History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: January, 1936 Vancouver Medical Association Jan 31, 1936

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 In This Issue:
APPENDICITIS  (Conclusion)
(With Cascara and Bile Salts)
. . FOR . .
Chronic Habitual
Western Wholesale Drug
(1928) Limited 1
(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.
203 Medical Dental Building, Georgia Street, Vancouver, B. C.
Editorial Board:
Dr. J. H. MacDermot
Dr. M. McC. Baird Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address
Vol. XII. JANUARY,  193 6 No. 4
OFFICERS  193 5-1936
Dr. C H. Vrooman Dr. W. T. Ewing Dr. A. C Frost
President Vice-President Past President
Dr. G. H. Clement Dr. W. T. Lockhart
Hon. Secretary Hon. Treasurer
Additional Members of Executive—Dr. T. R. B. Nelles, Dr. F. N. Robertson
Dr. W. D. Brydone-Jack Dr. J. A. Gillespie Dr. F. Brodie
Auditors: Messrs. Shaw, Salter & Plommer
Clinical Section
Dr. J. R. Neilson  Chairman
Dr. Roy Huggard    Secretary
Eye, Ear, Nose and Throat
Dr. H. R. Mustard  Chairman
Dr. L. Leeson   Secretary
Pediatric Section
Dr. G. A. Lamont Chairman
Dr. J. R. Davdbs '. Secretary
Cancer Section
Dr. J. W. Thomson     Chairman
Dr. Roy Huggard ~- Secretary
Library Summer School
Dr. G. E. Kidd Dr. J- W. Arbuckle
Dr. W. K. Burwell Dinner Dr. J. E. Walker
Dr. C A. Ryan Dr. Lavell Leeson Dr. H. A. DesBrisay
Dr. W. D. Keith Dr. J. E. Harrison Dr. H. R. Mustard
Dr. H. A. Rawlings Dr. A. Lowrie Dr. A. C Frost
Dr. A. W. Bagnall Dr. J. R. Naden
Publications Credentials
Dr. J. H. MacDermot Dr. H. A. Spohn
Dr. Murray Baird Dr. J. W. Thomson
Dr. D. E. H. Cleveland Dr. W. L. Graham
V. O. N. Advisory Board
Dr. I. T. Day &eP- io B' *-"• Medical Assn.
Dr. W. H. Hatfield Dr. Wallace Wilson
Dr. A. B. Schinbein
Sickness and Benevolent Fund — The President — The Trustees » I
Wm F
Diphtheria Antitoxin
Diphtheria Toxin for Schick Test
Diphtheria Toxoid   (Anatoxine-Ramon)
Scarlet Fever Antitoxin
Scarlet Fever Toxin for Dick Test
Scarlet Fever Toxin
Tetanus Antitoxin
Anti-Meningitis Serum
Anti-Pneumococcic Serum   (Type 1)
Anti-Anthrax Serum
Normal Horse Serum
Smallpox Vaccine
Typhoid Vaccine
Typhoid-Paratyphoid Vaccine
Pertussis Vaccine
Rabies Vaccine  (Semple Method)
Price List Upon Request
Connaught Laboratories
University of Toronto
Depot for British Columbia
MACDONALD'S prescriptions Limited
Medical-Dental Building, Vancouver, B. C. VANCOUVER HEALTH DEPARTMENT
Total Population  (Estimated)  244,329
Japanese Population   (Estimated) '.   8,037
Chinese Population  (Estimated)   7,803
Hindu Population (Estimated)  276
Total  deaths 	
Japanese deaths  _
Chinese deaths	
Deaths—Residents only :	
Birth Registrations—Male, 132; Female, 134.
Deaths under one year of age	
Death rate—per 1,000 births	
Stillbirths (not included in above)..
Rate per 1,000
November, 193 5 November, 193 5
         14 4
  5 2.6 14.5
  9 10
December 1st
-October, 193 5
Cases Deaths
Smallpox          0 0
Scarlet  Fever      53 0
Diphtheria        1 0
Chicken Pox       69 0
Measles          7  ! 0
Rubella          3 0
Mumps   ...     52 0
Whooping-cough         8 0
Typhoid Fever . '_ L      1 0
Undulant Fever     ■ 3 0
Poliomyelitis    -       0 0
Tuberculosis  _•- .46 10
Meningitis   (Epidemic)       0' 1
Erysipelas . -—       5 0
Encephalitis Lethargica        0 0
Paratyphoid   .—.       0 0
November, 193 5
Cases    Deaths
High Blood Pressure...
ffTbe -most effective therapy available."
Formula—Each 1 cc. Ampoule contains:
Pancreas    25 grammes of the fresh hypotensive principle
Anterior Lobe Pituitary 2 grammes of fresh substance
iHInbryonin    2 grammes of fresh substance
Biological and Research
Ponsbourne Manor, Hertford, England.
Rep., S. N. BAYNE
1432 Medical Dental Building       Phone Sey. 4239       Vancouver, B. C.
References: "Ask the Doctor who has used it."
Founded 1898
Incorporated 1906
Programme of the 3 8 th Annual Session
GENERAL MEETINGS will be held on the first Tuesday of the month
at 8 p.m.
CLINICAL MEETINGS will be held on the third Tuesday of the month
at 8 p.m.
Place of meeting will appear on Agenda.
General Meetings will conform to the following order:
8:00 p.m.—Business as per Agenda.
9:00 p.m.—Paper of the evening.
Dr. G. F. Strong: "Cardiac Pain."
Discussion opened by Dr. H. A. DesBrisay.
Dr. A. M. Agnew: "Vaginal Plastic Surgery."
Discussion opened by Dr. J. J. Mason.
November 5 th—GENERAL MEETING.
Dr. J. R. Naden: "Epiphyseal Injuries."
Discussion opened by Dr. F. P. Patterson.
Dr. J. H. MacDermot: "Early Medical History of the B. C. Coast."
Dr. Lyall Hodgins: "Diabetes."
Discussion opened by Dr. Wallace Wilson.
Dr. Frank Turnbull: "The Early Diagnosis of Brain Tumours."
Discussion opened by Dr. F. W. Emmons.
Dr. Walter M. Paton: "Tumours of the Head and Neck."
Discussion opened by Dr. H. H. Pitts.   '
Dr. B. J. Harrison: "Roentgenology of Cardiac Diseases."
Discussion opened by Dr. G. F. Strong.
Mr. J. W. deB. Farris: "Medico-Legal Problems."
Dr. C. E. Dolman: "Serum Therapy."
Discussion by Dr. Howard Spohn and Dr. A. Y. McNair.
THE death of Dr. J. M. Pearson came as a very great shock to all of
us who knew him. In some way we had come to regard him as more
or less a permanent institution in our medical world in Vancouver, and
if ever a man seemed certain to outlive the Psalmist's span of years, it
was he; one felt that he was the personification of hard, lean health. But
the "abhorred shears" of Atropos know no favourites. It makes one
realise what a very incidental thing death really is, it conies so easily,
almost by accident.
But he is a great loss to our profession here, and we shall miss him
very badly. Thinking over our impressions and ideas about him, gathered
through a knowledge of him extending over almost thirty years, perhaps
the characteristic of Pearson that stays most in one's mind was his
unswerving honesty, not alone in the ethical sense—that goes without
saying—but his mental and intellectual honesty. One could be quite sure
of one thing about him—whether one agreed with him or not, any conclusions to which he came, any opinion he expressed, was the outcome of
his clear, honest, painstaking thought: and independent thought, not in
any way influenced by any other person's expressed or implied opinion.
He could never be stampeded or swayed at all by outside pressure,
though characteristically he was extremely tolerant of other people's
opinions, to which he invariably gave due consideration and respect. He
was deliberate, even slow, in making up his mind about a subject, or
expressing what he thought, but one always felt that he had thoroughly
explored every nook and corner of it before he came to a definite conclusion.
He was our first Editor, and whatever the Bulletin is, or has done, is
chiefly the result of his 'work. He had very high ideals for the Bulletin,
and even after he gave up the active control of it, took a very keen
interest in it. Since it was not in him lightly to praise, or indeed to praise
at all unless he really meant it, his occasional pats on the back ■were very
precious and heartening to those who were striving to wear his mantle.
Looking back over early numbers and his editorials therein, one is struck
anew by the originality and individuality of his ideas. They were always
his own, minted in his own mental workshop, and expressed in a clear,
easy style, with an economy of -words that one sometimes envies.
As a medical man he was an artist, and had a keen appreciation of
the beauties of his art, as indeed he had of all beauty, whether it were in
poetry, to which he was much addicted, being especially interested in
modern poetry, which intrigued him greatly, or in language and the
written tongue. He was, too, much occupied with artistic work of his
own shortly before his death. And as was said above, he carried this into
his work. His was the thoroughness, the meticulous absorption in detail,
of the artist. To him a case was a mosaic, of 'which all the pieces had to be
found and fitted together to make a complete picture. So he would take
endless pains, spend unlimited time over one case, read and study, and
examine the patient over and over, quite regardless of other calls on his
attention, concerned only that no stone be left unturned, no avenue
unxplored, which might lead to the full knowledge and correct diagnosis
of the disease. His interest was scientific and not personal, and was quite
unaffected by the financial or other standing of the patient; so that the
indigent ward patient would engage hours of his time which might well
Page 72 have been spent on those who, in a money sense at least, would have been
far more profitable. In fact, one sometimes felt that he preferred the
indigent one, since he could work unhampered by any consideration save
that of thoroughness. Naturally, this does not make a fashionable physician, though it makes a very good one, and the highest and best kind of
one—which is exactly what he was. Without any display, without any
fuss about it, but constantly and unswervingly, he carried his torch high,
and reached and maintained the highest levels of his profession: and there
are none higher.
He was not an easy man to know—he could not easily be trapped or
held in anyone's net—but he was so completely reliable in his friendships that one felt free with him—free from any need for pretence, for
insincerity—and so comfortable and at home in the light of his personality. One could be conscious of a security, a reality, and an independence
of thought and action, that were always tonic and stimulating, encouraging others to aim at the ideals he himself attained so successfully and
•with so little apparent effort.
Christopher Wren put as his motto on the stones of St. Paul's
Cathedral, "Si monumentum reqtiiris, circumspice" (If you need a monument, look around you). So our late friend and colleague needs no words
to make his memory live amongst us. Everyone who enters and uses the
Library, of which we are so proud, may well give a thought to the man
who more than anyone in Vancouver is responsible for its foundation, for
its steady and prosperous growth to maturity, and for its high level of
excellence. The Vancouver Medical Association as an organization owes
him a tremendous debt. He was passionately loyal to its interests and
devoted to its wellbeing. As we have mentioned, the Bulletin is another
memorial stone set up to him. So he is still with us in those things that he
would most willingly have us associate with him.
"He has outsoared the shadow of our night . .  .
From the contagion of the -world's slow stain
He is secure, and now can never mourn
A heart grown cold, a head grown gray in vain."
The Extra Pharmacopoeia—Vol. 2, 193 5.
Dunbar, H. F.—Emotions and bodily changes.
Gradwohl, R. B.—Clinical laboratory methods and diagnosis.
Osler, Sir Wm.—Principles and practices of Medicine. Revised by Thos. McRae,
12 th edition.
Zondek, G.—Diseases of the Endocrines.
Medical Clinics of North America, November, 1935.
Fracastor—"Syphilis" a Poem. Translated by H. Wynne-Finch.
Goodman, N. G.—Benjamin Rush, Physician and Citizen.
Glasser, O.—Wilhelm Conrad Roentgen: a biography.
Reisman, D.—Medicine in the Middle Ages.
Ruhrah, J.—Paediatrics of the past.
Sabin, F. R.—Franklin Paine Mall: the biography of a mind.
Zitboorg, G.—The Medical man and the witch during the Renaissance.
I   ,
MacEachern, M.D., Chicago. Physicians Record Company, 193 5; pp.
968, Illustrated.   $7.50.
There have been other books published on this topic, but they dwindle
into insignificance compared with this monumental work which is profusely
illustrated with the various forms employed throughout the hospital field.
Most noticeable are the magnificent drawings which visualize each chapter.
It is well known in the hospital world that there is no one better qualified
from past experience to express an authoritative opinion on the subject of
hospital administration. The chapters on the history of hospitals are most
informative and worthy of a place in any reference library. From the chapters on promoting and building the new hospital to the final chapter on
Standing Orders, it seems that there is little more to be said.
The book is a mass of practical data useful in everyday hospital work,
and no doubt will be considered as a standard work to be found on the
Superintendent's desk, reference to which will be discovered to be a daily
The organization charts employed by the author are informative and
represent the opinion of leaders in the field as to the proper organization of
the various major hospital departments such as dietetics, business, power
house, laundry, Social Service, etc.
In addition to the publication of these most lucid charts, the duties
and authority of the heads of these various departments are detailed along
the lines of modern hospital administration.
There are fifty-two pages devoted to standing orders, which are of such
a detailed and general nature as to be adaptable to a hospital of any size.
Medical Records are gone into carefully. Staff relationships and the
organization of the medical visiting group are all splendidly handled, and,
last but not least, deserving of special mention are the elaborate check lists
of supplies and equipment necessary to the conduct of the hospital as a whole
or of each department.
To one who is personally acquainted with the author over a period of
many years, it would appear that the hospital field owes a deep debt of
gratitude to Dr. MacEachern.
A. K. Haywood, M.D.
General Superintendent, Vancouver General Hospital.
[The above review of Dr. MacEachern's work will command the attention of all hospital executives, to whom this book will, of course, especially
The Council, in view of the near appointment of a full-time Executive
Secretary, has found it necessary to raise the fees for the coming year.
By Dr. R. I. Harris
(Concluded from last issue)
Treatment of Acute Appendicitis.—From the standpoint of treatment,
as weffias that of pathology and clinical manifestations, acute appendicitis
presents two different phases; first, acute unperforated appendicitis, and
second, perforated appendicitis with (a) local or with (b) diffuse peritonitis.
Pathologically, clinically and therapeutically, they are entirely different
problems. In the unperforated cases, there can be no difference of opinion
as to treatment. The appendix should be removed as promptly as possible,
the earlier the better. Such treatment is followed by uniformly good results.
The mortality should be 1 % or less.
When perforation has occurred, the problem is entirely different. The
patient now is suffering from peritonitis, and whether this be local or diffuse,
it dominates the pathological and clinical picture and should dominate the
problem of treatment. The immediate removal of the appendix no longer is
necessary. The need for urgency has passed, 'since the disaster which urgent
operation seeks to avoid has occurred. It cannot be too strongly emphasized
that what the patient needs is treatment for peritonitis. Anything which is
done to his appendix will help him only insofar as it is of value in curing
him of peritonitis. Immediate appendectomy is not necessary. Indeed, it
may be and often is harmful since it focuses attention upon the appendix
which now is a minor part of his trouble and since the trauma of its removal
may actually make the patient worse.
If we agree that unperforated appendicitis and perforated appendicitis
with peritonitis are different problems and require different treatment it is
of some importance to be able to distinguish them. This is no easy problem,
but we have some important guide posts.
If the patient still has mid-abdominal pain, whether or not he also has
pain in the right lower quadrant, the appendix is still unperforated. This
pain is due to tension within the appendix and disappears when perforation
occurs. We have found hyperesthesia an important though not quite constant indication that the appendix was still intact. The exceptions to this
sign (no hyperesthesia with appendix still unperforated) can nearly all be
explained by the position of the appendix (pelvic appendix; appendix
wrapped in omentum).
Finally, the duration of the disease is of considerable importance. The
pathological changes follow in orderly sequence and require time for their
development. True, some cases progress with fulminating rapidity and some
progress slowly, but the majority present sufficient uniformity of progress
to make the time element a valuable aid to diagnosis. We can be reasonably
certain that perforation has not taken place at the end of twenty-four hours.
At the end of thirty-six hours most cases will still be unperforated. At forty-
eight hours many cases will have perforated and after that perforation will
be .the rule rather than the exception.
If we can recognize that the appendix is still unperforated it should be
removed at once. If there is any doubt as to whether or not it is perforated,
treat it as an unperforated appendix and remove it. If it is perforated it has
done so recently and the peritonitis is limited.
This leaves for our consideration those cases which are definitely corn-
Read before B. C. Medical Association, September, 193 5. plicated by peritonitis;  and these naturally divide themselves into two
groups—those with abscess and those with diffuse peritonitis.
Treatment of Perforated Appendicitis with Abscess.—Immediate operation is not necessary when the appendix has perforated and an abscess has
formed. If several days have elapsed since the onset of the attack, and if a
mass can be felt, we are justified in diagnosing appendicular abscess. There
is no necessity to get out in the middle of the night to operate upon such a
case. Perforation, the disaster which urgent operation might avert, has
already occurred. Peritonitis is being well handled by the patient's local
defences. These patients do best if they are treated for a time by the Ochsner-
Sherren method (Fowler position, fluids only by mouth, heat to abdomen,
and fluids intravenously). This puts the peritoneal cavity as completely at
rest as is possible, and permits it to wall off the infection still better. Under
such circumstances a considerable number of abscesses subside completely.
If they do so rapidly, operation during the acute stage is not necessary. The
appendix can be removed at an interval operation. If the abscess persists
after a few days, it should be drained, but care must be taken to drain it
without traversing clean peritoneum. This means a planned operation suited
for the individual case. If the appendix is readily seen and easily removed
without breaking down the wall of the abscess, it should be removed.
Otherwise the operation should consist of drainage of the abscess only. The
appendix is removed after an interval of two or three months.
The Treatment of Perforated Appendicitis with Diffuse Peritonitis.—
This is the group of cases in which the great mortality occurs. Improvement
in treatment here is of the utmost importance.
The greatest advance in the treatment of these cases has been the introduction of the delayed operation (Ochsner-Sherren). Removal of the appendix is not the first and most important step in treatment. The periton^R
constitutes the most urgent problem. Often the operation or removal of
the appendix actually is harmful to the patient and sometimes may determine his death. The patient usually is dehydrated, toxic and worn out. He
can be improved very greatly by adequate rest, abundant fluids administered intravenously continuously over several days, and heat to the abdomen.
If he is vomiting, a duodenal tube continuously in place keeps his stomach
empty and decompresses his distended intestine. Under this regime great
improvement can and usually does take place.
If we can obtain such improvement by the Ochsner-Sherren treatment,
must the appendix be removed? Yes, for two reasons. In gangrenous cases,
the mass of dead tissue is a constant source of reinfection. In perforated
cases there may be an outpouring of intestinal contents into the peritoneal
cavity. The appendix should be removed as soon as the patient is fit for
operation, usually after about two days of Ochsner-Sherren treatment.
With the greatest care and skill, the mortality in perforated appendicitis
with diffuse peritonitis is still high. The following are the figures for the
Toronto General Hospital and the Hospital for Sick Children.
Hospital for Sick Children
(abscess)                      Local Peritonitis
General Peritonitis
Mort.           Cases                   Mort.
Cases                    Mort.
52 .
     5.8%             73      1.37%
34   32.3%
Toronto General Hospital
Mass (abscess)                                                  G
:neral Peritonitis
Mort.          Cases
70 ..
 -    7.5%             97  	
_-         15%
Page 76
mtm It is evident that great improvement in the mortality rate from appendicitis would come most easily if we could operate upon such patients before
perforation occurred. There the mortaHtigis low. The responsibility for late
operations rests chiefly on the public. I believe doctors as a whole are at one
in believing that once diagnosed, appendicitis is a surgical problem. Delay
in treatment cannot be blamed on doctors. The public on the other hand
are very prone to treat the early stages of appendicitis lightly. The symptoms
may not be severe and there is nothing sufficiently outstanding to warn
them of the serious nature of the symptoms. They are prone to treat their
bellyache with a cathartic and this of course is the very worst thing they
could do. Appendicitis often derives its fiercest activities from the means
taken to treat it. No measure is likely to warn the public of their danger
other than a campaign of public education. In Philadelphia such a campaign
of education has been in existence since 1926 with definite improvement in
the results. The public should know that pain in the abdomen may mean
appendicitis; that appendicitis before perforation may be characterized by
very mild symptoms; that laxatives should never be given to a patient with
Chronic Appendicitis.—A word regarding chronic appendicitis. This is
a loosely used term which covers any form of appendicular pathology save
acute appendicitis. It may mean recurring attacks of low-grade appendicitis
or it may refer to attacks of appendicular colic.
I have previously stated that nearly every case of perforated and gangrenous appendicitis arises because the appendix is obstructed. This obstruction most often is caused by a f aecolith impacted on a band of fibrosis. Now
the very presence of a f aecolith in an appendix is an evidence that it is abnormal. Faecoliths arise because the appendix is not emptying properly. Faecal
material enters the appendix from the caecum but is not all expelled by the
peristalsis of the appendix. The fragment of faeces which remains behind
becomes inspissated by the absorption of water from it and increases in size
by the addition of fresh material. One can often demonstrate this layer
formation. Ultimately the f aecolith reaches such a size that it is mechanically
impossible for it to leave the appendix. The stage is then set for obstructive
The fault in the appendix which permits, a faecolith to form is some
mechanical interference with emptying. Most often this is a ring of scar
tissue or a stricture through angulation, or an external band may cause the
same mechanical fault. Annular fibrosis is due to scarring, and scarring is
due to past inflammation. Hence the presence of a f aecolith in an appendix
usually means that it has been the seat of catarrhal and ulcerative inflammation some time in the past.
Of greater importance is the fact that an appendix which contains a
f aecolith is potentially dangerous. It may become obstructed and give rise to
gangrenous appendicitis. It is oten possible to diagnose such cases, especially
in children, by recurring attacks of colicky pain which lasts a short time.
Such appendices should be removed.
If we can determine that the patient's chronic or recurring symptoms
are due to the appendix, it should be removed. A pathological appendix is
a constant menace. Its owner is in danger every time he goes away from the
reach of a hospital; every time he goes hunting or holidaying. We can all
recall cases amongst our own friends.
Dr. Charles Hunter, Winnipeg.
This is a hernia through the cesophageal opening, or Hiatus, of the
diaphragm; a small part of the fundus of the stomach pushes through the
hiatus into the posterior mediastinum; there is a hernial sac composed of
the diaphragmatic peritoneum, which may be fused with the serous coat of
the adjacent stomach; the sac gradually enlarges and pushes out behind the
mediastinal pleura into the posterior mediastinum, by the side of the oesophagus, exerting pressure on the heart. The hernia may be permanently fixed
in the thorax but more often is intermittent, sliding out when the tension
in the abdomen is heightened, as when the patient bends forward, or is lying
on his back, or sometimes after meals.
Previously described by Friedenwald and Feldman many years ago, hiatus
hernia has been brought into prominence recently by Von Bergmann, who
claims that it is exceedingly common, thoughi generally overlooked. Indeed,
Knothe, in Von Bergmann's clinic, was able to demonstrate this hernia in
300 patients in one year, and other German roentgenologists, using special
technique, also gave high figures. Doubt has been thrown on these figures
obtained mainly by x-ray examinations, confirmed as they were by few
operative or post mortem findings. But in the United States, quite independently, Chevalier Jackson has found hiatus hernia "a rather common
condition in our records," while Harrington, of the Mayo Clinic, has
recently given details of 43 hiatus hernias operated on at Rochester and has
systematically examined in 500 other abdominal operations the cesophageal
opening of the diaphragm; in these 500 cases, he found in 65% the diaphragm closed snugly around the oesophagus, with no appreciable space
between; in 35%, at least one finger could be placed between the oesophagus
and the margin of the diaphragmatic opening, irM4% two fingers, and, ha
exceptional cases, three fingers could be inserted in the space between. Harrington notes that in these latter cases, special x-ray examinations made
later showed occasionally a small hernia present. Looking specially for this
type of hernia in the last two years, Dr. McMillan, of Winnipeg, has demonstrated its presence in a number of cases; Hurst of London thinks Von Bergmann has greatly exaggerated its frequency but has himself given details of
a few convincing cases. Hedblom finds the lower end of the oesophagus has
generally prolapsed with a portion of the cardiac end of the stomach into
the thorax, while all observers admit that there is a condition of congenital
shortness of the oesophagus in which a portion of the fundus of the stomach
lies above the diaphragm, with the oesophagus entering it at its highest point.
(It should be noted that no account is being taken here of traumatic diaphragmatic hernia due either to direct injury to the diaphragm, as in gunshot wounds, or to indirect injury, as in a severe crus&bg accident.)
ILtiology: In hiatus hernia, a congenital embryological deficiency may be
present, but generally there seems to be a natural weakness of the cesophageal
ring; the increasing laxity of these tissues, with advancing years, accounts
for its relative frequency in elderly people, while in younger subjects, the
hernia particularly follows operations where severe vorMting has occurrd
during or after the anaesthetic, or where increased intra-abdorninal pressure
occurs, as in pregnancy or in violent physical strain. There is, according to
Address read at the Summer School of the Vancouver Medical Association, June, 193 5.
Page 7 8 Von Bergmann, a natural play of the oesophagus through the hiatus of one
or two centimetres.
The two vagi pass through the cesophageal opening; experimentally, in
animals, a small, bag placed in the hiatus and distended with air will press on
the vagi and cause reflexly a reduction in the coronary circulation by more
than one-half, without the general circulation or blood pressure being
affected. This probably accounts in part for the anginal symptoms sometimes
found in association with hiatus hernia.
Symptoms: Most cases of hiatus hernia, shown by x-ray, and a few
demonstrated by Harrington in the course of other abdominal operations,
have given rise to no symptoms; even when present, the symptoms are
usually slight, though exceptionally quite severe, when progressive incarceration of the stomach produces signs of obstruction or when serious reflex
symptoms like angina pectoris occur.
In mild cases, a feeling of pressure or of pain immediately behind the
lower sternum or xiphoid comes in attacks, during or immediately after a
heavy meal, or sometimes on bending forward as in lacing the boots, or even
while lying down. There may be a definite hint of difficulty in swallowing or
a sense of choking, with difficulty in getting a full breath; acid eructations
are common. The spell may be relieved by standing, stretching, or sometimes
by drinking a little aerated water or taking a little baking soda; belching of
gas or vomiting may relieve, suggesting cholecystitis. Exceptionally, the
pain may be severe, may radiate to the left chest and into the left arm, simulating angina pectoris; the hernial sac may become inflamed or even ulcerated, as Chevalier Jackson has frequently found in cesophagoscopic examination, with resulting haematemesis or blood in the stool. Weeks or months may
pass between attacks, the stomach not engaging in the cesophageal ring, but
when the fundus has become fixed in the chest by adhesions, the pain, gas
and vomiting may be prolonged and dangerous. Bock, Dulin and Brooke
have recently described 15 patients who suffered from repeated attacks of
anaemia of obscure origin which were associated with hiatus hernia; there
was no history or x-ray evidence of ulcer, but three of the patients operated
on and two examined post mortem revealed marked venous congestion of
the herniated stomach without definite ulceration. Small and frequent meals
may apparently relieve some—with the resultant diagnosis of ulcer.
Diagnosis: Other cesophageal disorders must be distinguished—the dys-
phagia of middle-aged anaemic women, the so-called cardiospasm, peptic
ulcer and peptic oesophagitis and especially carcinoma of the lower end of
the oesophagus.
The dysphagia of middle-aged anasmic women (the Plummet--Vinson
Syndrome) is referred high up to the entrance of the oesophagus instead of
to the lower end; it is associated with marked secondary anaemia, with
atrophic changes of the mucous membrane of the tongue, mouth and
pharynx, and often with splenic enlargement. 30-grain doses of iron & ammonium citrate, three times a day, cures the anaemia, while the difficulty of
swallowing is rapidly relieved by cesophageal bougies or sounds, guided, if
necessary, by a previously swallowed silk thread.
Cardiospasm is not liable to be confused if a satisfactory x-ray plate be
taken, showing the diffuse dilatation of the oesophagus and the smooth cigar-
shaped termination at the hiatus.
In peptic ulcer of the oesophagus, discomfort or pain may come behind
the lower end of the sternum and through to the back, during the swallow-
Page 79 I
i 11
ing of solid food, though, Chevalier Jackson found, generally not for half
an hour or longer after food; alkalies may give prompt relief. The x-ray
examination is often negative and diagnosis may be impossible without the
cesophagoscope, but in any case, the negative x-ray findings will exclude a
definite diagnosis of hiatus hernia.
Recently peptic oesophagitis has been differentiated, especially by Win-
kelstein and Chevalier Jackson, with symptoms similar to those of cesophageal ulcer—irregular spasm of the lower end of the oesophagus may be
present on x-ray examination, without dilatation above. The condition
improves with antacid and ulcer treatment, and this may, in doubtful cases,
confirm the diagnosis.
Carcinoma of the lower end of the oesophagus must be constantly
remembered in differential diagnosis but will not be taken up here.
With the suspicion of hiatus hernia aroused, a special x-ray technique
should be followed. The hernia may disappear with the subject erect, so that
the thickened barium should be drunk in the lying down position; others
recommend further, when the patient is on his back, pressing the upper
epigastrium firmly upwards and backwards so as to fill the fundus of the
stomach and squeeze some of the barium into the hernia. The folds of the
mucous lining of the stomach are comparatively thick and irregular, readily
distinguishable from the thin, fine parallel folds of the oesophagus—a point
of value in examining the x-ray plate. Of course, an expert with cesophagoscope or gastroscope may settle a doubtful diagnosis, but he is seldom
It is obvious that hiatus hernia should be considered when the symptoms
present are rather atypical of ulcer or cholecystitis; also, when at operation,
the expected lesion is not demonstrable, the hiatus ring should be carefully
investigated for a possible hernia.
Treatment: In the usual case with mild symptoms, the definite reassurance possible as to the comparatively minor disability, with relief from fear
of angina pectoris or carcinoma may help greatly, as Von Bergmann has
emphasized. Standing, stretching, or some special manoeuvre may give relief
instantly, the hernia slipping down into the abdomen; in other cases, air
swallowing or a mouthful of aerated water may have the same effect by
filling the fundus of the stomach. Anything likely to increase the intraabdominal pressure should be avoided; Hurst records a patient in which
attacks after breakfast could be prevented by putting on his boots only when
the feet were raised to the level of his buttocks, and other spells could be
avoided by sitting on a very low seat when writing, with the upright position
thus maintained. As both Hedblom and Harrington point out, operation
should be reserved for the exceptional cases when the hernia is large and
produces rather marked symptoms; in these cases, satisfactory closure of the
hiatus may be difficult even with a preliminary phrenicotomy.
Harrington, S. W.—Journal American Medical Association, Sept. 23, 1933.
Hedblom, Carl A.—Annals of Internal Medicine, August, 1934.
Von Bergmann—Functionelle Pathologie.
Hurst—Recurrent hernia of stomach through the Hiatus Oesophageus of the Diaphragm:
Guy's Hospital reports, January, 1934.
Hurst—Some disorders of the Oesophagus: Journal American Medical Association, February 24, 1934.
Bock, A. W.; Dulin, J. W., and Brooke, P. A.—Diaphragmatic Hernia and Secondary
Ana:mia (10 cases): Transactions of Association of American Physicians, vol. 48, p.
333, 1933.
Jackson, C, and Jackson, C L.—Journal American Medical Association, Jan. 26, 193 5.
Dr. Charles Hunter, Winnipeg.
This is a clinical entity, not uncommon but generally overlooked; it is
also described as chronic duodenal ileus or chronic duodenal obstruction;
compression of the duodeno-jejunal junction between the tight root of the
mesentery and the lumbar spine is the most familiar cause of the duodenal
stasis, which, as a permanent or intermittent state, constantly accompanies
the condition, whatever its origin may be.
Etiology: Most of the recorded cases, coming as they do from surgical
clinics, present duodenal obstruction at the duodeno-jejunal junction; here
enteroptosis is usually found, often associated with lack of supporting fat or
defective bodily posture—coils of small bowel or a mobile caecum and
ascending colon slip into the pelvis and drag on the mesenteric attachment
so that, especially if the mesentery be short, the bowel is compressed against
the spine and stasis of its contents results. In other cases, Lane's Kink or
chronic inflammatory thickening of the root of the mesentery is present; in
still other cases, tuberculous or even carcinomatous glands in the same
position may similarly narrow the gut.
But in recent years, many other types of duodenal stasis have been noted,
only a few of which can be touched on here. Feldman, particularly, has
described the "redundant duodenum," where the first part instead of bending down to the right and posteriorly from the cap to continue as the second
portion, elongates more or less horizontally from the cap for some centimetres and is supported by the hepato-duodenal ligament before dropping
abruptly into the descending portion of the duodenum. This lengthening
of the superior portion may cause an anomalous looping of the gut and so
give rise to duodenal stasis with sometimes associated ulceration. Again,
stasis may occur about the junction of the second and third portions of the
duodenum; Dr. McMillan, of Winnipeg, thinks this latter may be due to
undue laxity of the duodenum in the erect position, so that the cap and
descending portion sag down unduly, with resulting kinking. Congenital
bands and adhesions, sometimes from the gall bladder, sometimes from the
pancreas, sometimes connected with the colica media artery crossing the
second part of the duodenum, are evidently responsible in other cases.
Weinbren has recently described a number of cases of so-called right-
sided duodenum inversum, in which the third part of the duodenum, instead
of turning to the left and upwards, curves round to the right and so kinks,
as it comes to lie as high as or higher than the duodenal cap before passing
into the jejunum.
There is, lastly, no doubt that one form of duodenal stasis exists which
is not obstructive; a dilated duodenum, generally in the second part, has
been found repeatedly at operation by Wilkie, Judd and others, with no
||Pnking or stenosis present; this variety evidently results from some form
of neuro-muscular derangement and is analogous to the megacolon found
in Hirschsprung's disease.
Frequency: There is, of course, room for wide difference of opinion in
regard to the frequency of duodenal stasis; it can hardly be a rare condition, as I have personally seen in private practice 13 cases in the last year,
two confirmed at operation and the others reasonably certain from the
combined clinical and radiological examinations. Of these 13, 11 occurred
in women; the average age was 32, varying from 21 to 48 years; the average
weight of 7 of the number was 104 lbs., indicating sufficiently the type of
individual usually the victim; the average duration of symptoms was 3^4
Page SI years, ranging from 3 months to 10 years in individual cases. In 4 the
appendix, and in 1 the gall bladder had been removed without benefit. All
the patients were carrying on their duties and had not been confined to bed,
except occasionally for a few days at a time, though in several cases additional help has been necessary in the house and one man had done little for
many months.
Symptoms: There seems to be little difference in the symptomatology
of the different types of duodenal stasis above described. Epigastric fullness
and bloating, sometimes associated with marked nausea, comes on soon, generally within half an hour, after meals, though in three of my cases the distress did not appear till 2 to 3 hours after food, some relief being experienced
by eating again. The fullness and discomfort last a varying time, sometimes
for an hour or two, are more marked after a large or indigestible meal, are
helped by belching of gas and especially by lying down. Two of my patients
had discovered that they got relief by kneeling in the knee-chest position and
pressing with the hands below the navel in an up and back direction. The
epigastric distress sometimes amounts to a definite pain which is occasionally
severe, sharp or cramplike; it may come in spells of a few days' duration,
precipitated by overwork, worry or indigestible large meals, but later it
tends to recur practically every day.
Regurgitation of mouthfuls of food or of sour liquid is frequent after
the fullness has lasted for some time; occasionally, severe and recurring
vomiting of considerable quantities of liquid, sometimes persistently bile-
stained, may occur at intervals of weeks, and these so-called "bilious spells"
may persist for many hours or even for a day or two.
Constipation, sometimes severe, was specially noted in half my cases,
though no marked relief from the epigastric distress was obtained when the
bowels moved; discomfort, however, along the colon complained of by three
was relieved by action of the bowels. Lack of appetite was generally present
with inability to take a fair-sized meal; loss of weight was almost constantly
met with, amounting to 20 lbs. on an average. Spells of diarrhoea, noted by
several observers, were not met with in any of my cases.
Headache was complained of by seven; in two there was a family history of migraine; in six, the headaches antedated the digestive symptoms by
many years, were mainly of the migrainous type, ending in vomiting, had
become more frequent with the onset of indigestion; in one patient, daily
headache had been present for 14 months. The headaches were apt to come
when the patients were overtired, either from worry or overwork, but also
after indigestible food and especially after sweets and chocolates. I found
no evidence that animal food specially precipitated headaches, as has been
claimed by some writers; in women, the headaches might be associated with
menstruation but were usually independent.
All the patients complained of being tired; most were tired all the time,
two only at the end of the day's work. Many were nervous, irritable and
rather depressed, so that superficially they might pass readily as neurasthenics.
On physical examination, the patients were usually rather pale and obviously undernourished, at times quite emaciated, and the blood pressure was
low. Three were noted as of normal build; all the others were obviously
enteroptotic with the usual poor muscular development, long narrow chest
and sagging belly. Definite fullness in the lower epigastrium and just below
the navel was generally present with some tenderness; often splashing could
be elicited well below the navel some hours after food. Hayes claims, by
Page S2 steady pressure upwards and backwards on the abdomen below the navel
for some minutes, to be able to empty the duodenum into the bowel below
and so to remove the distension previously obvious. It is practically impossible to make out on physical examination the dilated duodenum, though
more marked sensitiveness and distension in the midline or immediately to
the right of the navel may arouse one's suspicion of the condition. A test
breakfast gave in every case free hydrochloric acid, within normal limits.
It should be specially emphasized that in the history, periods of comparative or absolute well-being alternated with spells of digestive distress
and lassitffiie, justifying Friedenwald's description of chronic intermittent
duodenal stasis with, presumably, periods in which even the x-ray would
show no abnormality.
Diagnosis: A definite diagnosis can be made only by x-ray examination,
but a provisional diagnosis of duodenal stasis was made in several of my
cases before confirmation was sought. The combination of recurring headaches, apparently migrainous in type, with rather indefinite epigastric distress, is particularly suggestive; the history of relief obtained by kneeling in
the knee-chest position or possibly by pressure below the navel may also help
especially when the age, sex and build of the patient is considered. Fullness
and bloating after meals naturally suggest cholecystitis, but the slight build
and youth of the average patient are against this diagnosis. In the exceptional case, duodenal ulcer is suggested by distress or pain, coming an hour
or so after meals, with partial or complete relief by food; there is rarely a
typical clear-cut history of attacks with complete relief in the interval, and
in the attack, soda may fail to give relief, inducing, some suggest, very
readily alkalosis. The possible combination of duodenal ulcer with duodenal
stasis must be remembered.
Every case of obstinate migraine, especially with somewhat anomalous
digestive symptoms, must be reviewed from the duodenal stasis standpoint.
It would seem that the old idea of intestinal intoxication, with absorption
of hypothetical toxins from the colon, now largely discredited, has its justification in the frequent association of weariness, depression and headache
with duodenal stasis. It is well known that high intestinal obstruction with
persistent vomiting will give rise to severe toxic symptoms, dehydration and
altered chemistry of the blood, while Brown, Eusterman and others have
reported toxic nephritis in duodenal obstruction.
X-ray Examination: In suspected cases of duodenal stasis, and indeed as
a routine in order to pick out unsuspected cases, the duodenum must be
examined fluoroscopically both in the erect and recumbent positions, the
oblique and lateral views being often particularly helpful. Too much attention has been concentrated on the duodenal bulb because of the frequency of
duodenal ulcer, and too little has been paid to the rest of the duodenum. In
mild cases, duodenal stasis may be obvious only in the erect position and can
be readily missed, especially if fluoroscopic examination, which shows clearly
antiperistaltic movements, be omitted. While variations occur in the x-ray
pictures according to the different etiological factors present, it may be said
in general that dilatation and stasis will be demonstrable in the duodenum,
with frequent peristaltic and antiperistaltic waves, carrying the duodenal
contents forwards and backwards from pylorus to the site of interference.
(Occasional antiperistaltic waves may be seen over the duodenum in the normal individual, it is said.) Stasis should generally be shown in plates taken
1J4 to 2 ]/? hours after the barium meal; usually in 5 hours, the stomach and
duodenum are empty (in two of my cases there was considerable residue
Page S3 at 5 hours) though in marked cases requiring surgical interference, a
considerable residue may remain. An irritable duodenal cap or one showing
definite radiological evidence of ulcer may accompany the duodenal stasis.
Visualization of the gall bladder by Graham's method will help in the differential diagnosis.
Treatment: Two of my 13 cases were operated on. One, a strongly
built man of 21, had enjoyed good health till a year previously, when after
severe right-sided abdominal pain with vomiting, for 12 hours, an appendix
said to be "only moderately affected" was removed. Thereafter, he was
nauseated after each large meal, had lost 40 lbs in weight; headaches present
in boyhood had recurred nearly every day and five quite severe attacks of
abdominal pain localized to the right iliac fossa had occurred, associated
with gas and vomiting. An x-ray taken a few months previously missed
the duodenal stasis; a second radiological examination, with duodenal stasis
specially considered, showed definite stasis of the second portion of the
duodenum—a finding confirmed at operation, when an inch long stump of
the imperfectly removed appendix was found, with also marked dilatation
of the descending portion of the duodenum, due to a tight band (? associated
with the colica media artery) crossing the duodenum in this position. The
patient has been very well since the operation, which involved removal of
the appendix stump and a duodeno-jejunostomy.
In the other case, a duodenal ulcer with a diverticulum of the first part
complicated the marked dilatation of the second portion of the duodenum;
here, too, Dr. Thorlakson performed a duodeno-jejunostomy. A third
patient, an emaciated, restless little woman who refused to follow medical
treatment, was advised operation but went instead to visit her mother in
Vancouver, where a physician was able to put her to bed, with considerable
improvement in her condition. Unfortunately, I do not know if this
improvement has been maintained since her return to Winnipeg.
Wilkie states that a drainage operation in cases of duodenal stasis due to
a neuro-muscular derangement, without any mechanical impediment to the
flow, is relatively ineffective.
The other 11 cases were treated on medical lines which naturally had to
be adapted to the individual circumstances. No doubt, in most cases, six
weeks' rest in bed with the foot raised 10 to 12 inches, would have been
advisable, combined with a smooth feeding-up diet and the prone position,
or knee-chest, after meals. But actually, unless the patients feel quite disabled, this ideal treatment is seldom practicable. Early hours, more rest in
general, help in the house in some cases, lying down in the prone or knee-
chest position after meals, the tilting of the foot of the bed some 10 or 12
inches, five smaller meals of the smooth feeding-up variety, liquid paraffin
for the bowels, adalin or medinal for sleeplessness, brief abdominal exercises
of the simple non-tiring type, possibly better adjustment to personal worries and problems—these measures are useful in the milder cases.
In an attack of abdominal distress or pain the knee-chest position with
pressure on the abdomen up and backwards below the navel may help, and
in severe attacks the stomach or duodenal tube may be used.
I give briefly the outline of one case with its medical treatment:
Mrs. C. G. M., age 24, seen in March, 1932. Fathier suffered from sick headaches till
about 50. She, herself, had suffered from sick headaches since childhood, which had got
much worse in the previous three months, coming every ten days—first nausea, on one side
or other, the head, mostly over the temple, begins to ache, with blurring of vision—
sometimes the headache is so bad she could bang her head. She usually vomits after three to
four hours—solid food, if present, then bile; there is no pain in the spell, which develops
Page S4
-T *um
especially with chocolates, greasy and fried things, being quite independent of menstruation. She complained also of general swelling of the abdomen, usually within half an hour
to an hour after food, lasting for half an hour or longer; there were sometimes gas pains
relieved by passage of gas, mostly downwards, and there was slight constipation.
The general physical examination then was quite niegative. She was healthy looking and
youthful in manner and appearance, but test meal was normal and a gastro-intestinal x-ray
was given as quite negative.
She reappeared in June, 1934, said that she was quite well while carrying her only
child, which was born in June, 1933, but after that the bilious spells recurred about once
in two weeks and were very severe. She still has to avoid cabbage, raw vegetables and fried
stuff to help to prevent the bloating after meals, and she finds, too, much sweet stuff also
will bring this on.
At this time it was noted that she had a rather long narrow chest with some sagging.
The gall bladder visualized normally and the duodenum was specially examined. The second
portion was found to be somewhat dilated and there was definite "slushing" movement in
the second portion, with stasis at the junction of the second and third portions.
She had been working hard, without help, and she secured help in the house, went to
bed early, rested an hour and a half in the afternoon; the foot of the bed was raised ten
inches, and she was put on a smooth ffeeding-up diet, five smaller meals a day with no
chocolates or sweets.
She was seen again at the end of March, 1935, when she had gained seven pounds in
weight, was feeling much better in spite of a hard winter with the baby sick and her mother
ill. She kept the maid for about four months and adhered closely to the diet till Christmas,
since when she has relaxed a little. She now gets the bilious spells only once a month, independent of menstruation, and has no indigestion. It should be noted that after meals she
usually lay on her stomach and that her gastric symptoms soon after meals have entirely
Judd, E. S., and Puestow, C. B.—Surgical Clinics of North America, August, 1933, p. 807.
Krass, E., and Beck, W. C.—Annals of Surgery, February, 1934, p. 311.
Friedenwald, I., and Feldman, M.—The American Journal of Roentgenology and Kaditcm
Therapy, August, 1934, p. 161.
Wilkie, D. P. D.—The American Journal of the Medical Sciences, May, 1927, p. 643.
Feldman, M.—The American Journal of the Medical Sciences, August, 1933, p. 198.
Portis, S. A.—The Medical Clinics of North America, March, 1930, p. 1277.
Morrison, T. H., and Feldman, M.—Annals of Internal Medicine, March, 1934, p. 1126.
Weinbren, M.—The Lancet, February 10, 1934, p. 280.
Rowlands, R. P.—The Lancet, May 27, 1933, p. 1107.
Andrews, K. S.—The Medical Clinics of North America, January, 1930, p. 1027.
Dr. Charles Hunter, Winnipeg.
The relation of gall bladder disease to heart disease may be considered
from different angles. As both diseases are extremely common in middle and
advanced age, they must often coincide in the same individual. Llewellys
Barker in his recent "Treatment of the Commoner Diseases," and Von
Bergmann in his "Functional Pathology" state that 30% of all men and
40% of all women, after the age of 40, who come to autopsy, are found to
have gall stones, and to these figures we must add the unknown but very
large percentage who have cholecystitis without gall stones. Blackford,
Ring and Sherwood estimate that more than 50% of adults past 30 years
of age have abnormal gall bladders and that about 20% have gall stones.
On the other hand, to emphasize the frequency of heart disease by middle
age, White points out that of 3000 physicians who died in the United States
during 1931, over 1000 died of heart disease. The association of cardiac with
gall bladder disease has long been recognized. Sir James MacKenzie, for
example, points out that the famous John Hunter was found at post mortem
to have both coronary disease and gall stones. MacKenzie found, from
Page S5 examination of Hunter's careful notes of his condition, that the gall bladder
attacks evidently existed for 17 years, while the anginal attacks dated only
from 6 years before death. Schwartz and Herman have recently found in
109 patients with cholecystitis, evidence of associated myocardial disease
in 63.3%.
Babcock, of Chicago, for many years emphasized his conviction, based
on personal experiences, that when chronic myocardial disease and gall bladder trouble co-existed, removal of the gall bladder had frequently a most
beneficial effect on the myocardium, provided close attention to the history
showed that active gall bladder disease in the form of colic or pain, associated or not with a gaseous dyspepsia, was present. Willius reports that, in
his cases of angina pectoris associated with gall bladder disease, 52% of the
patients experienced definite improvement of their angina by cholecystectomy, some indeed never having another anginal attack after the operation.
Butler, Feeney and Levine review over 400 cases with definite heart
disease (including 35 cases of angina pectoris) who were submitted to
operations, mostly major in type; they conclude that the surgical risk in
most cases of heart disease is not appreciably greater than in the normal
person. Thus 41 operations were performed on 3 5 patients with angina
pectoris, with only 3 unexpected deaths. Judd, of Rochester, does not hesitate to do a cholecystectomy on any case of angina pectoris, who would
otherwise require it, provided the patient is adequately prepared for operation. Obviously, however, as Butler's statistics show, if a patient is operated
on under the mistaken diagnosis of an abdominal emergency—acute pancreatitis, perforated ulcer or severe cholecystitis—when the symptoms are
really due to coronary thrombosis, the death rate will be exceedingly high,
though if the patient be successfully tided over for some weeks or months
after the coronary thrombosis, operation may be carried out with reasonable
It is clear that a correct diagnosis between sudden attacks of heart
disease and of gall bladder disease is of paramount importance. Previously,
when coronary thrombosis was little known, the mistake usually made was
to diagnose acute abdominal disease instead of cardiac infarction. But
nowadays, so deeply are physicians impressed with the frequency and seriousness of cardiac infarction, that this is sometimes diagnosed when only acute
gall bladder colic is present and angina pectoris may be suspected in other
It is to such mistakes (a number of which I have personally met with in
recent years) that I wish especially to direct your attention. It may be laid
down as an axiom that every case of suspected coronary occlusion or of suspected angina pectoris should be carefully reviewed from the gall bladder
standpoint—one must deliberately consider whether all the symptoms of the
supposed heart case might be due to gall bladder disease or at least whether
some of the attacks might be so explained, and if so, whether operation be
In the typical case of either malady, no great difficulty should arise in
the differential diagnosis. A painstaking history must be combined with a
careful examination and cool appraisal of the patient—an x-ray of the chest
and gall bladder and an electrocardiogram being often most valuable but
always subordinate to the history. 20-25% of all cases of angina pectoris,
for example, show no abnormality of circulation on physical examination,
on x-ray examination, or with the electrocardiogram. Hence, nothing can
replace a full and detailed history, the value of which is nowadays so often
Page S6 obscured here, as in other diagnostic problems by laboratory and x-ray short
cuts. In angina pectoris, a gripping pressing pain—in mild cases merely an
ache or sense of fullness—develops behind the sternum, on exertion especially
after a meal, or on exposure to cold or under great excitement. The substernal position, with possibly radiation to the left or, exceptionally to the
right arm, is characteristic—it does not spread downwards into the abdomen
or to the back, though it may pass up to the throat. The pain is not sharp
and stabbing, though its gripping quality may be modified to a numb burning or tingling sensation, especially in the arm; it is rarely if ever referred
to the apex of the heart or to the left costal margin. The distress is only
exceptionally accompanied by a sense of imminent death, in my experience.
It disappears rapidly when the patient stands still or slows up, and nitroglycerine, gr. 1/100, hastens its disappearance. The pulse rate and rhythm
are usually normal in an attack; the average blood pressure in 100 cases was
found by Levine to be 160 with a diastolic of 95; angina is much more
common in men over 50.
Gall bladder pain should rarely be confused, for its maximal site is
usually in the right upper quadrant or in the epigastrium, passing to the
back or right shoulder; it is more colicy in character, with often a sense of
extreme distension in high epigastrium, and it lasts much longer than an
anginal attack; exercise but rarely causes an attack of gall bladder colic;
the victims are more often women in middle age, with a history of gaseous
But it is often forgotten that anginal pain is not necessarily due to
organic changes in the coronaries or aorta, as many negative autopsies have
shown; it occurs whenever insufficient blood is supplied to the heart to meet
the passing demands of the body. Thus the anaemic patient may develop
angina pectoris, as the quality of blood supplied is insufficient to allow of
much exercise; mitral stenosis and aortic regurgitation even in the young
may be associated with angina; the hyperthyroid patient with increased
metabolic demands may exhibit angina with comparatively little exertion.
The varying, tone, maintained in the coronary arteries through the vagus,
allows increased or diminished flow to the heart, just as the capillaries of the
muscles of the legs are found to dilate in walking. Clinically, it would seem
that from the upper abdomen, especially from the gaU bladder, stimuli may
arise, which reflexly increase the tone of the coronary arteries, diminishing
the flow of blood through them to the cardiac muscle and so provoking
anginal pain. Certain it is that one sometimes gets a history of undoubted
cholecystic attacks, intermingled later with undoubted anginal seizures—
an angina which is relieved, or cured for years at least, by cholecystectomy.
Thus, on the one hand, angina pectoris and cholecystitis are often confused
and mistaken for each other, and on the other, the complete clinical picture
of angina pectoris may in certain cases disappear after removal of an infected gall bladder. Such facts challenge our diagnostic interest.
Summing up, we have to remember:
(1) Abnormal gall bladders are common in middle age, and thus nonvisualization of a gall bladder by Graham's method, and even negative
shadows of calculi in a gall bladder, may have no clinical significance, representing merely the silent gall bladder disease which is so often met with in
the post mortem room.
(2) The gall bladder may visualize and yet may be the culprit—due
sometimes to upset of the neuro-muscular mechanism of the extra-hepatic
Page S7 I
biliary tract, and sometimes to a calculus temporarily blocking the cystic
dust, but allowing at other times free flow of bile into a comparatively
normal-walled gall bladder.
(3) Abnormal electrocardiographic findings and even definite myocardial disease may be present; the symptoms may superficially appear entirely those of a failing heart with breathlessness as a prominent symptom;
the enlarged liver with tender edge may seem but the natural result of back
pressure from a failing myocardium, though other evidence of myocardial
failure in the shape of cedema of the legs or rales at the lung bases may be
curiously absent. Yet recurring attacks of high abdominal colic, or at least
distress, may antedate these cardiac disturbances which now dominate the
clinical picture; a sudden cholecystitis or a little jaundice following a low-
sternal, high epigastric pain of doubtful origin may reveal gall bladder disease, hitherto unsuspected. These are the patients about whom Babcock,
T. R. Brown and others have written, and in my own experience several
such cases have been greatly improved by cholecystectomy.
Evidently the gall bladder infection has weakened the myocardium,
which recovers considerably when the source of infection is removed. But
remember: the gall bladder disease must have shown evidence of activity;
the mere presence of a non-functioning gall bladder, or of gall stones demonstrable on x-ray examination, but accidentally discovered, is no reason at all
for operative interference, just because the heart shows signs of damage.
(4) Definite angina pectoris may be present, due not to unalterable
changes in the coronaries or aorta but to reflex influences from a diseased
gall bladder. Here, too, a searching history with a judicial appraisal of the
patient, and a detached analysis of cardiogram, x-ray of heart and of gall
bladder, should guide us; I know five or six such cases, entirely cured of
their angina by a timely cholecystectomy. We should regard angina pectoris
as a symptom, due generally to organic changes in the coronaries, but arising
at times from reflex disturbances whose site is in the upper abdomen, though
even in the latter cases, some associated narrowing of the coronaries is almost
always present.
Such considerations emphasize the limitations of the newer tests and
reinforce the oft-forgotten warning that a careful history and clinical
examination cannot be replaced by x-ray and laboratory findings. The
patient himself counts: a phlegmatic, easy-going individual is much less
liable to angina pectoris than a sensitive, unrelaxing, hard-living subject.
Especially necessary is it to distinguish between coronary thrombosis
and severe attacks of cholecystitis; one must remember that in coronary
thrombosis, the pain, as in gall bladder attacks, comes usually at rest, may
be confined to the high epigastrium, may last for hours and be accompanied
by restlessness of the patient and by rigidity of the upper abdominal muscles.
But the collapse, the feeble, sometimes rapid, heart, with gallop rhythm,
the breathlessness or even cyanosis, the possible history of preceding angina,
the frequent spread of the crushing pain upwards behind the sternum and
even into the arm, will usually guide one to the heart. A falling blood
pressure, sometimes within a few hours, a leucocytosis and rise of temperature later, with possibly a passing pericardial rub, may settle a hitherto
doubtful diagnosis; while if the right coronary be affected, the early onset
of right-sided cardiac failure with engorgement and tenderness of the liver
and icteric tinge of the conjunctivae may appear.
The Gastro-cardiac Syndrome: Just a few remarks on a symptom-complex, better known in Germany largely through Roemheld's writings, but
Page sn ■ I—
common enough in this country—the gastro-cardiac syndrome. This illustrates another relation between the digestive and circulatory systems and so
is described here. The condition is seen more often in men of middle or later
life, who live hard, eat hastily and take little exercise. Gastric anacidity, gall
bladder disease and spastic colon may complicate the picture, where the left
leaf of the diaphragm is pushed up, with displacement of the heart, by
accumulation of gas in the stomach or splenic flexure.
Symptoms: There is, especially after gassy food, a dull painful pressure
at the left costal margin, with shortness of breath and inability to take a
deep breath. The pain and pressure may extend up to the left chest and may
even pass into the left arm. Extra systoles, quite slow or rapid heart action,
dizziness and faintness may appear, with continued belching largely of
swallowed air, aggravating the condition and associated with nausea or even
hiccup and vomiting. The apex beat is displaced up and out, and a tympanitic
note on percussion may be noted unusually high on the left chest. On x-ray
exarnigation, there is an excessive accumulation of gas beneath the left
diaphragm, usually in stomach, sometimes in the splenic flexure. The patient
is rather breathless and becomes more aware of his heart, restricting his
exercise and so aggravating the condition—the fear of heart disease may be
a big factor in the case.
The treatment is satisfactory—reassurance re the heart; avoidance of
gas-producing articles of diet with generally reduction in weight; training
in abdominal breathing; abdominal massage; exercises and games. A specially
severe attack can be terminated by gastric lavage.
Miller, C. H.—Lancet, April 9, 1932, p. 767.
Palmer, W. L.—International Clinics, March, 1935, p. 111.
Brown, T. R.—Annals of Internal Medicine, September, 1934, p. 343.
Willius, F. A., and Brown, G. E.—American Journal of Medical Sciences, August, 1924,
p. 181.
Hamman, L.—Annals of Internal Medicine, October, 1934, p. 417.
Smith, H. L., and Plunkett, J. E.—Medical Clinics of North America, September, 1934,
p. 491.
White, P. D.—Annals of Internal Medicine, August, 1933, p. 218.
Riesman, David—Journal of American Medical Association, November 17, 1928, p. 1521.
Butler, S., Feeney, N., and Levine, S. A.—Journal of American Medical Association,
July 12, 1930, p. 8S.
Halstead, J. A., and Bauer, W.—Medical Clinics, of North America, January, 1933,
p. 951.
Faulknex, J. M., Marble, H. C, and White, P. D.—Journal of American Medical Association, December 27, 1924, p. 2080.
Robey, W. H.—Medical Clinics of North America, May, 1925, p. 1709.
MacKenzie, Sir Jas.—Angina Pectoris, London, 1923, p. 132.
Levyn, L., and Rose, W. J.—Radiology, May, 1934, p. 622.
McCrae, T.—American Journal of Medical Sciences, January, 1930, p. 16.
Barker, P. S., Wilson, F. N., and Collier, F. A.—American Journal of Medical Sciences,
August, 1934, p. 219.
Burns, G. R.—Canadian Medical Association Journal, October, 1931, p. 424.
Pardee, H. E.—Medical Clinics of North America, July, 1933, p. 67.
Winkelstein, A.—Medical Clinics of North America, July, 1933, p. 233.
Elliott, A. R.—Medical Clinics of North America, March, 1935, p. 1263.
Weiner, J. G.—Medical Clinics of North America, November, 1933, p. 823.
Roemheld, J.—American Journal of Medical Sciences, July, 1931, p. 13.
By Dr. R. I. Harris
Toronto, Ont.
Osteomyelitis in any of its multitudinous phases is a surgical problem of
first importance. Few conditions so endanger life or hold such a menace of
future disablement. Even when the first storm has passed the danger to life
is not entirely over. Recurrences may take place years later as virulent as the
primary infection, and death may result from the later flare-up of an infection laid down in childhood.
Though it is of the chronic phase of osteomyelitis that I desire to
speak today, it is necessary for me to spend a few minutes in discussing the
pathology and clinical course of the disease from its inception.
Acute haematogenous osteomyelitis is an infection of the long bones of
growing children by pyogenic organisms brought to the bone by the blood
stream. The staphylococcus pyogenes aureus is by far the most common
infecting organism. It invades the blood stream from skin infections and
abrasions. The primary focus very commonly is a boil. Other organisms,
however, may be the infecting agents—streptococci, pneumococci, typhoid
bacilli, or even colon bacill. Whatever the infective agent may be, the
essential background of osteomyelitis is a local focus of infection with
secondary invasion of the blood stream.
We have no clear knowledge of the factors which determine the selective localization in bone. It is a remarkable fact that an infection by pyogenic
organisms can under obscure circumstances invade the blood stream and
attack certain tissues and these only. Osteomyelitis is one of the most conspicuous examples of selective localization of infection, for once established
its various foci are almost exclusively confined to bone. This is the more
remarkable since the common infecting organism is one which under other
circumstances can produce infection in a variety of tissues.
Still more baffling is the remarkable constancy with which the infection
in bone is laid down in the metaphysis. No matter how widespread the disease
may become in a bone, it commences always in that part of the diaphysis
which lies immediately beneath the epiphyseal line—the so-called metaphysis.
It is probable that the vascular system has some part to play in the deposition
of the primary focus. The exact mechanism is obscure. I find it difficult to
believe that bacteria, even clumps of them, can ever occlude capillaries, since
they are so much smaller than the largest blood cells. Moreover, while one
primary focus in bone is being laid down, the metaphyses of all the other
long bones are exposed to the same blood stream infection and most of them
escape. The point of invasion cannot be explained on purely anatomical
What part does trauma play in the inception of a focus of osteomyelitis?
The evidence on this point is confusing. In some cases there seems a clear
history of injury. One might reasonably expect that injury would be an
important factor. Damage to blood vessels with haemorrhage would provide
an area in which infection could establish itself. On the other hand, innumerable cases develop fresh foci of osteomyelitis while lying in bed without
the possibility of trauma playing any part in their initiation.
Read at the Annual
September, 193 5.
Page 90
Meeting of the B. C Medical Association, VancSaover, B. C, The course of this acute infection in bone is unlike that of most infections and this is due chiefly to the nature of the tissue involved. The rigid
character of bone and the distribution of its blood supply favour extensive
necrosis by the shutting off of blood vessels. In the presence of infection
such areas of necrosis rapidly become infected. A common sequence of events
is as follows: The early focus in the metaphysis excites an inflammary reaction which spreads more or less uniformly in all directions. The epiphyseal
line, however, is a barrier which prevents its spread into the epiphysis.
Sooner or later the infection reaches the cortex and the products of inflammation accumulate beneath the periosteum. Here the resistance to spread is
slight and the subperiosteal abscess which forms spreads rapidly by stripping
the periosteum from the underlying bone. In so doing, it deprives the bone
of its periosteal blood supply and causes superficial flakes of bone to become
necrotic. These are the future sequestra. If the periosteum is stripped from
end to end, the nutrient artery may be thrombosed and this causes necrosis
of the whole shaft of a bone. The surviving bone is excited to an intense
inflammatory reaction, characterized by great increase in the cells and blood
vessels and absorption of the calcium ground substance. The necrotic bone
is slowly separated by the activity of the adjacent living bone until the dead
fragments lie loose as sequestra. Meantime osteoblasts which have been lifted
up with the cambium layer of the periosteum have multiplied and have produced a tube of new bone which overlies the sequestra. It is the mass necrosis
of bone by interference with its blood supply in the presence of infection
which constitutes the peculiar feature of osteomyelitis and gives rise to the
chronic phase with which we are concerned today.
The period of septicaemia and of invasion of bone may be called the
acute phase. Its outstanding problem is that of severe infection. The septicaemia may be so intense as to dominate the picture, the foci of osteomyelitis
being but insignificant incidents in an overwhelming and fulminating blood
stream infection. Such patients may die in forty-eight hours. The acute
phase may present itself in every gradation of severity from the fulminant
septicaemia which kills in forty-eight hours to the attenuated focus which
passes unrecognized at the time, only to be diagnosed as a Brodie's abscess
years later. In cases of average severity the deposition of multiple foci is the
rule rather than the exception. Many of these are not recognized until years
have elapsed. They constitute many of the cases of chronic osteomyelitis.
The urgent therapeutic problem in the acute stage is drainage of infection. The blood culture in nearly all cases is positive when first seen. If adequate drainage can be established the blood becomes sterile.
In the chronic stage of osteomyelitis the therapeutic problem is the
removal of infected sequestra and the disposal of the remaining bone in such
a manner that sound healing will ultimately take place. We may distinguish
two types of chronic lesion—open and closed. The open lesion is that which
has a discharging sinus which refuses to heal as long as the offending sequestrum remains. The closed lesion has no discharging sinus. Usually its sequestrum is small and the infection is so attenuated that frank suppuration is
held in abeyance for many years or does not occur at all. In principle they
are sirnilar but in practise they demand different treatment.
Active treatment of chronic osteomyelitis cannot be undertaken until:
(1) the sequestra are completely separated from the surrounding living
bone;  (2)  sufficient new bone has formed to maintain the integrity and
Page 91 tin
length of the bone. This requires at least three months and often longer.
Dense bone separates less readily than does cancellous bone. It is useless to
attempt the surgical cure of chronic osteomyelitis until the sequestra are
completely separated.
In principle the treatment of chronic osteomyelitis consists in: (1) the
removal of sequestra with as little damage to living bone as possible; (2)
the reshaping of bone cavities and spaces so that soft tissues may fall in upon
them and leave no dead spaces. Few operations in surgery require such
meticulous care as the radical cure of chronic osteomyelitis. Every sequestrum must be removed else recurrence will take place. Since there may be
many sequestra, and since some of them may be minute, and since they are
scattered widely throughout the bone, the complete toilet of an infected
bone is no easy matter.
The best plan of treatment is as follows: Operate with a tourniquet
wherever possible. This ensures a bloodless field which facilitates the search
for sequestra and safeguards the patient against loss of blood which might
otherwise easily take place. Expose the bone through an adequate incision.
The only satisfactory operation is one which is carried out under direct
vision, and this can only be obtained through large incisions. Raise the
periosteum no more than is necessary and remove all bone deprived of periosteum. It is easy to produce fresh necrosis from operative trauma and
extensive elevation of the periosteum invites this. With clean chisel cuts
remove such involucrum as is necessary in large masses. Do not chip it away
in small pieces. The fewer the chisel cuts the fewer will be the small spicules
which later will become sequestra. Having exposed the cavities in which the
sequestra lie by removal of the involucrum carefully lift out the sequestra.
Follow all the prolongations of the cavity in the search for minute sequestra.
Remove all the granulation tissue lining the cavity. Then remodel the cavity
in such a manner as to avoid overhanging edges or dead spaces.
When the operation is completed an important step is to determine the
exact manner in which after treatment will be carried out. Even though
perfect saucerization of the wound has been attained so that the soft tissues
will fall in and completely close the wound, it is inadvisable to attempt
primary closure. The trauma of operation almost inevitably causes devitalization of small spicules of bone which later separate and form small
sequestra. Provision must be made for their easy extrusion. Infection, moreover, is present in the widely opened wound and some means must be adopted
to deal with it.
Two methods are valuable: (1) Carrel-Dakin treatment of the wound
with secondary closure; (2) Winnett Orr's treatment with vaseline packs.
The treatment of the wound by the Carrel-Dakin method is excellent,
especially if some of the modern and stable forms of Dakin's solution are
used. It does, however, involve daily dressings and meticulous care. Its
advantage is the comparatively early closure of the wound which is attained.
The Orr treatment is extremely simple and, though prolonged, the results
are good.
A few words regarding Orr's treatment may be of value. Winnett Orr
of Lincoln, Nebraska, observed the results obtained in'war injuries by Fraser
Gurd, now of Montreal. Gurd, in attempting to devise some means of minimizing the incessant labour of wound treatment by the Carrell Dakin
method found that packing the wound permitted it to heal from the bottom
Page 92 *um
and required only infrequent change of dressing. The addition of vaseline,
bismuth and iodoform (B.I.P.) to the gauze provided a mild antiseptic
and facilitated the removal of the gauze. Orr's elaboration has consisted in
the use of simple paraffined gauze without any antiseptic, and of allowing
this to remain in place unchanged and undisturbed for three or four months.
The limb is enclosed in plaster and the wound completely covered. The
results of such treatment are surprisingly good. The wound becomes clean
and remains so. The patient's temperature falls to normal. The stench from
the dressing is very unpleasant, and in my opinion is unnecessary, and the
length of time required for cure is great.
Many of Orr's hypotheses are untenable but he undoubtedly has made
an important contribution to the treatment of chronic osteomyelitis. It is
unnecessary to use plain gauze. If the wound is packed with iodoform gauze
the unbearable stench is avoided, and one of the most important objections
to the method is overcome. The advantages are the avoidance of the frequent
painful dressings, the provision made for the extrusion of sequestra and the
certainty that the wound will heal from the bottom, so avoiding pockets
and recurrences.
We come now to a discussion of the closed forms of chronic osteomyelitis. This is a very important but little known aspect of the disease.
Closed lesions arise in two different ways: (1) They may be laid down as
subsidiary foci during the acute phase of osteomyelitis in another bone; (2)
they may arise as residual foci from the imperfect clearing out of an infected
Nearly every case of osteomyelitis of moderate severity is characterized
by the deposition of secondary foci in bones other than that first attacked.
These secondary foci are often less severe than is the first focus of osteomyelitis, and frequently are overlooked in the stress of attention which is
concentrated on the more obvious lesion. Often these secondary foci never
suppurate frankly. The patient's resistance to his infection increases and
he succeeds in holding the focus in abeyance though he never succeeds in
stamping it out. It grumbles on in quiet activity for an indefinite period
of time.
In a somewhat similar fashion, unnoticed pockets or minute sequestra
overlooked during the operation of sequestrectomy may heal over and become
quiescent foci which harbour infection for an indefinite period of time.
One of the distinctive features of chronic osteomyelitis is the ability of
such closed foci to harbour infection for an indefinite period of time. Forty
years is not an uncommon length of time for such foci to remain active.
In no other tissue of the body is this true. The explanation is not easy. It is
my impression that the persistence of infection is always due to sequestra.
These provide harbours in which organisms can hide immune from attacks
of the body's defensive mechanisms. In other tissues this is not true. Dead
and infected tissue is devoured by phagocytes. Sequestra cannot be disposed
of in such fashion. They are beyond the attack of phagocytes and osteoblasts,
and hence provide admirable culture tubes for bacteria.
The serious aspect of the closed focus of osteomyelitis is its ability to
flare into violent activity for unknown reasons. From time to time the
grumbling and innocent focus becomes the site of an intense inflammation
from which the blood stream may be infected. The fulminating flare-ups
may be fatal and often are. I have seen this happen most often after the
Page 93 osteomyelitis of war wounds, but it occurs also in haematogenous osteomyelitis.
The treatment of the chronic closed focus is often difficult. The prolonged irritation has led to dense sclerosis of the surrounding bone so that
localization of the cavity is difficult. Some form of block resection of the
involved area of bone is the ideal procedure when this can be carried out.
Unfortunately the mutilation involved often precludes such ideal treatment. If a fulminating recurrence takes place amputation should be given
serious consideration as a life-saving measure.
(The speaker closed with a reference to the treatment of osteomyelitis
with Dolman's staphylococcus antitoxin and toxoid.)
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Page 94 BBS
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Millions of people know of
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years of research in leading nutritional laboratories. Here are some
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question and answer form:
1. Is the "bulk" in bran irritating to
the intestines?
ANSWER: No, not for the normal
person. There are some individuals with highly sensitive intestines who should not eat "bulk" in
any form—either in fruits, vegetables or in bran.
2. Is bran effective In relieving constipation due to insufficient "bulk"?
ANSWER: Laboratory tests in universities with adult people substantiate the effectiveness of
Kellogg's All-Bran.
3. Does bran continue to be effective
over a period of months ?
ANSWER: Yes. Moreover, dosage
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with cathartics. In four laboratory studies on a group of healthy
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fuls of bran per person were eaten
daily, the laxative effect was as
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4. Is the "bulk" in bran more effective than that found in fruits and
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ANSWER: Yes, with many individuals. Laboratory tests indicate
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5. Is all bran more effective than part-
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ANSWER: Yes. It's the actual
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Kellogg's All-Bran provides
gentle "ttlk" to correct common
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FOR some while the Medical Profession has felt the need of a local
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COLONIC IRRIGATIONS are valuable in such cases as Constipation,
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Obstetrical cases are benefitted by internal baths at measured periods,
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We take pleasure therefore, in announcing to the Medical Profession
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