Chapter II: Introduction (1)

Having entitled this monograph "Jaundice, its Pathology and Treatment," it may, perhaps, be necessary for me to state at the beginning that by so doing it is not to be supposed that I regard jaundice as a disease _per se_. On the contrary, I look upon it in the same light as I do albuminuria, which is not of itself a disease, but only the most prominent symptom of several widely-differing pathological conditions. So also the peculiar state of body characterised by yellow skin, saffron-coloured urine, and pipe-clay stools, is itself but a symptom of morbid action. It may be asked, "Then why do you treat of jaundice as if it were a disease?" To this I reply, "Because, although {2} the condition called jaundice be merely a manifestation of morbid action, and one, too, requiring neither skill nor experience to detect, the proper comprehension of its true mechanism is of much practical importance to the physician, for without this knowledge it is impossible for him to treat it with any chance of success. Nay, even the remedies for jaundice become dangerous weapons, if unskilfully applied." In fact, it is almost unnecessary to apologise for treating of jaundice as a disease _per se_; for, notwithstanding all that has been written upon the subject, it is universally admitted that the simplicity of its diagnosis is only equalled by the obscurity of its pathology, and the uncertainty of its treatment; and no one at all conversant with the literature of jaundice can be in the least degree surprised at this statement. On the contrary, on glancing at the immense variety of morbid states, and known pathological conditions with which it is associated, he cannot fail to admit its truth.

Some of the pathological conditions are closely allied; others are widely separated--so widely, indeed, that at first sight it is impossible to discover from whence emanates the common symptom. We find jaundice connected with diseases of the liver, of the neighbouring organs, and of the general system. In some diseased conditions, {3} jaundice presents itself when least expected. At other times it is absent when, apparently, it ought to be present. On the other hand, again, there are cases in which jaundice is evidently merely a symptom, and others in which it seems to be in itself the disease. We have temporary jaundice from transient derangements, and we have permanent jaundice from stationary causes. There are cases in which the cause of jaundice is visible after death to the naked eye. There are others where the minutest research is baffled in ascertaining the cause. That this is no exaggerated view of the case the following table will show:--

JAUNDICE IS MET WITH,
Firstly, IN DISEASES AFFECTING THE LIVER--
_(a)_ Cancer.
_(b)_ Tubercle.
_(c)_ Cirrhosis.
_(d)_ Inflammation.
_(e)_ Atrophy.
_(f)_ Amyloid, and
_(g)_ Fatty degeneration.

Secondly, IN DISEASES OF THE BILE-DUCTS--
_(a)_ Congenital deficiency.
_(b)_ Accidental obstruction. The latter arising from gall-stones,
hydatids, foreign bodies {4} (such as cherry-stones and
entozoa) entering from the intestines.
_(c)_ Ulcer of the duodenum.
_(d)_ Tumours of the pancreas.

Thirdly, IN AFFECTIONS OF OTHER ORGANS OF THE BODY EXERTING AN
INFLUENCE ON THE BILIARY SECRETION--
_(a)_ Diseases of the nervous system.
_(b)_ Diseases of the lungs.
_(c)_ Diseases of the heart.
_(d)_ Imperfect establishment of the extra-uterine circulation
(infantile jaundice).
_(e)_ Dyspepsia.
_(f)_ Torpidity of the bowels, and consequent accumulation of fæces
in transverse colon.
_(g)_ Pregnancy.

Fourthly, IN A VARIETY OF ZYMOTIC DISEASES--
_(a)_ Typhus.
_(b)_ Yellow fever.
_(c)_ Ague.
_(d)_ Pyæmia.
_(e)_ Epidemic jaundice.

Fifthly, AS A RESULT OF THE INJURIOUS EFFECTS OF CERTAIN POISONS--
_(a)_ Snake bites. {5}
_(b)_ Alcohol.
_(c)_ Chloroform, etc.

Can it be wondered, then, that a state so easily diagnosed is nevertheless so difficult to comprehend?

Notwithstanding the apparent incongruity of the diseases with which the one common symptom of jaundice is associated, I trust to be able to reconcile these discrepancies, and prove that the seeming discord is but "harmony not understood."

All physicians, I think, admit that the peculiar state of the system to which the name of jaundice has been applied, is essentially due to some derangement of the biliary function, the exact nature of the derangement being alone the point of contention. I need not, therefore, waste the time of my readers, either by giving an account of the literature or a detail of the symptoms of jaundice. Even in discussing its pathology, I shall strictly limit myself to the consideration of the opinions at present held by the more advanced of our pathologists; the object of this monograph being, not to pourtray the views of others, but to give a brief _exposé_ of my own, and to point out how modern physiology, and chemistry have not only thrown a new light on its pathology, but have also given us a clue to its successful treatment.

{6} Frerichs, the most recent writer on this subject, in his elaborate treatise on diseases of the liver, says that jaundice may result from one of the three following conditions:--

Firstly,--Obstruction to the escape of bile.

Secondly,--Diminished circulation of blood in the liver, and consequent abnormal diffusion; both of these conditions giving rise to an increased imbibition of bile into the blood, and in both cases the liver being more or less directly implicated.

Thirdly,--Obstructed metamorphosis, or a diminished consumption of bile in the blood.[1]

[Footnote 1: Frerichs' "Clinical Treatises on Diseases of the Liver." New Sydenham Society's Translation, vol. i. p. 93.]

From this it is seen, that the pathology of jaundice, according to Frerichs, is very different from what we were formerly taught. For while he has entirely laid aside the theory of jaundice as a result of suppressed secretion, he has introduced two perfectly new elements--namely, abnormal diffusion, and diminished consumption. The latter theory, being, of course, founded on the supposition that bile, after playing its part in the digestive process, is re-absorbed into the circulation, again to perform another function in the animal economy, before its final excretion from the organism as effete matter. The theory of jaundice, hitherto most favoured in England, and which found {7} such an able exponent in Dr. Budd, is, that the disease may arise in two ways--firstly, by a mechanical obstruction to the passage of bile into the intestines, and the consequent re-absorption of the detained fluid into the blood; and secondly, by a suppression of the biliary secretion arising from some morbid condition of the liver itself, whereby the biliary ingredients accumulate in the circulation. Now, although I am not prepared to admit the justice of the views held regarding the origin and function of bile, on which these opinions are based, I nevertheless believe that in the following pages I shall be able, by the aid of modern medical science, to prove the correctness of the conclusions themselves. In order to do this, however, it will be necessary for me to begin by making a few remarks on the nature of bile, and the physiology of its secretion.

ON THE NATURE OF BILE.

In a few words, bile may be said to be composed of the following substances:--

Firstly,--Biliverdine, a green nitrogenized, non-crystallizable colouring matter, analogous to the green colouring matter of plants, and like it, leaving on incineration a distinctly ferruginous ash. This colouring matter appears, like {8} urohæmatine, and all other animal pigments, to be a direct derivative of the colouring matter of the blood.[2]

[Footnote 2: _Vide_ papers by the author on the colouring matter of the urine, Pharm. Journ., November, 1852. "Urohæmatine, and its combination with animal resin." Verh. d. Phys.-Med. Gesellschaft zu Wurzburg, Bd. V. 1854.]

Secondly,--Two peculiar substances, named respectively, glycocholic, and taurocholic acid--the former yielding, when in combination with soda, a crystallizable, the latter a non-crystallizable salt. Taurocholic differs still further from glycocholic acid, in containing a large percentage of sulphur, {9} and being, under the influence of hydrochloric acid, convertible into taurine, a beautiful white crystalline substance.

Thirdly,--Cholesterine, a crystalline, fatty matter, not, however, peculiar to bile, but found in various tissues, and secretions of the body.

{10} Fourthly,--A brown resinous substance resembling, in appearance and consistence, shoemaker's wax.

Fifthly,--Among the constituents of the bile, I may mention sugar, for both in the normal bile of man, and of the lower animals, the ox, and the dog, I have detected that substance. On one occasion, I even found torulæ in the bile twenty-four hours after its removal from the gall-bladder of a healthy dog.

Sixthly, and lastly,--a quantity of inorganic matter, consisting chiefly of soda, potash, and iron.

The specific gravity of bile fluctuates, of course, with the percentage of solid matter it contains. From my own observations, I consider that healthy human bile has an average specific gravity of 1020, and contains about six per cent. of solid matter, five per cent. of which is organic, and one per cent. inorganic substance. When fresh, bile is almost neutral; but it rapidly undergoes decomposition, and becomes alkaline.

In colour, human bile is usually of a brownish yellow hue; the colour, however, varies with its degree of concentration, the kind of food taken, and the state of the system. As regards the effect of food, if we may be allowed to form an opinion from experiments on dogs, it may be said that, as a {11} rule, animal food tends to give bile a yellow, vegetable food a green, tint.

Next, as regards the manner in which bile is secreted. For a long time it was thought, and, indeed, some people still think, that bile exists pre-formed in the blood, and that the liver only excretes it, as the kidneys excrete the urinary ingredients. Another class, running to the opposite extreme, believe that the liver is not merely the excretive, but also the formative organ of the bile. It appears to me, however, that neither of these extreme views is correct, and that the truth lies between the two.

It is, in fact, not at all difficult to prove that the liver manufactures certain biliary constituents, while it merely excretes others. Thus, for example, the two substances glycocholic and taurocholic acids are never to be found either in the blood, tissues, or fluids of the healthy organism, with the single exception of those of the liver and gall-bladder; and after extirpation of the liver neither acid is to be found in the body at all. On the other hand, such substances as cholesterine and biliverdine, are not peculiar to the liver or its secretion, but are the products of several organs, and are always to be detected in the blood, independently of the presence or absence of the liver. These facts, therefore, clearly show that the liver {12} is both a formative and excretive organ to some, and an excretive only to others, of the biliary constituents.

Lastly, the general opinion is that the secretion intermits, and, like the gastric, and pancreatic juices, bile is only formed during digestion. Were it so, however, where would be the necessity for a gall-bladder? Is it not to store up the secretion formed in the intervals of digestion, and to retain it until it is required? No doubt there are several animals, such as the horse, and the deer, that possess no gall-bladders; but there is undoubtedly in them some special arrangement of the digestive apparatus, rendering the presence of a gall-bladder unnecessary. In fact, it is easily shown that the biliary secretion in ordinary cases is continuous; for if in an animal possessing a gall-bladder a biliary fistula be established, and the secretion of bile carefully watched, it will be found that at no period of the day does it entirely intermit, although it is more active at one time than at another, the minimum of its activity being during sleep--the maximum during active digestion. The absolute quantity of bile secreted in the twenty-four hours is tolerably uniform, although the daily amount is slightly influenced by the kind of food.[3]

[Footnote 3: Arnold found that dogs secreted more bile on a bread, than on an animal diet. "Zur Physiologie der Galle," Mannheim, 1854.]

{13} IS BILE ESSENTIAL TO LIFE?

Several physiologists have given it as their opinion that bile is not essential to life, for animals have lived for many months after the artificial establishment of a biliary fistula, through which the bile was allowed to flow away, and be lost to the animal. Now, although this is perfectly true, yet it is at the same time evident that the uses of the bile cannot altogether be dispensed with, for all the animals with a biliary fistula lose flesh, become emaciated, and weak; the hair has a tendency to fall off, the bowels to become irregular; and a great and an almost constant discharge of foul-smelling gases takes place from the intestinal canal. At length, after a shorter or longer period, the animal sinks, and dies. The fatal termination can, however, be retarded by allowing him an additional quantity of nourishing food, for death from want of bile, as is too often seen in the human subject, is nothing else than death from slow starvation. The fact just related regarding the beneficial effects of an additional quantity of food in prolonging life, should never be lost sight of in the treatment of cases of obstruction of the gall-ducts, for, by attending to this circumstance, it is often in the power of the medical man to keep his patient alive for a considerable length of time.

{14} It may perhaps not be out of place if I here briefly enumerate the chief uses of bile in the animal economy. In order to live, not only must the individual particles of our frames die, but they must be continually replaced by new materials of a similar kind; and for the accomplishment of this important end, nature has endowed animals with a digestive apparatus in which their food undergoes the various physical, and chemical changes necessary to its absorption, and assimilation. In the animal laboratory or digestive apparatus there are five important agents constantly at work--saliva, gastric juice, bile, pancreatic fluid, and intestinal secretion, and each of these agents has a special and definite office to perform in the elaboration of the food.[4] At present, however, I must limit myself entirely to the consideration of bile.

[Footnote 4: For an explanation of these offices, see the author's article on "The Chemistry of Digestion," in the "British and Foreign Quarterly Review," January, 1860.]

Bile is the first digestive agent with which the food comes in contact on leaving the stomach and entering the intestines, and immediately on the acid chyme mixing with the alkaline bile, a white flocculent emulsion is formed, which emulsion has been described by many writers as a precipitation of the albuminose (digested albumen). Later {15} researches by myself and others have, however, shown that it is not the bile which precipitates the albuminose, but the acid of the chyme, which in reality sets free certain ingredients of the alkaline bile. In the majority of cases there is not even a true precipitation, for on throwing the milky-looking mixture upon a filter, I found that almost nothing remained behind, and the filtrate was nearly as white as the original liquid. Further, if the albuminose be separated from the chyme, and the chyme then brought into contact with the bile, the same flocculent-looking milkiness still appears. Nay, more, on adding equal parts of sheep's bile (fresh) to gastric juice drawn from a dog's stomach in full digestion, the apparent flocculent precipitate still appeared, although the acidity of the gastric juice remained unneutralized; and on throwing the whole into a filter, I found that the liquid that drained through was as milky and flocculent-looking as the original. The office of bile in the digestive process is neither to act on the albuminous[5] nor amylaceous portions {16} of our food; its chief action being to assist in the absorption of fats. When bile is mixed with neutral fat, little change is observed, but when brought in contact with the fatty acids, an immediate emulsion takes place. Lenz and Marcet[6] pointed out how the neutral fats of our food are transformed into fatty acids during their sojourn in the stomach; and Bidder and Schmidt[7] illustrated by experiments on dogs the important part played by the bile in their absorption. A dog, which in its normal condition absorbed on an average 7 grains of fat for every 2 pounds of its weight, absorbed only 3, or even as little as 1 grain, after the bile was prevented entering the intestines, in consequence of a ligature being applied to the gall-duct.

[Footnote 5: In speaking of the properties of the bile, I may mention that, although bile has no digestive power (properly speaking) over albuminous substances, yet, when injected into the subcutaneous cellular tissue of a healthy animal, it eats its way out through the skin, just as gastric juice or lactic acid does under similar circumstances. Even the muscles with which it comes in contact appear to be eaten away.]

[Footnote 6: _Vide_ a Discourse on the Chemistry of Digestion, by Dr. Marcet. Journ. of the Chem. Soc., Oct. 1862.]

[Footnote 7: "Die Verdauungssaefte und der Stoffwechsel." Leipzig, 1852.]

Further, these last-named observers found that, while the chyle in the thoracic duct of a healthy dog contains 32 parts of fat per thousand, that in the thoracic duct of a dog with a ligatured gall-duct, contains only 2 parts per thousand. These facts clearly prove that bile plays an important part in the absorption of the fatty portion of our food. Next comes the question, "In what manner does bile aid in the absorption of fatty matter?" {17} As is well known, fats or oils have no tendency to mix with water, and hence diosmose between an aqueous and an oily fluid is next to impossible. Matteucci has, however, shown that if an animal membrane be moistened on both sides with a weak solution of potash, it allows oil to pass through it. It has also been observed, that when the intestine is moistened with bile, it allows oil to pass through, which would not otherwise be the case. To illustrate this property of bile, I performed the following experiments:--

Firstly,--A clean piece of duodenum was filled with oil, ligatured at both ends, and suspended in water, holding in solution a small quantity of albumen. (The albumen was added to the water merely to imitate slightly the albuminous blood.) On examination, twenty-four hours later, no oil was found to have escaped through the intestinal walls.

Secondly,--A second portion of intestine had its internal surface moistened with sheep's bile before the introduction of the oil. It was then treated in the same manner as the preceding, and on being examined after the lapse of twenty-four hours, a small quantity of the oil was found to have penetrated through the intestine.

Thirdly,--Into a third portion of intestine was poured equal parts of sheep's bile, and chyme obtained from a dog in full digestion, through a {18} fistulous opening into its stomach. After being treated for the same length of time, and in precisely the same manner as the others, evident signs of the oily matters of the chyme having passed through the walls of the intestine were obtained, for they were seen as a scum floating on the surface of the albuminous water. Moreover, the fatty matters were not in the form of pure oil, but of a soapy substance.

The bile is thus seen to possess one of the more remarkable properties of the pancreatic juice. There is this important difference between the action of these two secretions on fats, however, that while bile merely emulsions and saponifies that portion of our food which enters the duodenum in the form of fatty acids, pancreatic juice, on the other hand, possesses the power, not only of emulsioning and saponifying the fatty acids, but also the neutral fats; indeed, its power seems chiefly to be exerted upon the latter. Hence it appears that both secretions are in a measure necessary to the complete digestion and absorption of the oleaginous constituents of our food.

On one occasion, while experimenting with bile at University College, I was surprised to hear Minton, the servant who was assisting me, say, that while he was travelling with Sir Andrew Smith in South Africa, he had oftentimes seen the {19} Caffres drink bile direct from the gall-bladders of the animals killed by the European party, and that, while passing the gall-bladder round to each other, they would rub their stomachs and say,--"Mooé-ka-kolla," signifying thereby, that it was very good. It certainly seems very extraordinary that any human being should not only drink, but drink with pleasure, a liquid so bitter and nauseating as bile. Perhaps the poor Caffres, however, drank the sickening tasted bile for the same reasons as the cattle in Caffreland, at certain periods of the year, go thousands of miles to drink at the salt-springs. There being scarcely any chloride of sodium in the earth, there is insufficient for the animal requirements in the herbage on which they feed, and they are forced to supply the deficiency by artificial means. Bile contains a large percentage of soda, and perhaps the Caffres drink it in order to obtain that substance, just as the animals drink the brackish water of the salt licks, feeling that it agrees with them, without knowing why.

THE MECHANISM OF JAUNDICE.

As said in the beginning of this paper, I believe, the pathology of jaundice may be embodied under the two heads, jaundice from suppression {20} of the biliary functions, and jaundice from re-absorption of the secreted but retained bile. These are at best, however, but vague terms, and in order to make the pathology of jaundice somewhat more definite it will be necessary for me to subdivide these two great classes in the following manner:--

(CLASS A.)--JAUNDICE FROM SUPPRESSION.
Arising from:--
(1) Enervation.
(2) Disordered hepatic circulation.
(3) Absence of secreting substance.

(CLASS B.)--JAUNDICE FROM RE-ABSORPTION.
Arising from:--
(1) Congenital deficiency of bile-ducts.
(2) Accidental obstruction of bile-ducts.

I shall now try to point out the pathology of these different states, and see how far they are able to explain the occurrence of jaundice under the various conditions already alluded to.

JAUNDICE FROM SUPPRESSION.

Although there can be no misunderstanding the meaning of the term "jaundice from suppression," there may, nevertheless, be some difficulty in comprehending how the skin becomes yellow, and the urine high coloured, when the secretion {21} of bile is arrested. In order to explain how this occurs, it will be necessary to recall to mind what was said regarding the nature of the biliary secretion. It will be remembered that I began by saying, that while some of the constituents of the bile are generated in the liver itself, there are others that exist, pre-formed in the blood.

If this view of the physiology of the biliary secretion be correct, it is perfectly evident that when the secretion of bile is arrested, those substances which the liver generates will be entirely wanting, while those which it merely excretes from the blood will accumulate there as soon as their excretion is prevented; just as urea accumulates in the circulation when its elimination by the kidneys is stopped. Hence it is that, as soon as the biliary secretion is in abeyance, biliverdine accumulates in the blood (until the serum is as it were completely saturated with the pigment), from which it exudes and stains the tissues, and produces the colour we term jaundice. At the same time, or even before the skin becomes yellow, the urine assumes a saffron tint in consequence of the elimination of the colouring matter by the kidneys.[8] From this it will be seen that I regard {22} the yellow skin and high-coloured urine of jaundice as simply due to the deranged secretion of biliverdine, quite independent of the presence or absence of the other constituents of the bile, the effects produced by which will be referred to elsewhere. Meanwhile we shall separately consider the further pathology of the three subdivisions of jaundice arising from suppression.

[Footnote 8: The true order of the occurrence of these changes is:--On the second day the urine becomes high-coloured; in a day or two later the skin assumes a yellow tint; and, in very severe cases, within the first week or two, the sweat, the milk, the tears, the sputa, and the serum in the thoracic and abdominal cavities, become of a more or less decided yellow hue.]

JAUNDICE AS A RESULT OF ENERVATION.

It is now a well-established fact that all secretions are under the direct influence of the nervous system. Stimulate a nerve supplying a gland, and secretion is accelerated; stop the nervous action, and secretion is as instantaneously arrested. Again, just in the same way as volition can produce or suspend muscular movement, mental influence can hasten or retard glandular secretion. As an illustration of this fact, I need only call to mind the influence the mere sight of food has in exciting the salivary secretion, and the effect of bad news in arresting it. Exactly the same influence as is here alluded to, is exerted by the mind over the biliary function. If, for example, {23} as Bernard first observed, a dog with a biliary fistula be caressed, the secretion of bile is actively continued; if, on the other hand, the animal be suddenly ill-used, the secretion of bile is instantly arrested. If he be again caressed, the secretion is re-established, and the bile flows drop by drop from the end of the cannula. Here the influence is entirely produced through the intervention of the nervous system; and if such effects as are above described occur in the dog, we can surely have little difficulty in understanding how the biliary secretion can be influenced in the highly-developed organization of the human being. Indeed, every one must have felt how quickly sad tidings received during a meal not only destroy the appetite and retard digestion, but occasionally alter the complexion. This effect, that all of us must have experienced in a slight degree in our own persons, several may have observed to a greater extent in the persons of others, even to the production of well-marked jaundice. At this very time I have under my care a young married lady, who during the last two years has twice suffered from an attack of jaundice induced by witnessing her child in convulsions, and this I regard as an example of jaundice from enervation.

One of the reasons, no doubt, why jaundice does not more frequently follow upon mental emotion is {24} simply on account of a certain amount of pigment being required in order to produce a visible tinging of the body, and it seldom happens that the emotional effect on the biliary secretion is sufficiently permanent to permit of the requisite amount of pigment accumulating in the blood. The reason, too, why mental emotion is more apt to cause jaundice immediately after a meal is, as will afterwards be better understood, on account of the congested state of the liver at that time favouring the stoppage of the secretion. A blow on the head, which is now and then observed to be suddenly followed by jaundice, acts, I believe, in the same way as fright, namely, by paralyzing the nerve force required for the continuance of the biliary secretion.

I now pass on to the consideration of the pathology of the second kind of jaundice from suppression, namely, jaundice resulting from hepatic congestion.

JAUNDICE ARISING FROM HEPATIC CONGESTION.

This is one of the most common causes of the disease; but as there are two kinds of hepatic congestion--active and passive--it will be necessary for me to make a further subdivision, and consider each of these separately.

{25} _Jaundice the Result of Active Congestion._

The mechanism of jaundice resulting from active congestion of the liver is readily explained on physiological grounds.

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:--

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.