is frequently absent in {26} cases of acute inflammation of the liver,
even running on to suppuration, and that the foregoing theory of the
pathology of such cases is therefore insufficient. At one time I was
puzzled to explain this apparent anomaly, but on subsequent
investigation the true cause became apparent, and instead of the above
fact detracting from, it tended rather to strengthen the theory. If,
for example, we closely examine cases of acute hepatitis without
jaundice, we find they are those in which only a portion of the liver
is affected. It matters not whether it be one lobe or two, the surface
or the centre of the organ, the disease is invariably circumscribed;
and there is enough hepatic tissue left in a sufficiently normal
condition to prevent the constituents of the bile accumulating in the
blood, and producing jaundice. This may even occur, as I have myself
observed, when the disease has run on to suppuration.
The most typical example of jaundice as the result of active
congestion, is to be found in those cases where it supervenes on an
attack of hepatitis, such as is met with in hot climates, where
indolent habits and high living favour portal congestion. It is
occasionally met with in England, however, and is frequently associated
with gastric derangement.
I had occasion to witness a good example of {27} this form of disease
in the person of a French gentleman, who was brought to me seven days
after his arrival in England, on account of his skin having assumed a
most intense yellow hue. It appeared that he had come to England on a
visit to some of his friends, and rather enjoying the novelty of an
English table, indulged too freely in a quantity and quality of food to
which he had hitherto been a stranger. The consequence was, that within
three days after his arrival he began to suffer from hepatic
tenderness, and dyspeptic symptoms; the skin at the same time assumed a
dusky hue, which soon merged into a decided yellowness. These symptoms
were accompanied by pipe-clay stools and saffron-coloured urine; on the
latter being tested it gave a distinct bile pigment, but no bile acid
reaction--a point which I shall afterwards have occasion to show, is of
a certain diagnostic value in obscure cases of jaundice. This
gentleman, under the influence of benzoic acid, perfectly recovered his
normal complexion in the short space of a week.
There is another form of jaundice from active congestion, viz., that
due to the presence of zymotic disease, such as ague, typhus, and other
fevers. As an illustration of this kind of affection, I shall cite one
arising from the first of these causes, namely, ague. And the best
example I {28} can give is one that has recently fallen under my
notice, and which occurred in the person of a member of our own
profession. The gentleman was for several years surgeon to one of our
large colonial hospitals, but in consequence of repeated attacks of
intermittent fever, was forced to resign the appointment, as well as a
lucrative practice, and return to England. He has now been at home for
two years, and although his general health has much improved, still
suffers from occasional attacks of his old enemy. On consulting me
regarding his case several months ago, he mentioned, that while
suffering from the above-named attacks, he occasionally suddenly passed
five or six ounces of urine as dark as chocolate, and this would recur
perhaps once in twenty-four hours, during two or three days, and then
as suddenly disappear. This urinary symptom being an unusual one, I
requested him to send me on the next occasion a specimen of the fluid.
In the beginning of last November[9] I received three samples of urine,
one passed at eight A.M., which was clear, pale, of a specific gravity
of 1025, of an acid reaction, deposited no lithates, and contained no
albumen, being in fact normal in every respect; another quantity passed
at two P.M., of {29} a chocolate brown colour, opaque, turbid, having a
specific gravity of 1032, of an acid reaction, depositing lithates,
containing albumen,[10] some sugar, and a large excess of urea (3·6 per
cent.) and urohæmatine; a third sample passed at night, of a specific
gravity of 1021, also with an acid reaction, depositing lithates in
small quantity, but containing no albumen. The percentage of urea in
this urine was exactly one-half (namely, 1·8) of what it was in the
preceding specimen passed at two P.M.
[Footnote 9: This was written last year, and therefore refers to
November, 1861.]
[Footnote 10: When examined with the microscope, this specimen of urine
was found to contain a large quantity of nucleated epithelium, and
granular cells; free granules of a hæmatine colour, granular
tube-casts, and a quantity of mucus; while the morning and evening
urines were perfectly free of any such substances.]
The varying conditions of these three urines clearly pointed to intense
congestion of the chylopoietic viscera, of a transient and periodic
character. Suiting the practice to the theory, mercurials were taken by
this gentleman in order to remove the congestion of the chylopoietic
viscera, and with the most favourable results, for, as I afterwards
learned, the jaundice and other disagreeable symptoms soon disappeared.
_Jaundice the Result of Passive Congestion of the Liver._
In this case the congestion, instead of arising from an increased flow
of blood to the liver, as {30} in the preceding, is the result of some
cause impeding the outward flow of blood from the liver. Thus for
example, passive hepatic congestion may arise from valvular disease of
the heart, or from any pulmonary affection obstructing the circulation
of blood through the lungs (pneumonia, &c.). Jaundice from the passive
form of hepatic congestion, is not so common as jaundice from the
active form, in consequence of the former being, as a rule, much
slighter than the latter. Its pathology is, however, I believe, exactly
the same, viz. the result of the engorged hepatic capillaries
compressing the secreting cells and tubes, and thereby annulling their
functions. Such being the case, it is unnecessary for me to do more
than merely allude to this cause of jaundice.
It may, perhaps, be asked--"If the foregoing statements regarding the
pathology of jaundice from congestion be correct, how does it happen
that it is not present in every severe case of gastric derangement,
fever, heart-disease, &c.?" This question is easily answered, for as
Dr. Budd has clearly put it, while speaking of the action of medicines
upon the liver--"In most persons, perhaps, a portion of the liver may
waste or become less active without sensible derangement of health,
they have more liver, as they have more lung, than is absolutely
necessary. In others, on the {31} contrary, the liver, from natural
conformation, seems just capable of effecting its purpose under
favourable circumstances." Persons inheriting this feebleness of liver,
"or in whom, in consequence of disease, a portion of the liver has
atrophied, or the secreting element of the liver has been damaged, may
suffer little inconvenience as long as they are placed in favourable
circumstances, and observe those rules which such a condition
requires;" but as soon as the balance of their hepatic circulation is
disturbed by causes like those above mentioned, jaundice makes its
appearance; such patients being, as Dr. Budd says, "born with a
tendency to bilious derangements."[11]
[Footnote 11: Diseases of the Liver, p. 55.]
JAUNDICE AS A RESULT OF SUPPRESSION CONSEQUENT UPON ABSENCE OF THE
SECRETING SUBSTANCE.
The pathology of this state is self-evident, for wherever secreting
substance is wanting, secretion cannot take place. If then, the tissue
which secretes bile be destroyed or transformed by disease, the biliary
function must be suspended, and the ingredients which it is the office
of such structure to separate from the blood, will accumulate in the
circulation, and give rise to the {32} usual chain of results following
suppression of the biliary secretion.
In cancer, tubercle, fatty and amyloid degeneration of the liver,
jaundice arises from the above-named cause. In these diseases it is
not, however, a constant symptom, and this is simply on account of
there being usually sufficient healthy tissue left to enable the
biliary secretion to be carried on. If the cancer, or other morbid
product, occupied the whole place of the secreting tissue, the biliary
function could no more be carried on by such product, than by the same
product occupying another organ of the body. In cases of jaundice
arising from absence of the secreting substance, the amount of the
jaundice depends on another cause besides the mere extent of the morbid
deposit. This is its situation. A large amount of diseased tissue may
exist in certain portions of the liver, and yet fail to produce
jaundice, while a much smaller amount of the same diseased tissue,
placed in another situation, may induce it. Should the morbid deposit,
for example, be so placed as readily to interrupt the flow of the
secreted bile, jaundice may rapidly occur, and be due as much to the
re-absorption of the secreted bile, as to the suppression of the
biliary secretion. This is, indeed, the true explanation of the fact,
that diseases affecting the {33} concave, are much more frequently
accompanied with jaundice, than those attacking the convex surface of
the liver. I might have chosen what at first sight appears a more
typical example of absence of secreting structure, namely, a case of
acute atrophy of the liver; for in such cases the hepatic tissues
sometimes dwindle down in the course of a few days to less than a
quarter of their original bulk, and give rise to intense jaundice. But
in such cases there does not appear to be a total arrest of the
secretion, until the very last stage of the disease, if it even occurs
then; and besides, if I dare form an opinion from one case, I should
say that, in consequence of the rapid disorganization of the parenchyma
of the liver, the circulation in the organ becomes much disturbed, and
gives rise to what Frerichs terms disordered diffusion. So that in
cases of acute atrophy of the liver, the jaundice, although chiefly due
to suppression, is complicated with re-absorption of the bile, as was
proved in a case I examined, by finding in the urine, not only those
products which are merely excreted from the blood, but also some of
those which are generated in the liver itself. It will be necessary for
me, therefore, to go more fully into this form of jaundice than I have
done in any of the preceding forms of the disease.
{34} JAUNDICE ARISING FROM ACUTE ATROPHY OF THE LIVER.
Acute, or yellow atrophy of the liver, is one of the most formidable of
human diseases. It is sudden in its onset, rapid in its course, fatal
in its termination. It is more common in women than in men; seldom
attacks those above thirty years of age, and occurs most frequently in
the earlier months of pregnancy. The immediate exciting cause of this
strange disease appears to be, in the majority of cases, mental
depression. The symptoms usually observed are jaundice, rapidly
followed by sickness, and vomiting; by febrile excitement, and cerebral
disturbance.
As the disease advances, the hepatic dulness diminishes; the urine
becomes scanty, and high-coloured; the bowels confined. Extravasations
of blood take place under the skin; and hæmorrhages from the nose,
vagina, or bowels are frequently observed. Lastly, delirium, or coma,
generally closes the scene, within a week after the commencement of the
violent symptoms, and within a month after the appearance of simple
jaundice. Frerichs, who has so well described these cases, even says,
"that in the severest forms, the disease may run its course, and end
fatally within twenty-four hours."[12]
[Footnote 12: "Clinical Treatises on Diseases of the Liver," vol. i. p.
197.]
{35} All cases of acute atrophy of the liver are, fortunately, not
necessarily fatal. In some the violent symptoms gradually disappear,
and recovery takes place after free evacuation of the bowels.
In every case of suspected acute atrophy of the liver, the urine ought
to be carefully examined for tyrosine, and leucine, two abnormal
products, which, according to Frerichs, are never absent. Some remarks
on the diagnostic value of these substances will be found at page 62.
Through the kindness of Dr. Wilks, I had the opportunity of examining
the liver, and analysing the urine, in a typical case of acute atrophy,
which he reported in the Pathological Society's "Transactions," vol.
xiii. p. 107. The brief history of the case is as follows:--E. K., aged
seventeen, a married woman, in the third month of pregnancy, was seized
with a bilious attack, and jaundice, after having a violent quarrel
with her husband, who accused her with infidelity. The patient was
first under the care of Mr. Bisshopp, of South Lambeth, who found her
suffering from jaundice, accompanied by some febrile symptoms, and
vomiting. In two days she became delirious, had violent screaming, and
convulsive fits, which were rapidly followed by unconsciousness. Next
day the patient was seen by Dr. Wilks; she was then quite insensible,
with slight stertorous breathing, {36} and foam on the lips. The pupils
were moderately dilated, and sensible to light. The pulse 120. The
hepatic dulness reduced to a narrow band over the lower ribs. No urine
had passed for twenty-four hours; a catheter was therefore introduced,
and twelve ounces of clear bilious-looking fluid were drawn off. This
urine I had the opportunity of analysing a few days afterwards. It was
then of a yellow-ochre colour, and contained a considerable deposit.
The analysis gave:
Specific gravity . . . . . . . . . . . . . 1028
Reaction . . . . . . . . . . . . . . . . . acid (?)
IN 1000 PARTS.
Water . . . . . . . . . . . . 948·860
Solids (organic, inorganic) . 51·138
=======
Urea . . . . . . . . . . . . . . . . . . . 30·000
Uric acid . . . . . . . . . . . . . . . . 0·375
Resin and mucus . . . . . . . . . |
Bile, colouring matter, and acids |
Urohæmatine . . . . . . . . . . . | . . . 14·575
Leucine, and tyrosine . . . . . . |
Inorganic salts . . . . . . . . . . . . . 6·188
======
The biliary acids (contrary to what Frerichs found in some of his
cases) were present in this urine in fair quantity. With Pettenkofer's
test (sulphuric acid and sugar) a decided purple colour was obtained.
{37} When a portion of the urine was concentrated, and allowed to
crystallize slowly, beautiful crystals of both tyrosine, and leucine
were detected in it by means of the microscope. The purified urine also
showed the presence of sugar in small quantity. When the organic solids
were burned, they had a strong odour, and gave off a smoky _flame_,
thereby showing that the urine contained a considerable quantity of
fatty resin.
As calculating the constituents of the urine by _percentage_ is a very
unsatisfactory method for scientific purposes, it may be useful for me
to give the analysis of the same urine as calculated for twenty-four
hours, viz., twelve ounces, the amount drawn from the bladder shortly
before death. In that case the analysis gives:
24 HOURS' URINE.
Quantity . . . . . . . . . . . . . 372·00 c.c.
Specific gravity . . . . . . . . . 1028
Reaction . . . . . . . . . . . . . acid (?)
Solids (total) . . . . . . . . . . 19·038 grammes.
Urea . . . . . . . . . . . . . . . 11·160 "
Uric acid . . . . . . . . . . . . 0·139 "
Resin, and mucus . . . . . . |
Bile pigment, and acids . . |
Urohæmatine . . . . . . . . | . . 5·441 "
Tyrosine, and leucine . . . |
Inorganic salts . . . . . . . . . 2·298 "
======
During the night before her death, the patient {38} aborted, and lost a
considerable quantity of blood by the vagina. The whole duration of the
disease was merely six days, and the more urgent symptoms only
manifested themselves two days before the fatal termination.
After death the liver was found to be very small in size, not
exceeding, as was supposed, 1½ pound in weight. It was deeply stained
yellow, and its cells were found to be small, and broken up; not an
entire cell could be detected by either Dr. Wilks or myself--nothing,
indeed, but a quantity of _débris_ of hepatic tissue, and fat. The
gall-bladder was contracted, and contained only a little mucus; the
urinary-bladder was empty.
Although jaundice the result of acute atrophy of the liver, might be
thought to be a typical example of jaundice arising from a suppression
of the biliary function--the diminution in secreting substance
naturally inducing a diminution in secreting power--I have, as was
before said, been led to view it differently; because, although less
bile than usual is secreted, there is nevertheless nothing like an
entire suppression of the biliary function, as is proved,--
Firstly,--By the absence of pipe-clay stools.
Secondly,--By the deep staining of the hepatic tissue with bile
pigment, just as occurs in jaundice the result of obstruction.
{39} Thirdly,--By the presence of the biliary acids in the urine.
Fourthly,--and lastly, the violent symptoms of bile-poisoning lead to
the same conclusion, for it is not bile pigment, but the bile acids,
that induce the fatal symptoms of bile-poisoning.[13]
[Footnote 13: Six grains of pure glycocholate of soda killed a small
dog, into whose femoral vein I injected it, in the course of two hours.
In experimenting on animals, I have made the curious observation, that
although bile has the property of retarding or arresting putrefaction,
both in the intestinal canal, and out of the body, yet, when injected
into the subcutaneous cellular tissue of a healthy animal, it causes
the surrounding tissues to decompose, and become foetid, and an
artificial disease is thereby set up, whose most peculiar feature is
the engendering of a rapid putrefaction of the body after death.]
CLASS B.
THE MECHANISM OF JAUNDICE ARISING FROM THE RE-ABSORPTION OF THE
SECRETED, BUT RETAINED BILE.
In cases of this kind, the obstruction is not usually to be found
within the liver itself, but in the ducts after their exit from the
hepatic organ. The seat of the obstruction, too, is much more
frequently found near to, or at the termination of the common duct,
than close to the liver. The obstruction may be of three kinds:--
{40} Firstly,--A congenital deficiency of the bile-ducts.
Secondly,--An accidental obstruction in the course of the ducts, as
from gall-stones, hydatids, or the entrance of foreign bodies from the
intestines.
Thirdly,--From closure of the outlet of the common duct, as, for
example, from the pressure of the pregnant uterus, or distended
transverse colon, or from organic disease of the pancreas, or
neighbouring organs.
First, as regards cases of jaundice from congenital deficiency of the
ducts. Cases of this kind are rare. The best with which I am acquainted
is the one that was brought before the Pathological Society last year,
by Dr. Wilks. "The child had never passed any meconium, the motions
always being of a white colour. When a fortnight old, jaundice came on,
and continued until death, at the age of six weeks. After death, the
liver was found of a dark green colour, and, apparently, the
gall-bladder was absent. On further examination, however, the cellular
tissue, which appeared to occupy its place, was found to be occupied by
a small canal, just large enough to contain a bristle; to this,
however, no outlet could be found, and on endeavouring to discover the
hepatic ducts, these, in like manner, could not be made {41} out. The
opening of the common duct in the duodenum was natural, but no hepatic
duct could be found joining the pancreatic. It appeared, therefore, as
if the larger ducts had become shrunken and obliterated."[14]
[Footnote 14: "Medical Times and Gazette," 29th March, 1862.]
Through the kindness of Dr. Wilks, I had the opportunity of making a
microscopical examination of the liver. The hepatic cells were very
small in size, much broken up; very few possessed nuclei, and all were
deeply tinged with brownish yellow colouring matter. Scattered
throughout the hepatic tissue, I found numbers of well-formed
cholesterine crystals, like those represented in Fig. 3.
I must here mention, that jaundice does not necessarily follow upon
absence of the gall-bladder; just as in the horse, the deer, the rat,
and other animals that possess no gall-bladders, the biliary function
is perfectly well carried on, so it may be in the human subject,
labouring under a congenital or accidental deficiency of the
gall-bladder. In such cases, the hepatic ducts are pervious, and
consequently the secreted bile finds no difficulty in reaching the
intestines. In the "Edinburgh Medical Journal" (May, 1861, p. 1045,)
Dr. Alexander Simpson reports a case of {42} this kind occurring in a
child, which died when only a few weeks old. There was no trace of the
existence of a gall-bladder; but on laying open the duodenum, the
orifice of the bile-duct was at once seen in its ordinary situation,
and a drop of pale bile was expressed from it. On tracing the duct to
the liver, it was found to pass up undivided into the horizontal
fissure, where it at once broke up and branched into the hepatic tissue
of the right, and left lobes.
I shall delay entering into an explanation of the mechanism of jaundice
from obstruction, until I come to the consideration of what may be
termed _Permanent Jaundice_, as in that case one explanation will do
for all.
JAUNDICE AS A RESULT OF THE ACCIDENTAL OBSTRUCTION OF THE BILE-DUCTS.
The second class of cases, namely, those in which the obstruction is in
the course of the ducts, are of frequent occurrence, and in them the
jaundiced state is usually merely transient, for no sooner has the
obstruction been removed, than the jaundice begins to disappear. The
most common cases of this kind are those arising from gall-stones. As
every one is familiar with their history, I may merely mention, that we
may have gall-stones, and even all the most painful {43} symptoms of
gall-stones, without the slightest trace of jaundice. This, I believe,
arises in the following manner:--
Firstly,--The majority of gall-stones are formed in the gall-bladder;
their formation being due to the accidental deposition of the less
soluble parts of the bile, either as a consequence of these ingredients
being present in excess, or in consequence of the solvent, whose duty
it is to retain them in solution, being in reduced quantity. The
deposition or formation of gall-stones follows exactly the same law as
the deposition or formation of stone in the bladder.
Secondly,--In some cases the gall-stone, or stones--for there may be
many, even hundreds, remain in the gall-bladder during the whole life
of the individual, without giving rise to any disagreeable results,
either as regards pain, or jaundice. In other cases, the
gall-stones--and this usually happens when they are small--get into the
cystic duct, and become lodged there; and in such a case, although the
patient may suffer intense pain, there is still no jaundice. Moreover,
it is not until the stone or stones have passed down into the common
bile-duct, that jaundice is at all likely to be induced by them. For
while a stone remains in the cystic duct, although it may completely
block it up, and effectually prevent the bile either {44} entering into
or escaping from the gall-bladder, yet, as in this situation it cannot
offer any obstacle to the direct flow of the biliary secretion from the
hepatic tissue into the intestines, there is no retention, and
consequent absorption of bile. In fact, the presence of the stone in
this position, in as far as the biliary function is concerned, only
reduces the patient to the state of a person in whom the gall-bladder
is accidentally absent; or to that of a horse, or other animal, in
which the absence of the gall-bladder is a normal condition.
Thirdly,--There are yet other ways in which gall-stones may give rise
to great discomfort, and even imperil life, without inducing jaundice.
For example, a calculus may remain in the gall-bladder until it attains
a very large size, and then ulcerate its way into the stomach,
intestines,[15] peritoneal cavity, or even out of the body through an
opening in the abdominal parietes.[16]
[Footnote 15: _Vide_ a case of this kind published by the author in the
Pathological Society's "Transactions" for 1857, p. 235.]
[Footnote 16: _Vide_ a case published by Mr. Hinton in the "Brit. Med.
Journ." of August 4th, 1860, p. 603, and one by Mr. Sympson in the same
Journal of the 7th February, 1863, p. 139.]