of Directors, January, 1939	
President's   message	
BROWN, C. E.—Plummer Vinson syndrome	
Regional obesity	
Letter from Dr. H. H. Millburn	
Annual meeting, 1939 _	
CLEVELAND, D. E. H.—Scabies, a new method of treatment.
DAGENAN AND PNEUMONIA—B. M. Fahrni  146, 250
DAVIDSON, J. R.—Problems of contract practice     63
DAVIES,   C.   E.—Strabismus  302
DOLMAN, C. E.—-Compulsory pasteurization of milk  319
Public Health Laboratory tests  292
DORRANCE, G. M.—Educational advantages of the Tumour Clinic  103
EDITORIALS  2, 26, 58, 90, 123, 153, 192, 230, 260, 284, 312,  342
ESOPHAGUS—R. Scott Moncrieff     75
EPILEPSY—R. Glen Spurling     15
EPILEPTICS, SURVEY OF—S. E. C. Turvey     52
FAHRNI, B. M.—Some points in the treatment of pneumonia cases with Dagenan   146
Further report on treatment with Dagenan  250
FRASER, C. A.—Radiation treatment of carcinoma of the skin  301
GRAHAM, W. G.—Some aspects of hepatic and gall bladder disease
HAIG, KARL—Congenital dislocation of the hip     95
HARRISON, B. J.—British Columbia Cancer Institute  243
HENRY, A. T.—Common rectal conditions  184
HYDRONEPHROSIS, CASE—Millburn, H. H., and Hall, E. R  223
KENNING, G. C.—Coronary thrombosis  178
KIDD, G. E.—Points in physical anthropology 1 1  159
LENNIE,  T.  H.—Post-operative  treatment M..	 M
MACDERMOT, J. H.—The Layman and the Doctors  198
McKECHNIE, R. E., II—Pelvis disease following subtotal hysterectomy  225
McNAIR, A. Y.—Cancer organization  and activities  72
Canadian Society for the control of cancer.  246
NEUROSYPHILIS, Malarial treatment of—S. E. C. Turvey  308
Dr. W. D. Brydone-Jack :       9
Dr. F. X McPhillips     94
Dr. D. W. McKay  127
Dr. J. M. Robertson -  127
Dr. S. E. Beach  157
Dr. Neil McDougall .  197
Dr. F.  G. Logie  233
Dr. G. B. Henderson ,  264
Dr. L. N. Beckwith - - -  264
OLFACTION—R.   Scott Moncrieff  266
OSLER LECTURE,  1939—J.  H. MacDermot  198
PELVIS DISEASE—R. E. McKechnie, II  225
PITTS, H. H.—Blood sedimentation tests  148
PREVENTIVE MEDICINE SECTION  81, 105, 173,  319,  361
PRIMARY CANCER OF THE LIVER—C. H. Vrooman and A. Y.^McNair  337
PUBLIC HEALTH—S. S. Murray..  137
RADIATION THERAPY—H. H. Murphy....     44
"RHEUMATISM"—M.   McC.   Baird  163
ROBERTSON, H. A.—Case of adenocarcinoma of the ovary  367
ROXBURGH, D. B.—Pathology of cancer of the cervix  255
SCOTT-MONCRIEFF, R.—Olfaction  266
Sense of taste  218
The   Oesophagus     75
SMITH, J. A.—Operative treatment of ocular deviations  304
SPOHN, A. H.—Two cases of cretinism  116
SPURLING, R. G.—Epilepsy      15
ST.  PAUL'S HOSPITAL  SECTION  86,  111,  188,  223,  337,   367
STRABISMUS—C. E. Davies   302
TASTE, SENSE OF—R. Scott Moncrieff 1  218
TRAPP, ETHLYN—Department of cancer control 1  238
TURNBULL, F.—Tumours of the pituitary and parapituitary region  30
TURVEY,  S. E. C.—Examination of cerebrospinal fluid in syphilis  361
Malarial treatment of neurosyphilis  308
Preliminary report on 452 cases of neurosyphilis  174
Survey of epileptics from outpatient department  52
71, 335
Case reports  22, 23, 54, 82, 83, 109,  110, 111,  150, 221, 276,  332,  364
Educational facilities of the out-patients'  department     20
Medical records—F. J. Fish     20
Medical ward rounds     21
Anniversary Dinner     29
Annual Dinner, 1938     62
Annual Meeting, 1939 ...  235
VENEREAL DISEASE CONTROL—D. H. Williams......     49
VICTORIA MEDICAL SOCIETY SECTION   75,  106,  150,  178,  255,  278,  306
VROOMAN, C. H., and E. R. HALL—Primary cancer of the liver „  337
WILLIAMS, D. H.—The physician and venereal disease in B. C _     49
Founded 1898     ::    Incorporated 1906
GENERAL MEETINGS will be held on the first Tuesday of ithe month at 8:00 p.m.
CLINICAL MEETINGS will be held on the third Tuesday of the month at 8:00 p.m.
Place of meeting will appear on the Agenda.
General meetings will conform to the following order:
8:00 p.m.—Business as per Agenda.
9:00 p.m.—Paper of the evening.
Programme of the 42nd Annual Session (Fall Session)
October   3—General Meeting.
Dr. Howard Spohn: "Some observations on Pediatric practice in Europe."
October 17—Clinical Meeting.
November   7—General Meeting.
Major H. A. DesBrisay: "Biliary Tract Diseases."
November 21—Clinical Meeting.
December   5—General Meeting.
Dr. W. A. Dobson: "Diagnosis of early Schizophrenia."
Dr. J. M. Jackson: "Treatment of early Schizophrenia."
December 19—Clinical Meeting.
The New Synthetic Antispasmodic
Trasentin "Ciba"
Tablets—bottles of 20 and 100. Ampoules—boxes of 5 and 20.
1 tablet or 1 ampoule contains 0.075 grm;
v.&* of the active substance.
Page 4 .Ufi:
Iron is the oldest and still one of the
most effective treatments for anaemia;
but the most potent form of iron medication was not definitely known until
In the past, hundreds of organic and
inorganic compounds of iron have
been tried clinically with widely varying results. This variation of result
caused investigators to continue the
study of iron absorption in anaemia.
Their recent investigations confirmed
the previously observed fact that ferrous salts are more readily absorbed
than other forms of iron, and that all
ingested iron is converted into the
ferrous state before absorption, cf.
Journal C.M.A. March '33. Lucas and
P. Hendrycb and K. Klimesch, Arch.
Exptl. Path. Pharmakol 178, 178-88,
1935, regard ferrous chloride as the
physiological form of iron. They find
that it does not cause chronic poisoning when administered orally, but
that ferrous carbonate and ferric citrate cause characteristic liver damage.
But ferrous chloride is unstable and so
unpalatable that many patients refuse
to continue treatment long enough to
raise the haemoglobin to normal.
Former objections to the use of ferrous
chloride have been overcome in Ferrochlor E.B.S. which presents ferrous
chloride in permanent and palatable
form. Each teaspoonful dose of Ferrochlor contains 2 grains of ferrous
chloride, equivalent to 30 grains of
reduced iron.
"Ferrochlor E.B.S. builds haemoglobin rapidly."
Ferrochlor is also supplied in tablet form for patients tcho prefer this form of iron medication.
We extend the hand of heartiest congratulation to the British Columbia Medical Association for the very great success of their Annual Meeting held last month. We feel that
the officers and directors of the Association did very wisely when they decided that the
meeting should be held as arranged, in spite of the war. Perhaps even more because of the
war, since this meeting gave an opportunity to us all to discuss amongst ourselves our
duties and responsibilities in this national emergency.
Moreover, morale is everything, and we feel that normality and sanity of thought and
behaviour are essential at this very critical moment. The world goes on: people do not
stop being sick in a purely civilian manner, just because there is a war, and we still need
the refreshment and stimulation that we received in such generous measure from this
This note of normality, of the need for a sense of proportion, was perhaps especially
evident in the special meeting that dealt with "The Role of the Physician in War." There
could be no slightest doubt of the wholehearted desire of us all to serve as best we can, and
to do all that lies in the power of each one of us to help the cause—but there was a definite
difference in the atmosphere as compared with the last war. Then men volunteered here,
there and everywhere, with no regard for selection—no supervision or control, based' on
the fitness of each one for any particular job—and the result was very often serious dislocation and grave inconvenience.
Today the spirit of loyalty and anxiety to serve is just as strong—but there was quite
evident a feeling that every precaution should be taken to avoid these former errors—and
that men should be chosen for work as required, and according to their several abilities—
that nothing should be done, if possible, that would gravely upset civilian needs and
arrangements—and that order and discipline should prevail. This is as it should be. Canada
has not as yet got firmly into her stride as regards her share in the prosecution of the war.
It is difficult, perhaps impossible, at this stage, to see clearly just what our individual
duties will be in this shares—but meanwhile it would seem to us that it is wisest and best
to wait patiently till we are given the lead which is bound to come sooner or later. A
certain degree of impatience is perhaps natural, but we must curb it. There is no doubt
that there will be work for each one of us in some capacity or another.
October is the beginning of our year, as far as regular meetings go: and we feel as the
schoolboy does, at the start of a new term. The holidays are over, and it is time to get back
to work. We wish all our readers a happy and profitable year of it, and we would like to
remind them that success in these directions is not entirely the responsibility of our officers
and committees. They merely get the meals ready: but if the meals are to do any good and
not be mere waste, they must be consumed by us as members of the Association. Our part
is just as important: to attend meetings regularly, to take part in discussions: to be willing
and ready to do our share of committee work, if called on. We are moved to this outburst
by observations over the past few years, of scanty attendances and empty seats. Those
who fail to attend, and to take part, are the losers: let them think it over, and mend
their ways.
Dr. R. V. McCarley of North Vancouver is travelling in the East. He will leave his
son John at Queens University and then visit in Montreal before returning.
•■^ »'. «'. *L
*r *C *r *tr
Dr. J. W. Lang of West Vancouver has returned from a motor tour of Interior points.
Dr. and Mrs. Alan Hall are spending a month's vacation in Montreal.
5^ *P *P ws"
Dr. R. W. Garner of Port Alberni is off on a two weeks' expedition into the Cariboo
hunting bears. During his absence Dr. J. C. Thomas is doing locum tenens.
The officers of No. 13 Field Ambulance are to be congratulated on the reciept of the
Ryerson Cup for general efficiency. This was won in competition with all Field Ambulance
Units in Canada. The officer personnel consists of Lt.-Col. G. C. Kenning, Officer Commanding; Major S. G. Kenning, second in command; Capts. C. A. Watson and L. W.
Bassett; Lieuts. J. S. McCannell, W. R. Caverhill, Andrew Turnbull, Douglas Roxburgh,
R. Scott-Moncrieff, and Major and Quartermaster H. A. Davenport.
No. 13 Field Ambulance has been mobilized and officered by Lt.-Col. G. C. Kenning,
Capt. C. A. Watson, Lieuts. J. S. McCannell, W. R. Caverhill, R. Scott-Moncrieff, and
the Quartermaster, Major H. A. Davenport, all of Victoria.
Dr. J. M. Hershey of Pouce Coupe has been transferred by the Provincial Board of
Health to Kelowna.
Dr. R. Millar Tait has gone to California for a short holiday.
Dr. W. D. Higgs of Port Alberni left for Calgary to join his former unit, No. 8 Field
Dr. P. M. McLean is now associated with Dr. R. N. Dick at Chemainus.
**. *t **• *»-
*c *tt *i" «r
Dr. McKenzie Morrison of Stewart attended the Annual Meeting and is completing his
vacation.  Dr. H. A. Whillans is doing this locum.
Dr. A. E. Kydd is doing locum for Dr. H. D. Galbraith at Bella Coola.
3?* 55- 2%: 55-
Dr. J. G. Robertson of Tofino has left to do post-graduate work. During his absence
Dr. H. Cantor will carry on the practice.
Dr. Gordon James of Britannia is having a well-earned vacation.   Dr. H. Ostry is
doing locum for him.
The following doctors, who reside
minster, were registered at the Annual
R. N. Anderson, Ladner.
F. M. Auld, Nelson.
W. K. Blair, Nelson.
E. W. Boak, Victoria.
B. F. Bryson, Essondale.
H. L. Burris, Kamloops.
outside of Greater Vancouver and New West-
Meeting of the British Columbia Medical Asso-
Gordon C. Kenning, Victoria.
Stuart G. Kenning, Victoria; q
G. M. Kirkpatrick, Essondale.
W. J. Knox, Kelowna.
Wilfred Laishley, Nelson.
E. J. Lyon, Prince George.
Page 6 H. Baker, Salmon Arm.
N. B. Ball, Oliver.
W. T. Barrett, Victoria.
D. W. Beach, Langley Prairie.
G. A. Bird, Victoria.
C. C. Browne, Nanaimo.
E. A. Campbell, Essondale.
T. G. B. Caunt, Essondale.
R. Franklin Carter, New York City.
H. A. Cave, Montreal, Que.
G. A. Cheeseman, Field.
L. S. Chipperfield, Port Coquitlam.
W. G. Cosbie, Toronto, Ont.
P. A. C. Cousland, Victoria.
H. B. Cushing, Montreal, Que.
J. Stuart Daly, Trail.
G. E. Darby, Bella Bella.
R. N. Dick, Chemainus.
G. R. F. Elliot, Essondale.
E. D. Emery, Nanaimo.
Richard Felton, Victoria.
G. H. Francis, Pioneer Mine.
A. Francis, New Denver.
W. A. Fraser, Victoria.
Alexander Gibson, Winnipeg, Man.
A. F. Gillis, Merritt.
V. B. Goresky, Castlegar.
Roscoe R. Graham, Toronto.
George Hall, Victoria.
N. B. Hall, Campbell River.
B. J. Hallowes, Alexis Creek.
D. P. Hanington, Ladysmith.
T. C. Harold, Ladysmith.
C. T. Hilton, Port Alberni.
Gordon James, Britannia Beach.
Thomas McPherson, Victoria.
I. Martianoff, Steveston.
A. H. Meneely, Nanaimo.
R. L. Millar, Victoria.
George More, Shawnigan Lake.
Osborne Morris, Vernon.
M. Morrison, Stewart.
G. Morse, Haney.
A. B. Nash, Victoria.
L. A. C. Panton, Kelowna.
F. R. Patton, Spokane, Wash.
N. J. Paul, Squamish.
W. B. Penney, Tacoma, Wash.
R. C. Riley, Calgary, Alta.
G. A. C. Roberts, Chilliwack.
A. O. Rose, Langley Prairie..
E. S. Sarvis, Sumas, Wash.
E. P. Scarlett, Calgary, Alta.
F. D. Sinclair, Cloverdale.
D. L. Stokesbary, Ferndale, Wash.
P. L. Straith, Courtenay.
J. Bain Thorn, Trail.
A. J. Tripp, Fernie.
A. S. Underhill, Kelowna.
J. P. Vye, Victoria.
S. A. Wallace, Kamloops.
W. H. White, Penticton.
H. G. Willard, Tacoma, Wash.
S. L. Williams, Nanaimo.
F. L. Wilson, Trail.
G. H. Worsley, Alert Bay.
R. J. Wride, Princeton.
T. W. Walker, Victoria.
E. C. Yoder, Tacoma, Wash.
H. E. Young, Victoria.
The Library has secured a reprint of an article by Dr. Frank Turnbull published in the
Yale Journal of Biology and Medicine, v. 11, May, 1938, entitled "Cordotomy for
Thalamic Pain," a case report, from the sub-department of Neurology and Neurosurgery,
Vancouver General Hospital. Dr. Turnbull notes that he is indebted to Dr. S. E. C.
Turvey for assistance in the diagnosis and treatment of this case. The account of this case
was presented by Dr. Turnbull at the Eighth Annual Meeting of the Harvey Cushing
Society, April 6-8, 1939, at New Haven, Connecticut.
The results of Staff
Bierman, Wm.—Medical applications of short wave current.   1938.
Wilson, Philip D., ed.—Experience in the Management of Fractures:
of Fracture Service in the Massachusetts General Hospital.  1938.
Fulton, John F.—Physiology of the nervous system.  1938.
Still, Sir Frederick—Common happenings in childhood.
Prinz, H, and Greenbaum, S.—"Diseases of the mouth and their treatment."  1939.
Gordon, S. M.—"Dental science and dental art,"   1939.
Page 7
»M Long, P. H., and Cliss, E.—"Clinical and experimental use of sulfanilamide."   1939.
Kanavel, A. B.—"Infections of the heart." 7th ed., 1939.
From the Nicholson Fund
MacDermot, H. E.—Sir Thomas Roddick.  1939.
Carrell, Alexis and Lindberg, CA.—Culture of organs.   193 8.
Book Review
A.B., M.D., D.P.H. (Industrial Health Book Co., Chicago, 111.)
This is quite a complete summary of the various phases of occupational diseases. It
deals with the industrial side of the subject—giving causes, standards of permissible
exposures to irritants and poisons, control of exposures, and the cost of occupational
disease. It is interesting to note that silicosis in every case is the cause of the highest
indemnity paid: this, no doubt, mainly on account of its long duration) and so frequently
fatal ending: but it shews the immense importance of controlling this disease.
The work then takes up Insurance and Prevention—dealing with the questions of pre-
liminary medical examinations—and goes on to the medical aspects of the subject. There
is much in this that each of us might do well to read, andi one is amazed at the long list of
causes of disability due to occupation. The part played by noise, fatigue, heat and cold,
bad lighting, bad air, is very great and demands more attention than we usually give it.
Lastly, comes the legal aspect of occupational disease, and we are taking the liberty of
reproducing a chapter which we consider as good an article as we have read on the "Physician as a Witness." To all of us, except a few trained by long experience, the witness-box
is an unknown land, and as such full of terrors and discomfort. The advice given in this
chapter is excellent and will help us all, including justice.
This book is a worthy addition to our bookshelves. —J. H. M.
Extracted from "Medico-Legal Phases of Occupational Diseases/'
by C. O. Sappington, A.B., M.D., D.P.H.
(See Book Review)
It is common practice to give advice to physicians who go on the witness stand to give
testimony; in fact, almost every technical paper on the subject of medical jurisprudence
includes either some direct or indirect suggestions to the physician who is employed either
in the capacity of a witness to the facts or as an expert witness.
Sir John Collie, the eminent British authority, has taken the trouble to outline what
he calls the rules for giving evidence, and although these apply mainly to the British custom, there may be some principles among them which are useful in American experience.
"1.   Speak slowly and distinctly.
"2.   Watch the Judge's pen. When he stops writing, resume your evidence.
"3. Look at counsel as he propounds his question, but direct your reply to the Judge
and Jury.
"4. Answer the exact question put. If any explanation or amplification is necessary,
the witness has a right to give it after having given a direct answer.
"5. In giving medical evidence, one must be careful not to give the Court the impression that you know that it has not any real sound knowledge on medical subjects.
"6\ Nothing is more effective than to take into the witness-box a model or picture.
This always impresses both the Judge and the Jury. One can often make a fracture quite
clear by showing a bone.
"7. A medical witness can always take his notes with him into the witness-box and
refresh his memory from them // and only if they are the original notes which he took at
the time of his examination. They cannot possibly be objected to. I have seen typewritten
copies of notes successfully objected to.
"8.    Seldom, if ever, use technical language; if it is imperative to do so, explain it.
Page 8 "9. Make sure that your process of reasoning is abundantly clear.
"10. Put aside all bias, and be absolutely candid. Remember that you have sworn not
only to tell 'the truth' but 'the whole truth.' This, I take it, refers to suppressio vert. Do
not hesitate to admit a fact which may at first sight appear to be against your contention;
you will probably be able to demonstrate that it is not so in reality. In any event the admission will demonstrate such fairness that the remainder of your evidence will have an
enhanced value.
"11.   A medical witness should be scientifically exact, lucid, and succinct.
"12. Remember that, in medicine at any rate, anything is possible, therefore get the
credit of willingly admitting it.
"13.   Never give evasive answers.
"14.   Never guess."
A little later on in his discussion concerning the medical witness, Collie also states:
"Above ally never lose your temper; however irritated. Remember that the object of cross-
examination is to test your knowledge or your candour. It always pleases cross-examining
counsel if he succeeds in making a witness angry. Do not be offended if counsel insinuates
that you are a gross perjurer, or the Judge sums up with an insinuation that you are either
very unobservant or much misguided. Remember that the case must go against somebody,
and that, if you do have these pleasantries; levelled at your head, your medical friend who
is opposed to you has been saved what he possibly might have been f oolish enough to take
There is, of course, a great deal of difference in the method of attack on the same
problem, by the legal and medical professions. Sometimes these differences bring about
considerable difficulty in the co-operation of the members of both professions. Springstun
has made the following comments on this point: "The mere difference in the language of
medicine and law is enough to bring about friction when these professions meet in the
courtroom. The lawyer asks technical legal questions and the doctor gives technical medical answers, with the result that in many cases little or no information is imparted to the
jury. The lawyer knows what he wants to find out by his question and the doctor knows
what he wants to impart by his answer, but it is often the case that while the answer would
convey information to a jury of doctors, it means absolutely nothing to a jury of laymen,
either because of the qualifications contained therein or because of the medical terminology
used. Words which are usual to the doctor often mean nothing to the layman. The Latin
and Greek terminology and phraseology which is part and parcel of the medical language
is just so much gibberish to the man in the street who sits on the jury as one of the peers
of the accused. To the lay or legal mind it often seems that the words used by doctors in
answer to questions in court are for the purpose of obscuring thought and concealing information rather than for imparting information and clarifying thought. If a medical witness wishes his testimony to have any effect he must take pains to couch it in language
which he knows the jury will understand. If he does not do this, he might just as well
refrain from testifying. The average doctor on the witness stand is natural and modest,
neither aggressive nor afraid; and if his language was in accord with his manner he would
be a much more effective witness. The average layman is not especially alert intellectually,
anyhow, and if he is to be driven in any direction by medical testimony it usually has to
be in words of one syllable if it is to sink into his consciousness and make any impression
upon his mind. . . . Testifying in court is a good deal like playing golf. If a doctor
takes a good stance, keeps his eye on the ball, gets a good swing and follows through he gets
along pretty well; that is, if he sits squarely and comfortably in the witness chair, doesn't
squirm or fidget, keeps his voice up and watches his questioner, responds clearly and frankly
to the questions, and takes care to make his answers understandable to those not in his
profession—he has no difficulty and serves a useful purpose on the witness stand; but if
he stammers and stutters, twists and squirms, whispers his. answers and speaks so that his
words are unintelligible, evades or fulminates, or does any of the things which tend to
detract from his professional knowledge, prestige and presence, he is likely to have a
tough time of it and his testimony will be worthless in direct proportion to the extent of
such actions."
Page 9
111 A great deal has been said about the judicial temperament that the doctor should
possess in testifying, and also the co-operation between the advocate and the physician.
Oppenheimer has stated: "We may epitomize it all by saying that the value of the physician's testimony depends far more upon its form than upon its content,—more upon the
manner in which it is given than upon its scientific worth or exactitude. His education
and training—his opportunities for study and observation which especially qualify him to
testify as an expert—may make it possible for him to be particularly impressive; but these
may also become instrumentalities1 for rendering him. ridiculous in the sight of those untrained jurors who, by reason of their own limitations, may be unable to understand or
appreciate him. ... It would scarcely be fair to omit a word concerning the part which
is necessarily played by the advocate who calls the physician to the witness stand. He, too,
must be possessed of at least a modicum of knowledge concerning anatomy, surgery and
pathology—sufficient, in any event, to enable him to lead his medical witness along the
proper paths, as well as to outline to them in advance the subject concerning which they
are to be interrogated. The most pathetic and helpless figure in any courtroom is an attorney who, knowing little or nothing of the scientific or technical matters around which a
controversy may revolve, seeks to examine or cross-examine an expert witness who is
thoroughly familiar with them.
"And it is well, in most cases, for the physician who is about to be called into court to
require beforehand of counsel some information concerning the subject matter which is
to be discussed, and to familiarize himself (if he should not already* be entirely* familiar)
with the available literature, so that he may be adequately prepared to meet the attempted
cross-examination of some impertinent counsel who is wholly destitute of the requisite
scientific knowledge, but who has learned a few technical terms or the titles of a few books
which he does not hesitate to use indiscriminately, and with which he may vastly impress
gullible and giddy jurors."
The importance of the attitude of the medical and legal professions relative to the
establishment and proof of claims is also significant. Many physicians of good reputation
and high professional standing are loath to give expert opinion and testimony because of
distasteful experiences involving the distortion of scientific data; others, less well-informed,
have, probably because of financial pressure, and acceding to the overtures of ill-advised
but well-intentioned attorneys, given evidence leading to decisions based upon an erroneous
interpretation of incomplete technical material. Nevertheless, many instances may be cited
in illustration of cases where counsel for either or both sides has functioned honestly and
adequately, giving the best possible interpretation of the facts presented, under the circumstances.
To those who have had experience in the courts and before commissions, it is evident
that both the medical and legal professions are too little acquainted with the customary
procedures of the other; to achieve the desired results and to cause the commission or jury
to understand the important factors in any given case, involves the use of sincere and
honest motives and the detailed study of all factors concerned, together with a scholarly
evaluation on the part of the representatives of both professions.
It is not always easy to accomplish these results; important evidence may be missing or
unobtainable; expert testimony, even in the hands of those who should know, may be
contradictory; but perhaps the most important single point in the adequate achievement
of justice is a proper interpretation and use of the facts which are available. Perhaps the
most important guiding principle is the thorough co-operation of a capable industrial
physician, who has a wholesome regard for scientific data and can use them to good advantage,—with an attorney who has similar high regard for legal procedures, and the adaptation of the physician's ability, experience, and scientific interpretation, to the case in
Before this principle can be put into effect, it is necessary to have at least a certain
amount of fundamental information to be used as the basis for the development of further
ideas and the adaptation of them as found expedient.
It has been the purpose of this monograph, therefore, to outline some of the more
important conceptions which can be used in the ways indicated.
Page 10 British  Columbia  Medical   Association
(Canadian Medical Association, British Columbia Division)
President Dr. F. M. Auld, Nelson
First Vice-President Dr. E. Murray Blair, Vancouver
Second Vice-President Dr. C. H. Hankinson, Prince Rupert
Honorary Secretary-Treasurer Dr. A. H. Spohn, Vancouver
Immediate Past President Dr. D. E. H. Cleveland, Vancouver
Executive Secretary . Dr. M. W. Thomas, Vancouver
Dr. P. A. C. Cousland, Victoria; Dr. Anson G. Frost, Vancouver; Dr. Herbert McGregor,
Penticton; Dr. P. L. Straith, Courtenay; Dr Wallace "Wilson, Vancouver.
Dr. W. E. Ainley, Vancouver —Representative, College of Physicians
and Surgeons of British Columbia.
Dr. L. H. Appleby, Vancouver Representative, College of Physicians
and Surgeons of British Columbia.
Dr. L. H. Leeson, Vancouver Vancouver Medical Association.
Dr. W. Allan Fraser, Victoria Victoria Medical Society.
Dr. F. R. G. Langston, New Westminster Fraser Valley Medical Association.
Dr. D. P. Hanington, Ladysmith Upper Island Medical Association.
Dr. C. H. Hankinson, Prince Rupert Prince Rupert Medical Association.
Dr. J. Stuart Daly, Trail , West Kootenay Medical Association.
Dr. F. E. Coy, Invermere East Kootenay Medical Association. •
Dr. J. C. M. Willoughby, Kamloops District No. 4 Medical Association.
Dr. R. V. McCarley, North Vancouver North Shore Medical Society.
Sept. 18-21 Inclusive
Both in quantity and quality, and especially in the latter, this year's meeting has set
a very high standard. One heard from every side remarks to the effect that it was easily
the best meeting we have ever held.
Many things contributed to this. First, the pre-operative preparation, to use a technical
phrase, was extremely thorough and painstaking: this is the more remarkable, perhaps,
since the man chiefly responsible is a very well-known internist, and not a surgeon. Perhaps there is something, after all, in the suggestion that the pre-operative care of our
patients would be best undertaken by an internist rather than by the surgeon.
In any case, Dr. G. F. Strong, Chairman of the Committee in Charge of Programme
and Arrangements, did excellent work, assisted by a very loyal Committee, and, we need
hardly say, by our Secretary, Dr. M. W. Thomas. It is, of course, axiomatic that no amount
of enthusiasm, or effort is of any value unless it is adequately translated into action, and
it is here that Dr. Thomas comes in. Our President, Dr. D. E. H. Cleveland, feelingly
referred to him as the "human gadfly." It is not possible for honest Chairmen of Committees (we were one) to get a good nap as long as Herr Gadfly Thomas is around, and he
shares with Father O'Flynn of pious memory the faculty of "helping the lazy ones on wid
a stick."
Anyway, there was excellent preparation, and that was more than half the battle, and
we feel grateful to these organizers of success. To Dr. Thomas particularly, this Annual
Meeting is the culmination of a year's effort and work on behalf of the medical profession,
and the reports and discussions shewed that a great deal was done of a really constructive
nature. Those responsible for the meeting will be feeling greatly gratified at the results
which crowned their work, and they earned both our thanks and congratulations. Every-
Page 11 thing went very smoothly: projectors worked—there were no hitches.   These things do
not just happen: they have to be worked for.
The place of meeting was, too, largely responsible for the success of this; convention.
The new Hotel Vancouver is, beyond doubt, an ideal place for such affairs. We had a floor
practically to ourselves—the elevator and other service was excellent—and the "layout"
was especially good from our point of view, as it was quickly and easily reached, and very
convenient. An important advantage, too, was that all exhibits enjoyed a very favourable
position. Instead of having to be sidetracked off the main line of traffic as they have always
been hitherto, they were right where everyone had to pass them, and! the comments from
the exhibitors, as far as we heard them, were most favourable and appreciative. Perhaps one
of the greatest advantages we found this time was the admirable system of built-in loudspeaker arrangements that obtains all through the public rooms of this Hotel. Nobody had
to strain either their voices to be heard, or their ears td hear. The speakers could talk in
their natural voices, and everyone heard clearly.
One thing that we did hear unfavourable comment on, and, we honestly believe, the
only thing, was the chairs. They were too prim and stiff—there was no chance to relax
(perhaps this was intentional) and no place to put one's feet. Stillr this is a minor matter.
The papers and addresses were unif ormly excellent, and there is little choice between
them: from Dr. Cosbie of Toronto, who arrived as the meeting opened, had to change from
golf clothes, and was apologetically a few minutes late, through) Drs. Graham of Toronto,
Cushing of Montreal, Gibson of Winnipeg, to Scarlett of Calgary. Every paper was worth
hearing (we know, because for the first time in history we heard them all, except one)
and every paper reflected a great deal of care and trouble on the part of the speaker. These
papers, or abstracts and summaries, will later be published by the Bulletin.
The Round-Table Discussions, on Obstetrics, Nutritional Diseases, Fractures, etc.,
were admirable, well-led and most profitable. Discussion was free and much was gained
by these meetings, which constitute a vital feature of our annual gatherings.
The Public Health and Preventive) Medicine Section of our profession also contributed
greatly to this meeting, and al long afternoon given up to their talks and demonstrations
was one of the" best-spent periods of the whole affair.
Then Mr. Hugh Wolfenden, the Consulting Actuary to the Canadian Medical Association, who so fully won our affection and confidence by his admirable talks, his delightful
manner, and his complete ease and friendliness with us all. We could never have hoped to
be so completely at ease with one of these numerological wizards. Talking to him, listening
to him, discussing questions with him, one is apt to forget or overlook his eminence in his
domain, so simple and unaffected is hisf demeanour, and so friendly and kindly his personality. There is no doubt of the wisdom that asked him to become consultant to our profession, and we feel that his help and advice are going to be of quite indispensable value to us.
All that part of the meeting that was given up to the discussion of Medical Economics
was very good. Of course, there were- occasional differences of opinion, but on the whole,
very marked harmony was observed, and much was done: here again Mr. Wolfenden was of
great assistance to us in keeping our feet on the grounds pointing in a right and practicable
A highlight of the meeting was the Dinner (the Dinner, as there were several others)
held on the last evening: in the Banquet Room. Some hundrd or more men had been
playing golf that afternoon, over the beautiful Capilano Golf Course, and they arrived
hungry and thirsty. Both phases of appetite were adequately dealt with—and it was a
contented and happy crowd that turned, dinner over, and' tobacco well alight, to listen to
our honoured guest, the Hon. R. L. (Pat to you) Maitland, K.C., as he rose to make his
speech. It was an excellent and a timely speechl—as one has learned to expect from his well-
known speaker. A professional man himself, he appreciates the special needs and weaknesses of professional men: the dangers that "do so readily beset us," as the Book of Common Prayer has it—the dangers of haste and mechanical speech, of failure to keep one's
mind and brain and heart alert for the reactions of other minds and hearts, and, as he said,
even souls, to our speech and daily conduct—the need for kindliness and gentleness and forbearance: and with easy wit and humour he enlarged on this topic—"the power of words,"
our most commonly used tool.
Page 12 The retiring President, Dr. D. E. H. Cleveland, who has given so unsparingly of his
time and energy for the past year, acquitted himself nobly. He was everywhere, and to his
steady guiding hand is due much of the the unobtrusive ease with which the machinery
worked. In his introductions, short addresses, and so on, he was always happy and apposite
in his choice of words and phrases: and we congratulate him. personally on the success of his
meeting. To Dr. J. M. Auld, his successor, we tender our best wishes', for success.
Nelson was chosen as the venue of the next Annual Meeting for 1940: and we may as
well start making our plans now.
Any account of this meeting would be incomplete without a grateful acknowledgment
of the work of two people who really contributed' indispensable service to the Association.
We refer to Mrs. Bender, secretary to the College of Physicians and Surgeons, and Miss
Smith, the stenographer of the Association offices. We cannot recall going past the
door without seeing Mrs. Bender there. Apparently she neither eats nor sleeps, and yet manages always to preserve complete self-possession, and to be entirely efficient. Perhaps the
pleasantest memory many of our visitors will carry away with them will be thei gracious
courtesy and help they received unfailingly from this lady, and, too, from her assistant,
Miss Smith. These two ladies had a very great deal of work to do, and did it extremely well.
We had a large attendance. Some three hundred and forty-odd registrations are
recorded, and many local men came in without registration. Every part of the province
sent its representatives, and we met many visitors from our Southern neighbour, the United
States. As always, we were delighted to have them.
So, till another year rolls round, to all who helped to make this meeting the helpful and
constructive affair it was, thanks and farewell.
The Tournament was held this year at the Capilano Golf Course, the weather was perfect and there was an excellent turn-out of about 100) players, so that the whole affair was
most successful. Drs. D. F. Murray and J. P. Bilodeau were in charge of all arrangements,
and had a total of twenty-six prizes to award at the? Dinner! the following evening. The
Mead Johnson Cup for the best low net score was Won by Dr. Neil' McNeil, with score of
91 less 24—67. Dr. Bilodeau won the low gross with a score of 79, and Dr. Morton of
the Vancouver General Hospital came next with a low gross of 80. Dr. Leith Webster
won the second prize for low net with a net score of 69. Dr. Morton came next in the low
net score, as his handicap of 9 brought his net score down to 71.
When the prizes were awarded a fine box of chocolates was awarded! to Dr. M. W.
Thomas,, not because he played golf, but because during the whole meeting he was "hitting
the ball." To Mr. Pat Maitland was also awarded :a box of chocolates, not because he was
the best lawyer, not because he was the best speaker, but just because he was "Pat Maitland."
Arrangements for this are in the hands' of Drs. G. A. Davidson and H. H. Pitts.
m ■RSlIAND treatment* ;|
By Dwight L. Wilbur, M.D.
San Francisco.
The concept that disease may be due to deficiency of vitamins has received such widespread proof, and has been so universally accepted, that our clinical interest must now turn
to means of recognizing and treating vitamin-deficiency states as well as to a study of the
events leading to development of them.
Character of Deficiency States
For purposes of a clearer understanding of deficiency diseases and the difficulties surrounding recognition of them, a simple grouping is of considerable value. In the first
group are those patients who, with a marked degree of deficiency, present a classical
deficiency disease, as xerophthalmia, beriberi, or pellagra, all rare in this country.
In a second group may be placed those diseases which are usually due to a moderate
degree of deficiency, such as the multple neuritis of chronic alcoholism, nutritional night
Table 1.—The Character of Vitamin-Deficiency 'States
Degree of
Clinical Signs
Essential Changes
Classical Deficiency
Clinical findings
Pathologic and
Physiologic '
Clinical findings
Laboratory tests
Laboratory tests
blindness, certain types of macrocytic anaemia and glossitis. In these cases the deficiency
is less marked than in the, cases of the preceding group, the symptoms depend on physiologic and pathologic changes, and the diagnosis may rely on the use of special diagnostic
In many respects the sequence of events in these two groups of "deficiency states" may
be likened to those occurring in patients with diabetes, nephritis or cardiac disease. Patients
with a marked degree of vitamin deficiency may be said to be analogous to diabetic or
nephritic patients who are in coma, or to cardiac patients who are decompensated and in
whom the pathologic changes are extensive and the diagnosis may be made by clinical
means alone. Patients with less marked degrees of deficiency, in whom the pathologic
changes are less obvious but the physiologic ones very definite, may be considered analogous
to patients with definite diabetes, nephritis or heart disease, in whomi the symptoms may
depend as much on physiologic as on pathologic changes, and in which special tests may
or may not be required before a diagnosis can be established.
In a third group may be placed those conditions in which the deficiency is mild and in
which recognition of the deficiency may be said principally to depend upon physiologic or
chemical alterations rather than on pathologic ones. In fact, recognition of this group of
cases in which clinical changes are often absent has depended on the develpoment of special
tests, such as the biophotometric determination of dark adaptation of the eyes in vitamin
A deficiency and the chemical measurement of the saturation of the tissues with vitamin C.
The clinical significance of this group of "deficiency states" has not been settled. To carry
further the previous mentioned analogy, one might say that this group corresponds to
those diabetics in which the diagnosis can be made only after careful studies of the toler-
* Reprint from California and Western Medicine: March, 1939, Vol. 50, No. 3; April, 1939, Vol. 50,
No. 4: 450 Sutter Street, San Francisco.
Page 14 ance to dextrose, or with those nephritics who do not present clinical signs of renal disease
and in whom the diagnosis depends on careful study of the urinary sediment or of the
ability to concentrate urine.
Methods of Production of Deficiency Diseases: Types of Patients
It is commonly believed that vitamin-deficiency diseases occur only when the diet is
inadequate. While this is probably the most common cause of deficiency disease, there may
be other factors of etiologic importance, such as an increased demand for vitamins during
pregnancy, during fever and when the basal metabolism is increased, such as loss of or
destruction of vitamins after ingestion, and such as abnormalities in gastro-intestinal
function. (Table 2.)   During pregnancy and lactation, for example, the need for certain
Table 2.—Vitamin. Protein and Mineral Deficiency States May
Be Produced as a Result of:
1. Inadequate intake of essential substances in the diet.
2. Increased   requirements   during   periods   of   rapid   growth,
pregnancy, infections, fever, elevated basal metabolic rates.
3. Impaired or altered gastrointestinal function.
4. Altered metabolism of the vitamin.
vitamins may be increased from 10 to 100 per cent, or even more, above the requirement
for the normal person.
Vitamin-deficiency states should be looked for particularly among those patients who
have been on an adequate diet in an attempt to reduce weight, or (due to alcoholism, economic difficulties, faddism, or to poor therapeutic dietary advice, such as long-continued
elimination diets, diets for gastro-intestinal diseases, allergic conditions, and so forth.
(Table 3.)
The Diagnosis of Deficiency States
In considering the diagnosis of deficiency disease it is important to keep in mind the
fact that the clinical features of a deficiency disease may vary within wide limits. This is
due to the fact that there is great individual variation in the response of patients and also
Table 3.—Suspect and Look for Deficiency States
Wlien the diet is inadequate because of:
1. Economic difficulty.
2. Eccentricities, f addism, ignorance, alcoholism.
In association with or during
1.   Gastro-intestinal diseases.
3. Anorexia, dyspepsia, dysphagia, pain.
4. Therapeutic dietary inadequacy.
2.   Pregnancy, Infection, Hyperthyroidism.
experimental animals to the same deficiency diet, and that it is questionable if a vitamin-
deficiency state ever exists in pure form. There is almost always deficiency of more than
one of the vitamins in a single patient. In fact, McCollum and Simmonds pointed out some
time ago that it is questionable if a pure vitamin-deficiency state, with the possible exception of scurvy, ever has been produced in the experimental' animal.
The diagnosis of vitamin-deficiency states depends principally on clinical observations,
although there is rapidly accumulating laboratory evidence to suggest that certain chemical
or biologic tests may be useful in substantiating the diagnosis, or in establishing it in the
absence of clear-cut clinical findings. A therapeutic test also may be of considerable value
as diagnostic procedure, for now that some of the vitamins may be obtained in crystalline
form, the specific response to use of a pure form of a vitamin may be considered significant
in establishing a diagnosis in some cases.
Vitamin A Deficiency
Symptoms.—The most readily appreciated clinical symptoms of vitamin A deficiency
have to do with changes occurring in the eyes.   These symptoms consist principally of
night blindness or inability to see clearly in dusky light, and of irritation of or lesions? of
Page 15 the conjunctivae. In its most exaggerated form, xerophthalmia (which is rarely observed
in this country), there may be dryness of the conjunctival tissues, conjunctivitis, softening
of the cornea, infection of the eyeball, and blindness.
Night blindness, which occasionally may be due to intra-ocular disease such as retinitis
pigmentosa, is usually manifested by difficulty or inability of the patient to adapt his vision
to faint illumination, although during the daytime or in bright light he may see perfectly.
In questioning a patient in regard to night blindness, particular attention should be paid
to vision while driving a car at night, while in a theatre or? the movies, while walking at
night or in the dark, or on entering a house from the bright sunlight. Such patients are
apt to bump into things while walking at night, to have difficulty-in driving a car at night
because they cannot see the road or are dazzled by the lights of an approaching car, or to
have difficulty in distinguishing facial features, the hands of a clock, or details of a picture,
on entering a dimly lighted room.
A history of conjunctival irritation or dryness, which cannot be explained otherwise,
may be obtained in some patients with vitamin A deficiency. Examination of the conjunctiva; may reveal pigmentation, or there may be dryness or a granular appearance to
the conjunctiva if the lids are held away from the eyeball for a few moments.
There has been discussion of the relation of vitamin A deficiency to cutaneous lesions,
to lesions of the genital or urinary tract, and to states of lowered resistance to infections.
Since deficiency of vitamin A characteristically leads to thickening or keratinization of
epithelial tissues, followed frequently by secondary infection, it might be anticipated that
cutaneous lesions would occur in vitamin A deficiency. The characteristic change, which
is considered by some authorities to be the first manifestation of deficiency, consists of
keratinization of a hard, dry, papular type that resembles goose flesh and is most marked
on the exterior surfaces of the forearms, legs, and thighs. A somewhat similar keratinization of the mucous membrane of the vagina, leading to a lesion resembling that of atrophic
Table 4.—Vitamin A Deficiency
Degree of Deficiency
Clinical Signs
Very rare
Night blindness
Skin lesions
Conjunctival lesions
Epithelial lesions of mucous surfaces
1. Biophotometer
2. Scrapings of
mucous surfaces
Mild  (Preclinical?)
25 to 75 per cent of all
children and adults?
3.   Therapeutic
or senile vaginitis, has been reported in vitamin A deficiency. The relation of vitamin A
deficiency to renal lithiasis in man is still indefinite, and while there is evidence to substantiate the view that in some cases renal lithiasis may be related to deficiency of vitamin A,
in most instances of stone this does not seem to be the case.
The only recognized anti-infective influence vitamin A possesses is in maintaining
normal epithelium, which will act as a barrier to infection; and since, so far as is known,
the vitamin does not have any influence on immunological processes, it seems obvious that
vitamin A in reality is not an anti-infective vitamin.
Diagnosis.—Principal interest at present in the diagnosis of vitamin A deficiency is in
the detection of states of mild or partial deficiency in which the clinical diagnosis is not
easy. (Table 4.) When the physician is confronted by a patients who he suspects may
have vitamin A deficiency, he should inquire into the presence of night blindness; and on
examining the patient he should look for dryness ot pigmentation of the conjunctivae and
for a papular cutaneous eruption involving particularly the limbs, especially the exterior
If vitamin A deficiency is suspected, there are three methods of diagnosis which may
be employed in an attempt to confirm the clinical history suggesting that a deficiency exists
Page 16 or to suggest its presence in the absence of clinical findings. There are: (1) a study of the
sensitivity to light following partial adaptation to darkness, as determined by biophoto-
metric methods of Jeans and Zentmire; (2) scrapping of the conjunctival, nasal or vaginal
mucous membrane, making smears and examining them for keratinized epithelial cells;
and (3 ) administration of vitamin A in crystalline or concentrate form. These methods
are all relatively indirect, but if either of the first two test9 proves to be positive, and if
there is disappearance of these signs or of previously noted night blindness or cutaneous dr
conjunctival symptoms following administration of vitamin A or carotene, the diagnosis
of vitamin A deficiency seems reasonably well established.
The diagnosis of very mild or "preclinical" deficiency of vitamin A in which clinical
signs are absent is made at present only by use of the biophotometer. Patients who have no
clinical evidence of vitamin A deficiency, but who have defective adaptation to darkness
as revealed by this test, and who have normal adaptation after administration of vitamin A,
are considered by some observers to have mild deficiency of vitamin A.
Treatment.—Deficiency of vitamin A usually may be prevented by the use of adequate
amounts of the following foods rich in vitamin A or carotene: butter, cream, eggs, cod-
liver oil, carrots and spinach. Fish-liver oils which are particularly rich in vitamin A are
those of the halibut, cod, turbot and tuna.
The daily optimal requirement of vitamin A is not known, but it is probably in the
neighborhood of 6,000 to 10,000 U.S.P. units. In the treatment of vitamin A deficiency
states, the following measures are of value: (1) a diet containing many foods rich in vitamin A; (2) supplements to the diet of vitamin A ini cod or halibut-liver oil in amounts
of 10,000 to 25,000 U.S.P. units daily (Jeghers suggests) 70,000 U.S.P. units orally for
two weeks, and then 25,000 units until the patient is normal); (3) in rare instances by
intramuscular injection of cod-liver oil or other substances rich in vitamin A.
Vitamin Bi (Thiamin) Deficiency
Symptoms.—Thiamin is a catalyst essential for the oxidation of carbohydrates, and
when it is not present in adequate amounts in man the characteristic symptoms of peripheral neuritis, circulatory failure and beriberi occur. (Table 5.)
As Strauss and others have indicate, the diagnosis of alcoholic, diabetic, biliary, gastro-
genic and postinfective polyneuritis, polyneuritis of pregnancy, and of Korsakoff's syndrome, have all concealed the true diagnosis of thiamin (vitamin Bi) deficiency.   While
Table 5.—Thiamin Deficiency (Vitamin B\)
Degre of Deficiency
Clinical Signs
Peripheral neuritis
Cardiovascular disturbances
Gastro-intestinal dysfunction?*
1. Calculations
Cowgills Formula
2. Therapeutic
3. Amounts of Thiamin in blood and
Mild  (Preclinical?)
Changes in these organs are very frequently associated with thiamin deficiency, but are probably
due to deficiency of components of the vitamin B complex other than i thiamin.
symptoms of these conditions may be sudden in onset they are generally insidious, and the
earliest manifestations usually are heaviness in the legs and tendernessf of the calf muscles
when they are squeezed. Weakness of the limbs, burning of the soles, and numbness of the
dorsum and lower part of the ankles are next to appear, followed by hypaesthesia, which
advances up the leg and thigh, and by atrophy of the muscles and of the skin. With these
symptomatic changes there usually are associated diminished or absent reflexes in the
involved extremities and various degrees of muscle weakness.
Page 17 The cardiovascular manifestations of thiamin deficiency have been extensively studied
by Weiss and Wilkins, and consist principally of dyspnoea and palpitation on exertion,
tachycardia, and cedema. In cases in which the deficiency is greater the clinical picture
may be that of cardiac failure with an enlarged area of cardiac dullness or an enlarged
shadow on the roentgenogram, signs of right or left heart failure^ and extensive cedema or
anasarca with or without signs of peripheral neuritis. It is obvious that in the absence
of marked changes these manifestations do not, for the present at least, constitute a rigid
and easily recognized clinical syndrome.
Other manifestations of thiamin deficiency which have been reported over a period
of years include gastro-intestinal changes such as anorexia, glossitis, achlorhydria and
diarrhoea, and changes in the blood such as those indicating anaemia. As Strauss has pointed
out, there is considerable evidence to suggest that these phenomena are, at least in part if
not entirely, manifestations of a deficiency of some portion of the vitamin B complex
other than thiamin.
Diagnosis.—The diagnosis of well-established thiamin deficiency is simple if the
characteristic triad of symptoms of beriberi, namely, cedema, peripheral neuritis and
cardiac failure, is present.
The diagnosis of a moderate degree of thiamin deficiency is usually not difficult, and
with increasing recognition of the fact that peripheral neuritis is usually due to thiamin
deficiency, the diagnosis is being made much more commonly than it was a few years ago.
Recognition of cardiovascular symptoms as being due to thiamin deficiency has been a
much more recent development and, because of this fact and the nonspecific character of
the symptoms and findings, namely, dyspnoea and palpitation on exertion, cedema, and
circulatory failure, the diagnosis is more difficult to establish.
Thiamin deficiency is usually to be found in chronic alcoholics, among patients who
have been on a limited diet as a result of economic disability, f addism, ignorance or in an
attempt to reduce weight, and during pregnancy and lactation.
There are no laboratory procedures which are helpful in determining the adequacy of
the thiamin metabolism of a patient. Recently, several biologic tests revealing the apparent
thiamin content of tissue fluids or of urine have been developed, but they are not of sufficient simplicity and perhaps accuracy to permit their use in the ordinary clinical laboratory. However, there are two other methods which will enable the physician to suspect
that symptoms of his patient are due to thiamin deficiency. These are the calculations of
Cowgill's formula and the therapeutic test. In cases in which the previous diet is known,
an estimation of the adequacy of the tlnamin content of the diet, as compared' with the
requirement of the patient, may be made by Cowgill's formula. Cowgill has shown that
the requirement for thiamin is proportional to both intake of calories and body weight.
The therapeutic test with thiamin may be very useful in establishing a diagnosis of
previous deficiency, but great care must be exercised in regard to the interpretation of the
clearing up of cardiovascular symptoms, because frequently associated methods of treatment, such as rest in bed, sedatives, digitalis, and psychic mfluences, may be the significant curative factors.
Evidence for thiamin deficiency of very mild character has not been established because
of lack of chemical or other direct methods of determining the status of thiamin metabo;
lism in patients with clinically recognizable deficiency.
Not infrequently, in association with thiamin deficiency, will be found evidence of
deficiency of other components of the vitamin B complex, such as gastro-intestinal symptoms or macrocytic anaemia. These symptoms and findings may prove helpful in establishing the correct figures.
Treatment.—In the treatment of thiamin deficiency the exhibition of all of the following measures will be found most helpful: an adequate diet high in vitamin B content,
preparations of brewers' yeast or wheat germ and crystalline thiamin chlorid. While
crystalline preparations are available they should not, for two reasons, be used exclusively
in the treatment of thiamin deficiency: first, because, as has been pointed out, most patients
with thiamin deficiency have evidence of deficiency of other components of the B complex,
and secondly, because crystalline thiamin chloride is still quite expensive.
Page 18 For those patients with only moderate deficiency, and without evidence of impairment
of gastro-intestinal function, the use of 30 grams of powdered brewer's yeast of good
potency, or 6 grams of autolyzed yeast, administered three times daily, is generally adequate. Along with this should be a high caloric, high vitamin diet, if it can be tolerated,
and from 10 to 40 milligrams of thiamin chloride daily, intramuscularly or orally administered. For those patients with severe cardiac symptoms, daily intramuscular or intravenous injections of similar doses of thiamin may be advisable. In addition, dilute liver
extracts, suitable for intramuscular injection, given in doses of 10 to 20 cubic centimeters
or more daily, are helpful in controlling glossitis and cutaneous manifestations of the type
associated with pellagra. As soon as the patient shows evidence of distinct improvement,
the dose of crystalline thiamin may perhaps be reduced to 10 to 15 milligrams daily; but
Table 6.—Vitamin B deficiency (Other than in Thiamin)
Clinical Changes
Deficiency of
Nicotinic  acid
Other factors?
Therapeutic only
Macrocytic ansemia
Therapeutic only
Therapeutic only
it is advisable to maintain large doses of thiamin and other portions of the vitamin B
complex, in the form of food and of yeast and wheat germ.
Deficiency of Vitamin B (Other than Thiamin)
The vitamin B complex consists of a variety of factors/ other than thiamin, such as
riboflavin, the P-P factor (nicotinic acid?), a filtrate factor, vitamin B^, and others.
However, so far only two members of the complex, namely, thiamin and the P-P factor,
have been linked unquestionably with deficiency disease in man. (Table 6.)
Deficiency of P-P Factor (Vitamin G, B2, Nicotinic Acid?)
Symptoms.—Efficiency of this factor leads to the development of pellagra, the characteristic symptoms of which are three D's—diarrhoea, dementia, and dermatitis—but these
occur simultaneously in severe cases only. Perhaps the most characteristic feature is the
dermatitis, without which the diagnosis is questionable. The, cutaneous lesions consist of
a dermatitis suggesting sunburn; a reddened, dirty brown skin, parchment-like, rough and
scaling and affecting principally the exposed surface, especially the backs of the hands,
wrists and forearms/usually in a symmetrical fashion. The face, neck, genitalia, and legs
may be similarly affected. Gastro-intestinal symptoms which accompany pellagra are
variable, although severe glossitis and diarrhoea are the most common. The stomatitis may
consist of a brick-red colour of the tongue, gums and cheeks, or there may be, in addition,
considerable oedema, ulceration, and exudation. Diarrhoea may be intractable. Anorexia,
vague abdominal distress, and, at times, constipation may be present. Loss of weight is
common, as are also nervous symptoms such as those of peripheral neuritis or of neurasthenia, namely, exhaustion, lassitude, and insomnia. The occurrence of any of these
symptoms, accompanied by dermatitis of the type mentioned, should suggest the possibility of pellagra.
Diagnosis.—The diagnosis of pellagra depends entirely on the symptoms. While diagnostic and laboratory tests have not been developed, therapeutic test with nicotinic acid is
proving of considerable diagnostic value.
Mild degrees of deficiency of the P-P factor are not clear-cut and little is known about
them. The occurrence of otherwise unexplained glossitis, or vague gastro-intestinal symp-
Page 19 toms with diarrhoea, with or without symptoms referable to the nervous system, have been
thought by some observers to be due to early pellagra or deficiency of vitamin G (B2) •
The therapeutic effect of nicotinic acid in such cases may be of considerable diagnostic
value if psychic influences can be controlled.
Treatment.—The daily requirement of the P-P factor or of nicotinic acid is unknown;
nevertheless, the treatment of pellagra has become very effective, largely as a result of
the work of Spies and his associates. It has been shown that the effective measures in treatment are a diet high in calories, proteins and vitamins (3,500 to 4,000 calories), supplemented by nicotinic acid in doses of 500 to 1,000 milligrams, by thiamin chlorid in doses
of 20 to 50 milligrams, by powdered brewers' yeast in doses of 75 to 150 grams, or by
dilute liver extract in doses of 25 to 75 cubic centimeters daily. Early in the course of the
treatment the vitamin supplements may be administered parenterally to those patients who,
because of a sore mouth or vomiting, cannot tolerate an adequate diet. Bed rest, good
nursing care and symptomatc treatment, consisting of sedatives, antiseptic solutions (such
as potassium permanganate 1:5000 applied to the skin, and tincture of opium in large
doses to control diarrhoea), are also valuable adjuncts in treatment.
Since pellagra of the secondary type occurs not uncommonly in association with organic
lesions in the gastro-intestinal tract, particularly with those which produce obstruction
and with malignant disease of the stomach and colon, it is important to exclude gastrointestinal disease before dismissing the patient.
Anamia—Abnormalities in the Gastro-intestinal Tract.—Little is known of the etio-
logic factor or factors leading to the development of macrocytic anaemia, which is commonly observed in pellagra, beriberi, and other cases of deficiency of the vitamin B complex. The relation between this type of anaemia and that of pernicious anaemia is also not
clear. However, some factor in the vitamin B complex, but not thiamin, seems responsible
for the macrocytic anaemia of pellagra, beriberi and similar deficiency states.
Apparently gastro-intestinal symptoms, such as anorexia, glossitis, achlorhydria, hypomotility and hypotonicity, particularly of the small intestine, and diarrhoea, are commonly
associated with deficiency of the vitamin B complex. In some patients the clinical picture
is characteristic of pellagra, in others it is not. Whether deficiencies of thiamin and of
nicotinic acid will explain all of these symptoms is not clear.
Vitamin C
Symptoms.—The most readily appreciated symptoms of deficiency of the antiscorbutic
vitamin have to do with haemorrhagic phenomena. This is due to the fact that the? fundamental pathologic change in vitamin C deficiency is in the intercellular substance, particularly of the blood vessels, with softening of this substance which leads to haemorrhage
into the subcutaneous, subperiosteal, gingival and other tissues. It has been observed that
the intercellular substance, which ordinarily exists as a solid or gel, under circumstances
of vitamin C deficiency may soften and become a liquid. Consequently, there has been
much discussion of the possible role of vitamin C deficiency in acute and chronic haemor-
Table 7.—Vitamin C Deficiency
Degree of deficiency
Clinical Signs
1. Capillary resistance
2. Urinary excretion
Mild  (Preclinical?)
Infantile scurvy
Hemorrhagic states
Dental caries
Increased susceptibility
to infections
3. Plasma levels
4. Intradermal
5. X-ray of bones
6. Therapeutic
' Above in milder form
Page 20 rhagic phenomena of the so-called "essential" or idiopathic type, and as to whether vitamin
C deficiency may be a contributing factor in leading to haemorrhages in cases of peptic
ulcer, menorrhagia, essential haematuria, subdural haematoma, and soi forth. (Table 7.)
Vitamin C deficiency has also been connected with dental caries, anaemia, and with
increased susceptibility to infections. Most patients with infections! require vitamin C in
larger than usual quantities if normal levels are to be maintained in the blood and if normal
quantities are to be excreted in the urine. Most observers are inclined to the opinion that
this is due to the increased demand for vitamin C as a result of the infection, while others
are inclined to the belief that a state of partial vitamin C deficiency may have predisposed
to the development of the infection.
Diagnosis.—The clinical diagnosis of scurvy is relatively simple in a well-developed
case. However, the clinical diagnosis of latent or preclinical scurvy isi not so easy, although
it may be suspected in patients who have unexplained haemorrhages of any type or in any
situation, who have long-continued infections, or who have considerable dental caries.
It is exceedingly important to emphasize that such conditions do not establish the diagnosis
of vitamin C deficiency, but only suggest the possibility of it.
Fortunately, we possess better methods of determining the presence or absence of
partial deficiency of vitamin C than of any other vitamin. These methods include the
capillary resistance test, roentgen-ray studies of bones, intradermal test, studies of the
levels of vitamin <-C in plasma and of the excretion of the vitamin in the urine, and vitamin C tolerance tests.
One simple method of performing the capillary resistance test in the office is to mark
an area on the skin, 60 millimeters in diameter, in the anticubital fossa of one forearm.
Following this, venous stasis is produced for fifteen minutes with a sphygmomanometer
cuff at a pressure of 50 millimeters of mercury. If more than! eight petechiae develop on
the marked area the test is positive; if less than five develop, it is negative. Although this
test is not specific, it is suggestive, and if positive in a case in which vitamin C deficiency
is suspected, it should lead to studies either of vitamin C saturation or to treatment with
vitamin C.
Methods of determining the vitamin C content of the plasma and the urine depend on
the titration of these fluids with the indicator, 2-6 dichlorophenoHndophenoll. The titra-
ton of the urine is relatively simple and may be done in the physician's office if proper precautions are taken to preserve the urine in a dark bottle containing 10 per cent by volume
of glacial acetic acid. The amount of vitamin C excreted in the urine by the normal individual in twenty-four hours is approximately 20 to 30 milligrams, while the vitamin C
content of the blood plasma of the normal individual is in the neighborhood of 0.7 to 1.3
milligrams per hundred cubic centimeters of blood.
The most satisfactory method of deterrnining vitamin C deficiency is in a measure of
these levels and in an estimation of the tolerance of the patient to a test dose of vitamin C.
The diagnosis of very mild states of vitamin C deficiency depends entirely on such a
chemical determination because clinical symptoms are lacking in these cases. There has
been considerable discussion of the real clinical significance of such abnormal tests, for,
as Finkle has pointed out, a fairly large proportion of the population suffers from an under-
saturation of vitamin C. He believes that as yet there isi no evidence to justify the conclusion that vitamin C deficiency has a causal relation to1 any pathologic condition other
than scurvy.
Treatment.—Vitamin C deficiency may be avoided by intake of a diet adequate in
fresh fruits, particularly of the citrus variety, and vegetables. The minimal intake necessary to prevent signs of deficiency is not certain, but probably approximates 20 to 40
milligrams daily.
In the treatment of deficiency the diet should be high in its content of the above-noted
foods, which may be supplemented by the administration of vitamin C in synthetic crystalline form, by mouth or intravenously, in doses of from 50 to 200 rnilligrams. In cases with
haemorrhage n which rapid saturation of the tissues with vitamin C is desired, larger doses,
such as 1000 rnilligrams, may be given daily for two to three days and then reduced to
levels of from 100 to 300 milligrams daily until the therapeutic response is complete.
Page 21 Vitamin D Deficiency
Symptoms.—Vitamin D is the antirachitic vitamin which plays an essential role in the
metabolism of calcium and phosphorus, and has to do in particular with the retention of
Table 8.—Vitamin D Deficiency
Degree of Deficiency
Clinical signs
1. X-ray of bones
2. Blood phosphatase
3. Therapeutic
Dental caries
Inadequate mineralization
of bone
(50-90 per cent of
Mild  (Preclinical?)
(Above in milder forms?)
calcium and phosphorus in the body, in the deposit of these substances in bones and, perhaps, in the concentration of these elements in the blood. (Table 8.)
Rickets is such a widespread condition in infancy ( 5 0 to 90 per cent of infants are stated
to have it) that it may be classified as probably the most common deficiency disease. Vitamin D deficiency in adults may lead to osteomalacia, which is very rare in the United States.
It is probable also that certain forms of osteoporosis, of tetany, and possibly of dental
caries, are the result of vitamin D deficiency, either because of an inadequate diet or
because of interference with absorption of the vitamin or of calcium from the intestine.
Diagnosis.—The diagnosis of rickets is usually simple. When the classical symptoms
are present, the diagnosis is obvious clinically. In cases in which the symptoms are less
clear-cut, the diagnosis may be suspected clinically and confirmed by roentgenologic
studies of the bones. Further confirmatory evidence may be obtained by determination of
the blood phosphatase, which usually is increased in rickets. The therapeutic test with the
administration of vitamin D may be helpful in establishing the diagnosis.
States of partial deficiency of vitamin D may be suspected if persons have dental caries,
tetany, frequently occurring fractures or osteoporosis of the bones. During pregnancy or
lactation, and among patients who are jaundiced or who have abnormalities of intestinal
absorption such as occur in celiac disease and sprue, deficiency of vitamin D is most likely
to be present. Whether the deficiency in such cases \s the result of deficiency of calcium
or phosphorus, or of abnormalities in function of the parathyroid glands may be difficult
to determine. The administration of vitamin D may be helpful in distinguishing osteoporosis which is on a basis of deficiency from other types of osteoporosis, but a satisfactory
response does not necessarily prove that the osteoporosis is attributable to vitamin D
deficiency alone.
Treatment.—While there are at least ten different sterol derivatives which exhibit the
properties of vitamin D, only two of these are known to be of prime importance in medicine. These are activated ergosterol or calciferol, which is the vitamin D of viosterol,
irradiated yeast and yeast milk, and 7-dehydrochlosterol, which is the chief sterol of animal fats.
Rickets may be prevented by supplying the infant each day with one of the following:
(1) two standard teaspoonfuls of cod-liver oil, which meets the requirements of the New
and Nonofficial Remedies (1936); (2) one quart of milk containing 400 U.S.P. units of
vitamin D to the quart; (3) five drops of viosterol (1.125 U.S.P. units) ; (4) irradiation
of the skin with ultraviolet light.
In the treatment of rickets, a dose of twenty drops of viosterol (4500 U.S.P. units) or
a similar number of units of vitamin D in another form is effective. Vitamin D may be
supplied also in the form of fish-liver oils, or irradiated yeast, milk and cereals, of milk to
which a concentrate of vitamin D had been added, or by irradiation of the skin.
Page 22 In adults with senile osteoporosis, ten drops of viosterol three times daily in conjunction
with four drams of calcium lactate or tribasic calcium phosphate three times daily often
will relieve symptoms.
Deficiencies of Other Vitaminss Vitamin E
At least three substances possess the effect of vitamin E, but as yet it has not been
clearly demonstrated that any of them is required by man for normal health or reproduction. Of principal clinical interest is the possible etiologic role of deficiency of vitamin E
in threatened and spontaneous abortion, and of an excess of the vitamin in malignant
disease. It is difficult to obtain proof that vitamin E is of value in the treatment of
sterility and habitual abortion in human beings, and much more evidence is greatly needed
to establish the usefulness of vitamin E in abnormal human reproduction.
Vitamin K
Apparently the antihaemorrhagic factor, known as vitamin K, may play some role in
the production of prothrombin, for in certain species of animals deficiency of vitamin K
leads to a decrease in the prothrombin content of the blood. In considering the possible
therapeutic use of vitamin K in patients with jaundice it has been suggested that it is of
value because the prothrombin deficiency of such patients may be due to deficiency of
vitamin K, since vitamin K is fat-soluble and there is frequently interference of absorption of fat in patients with jaundice. Vitamin K is not available on the market, but substances rich in it are green vegetables, pig-liver fat, hemp seed, and alfalfa.
Use 'of Vitamins
Use of Vitamins in Persons Who Are Chronically Fatigued, Rundown, Underweight,
Below Par or Subject to Frequent Infections.
The diagnostic and therapeutic problems presented by patients who fall into this group
are often very difficult to solve. It goes without saying that great care must be used to
exclude the presence of an underlying organic disease when these symptoms are present,
and adequately to treat it. It is probable that, of the patients who fall into this group,
a certain number will present no distinguishable organic disease. Some of this latter group
of patients may be benefited by administration of vitamins while other patients may not,
depending on whether or not in a particular case the symptoms are due to vitamin deficiency
and depending to some extent on psychic influences.
How is one to tell which patients will do well and which poorly on vitamin therapy?
There is no clear-cut way to distinguish between these groups at the present time. However, the history of an inadequate diet, the presence of symptoms or findings of mild
deficiency states or the occurrence of abnormal responses to some of the diagnostic tests
previously mentioned may be helpful in determining the patients who may benefit from
vitamin therapy.
Table 9.—Vitamin Deficiencies
Average Daily Requirement
Average Daily Therapeutic Dose
International Units
International Units
G (B2)
300-500 milligrams nicotinic acid
10-100 grams brewer's yeast
10-75 cubic centimeters dilute liver extract
Mg. of synthetic HCl.    1 Average full-term infant.    2 Premature infant.    3 Adult and child.
Page 23 It is important to recall that the conditions we are discussing are symptoms rather than
diseases, and that it is essential to treat any underlying cause of them. It is no more sensible
to give vitamin therapy to all such patients than it is to give aspirin to all patients with
headache, codein to all who cough, or opium to all who have diarrhoea.
Table 10.—Protective Poods Which Serve as a Foundation for a Normal Diet
(Daily Quantities)
1 pint
3 large servings, besides potatoes (one a green leafy vegetable)
2 servings (one raw)
Meat, fish or fowl
1 serving  (about 2 ounces)
1 tablespoonful
Finally, too much stress cannot be placed on the importance of an adequate diet in the
prevention and treatment of deficiency diseases. It has been well said that the grocery store
is more important than the drug store.in the prevention and treatment of these conditions.
In the treatment of some deficiency states, crystals and concentrates of some of the vitamins are available and, while these products are extremely useful, they should always be
supplemented by vitamins in the natural state, i.e., in foods, yeast, cod-liver oil, and so
forth, not only because this is the way in which vitamins ordinarily are obtained by normal
persons, but especially because there are present in foods certain essential substances which
have not only been synthesized or concentrated, but of which at present we are only
vaguely aware. (Tables 9 and 10.)
By Gillean MacKinnon, M.D.
This study was undertaken to ascertain' the incidence of Bright's disease in the wards
of the Vancouver General Hospital.
During the year 1937 there were seventy-eight charts bearing the diagnosis of
nephritis. This heading did not include pyelonephritis, pyelitis, focal nephritis, nephroses
or traumatic lesions. It did include all forms of nephritis, acute and chronic. During 1937
there were seven cases of nephrosis.
The charts were studied for the following facts: Age, sex, clinical diagnosis, other
diagnoses, recovery or otherwise, whether or not an autopsy was done, the post-mortem
diagnosis, laboratory investigations (the N.P.N., kidney function tests, haemoglobin determination), urinalysis (presence of albumen, casts, and the specific gravity range as an
index of kidney function). We also noted whether the post-mortem diagnosis tallied with
the clinical diagnosis, whether the case was a private or a staff case, and the treatment
given. Finally, we appraised each case from the standpoint of adequate investigation. To
make a diagnosis of nephritis arbitrarily required that this should include determination
of the non-protein nitrogen, some indication of the specific gravity range, more than one
urinalysis, a haemoglobin determination and some kidney function test, preferably a urea
clearance test, although other tests were accepted.  Each case was considered on its own
Page 24
■ merits, and extenuating circumstances were remembered when assessing the adequacy of
Ant attempt was made to classify the cases of Bright's Disease. This was not easy in
view of the great variance of clinical and laboratory findings even in the same variety of
nephritis. Feeling that Prof. Boyd's text, "The Pathology of Internal Diseases," was both
authoritative and familiar, we adopted his classification:
I.    Bright's Disease: First stage—acute nephritis; second stage; subacute nephritis;
third stage; chronic nephritis.
II.    Arteriosclerotic kidney: (a) Senile arteriosclerotic; (b) hypertensive arteriosclerotic.
Bright's original account is contained in Major's work, "Classic Descriptions of Disease."
Richard Bright was born in Bristol in 1789 and was graduated from Edinburgh in the year
1813. In 1820 he became assistant physician to| Guy's Hospital, London, and in that city
he achieved a spectacular career, being renowned for the careful and minute records of
his cases. He died in 1858, the most widely known British physician.of his day. In 1827,
when he was thirty-eight years of age, he published his epoch-making work, "Reports of
Medical Cases, Selected with a View of Illustrating the Symptoms and Cure of Diseases by
a Reference to Morbid Anatomy." Speaking on "Dropsical Effusion," he says: "There are
other appearances to which I think too little attention has hitherto been paid. They are
those evidences of organic change which occasionally present themselves in the structure
of the kidney; and which, whether they are to be considered as the cause of the! dropsical
effusion or as the consequence of some other disease, cannot be unimportant. Where those
conditions of the kidney to which I allude have occurred, I have often found the dropsy
connected with the secretion of albuminous urine more or less coagulable onl ,the application of heat." And again, "I have in almost all instances found a great tendency to throw
off the red particles of the blood by the kidneys, betrayed by various degrees of haematuria,
from the simple dingy colour of the urine, ... to the completely bloody urine, when the
whole appears to be little but blood."
Thus, Bright's Disease, as originally described, would necessarily include the Nephroses,
the acute and chronic Nephritides, as well as the arteriosclerotic1 kidney.
Our findings, after the analysis of the three large groups of kidney lesions, as are shown
in the following table:
Type Number Deaths P. M. Investigation
-Acute . 20 5 2 8]
Subacute  3 2 1 1 33%
Chronic  25 13 2 7 J
Nephrosis  7 2 1 2 28%
Arteriosclerotic Kidney:
Senile £ 11 5 3 2 [
Hypersensitive | 6 2 2 0 5 11 %
Of the seventy-eight charts diagnosed "Nephritis," we rejected thirteen, for they were
either inadvertently included with the nephritis cases, were an allied kidney disease such
as pyelitis, or secondary kidney disease such as chronic passive congestion, or else it was
felt that there was not sufficient evidence to justify a diagnosis of nephritis. Of the sixty-
five cases of nephritis, twenty were of the acute variety, three were sub-acute, and th|e
remaining twenty-five cases were of chronic nephritis. Five out of the twenty cases of
acute nephritis died, two out of the three cases of subacute nephritis died, and of the
twenty-five chronic cases thirteen died.
Considering Boyd's second group, the arteriosclerotic kidney, there were eleven cases
of the so-called senile arteriosclerotic type, of which five proved fatal; six cases appeared to
be hypertensive in origin, and two of these died.
Boyd's third class in the group of kidney lesions includes die) I nephroses, and of these
there were seven cases, two of whom died. Only one of these cases came to post-mortem.
As for sex distribution, there were five males and two females. These showed no particular
age-incidence, the cases ranging from a four-weeks-old infant to an eighty-four-year-old
man.  It was decided that adequate investigation should include the basal metabolic rate,
Page 25 Wm a blood cholesterol determination and an albumen-globulin ratio. The nephrosis cases were
not thoroughly investigated and only two even approached the required standard.
In the nephritic cases, including the arteriosclerotic kidney, the sex distribution was:
males 41, females 24. Mortality was about 30%, twenty-six out of the sixty-five being
fatal cases. Only twelve cases came to post-mortem. Out of the sixty-five, only twenty-
three fulfilled the stipulations of "adequate investigation." Of these cases which were
adequately investigated, sixteen were "staff" cases.
1. "Staff" cases are more thoroughly worked up than "private," as one might anticipate, for economic reasons.
2. No definite age incidence could be remarked, apart from that fact that acute
nephritis tends to occur in the younger age groups.
3. There is a preponderance of male cases as compared with females in the nephritis
cases, the male cases comprising 63 %.
4. Only about a third of the cases were considered to have "adequate investigation."
The writer wishes to thank Dr. S. E. C. Turvey for help and suggestions in the preparation of this paper and also wishes to thank Mr. Fish of the Records Department for valuable assistance in placing the hospital files at his disposal.
Note: By B. M. Fahrni, M.D.
It is interesting to note the difficulty encountered by Dr. MacKinnon in attempting to
compile representative figures from the hospital charts. This may be the result of an
unsatisfactory classification nomenclature, briefly, "What exactly do we mean by the
term 'Bright's Disease'?" When we consider that only one-third of the cases in this seres
had a niinimum of investigation necessary for confirmation of the diagnosis, the difficulty
of a satisfactory scientific analysis of such charts is obvious.
When the question as to how many cases of acute nephritis progress to true chronic
(third stage) nephritis is so unsettled today, we should keep a closer check on our cases
here in an endeavour to help solve this problem. At present opinion varies from the school
of Aldrich, who believes that a case of acute nephritis clinically well is cured permanently,
providing the follow-up routine urinalyses are negative. At the other end of the swing
are men such as Addis, who by means of his cell count in the urinary sediment was the
first to trace closely the progression of cases of nephritis from the acute to chronic stage.
He feels that probably fifty per cent of all cases of acute haemorrhagic nephritis in children become latent and chronic cases. When routine analyses fail to show any evidence of
haematuria following the acute stage, red blood cells can frequently be demonstrated by
means of an Addis count of the urinary sediment of an overnight specimen of urine following a day of restricted fluids. Certainly such a procedure would be of inestimable benefit
in deterniining the diagnosis and prognosis of any case, and should probably be tried here.
50 West 50th Street, New York, N.Y.
Thirty-five hundred health officers, nurses, engineers, school physicians, laboratory
directors and other health specialists will attend the 68 th Annual Meeting of the American
Public Health Association and meetings of related organizations in Pittsburgh, Pa., beginning Sunday, October 15, and ending Friday, October 20.
Every state in the Union, Canada, Cuba and Mexico, and many European countries
will send their health leaders to participate in a scientific programme embracing the official
public health activities of the North American continent.
On Sunday, October 15, the Sixth Institute on Public Health Education begins. The
Institute continues on Monday, October 16, and the International Society of Medical
Health Officers, the American School Health Association, the Association of Women in
Public Health, and the National Organization, for Public Health/ Nursing also meet. Five
conference groups convene Monday: State Laboratory Directors, State Sanitary Engineers,
Municipal Public Health Engineers, Directors of Local Health Service and State Directors
of Public Health Nursing.
Six general sessions throughout the week will engage the attention of all delegates.
Page 26 Medical Care, Cancer, Professional Education, The American Way as Seen from Abroad
are among the subjects chosen for the general assemblies.
The ten Sections of the Association have arranged an extensive series of joint and individual meetings covering topics of interest to health officers, laboratory workers, vital
statisticians, industrial hygienists, public health engineers, food and nutritionists, child
hygienists, public health education experts, epidemiologists and public health nurses.
Other organizations meeting during the week are the Pennsylvania Public Health
Association, the Tri-State Food and Health Officials, the American Social Hygiene Association, Delta Omega, and the American Association of State Registration Executives.
An extensive Health Exhibit featuring commercial and scientific displays is an important part of the meeting.
Headquarters will be the William Penn Hotel.
The preliminary programme has been reprinted from the August issue of the American
Journal of Public Health and may be obtained from the American Health Association,
50 West 50th Street, New York, N.Y.
Victoria  Medical   Society
Officers, 1938-39.
President ; Dr. P. A. C. Cousland
Vice-President Dr. W. Allan Fraser
Hon. Secretary Dr. W. H. Moore
Hon. Treasurer Dr. C. A. Watson
G. A. McCurdy, M.D. Royal Jubilee Hospital, Victoria, B. C.
Perhaps no other haematological diagnostic procedure is so neglected as is the examination
of the bone marrow. Very often the clinician, in trying to understand an obscure blood
dyscrasia, has the peripheral blood examined in every possible way and the diagnosis still
remains doubtful; whereas if the bone marrow were examined the true nature of the condition would very often be revealed.
There are several reasons why the study of the bone marrow is not resorted to more
often. One reason is that many clinicians still believe that the peripheral blood always
reflects the changes which are continually going on in the bone marrow. Another reason
is that there exists, in the minds of many doctors, the idea that a bone marrow biopsy is a
radical procedure and the findings, while of academic interest, ana of little practical value
in their daily practice. Another reason is that, because of supposed technical difficulties,
the doctors are unwilling to subject their patients to thisi procedure. The answer to these
objections will, I hope, be made clear in what follows.
The routine clinical study of the bone marrow is a comparatively recent innovation,
for it was only in 1923 that Seyfarthl introduced a method utilizing the sternal marrow.
Previous to 1923 the tibial marrow was used', and not only was the approach difficult, but
the results were unsatisfactory and also misleading.
Technique of Sternal Puncture:
There are two satisfactory methods of obtaining sternal marrow. First, that of Dame-
shek, who uses a modified Seyf arth trephine (Codman & Shurtleff, Boston). The skin over
the sternum in the region of the third or fourth interspace is sterilized and then infiltrated
with 1% novocaine. A 2-4 cm. incision is made on the mid-line and the edges of the
incision are retracted with Allis forceps. The periosteum, after being infiltrated by novocaine, is incised and retracted. The bone is then trephined until it "gives." The trephine
is then removed with its enclosed plug of bone. The resulting cavity! is then scooped out
with a small curette and the marrow thus obtained is spread on clean sterile slides as in
making a blood film. Touch preparations' are also made. The small plug of bone is placed
Page 27 in Zenker-acetic fixative and prepared for sectioning. After the requisite amount of
marrow has been removed the wound is closed by one deep silkworm gut and two to four
horsehair skin sutures.
The second method is that proposed by Osgood and Young. Prepare the skin over the
sternomanubrial junction with iodine and alcohol. Using aseptic technic infiltrate the
skin, subcutaneous tissue and periosteum with about 4 cc. of 1 % procaine hydrohcloride.
The landmarks are the jugular notch for the midline and the ridge opposite the second ribs
for the sternomanubrial joint. When anaesthesia is complete, introduce the sternal puncture needle (16 gauge needle cut off to 3.5 cm. and rebeveled) vertically into the mid-line
of the joint. Then tilt the needle to an angle of 30-60 degrees with the sternum, and,
standing at the patient's head, introduce it into the marrow cavity by rotating the needle.
When the needle has entered the bone, remove the stylet and attach an absolutely tight 10
cc. syringe. With the syringe aspirate 1 to 2 cc. of marrow, loosen the syringe from the
needle and introduce the marrow into a 4 x l/z -inch test tube containing 2 to 4 mgm. of
dry potassium oxalate. Cork and mix thoroughly. Replace the stylet in the sternal puncture needle and withdraw needle quickly. Place a drop of collodion over the point of
The oxalated marrow should1 be sent at once to the laboratory, where thin smears are
made and stained.
Either of these methods will give satisfactory results. The advantage of the Dameshek
method is that one is able to prepare a section of the bone marrow and study the histological relationship of the various cells. The advantage of the aspiration method is that it
it simpler to perform, but has the disadvantage that the reticulo-endothelial cells and other
cells firmly fixed in place will not be aspirated.
In the study of marrow slides the following nucleated cells of the red cell series must
be noted: normoblasts, erythroblasts, pro-erythroblasts, megaloblasts and pro-melagoblasts.
The latter three cells are characteristic of pernicious anaemia. The other cells to be classi-.
fied and enumerated are as! follows: mature neutrophiles 2-5%,metamyelocytes.20-40%,
myelocytes 30-50%, premyelocytes and myeloblasts 1-5%, eosinophiles 1-5%, histiocytes,
1-2%, and megakaryocytes 0.7-3.3%.
Almost every blood dyscrasia is a result of some ^change in the bone marrow, and it is
only by a consideration of these changes that an understanding of the condition is possible.
Very often an examination of the peripheral blood will give one a good idea of the conditions existing in the marrow. For example, in haemolytic jaundice, the presence of sphero-
cytes, normoblasts and reticulocytosis informs one that the marrow is undergoing normoblastic hyperplasia due to the production of an unduly fragile) erythrocyte. It often happens, however, that one cannot so easily visualize what is occurring in the marrow. For
example, take those cases where it is almost impossible to differentiate between gastric carcinoma and pernicious anaemia by an examination of the peripheral blood. However, when
one examines the marrow, cases of pernicious anaemia will be found to be accompanied' by
a megaloblastic reaction, while cases of anaemia due to carcinoma of stomach show a
normoblastic reaction.
It is perhaps in dyscrasias of the granulopoietic system that a study of the bone marrow
will be of the greatest assistance. We are very accustomed to think of the leukaemias as
always being accompanied by a great increase in the white cells of the peripheral blood.
However, there are numerous cases of aleukaemic leukaemia being reported every year.
Dameshek even goes so 'far as to say that the majority of cases of leukaemia in his experience have been associated with a normal or low white blood cell count. Previous to bone
marrow studies many of these cases were reported as: typhoid fever, agranulocytosis,
miliary tuberculosis, malaria, purpura haemorrhagica, pernicious anaemia, lymphosarcoma,
etc. In this regard I would like to emphasize that in these cases complete blood counts were
performed, but it was only when the bone marrow was studied that the true nature of the
conditions was revealed. According to Dameshek the association of anaemia, leukopenia
and thrombocytopenia usually points towards a destructive lesion of the bone marrow,
very often leukaemic in type.
Again, in those cases where splenomegaly is a prominent feature, if there is an associated anaemia, one is very apt to diagnose the condition as splenic anaemia and let it rest
Page 28 there. However, if the marrow is studied, many of these cases will turn out to be something entirely different, such as lymphosarcoma, Hodgkin's disease, Gaucher's disease or
myelogenous leukaemia. One is apt} to think twice before puncturing the spleen, so why
attempt it before doing a sternal biopsy when in a large number of cases as much can be
learned by this simpler procedure.
With these general remarks in mind, I will now give a brief summary of the changes in
the sternal marrow associated with the more important blood dyscrasias.
Pernicious Ancemia: The characteristic picture here is a marked erythroblastic hyperplasia of the megaloblastic type. There are great numbers of megaloblasts and pro-megalo-
blasts all undergoing active proliferation, and mitotic figures are numerous. Another cell
which is typical of pernicious anaemia is the erythrogone, a small cell with a large nucleus
and scanty cytoplasm, which resembles the small lymphocyte. Histiocytes are also increased in numbers and many are found containing phagocytosed red cells. The granulopoietic marrow shows an increase in myeloblasts. The nuclei of the myelocytes undergo
excessive lobulation and the resulting neutrophiles havej nuclei which are intricately segmented. In addition to the nuclear change, many of the neutrophiles are larger than
Other Macrocytic Anamias: The findings in sprue simulate these in pernicious anaemia
though the megaloblastic hyperplasia is not nearly so marked. The macrocytic anaemic
associated with diseases of the liver are not accompanied by a megaloblastic reaction of the
bone marrow.
Hypochromic Amentias: The bone marrow findings in the hypochromic anaemias will
depend very much on the etiological factors involved. For example, in anaemias due to a
chronic loss of blood such as one sees in cases of a bleeding gastric ulcer, etc., a normoblastic reaction will be found, the degree of hyperplasia will depend on the amount of blood
lost. The reaction here is really one of compensatory hyperplasia. In cases of the iron
deficiency anaemias, whether the deficiency is due to a chronic loss of blood, inability to
absorb iron or inability to utilize iron, the bone marrow will present a normoblastic reaction, the erythrocytes produced will be smaller than normali and will contain less haemoglobin than normal. In anaemias due to a depression of the bone marrow by some toxin or
in chronic nephritis, there will be hypoplasia of the erythropoietic tissue and an increase
in fat.
Aplastic Ancemia: In aplastic anaemia the erythropoietic marrow is almost entirely
replaced by fat. The cells remaining do not appear to be active, mitotic figures are absent
and there is a great dirninution in normoblasts.
Myelogenous Leukaemia: In acute myelogeneous leukaemia the bone marrow is overrun by myeloblasts which are present in great numbers, crowding out the erythropoietic
tissue and filling up the spaces which normally contain fat. In the subacute and chronic
cases there is dirninution in the numbers of myeloblasts and an increase in the myelocytes
and neutrophiles. The state of the bone marrow is not always reflected in the numbers of
leucocytes in the peripheral blood, for with the same degree of hyperplasia the white blood
cell count may be either high, low or normal.
One must also bear in mind that long standing cases may lead to exhaustion of the'
granulopoietic marrow and the marrow becomes replaced by connective tissue or bone.
Lymphatic Leukcema: According to Jaff e the bone marrow in most cases of lymphatic
leukaemia resembles lymphoid tissue. Granulopoietic and erythropoietic tissue persists in
the form of small islands. However, in the presence of complicating infections these
islands of haemopoietic tissue undergo hyperplasia and replace the) lymphoid tissue.
Monocytic Leukcemia: Two forms of this type of leukaemia have been described, vi.,
acute and chronic. The acute form is characterized by marked proliferation of the histiocytes with no overgrowth of reticulum. In the chronic form there is marked overgrowth
of reticulum and numerous giant cells are presnet.
Agranulocytosis: In some cases of agranulocytosis there is almost complete absence
of granulopoietic marrow, the few cells remaining being small islands of myeloblasts. In
the majority of cases there is active proliferation of myeloblasts with failure of these cells
to mature into myelocytes and neutrophiles. Thus the peripheral blood' receives very few
Page 29 Polycythemia Vera: In this condition there is marked hyperplasia of both granulopoietic and erythropoietic elements and also an increase in megakaryocytes. The relation
between erythropoietic and granulopoietic elements remains normal, i.e., 1:1.
Thrombocytopenic Purpura: The granulopoietic and erythropoietic elements show no
abnormalities in this disease in its pure form. The megakaryocytes! are usually found to
be normal in number, but many authors report them to be smaller than normal and their
fine azurphilic granulations are often missing. Falconer and Morris advise against biopsy
in cases of purpora because of the danger of haemorrhage. This is greatly reduced, however,
if one uses the aspiration method.
Hodgkin's Disease: In most cases of Hodgkin's disease there is hyperplasia of the
granulopoietic elements with an increase in the percentage of immature forms. The percentage of histiocytes varies greatly, a definite increase being the most common finding.
In some cases actual histological evidence of Hodgkin's disease may be found.
Lymphosarcoma: When lymphosarcoma has metastasized to the bone marrow the
biopsy will show almost complete replacement of the normal elements by lymphoblasts
and lymphocytes.
Gaucher's Disease: In this condition the typical Gaucher cell—a large histiocyte filled
with lipoid material giving it a foamy appearance—will be found in varying numbers. The
cells are diagnostic of Gaucher's disease and the presence establishes the diagnosis.
Bantu's Disease: The findings in this disease are not specific. Some report a mild degree
of hyperplasia of the granulopoietic elements.  Others report no changes at all.
1. Custer, R. P.: Am. J. Med. Sci., 189:507, 193 5.
2. Dameshek, W.: Ibid, 182:520, 1931; 190:617, 1935.
3. Falconer, E. H., and Morris, L. M.: M. Clin. North America, 6:3 53, 1922.
4. Jarre, R. H.: J. A. M. A., 107:124, 1936.
5. Reich, C: Am. J. Med. Sci., 189:515. 1935.
6. Vogel, P., Erf, L.A., and Rosenthal, N.: Am. J. Clin. Path., 7:436 and 498, 1937.
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