Georges Dieulafoy.

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increased virulence, enter the appendicular veins, and reach the great mesen-
teric vein, the portal vein, and the Uver. In some cases, as in my patient,
the infected veins form a varicose network. Some small veins are throm-
bosed ; others are not. Phlebitis sometimes affects the larger venous trunks,
such as the great mesenteric vein, which receives the appendicular veins,
and even the trunk of the portal vein, which starts from the mesenteric

I would remind the reader how this hepatic infection announces itself.
The patient has been suffering from appendicitis, and it matters little whether
the attack has been severe or mild. Sometimes, indeed, an operation


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has been performed (too late), and the patient is on the highroad to cou-
valescence. And yet rigors, temperature rising to 104° F.,and profuse
sweats open the scene. The attacks return daily, and the fever is con-
tinuous. The attacks of fever are accompanied by hepatic or epigastric p^n,
jaundice, gastric intolerance, and vomiting. These symptoms are accom-
panied by rapid swelling of the liver, which may become enormous. The
spleen remains normal. Diarrhoea is as frequent as constipation. In one of
my cases it was exceedingly profuse. Jaundice may be early or late, slight
or intense. The general symptoms are those of the typhoid state. The
pulse is quick, the tongue is dry and red, and the attacks of fever persist
for one or two weeks. Sometimes the fever improves, and there is a tem-
porary remission, but in the end the patient succumbs in a state of adynamia,
collapse, or syiKJope, or with symptoms of icterus gravis, multiple haBmor-
rhages, albuminuria, and anuria.

The hepatic infection is always consecutive to the acute phase of appen-
dicitis. It is not to be feared when the active process of appendicitis has
been extinct for some time. On the other hand, I do not know of a single
example where hepatic infection supervened quickly during the early stage
of appendicitis. The migration of the microbes into the veins of the
appendix never commences — at least, so I believe — before the fifth or sixth
day. Surgery has, therefore, ample time to intervene before the conunence-
ment of the appendiculo-portal migration.

This hepatic infection is one of the most terrible complications of appen-
dicitis, because I am only acquainted with two cases of recovery (Koerte,
Loison). The operation was successful because, extraordinary to relate,
there was a solitary hepatic abscess. In Loison's case radioscopy gave
considerable support to the diagnosis. Sunmiary : Except in very rare
cases, medicine and surgery are powerless to avert the evil once it has
declared itself. As a matter of fact, however successful the surgeon may
be in solitary abscess of the liver, intervention is hopeless in appendicular
infection, where abscesses of the liver are almost always counted by dozens.
What a lesson, however, for those who say that we must only perform
interval operations ! Once again I protest against such an assertion. In
appendicitis we must never wait, for we can never know what the future
has in store for us.


Structure and Formation of GaU-Stones.— The production of gall-
stones is one of the most common troubles in the human race (Cruveilhier).
They may be formed in the intra- or extrahepatic ducts, or in the liver,
but the gall-bladder is the most common situation.

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Biliary concretions of all sizes are found in the gall-bladder, from gravel
to calculi larger than an egg. They may be solitary, multiple, or indefinite
in number. The soUtary calculus has no facets, and may be oval or pear-
shaped. Multiple calcuU are rounded or pyramidal and faceted from the
rubbing and pressure of neighbouring calculi. They are elongated when
they have been long in the common duct. Their colour is brown, greenish-
yellow, or blackish. It is whitish in the case of calculi of cholesterin.
Their density, though low, is greater than that of water. When they have
not been dried, their structure varies, according as they are simple or com-
pound. The compound calculi have a nucleus and a crust. The nucleus
is formed of bile pigment, chalk, epithelial cells, and rarely foreign bodies. It
is surrounded by a middle radiating layer, in which crystals of cholesterin
predominate. The crust is stratified and composed of cholesterin, bile
pigment, or chalk. Calculi without a crust may be met with. Others,
again, called simple calculi, are homogeneous throughout their whole thick-
ness. The calculi contained in the same gall-bladder are identical as regards
structure, colour, and chemical composition. Agglomerated and frag-
mented calculi are found. The consistency of the biliary concretions is
moderate, and the most resistant ones are formed of pure cholesterin. The
calculi are free in the bladder. They may sometimes be adherent to the
wall. They are then let into the walls of the gaU-bladder which have
become alveolar, as Terrier observed when performing cholecystotomy.
The chief components of gall-stones are crystalline or amorphous chole-
sterin, and neict the colouring matters of the bile and the calcareous salts.
It is curious to note that cholesterin and chalk, which are found in very
small quantities in the bile as compared with the other elements, form the
chief constituent parts of the calculus. Thus, cholesterin, on an average,
forms 70 per cent, of the constituent parts of the calculus, whilst the bile
barely contains 2 per cent. The salts of potassium and of sodium, which
alone form some calculi, are found in very small quantities in the bile.
Throughout the whole thickness of the calculi there is a land of organic
albuminoid web, which indicates the participation of the mucosa in the
formation of calculi.

The exact manner in which the stones are formed is still imperfectly
known. The substances contained in the bile must be precipitated and
agglomerated, and must be kept agglomerated. It is supposed that chalk is a
product of the secretion of the gall-bladder (see Catarrh of the Gall-Bladder).
Catarrh of the gall-bladder is said to have the power of acidifying the bile,
and the acidity of the bile is said to split up the bile salts ; by the dissolution
of the salts, cholesterin and bilirubin are set free and precipitated — the
former in a crystalline form ; the latter either in a crystalline form or mixed
with the chalk.

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It is admitted that microbic infection plays an important part in the pro-
cess, by favouring cholecystitis, altering the composition of the bile, and
contributing to the formation of the nuclei. It may, perhaps, be that
typhoid fever and other infectious diseases which affect the gall-bladder
are, by reason of the microbes, the remote origin of biliary calculi (Dupre).
Dufour was able to collect fourteen cases of patients of various ages who
had hepatic colic some months after an attack of typhoid fever, while they
had had no symptoms of gall-stones prior to the fever. Several writers accept
this pathogenesis of biliary lithiasis (Chiari, Gilbert), and Hanot thus sums
up the question : " If the intestinal catarrh spreads to the biliary passages
and becomes lithogenous catarrh — that is, if the micro-organism of typhoid
fever is, after all, capable of causing biliary lithiasis — the question of a
microbic origin is settled. It would, then, remain to be decided which
microbes, other than those of typhoid fever, intervene. It may be possible
that every microbe, from the very fact that it swarms in the bile-ducts,
causes chemical changes leading to the deposit of the mineral principles.
Thus, Galippe actually saw the formation of crystals of carbonate of lime
in saliva placed in a flask, around masses of micro-organisms which were
growing therein."

*' Biliary lithiasis would, then, result from the mode of penetration of the
micro-organisms into the bile-ducts, from their greater or smaller number,
and particularly from the constitution of the mucus, which is more or less
readily deposited. If this last theory is true, the soil is more important
than the seed, and biliary lithiasis would no longer be an accidental
phenomenon, but would remain the expression of a previous state of
the organism, of a hereditary or congenital modification, totius substanticB
— that is, of a diathesis." My ideas agree absolutely with those ex-
pressed by Hanot — that the diathesis is the factor in the pathogenesis of

etiology. — Biliary lithiasis is more frequent in women ; it is most prone
to occur in heavy eaters, in fat people who take Uttle exercise, and in indi-
viduals past middle life. Often, says Trousseau, the real causes of the
disease escape us, and a clear point is that these causes, no matter what
they be, are dominated by a predisposition special to the individual. As a
matter of fact, biliary lithiasis is often associated with the diathetic condi-
tions that form a part of the group of arthritic diseases — migraine, gout,
or rheumatism, urinary lithiasis, obesity, asthma, diabetes, and eczema—
which have been described by Bouchard in his work on '* Les Maladies par
Ralentissement de la Nutrition." Urinary lithiasis is closely related to
hepatic lithia«is, and these two manifestations may occur successively in
the same individual, or exist simultaneously in one family, where they are
hereditary. The same remark applies to appendicular lithiasis, and the

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numerous cases quoted under Appendicitis show that hepatic, intestinal,
renal, and appendicular lithiasis belong to the same pathological family.
After the diathetic causes, or side by side with them, come infections of
microbic origin, as I have mentioned above.

Pregnancy— Puerperal Condition.— Pregnancy plays a large part in
biliary lithiasis. I have devoted a clinical lecture to this question.* Hepatic
colic is frequent in pregnant women. In a comprehensive work, the first
which has appeared on the subject, Huchard has published several cases.
The cases of Depaul, Tamier, and Pinard are positive evidence. I have
reported several cases. According to Leyden's statistics, in one hundred
cases of women suffering from hepatic colic, concomitant or anterior preg-
nancy has been noticed in ninety of them. Authorities are not absolutely
agreed as to what period of the puerperal state is most favourable to the
appearance of hepatic colic. Some maintain that it is during pregnancy ;
others that it is during accouchement. Cyr has published the following
statistics : In fifty-one women with gall-stones, hepatic colic has been noticed
eleven times during pregnancy, four times after miscarriage, and thirty-six
times after accouchement. The period between the accouchement and the
attack of colic varied from one day to a month in twenty- two cases, and from
one to twelve months in fourteen cases. In the statistics sent me by Bou-
loumi6, of Vittel, hepatic colic figures as follows : twenty-two times during
pregnancy, and fifty-five times from a day to a year after accouchement.
In the statistics forwarded to me by Deleage, of Vichy, hepatic colic figures
as follows : fifty-nine times during pregnancy, and forty-five times after

Whether hepatic colic appears during pregnancy or after deUvery, it is
none the less true that the puerperal condition has a great influence in the
pathogenesis of biliary lithiasis. Hepatic colic appears in various ways.
First variety : A young girl who has never hid hepatic colic marries ; during
her first pregnancy hepatic coUc appears, and reappears during subsequent
pregnancies ; but never apart from the puerperal condition. Second variety :
A woman who has never had hepatic colic, either as a girl or later during
pregnancy, is seized with hepatic colic some days or weeks after delivery.
The colic recurs after subsequent deliveries, and is never present except at
this time. Third variety : Hepatic colic appears, either during pregnancy
or after labour, and again later, at indeterminate periods, when the woman
is not pregnant.

Hepatic colic during pregnancy or after delivery does not differ from

the ordinary form. The diagnosis is generally easy ; nevertheless, when it

appears during pregnancy, it may, for want of clear symptoms, be mistaken

♦ '* La Grossesse et les Lithiases " (Clinique Medicale de V Hotel-Dieuy 1898,
15rae le^on).

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for a miscarriage. When it appears after delivery, it may, for want of atten-
tion, be looked upon as commencing peritonitis.

Many theories exist regarding the occurrence of biliary lithiasis during
pregnancy. Pregnancy is said to favour stagnation of bile in the bile-ducts,
and, as a consequence, the formation of calculi. It has been said that preg-
nancy favours mobility of the kidneys and liver. On account of the flaccidity
of the abdominal walk, the gall-bladder, since its means of fixation have
been relaxed, tends to swing backwards, and the conmion bile-duct being
dragged on by this swinging movement, becomes narrowed ; this narrowing
favours stagnation of the bile in the gall-bladder. Pregnancy, according to
Heidenhain, is also said to provoke stagnation of the bile, by hindering the
play of the diaphragm, especially as the corset fixes the costal insertions of
the muscle. This pathogenesis might be classified under the mechanical
causes, but the chemical causes (malnutrition), the bacteriological causes
(action of the microbes in forming calculi), and the constitution of the
patient (arthritism, heredity), have also to be considered. All these theories
are possible, but not one seems to me to be sufficient. The undeniable
clinical fact is that the puerperal condition excretes a considerable influence
on the pathogenesis of gall-stones.

After having shown the influence of pregnancy on the pathogenesis of
hepatic colic, let us invert the question and inquire what influence hepatic
colic may have on pregnancy and the sequelse of labour. The prognosis in preg-
nancy is scarcely affected by hepatic colic ; severe and repeated attacks of colic
do not interrupt it. The jaundice which in many cases follows hepatic colic
is not dangerous to the pregnant woman ; it is merely jaundice by retention,
which habitually ceases a few days after the colic, and does not injure the
cells of the liver. If, however, it lasts too long, as in permanent obhteration
of the common duct, the normal activity of the cell may suffer, and for-
midable miechief may ensue. Hepatic colic and jaundice do not, as a rule,
render the prognosis serious, either in the pregnant woman or the recently
delivered woman. And though jaundice due to a stone is not, as a rule,
dangerous in the pregnant woman, this is not the case in the other
varieties included under infective jaundice. It matters little what theon^
is formulated to explain the affection of the hepatic cell. As soon as the
cell participates in the toxic process, it imdergoes a change which under
other circumstances might not have serious consequences, but which in
the gravid condition is always to be feared. Jaundice supervening in a
pregnant woman, therefore (I speak of jaundice apart from hepatic cohc),
is always a suspicious symptom, because it points to possible hepatic
insufficiency, with all its consequences. This question will again be re-
ferred to under Jaundice, when we shall consider the relations between
pregnancy and infective jaundice.

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Symptoms and Complications of Gail-Stones.— In some cases (in old
people particularly) gall-stones cause no symptoms. At a post-mortem
examination it is by no means rare to find a calcified and enlarged gall-
bladder, containing numerous calculi, in people who have shown none of
the symptoms of gall-stones. More frequently, however, the stones cause
various troubles and more or less grave complications, divisible into several
groups :

1. Migration of the calcuU into the large bile-ducts — hepatic colic.

2. Migration and arrest of the calculi in the intestine — obstruction of
the pyloric orifice.

3. Persistent obUteration of the large ducts — biliary cirrhosis.

4. Infection of the ducts — angiocholitis, cholecystitis, hepatitis, endo-

5. Passage of the calculi outside the natural passages — perforation of
the gall-bladder and bile-ducts, peritonitis, biliary fistulae.

1. Hepatic Colic.

Anatomy. — Hepatic colio is the most common complication of gall-stones. In order
to understand the mechanism, it will be well to mention certain anatomical factfi con-
cerning the ducts through which the calculus has to pass.

In the normal condition the gall-bladder contains about 2 ounces of bile, but its
walls are capable of such distension that it may contain more than 2 pints without
rupture. The gall-bladder ends in a neck, which is very flexible, and is continuous
with the cystic duct. The neck of the bladder presents a swelling, or pelvis. In an
opened bladder we see that this swelling is limited above by a valve, which considerably
narrows the orifice, and below by a second and less important valve. The gall-bladder
is contractile, and possesses muscular fibres, forming a muscularis mucosse, which
becomes hypertrophied in biliary hthiasis. The mucosa shows both temporary and
permanent folds. The former disappear as soon as the bladder is sufficiently distended ;
the latter anastomose, and circumscribe areolae of various forms.

The cystic duct is the continuation of the neck of the gall-bladder. It is nearly
2 inches long and \ inch in diameter ; it opens into the common duct. On opening the
cystic duct we see that its internal walls show projections (the semilunar valves of
Heister), which prevent the migration of calculi. The common duct is formed by the
fusion of the cystic and hepatic ducts. It is 3 inches long and about \ inch in
diameter ; it opens into the duodenum at Vater's ampulla, in common with the pancreatic
duct. The common duct is not provided with valves, but at its entrance into Vater's
ampulla it possesses a sphincter, composed of muscle fibres. As a matter of fact, the
real opening is situated at the duodenal opening of Vater's ampulla, and at this point
there is a very marked constriction, which is a final obstacle to the calcuh coming from
the bladder. The cystic and conunon ducts possess longitudinal muscle fibres, which
disappear late in hfe. They are capable of such distension that they may allow the
passage of calculi as big as a hazel-nut. The common duct when distended may be as
large as a coil of bowel.

Hepatic Colic. — The contraction of the gall-bladder, bile-duct, and abdo-
minal muscles causes a calculus to engage in the cystic duct. If the stone
is neither large nor angular, it will pass through the cystic and common ducts

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into the intestine without causing colic ; if the stone is larger than the
lumen of the bile-ducts, it produces in its migration the symptom-complex
of hepatic colic.

In the struggle between the calculus and the ducts, the former is pushed
onwards, but causes, in its migration, spasm and contraction of the latter.
It meets with numerous obstacles to its passage : in the cystic duct, which
is of small calibre, it must pass a series of valves ; and in the common duct,
which is larger, it meets, at the last moment, with the narrow orifice of
Vater's ampulla. Hepatic colic appears most frequently a few hours after
a meal, fost prandium, probably because at this moment the gall-bladder
contracts, in order to empty the bile into the intestine. The onset is sudden,
and the subject complains of sharp pain, radiating in several directions : to
the pit of the stomach (epigastric point), around the umbilicus, to the right
hypochondrium, the right shoulder, and the lower extremity of the scapula
on the same side (scapular point). The pains rapidly become very severs,
and cause the patient intense agony. They may be continuous or inter-
mittent, following one another at more or less close intervals, and consti-
tuting an attack of hepatic colic. The attack lasts, on an average, from six
to twelve hours, though it may persist for several days. It is most fre-
quently apyretic, but in some cases fever is also present.

Hepatic colic is, as a rule, accompanied by vomiting, which is at first
alimentary, if the colic appears soon after a meal, and subsequently becomes
glairy and bilious. As long as the calculus remains in the cjrstic duct, the
vomit may be bilious, because the bile continues to pass into the intestine,
whence it regurgitates into the stomach ; if, however, the calculus is arrested
in the conmoion duct, the passage of the bile into the intestine is interrupted,
and bilious vomiting cannot occur. The same remark applies to the de-
coloration of the ffiDces. As long as the calculus remains in the cystic duct,
the bile flows freely into the intestine^ and the faeces are coloured ; but if
the calculus is impacted in the common duct for some time, the faeces become
colourless, and the yellow colour of the skin and of the urine reaches its
maximum. Generally speaking, the attack of hepatic colic ceases suddenly,
and the patient at once feels a delightful sensation of relief. The calculus
has, then, gone back into the gall-bladder, after a vain attempt to pass through
the cystic duct, or has reached the duodenum, after a painful migration
through the ducts. The end of the attack is often accompanied by the
passage of much watery urine (nervous urine). During the attack the liver
is often enlarged, and the region of the gall-bladder is extremely tender on

When the colic has been long and severe, the liver remains enlarged and
painful for several days ; it reaches below the false ribs, and is so tender on
pressure that women cannot wear their corsets.

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I have just described a severe attack, but hepatic colic is often much less
acute. Many people with gall-stones merely complain of cramp in the
stomach, which may be looked on as gastralgia, but is, in reality, rudimentary
hepatic colic. The yellowish tint which often follows this so-called cramp in
the stomach explains the nature and the origin of the mischief.

Jaundice is a frequent symptom of hepatic colic, provided the calculus
blocks the common duct completely and for a sufficient time. The result is
jaundice by retention some hours after the colic. If the obliteration of the
common duct lasts long enough, the faeces have a whitish look, due partly
to the absence of bile and to the presence of non-emulsified fats. The urine
is loaded with bile pigment, and has a characteristic mahogany colour.
Jaundice is, however, not constant : in forty-five cases of hepatic colic
analyzed by Wolff where gall-stones had been found in the stools, jaundice
was absent in twenty-five, proving that the stone may traverse the common
duct without, however, completely obliterating it. The icteric tint may
be very slight, and must be looked for carefully. We must not forget, too,
that the seat of the trouble may be the cystic duct, in which case there will
be no jaundice. Finally, we must remember that attacks of pain, mistaken
for hepatic coUc without icterus, may in reality be due to cholecystitis.

If the stools are examined by sifting them, the calculus or the calculi
which have caused the complications, will be found, unless the calculus in the
cystic duct has passed back into the gall-bladder, or has been pushed back
from the duodenum into the stomach and rejected by vomiting. The
calculi may not appear in the stools till three or four days after the att*ack.
To find them, the stools must be carefully sifted ; otherwise the calculi may
pass unnoticed. The syndrome of hepatic colic may likewise be caused by
worms or by hydatids impacted in the excretory canals, but these cases are
very exceptional.

Accompanying Symptoms.— I have given the name of " satellite symp-
toms " to certain phenomena which sometimes accompany hepatic colic, or
which may, indeed, exist without typical colic ; in the latter event we have to
deal with defaced hepatic colic.

Vertigo is one of these symptoms, and I may say that it is frequent,
if trouble is taken to seek it. I do not know the exact pathogenesis, but it
is certain that a fair number of persons with gall-stones suffer from vertigo,

Online LibraryGeorges DieulafoyA text-book of medicine, Volume 1 → online text (page 119 of 129)