Jaundice: Its Pathology and Treatment With the Application of Physiological Chemistry to the Detection and Treatment of Diseases of the Liver and Pancreas

Part 4

Chapter 44,020 wordsPublic domain

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.]

In fact, jaundice only appears as a complication of gall-stones when they chance to block up the common duct, and thereby prevent the bile entering the intestinal canal. Hence, also, the reason {45} why jaundice, as a result of gall-stones, is more frequently transient than permanent. If it chances to become permanent, it sooner or later leads to a fatal termination--usually within eighteen months after complete obstruction. Lastly, it may be mentioned that, although gall-stones are liable to form in almost every constitution, yet it is generally considered that they are most frequent in persons of the tubercular, cancerous, and gouty diathesis, either hereditary or acquired.

There are other substances besides gall-stones which, by their accidental presence in the bile-ducts, may give rise to jaundice. Thus, for example, foreign bodies, such as cherry-stones, have found their way from the intestine into the bile-duct, and given rise to jaundice. Intestinal worms have been observed to do the same thing, and recently an interesting case of jaundice, occurring in a girl aged 16, who died after a few weeks' illness, has been reported, which resulted from the presence of hydatids in the ductus hepaticus, and ductus communis choledochus.[17] Hydatids of the liver itself seldom give rise to jaundice, their position being usually such as not to interfere with the biliary function.

[Footnote 17: Dr. Dickinson has reported this case in the Pathological Society's "Transactions," p. 104, vol. xiii. 1862.]

There are still other cases where we find {46} transient jaundice arising from accidental obstruction of the bile-ducts; but in them, instead of the closure of the ducts resulting from plugging from within, it arises from the application of pressure from without. Thus, for example, transient jaundice is met with as the result of closure of the common bile-duct, by pressure exerted upon it by the pregnant uterus, or by impacted fæces in the transverse colon. Certain permanent abdominal tumours may also lead to the same result, but these will with greater propriety be considered under the next head.

PERMANENT JAUNDICE FROM OBSTRUCTION.

In order to give as clear a view as possible of the pathology of permanent jaundice from obstruction, it will be necessary for me to give the history of a case of closure of the outlet of the common bile-duct in consequence of organic disease--such, for example, as cancer of the head of the pancreas. A case of this kind has the further advantage of at the same time furnishing us with a typical example of jaundice arising from the re-absorption of the secreted, but retained bile.

When cancer of the head of the pancreas involves the orifice of the common bile-duct, as the tumour grows, the duct slowly, and gradually becomes impervious to the passage of bile into the {47} intestines, until at length the flow is completely arrested. As this gradual process of occlusion of the outlet goes on, the duct itself becomes more and more distended by the retained bile, till it at length attains an enormous size. The gall-bladder being equally prevented from emptying itself, likewise becomes stretched and dilated, until it may at last become not only palpable to the touch, but even apparent to the eye through the abdominal walls. This was the case in the patient whose liver, and occluded ducts are represented in Plate I.

The distention of the bile-ducts is not limited to those situated external to the liver, but also affects those in the substance of the organ; and to such an extent may this be the case, that, on making a section of a liver that has long had its common duct obstructed, a number of large excavations are observed all over its surface, which excavations are nothing more than the open mouths of the transverse sections of the dilated ducts. Such a state of matters is tolerably well represented in the section of the liver in Plate I. Further, the effect of this obstruction to the exit, and consequent accumulation of the biliary secretion, is not confined to the mere distention of the ducts, but causes various changes to occur in the parenchyma of the liver itself. The first of these is an increase {48} in the size of the organ, arising partly from the accumulation of the bile, and partly from the congestion caused by the pressure exerted on the vessels by the distended ducts. In the second place, gradually as the state of matters here described progresses, the parenchyma of the organ becomes itself affected, partly from the direct pressure exercised upon it, and partly from the derangement of its nutrition, produced by the interruption to the hepatic circulation; so that, after a time, the enlarged liver slowly, and by degrees diminishes, until it at length regains its natural size, thereby rendering, at this period of the disease, the diagnosis of the case extremely difficult. This state of matters is not, however, of long duration; for, in consequence of the continued compression of the blood-vessels and parenchyma, the nutrition of the liver is so disordered, as to lead to a gradual shrinking of the entire substance, or, in other words, to a general atrophy of the organ.

It is thus seen how in _permanent occlusion_ of the common gall-duct the liver may be found _hypertrophied_ in the _first_, of _normal dimensions_ in the _second_, and _atrophied_ in the _third_ and _last stage_ of the disease.

In cases of the kind here described, it is not at all unlikely that the enlargement of the liver in the earlier, as well as its atrophy in the later {49} stages of obstruction, may be mistaken for the cause of the jaundice, instead of the result of the arrest of the flow of bile, and thereby lead to a grave error in treatment. The history of the case, together with a knowledge of the above facts, will, however, tend to facilitate the diagnosis. Thus, it must be ascertained:--

Firstly,--If the jaundice preceded the alteration in size of the organ.

Secondly,--If there is an absence of any history of hepatitis; and,

Thirdly,--If there is no evidence of any pulmonary or cardiac mischief likely to lead to passive congestion of the hepatic tissue.

Even with a knowledge of all these facts, however, it often baffles the skill, and acumen of the ablest physicians to discover the cause of jaundice. Every now and then cases are met with, where the patient tells us that the jaundice has gradually come on without any assignable cause, and where, after the most careful examination of his history, as well as of his physical condition, we fail to detect a clue to the diagnosis. Cases of this kind are far from uncommon, and this is the more to be regretted, seeing that unless we have a clear appreciation of the cause, it is not only difficult, but even dangerous to treat the symptom. The injudicious administration of {50} a remedy here, may hasten the termination we most desire to retard. The truth of this remark will, however, be better appreciated when I come to consider the rationale of the treatment of jaundice. Meanwhile, it may be advisable to point out a method capable of yielding most important information, when all the ordinary means of diagnosis fail. I allude to the chemistry of the excretions. Although the pathological chemistry of the excretions is as yet in its infancy, it has already given the scientific physician a key to the detection of several diseases, and I trust to be able to show, that even in the obscure cases of jaundice above alluded to, it not only gives us a clue to their cause, but presents us with a guide to their treatment.

In jaundice arising from obstruction, the pipe-clay stools are, as in the case of jaundice from suppression, entirely due to the absence of bile from the intestinal canal. The yellowness of the skin is in like manner caused by the accumulation of the bile pigment in the blood, from whence it exudes, and stains the tissues; and, lastly, the saffron-coloured urine results in a similar way from the elimination of the pigment from the blood by the kidneys. Instead, however, of these three conditions arising, as in the case of jaundice from suppression, from the arrest of the biliary functions {51} allowing certain of the constituents of the bile to accumulate in the circulation, they are, in the first place, the result of the re-absorption of the secreted bile from the distended ducts, and gall-bladder. So that while in jaundice from suppression, only those biliary products which exist pre-formed in the blood accumulate in the circulation, in cases of jaundice from obstruction, the biliary products which are manufactured in the liver, equally with those which are pre-formed in the blood, find their way back into the circulation, to be from thence eliminated with the excretions. If then, we could ascertain the presence or absence of these products in the excretions, we should be enabled to distinguish between jaundice resulting from suppression, and jaundice arising from obstruction. Let us now see what the chemistry of the excretions teaches us; and to begin, we shall take the intestinal excretion.

ANALYSIS OF THE INTESTINAL EXCRETION AS AN AID TO THE DIAGNOSIS OF OBSCURE CASES OF JAUNDICE.

The intestinal excretion, in the natural state, consists, firstly,--of those portions of our food which have resisted the action of the digestive juices; secondly,--of the excess of the modified food remaining unabsorbed; and, thirdly,--of the excess, {52} as well as of the effete portions of the digestive secretions themselves. Consequently, if from any cause the digestive secretions do not act properly, the evacuation immediately becomes abnormal, and we can discover by analysis which of the secretions is at fault. Thus, for example, we know that the saliva acts upon the starchy matters of our food, the gastric juice on the albuminous, the pancreatic on the fatty, and that the biliary secretion so modifies the chyme as to allow of its rapid absorption by the lacteal, and portal vessels. If then, from any cause the elaboration, or excretion of any of these digestive juices be interfered with, more of the particular kind or kinds of food on which it acts, passes unchanged through the intestines. Thus, if the salivary secretion be affected, an unusual amount of unmodified starch is found in the stool. If the gastric juice is defective, more albumen than is normal passes away unchanged, and so on with the others.

It is clear then, that an examination of the stools must afford us important information regarding the presence, or absence of the normal secretions. A simple inspection of the stool will sometimes at once tell us whether or not bile is present. If it be present, the stool varies from a pale yellow, to a dark olive-green hue, according to the kind, and quantity of biliary colouring matter present, and {53} the nature of the food. It must not be forgotten however, that unless care be taken, the colour deducible from highly-coloured food may be mistaken for an excess of bile. This remark is still more applicable to medicines, for mercury, bismuth, iron, and some other mineral remedies, give rise to dark evacuations so closely resembling bilious stools in appearance, that the only way to distinguish them, is by chemical analysis; when, the presence of the mineral, together with the absence of the bile pigment, and the biliary acids (which are always to be found in normal evacuations), will at once reveal the true nature of the case. I have seen a mistake of this kind happen, and that too, where a patient labouring under jaundice from obstruction, was thought to be passing the usual amount of bile in his stools, when in reality not a particle of bile pigment was present. The colour was in this case entirely due to the food, and ferruginous remedies. Blood from the stomach or bowels, is also apt to be mistaken for biliary matter, more especially when acted on by the gastric juice, which has the property of turning red blood brown. With these exceptions, the absence of bile from the stool, is usually very easily ascertained. For if the patient be taking no highly-coloured food, or any of the medicines above indicated, the stools are of a {54} dirty pipe-clay colour. This is not due to the presence of any new or foreign matter, but solely to the absence of bile pigment. In these cases the evacuations, besides being white, are usually of a most offensive odour, for, among other things, bile checks intestinal putrefaction, and the development of offensive gases.

In addition to the colour, and odour of the fæces, in cases of jaundice, another important indication is to be found in the presence of fat. The presence of fat in the stools was at one time looked upon as evidence of pancreatic, at another time of hepatic disease; now, however, experimental physiology has taught us, that it in some measure depends upon both. For while, on the one hand, the pancreatic secretion emulsions the fatty part of our diet, and thereby renders it capable of absorption, recent researches, as has been already pointed out, have established the fact that the biliary secretion also plays an important part in the absorption of the oleaginous constituents of our food. Bidder and Schmidt, as was before said, have shown that a dog, after ligature of the gall-duct, absorbs less than half the average normal quantity of fat; and by experiment it has been found that this arises from the circumstance that bile emulsions only the acid fats, while pancreatic juice transforms the neutral as well as the acid {55} oleaginous matters. The presence of fat in the stools may be due, therefore, partly to hepatic, partly to pancreatic derangement; and I shall immediately point out how we can turn this fact to account in diagnosis, and discover in cases of jaundice from obstruction, whether the seat of the obstruction be at the outlet or in the course of the duct.

EXAMINATION OF THE RENAL SECRETION.

The urine affords us important information in all cases of jaundice. In fact, an examination of it alone would in many cases enable us to discover the presence or absence of this affection.

_Diagnostic Value of the Colour of the Urine._

The urine of jaundice has invariably a peculiar tint, ranging from a saffron-yellow to a dark olive-green, or almost black hue. It must not be forgotten that the colour of normal urine varies with the degree of concentration. Where little is passed, being of a high, where much is passed, of a pale colour; the depth of colour depending on the degree of dilution of the urohæmatine. Again, it must also be remembered that there are many diseases, which change the colour of urine very materially, some only deepening, others actually changing the tint. Foods, and medicines also, {56} alter the colour of the renal secretion. Rhubarb, and santonine give to it a saffron hue, arsenious acid gas a black colour. Bearing in mind these facts, one would hesitate before giving a decided opinion as to the presence or absence of icterus from a mere inspection of the urine. For this reason, it is generally recommended in cases of jaundice to pour a little of the urine on a white plate, and watch the play of colours produced by strong nitric acid. This method, however, is not always satisfactory, for the play of colours depends on the different stages of oxidation through which the pigment passes, and other animal pigments, besides biliverdine, unfortunately act in a somewhat similar manner.

A very simple, and more convenient way of testing the pigment without changing its physical characters, is to separate it in combination with uric acid. This is readily done by simply acidulating the urine with a few drops of hydrochloric acid, and setting it aside for twenty-four hours to crystallize. The white uric acid in crystallizing takes up the colouring matter, and assumes the hue of the pigment present in the urine. I have thus obtained crystals of all the different hues from a bright golden yellow tint through the intervening shades of red, brown, blue, olive, to a dark, almost black colour. This experiment {57} has another advantage, for if we take a measured quantity of urine, and collect, dry, and weigh the uric acid obtained from it, we can readily calculate the total quantity passed in the twenty-four hours, and thereby assist in diagnosing the presence or absence of malignant disease of the liver, as I shall afterwards have occasion to point out.

The urine of jaundice is generally described as being of a saffron colour; but if I may be allowed to form an opinion from my own observations, which are tolerably numerous, I should say that it, in colour, much more frequently resembles old ale than anything else with which I am acquainted. On standing, the colour changes very considerably, in consequence of the pigment becoming slowly oxidized by its exposure to the air. When there is a very great excess of bile pigment present in the blood, the kidneys have some difficulty in eliminating it. Occasionally even, it chokes up the renal capillaries, and thereby complicates the jaundice by inducing secondary disease in the kidney. In such cases the external surface of the kidney, after the removal of the capsule, looks as if it had been sprinkled over with ink. The black specks vary in size from the minutest visible point to that of a pin-head. The accompanying chromo-lithograph (Plate II.) represents a kidney in this condition. {58} It will also be observed that it is studded over with a number of small abscesses; but whether these resulted from the blocking-up of the capillaries just alluded to or not, it is impossible to say. In the case in question no albumen was detected in the urine during life, and it was only on careful analysis, after the post-mortem had revealed the above state of matters, that a small quantity was discovered; and even then, had not the experiment been carefully performed, the presence of albumen might have been overlooked.

_Diagnostic Value of the presence of the Bile-Acids in the Urine._

All acquainted with the recent literature of jaundice know how hard a battle is being fought between two sets of observers in Germany, regarding the presence of bile-acids in urine. One class, with Frerichs and Städler at their head, believe that the biliary acids are decomposed in the blood, and are consequently never to be detected in the urine. The other class, headed by Kühne, state as positively that they have detected these substances in the urine. Indeed, Kühne states that by adopting Hoppe's method,[18] he never fails to {59} detect the presence of the biliary acids in the urine of patients labouring under icterus, as well as in the urine of dogs with the bile-duct ligatured. When first studying this question, I was very much perplexed by these contradictory statements, for neither the judgment, nor the power of observation of either of the authorities could for a moment be called in question; and on experimenting for myself, so unsatisfactory were the results obtained, that I almost threw the question aside in despair. On one occasion, however, I at length met with such unmistakeable evidence of the presence of bile-acids in the urine, that I could no longer doubt the fact of their existence, and was forced to search for an explanation of the previous contradictory results. Fortunately, it was not very long before a solution to the difficulty was obtained, and, what was of still greater importance, led to the observation that the contradictory results arose from a circumstance which might be turned to account, as a means of differential diagnosis. The discovery was, that in certain cases of jaundice not a trace of the biliary acids is to be detected in the urine, although the {60} bile pigment is present in abundance; while in certain other cases both biliary acids, and bile pigment occur in notable quantity. What, then, is the cause of this difference? Simply this. In jaundice from suppression the liver does not secrete bile; consequently no bile-acids being formed, none can enter the circulation, and they are therefore not to be detected in the urine. In jaundice from obstruction, on the other hand, bile is secreted, and absorbed into the blood; and the bile-acids not being all transformed in the circulation, as Frerichs supposed, are eliminated by the kidneys, and appear in the urine, where they can be detected by Hoppe's method, or even, with proper precautions, by simply adding sulphuric acid and sugar. Here, however, some skill and experience are requisite, in order not to confound the colour produced by the action of the reagents on other substances with the fine purple produced by the biliary acids. As the majority of cases of jaundice result from suppression of the hepatic function, and as many of the cases of obstruction ultimately merge into the former, it is easily understood how the existence of the biliary acids in the urine has been so frequently denied. I have myself seen, in a case of obstruction of the common duct, the biliary acids slowly and gradually diminished in the urine, until they at length almost entirely {61} disappeared as the case approached a fatal termination. Here the disappearance of the biliary acids went on step for step with the impairment of the secreting powers of the liver, in consequence of the pressure exercised on its parenchyma by the retained bile.