Part 3

The congested condition of any gland is unfavourable to secretion. We all know, for example, that congestion of the kidney is accompanied by a suppression of the urinary secretion, and that the secretion is re-established as the congested condition of the organ diminishes. The suppression of the renal secretion is no doubt due to the engorged capillaries pressing upon the secreting structure, and ultimate ramifications of the urine tubes, and thereby annulling their functions. A similar explanation is equally applicable to the biliary secretion; and just as it happens in the case of the kidney, that it is exceedingly rare for a total suppression of its functions to take place, so with the liver it seldom happens that the congestion is sufficiently severe to induce complete arrest of the biliary secretion. We find, therefore, that although there may be yellowness of the skin and high-coloured urine in such cases, pipe-clay stools are frequently absent, sufficient bile to tinge the fæces still finding its way into the intestines.

Undoubtedly it must have occurred to many of my readers, that jaundice 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:--