History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: November, 1947 Vancouver Medical Association Nov 30, 1947

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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.
No. 2
Db. G. A. Davidson
OFFICERS, 1947-48
Db. Gobdon C. Johnston
Dr. H. A. DesBbisay
Past President
Db. Gordon Burke
Hon. Treasurer
Db. W. J. Dorrance
Hon. Secretary
Additional Members of Executive: Dr. Roy Huggard, Dr. Henry Scott
Dr. A. M. Agnew Dr. G. H. Clement Dr. A. C. Frost
Auditors: Messrs. Plommeb, Whiting & Co.
-Gtenieal Section
Db. Reg. Wilson Chairman Db. E. B. Trowbridge Secretary
Eye, Ear, Nose and Throat Section
Dr. Gordon Large Chairman Dr. G. H. Francis Secretary
Paediatric Section
Db. J. H. B. Grant Chairman Dr. E. S. James_ Secretary
Orthopaedic and Traumatic Surgery Section
Dr. J. R. Naden Chairman Dr. Clarence Ryan Secretary
Neurology and Psychiatry
Dr. J. C. Thomas Chairman Db. A. E. Davidson Secretary
Db. J. E. Walker, Chairman; Db. W. J. Dobbance, Db. D. E. H. Cleveland,
Db. F. S Hobbs, Db. R .P. Kinman, Db. S. E. C Tubvey.
Db. J. H. MacDebmot—Chairman; Db. D. E. H. Cleveland, Db. H. A.
DesBbisay, Db. J. H. B. Gbant, Dr. D. A. Steele.
V. O. N. Advisory Board:
Db. Isabel Day, Db. H. H. Caple, Db. E. J. Cubtis.
Summer School:
Db. A. B. Manson, Chairman: Db. E. A. Campbell, Db. J. A. Ganshobn,
Db. G. Large, Db. D: S. Munbo, Db. D. A. Steele.
Db. H. A. DesBbisay, Dr. H. H. Pitts, Dr. Frank Turnbull.
Representative to B. C. Medical Association : Dr. H. A. DesBrisay.
Sickness and Benevolent Fund: The President—The Trustees.
TABLETS (No. 830)
Each tablet contains:
Ferrous Sulphate
Exsiccated 162 mg. (2.5 grains)
Liver Concentrate - - equivalent to
1 Gm. fresh liver
Thiamin Chloride - -
Riboflavin ....
Niacinamide ...
Pyridoxine ....
Calcium d-Pantothenate
1 mg.
0.66 mg.
3.34 mg.
0.34 mg.
1.84 mg.
In bottles of 100, 500 and 1000
„ >■■ _^i
SYRUP (No. 944)
Each millilitre contains:
Ferrous Chloride
(Citrated) 30 mg. (0.468 gr.)
Copper Sulphate 0.228 mg. (0.003 gr.)
Liver Concentrate - - equivalent to
0.246 Gm. fresh liver
Thiamin Chloride - - 0.029 mg.
Riboflavin .... 0.038 mg.
Niacinamide      ...      0.475 mg.
In bottles of 16 ounces
Biological and Pharmaceutical Chemists
446 January 6th
January 20 th
February 3rd
Founded 1898    :    Incorporated 1906.
Programme for Fiftieth Annual Session
(Spring Session)
GENERAL MEETING, Auditorium, Medical-Dental Building.
"The Problem of Dizziness"—Dr.  Laurence  Selling,  Professor of
Medicine and Neurology, University of Oregon Medical School.
CLINICAL MEETING—Vancouver General Hospital, Lecture Room.
GENERAL MEETING, Auditorium, Medical-Dental Building.
"The Treatment of Burns, as Practised at St. Paul's Hospital"—
Dr. P. B. Guttormson.
Discussion Led by Doctors B. T. H. Marteinson and A. S. Mc-
February 17th    CLINICAL MEETING—St. Paul's Hospital, Nurses' Auditorium.
March    5th (Friday)     OSLER DINNER AND LECTURE—Hotel Vancouver, Banquet Room.
Osier Lecturer—Dr. Murray Blair.
CLINICAL MEETING—Children's Hospital.
GENERAL MEETING—Auditorium, Medical-Dental Building.
Speaker—to be announced.
CLINICAL MEETING—Place of meeting to be announced.
ANNUAL MEETING—Auditorium, Medical-Dental Building.
March 16th
April    6th
April 20th
May    4th
Breaks the vicious circle of perverted
menstrual function in cases of amenorrhea,
tardy periods (non-physiological) and dysmenorrhea. Affords remarkable symptomatic
relief by stimulating the innervation of the
uterus and stabilizing the tone of its
musculature. Controls the utero-ovarian
L    circulation and thereby encourages a    i
1%   normal menstrual cycle. Jr
Ik Wm JT
^ ISO IMMMIt S T t tit. NCW TO«K. N. T. J&
Full formula and descriptive
literature __• request
Dosage:   l to 2 capsules
3 or 4 times daily.   Supplied
in packages of 20.
Ethical protective mark MHS
embossed on inside of each
capsule, visible only when capsule is cut in half at seam.
PERTUSSIS VACCINE (For Prevention of Whooping Cough)
A modification in the concentration of pertussis vaccine has recently
been made by the Connaught Medical Research Laboratories, so that the
vaccine formerly containing 15,000 million killed organisms (H. pertussis
from strains in Phase 1) per cc. now contains approximately 22,500 million
killed organisms per cc, permitting the administration of three doses of 1 cc.
at monthly intervals, and a reinforcing dose of 1 cc. after an interval of at
least three months.
Diphtheria toxoid has been combined with the new concentration of
whooping cough vaccine. The new combined product is also administered
in three doses of 1 cc, with a reinforcing dose of 1 cc.
For protection against tetanus as well, a triple antigen has been introduced by the Laboratories. This product contains diphtheria and tetanus
toxoids combined with the new concentration of whooping cough vaccine and
is administered in three doses of 1 cc, followed by a reinforcing dose of 1 cc.
ADVANTAGES    f| ;^p:
Two  important advantages have  been  made
possible by this change:—
A dose of 1 cc. replaces the dose of 2 cc. as formerly
The reinforcing dose is included in each package.
For the inoculation of one child—Package containing Four 1-cc. Ampoules.
For a  group  of  nine children—Package  containing  Six  6-cc   Ampoules.
University of Toronto Toronto 4, Canada
Total Population—Estimated 	
Chinese Population—Estimated
Hindu Population—Estimated _
Total deaths 292
Chinese deaths /     \6
Deaths, residents only     277
Rate Per 1000
INFANT MORTALITY: Sept., 1947 Sept., 1946
Deaths under 1 year of age       23 15
Death rate per  1000 live births       36.9 20.9
Stillbirths   (not included above) 1__ 6 9
Scarlet Fever
Diphtheria Carrier
Chicken Pox 	
Whooping  Cough	
Typhoid  Fever	
Typhoid Fever Carrier
Undulant Fever 	
Poliomyelitis    ,	
Meningococcus   (Meningitis)
Infectious Jaundice 	
Salmonellosis  (Carrier)	
Dysentery  (Carriers)	
Cancer (Reportable):
Non-Resident —
ber, 1947
, 1947
0 !
Page 47 Demerol hydrochloride ranks between morphine and
codeine in analgesic power. Furthermore, it possesses
marked spasmolytic and miid sedative action. It causes
less nausea and vomiting and less urinary retention than
morphine, and no constipation. The danger of respiratory
depression is also greatly reduced with Demerol hydrochloride. Warning: May be habit forming. Ampuls of 2 cc.
(100 mg.) and tablets of 50 mg. Narcotic blank required.
Write for detailed literature
H V D R I C H I 0 lil E
Brand of meperidine hydrochloride (isonipecaine)
DEMEROL, trademark Rag. U.S. Pat. Off. & Canada
New York 13, N. Y.     •     Windsor, Ont. Ike ZdUo>& Paae
To allits readers the Bulletin wishes a very Merry Christmas and Happy New
Year. Our family is growing steadily and fairly rapidly—this issue will amount to
some seventeen hundred copies—and may they all prosper and achieve success in the
coming years.
Our next copy will appear in a new cover. The Publications Committee has felt
for some time that a change should be made in this, and we hope it will be felt to be
an improvement. We have kept the journal at its present size and shape, as being the
handiest and most convenient, and the type and arrangement of the pages will be the
same. We hope to go in for more illustrations, in the way of cuts, etc., and would
suggest to those who contribute articles and papers that if they have any illustrations
that they feel* would enhance the appearance and value of their contribution, we shall
be very glad to have these, and to reproduse them. We can afford to do this now—
in times gone past the shadow of the Auditor hovered too closely for us to take any
chances, and we had to be careful—but we have always looked forward to the day
when we should be able to illustrate our pages with appropriate cuts and pictures—
these do undoubtedly add a great deal, not only to the attractiveness of the pages, but
also to ease of reading, and a greater clearness of presentation.
Some of our readers who subscribe to Maclean's Magazine may have noticed an
editorial printed in the December 1st issue "Calling Dr. D. P." The writer, in this short
editorial article, attacks the Canadian medical profession for its supposed opposition to
the admission to Canada of refugee doctors from Europe. He ascribes to the General
Secretary of the Canadian Medical Association the expression .of his belief that these
men should not be admitted.
He objects that this is "discrimination in favour of Canadian doctors," and ends his
article by saying that where there is such a need, "especially in rural areas," for more
medical men, "we cannot afford to waive, at the behest of a particular profession, a
principal which has national acceptance."
Any stick, of course, will do to beat the medical profession with, but we consider
that Maclean's Magazine has gone too far in this matter. The writer is probably referring, not to any utterance of Dr. Routley's, for he has been out of Canada for over a
year, and has not, at least to our knowledge, made any such categorical statement as that
attributed to him—but to certain public utterances made by Dr. A. D. Kelly, his assistant and associate secretary.
One has only to read Dr. Kelly's statement, published in the September number of
the Bulletin, to see how unfair and inaccurate is the Maclean editorial, and how completely it ignores all his arguments. Dr. Kelly gives very excellent reasons why Canada
should be very careful about admitting "refugee doctors." We feel that every Canadian
doctor will agree strongly with Dr. Kelly's very carefully-worded article, and will feel,
as we do, that the Canadian medical profession cannot justly be accused, either of lack
of sympathy with these unfortunates, or of self-interest in their hesitation to admit
them. Nor would a wide open policy meet the needs of Canada, nor be good for Canadian conditions, as Dr. Kelly points out.
We wrote to Maclean's Editor, pointing out these things, and sending him a copy of
Dr. Kelly's article. We are confident that it was merely a failure to understand the real
' facts of the case that led the editorial writer to say what he did, and not any animus
against the medical profession, and we are sure that he will be glad to be corrected in
this matter. A fair and impartial reading of what Dr. Kelly said in his address will leave
no room for any charge that we are opposing aid to refugee doctors, not to speak of
Page 48
—- improvement of medical conditions in Canada, on any selfish grounds; and we believe a
clearer understanding of the facts will be for the good of all concerned, not only in our
own country, but in the other countries of the world.
*      k-      *      *
So many requests have been made for the concise summary that Dr. Cleveland drew
up some time ago, as a guide to those who contribute papers for publication, that the
Bulletin has secured an ample supply of reprints of this, and they are being kept at
the Library. Any member who would like to make one of these may have it for the
asking. It will be found very useful, and a careful attention to the suggestions found
therein will be of great assistance, not only to the author, but to the Editorial Board in
its use of the article contributed.
Monday, Wednesday and Friday  9:00 a.m. to 9:30 p.m.
Tuesday and Friday  9:00 a.m. to 5:00 p.m.
Saturday    9:00 a.m. to 1:00 p.m._.
Medical Clinics of North America, Symposium on Respiratory Diseases, Philadelphia
Number, November, 1947.
Wm. Beaumont's Formative Years (Two Early Notebooks), Annotations and introductory essay by Genevieve Miller.
The Reception of Wm. Beaumont's Discovery in Europe, by George Rosen.
(Historical and Ultra-Scientific Fund.)
No.  193    The influence of positive pressure breathing on the circulation in man.
No.  194    The coagulation of blood—investigations on a new clotting factor.
No. 195 The cardiological anoxemia test with special reference to its standardization.    A clinical and physiological study.
No.  196    Hilding Berglund (60th birthday anniversary number)—Various authors.
No.  197    Tuberculosis and pregnancy.
No. 198 Dietary factors and quantitative morphology of the Islets of Langerhans—
an experimental study of the influence of the Islets of Langerhans and
an analysis of the relation between the volume of islet tissue and the
number of islets in the rat.
No. 200 Studies on the formation of cellular substances during blood cell production.
Mr. H. L. Campbell, Chairman, Junior Red Cross, Provincial Department,
has written to the British Columbia Medical Association appealing to the doctors
for reduced fees regarding the care of Junior Red Cross handicapped children.
Members of the Junior Red Cross consist of 47,484 pupils in the schools
of British Columbia, who raise and maintain a fund which is used to assist
needy crippled and handicapped children in this Province obtain necessary
medical care and treatment.
They have played an important role in Junior Citizenship and are now
appealing to the doctors of this Province to assist in every way possible.
K. R. TRUEMAN, M.D., M.Sc.  (Minn.)
Winnipeg, Man.
(Read Before B. C. Medical Association Annual Meeting)
Gall bladder disease can usually be diagnosed on a clinical basis when it is frankly
and fully developed. The classical features of such an advanced state include attacks
of severe pain or colic associated with restlessness and requiring morphine for relief.
The pain generally is felt in the right upper quadrant, and may radiate posteriorly
to the scapula or shoulder. Vomiting may be present. Jaundice may occur without a
stone in the common duct and be due to inflammation or dysfunction of the adjacent
tissue. It may be obvious or subclinical when its presence can be detected only by
laboratory means. Following the attack, residual tenderness is noted in the gall
bladder area. So frequently are the attacks produced by, or are coincident with the
use of articles of a fatty nature that the patient may develop a fear of food, and his
reduced diet leads to a steady decline in weight. For years, the cholecystogram has
supported or helped to rule out the diagnosis of gall bladder disease with a high degree
of perfection. More recently, the introduction of improved dye, the standing position
and increased speed of exposure have increased the incidence of correct diagnosis in each
It is the surgical treatment of such advanced disease of the gall bladder in which
all the clinical criteria for operation have been met which is acknowledged to be so
successful. Here there should be a full measure of agreement, not only in diagnosis
but in treatment. There are, however, other lesser degrees of gall bladder involvement
where a conflict of opinion as to the ideal method of therapy may exist. The solution
will probably never be decisive or simple, and the individual cases must be decided on
the basis of certain distinctions.
It is well known that many persons may conceive gall stones and remain unaware
of their silent' presence for years until some related event discloses them.    A certain
proportion are found to have stones, during the course of an examination, because of
some complaint not associated with gall bladder disease.   In many of these cases, the
question must arise as to whether surgical intervention is warranted.   It is, of course,
impossible to foresee which of this group will remain free of trouble until the end of
their time, and who will at some period develop a full blown picture of gall bladder
disease—as some must.  Of these latter, the effects may develop gradually, and assistance
can be sought in an elective manner.   On the other hand, others may be suddenly
stricken at such a time or place or age that treatment is not available or satisf actpry,
and there follows a prolonged and dangerous illness which may terminate unsuccessfully.
It is no doubt impractical to advise the removal of all silent gall stones when discovered.   This is so despite the easy technical problem and the fact that the morbidity
and mortality would be reduced almost to a fantastic figure in such cases.   There are
obviously good reasons to contra-indicate such a practice.   How worthy and justifiable
these reasons continue to be held will vary, doubtless, with what recent experience the
medical and surgical consultants have had with some of the more advanced and serious
states of gall bladder disease.   Nothing can be more worrying or unsettling than the
care of such a case when the successful outcome hangs in the balance.   This is especially
so when the patient is precipitated into trouble after a period of successfully getting
by on the counsel that silent stones are innocent stones.   It is following an unhappy
example of this nature that both physician and surgeon are likely to believe that never
again will they permit themselves to suffer such a trial.   However, so changeable is
human nature that in time this attitude softens, and silent gall stones are allowed to
rest in peace, and it is only with a further bitter experience that the resolve to remove
all calculi is reborn.
Page 50 Some day possibly the prophylactic removal of all gall stones may be widely practiced
and without criticism. By analogy one might point to the treatment of adenoma of
the thyroid. In the large centres great experience has taught that a certain proportion
of these undergo changes which are toxic or malignant. The teaching has further
spread that it is reasonable to remove the great majority of these before a condition
arises which may imperil the patient, despite the fact that many would remain unaffected
if left alone. Similarly, the urologist should show little hesitation in dealing with a
symptomless stone discovered by accident in the renal pelvis because of the fear of
possible consequences. Much the same argument may be directed to the repair of
hernia, which in the early stages is so successful.
As already noted, it may be impractical to advise removal of all silent stones.
Nevertheless, it is well to distinguish between certain conditions. Thus a normally
functioning gall bladder by cholecystogram, containing one or two moderately large
cholesterol stones, represents a less urgent problem than such an organ containing
multiple small stones. The great danger obviously in the latter case is the possibility
of a small stone entering a duct and causing obstruction with major ill effects. Such
a situation is regarded by some as a definite indication for operation, and the argument
appears reasonable, despite absence of symptoms. Generally it may be argued that
other future hazards due to gall bladder disease will be reduced. These include, in
addition to biliary obstruction, acute cholecystitis, which may progress to gangrene
and perforation, too often carcinoma, which almost invariably is associated with gall
stones, cirrhosis of the liver, pancreatitis, and possibly serious effects from cholecystitis
having some relationship to a greater degree of arteriosclerosis. As a basis for concern
regarding silent gall stones was the finding in a recent series of choledochotomies at the
Winnipeg Clinic. Of thirty cases of common duct stone, 50 percent had had symptoms
referable to the biliary tract for less than one year.
Another problem involves combinations of mild or moderate symptoms suggestive
of gall bladder disease. In such cases may be found a functioning gall bladder with
one or more large cholesterol stones or a gall bladder which functions poorly or not
at all in the cholecystogram. None of the urgent symptoms of gall bladder disease
has been present. The treatment of these cases constitutes a problem. Although
cholecystectomy may be indicated because of the presence of stones alone, this measure
does not always produce the symptomatic relief expected. The resultant disappointment
must be shared alike by patient and doctor, and too often the lack of improvement
is attributed to the surgical procedure and not to the true circumstances, namely, the
possibility of associated conditions.
The presence of more than one abnormal condition is not uncommon in patients
of middle age or over, and they may be functional or organic in nature. Frequently,
coronary heart disease, oesphageal hiatus hernia, gastric and duodenal lesions, pancreatitis,
appendicitis and diverticulosis of the colon may in their way mimic cholecystitis.
Furthermore, mild gall bladder disease may be associated with but not always responsible
for hypermotility of the stomach and irritable colon.
It is well know that gall bladder disease may simulate coronary heart disease, and
the reverse is also true, while the two conditions may exist together. It is, therefore,
proper in the older patient who has some hypertension and some evidence of arteriosclerosis and whose heart is enlarged in the routine chest film, to obtain an electrocardiogram. The evidence of a recent myocardial infarction may change one's mind towards
the part played by the gall bladder regarding that attack of epigastric pain associated
with so much gas and relieved by soda. The problem is a substantial one as evidenced
by the fact that at the Mayo Clinic in 25 percent of cases of angina pectoris gafll
stones are present. It has been advised by Barnes1 that when angina pectoris and
cholecystitis co-exist, the surgical attack on the gall bladder should be performed only
if the symptoms of cholecystitis are severe and unendurable, if the risk of operation
is recognized as considerably increased, and if little prospect is held out to the patient
that the surgical procedure will relieve him of angina pectoris.
Page 51 Because so many of these cases present a history suggestive of gall bladder disease,
a cholecystogram is the most likely roentgenological procedure to be performed in
their investigation. However, since the full truth has been missed so often, our
principle is that because in upper digestive tract disease one condition may simulate
or mask another, or more than one lesion may be present, the examination is not
complete without both a barium meal and a gall bladder visualization. From our
experience, cholecystititis is a common associate of hiatus hernia, occurring as it does
frequently in older and obese patients. The incidence of this condition is over one
percent of all cases with symptoms referable to the biliary or upper gastro-intestinal
tract.2 It is interesting to note that 25 percent of our cases of hiatus hernia had
undergone cholecystectomy before a diagnosis of hernia was made and their symptoms
had failed to be relieved in a satisfactory manner. It is recommended that the oesophageal
hiatus be examined during the abdominal exploration performed in every case of cholecystectomy to determine if the opening is abnormally large.
Another cause for the post-operative persistence of these symptoms which led to
cholecystectomy is the presence of a peptic lesion apart from gastritis. The association
of peptic ulcer in gall bladder disease as found in a review of 277 recent cases undergoing cholecystectomy was between 3 and 4 percent, and in some series the incidence
is higher.
The condition of irritable colon may produce symptoms as variable as those of
cholecystitis. Common complaints according to Wilkinson3 include epigastric distress,
gas, belching, distention, and abdominal pain. The last is usually referred to the sigmoid
area, but may be felt in either colonic flexure. One of the chief symptoms is constipation, the stool being fragmented or inspissated. The condition may be associated
with hyperacidity or achlorhydria, which in turn may produce sourness, gnawing
sensations, nausea, and perhaps vomiting. The barium enema generally will reveal little
to assist the diagnosis in a specific manner. Diagnostic, perhaps, is the relief of pain
which usually follows flatus escape.
Where the diagnosis of gall bladder is not supported by a history of colic or
jaundice, the possibility of spastic or irritable colon should be considered. Certainly
in such cases the urgency for surgical intervention is not great. Time is available
for a therapeutic trial of the methods considered useful in the treatment of this
condition. The frequent improvement in symptoms, it has also been observed, may be
associated with the return of gall bladder function, as evidenced by the normal cholecystogram.
In view of the foregoing, it is therefore well to reserve one's judgment as to the
part played by a diseased gall bladder if the picture is not supported by a classical
symptoms complex of gall stone colic. If it is not present, it should be accepted that
possibly only a partial diagnosis has been established, and although it is known that
50 percent of all those patients suffering from indigestion have gall bladder disease,
there may exist in a large proportion a combination of exciting factors. This, then, is
a plea for thorough investigation of cases. It is not meant to detract from the decision
to remove gall stones, which is based upon other principles. Rather it is an attempt
to avert disappointments and to prevent discredit from falling upon the operation and
the operator by failure to fulfil what has been so eagerly expected by the patient.
The need for complete diagnosis to determine the possibility of associated conditions
has already been mentioned. Despite the fact that the mortality in cholecystectomy
has been greatly reduced in the uncomplicated type of case, it still remains high where
other unusual factors exist. Only by close attention to details will these difficult cases
be treated successfully. Chronic pulmonary sepsis, cardiovascular disease, anaemia and
impaired liver and renal function must be kept in mind and corrected if possible.
Where a major complication looms as a possible result of surgery, the judgment of the
Page 52
It I* *, '.•■*■
'I &#%
medical consultant and the surgeon should be reached with care, and operation delayed
to permit optimum preparation.
In the event that the need for cholecystectomy follows a prolonged and perhaps
serious illness, the factor of malnutrition may be present and protein reserves
be depleted. This possibility may be suspected where the diet has been inadequate or
if there has been vomiting. A diet rich in protein or supplemented by the parenteral
| administration of amino acids to provide up to 150 grams of protein should be available.
The main difficulty is to secure adequate caloric intake which will prevent amino
acids, which necessary for tissue building, from beoig deflected to meet energy requirements. Therefore, free use of glucose should be made. In the liver it is converted
into glycogen, and held there if thiamine chloride (Vitamin B) is available in satisfactory
amounts. The possibility of haemorrhage in cases of liver damage associated with
obstruction and jaundice is controlled by the intravenous or oral administration of
Vitamin K. By such methods the liver and other tissues may be supported and recover
in the face of the ill effects of disease and faulty nutrition, and this an important
hazard in gall bladder disease may be eliminated.
The technique of cholecystectomy has been well developed. Most surgeons practice
the same procedure employing minor variations. In the uncomplicated case usually
. little difficulty arises, but where anomalies are present or where extensive pathology
exists, good judgment must support technical skill in the solution of the problem.
Generally it is felt that a right paramedian incision of generous length, namely from
the xiphisternum to below the level of the umbilicus is satisfactory. Thus space is
obtained to permit proper exposure of the gall bladder and the bile ducts. A small
incision with limited visibility may obscure the field and lead to an accident, while
nothing is gained by this economy except possibly some flattery to the surgeon's
prowess. The subcostal incision of Kocher is no longer commonly used, but in the
obese patient with wide flaring costal margins it may be of distinct advantage.
Surgeons also differ in their method of actually removing the gall bladder. Thus it may
be preferred that this be done from the cystic duct outward or from the fundus down
to the cystic duct, and each method has its advantages. It is felt that less bleeding and
so better visualization and less hazard result from the dissection and control of the
cystic artery and duct at the outset. Concerning the cystic duct and artery, certain
problems may arise because of anatomical variations.
The anomalies of the bile ducts and branches of the hepatic artery as they are
related to the dissection of the gall bladder are well known because of the special studies
on this subject. The brief review of this sub jet which follows is based upon the
investigation of I. M. Thompson, Professor of Anatomy at the University of Manitoba:4
(a)  The right hepatic artery
1. In seventy percent of cases it arises from the main hepatic trunk and reaches
the liver by passing behind the common hepatic duct.
2. In twelve percent of cases the right hepatic artery crosses anterior to the hepatic
duct or even the common duct.
3. In ten percent of cases the right hepatic artery may be closely associated with
the cystic duct and the neck of the gall bladder. It could be easily included in the
clamp applied to the cystic duct.
4. In eight percent of cases the right hepatic artery crosses the right border of
the hepatic duct or even forms a ring around the hepatic duct.
Page 53 (b) The cystic artery
1. In eighty-eight percent of cases there is a single cystic artery and in eighty-two
percent of cases it arises from the right hepatic artery.
2. In a few percent the cystic artery arises from the gastro-duodenal artery. It
must cross the common bile duct to reach the gall bladder. If injured, it may retract
considerably and the source of bleeding be difficult to determine.
3. In most cases the cystic artery arises to the right of the main hepatic duct.
In twenty-seven percent of cases the cystic artery arises to the left of the hepatic or
common duct and must cross one of each to reach the neck of the gall bladder. In
two percent, the cystic artery passes behind the main hepatic duct and should it retract
the duct may be included in the forceps.
4. In twelve percent of cases there may be an accessory cystic artery of variable
origin.   Failure to recognize such an additional artery may lead to serious haemorrhage.
(c) The bile dudts
In about seventy-five percent of cases the cystic duct joins the hepatic duct at
something like a right angle. In seventeen percent, the ducts pursue a parallel course
before they unite. They are bound togther by fibrous tissue and it may be possible to
dissect them from each other for as much as two inches or more. The point of actual
union may be only 0.5-1 cm. above the ampulla. In eight percent the cystic dudt
spirals in front of the hepatic duct before they unite—or the cystic duct may run
for a distance behind the hepatic and enter its left side.
(d) Accessory bile duct
This is found in eighteen percent of cases. It usually arises from the right lobe of the
liver and lies at a deeper plane than the cystic duct at first. The accessory duct may
join the right hepatic duct at a relatively high level and be out of danger. It may
enter the surgical field because its union is near that of the cystic and common ducts
and therefore it is exposed to injury. Finally, it may enter the junction of the cystic
and common hepatic ducts in such a manner as to avoid detection but not injury.
Actually, although the incidence of anomalies appears high from anatomical studies,
one recognizes or encounters them in a surprisingly small proportion of cases. The
great concern, of course, is that an anomaly may pass unnoticed, either through unnecessary haste or where the position is too obscured by the results of disease to permit
a free view of the tissue under consideration.
Accident or oversight may lead to the production of three serious conditions during,
the dissection of the cystic duct. The first of these is injury to the common hepatic or
common bile duct. It is known that the great majority of benign strictures result
from a surgical accident occurring during cholecystectomy. The reasons for such a
complication include poor anaesthesia with impaired working conditions, an incision
that is made too small, and the effects of long-standing disease and inflammation.
Very often the history of the operation reveals that the case was a most simple one
to do. In such an instance, the surgeon may employ undue haste and fail to observe
proper precautions. In other cases there may be an extensive haemorrhage from a torn
cystic or anomalous vessel. In desperation, the anxious operator may blindly seek to
control the bleeding with a haemostat. The bleeding point may be controlled in this
way, but often the forceps is found later to be across the common or hepatic duct.
The great danger in the very easy case arises when the gall bladder is lifted upwards
and, where the cystic duct is short, the common duct may be tented and a forceps is
placed across this angulated portion which provides the illusion of being the cystic
duct. The damage is aggravated- by the application of a ligature which in turn involves
more of the common duct.
Safety in clamping the cystic duct demands proper exposure and lighting. There
will no doubt be less bleeding if the removal of the gall bladder is commenced at the
cystic  duct  with  early  control  of   the   cystic   artery  in  order   to   reduce  or   avoid
Page 54
re *_£_!
Hfc" ft haemorrhage. Once the cystic duct is found, it should be dissected free of its surrounding tissues until it reaches the common duct. Both the latter and the hepatic duct
should be distinguished below and above the junction. When the clamp is finally
applied, the gall bladder and the cystic duct should be relaxed to prevent any tenting
of the common duct. In this manner the possibility of any involvement should be
prevented. Should it be damaged and the injury recognized, immediate repair is
The second condition involves extraordinary haemorrhage during cholecystectomy
due to iniury to two vessels. The first of these is the right hepatic ar-tery. This
structure is occasionally so closely related to the cystic duct and the neck of the gall
bladder that it may be torn during the dissection. It is said that loss of the right
hepatic artery leads to a fatal outcome in fifty percent of cases. The other vessel
which might be unrecognized and traumatized is an accessory cystic artery of obscure
origin. A well known and frequently described manoeuvre is a satisfactory method
for control of bleeding. The hepatic artery can be palpated and compressed by placing
the finger in the foramen of Winslow and the thumb over the artery long enough to
remove the accumulation of blood and visualize and control the bleeding point with
Finally, a cause for persistence or recurrence of symptoms of cholecystitis following
removal of a diseased gall bladder relates to an unusually long cystic duct which may
sometimes be present. Such a duct may be so intimately bound to the common duct
that the condition cannot be distinguished readily. If it is suspected, it may be
demonstrated by passing a probe through the cut end of the cystic duct to explore
its length. The lengthy remnant may produce symptoms because of the presence of
a stone or chronic inflammatory changes. Our experience with this condition includes
four cases which required secondary operation following cholecystectomy. The preoperative diagnosis in these instances was stone in the common bile duct. The findings
revealed that the remnant of the cystic duct had become dilated to such a degree that
it resembled a tiny gall bladder. One contained a calculus, and sandy material was found
in the remainder. Tissue examination revealed chronic inflammatory change. Relief of
symptoms followed their removal.
A further problem in surgery of the gall bladder may be the necessity of exploring
the common bile duct. The indications for this procedure may be based upon the
patient's history. Thus the characteristic combination may be based upon the patient's
history. Thus the characteristic combination of colicky pain followed soon by
jaundice which varies in intensity and possibly chills and fever, is likely evidence of
a common duct stone. However, a review of cases of common duct stone actually
removed at operation demonstrates that this group of symptoms may be wholly or
partly absent. Thus, in a series of two hundred and nineteen cases of this condition
reviewed at the Mayo Clinic (in 1939), it was noted that jaundice was absent in nearly
thirty-five percent of cases.5 In addition, fever and chills were not a complaint in an
even larger proportion of cases. Further criteria, therefore, must be sought in deciding
if interference with the bile duct is necessary. This can be determined only by a
careful examination of the cystic and common ducts at the time of the operation.
The experienced operator is familiar with the normal calibre of these structures. Therefore if the well known clinical picture of common duct calculus is absent and even
if one cannot palpate a stone in the cystic or common duct, yet if the lumen of the
cystic duct is larger than usual or if the common duct is dilated, exploration of the
latter is indicated. If this principle is followed, the finding of unexpected stones will
more than compensate for the additional work involved in exploring all ducts when
definite and suggestive changes are noted even though stones may not always be found.
When the abdomen is opened on a diagnosis of gall bladder disease, peptic ulceration
or chronic appendicitis, the surgeon should be prepared to encounter almost any type
of disease, He -may expect to find one or all of these three conditions present. This
is  so despite the  most  careful  pre-operative  investigation.    It  is  not  uncommon   to
Page 55 discover at cholecystectomy a badly inflamed appendix which would be dangerous to
leave. Removal through the gall bladder incision may be difficult. In such a case a
separate incision may simplify the situation. The pancreas, which is an unsatisfactory
organ to investigate, is capable of providing surgical problems which may be encountered
at cholecystectomy. Thus pahcreatitis and carcinoma of the head may be the cause
of biliary obstruction. In such cases the need for anastomosis between the gall bladder
or the common bile duct and the gastro-intestinal tract must be met. Recently, despite
a normal cholecystogram, I planned a cholecystectomy because of severe colic and
vomiting in a fourteen year old girl. The gall bladder was normal, but a cyst in the
head of the pancreas was found. The symptoms were relieved following drainage of
the cyst.
The finding of a gastro-duodenal lesion at cholecystectomy is relatively common,
and it is also relatively common for the operator to overlook it. Carcinoma of the
stomach is an unpleasant surprise, especially if the barium meal has been negative.
Nevertheless, the operator should be prepared to perform a resection. A stenosing
duodenal ulcer may be satisfactorily treated with gastroenterostomy supplemented
by sub-diaphragmatic vagotomy. The approach for the latter from a right rectus
incision is difficult but possible. The exposure can be improved by performing a
transverse incision across the epigastrium to meet the centre of the original incision.
Formerly an uncomplicated duodenal ulcer was usually left alone, and often the
patient's symptoms continued because of it. Now the combination of cholecystectomy
for a diseased gall bladder and subdiaphragmatic vagotomy for duodenal ulcer without
obstruction should not be considered a prohibitive undertaking.
In conclusion, a plea for earlier surgery in the treatment of cases suffering from
biliary colic is still indicated. Delay in these cases is responsible for the continuing
high degree of morbidity and mortality which still exists across the country in contrast
to the satisfactory operative results in earlier treated cases. The development of fine
technique and operating ability and the advances in anaesthesiology cannot at times
match the ravages of disease.
Often these cases require an urgent operation without proper time for preparation.
The surgeon may then be faced with a procedure that must be performed with despatch
because of some associated disease while the gall bladder situation has become difficult
and requires a time-consuming dissection. The result must be an incomplete operation,
or else the undertaking is completed in the face of serious danger to the patient.
1 BARNES, A. R., nd PRUITT, R. D.:Problems in the Differential Dianosis of Coronary Sclerosis,
/. Michigan M. Soc, Nov., 1942.
2 TRUEMAN, K. R., Diagnosis and Treatment of Para-esophageal Hiatus Hernia, Canad. M. A. J.,
56:   149,  1947.
3 WILKINSON, S. A., Chronic Cholecystititis vs.  Irritable Colon, J.A.M.A.,   109:   1012,  1947.
4 THOMPSON, I. M.: On the Arteries and Ducts in the Hepatic Pedicle.   Univ. of Calif. Publications in Anatomy, Vol.  1, 55-160,  1933.
5 TRUEMAN, K. R.: Symptoms of Common Duct Stone: "Review of 219 Cases.   Proc. Staff Meet.,
Mayo Clinic,   15:283,   1940.
Division of V.D. Control
Owing to the rapid changes and recommendations in penicillin therapy in Syphilis,
it is not possible to contact all physicians in this province when such changes occur.
Through the kindness of this Bulletin it is planned to present such changes and
recommendations  as  they occur.
It is important that the diagnosis of syphilis be established and treatment begun
early in pregnancy.
We recommend that all cases of syphilis in pregnancy, irrespective of previous
treatment, be hospitalized for penicillin therapy, i.e., intramuscular injections of 40,000
units every three hours for eight days. This treatment is then followed by regular
weekly injections of alternating courses of matharsen and bismuth. The courses
of bismuth after the fifth month of pregnancy should not exceed four consecutive
injections and the last six to eight injections before term should be arsenicals. Blood
pressure and urinalysis are recommended weekly while the patient is receiving arseno-
therapy and haemoglobin taken every three months. The serology should be followed
monthly, and if there is any evidence of a rising titre we would recommend that
consultative service be requested with the view to possibly repeating the penicillin
If the cerebrospinal fluid has never been taken and if it is indicated in the routine
follow-up of these patients, the Division recommends that advantage be taken o£ the
woman's hospitalization (at delivery) and the spinal tap be performed during this
postpartum period rather than in the prenatal period.
It is recommended that a routine Cord Kahn be taken at birth. If this is negative
the infant's blood test should be repeated at six weeks and three months of age.
If the Cord Kahn is positive, treatment should not be given unless there are
confirmatory clinical or X-ray evidences of infection. In many cases the positive Cord
Kahn is due to carry over of reagin from the mother. These patients should have
repeated quantative Kahn tests. If the titre is rising the diagnosis is confirmed and
treatment should be started. If the titre falls the child should be kept under observation
until freedom from infection is established.
(For details of Management of Prenatal Syphilis refer to Symposium dated June
1947, and distributed to all members of the medical profession in B.C.)
Note: The use of Penicillin in Oil and Beeswax is not recommended for syphilis
in pregnancy and in particular late pregnancy. Preliminary evidence suggests that
penicillin levels with use of this product are too low to penetrate the placental barrier
in sufficient concentration to adequately prevent development of prenatal syphilis in a
percentage approximately that obtained with aqueous penicillin.
Page 57 VaHcauAten, Qene/ixU ^oA^utcu Section
Aortic aneurysms have for many years been an interesting lesion to clinicians and
surgeons. The first were described by Galen in the second century, and since that time
many reviews have been published concerning diagnosis and therapy. However, though
our knowledge of them has increased immensely, the treatment has been unsatisfactory
and, in the main, unsuccessful. With the advent of anticoagulants in vascular surgery
and with the refinements of endoaneurysmorrhaphy1, combined with wiring and galvanism, it is probable that the operative procedures on these lesions will meet with more
and more success. It is for this reason that this pathological review has been undertaken.
In addition, a number of the more unusual cases will be presented more fully. No
attempt has been made to carry out a full clinical review, as this has been recently and
excellently done by Mills and Horton2, on many more cases than are here presented.
Aortic aneurysms, in the main, are of two etiological types, atherosclerotic and
luetic. Other types have occurred but are extremely rare, such as those following severe
injury and mycotic aneurysms arising from infected emboli lodging in the vasa-vasorum.
Incidence and Material.
The incidence of aneurysm varies markedly in different localities depending on the
incidence of syphilis and the adequacy of the antiluetic therapy. The material for this
discussion was discovered in 8044 consecutive autopsies at the Vancouver General Hospital from the years 1936 to 1945, inclusive. In this number there were 82 persons with
some type of aortic aneurysm. These autopsies consisted of approximately twice the
number of males as females, of all ages, and it is seen that in this locality the incidence
of aortic aneurysms is approximately one percent.
Of the 82 aneurysms, 72 (87.8%) occurred in males and 10 (12.2%) occurred in
females. This ratio, when corrected for the preponderance of autopsies on males, is
approximately the same as that previously reported by other authors2. In 23 cases the
aneurysm was a contributory finding and not the primary cause of death.
Age. Aortic aneurysm is a disease of the older age groups and in this series 93.7%
occurred after the age of 50. The youngest patient was 36 and was victim of an atherosclerotic dissecting aneurysm involving the whole of the aorta. The oldest patient was
84 and his demise was caused by a rupture of an atherosclerotic fusiform aneurysm of
the abdominal aorta. However, it would appear that the commonest age group for aortic
aneurysm of either luetic or atherosclerotic etiology is from 55 to 75.
Etioolgy. In this series, 33 cases (40.2%) were of a luetic etiology while 49
(59.8%) were on an atherosclerotic basis.
Types. Aortic aneurysms can be classed in anatomical types; i.e., fusiform, saccular
or dissecting. In addition, they may be multiple and consist of any combination of those
types. It has been previously pointed out that a dissecting aneurysm is an extremely
uncommon occurrence with a luetic aortitis because of the extensive fibrosis, which
takes place in the adventitia and media3. This phenomena was again seen in this series
as we discovered no dissecting aneurysms occurring in a luetic aortitis.
From the Department of Pathology, Vancouver General Hospital, Vancouver, B. C.
The author expressed his appreciation to Dr. H. H. Pitts, Director of Laboratories, Vancouver General Hospital, for his assistance in preparing this paper. |?|*
Presented to the Staff Clinical Meeting of the Vancouver General Hospital, February 25 th, 1947.
Page 58
mm A true dissecting aneurysm is one in which the dissection takes place between the
middle and outer thirds of the media4. In some of our cases the dissection was evident,
but the eventual laceration had been so severe that it was impossible to tell whether the
tracking was wholly within the layers of the media and indeed in some sections it appeared to be tracking between the adventitia and media. However all cases where a
definite dissection between any coats of the aorta could be found were classed as dissecting aneurysms.
In this series, 42.7% had a single saccular aneurysm, 24.4% a single fusiform
aneurysm, 20.7% dissecting aneurysm and 12.2% showed multiple aneurysms. The
incidence of multiple aneurysms is slightly greater than previously reported.
Position. The position of the aneurysms in the aorta is important both for diagnosis
and therapy. To denote position in this discussion the aorta was divided into five anatomical areas as follows:
Area 1.   between the aortic cusps and the innominate artery. |pf|
Area 2.   between the innominate artery and the left subclavian artery.
Area 3.   between the left subclavian artery and the coeliac axis.
Area 4.    between the coeliac axis and the inferior mesenteric artery.
Area 5.   between the inferior mesenteric artery and the bifurcation of the aorta.
It can be readily seen that many of the aneurysms will be placed in more than one
area, particularly those of the dissecting variety, some of which extended throughout
the whole length of the aorta.
Of the 35 cases of single saccular aneurysms 17 were of luetic origin and 18 of
atherosclerotic origin. In the 17 of luetic origin, 5 were in Area 1, 4 in Area 2, 6 in
Area 3, 1 in Area 5, and 1 case involved more than one region; i.e., Area 1 and Area 2.
Thus saccular luetic aneurysms are nearly completely confined to the arch and descending thoracic portions of the aorta, with a slight predilection for the ascending aorta and
thoracic descending aorta over the actual arch. There is only one case of a single saccular luetic aneurysm occurring in the abdominal aorta.
Now in considering the saccular aneurysms of atherosclerotic origin, we find that
of the 18 cases, 5 were in Area 1, 1 in Area 2, 2 in Area 3, 4 in Area 4, and 4 in Area
5. Two involved more than one area, 1 in Areas 1 and 2, and 1 in Areas 4 and 5.
From this it is seen that atherosclerotic aneurysms are commonest at both ends of the
aorta and tend to be more common in the abdominal aorta than in the thoracic. This
is as would be expected, as the earliest appearing atherosclerosis is usually seen in the
ascending aorta and towards the bifurcation of the aorta.
When the single fusiform aneurysms are reviewed it was found that of the twenty
cases, 10 were of luetic origin and 10 of atherosclerotic etiology. In those of luetic
etiology 5 occurred in Area 1, 1 in Area 3, and 4 cases involved more than one area,
3 involving Areas 1 and 2, and one involving Areas 2 and 3. In the fusiform atherosclerotic aneurysms, 1 occurred in Area 1, 1 in Area 2, 1 in Area 3, 1 in Area 4, 3 in
Area 5, and three showed involvement of more than one area, 2 involving Areas 1 and
2, and 1 involving Areas 4 and 5. Thus the fusiform aneurysms have an identical distribution to the saccular aneurysms, the luetic ones occurring mainly in the ascending
arch, and to a lesser extent the descending thoracic aorta, while the atherosclerotic ones
tend to occur at both ends of the aorta. The fusiform aneurysms show a greater tendency to involvement of more than one segment of the aorta than do the saccular.
In reviewing the dissecting aneurysms, as stated previously, they were all of atherosclerotic etiology. They were, as would be expected, found frequently involving more
than one segment of the aorta; 3 were wholly situated in Area 1, 1 in Area 2 and 2 in
Area 3. In the remaining dissecting aneurysms 9 began their dissection in Area 1 and
extended for a variable distance, some as far as the bifurcation; 1 originated in Area 2
and 1 in Area 4. Thus it may be concluded that a dissecting aneurysm nearly always
originates in the ascending, arch, or upper portion of the descending thoracic aorta.
However it may extend for a variable length, even to involving the whole of the aorta.
Page 59 The length of extension depends entirely on where it ruptures, either externally or back
into the aortic lumen.
Multiple aneurysms were seen to be of luetic etiology in 6 cases and of atherosclerotic etiology in 4 cases. In the luetic cases they occurred as saccular or fusiforsn
dilatations or combinations of these with no particular rhyme or reason. All but two
occurred above the diaphragm. In one case there were seen five separate saccular
aneurysms, one occurring in Area 2, three in Area 3, and one in Area 4. These
aneurysms, particularly those of the saccular variety, tended to be smaller than the
single large ones usually seen, and appeared as golf-ball sized out-pouchings of the aorta.
In the multiple aneurysms of atherosclerotic etiology the majority appeared in Areas
4 and 5; i.e. below the diaphragm. One cases showed a fusiform aneurysm in the ascending aorta and two saccular aneurysms near the bifurcation. Two of the cases showed a
dissecting type of aneurysm along with the other either fusiform or saccular varieties.
In these cases the dissecting type of aneurysm originated in Areas 3 and 4 respectively.
Involvement of Great Vessels.
It would appear that in any therapeutic attack on aneurysms the relation to the
ostia of great vessels would be of importance as the patency of these must be maintained. For this reason an attempt was made to determine the number of times great
vessels were found originating from the sac. This portion of the review was confined
to those aneurysms of the fusiform or saccular variety. Including those cases of multiple aneurysms 62 fusiform or saccular lesions were identified. Of these 38 had no
great vessel originating from the sac wall and 24 had a vessel originating from the sac.
In the cases of those aneurysms in Area 1 the coronary arteries were the vessels of concern. In general, the usual aneurysms in this area began above the coronary ostia. However in several of the luetic lesions, intimal proliferation had occluded the openings.
As would be expected, Area 2 showed the highest rate of involvement, nearly all
enourysms having a vessel originating from the sac. Only the occasional sac was found
on the inferior surface of the arch. Areas 3 and 5 were singularly free of vessel involvement with only the occasional Area 5 aneurysm showing one or both of the common
iliac arteries originating from the sac. Area 4 showed the next highest great vessel
involvement after Area 2. In this case the usual vessels involved were the renal arteries,
the inferior mesenteric artery or the superior mesenteric artery. The coeliac axis was
singularly free of involvement in lesions of this area.
Lamination and Clotting
Nature's reparative attempts in aneurysmal lesions consist of laying down of tough,
organized, laminated thrombus along the lining of the sac. It would appear that both
the ability of the human to form this thrombus, and the quality of the thrombus
formed, have much to do with the life expectancy of that individual. As thrombus is
laid down and the lumen of the vessel decreased, it is seen from the laws governing
the flow of liquids in tubes, that the lateral pressure on that portion of the aorta will
likewise be decreased. This statement is derived from the following laws: (1) Lateral
pressure is inversely proportion to the velocity; (2) pressure head remaining constant
then the velocity is directly proportional to the sectional area of the tube (part of
Poiseuille Law).
In nearly all cases which were autopsied because of a rupture of a fusiform or saccular aneurysm, one either found an aneurysm in which there was no thrombus, or an
aneurysm in which there was laminated thrombus which in one area showed a softening
with resultant break-through of the clot and underlying aortic wall. It is probable
that any therapeutic attempt on aneurysms will probably depend on the ability of the
procedure to lay down clot in the sac or increase the toughness of the clot laid down.
It is for this reason that the organization of the clot in the aneurysm sac was studied!.
To facilitate the classification of thrombus formation, the clot was classed as minimal,
with only a few shreds of thrombus attached to the sac; moderate, with a definite layer
Page 60
iff*-- • •"
p&h of firm clot; or marked, with a nearly complete filling of the sac by firm, well organized laminated thrombus.
It was possible to review 78 of the aneurysms of both saccular and fusiform varieties in this respect. There were 48 saccular aneurysms of which 15 showed marked, 21
moderate and 12 minimal thrombus formation. There were 30 fusiform aneurysms of
which 2 showed marked, 3 moderate and 25 minimal thrombus formation. From these
figures, it is seen that approximately 75% of saccular aneurysms have good thrombus
formation and therapy should be directed at strengthening this thrombus; whereas 83%
cf fusiform aneurysms show poor clot formation and therapy should be directed at
laying down new thrombus. With the refinement of technique of arteriography, it
will be possible to study the thrombus formation and aneurysms and possibly introduce
the required therapy.
Bony Erosion.
Evidence of erosion of adjacent bony structures by aneurysms was looked for in all
cases of fusiform or saccular aneurysms. Six cases of bony erosion were found. As has
been previously reported, the luetic aneurysm is the main offender in this respect. In
five cases, the aneurysms were of luetic origin. Four occurred in Area 3 and eroded
underlying vertebrae, while one occurred in Area 2 and eroded sternum, ribs and
clavicles. One of these cases showed a fusiform aneurysm, while the other four showed
saccular aneurysms.
The case of an atherosclerotic aneurysm eroding the vertebrae is very interesting
and will be reported more fully below. It was a saccular aneurysm of Area 2 which
protruded medially to erode the adjacent vertebrae. Microscopic sections through the
vetrebrae however showed the picture of a plasma cell myeloma. It would appear that
atherosclerotic aneurysms, for some reason, will not erode normal bony structures.
Site of Rupture.
In all cases of ruptured aneurysms, fusiform, saccular or dissecting, the site of rupture was studied to determine if any particular portion of the aortic trunk were more
liable to rupture than any other portion, and also to help determine what bizarre sym-
tom complexes may be expected following rupture. Altogether there were 50 aneurysms
of all types which ruptured and the tissues into which they ruptured are as follows:
Dissecting Aneurysms—11 Cases
10 ruptured into pericardium.
1  ruptured into post mediastinum.
Eaccular and Fusiform Aneurysms
In Area 1—6 cases
- ruptured into right pleural cavity.
1 ruptured into right lung parenchyma.
3 ruptured into pericardium.
1 ruptured into superior mediastinum.
In Area 2—5 cases p||
2 ruptured into posterior mediastinum.
1 ruptured into left pleural cavity.
1 ruptured into trachea.
1 ruptured into pericardium.
In Area 3—II cases
5 ruptured into left pleural cavity.
2 ruptured into posterior mediastinum.
1 ruptured into right main bronchus.
2 ruptured into left upper lobe bronchus.
1 ruptured- into oesophagus.
Page 61 In Area A—5 cases
5 ruptured into retroperitoneal tissues.
In Area 5—7 cases.
5 ruptured into retroperitoneal tissues.
1 ruptured into inferior vena cava.
1 ruptured into peritoneal cavity.
Saccular and Fusiform Aneurysms Involving Multiple Areas—5 Cases
2 in Areas 4 and 5—ruptured into retroperitoneal tissues.
1 in Areas 3 and A—ruptured into posterior mediastinum.
1 in Areas 2 and 3—ruptured into left pleural cavity.
1 in Areas 1, 2 and 3—ruptured into left lung parenchyma.
From the above figures it may be concluded that the tendency of an aortic aneurysm
to rupture is no more frequent in one site than another. However it may be mentioned
that it is my personal observation that the actual site of rupture is more likely to be
at the point where a great vessel joins the aorta; e.g. junction of a renal vessel to aorta.
It can also be seen that a ruptured aneurysm is not necessarily a cause for sudden death,
because of the formation of a false sac. The author has recently seen a case of an atherosclerotic aneurysm of the abdominal aorta in Area 4 which ruptured into the retroperitoneal tissues and the patient remained alive for several days. During this time she
began to develop a haematuria which suddenly increased in its severity and the patient
died. In this case, at autopsy the ruptured aortic aneurysm was found; then an area
of false sac and further, lateralward, a rupture of the false sac into the left renal pelvis.
A few of the more unusual aneurysms will be recorded below.
Case 1. A 47-year-old white male logger, of Swedish extraction, was admitted to
hospital 21 July, 1939, complaining of swelling on front of neck—4 months; dysphagia
—2 weeks; cough—2 weeks; and hoarseness—1 week. Twenty years before admission
he had had an urethral discharge but no history of treatment could be elicited. The
physical examination revealed a midline episternal swelling, approximately 11 x 9 x 13
cm., between the sternal notch and thyroid cartilage. Skin over this area was tense and
red but the color faded on pressure. The mass pulsated with each heart beat with an
expansile thrust in all directions. The examining fingers could be pushed into the mass
and pulsations were felt to be increased. Th eremainder of the physical examination
was negative. On 1 Aug., 1939, the right arm showed a lymphoedema above the middle
of the forearm. Blood pressures recorded in both arms at this time showed R. 114/82
and L. 125/80.   On 10 Aug., 1939, the patient died of what appeared to be asphyxia.
At autopsy a large saccular aneurysm arising from the uppermost portion of the
aortic arch was discovered. The left common carotid artery and the left subclavian
artery originated from the sac. The sac itself had a moderate thrombus formation. Both
clavicles were eroded, the ends projecting into the sac. All ribs down to the sixth on
the left and fifth on the right projected into the sac. At this level there was no sternum
found and in the clot itself were discerned a number of small bits of cancellous bone.
The trachea had been nearly completely compressed in the superior mediastinum. The
remainder of the aorta showed in a number of areas in the ascending and thoracic portion the typical longitudinal puckering of luetic aortitis. The Kahn test was positive.
Diagnosis: Massive saccular aneurysm of the arch of the aorta eroding sternum, left
upper five and right upper four ribs and clavicles and compressing the trachea.
Case 2. A 41-year-old white male came to autopsy on 18 Oct., 1939. No history
was available as this was a case of sudden death. At autopsy the heart was hypertrophied
and dilated, weighing 780 gms. A valved but patent foramen ovale was discovered; the
aortic valve consisted of two cusps only. At the uppermost part of the ascending aorta
was a split in the intima and a typical dissecting aneurysm was present tracking down
the ascending aorta to rupture into the pericardial sac. Just distal to the innominate
artery the aorta was coarctate for a distance of 1.5 cms. Just distal to the coarctation
was a persistent ductus arteriosus and distal to this the left common carotid and left
Page 62 subclavian artery were seen arising from the aorta. A marked degree of atherosclerosis
was present in the aorta proximal to the coarctation while virtually none was present
in the distal portion. The right internal mammary artery was over twice the size of
the left internal mammary and showed definite atherosclerosis. Diagnosis: Haemoperi-
cardium, dissecting aneurysm of the ascending aorta, coarctation of the aorta, patent
ductus arteriosus.
Case 3. A 68-year-old white male was admitted to hospital on 17 May, 1941, complaining of distended abdomen, cough and mid-back pain. All symptoms had been
present for eight weeks. There was a past history of syphilis and gonorrhoea contracted
40 years previously. The syphilis had received some treatment. Physical examination
showed a well nourished man with distended, and in some cases thrombosed, superficial
veins present over the left anterior chest wall extending up into the left axilla and
suprasternal notch. An aortic systolic and diastolic murmur were present and a pitting
oedema of both lower legs. Blood pressure was 160/70 in both arms. An electrocardiogram showed a bundle branch block and an X-ray of the heart great vessels and spine,
a left-sided widening of the aortic arch and a concavity of the anterior surface of the
ninth thoracic vertebra.
At autopsy on 26 May, 1941, a saccular aneurysm of Area 2, measuring 6x4x2
cms. and eroding the left antero-lateral portions of the third and fourth thoracic vertebrae, was found. In the aneurysm was a moderate quantity of laminated thrombus.
In addition a number of white cellular lymph nodes and similar white cellular plaques
present on the mesentery were discovered. On microscopic examination the aneurysm
was of atherosclerotic etiology and the underlying vertebrae, the lymph nodes and the
mesenteric plaques showed typical plasma cell myeloma. No evidence of any luetic
process was discovered.
Case 4. A 50-year-old white male was admitted to hospital on 4 April, 1943, with
the complaints of "influenza feeling" and a severe, hacking, non-productive cough—
6 weeks; weakness—3 weeks; pains in the legs—2 weeks. He had lost seventeen pounds
of weight since his onset of symptoms. Physical examination revealed a sick-looking
but fairly well nourished man. Temperature was of a spiking variety with a high in
the evening up to 103° F. Pulse 100; respirations 20. There was a pitting oedema of
both ankles and feet. Cardiac examination revealed a loud blowing systolic mitral
murmur and a systolic aortic murmur. The white blood count during his hospital stay
was consistently elevated in the region of 18,000 per cmm. His red blood count showed
a severe hypochromic anaemia down to 2,500,000 per cmm. Repeated blood cultures
were consistently negative. Kahn was negative and repeated urinalysis showed a plus 3
albuminuria and a variety of casts, red and white blood cells and sediment. Electrocardiogram showed a sinus tachycardia and X-ray of the thorax revealed nothing of
note. The treatment consisted of repeated blood transfusions. On 26 April, 1943, he
became markedly dyspnoeic and began to cough up frothy bloody spuutum and on 28
April, 1943, he expired.
At autopsy the lungs were markedly congested. The mitral and aortic valve showed
some fibrous thickening along the bases of the cusps. • In the ascending aorta just above
the left coronary ostium was an atherosclerotic aneurysm 3 cm. in diameter. Lining the
sac was a moderate layer of laminated thrombus and over this and attached to the edges
of the aneurysm was a soft, friable, typical bacterial vegetation. Cultures of this were
spoiled but there was no doubt that this vegetation was infected. Infarcts were found
in the spleen and left kidney.
Case 5. A 70-year-old white male was admitted to hospital 11 Jan., 1944, complaining of gangrene of right small toe. Four weeks previously he had a severe cramp
in the right calf muscles which was followed by swelling of the right foot and ankle
and sloughing of the skin between the toes. On physical examination all the toes of the
right foot were swollen and tender to touch. There was a blackened area along the
outside of the small toe and extending for a short distance along the lateral surface of
Page 63 the foot. In addition there was a small black area on the tip of the great toe. Dorsalis
pedis and posterior tibial pulsations were equivocal. Dermotherm readings showed a
very slight response following lumbar sympathetic injection with novocaine anaesthesia.
While waiting in hospital for a definite line of demarcation to form before doing
definitive surgery, this mas was seized with a sudden abdominal pain which proved to
be a perforation of an anterior duodenal ulcer. This latter condition caused his demise
on 9 Feb., 1944.
At autopsy a subphrenic abscess and the perforated duodenal ulcer were found. In
addition there was found involving Areas 4 and 5 an atherosclerotic saccular aneurysm
14 cm. in diameter. The iliac vessels originated from the inferior edge of this aneurysm.
The sac was nearly completely filled with well-laminated thrombus and this thrombus
completely occluded the right common iliac artery and partially occluded the left common iliac artery. The right leg from the ankle to the groin was reddened, swollen and
oedematous.   The small toe had sloughed off.
Case 6. This was a case of sudden death and no history was available. The patient
was a 62-year-old white male who expired suddenly on 14 Sept., 1944. Both lungs were
found to be markedly congested and oedematous while in the pulmonary artery were
found a number of large chunks of well organized thrombus, obviously of ante-mortem
quality. These were completely blocking the artery and the patient had obviously died
of a massive pulmonary infarction. A typical luetic aortitis was found in the aorta
while in Area 5 there was present a saccular aneurysm 20 sm. in diameter which was
lined by irregular quantities of laminated thrombus. At the posterior margin of this
aneurysm the sac was adherent to the inferior vena cava and an arterio-venous fistula
was present between these two structures. Through this perforation bits of thrombus
lining the aneurysm had passed to form the massive pulmonary emboli previously
(a) Eighty-two cases of aortic aneurysms which have come to autopsy have been reviewed as to incidence, s age, sex, etiology, anatomical type and position.
(b) An attempt has been made to study great vessel involvement, bony erosion and
(c) A study has been made to ascertain at which sites an aneurysm is most likely to
(d) A suggestion, has been made as to the form any therapeutic attack should take on
saccular and fusiform aneurysms. This therapy would be in addition to the treatment of the underlying cause.
(e) Six cases of unusual aneurysms have been presented more fully.
1. Blakemore: Nelson Looseleaf Surgery, 1: Xlt B; 785.
2. Mills and Horton: Arch. Int. Med., 62: 949, Dec, 1938.
3. Shapiro: Can. Med. Assn. Journal, 19: 408, Nov., 1943.
4. Boyd: Textbook of Pathology, 4th ed., 401, 1943.
If" ^KPWfl
Page 64
-   ■•"
, ji'.-v-i-it;
■ #N
The presentation of this paper tonight on the subject of splenectomy stemmed
primarily from a desire to determine as far as possible the end results to be anticipated
following the removal of a diseased spleen. It was the intention at first to review the
end results of splenectomy in all forms of splenic disease, but once a perusal of the
literature was started it was quickly realized that a very large and a very controversial
subject was being studied and that it would be impossible to discuss adequately the
problem in this short paper. For that reason it was determined to review the results
of splenectomy only in the splenopathies where the indications for splenectomy are most
clear-cut, namely splenic anaemia, thrombocytopenic purpura, haemolytic icterus and
primary splenic neutropenia. It is assumed that the correct diagnosis has been made
and no discussion will be entered into in regard to the physiology, haematology and
differential diagnosis involved.
The classification outlined by Pfeiffer seems to be fairly widely accepted. He has
separated the various diseases with splenogemaly into three groups:
A. Conditions for which splenectomy is of decided value:
(1) Traumatic lesions and .non-traumatic rupture.
(2) Anomalies of position and mechanical accident (tumours and movable spleen).
(3) Abscess (certain cases).
(4) Cysts and haemangiomas.
( 5 ) Neoplasms.
(6) Aneurysm of the splenic artery.
(7) A large spleen causing mechanical distress (certain cases).
( 8 )   Schistosomiasis.
(9) Congestive splenomegaly, splenic anaemia, Banti's syndrome.
(10) Spherocytic haemolytic jaundice.
(11) Thrombocytopenic purpura.
(12) Chronic neutropenia.
B. Conditions in which splenectomy is of possible value:
(1) Gaucher's disease.
(2) Erythroblastic anaemia (Cosley, Van Jackson).
(3) Sickle cell anaemia.
(4) Cirrhosis of liver.
( 5) Tuberculosis.
C. Conditions for which splenectomy is of no value:
(1) Syphilis.
(2) Amyloidosis.
(3) Kala-azar.
(4) Malaria (tropical splenomegaly).
(5) Polycythemia vera.
(6) Leukaemia.
(7) Hodgkins' disease.
( 8 ) Haemochromatosis.
(9) Anomalies.
(10)  Other diseases.
Group A is where splenectomy is definitely of value. Of this group the first eight
diseases listed have almost self-explanatory indications for splenectomy and the prognosis
is equally clear-cut. The remaining four diseases are the subject of this paper and will
be discussed later. Groups B and C will not be discussed further tonight and are only
mentioned to round out the classification.
In searching for information in reference to the four diseases I was interested in, I
first turned to the records of the Vancouver General Hospital and, with the kind co-.
Page 65 operation of Mr. Fish and his excellent Records Department, all the records of patients
having splenectomies during the years from 1935 to 1946 inclusive were reviewed.
Splenectomies at the Vancouver General Hospital (1935-1946 inclusive):
No. of Hospital
Cases Deaths
Splenic  anaemia       9 3
Thrombocytopenic purpura   13 0
Haemolytic icterus     9 0
Primary splenic neutropenia      0 0
31 3
Traumatized spleen   11 3
Cyst of spleen     1 0
Spleen included in tumour mass     1 1
13 4
Total I  44
It will be noted that there were only 31 splenectomies for diseased spleens during
that time interval, or an average of less than three splenectomies per year. Unfortunately, the recorded clinical data in their records was often incomplete and for that
reason, plus the paucity of cases, the material was not considered sufficiently enlightening to warrant detailed study.
The text-books and medical journals were turned to next in the search and review
made of a large number of articles. From reading, it can be realized that the problem
of the enlarged spleen is confusing and that many writers are drawing erroneous conclusions from inadequately studied and too small series of cases. Thus it was determined
to concentrate on a search for opinions on splenectomy given by responsible persons or
organizations who have studied a sufficient number of well-worked-up and adequately
followed cases to make these opinions of value. These criteria immediately brought the
groups studied down to a very small number:
(a) Combined Spleen Clinic—Columbia Presbyterian
Medical Centre, New York — 316 cases
(b) Mayo Clinic (Pemberton) 1 760 cases
(c) Eliason and Stevens of the Surgical Service of the
University of Pennsylvania at Philadelphia 1     63  cases
(d) Diamond of the Department of Paediatrics at Harvard University 52 cases*
Total   -  1191
* Children.
There are undoubtedly other very sound organizations giving considered and valuable opinions, but these four groups have been selected as having the most to offer.
The following is a discussion of their conclusions.
Splenic Anaemia (Banti's Syndrome, Congestive Splenomegaly).
This disease has never been well understood and the etiologic factors involved have
not been clear. As is usual when such conditions prevail, there tends to be a confusion
of ideas and much misunderstanding.
However, in recent years a considerable amount of study has been devoted to the
disease and some interesting ideas have been evolved. The Combined Spleen Clinic have
been most progressive in this study and they have advanced the idea first propounded
by Larrabee in 1934 that the so-called toxic splenomegaly of Banti's disease is in reality
a congestive splenomegaly secondary to venous congestion in the portal system. Reason-
Page 66
1'^ V'feft'-
•:;  >■:.> r ing from there they anticipate that if this theory is correct the splenic vein should
appear congested, that the venous blood pressure of the splenic vein should be increased
and that the cause for obstruction should be found in many cases. Rousselot (of the
Combined Spleen Clinic) noted definite distension of the splenic vein at the time of
operation. He also found the venous pressure of the splenic vein to be considerably
higher than that of the peripheral venous pressure of the same patient.
Comparative Venous Pressures
Vein Pressure
(1)   Banti's Syndrome—Laennec's Cirrhosis 275 mm. H2O
(1)  Typical Haemolytic Jaundice.-           105 mm. H2O
Simultaneous Arm
Venous Pressure
12 mm. HoO
(2) " I j            125     I " 130
(3) jj j I        120    I I 85
The third factor in determining the cause of the obstruction was not so easy. He
considered cirrhosis of the liver when present to be sufficient of an obstructing factor
to cause portal hypertension. When cirrhosis was not present, he felt that there was an
obstructing factor in the portal system and reported 15 cases that all had the characteristic features of Banti's syndrome and all had gastrointestinal bleeding but none had
or developed cirrhosis of the liver over a long period of time up to 19 years after
operation. In eight of these cases, the cause and site of venous obstruction was definitely
Nature of Obstructive Factor in Eight Cases
Case 5—Thrombosis of Splenic Vein (traumatic).
Case 11—Same  (at junction with portal vein), traumatic.
Case 9—Same non-traumatic).
Case 1-4—Same.
Case A—Stenosis of portal vein (upper end) just below liver.
Case 12—Same (lower end) above entrance of splenic vein.
Case 6—Cavernous transformation of portal vein.
Case 7—Same, at junction of portal and splenic veins.
Of the other authors considered, Pemberton of the Mayo Clinic did not advance an
original theory as to the cause of the so-called Banti's syndrome. Eliason and Stevens of
the University of Pennsylvania and Diamond of Harvard more or less agree with the
congestive theory as discussed by Roussellot.
Results of Splenectomy in Splenic Anaemia
Pemberton of the Mayo Clinic believes that the chief benefit of splenectomy in this^
disease is to lessen the volume of blood circulating in the portal system and to establish
a collateral circulation by means of adhesions and an omentopexy. He found that about
half of those that haemorrhaged from the gastrointestinal tract pre-operatively, also
haemorrhaged after the operation. He does not believe that ligation of the coronary
vein is of much value in preventing haemorrhages from oesophageal varices. He does
report a series of 215 cases with splenic anaemia and a hospital mortality of 9.8% and
a gratifying life expectancy record: 54.6% lived 5 years plus, 41.5% lived 10 years
plus, and 20.4% lived 20 years plus. He advocated splenectomy even in the presence of
moderate cirrhosis of the liver.
Diamond reported  8  cases in children diagnosed as splenic  anaemia by reason of
splenomegaly of unknown origin, chronic progressive hypochromic anaemia, a constant
Page 67 leucopenia and thrombocytopenia. Splenectomy was followed by rapid improvement and
6 of the 8 lived normally from 6 to 10 years.
Eliason and Stevens reported 28 cases who underwent splenectomy for splenic
anaemia with a mortality rate of 25%. 28% of survivors lived 5 years and 21% lived
10 years plus.
Roussellot (Spleen Clinic) reported 55 splenectomies with a 14.5% mortality, the
mortality rate being highest in those cases associated with cirrhosis of the liver. 20%
of the remainder lived 5 years and 10% lived 10 years or more. He believes that the
prognosis and variations in clinical behaviour are dependent on two factors: the site of
the obstruction in the portal system and the variants in the venous pattern.
Variations in the anatomical pattern of the portal system illustrating how an
obstructive factor of the same site in different individuals may result in marked
differences in clinical behavior.
In confirmation of his theory, Roussellot describes one of his patients on whom a
splenectomy had been performed at the age of 5 years and who died of haemorrhage
thirteen years later after haemorrhaging 21 times via the oesophagus and 10 times per
rectum. A diagnosis was made of a portal vein obstruction close to the liver causing
back pressure on the splenic, coronary, and mesenteric veins. Cirrhosis was ruled out
by the normal liver at operation and a normal bromosulphathalein test on numerous
occasions.   Autopsy confirmed the diagnosis.
Thrombocytopenic Purpura.
There is general agreement amongst most authors that primary idiopathic thrombocytopenic purpura responds very satisfactorily to splenectomy. The Spleen Clinic found
that 18 (85.7%) of a series of 22 cases had excellent results from splenectomy. Two
improved but were not symptom-free and one died of the disease 18 months after the
operation. A control group of 20 cases were treated conservatively with snake venom,
Vitamin C, sesame oil, progynon, transfusions, etc., and only two cases appeared to have
had the disease arrested.   The remaining 18 cases were not improved.
Accessory spleens are blamed in some cases for a tendency for recurrence of symptoms after a successful operation. Secondary operations have at times demonstrated their
presence and removal relieved the symptoms.
Pemberton and Kiernan believe that in the very mild cases with few symptoms of
thrombocytopenic purpura medical measures such as removal of foci of infection may
be sufficient. However if the disease advances beyond the mild stage and causes even
moderately severe symptoms, then splenectomy is indicated to relieve the symptoms and
prevent acute exacerbations of the disease. In splenectomy done on 153 cases, they
report a mortality rate of 5.9%. In 82 patients traced 5 or more years, 56.6% survived
5 years and 79% survived 10 years. Two cases only were traced 20 years and they were
alive and well.
Diamond in 28 cases of children with idiopathic thrombocytopenic purpura haemorr-
hagica was able to control 20 cases medically. Of the remaining eight cases all but two
obtained complete relief of symptoms from splenectomy.  Mortality rate was 0.
Elias and Stevens in 15 cases had a mortality rate of 6.6% (one case) and this was
a case with an erroneous diagnosis. Their follow-up showed 50% alive at 5 years and
21% at 10 years. jp|
Haemolytic Icterus
The removal of the spleen in this disease is, for practical purposes, a curative procedure, and since there is danger of possible complications incident to neglect, such as
the development of recurrent crises, gallstones and hepatic damage, splenectomy is definitely the treatment of choice in all cases. The removal of the spleen does not vary
the blood picture. The operation only removes the site of destruction of the more fragile
and characteristic spherocytes in the blood. These small spherical red cells are, accord-
Page 68
ft-    '-. ing to the work of Haden, alone responsible for the fragility changes in this disease and
are found in all active cases and in their relatives who have the latent disease in a percentage of about 10% to 25% of the total red blood cell count.
In atypical haemolytic jaundice presenting an acholuric jaundice, anaemia with
evidence of regeneration and splenomegaly but with no spherocytes present in the blood,
splenectomy is of no value. The Spleen Clinic studied 15 cases of this type and although
they followed three family groups that showed a familial tendency to acholuric jaundice
without spherocytes they were unable to demonstrate the cause of the disease or that
there was benefit to be obtained by splenectomy.
The Mortality rate following splenectomy in this disease is consistently low:
Mortality Rate
Pemberton    3.3%
Roussellot     6.6%
Eliason  and  Stevens  9.0%
Diamond    I  5.0%
Primary Splenic Neutropenia
I have little to say about this disease as I know little about it. This disease is one
in which the patient complains chiefly of weakness, fever, coryza or angina. They show
a marked leukopenia and granulocytopenia together with a progressive enlargement of
the spleen. Leukaemia and ordinary malignant neutropenia are ruled out by sternal
puncture which shows active hyperplasia of the neutrophilic myelocytes. The spleens,
when removed, show an extraordinary ingestion of neutrophilic leukocytes by the
splenic phagocytes. The cause of the disease is believed to be an accentuation of the
normal function of the spleen to destroy white blood cells. This accentuation of function may also extend to the destruction of red blood cells and platelets and there is, in
those cases, an associated anaemia and thrombocytopenia along with the neutropenia.
Wiseman and Doan reported five cases of neutropenia associated with splenomegaly-
completely cured by splenectomy.
A review has been made of the end results of splenectomy in splenic anaemia,
thrombocytopenic purpura, haemolytic icterus and primary splenic neutropenia.
It has been pointed out that in splenic anaemia, the hospital mortality rate of the
operation of splenectomy varies from 9,8% to 25%, the highest mortality being amongst
those cases with cirrhosis of the liver. The longevity records after operation revealed
20% to 54% alive after 5 years, 10% to 41% alive after 10 years, and 20% after
20 years. It can be anticipated that about half of the cases that had gastrointestinal
haemorrhage pre-operatively will have the same symptoms post-operatively. The symptoms vary with the site of obstruction in the portal system.
In primary idiopathic thrombocytopenic purpura, splenectomy is the operation of
choice in all cases that have other than very minimal symptoms in order to relieve the
symptoms and prevent acute exacerbations of the disease. Splenectomy is of no value
in purpura caused by toxic factors. The operative mortality is, low, varying from
0% to 5.9%.
In haemolytic icterus with spherocytes present, splenectomy is indicated to relieve
symptoms, prevent recurrent crises of the disease and the development of gallstones and
liver disease. The mortality rate is again gratifyingly low, varying between 0% and
6.6%, and the results are excellent. Splenectomy is of no value in haemolytic icterus
in the absence of spherocytes, even when a familial tendency is present.
Primary splenic neutropenia is mentioned as a disease responding most satisfactorily
to splenectomy.
W. N. BELL, M.D.
The purpose of this paper is to present a brief review of certain aspects of the physiology of peptic ulcer with the idea of indicating their actual or possible relation to the
treatment of the ulcer problem. No attempt will be made to list and evaluate the
numerous theories of the genesis of ulcer.
The matter will be divided into three main sections. The first will deal with the
physiology of gastric secretion and abnormal factors which may influence it; the second
with the motor physiology of the stomach, pylorus and duodenum; and the third with
the pain mechanism in peptic ulcer. In conclusion, I shall try and point out theamport-
ance of adhering to physiological principles in the treatment of peptic ulcer.
(a)   The normal physiology of gastric secretion:
Beaumont and Pavlov are probably mainly responsible for the view that in the absence of food or psychic stimuli the gastric glands are quiescent. Carlson showed in
1923 that a continuous secretion of gastric juice is a normal phenomenon and occurs
even in prolonged fasting. The cause is unknown. Presumably it might be due to a
persistent secretory tonus in the vagi, the production of secretagogues through the auto-
digestion of the gastric juice, the endogenous production of histamine-like substances or
a combination of these factors. The normal rate of this secretion in man has been
reported to be between 30 to 60 c.c. per hour. Recently, particular attention has been
directed towards this continuous secretion by Dragstedt and his associates who claim
that an increase in this secretion is the most important factor in the pathogenesis of
ulcer. They state that this excessive secretion appears to be due chiefly to an abnormally
great secretory tonus in.the vagus nerves and is reduced to normal values by complete
vagus section.
The digestive period of secretion is conveniently divided into three phases — the
cephalic, the gastric and the intestinal. Each phase denotes the region in which the
stimuli are acting to excite gastric secretion.
The cephalic phase is provoked by the seeing, smelling or tasting of palatable food,
provided the state of hunger and appetite is present. It is, therefore, a conditioned
reflex. Pavlov and his pupils demonstrated that the vagus nerves constitute the sole
efferent paths for this reflex. The gastric juice of the cephalic phase is highly acid and
possesses considerable peptic activity. With regard to the long latent period of the
reflx gastric secretion, no satisfactory explanation of this unique phenomenon has been
found. The amount of secretion in this phase is variable but by the intravenous insulin
method it has been found to be about 140 c.c. per hour. The insulin test, which has
recently been stressed by Hollander, has been employed in the vagotomy routine to determine if all the vagus secretory fibres have been cut. The test depends upon the fact
that the hypoglycaemia induced by an adequate dose of insulin stimulates the vagus
secretory fibres to the stomach, probably by an effect on the central nervous system. As
a rule the injection of 20 units of insulin in a normal adult produces a fall in the blood
sugar to 40 mgm. or lower, and in about 30 minutes to an hour, a marked augmentation
in the rate and acidity of the fasting secretion results. No effect whatever occurs if
the vagus section has been complete. The test must be controlled by estimation of the
blood sugar before and one hour after the injection of insulin. The sugar must fall to
50 mgm. or lower or no stimulation of the vagi is produced.
The gastric phase of secretion can be stimulated by mechanical distension and secretagogues, either present in the food or arising as products of the digestion of food. These
may act per se or through the liberation of a gastric hormone.   The exact mechanism of
Page 70
m this phase is unknownJlTThere are no accurate statistics on the volume of secretion
produced during this phase.
The intestinal phase of gastric secretion is provoked by the presence of secretagogues
in the intestine, mild distension being without effect.
Two types of mechanism are concerned in the normal inhibition of gastric secretion.
First, there is nervous inhibition; both the vagi and the splanchnic nerves contain inhibitory fibres, and mental states may inhibit gastric secretion through these pathways.
Overdue distension also inhibits gastric secretion, probably reflexly. The second is
humoral inhibition, in which the hormone, enterogastrone, is concerned. The normal
mechanism for the release of enterogastrone is the presence of fat in the intestine. It
inhibits gastric secretion and motility and has shown considerable promise in the therapy
of peptic ulcer. Under certain conditions acid in the stomach and duodenum inhibits
gastric secretion. Sandweiss and his associates have isolated a substance from pregnancy
and normal female urine which has been found to inhibit acid secretion. It may be
related to uragostrone which was isolated by Ivy.
The composition of the secretion from the various parts of the stomach varies according to the distribution of the various seceetory cells in the stomach. Generally, the
secretion of the cardia is alkaline and consists in great part of mucus; that of the fundus
is acid and contains much pepsin and some mucus; the pyloric portion of the stomach
secrets an alkaline mucus with no acid, but apparently the pylorus is important, though
not essential, for the humoral phase of gastric secretion.
The total volume of gastric secretion has been estimated at 2Q00-3000 c.c. daily but
this varies with the type of food eaten.
(b) Abnormal Factors which influence gastric secretion:
Decrease in Increase in
Gastric Secretion Gastric Secretion
1. Organic Factors:
Hyperthyroidism and Hypercalcemia X
Poor Liver Function X
2. Nutritional Factors:
Irradiated ergosterol, thiamine deficiency and vitamin A deficiency X
3. Drugs:
Alcohol, histamine, tobacco and X
Sulphanilamide X
4. Others:
X-ray, fever, anaemia, anoxaemia X
Burns X
5. Psychic Factors:
Recently, peptic ulcer has been called a psychosomatic disease. After reviewing many
of the pros and cons, it would appear that, in addition to mental stress of strain, some
inherent nervous or psychical factor must predispose to hypersecretion as it has been
shown that stress and strain do not cause increased secretion in all people.
(c) Gastric Secretion in the presence of ulcer and its relation to the Causation of Ulcer:
Acid values higher than those usually found in normal subjects are common in the
presence of ulcer, particularly duodenal ulcer. An increase in the cephalic phase of
secretion in patients with ulcer has been reported and Babkin has expressed the view that
the vagus may play an important role in the genesis of ulcer. This is.supported by
Cushing's observations of various types of ulcer in the presence of lesions of the midbrain, although the occurrence of ulcer under such conditions is not a uniform experimental finding.    All the physiological vagal mechanisms for gastric secretion can be
Page 71 completely annulled by atropine. The hypernormal interdigestive secretion in peptic
ulcer patients cannot be abolished by ordinary doses of atropine. Therefore, if this
hyper secretion is due to a vagal mechanism, it is some type of normal vagal effect which
is unaffected by atropine unless the factor of the dosage required is concerned. The
emptying time and mucus formation are often interfered with in the presence of ulcer
and these exert an influence on gastric acidity.
Much emphasis has been placed on the acidity of the gastric juice without regard to
peptic activity. Ulceration of the gastrointestinal tract has never been produced by
physiological concentrations of acid in the complete absence of pepsin. That pepsin
may play a significant role is further indicated by the high incidence of hyperpepsinia in
connection with duodenal ulcer. It seems desirable to use some therapeutic agent that
will neutralize acid and be able to inactivate pepsin. Some aluminum compounds have
these properties.
It has been demonstrated that pure gastric juice can destroy and digest living tissues
including the stomach and duodenum itself, producing in this case a defect which appears
to be identical with the lesion encountered in man. Under normal conditions the gastric
wall is not digested away apparently because it is not exposed to pure gastric juice for
long periods. Food, which in the normal individual is the stimulus for the formation of
gastric juice, is also the chief factor which protects the tissues against its corrosive
activity. Pancreatic juice, gastric and intestinal mucus and bile constitute an additional
mechanism which protects the duodenal and, to a certain extent also, the gastric and
jejunal mucosa. These acid-neutralizing and mechanically protecting secretions are
clearly of the greatest importance when-considering gastric juice is formed in the absence
of food taking. Thus when excessive volumes of normal gastric juice are secreted continuously in experimental animals, this defensive mechanism is overcome and an ulcer
is produced.
Clinically, peptic ulcer develops chiefly in the distal part of the oesophagus, the
stomach and the proximal part of the duodenum. These organs have as a common
function the transportation of food, and, in the oesophagus and duodenum, this propulsion is the paramount motor function. In addition to propulsion, the stomach has the
important motor task to store food, to break it up into fragments and to mix it with
gastric juice. The normal stomach in man does not remain inactive in the interdigestive
phase, but exhibits a periodic activity which gives rise to the hunger sensation. According to Carlson, the pressure variations in the stomach are caused by (1) a tonus rhythm,
(2) hunger contracti6ns and (3) respiratory and pulse pressure changes. Hunger contractions develop in the empty stomach at a variable interval after gastric emptying.
These are peristaltic in nature an4 start weakly in the region of the cardia, sweep with
augmenting strength over the entire stomach, the ordinary contractions produce intermittent distress or gnawing sensations, while the incomplete tetany which frequently
terminates the period is definitely painful. The presence of food in the gastro-intestinal
tract, especially in the duodenum, promptly relieves hunger contractions, in the latter
situation by the enterogastric reflex and through enterogastrone. The mechanism controlling the,spontaneous initiation and termination of hunger contractions is unknown.
Nevertheless, hunger contractions occurring in the completely denervated stomach are
strikingly similar in the transplanted gastric pouch and the .main stomach from which
it was made. This indicates the action of an unidentified humoral factor. The evidence
is convincing that hunger contractions, through mechanical trauma to the area involved,
may give rise to considerable distress in the patient with ulcer and may also prevent
healing of the ulcer. Animals appear to experience hunger after extirpation of the
stomach, denervation of the stomach and also after vagotomy, splanchnicectomy and
coeliac ganglionectomy. This and other related evidence suggests that a mechanism,
probably centrally located, in addition to the hunger contractions, produces the hunger
sense and behaviour in the normal person.
Page 72
ii1,i.i .~»« There is evidence to indicate that the vagus nerve may be both motor and inhibitory
to the stomach. However, the vagus appears to be the primary motor nerve to the
human stomach. It would seem that the occasional variability in the gastric motility
observed during the control period and subsequent to vagotomy is due to the dual
innervation to the stomach. Apparently the frequency and strength of the stimulation
is an important factor in the result obtained. The results reported in the literature
regarding the effect of stimulation of the vagus nerve on the pyloric sphincter are conflicting. The evidence indicates that the vagus and splanchnic nerves carry both motor
and inhibitory impulses to the stomach as a whole as well as to the pyloric sphincter and
that the subsequent result of stimulation is governed by the tonus or peripheral mechanism at the time of stimulation. Inhibitory fibres are apparently found more in the
splanchnic nerves than in the vagi.
The motor activities of the stomach during digestion consist of the reception of a
meal, the maceration, the fragmentation and the mixing of the food with the gastric
juice and the discharge of chyme into the duodenum. The food in the stomach is held
chiefly in the body and fundus. Here it undergoes but little mixing and is gradually
liquefied by the specific enzymes. Periodically, a portion of the mass is forced into the
pyloric antrum where it is mixed and broken up into fragments by powerful peristaltic
waves which pass toward the sphincter. The contractions starting near the incisura
require about 3 Oseconds to reach the pylorus. Fluids usually begin to leave the stomach
promptly (1-4 minutes after ingestion), but more solid material makes its first appearance in the duodenum after a longer period. The factors governing this early evacuation
are not definitely known, but in general, materials which might be irritating to the
duodenum are retained and modified to make them more acceptable. The rate of gastric
evacuation is largely determined by the antral tonus, the antral contraction waves, the
activity of the pyloric sphincter and the character of the food. The pyloric sphincter
is probably more effective in preventing duodenal regurgitation than in blocking gastric
Interference with either gastric evacuation or regurgitation can produce stagnation,
hyperacodity and, finally, peptic ulcer. Certain types of stagnation exaggerate and prolong gastric motility and gastric secretion; this favours the production and maintenance
of ulcer. Various surgical procedures have been attempted to rectify these conditions
and have met with varying success probably because interference with free communication between the stomach and intestine did not always obtain pre-operatively. It is
generally believed that the presence of hyperacidity produces pylorospasm and thus sets
up a vicious circle. This theory may be questioned since it was based on indirect evidence which indicated that acid in the duodenum caused firm closure of the pyloric
sphincter. It has been shown by direct methods that hydrochloric acid in the duodenum in concentrations similar to or even exceeding that of chyme does not produce
pylorospasm. In fact, the predominant effect is inhibition of the entire region of the
Trauma to the digestive tract is not essential to the formation of ulcer. However,
in many cases, trauma appears to be a contributing factor or occasionally even the
major factor in the development and maintenance of ulcer. In this connection it is
interesting to note that Beazell and Ivy were able to produce a chronic peptic ulcer in a
completely vagotomized animal by the feeding of a rough diet. It has been observed
both clinically and experimentally that when gastric contents are expelled in such a
manner that they strike a region with some force, an ulcer may be induced or, if already
present, may fail to heal. According to Mann and Bollman the first step in the process
of ulcer healing consists of the formation of a delicate membrane over the ulcer and this
film is readily removed by a variety of mechanical and chemical factors.
The impression is current that successful treatment of ulcer involves reducing the
motor drive of the stomach, keeping the pyloric sphincter patent and promoting gastric
I have chosen to discuss the pain mechanism under a separate heading as, at present,
it constitutes one of the most controversial aspects of the vagotomy operation. Until
recently it has been generally accepted, without definite proof, that pain sensations were
transmitted by the vagi. This probably represents the theoretical reasoning of Exner,
who, in 1912, performed subdiaphragmatic vagotomies on 20 patients with gastric
crises for the relief of pain with a 50 per cent cure. Recently stimulation of the central
ends of the vagus nerves in a transthoracic vagotomy has failed to demonstrate the presence of pain fibres in these nerves.
There is no general agreement as to the mechanism whereby the pain is produced.
It is gnerally conceded, however, that it is not due to the direct stimulation of pain
endings in the ulcer by acid or food. Nevertheless the acid plays some part as shown by
Palmer who exposed an ulcer under local anaesthesia and produced pain by putting l/z
per cent of hydrochloric acid directly on the ulcer. Disturbances of the motor mechanism of the stomach or duodenal cap dependent upon reflexes initiated from the irritable focus are believed to be directly responsible for the pain. There is no general agreement, however, as to the precise nature of the motor disturbance. Pylorospasm, achalasia of the pyloric sphincter and antral peristaltic waves have been postulated. If such
is the case, why does soda bicarbonate or food relieve the pain? Ryle suggests that the
ingested food, or the evolved gas, by increasing the volume of the gastric contents
ablishes the pain by causing an adaptive relaxation of the gastric walls. As Dr. Ivy has
pointed out, we should distinguish between gastric hunger pains and other subjective
sensations associated with hunger on one hand, and appetite on the other. Section of
the vagi abolishes gastric hunger contractions on tone but does not abolish gastric
hunger peristaltic activity. With regard to the precise mechanism of the production of
pain, it seems clear that the first essential is a lowering of the pain threshold of the nerve
endings, presumably as a result of inflammation. This might explain why certain individuals with a high pain thershold may have no pain associated with an ulcer process.
de Takats has presented evidence that the sympathetic nerves may play a role in the
transmission of pain. He found that by blocking the sixth to ninth left dorsal sympa-
thetics he Was able to relieve the deep, boring and continuous pain of an early penetrating
lesion unless somatic intercostal fibres were involved by peritoneal involvement.
It is hard to say why the pain disappears so promptly following vagotomy. / Pain is
no longer produced by putting acid directly on the ulcer, suggesting some diminution in
sensitivity of the mucosa but the fact that inflated balloon distension of the oesophagus,
stomach or duodenum still produced pain and the fact that an intestinal obstruction after
vagotomy caused much pain shows that the sensory pathways have not been interrupted.
Moore noncommittally sums it up by saying that the relief of pain "results from a fundamental alteration in some aspect of the ulcer producing mechanism."
Medically, these may be summarized briefly as the use of frequent feedings to reduce
gastric acidity and to furnish digestive products (probably peptones) which exert a protective action against the action of acid, according to Mann and Bollman; a high fat
intake, eg., milk and cream to increase the action of enterogastrone and to increase the
output of bile and pancreatic juice so as to reduce the acidity of the duodenal contents;
the limitation of highly seasoned foods and foods high in extractive, e.g. meat and alcohol
which stimulate the gastric glands; the omission from the diet of coarse indigestible
articles which are likely to cause mechanical irritation of the ulcer; the administration of
alkalies or mucin for their mechanical protection and their high acid combining power;
the possible use of atropine to reduce secretion and the avoidance of overwork, mental or
physical fatigue, work or any psychic state likely to bring the neurogenic factor into
play. »
glli Page 74
.fi* i
I A Surgically, various operative procedures have been suggested and tried. Vagotomy,
the newest of these, will certainly knock out the cephalic phase of gastric secretion but
will be ineffective in reducing the gastric or intestinal phases. Thus, in selecting cases
for vagotomy, the ideal subject would be one whose ulcer can be laid at the door mainly
of vagal activity. To reduce the gastric phase partial gastrectomy has been employed.
If the gastric phase is increased because of stagnation of gastric contents, as sometimes
happens following vagotomy, gastro-enterostomy with adequate drainage may be of benefit. Pyloroplasty has also been used in conjunction with vagotomy to remove the ulcer
area and to ensure adequate gastric emptying.
As the march of therapy in peptic ulcer advances it becomes increasingly evident that
physiological reasonings form the framework for progression.
1. PHYSIOLOGY OF GASTRIC SECRETION, Schiffrin, M. J., and Ivy, A. C, Arch. Surg. 44:399
(March)  1942.
Arch. Surg. 44:414   (March)   1942.
3. VAGOTOMY IN THE THERAPY OF PEPTIC ULCER.    Weinstein et al S. G. O. 79:297, 1944.
4. VAGOTOMY FOR GASTRODUODENAL ULCER.    Dragstedt, L. R., Annals of Surgery 122:973,
IN THE DOG, Beazel, J. M., and Ivy, A. C, Arch. Path. 22:213   (August)   1936.
ULCER.    Dragstedt, L.  R., and Schafer, P. W., Surgery  17:742,  1945.
7. SUPRADIAPHRAGMATIC   SECTION  OF   THE   VAGUS   NERVES.     Thornton,   T.   F.,   Storer,
E. H., and Dragstedt, L. R., J.A.M.A.  130:764   (March 23)   1946.
8. SUPRADIAPHRAGMATIC SECTION OF THE VAGUS NERVES.   Dragstedt, L. R., et al, Gastroenterology 3:450,  1944.
L. E., and Curtis, G. M., Arch. Surg. 34:1132   (June)   1937.
Grimson, K. S., et al, South, M. J.,  39:460   (June)   1946.
Inc., 1944.
12. PHYSIOLOGICAL BASIS  OF MEDICAL  PRACTICE.     Best  &  Taylor,   3rd Edition,  Williams &
.  Wilkins, p. 742 and 810,  1943.
Locums and Assistantships Available
There are a number of vacancies in the Province for assistants to established
doctors and clinics, and for men who are available for locum tenens work.
Certain of these posts offer opportunity for permanency after a probationary
Anyone available please contact the undersigned.
Executive Secretary,
College of Physicians and Surgeons of British Columbia.
Room 203, Medical-Dental Building, Vancouver, B. C.
Vancouver General Hospital
Presented: May 27, 1947
Miss B. W., age 19, was admitted to the Vancouver General Hospital on April 19th
as an emergency patient complaining of severe lower abdominal pain with accompanying
nausea and vomiting.   Family history was essentially negative.
Past Personal History: Infectious diseases—measles, chickenpox. Bilateral mastoiditis in infancy with mastoid operation. She has had no other serious illnesesses, injuries
or operations.
Menstrual History: Onset at 17. Flow has been regular every 28 days and of 4 days'
duration. There has been some dysmenorrhea since the onset but it has been more
marked during the past year necessitating bed rest on occasions. She has noted that the
pain would tend to persist for a day or so after the flow had ceased. There had been
no severe pain however until April 18th (the day before admission) when coincident
with the onset of her menstrual period, she began to experience severe, cramp-like, lower
abdominal pain which was soon accompanied by nausea and vomiting. There was some
partial relief during the morning of April 19th but it recurred again with increased
severity during that afternoon and she was admitted to hospital by ambulance. On
direct questioning she admitted that she had recently noted the presence of a swelling
of the abdomen low on the right side but this had apparently given her little concern.
Physical Examination: The patient is a tall, rather thin young woman of good
physique, in acute pain. There is frequent vomiting and retching. Temperature 99.2
and pulse 96. The abdomen is distended in the lower half where there is a rounded,
hard, smooth, very tender, tumor mass apparently arising from the pelvis and roughly
the size.of a five months' pregnancy. There is considerable increased resistance over the
entire abdomen but no true rigidity.   The flanks are clear.
Pelvic Examination: Virginal introitus which does not admit one finger. There is
no evidence of a vaginal septum. Per rectum, the abdominal mass apparently extends
into the pelvis as a hard, smooth, fixed tumor completely filling the pelvic cavity.
Laboratory Examinations: Catheter specimen of urine, negative. There was a slight
leucocytosis, 9,500 with 75 per polys.
Because of the urgency of the condition, an emergency operation was arranged with
the pre-operative diagnosis of an impacted ovarian cyst with torsion of the pedicle. At
operation, the tumor was seen to consist of a large, bicornuate uterus with a haematosal-
pinx on the right side. The uterine horns were apparently equal in size and were about
3 to 4 cms. in diameter Below their attachments the uterine body and lower segment
was ballooned out and densely hard resembling the appearance that might be produced
by a large myoma growing from the lower uterine segment. The bladder fold of peritoneum was stretched over the tumor and firmly attached high on the anterior surface
of the uterus. In spite of the obvious bi-cornuate uterus and the fact that the right
haematosalpinx suggested a haematometra, it was believed that there might be a large,
solid uterine tumor such as a myoma in the lower segment which was interfering with
uterine drainage. This conclusion was based on the fact that the lower part of the
uterus was symmetrically enlarged and seemed to involve chiefly the anterior wall. In
addition the whole mass could not be delivered out of the pelvis. The possibility of
incising the mass to determine its exact nature was considered but it seemed possible
that the uterine contents might be infected. Moreover the whole organ was so deformed
and dilated that it appeared doubtful that a useful uterus with respect to child-bearing
could be left were a plastic operation attempted. Accordingly a total hysterectomy
was performed leaving a normal left ovary.   The operation was difficult because of the
Page 76
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f M-»ft-
lack of working room in the pelvis.    Upon removal, the tumor was incised with the
escape under tension of about a liter of dark, chocolate-coloured menstrual blood.
The patient made a somewhat slow but uncomplicated recovery from her operation
and was discharged on the twelfth post-operation day.
The various congenital abnormalities of the uterus due to failure of complete union
of the two Miillerian ducts may result in considerable difficulty and danger, particularly
during pregnancy. The rarity of the condition, occurring about once in 1500 obstetrical
cases and once in 2000 gynaecological cases, accounts for its frequent lack of recognition.
All degrees of failure of fusion of the Miillerian ducts may exist, from the simple
uterus arcuatus or notched uterus to two complete sets of genital organs. Thus the
uterus may be divided completely or incompletely by a septum and likewise the cervix
and vagina may be partially or wholly divided. In general, one duct tends to develop
to a greater extent than the other. Many confusing classifications of the various
anomalies have been listed.
Taylor suggests a simplified classification as follows:
1. Uterus arcuatus.
2. Double uterus with a single cervix.
3. Septate uterus.
4. Double uterus with double cervix.
5. Uterus with rudimentary horn or absence of one horn.
A septate vagina should make one suspect further abnormalities higher up though it
may exist alone. In the gynaecological patient an exact diagnosis may be established by
an injection of an opaque medium into the uterus as in utero-salpinography. However
a rudimentary horn or closed half of a septate uterus may be missed even by this method.
The anomalies may cause considerable disturbance in the function of child-bearing.
Abortions are frequent and in the woman who repeatedly aborts an abnormality of the
uterus should be considered as a possible cause. Pregnancy in a rudimentary horn or
situated high in a bicornuate uterus may result in rupture simulating an ectopic pregnancy with profuse intra-abdominal haemorrhage.
In labour, many difficulties may arise. Uterine inertia and inefficient contractions
are common. The non-pregnant portion of the uterus or the septum may obstruct the
presenting part. Rupture of the uterus may occur. In the third stage of labour post
partum haemorrhage and retention of the placenta are relatively frequent. In spite of
these dangers, a conservative plan of management in labour is usually advocated since
many women with such uteri may have comparatively normal labours and deliveries.
Caesarean section may be required, however, because of malpresentation, inertia or failure
of engagement or descent of the foetal head.
I have found little material in the literature concerning the advisability or feasibility
of plastic surgery in these malformations of the uterus. This is probably due to the fact
that few gynaecologists have had sufficient experience to establish authentic criteria for
operative treatment. Obviously when a rudimentary accessory horn is found at operation it should be removed. With respect to plastic surgery on the septate uterus, a few
cases have been reported by certain German gynaecologists, notably Strassmann, in which
the uterus has been opened and the septum partially or wholly removed. Some of these
operations have been followed by full-term pregnancy and normal delivery. Up to 1933
nine cases of successful pregnancies following metroplastic operations have been reported. The possible danger of uterine rupture during pregnancy or labour following
such plastic procedures is emphasized. On the other hand, Norman Miller states that a
large accumulation of menstrual blood in the atresic half of a septate or double uterus
may require hysterectomy and cites such a case. A closed or poorly draining accessory
horn may cause haematometra, pyometra or pelvic endometriosis. The fact that menstruation is occurring regularly from the other portion of the uterus may be misleading
in the diagnosis.
Page 77


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