Georges Dieulafoy.

A text-book of medicine, Volume 1 online

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syndrome. This form of ascites never proceeds in an identical manner.
The stages of the process differ in aspect and in duration, but the termination
is always fatal. Momentary arrest and remissions have been observed.
In most cases, after a year or eighteen months, during which the tappings
follow at closer and closer intervals, the patient dies of cachexia. This
fatal prognosis is perhaps the only point of difference between lactescent
and ordinary ascites. Ascites with citron-like effusion can recover when
the causative lesion is cured. Such cases are not imcommon.* Lactescent
ascites is never cured.

Diagnosis. — Lactescent ascites may be diagnosed by examination of
the liquid. Fatty granules and leucocytes must be sought for, and the
formula of the latter must be determined. Strauss^'s experiment (ingestion
of large quantities of butter) might be tried, and does not present the
slightest danger. As to the diagnostic value of lactescent ascites, it is of
but small importance. It must be remembered, however, that it has been
specially observed in tuberculosis and cancer of the peritoneum.

♦ Dieulafoy, Cliniques de VHotd-Dim, 1898, 1899, 19'» le(?on.

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Anatomy. — Before describing the lesions of the Hver, the cirrhoses which play snch a
large part in the pathology of this organ, the degenerations of all kinds (fatty, pig-
mentary, amyloid) which affect the cell in various ways, the changes in the bloodvessels
and biliary canals, etc., it is essential to describe briefly its normal structure and

The liver occupies the right hypochondrium, and weighs about 50 ounces. It
receives two kinds of afferent vessels : (1) the hepatic artery for purposes of tissue
nutrition ; and (2) the portal vein, which brings the venous blood from the intestine,
stomach, and spleen to the liver. It has only one set of efferent vessels— the
hepatic veins, which pour the blood into the vena cava. In a section of the liver the
portal veins may be easily distinguished from the hepatic veins. The portal veins are
accompanied by the ramifications of Glisson's capsule, do not adhere to the tissue of
the liver, and collapse, whereas the hepatic veins adhere to the tissue of the liver and
remain open. On section of the liver we can observe with the naked eye or with a
low-power microscope a number of small islands, coloured deeper at the centre than
at the circumference, and giving to the liver a grained appearance. These islands
represent the hepatic lobules.

The liver is formed by the union of lobules, and, according to Sappey, contains
1,200,000. If, therefore, we know the structure of one lobule, we know the structure
of the whole hver. The hepatic lobules sure small masses I millimetre wide and 2 milli-
metres long, and fixed on to the divisions of the hepatic vein like glandular acini to
their excretory ducts. The polyhedral form of the lobules is due to mutual pressure.
They are separated from one another by fissures and by triangular spaces caused by
the blunting of their angles. In the centre of the lobule we find the suprahepatic vein,
which is adherent to the tissue of the Uver, and penetrates the lobule. It is a short
branch of the extralobular hepatic vein. The suprahepatic vein is formed of fibro-
elastic tissue, with a few smooth muscular fibres, and is hned with epithelium. In
pathological conditions this fibrous thickened vein is an important histological land-
mark. Around the lobule, in the triangular spaces and fissures, are the portal veins,
the hepc-tic artery, the biUary ducts, and the lymphatic vessels, bound together by con-
nective tissue. The importance of these fissures and spaces in the pathological anatomy
of the hver will be already apparent. Between the hepatic vein, which is central, and
the portal veins^ which are peripheral, we find capillaries carrying the blood from the
circumference to the centre of the lobule, forming a venous network in the interior of
the lobule, and united with one another by transverse anastomoses. In pathological
conditions these capillaries are often obstructed by red corpuscles and microbes. In
the meshes of this capillary network are the hepatic cells, directly connected with the
network of the bihary canalicuU.


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1. The hepatid cells constitute the eesential and speoifio element of the liver. They
are smaU blocks of a soft and granular substance, and their variety of shape is due to
the pressure exerted on them by the surrounding cells and vessels. After a fast the
eellfl are small and somewhat ill-defined, but during digestion they become large and
very distinct. They are readily isolated. They are flattened, polygonal, so that each
cell is in contact with six or seven of its neighbours, as weU as with the blood and bile
capillaries. The hepatic cells do not appear to have an envelope, and are formed of
granular protoplasm containing one or two nuclei. They contain yellow granules of
biliary pigment, with red granules of blood pigment and fatty granulations. They
contain glycogen and the ferment by which the glycogen is transformed into sugar.
This glycogenic matter is especially abundant in the cells at the centre of the lobules.
It appears in little amorphous masses, which are almost fluid, and turn a mahogany-rod
colour with tincture of iodine. The cells radiate from the centre towards the circum-
ference, thereby foUowing the disposition of the vascular meshes, and are placed in a
network at the periphery of the lobule (Frey).

The radiation of the cells gives them the appearance of little columns, sometimes
called trabeoulse. Eberth has compared these trabeculsB with tubes, the tube being
formed of hepatic cells surrounded by a membrane. This tubular disposition of the
liver, which exists in some animals, especially in the seal, is seen in man in pathological

2. The portal veins which surround the hepatic lobule run in the spaces and fissures
between the lobules. Each lobule is penetrated by capillaries derived from several
portal vessels. These capillaries make their way in a radial direction from the periphery
towards the centre of the lobule (KoUiker). They are imited one to another by tians-
verse anastomoses, and they anastomose with the capillaries of the central hepatic
vein. It is by means of this network that the blood of the peripheral portal veins,
after having traversed the mass of the cells, pours into the hepatic vein. It is in this
network that the hepatic cells are contained. The blood capillaries make their way
in the gutters hollowed out at the junction of the vertical edges of the hepatic cells.
Hence, in a section of the fiver perpendicular to the capillaries of the lobule, the hepatic
cells have four sides, and their excavated angles receive a blood capillary, whereas
the bile capillaries travel over the faces, and not over the angles, of the colls.

3. The biliary eanals surrounding the hepatic lobule are formed of & thin enveloping
membrane, fined internally by cubical epithefial cells. These canals are the terminal
portions of the intralobular bifiary canalicufi. The intralobular canaficufi make their
way through the hepatic cells, forming narrow meshes. Their path is rectifinear, and
their meshes are somewhat elongated, fike those of the blood capillaries. " The bifiary
canaficufi pass between the faces of the ceUs, and consequently do not meet the
capillaries of the blood, from which they are distant by at least half the fare of a
hepatic cell."

Some doubt exists regarding the structiire of the intralobular canaficufi. Some
authors assign to them a wall of their own, formed of juxtaposed flat cells (Legros) ;
others say that they hi. ve only a borrowed wall, " formed by the condensation of the
surface of the hepatic cells into a cuticle." The hepatic cell, without a proper wall,
is said to be a simple modification of the epithefium of the bifiary canaficufi, and to
circumscribe them, after the manner of the secretory celb (Faraboeuf). In any case,
these intralobular canaficufi serve some purpose in the bifiary secretion. They receive
the bile secreted by the hepatic lobule.

4. The eonneetive tissue of the hepatic lobule is derived from Gfisson's capsule.
On the siu^ace of the fiver this envelope is formed of two layers — tho one superficial,
serous, and covered by the endothefial cells of the peritoneum ; the other deep, thicker,
and formed of fibrous tissue. From this capsule bundles of connective tissue accom-
pany the interlobar vessels, and help to fill the fissures and spaces between the lobules.

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The perilobular connective tissue, in its turn, sends out an intralobular network which
is adherent to the wall of the capillaries or extends between the capillaries in the form
of a reticulated tissue. This tissue, united with the blood capillaries, forms a woof
supporting the hepatic cells.

The perilobular lymphatie vessels form networks that accompany the portal vein.
These lymphatic vessels are probably formed by lymphatic capillaries arising in the
interior of the lobule (MacGillavry). The hepatic artery (nutrient vessel) supplies the
lobules and the walls of the veins and biliary canals.

The hepatic lobule forms an anatomical unit, but this unit in no way corresponds
to the ordination of pathological lesions. If we wish to discover our bearings in many
lesions of the liver, we must come back to the conception of Eberth, who looks upon
this organ as a tubular gland. His conception is borne out by comparative anatomy
and embryology. The hepatic lobule constitutes in the human species the anatomical
unit, but the pathological unit is the biliary lobule (Sabourin). The biliary lobule,
the liver being considered as a tubular gland, *' has as its glandular domain the paren-
chyma grouped around a portal space — a domain extending excentrically as far as the
first system of subhepatic veins. This domain is not homogeneous, because it is com-
posed of several hepatic lobules. Each hepatic lobule is, therefore, formed of distinct
segments, each one belonging to different biUary lobules " (Sabourin).

Physiology. — ^The liver performs multiple functions, some well known, others still
under study. I shall review them briefly.

1. The liver makes bile. It is not made, as was formerly held, by the biHaiy glands
contained in the bihary canals. The biliary canals, no matter what their size, are only
excretory ducts. The secretory organ of the bile is the hepatic oelL BUlgenesis is
one of the most important functions of the hepatic cell, which, bathed in the blood of
the portal vein, extracts and elaborates the primary matter of the biUary excrements.
The bile made by the cell is poured into the biliary canaliculi, which in turn lead it
into the larger excretory canals.

It is chiefly during periods of fasting that the liver accomplishes its biligenic fonction,
and it is towards the end of the meal that the excretion of bile into the intestine takes
place. Man secretes about 40 ounces of bile in twenty-four hours, but a portion is
reabsorbed. Fresh bile has a beautiful yellow colour, due to bilirubin. The first stage
of oxidation causes the yellow bile to become green, the bilirubin being converted into
bihverdin. Bilirubin is derived from the haemoglobin of the blood, which is converted
into hsematin by the bihary acids, takes up water, and loses its ferruginous elem^ts.
Haemoglobin is not present in normal bile. In the spectroscope bilirubin extends to
the left of Frauenhofer's B line.

The biliary acids are likewise formed by the hepatic cells. Cholic and oholeic acids
are eliminated as salts of soda.

The bile shares with the pancreatic juice the power of emulsification and absorp-
tion of fat. A fatty condition of the faecal matter is therefore seen in obstrnctive

As the bile passes through the intestine, it has been thought to act as an antiseptic
(Charrin and Roger).

The bile is a toxic liquid, and the intravenous injection in an animal of 5 or 6 grammes
of bile per kilogramme of weight produces convulsions and death. The toxic action
depends on the acids and colouring matter.

2. The hver makes glycogen, and the hepatic cell is charged with this important
function. The question of hepatic glycogenesis, first discussed by Claude Bemtuxi, will
be treated in greater detail under Diabetes.

The hver possesses the power of making glycogen from every kind of food. I say
every kind advisedly, because the formation of glycogen takes place in the hepatic cell,
no matter what the kind of food may be, and apart from any starch and sugar.

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Glycogen, or animal staroh, is not the simple result of a transformation, but of a
formation which is effected throughout the whole animal series by a mechanism analo-
gous to that observed in the vegetable kingdom.

The sugar, absorbed by the intestine, does not remain in the liver as sugar, but is
immediately transformed into glycogen, which is in its turn transformed into glucose,
and poured into the general circulation as the economy demands it for nutrition and
heat production.

In the formation and evolution of the immediate sugar principle there are two
distinct phenomena: (I) The creation of the amylaceous matter in the hepatic cell —
that is to say, the secretion of glycogen ; (2) the chemical phenomenon, causing this
principle to undergo successive transformations. A portion of the glycogen contained
in the cell is stored there as a reserve ration ; another portion is continually subject to
the action of a ferment produced in the liver. By this ferment the glycogen is con-
verted into glucose, which passes into the hepatic veins, and so to the whole system,
to aid in the general nutrition and production of heat. Glycogen appears to imdergo
other successive transformations (carbonic acid, lactic acid, and no doubt fat).

During hfe these two phenomena — the secretion of glycogen and its transformation
by the ferment — take place at the same time ; after death the secretion of glycogen,
which is the vital act, stops, whibt its decomposition into secondary products, which
is the chemical act, continues. Accordingly, the liver of an animal may be washed
several times, and still yield traces of glucose.

Writers have wished to make the glycogenic function general. Rougey, having
found glycogen in other tissues — in the muscles, for example — though only in small
proportions, wished to make glyoogenesis a general nutritive act, and not a particular
function of the liver. I cannot enter here into the full details of this question, but it
is certain that the presence of glycogen in the muscles, testicles, ovaries, and placenta
has not the importance formerly attributed to it. " These are phenomena subject to
all the eventualities of feeding, and to all the varieties that are observed in the acci-
dental phenomena of the economy, and must be distinguished from the constant
functions " (Claude Bernard). The constant, invariable, and necessary function has
devolved on the liver.

3. The formation of fat in the liver (I am not speaking of fatty degeneration) seems
to result from a change in the glycogen similar to the production of wax by bees which
nourish themselves on sugar, and the production of fat in geese, who, after an exclusive
diet of starch and sugar, end by having an enormous liver (Persoz). The formation
has not its exclusive seat in the liver, but this organ participates largely therein.

4. Lehmann's view that the liver is concerned in the production of the red corpuscles
is no longer admitted. It is now held that the liver is an organ in which the red cor-
puscles are destroyed.

5. The theory advanced by several authors, and notably by Murchison, that the
liver may be charged with the production of urea, has been upheld in France (Brouardel).
According to the old theory, urea, considered as a phenomenon of combustion, or as
the result of organic splitting up, was produced in the tissues of the whole economy.
According to the new theory, urea, considered as the result of organic spUtting up, is
produced exclusively in the liver. We see the deductions which result therefrom.
Pathological conditions, which exaggerate the normal functions of the organ, favour the
increased production of urea. Pathological conditions, which tend to impair or destroy
the function of the Uver (acute atrophy), produce a noticeable diminution in the quantity
of urea excreted in the urine. We shall see in the course of the following articles that
this theory is not absolutely in accordance with facts, but we must nevertheless recog-
nize that physiologicaUy the Uver takes an active part in urogenesis.

6. According to Schiff, another function of the liver is to arrest, neutraUze, or
destroy, the toxic substances absorbed in the intestine and cont-ained in the portal

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vein. The hepatic cell has to stop in part the alkaloids resulting from the putrid
fermentation that goes on during intestinal digestion.

** In the intestine infection is constant. In every man and at every hour the agents
of intestinal putrefaction are found in the intestinal cavity giving hirth to toxic products
which the intestine ahsorbs, and intoxication in various degrees is extremely frequent.
If this intoxication is not more frequent, or if it is not of daily occurrence, it is because
the organism is suppUed with the means of self -protection. The liver arrests, destroys,
or converts a part of the poisons absorbed by the intestine ; the blood bums a part, and
the kidneys eUminate the surplus " (Bouohe^).

** The poisons of the gastro-intestinal tract are to a large extent produced by
microbes which decompose the tertiary and quaternary substances of food. On the
other hand, these very microbes produce toxines, so that infection and intoxication are
thus intimately connected " (Hanot).

" The intestine is generally the open door for the poisons of intoxication, but the
liver protects the organism by arresting the passage of the poisons in order to neutralize
them or to return them into the intestine " (Bouchard).

** The liver, then, is not only the storehouse for the organism : it is also the advance
fortress against intoxication. The recognition of the antitoxic power of the liver and
of the auto -intoxication of intestinal origin show the pathological relations between the
liver and the intestine " (Hanot). The Hver arrests the vegetable alkaloids (morphia,
quinine, curare) in the proportion of 50 per cent. It arrests the toxic substances of
the bile which have been reabsorbed into the intestine.


The extreme vascularity of the liver and the richness of its double
system of capillaries, interposed between the general venous circulation
and the heart, are favourable to congestion. In congestion of the liver,
as in that of the lungs, or of the other viscera, we have not to describe a
definite morbid entity, but only a morbid condition, made up of dissimilar
elements. This chapter in pathology is therefore an enumeration of facta,
most of which have no connection one with another, and in order to group
these facts it is customary to unite them into active and passive congestion.
The latter has acquired such an importance in connection with "the
cardiac liver " that I shall devote a special section to it« description.

Active Congestion. — Active congestion is caused by an excess of
pressure in the afferent vessels (portal veins). The fullness of these vefwels
causes a marked increase in the size of the liver. Heavy meals, errors of
diet, alcoholic excess, and purgatives, modify the portal circulation and
stimulate the hepatic cells, causing vaso-dilatation and congestion. I may
say the same of affections of the small intestine (tuberculosis) and of the
colon (dysentery), in which case the portal blood carries irritating substances
(microbes or toxines) to the liver. Congestion of the liver is frequent in
the intermittent fevers and in the bilious remittent fevers of hot countries
(Dutrouleau). It forms the first stage in certain diseases of the organ
(cirrhosis, hepatitis). Suppression of the menses or of a hc&morrhoidal flux

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may cause congestion of the liver. An attack of gout is sometimes preceded
by congestion of the liver.

Amongst the causes which produce congestion of the liver, I may mention
dyspeptic troubles and auto-intoxication of gastro-intestinal origin.

Dilatation of the stomach enters into the pathogenesis of hepatic con-
gestion. " In 389 personal observations of dilatation of the stomach,"
says Bouchard, " I found swelling of the liver in the proportion of 23 per

Congestion of the liver shows itself by a feeling of discomfort and heavi-
ness in the right hypochondrium. Slight jaundice may be present, and the
urine contains urobilin or biliary pigments. The liver is tender on pressure,
and can be felt beyond the false ribs. Percussion gives an increase of several
centimetres in the vertical diameter. This swelling increases or diminishes ;
it Ls subject to recurrences, and is sometimes the first stage of a commencing

The treatment of hepatic congestion varies according to the cause.


Pathogenesis. — Passive congestion of the Uver is caused by increased
pressure in the efferent vessels (sublobular veins, vena cava). This venous
stasis is due to many causes — diseases of the heart (lesions of the mitral
and tricuspid valves), diseases of the lungs, which diminish the field of
hsematosis (emphysema and fibrosis), intrathoracic tumours, which impede
the circulation in the inferior vena cava — but the most frequent causes
are lesioas of the mitral valve and changes in the cardiac muscle. When
mitral lesions are ill-compensated, when the cardiac muscle Ls affected, and
the left auricle is not completely emptied, there results an obstruction
which extends throughout the whole of the lesser circulation to the vessels
of the lungs, the right ventricle, and the right auricle. This blood-stasis
hinders the return circulation in the inferior vena cava, and the hepatic veins
and causes congestion of the Uver. This congestion, which is at first
temporary, ends by becoming permanent, and causes the anatomical changes
of the cardiac liver.

The value of this mechanical theory for the cardiac liver, as created by
Beau and Gendrin, must not be exaggerated. Defective hydraulics, due to
the cardiac lesion, certainly play a large part in the determination of the
hepatic changes, but the mechanical obstacle to the circulation is not the
only cause. It is not rare to find people suffering from disease of the heart
in whom the liver is attacked before the intermediary circulation — that of
the lungs, for instance — and before the peripheral circulation (oedema of
the legs) has been influenced by the cardiac lesion. In such a case it might

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be held that the liver, having, under the influence of multiple causes, become
an organ of minoris resistetUiWy is more liable than the other organs to
feel the cardiac lesions.

These considerations are absolutely applicable to the auto-intoxications
of intestinal origin, prolonged gastro-intestinal dyspepsia, alcoholism,
malaria, gall-stones, and more or less general arterio-sclerosis. The liver
withstands the effect of the cardiac lesions the better as it is prepared by
its relations.

Symptoms. — The clinical picture of the cardiac liver varies. Let us
select the most common types. In one variety the cardiac lesion is not
advanced. The patient suffers sUghtly from palpitation, and can neither
ascend a staircase nor walk quickly without getting out of breath. Malleolar
oedema is common, but there are as yet no serious symptoms. Later, in
consequence of fatigue, of excesses in the use of drink and food, or even
without any appreciable cause, the patient suddenly experiences digestive
troubles, distension of the belly, and a feeling of weight in the liver. He
complains of sharp pains in the right hypochondrium, and has " a weight
on his stomach." The dyspnoea and the cardiac arrhythmia grow worse,
as if the liver, in its turn, reacted on the cardio-pulmonary circulation
(Potain). On examining the patient, we notice a yellowish tint of the con-

Online LibraryGeorges DieulafoyA text-book of medicine, Volume 1 → online text (page 107 of 129)