Chapter I: Functional Disorders

Biliousness.

DEFINITION.--The term biliousness is used to signify a disturbance of the gastro-intestinal digestion, with coincident excess in the production of bile. According to the popular conception, both lay and medical, the excess of bile is the cause of the symptoms; but when the whole subject is carefully examined it will be found that biliousness is made up of several factors, and that the hepatic disorder, if it exist at all, is a mere incident.

PATHOGENY.--From the time of Galen biliousness has been regarded as a morbid entity and the liver as the organ affected. Stoll, amongst moderns, first revived the Galenical doctrines. Abernethy[1] was amongst English physicians the most conspicuous advocate of the condition called biliousness, and was the apostle of blue pill and black draught. Copland in his great dictionary[2] more distinctly formulated the views of the English school--especially that portion of it influenced by the results of Indian practice--than had been previously attempted, and hence his work best represents the opinions and practice of the time amongst the English-speaking peoples. In this country the great Rush first promulgated the notions of biliousness which have since so dominated the medical opinion of this continent. A large part of the United States has proved a fruitful soil for the cultivation of theories of biliousness, since the condition known under this name is a frequent accompaniment of malarial poisoning. To this fact must be attributed the preponderating importance of biliary derangements in the practice of the physicians of India also.

[Footnote 1: _Surgical Works_, London, 1811, vol. i. p. 36.]

[Footnote 2: _A Dictionary of Practical Medicine_, vol. ii. p. 723.]

It is a fact which will be hereafter more fully developed that malarial infection may, and often does, derange the hepatic functions without producing fever. The malarial poison irritates the liver, and thus more bile is produced, but the quality deteriorates with the increase in quantity. The functions of the liver are more disturbed during an access of intermittent fever: the organ is swollen, the skin is muddy, the eyes yellow, the tongue coated with a thick yellow fur, and the urine is deeply tinged with bile-pigment.

Many of the metals employed as medicines and as poisons, as gold, {966} silver, antimony, arsenic, phosphorus, etc., irritate the liver both in their entrance and in their exit from the organism, and cause biliousness; and the same fact is true of some vegetable alkaloids and animal poisons. The liver excretes many of these substances, and in their passage out from the blood the hepatic cells are irritated and an increased production of bile is a result. Improper food, indulgence in fats, sweets, condiments, and all kinds of fermented and alcoholic liquors, intestinal indigestion arising from any cause, and gastro-duodenal catarrh, are the most usual and obvious pathogenic factors. In respect to food and indigestion as etiological factors there are several points requiring more explicit statement. When nitrogenous elements (albuminoids) are in excess in quantity or as respects the power to digest and convert them, immature products, of which uric acid is the chief, accumulate in the blood. When the fats, sugars, and starches are in excess of the requirements of the organism or are imperfectly disposed of in the small intestines, a local irritation of the mucous membrane is produced, and various complicated, immature products enter the blood. With these troubles and faults of intestinal digestion a gastro-duodenal catarrh is usually associated. Without the production of catarrhal jaundice, gastro-duodenal catarrh, with the forms of indigestion accompanying it, keeps up a reflex irritation of the liver. Just as the presence of normal chyme induces the flow of bile, so the unhealthy products of intestinal indigestion excite an irritation of the liver. The continued operation of this cause maintains an abnormal activity of the liver, and more bile is produced than is easily disposed of.

SYMPTOMS.--The condition of biliousness, as now understood, is made up of derangement of the gastro-duodenal mucous membrane, with bile-production in excess and bile-absorption probably delayed. The symptoms are the product of these complicated conditions. The complexion is muddy; the conjunctivæ are yellow; the tongue is heavily coated with a yellowish-white fur; a bitter taste persists in the mouth; the breath is heavy in odor, even fetid; the appetite may be keen or there may be complete anorexia; a sensation of nausea, of heaviness, and fulness of the stomach is experienced, especially after eating; the bowels are confined usually, but occasionally the movements are relaxed, bilious in appearance, and cause heat and irritation about the anus; headache is constantly present to some extent, and there is a sense of fulness with more or less dizziness, and singing in the ears; vision is rather blurred, and there is a hebetude of mind; the urine is high-colored, high in specific gravity, and deposits lithates abundantly on cooling. When these symptoms are conjoined with hemicrania, nausea, and vomiting, the case is called bilious sick headache, and when diarrhoea supervenes, the discharges apparently containing much bile, it is bilious diarrhoea. The symptoms which above all others give the character to the morbid complexus are the muddy (bilious) complexion, the yellow-coated tongue, the yellow conjunctivæ, and the high-colored urine. The first departure from the normal may be scarcely observed. Gradually, owing chiefly to errors of diet, to climatic changes, or to malarial influences, or to these several factors combined, the affected person drifts into the condition of biliousness above described. Besides the general malaise, he experiences no little despondency, inaptitude for exertion, and indeed actual weakness. Finally, he is unable to apply himself to business, relinquishes the effort, and seeks advice.

{967} COURSE, DURATION, AND TERMINATION.--Those who are accustomed to experience attacks of biliousness suffer from them at certain intervals which may be tolerably regular--at intervals of a few days, two, three, or four weeks--when the cause is uniform; but they may happen very irregularly when the conditions producing them are variable. The duration of an attack is from two days to a week or more, according to the severity of the symptoms and to the character of the measures instituted for relief. The termination is in a return to the normal state. If the conditions which produced it continue, when one attack is ended the preparations for another begin at once, and at length sufficient derangement of the organs concerned arises to constitute the morbid complexus of biliousness.

TREATMENT.--Prophylaxis has great importance, since the causes of the malady are to a considerable extent, at least, preventable. Errors of diet in respect to the use of condiments, fats, meat, pastry, etc. must be corrected. When there is pronounced gastro-duodenal catarrh and acid fermentation in the duodenum, the saccharine, fatty, and starchy elements of the food must rather be excluded and lean meats allowed. Abundant exercise, bathing, and an open-air life in general should be directed. Whenever a malarial infection is causative a change of climate becomes imperative. Heredity cannot, of course, be excluded, but the tendency to hepatic derangement can be rendered inoperative by an abstemious life.

The remedial management includes the dietetic as well as the medicinal treatment. When the distress has reached sufficient proportions to justify such an extreme measure, the patient should be restricted to a diet exclusively of skimmed milk, of which he is directed to take a gill or more every three hours. This serves a double purpose, as aliment and as a depurative agent, for this considerable quantity of fluid promotes the urinary excretion and the elimination of waste products. If the case is not severe enough to allow of such an expedient, the diet should in any event be restricted to skimmed milk hot, milk and hot water, hot lemonade, a little chicken or mutton broth, a bit of dry toast, etc. As a rule, although not so palatable, hot drinks are more beneficial than cold, but if the preference is decidedly for cold, they may be allowed. After the more severe symptoms have subsided a little lean meat broiled may be added, and as the cure proceeds the succulent vegetables and acid fruits may be permitted. Abstinence from potatoes, hominy, cracked wheat, and oatmeal should be enjoined during the convalescence of those who suffer from habitual attacks.

Medicines may not be necessary to those who have the resolution to adhere to skimmed milk for several days or who can abstain from food altogether for a day. Many experienced sufferers, especially through the South and West and in England, procure rather prompt relief from a blue pill of ten to fifteen grains or from one to five grains of calomel at night, followed by a Seidlitz powder, Rochelle or Epsom salts, or phosphate of soda on the following morning. Such patients find that no other treatment is as serviceable. They get relief from other measures, it is true, but neither as promptly nor as satisfactorily. It is held by the advocates of this practice that the mercurial acts on the liver--that the surplus bile is carried off; and they point to the peculiar stools and to {968} the relief experienced in evidence of the truth of this theory. Without entering on the argument, which would occupy too much space, it must suffice here to state that calomel and blue pill do not increase bile-production,[3] but they do stimulate the intestinal glands and increase excretion from them. The peculiar greenish stools produced by these mercurials do not owe their characteristic appearance to the presence of bile, but rather to the chemical transformations of the mercury itself and to the waste products excreted by the intestinal glands. Since the researches of Rutherford have been published, euonymin has been much prescribed in cases of biliousness. From three to five grains are taken at the bed-hour, and a mild laxative in the morning. In the same group of cholagogues are ipecac, iridin, sanguinarin, and especially podophyllin; but the serious objection to their use is that they stimulate the liver when this organ is in an irritable state. As calomel and blue pill have a sedative rather than a stimulant action on the liver, they are more useful in biliousness than are the true cholagogues. It should be borne in mind that one-half of a grain of calomel will have a distinct purgative action on many persons, and that one grain will rarely need to be exceeded.

[Footnote 3: That calomel, the type of a mercurial purgative, does not increase the discharge of bile has been demonstrated on dogs by Röhrig and Rutherford, and confirmed by observation of the effects of 20 grains on Westphalen's case of biliary fistula in man--a case in which, for a time, all the bile escaped externally, and none apparently entered the intestine (_Deutsch. Archiv f. klin. Med._, 1873, Band xi. pp. 598 and 600).]

In general, notwithstanding the unquestionable utility of the mercurial, it is better to relieve cases of biliousness by less objectionable measures. A saline which acts at the same time on the intestines and kidneys, as Rochelle salts, is usually effective in bringing relief. A bottle of solution of magnesia citrate, of Saratoga water (Congress, Hathorn, or High Rock), and of Blue Lick, the famous sulphurous laxative of Kentucky, may remove the disorder in mild cases if at the same time a suitable diet is enjoined. Phosphate of soda in laxative doses, with or without Vichy water, is also a good remedy, if somewhat slow. The warm purgatives, rhubarb, colocynth, aloes, etc., are useful when there is pronounced constipation.

Lithæmia.

DEFINITION.--By the term lithæmia is meant a condition of the system in which uric (lithic) acid is produced in excess, and in which certain derangements occur in consequence of the accumulation of this material in the blood. Uricæmia was the term first suggested by Flint, Sr.,[4] to express this state, and subsequently lithæmia was employed by Murchison.[5] The latter has been more generally accepted. In one of the most recent and valuable contributions to this subject by DaCosta[6] lithæmia is the term used to designate the complex of symptoms produced by uric acid in excess.

[Footnote 4: _The Principles and Practice of Medicine_, Philada., 1882.]

[Footnote 5: _Clinical Lectures on Diseases of the Liver_, 2d ed., p. 565.]

[Footnote 6: _The Medical News_, vol. ii., 1883.]

PATHOGENY.--The ultimate product of albuminoid substances in the organism prepared for final excretion is urea. That this substance is {969} finally formed in the liver, to be excreted by the kidneys, seems now well established.[7] In acute yellow atrophy of the liver, with the disappearance of the proper structure of the organs urea ceases to be produced, and instead leucin and tyrosin are excreted. In certain states of the system characterized by deficient oxidation urea is not sufficiently formed, and instead uric acid, a lower grade of oxidation and a product of the disintegration of albuminoid substances, results. An excess of urates is not always pathological. Their excretion seems to be in a certain sense a safety-valve function. When albuminoid matters are taken in excess of the power of the system to convert them, or when the supply of oxygen to the blood is deficient from any cause, urea is not formed, but uric acid and urates are abundantly excreted by the urine.[8] Imperfect digestion of the albuminoids when they are not taken in relatively too large an amount, and limitation below the normal of the oxidation process when the supply of oxygen is not insufficient, will have the same effect: in place of urea, uric acid and urates will be formed and excreted. One of the early results of the persistent presence of an excess of uric acid is the production of lithæmia, the morbid complexus of which this excess is at once the cause and the proof.

[Footnote 7: This proposition is not universally accepted. Valmont (Thèse de Paris, _Étude sur les Causes des Variations de l'Urée dans quelques Maladies du Foie_, 1879) has carefully studied the excretion of urea in several diseases in which the proper structure of the liver is damaged--in atrophic cirrhosis and in cancer. As in these maladies not all the secreting portion of the organ is destroyed, the argument is so far weakened. His conclusions are as follows: "1. Patients with cirrhosis or cancer of the liver who eat little excrete but little urea. If they eat and do not absorb, or vomit or have diarrhoea, the result is the same. When they partake largely of nitrogenous aliment the proportion of urea rapidly increases. 2. In a cachectic or simply anæmic patient the urea falls, apparently in proportion to the state of the general nutrition and of the work done by the organic functions. 3. Absolute immobility of the patient seems to have an influence on the amount of urea excreted. 4. In sclerosis or cancer the quantity of urea falls rapidly on the occurrence of ascites or oedema, when a notable quantity of urea is found in the fluid. 5. The digitalis often used in the treatment also contributed to the loss of urea." If these conclusions are verified, the formation of urea must depend on some other function.]

[Footnote 8: Genevoix, _Essai sur les Variations de l'Urée et de l'Acide urique dans les Maladies du Foie_, Paris, 1876.]

The persons who suffer from lithæmia are usually those who indulge in the pleasures of the table and habitually consume much meat, pastry, and highly-seasoned and rich food of all kinds. The idle, luxurious, and indolent, literary men of sedentary habits, men who have led active lives, but on retiring from business have continued to indulge in a full diet, are apt to suffer from this malady. Women are less disposed to it, but if subjected to the same conditions may also be similarly affected. Especially do those suffer from lithæmia who indulge in malt liquors or in alcoholic drinks of any kind. These substances act by deranging digestion, and thus preventing the proper conversion of the albuminoids, by inducing congestion of the liver, and also by interfering with the process of oxidation.

SYMPTOMS.--The symptoms of lithæmia include derangements of the digestive organs and of the liver, of the circulation, and of the nervous system. As these subjects suffer from gastric and gastro-duodenal catarrh, they present the usual symptomatology of these affections, as a sense of weight and oppression at the epigastrium, acidity, pyrosis, a capricious--sometimes voracious, sometimes good--appetite, a coated {970} tongue, a bitter taste, etc. The bowels are irregular, sometimes constipated, occasionally relaxed, with scybalæ. The stools may be liquid, almost black or light-yellow and grayish. The motions are apt to be offensive, and a good deal of offensive gas is discharged with them. Hemorrhoids are often present, and there may be heat and irritation about the anus, and not unfrequently intolerable itching. After meals there is much depression, and often an insupportable drowsiness. Irregularity in the rhythm, even intermissions, of the pulse are not infrequent.

The nervous symptoms, as DaCosta has lately insisted on, are the most important and pronounced. The connection between oxaluria and mental despondency has long been known, but the nature of the relation remains undetermined. Headache, frontal and occipital, especially the former, dizziness, tinnitus aurium, suffusion of the eyes, ecchymoses of the conjunctiva, are usually present. Not unfrequently the subjects of this affection experience sudden attacks of vertigo, accompanied by dimness of vision and intense headache, and are supposed to have some organic lesion of the brain. They are irritable, despondent, and often intensely hypochondriacal, almost suicidal--are subject to neuralgic attacks, and have aching in the limbs, a sense of weariness, and more or less burning in the palms and soles.

The skin is rather dry and the complexion muddy. Urticaria is of frequent occurrence, and sudden attacks of nausea, vomiting, and intestinal pain coincide with the appearance of the eruption on the skin.

The urine is usually rather increased in amount, its color heightened, its acidity above normal, and floating in it, usually visible to the naked eye, are reddish masses composed of uric acid. More or less pain in the back, referable to the situation of the kidneys, and sometimes extending along the course of the ureters, is common. The bladder is rather irritable, and the passage of the urine produces heat and scalding. The testicles are apt to feel sore and are somewhat retracted. On standing, the urine may deposit uric acid and the urates copiously, or the acid may be seen to form a cloud which slowly subsides.

COURSE, DURATION, AND TERMINATION.--The course and duration of lithæmia are much influenced by the habits of life of the person affected. When unopposed by treatment and no change is made in the conditions producing it, a gradual increase in the various disturbances takes place. After a time structural changes occur in the liver; the organs of circulation early undergo atheromatous degeneration; various cerebral disorders due to degenerative changes arise; and acute intercurrent affections may terminate life. Amongst the secondary maladies due to lithæmia are gout, diabetes, renal calculi, and nephritic colic. If the cases are subjected to appropriate treatment, curative results may be certainly obtained. The prognosis, then, will be influenced materially by the moral strength of the patient. If he is one who can surrender his appetites and live abstemiously, a cure may be promised. The case is far different with those who will continue the use of malt, vinous, or alcoholic drinks, and will persist in indulging in the pleasures of the table.

DIAGNOSIS.--The differentiation of lithæmia from other affections offers no special difficulties. From gastro-duodenal catarrh it is separated by the {971} excess of uric acid in the urine only, the other symptoms being for the most part the same. The cerebral symptoms--the vertigo, headache, etc.--are to be distinguished from the same due to actual disease of the brain by the previous history, by the absence of changes seen on ophthalmoscopic examination and of other signs of brain disease, and by the subsequent behavior. Cases of cerebral mischief producing such effects would rapidly develop into serious states, whereas in lithæmia there are great fluctuations, but no apparent progress in many months. In lithæmia also there are no changes in the fundus oculi, whereas in brain diseases choked disk, hemorrhage into the retina, white atrophy, etc. are often discovered. Further, in lithæmia there are no disorders of sensibility, of motility, or of intellection, whilst these are ordinary evidences of cerebral mischief.

TREATMENT.--Attention to diet is of the first importance. As uric acid is an intermediate product in the metamorphosis of albumen, it might be supposed that to diminish the quantity of this constituent of the food would be sufficient. In some cases this suffices, but usually attention must be given to the peculiarities of digestion characteristic of each patient. More frequently trouble arises from indulgence in the starchy and saccharine constituents of the diet; in some a very considerable gastro-duodenal catarrh exists, and the mucus, acting as a ferment, sets up an acetic fermentation in the starchy and saccharine substances, with the necessary production of much carbonic acid gas. If the fats disagree, the butyric fermentation also takes place, and very irritating fat acids result. In these cases there is usually much gas formed in the stomach and intestine, and an immediate ratio appears to exist between the degree of mental despondency and the quantity of gas in the intestinal canal. It follows, then, that in cases of lithæmia the saccharine, starchy, and fatty constituents of an ordinary diet should be omitted from the food of such subjects. Bread should be partaken of very sparingly, and the foods containing starch, sugar, and oil ought not to be partaken of at all. The succulent vegetables, as lettuce, spinach, celery, cole-slaw, tomatoes, etc., ought to be substituted. Lean fresh meats, poultry, game (plainly cooked), fresh fish, oysters, eggs, etc. should constitute the basis of the diet. On the other hand, there may be those who do better on a diet of vegetables and fruit, excluding meat. In such we may suppose the fault lies in the stomach digestion, where the albuminoids are converted into peptones, the intestinal digestion being active and normal. All kinds of wine and malt liquors should be prohibited. Coffee and tea must also be relinquished. Without the carefully-regulated diet medicines can accomplish but little; hence he who would obtain curative results must give careful attention to every dietetic detail.

As deficient oxidation is an important factor in developing lithæmia, active exercise must be enjoined. The amount of exercise must be determined by the condition of the individual and the time, regulated as far as may be by the period after meals. As when the food prepared for assimilation is entering the circulation oxygen is needed to perfect the final changes, it seems clear that exercise should be taken three or four hours after the process of digestion has begun. Walking exercise is better than any other for this purpose, but it should not be carried to the point of exhaustion from fatigue. Sea-air and sea-bathing are oxidizing agents of considerable value, and are especially useful to the {972} subjects of lithæmia suffering at the same time from malarial infection.

Medicines are administered with the view to accomplish two purposes: to correct the disorders of digestion, to promote oxidation. One of the most useful remedies is nitric acid, five to ten minims of the official diluted acid being given before meals. It is more especially effective when there is an excessive production of acid. The fermentation which produces acid and the diffusion of acid-forming materials from the blood are alike prevented by it. The injunction to administer it before meals must be borne in mind when these purposes are to be subserved. Nitric acid, as well as the other mineral acids, but in a greater degree, promotes the flow of bile. This well-known clinical fact has been confirmed by experiments. Under the use of nitric acid, as above advised, uric acid and the urates disappear from the urine, being excreted as urea, and hence this remedy accomplishes both of the objects for which medicines are administered in this disorder. No other mineral acid can fill its place in this connection.

Alkalies possess very decidedly the power to promote oxidation. The soda salts are objectionable, for, combining with uric acid, they form the insoluble urate of soda. The salts of potash and lithium, on the other hand, form soluble combinations, and they also increase elimination. Much depends on the time at which they are administered, as Bence Jones,[9] and since Ralfe[10] especially, has shown. To increase the alkalinity of the blood and urine, they must be taken after meals, for then the acid materials of digestion are pouring into the blood. For the same reason, if alkalies are administered to neutralize the acidity of the intestinal canal, they must be given after meals. The most useful alkaline remedies are liquor potassæ, bicarbonate of potash, Rochelle salts, citrate of lithium, etc. The effervescing preparations of potash and of lithium are elegant and palatable forms in which to administer these remedies. They may also be taken dissolved in Vichy water, in our Saratoga Vichy, or in Carlsbad or Bethesda. When the use of mineral waters is not contraindicated in the state of the digestive organs, great good is accomplished by the persistent use of Vichy, foreign or domestic, of Carlsbad, and the alkaline waters of Wisconsin.

[Footnote 9: _Lectures on Pathology and Therapeutics_, by H. Bence Jones, London, pp. 90, 280.]

[Footnote 10: _Physiological Chemistry_, by Charles Henry Ralfe, London, 1883.]

The so-called cholagogues are unquestionably useful, but they become less and less necessary according to the success achieved in the dietetic course. Phosphate of soda is one of the most effective of this group of medicines. As it acts as a compound, and not as a salt of soda merely, it does not come within the prohibition against the use of soda salts. It promotes the flow of bile and appears to remove the catarrhal state of the mucous membrane. A teaspoonful three times a day is the quantity usually required. Under some circumstances it may be advantageously combined with arseniate of soda. Mercurials were formerly almost universally used, but they have been largely supplanted by podophyllin, euonymin, baptisin, etc., and by the phosphate of soda above mentioned. Podophyllin is indicated when constipation is a symptom. An efficient mode of giving it is in the form of granules, but it must be continued without intermission for some time or during the existence of {973} the lithæmia. The quantity given should be sufficient to maintain the evacuations in a soluble state. Good results are obtained from a combination of podophyllin with extracts of physostigma, nux vomica, and belladonna. When distinct torpor of the liver without constipation exists, euonymin, combined with physostigma, may be advantageously used. For the vertigo and hypochondriasis no remedy is more beneficial than arsenic (Fowler's solution) in small doses kept up for some time, and it is also distinctly curative of the catarrhal state of the mucous membrane. When malarial infection is the cause of lithæmia, quinine becomes indispensable.

Topical agents in some cases render important aid to the other curative measures. A daily sponge-bath, the water made more stimulating by the addition of sea-salt, is very useful in the absence of sea-bathing. Friction of the hepatic region with the official ointment of the red iodide of mercury unquestionably stimulates the hepatic functions. General faradization and faradic and galvanic excitation of the chylopoietic system promotes activity of the digestive apparatus and of the organic functions in general.

Hepatic Glycosuria (Temporary).

DEFINITION.--By the term hepatic glycosuria in this connection is meant a temporary glycosuria due to excessive formation of glycogen. The liver, unduly stimulated, produces more glycogen than can be disposed of, and hence it is excreted by the kidneys as grape-sugar.

PATHOGENY.--In the normal condition it is supposed that the glycogen produced by the liver is converted into grape-sugar, and soon oxidized and thus consumed. One theory of diabetes maintained that in some way the conversion of glycogen into grape-sugar was excessive and beyond the oxidizing power of the blood, and hence this substance was discharged in the urine. The recent discovery by Pavy[11] of glycogen in considerable amount in the blood of all parts of the body renders it certain that there are peculiar conditions necessary to the formation of grape-sugar in sufficient quantity to constitute diabetes. It is tolerably certain that an excess of acid in the intestinal canal, diminishing thus the alkalinity of the blood, will have as a symptom sugar in the urine. Persons disposed to the accumulation of fat, and eating freely of sugar and starchy food, are apt to have intestinal indigestion, and the acid produced by the fermentation of these substances will, after its absorption, hinder the conversion of any food-sugar. In such subjects also there may be an increased conversion of the glycogen of the blood into sugar under the same conditions. Such a glycosuria must necessarily be temporary and a purely functional disorder.

[Footnote 11: _The Lancet_, vol. ii., 1883.]

SYMPTOMS.--The subjects of the malady under consideration are of full habit, even obese. They habitually consume considerable quantities of malt liquors and a diet composed largely of the starchy and saccharine foods. If not in malt liquors, they at least indulge freely in bread, potatoes, pastry, cakes--in all forms of farinaceous food, fats, and sweets. They have a keen appetite, eat largely, and drink freely of fluids. As {974} a rule, these subjects are but little disposed to physical exercise and lead rather sedentary lives. Indulgence in such a mode of life tends to increase the accumulation of fat, weakens the muscles, and with them the heart-muscle, and slowly induces a gastro-intestinal catarrh accompanied by stomachal and intestinal indigestion. At first, heaviness, oppression, and drowsiness after meals are experienced; then acidity, pyrosis, and eructations follow; and ultimately the evidences of intestinal indigestion--flatulence, pain, irregular and unhealthy evacuations, etc.--come on. Meanwhile, the appetite is not usually impaired, and the disposition to drink fluids increases; the amount of urine voided is greater, and to rise during the night for the purpose of emptying the bladder comes to be a fixed habit. The urine under these circumstances is copious, high-colored, acid, and deposits on cooling abundantly of uric acid and urates. The amount passed in twenty-four hours will reach sixty, eighty, or more ounces, and the specific gravity will range from 1025 to 1035. On testing in the usual way, traces of sugar, more or less distinct, will appear,[12] but not constantly, and hence repeated examinations are necessary to determine the quantity. As a rule, the evidence of the presence of sugar in small amount is satisfactory.

[Footnote 12: In testing for sugar, when the urine contains the urates in such abundance there is danger of error. In using Trommer's, Fehling's, or Moore's test, on heating, the urates will effect a reduction of the copper or bismuth. It is necessary, therefore, to separate them before applying the test. This is accomplished as follows: The urine is evaporated to dryness on a water-bath; the sugar in the evaporated residue is dissolved out by absolute alcohol, and then an aqueous solution is prepared, to which the test is applied. An experienced operator will not need to take such precautions, for, familiar with the reactions, he can readily judge of the results.]

Various affections of the skin appear in the subjects of this malady, and urticaria, prurigo, eczema, and boils are the forms most usual.

COURSE, DURATION, AND TERMINATION.--Slow in developing, this temporary glycosuria is also slow in its course. It remains nearly stationary for months, even years. Meanwhile the degenerative changes associated with it slowly develop on all sides. The quantity of sugar does not greatly increase, for its amount, being apparently dependent on the quantity of acid entering the blood from the intestinal canal, must continue nearly at the same standard. It is comparatively rare for true diabetes to develop out of this state, although such a termination must be regarded as a natural outcome. One reason, it may be, why such a conclusion is not often reached is because of intercurrent maladies. It is an important fact that acute serous--less often parenchymatous--inflammations are very apt to occur during the existence of even temporary glycosuria. Under appropriate management this disorder is readily amenable to treatment. Hence the prognosis will be favorable or not according to the skill exhibited in its treatment.

DIAGNOSIS.--This malady offers no special difficulty in diagnosis. From gastro-duodenal catarrh and from lithæmia it is distinguished by the saccharine condition of the urine. From diabetes it is separated by the rate of progress, by the protracted duration of the case without any distinct advance, and by the temporary and fugitive character of the glycosuria.

TREATMENT.--To carefully regulate the diet is the first consideration. The traces of sugar and the excess of urates rapidly disappear when the {975} starches, sugar, and fats are withdrawn from the diet. Indeed, the rule as to alimentation must be as rigidly enforced as in true diabetes, but after the gastro-intestinal catarrh has subsided the ordinary mixed diet--that before the disturbance began--may be returned to gradually. Active exercise must be enjoined under the same conditions and for the same purpose as in the treatment of lithæmia. In these obese subjects, unaccustomed to movement, exercise must be cautiously undertaken; beginning with short excursions, it must be gradually increased. Horseback riding is an excellent expedient, but should not take the place of walking.

The merely medical measures have a twofold direction: to remove the gastro-duodenal catarrh; to promote oxidation of the sugar in the blood or prevent the conversion of glycogen into grape-sugar. Vichy water, the potash salts, and alkalies generally serve to accomplish the latter, and phosphate and arseniate of soda, tinctures of nux vomica, and of physostigma, bismuth, and carbolic acid, relieve the former. Small doses of Fowler's solution (two drops ter in die), and a minim three times a day of a mixture in equal parts of tincture of iodine and carbolic acid, are effective remedies in gastro-duodenal catarrh.

Jaundice (Icterus).

DEFINITION.--The term jaundice has its origin in the French word jaune, yellow. Icterus, which has come to be a more technical word, is of uncertain Greek origin, and is much employed by French writers as ictère. The common German name is Gelbsucht, a highly expressive designation. Jaundice signifies a yellow discoloration of the skin caused by the presence of bile. It is a symptom rather than a disease. As a symptom it will receive much consideration in the pages to follow, but there is also a functional disorder--a jaundice due to a disturbance in the biliary functions, without evidences of structural change--which must be discussed here. This preliminary statement of our present knowledge of jaundice will facilitate the comprehension of it as a symptom, and will render unnecessary explanations that will be merely a repetition of previous ones.

CAUSES.--The theories of the causation of jaundice may be reduced to three: 1, that it is due to a disorganization of the blood in which the coloring matter is set free, and hence is known as hæmatogenous; 2, that the materials of the bile, which it is the office of the liver to remove from the blood, are not so disposed of; 3, that the bile, after being formed by the liver, is absorbed into the blood because of an obstacle to its escape, and hence this is called hepatogenous jaundice.

The modern view of hæmatogenous jaundice had its origin in the supposed discovery of the identity of hæmatoidin with bilirubin. If the pigment of the blood has the same composition as the pigment of the bile, hæmatogenous jaundice will be produced whenever hæmatoidin is set free in the blood. Virchow[13] was the first investigator to show the close resemblance between these two pigments. Since his observation was made an identity of hæmatoidin and bilirubin has been maintained by Zenker, Valentiner, Kühne, and others, and as strenuously denied by {976} Städeler, Preyer, Young, and others. At the present time it appears to be established that although the blood- and bile-pigments are closely related, they are not identical.[14] Nevertheless, a hæmatogenous jaundice is still admitted to exist by Leyden,[15] Immermann,[16] Gubler,[17] Ponfick,[18] and some others. The existence or non-existence of this form of jaundice is, however, of little importance in this connection, since, if it ever occur, the malady of which it is a symptom is not an affection of the liver, but of the blood, as phosphorus-poisoning, pyæmia, etc.

[Footnote 13: _Archiv für path. Anat., etc._, Band i. p. 370, 1847.]

[Footnote 14: Legg, J. Wickham, _On the Bile, Jaundice, and Bilious Diseases_, p. 243.]

[Footnote 15: _Beiträge zur Pathologie des Icterus_, Berlin, 1866, p. 6.]

[Footnote 16: _Deutsch. Archiv für klin. Med._, Band xii. p. 502.]

[Footnote 17: _Union médicale_, 1857, p. 503.]

[Footnote 18: _Ziemssen's Cyclopædia_, vol. ix. p. 24.]

The second theory, that the bile is preformed in the blood and separated by the liver, and that jaundice results because of the failure of the liver to perform this office, is no longer entertained, although largely held down to within a very recent period. As the bile acids and bile-pigments are not to be found in the blood, chemistry lends no support to the theory of jaundice by suppression of the hepatic function. As they do not exist in the blood and are found in the secretion of the liver, there can be no other view held than that they are formed by this organ.[19]

[Footnote 19: The old doctrine of jaundice by suppression, which has always been maintained by Harley (_On Jaundice_, London, 1863, p. 20 _et seq._), has been again restated and strongly advocated by him in his treatise on _The Diseases of the Liver_, p. 83, which was issued in 1883. In the two following postulates he formulates his view:

"1. The biliary secretion can be actually retarded, and even totally arrested, without alteration of hepatic tissue.

"2. When the liver strikes work and secretes no bile, the animal body becomes jaundiced as a direct consequence thereof."

This view, he affirms, "can be made comparatively easy of absolute proof."

The evidence on which he chiefly relies is exceedingly fallacious. It rests on two facts: the existence of a case of jaundice in which the ducts and gall-bladder contain no bile, but only ordinary mucus; the appearances presented by a liver in a case of jaundice due to obstruction of the common duct. The evidence afforded by the former is entirely fallacious, because in an old case of jaundice with catarrh of the bile-ducts such changes take place in the bile that it loses all of its distinctive characteristics. This may be seen in an ancient example of obstruction of the cystic duct, where the bile which the gall-bladder contained is ultimately transformed into a whitish or colorless mucus. The changes which occur in the so-called cysts of the arachnoid are comparable, and exhibit the entire transformation of blood-pigment, which is closely allied to bile-pigment.]

The third theory of jaundice--that which refers the disease to an absorption of the bile into the blood after it has been formed by the liver--is the one now most generally held, and, indeed, as one of the causes is universally held. The bile is absorbed into the blood because an obstacle to its passage by the bile-ducts exists at some point in their course. This is the principal, but not the only, cause of absorption. When the pressure in the vessels falls below that in the ducts, bile will pass toward and into the vessels. Again, it sometimes happens that a considerable part of the bile discharged into the intestines is reabsorbed unchanged, and enters the portal vein and the general circulation, thus causing jaundice.

The disturbances of the liver causing jaundice are various. It sometimes occurs without cause, and the first intimation of it is the peculiar tint of the skin. It is certainly true that powerful emotions are causative; thus, a violent anger has brought on an attack. In such a case we must suppose a depression of the vaso-motor system, and such a lowering of the blood-pressure as to favor the passage of bile into the {977} veins rather than into the bile-ducts. Thus, it has been abundantly shown that a slight difference in pressure will divert the bile in either direction. Heidenhain[20] has demonstrated that the bile passes in the direction of least resistance, and in the case of the considerable vaso-motor depression caused by extreme emotion the least resistance is in the direction of the vessels. More frequently than moral emotion is catarrh of the bile-ducts. It is not necessary for the catarrhal swelling of the mucous membrane to close the ducts to have the bile pass into the veins; such a degree of swelling as to make the passage of the bile somewhat difficult suffices. A simple hyperæmia of the mucous membrane may cause sufficient obstruction of the bile-ducts to give rise to jaundice. Gastro-intestinal catarrh plays an important part in the production of simple jaundice. Frerichs[21] ascertained that of 41 cases, gastro-duodenal catarrh existed in 34. Ponfick[22] considers catarrh of the ducts the principal factor. In fact, at the present time there is but one dissenting voice on this point.[23]

[Footnote 20: Quoted by Legg, _supra_, p. 253.]

[Footnote 21: _Diseases of the Liver_, Syd. Soc. ed., by Murchison.]

[Footnote 22: _Ziemssen's Cyclopædia_, vol. ix., _supra_.]

[Footnote 23: Harley, _Diseases of the Liver_, 1883, p. 440 _et seq._]

Gastro-duodenal catarrh extends by contiguity of tissue to the mucous lining of the bile-ducts. The catarrhal state of the mucous membrane is produced by errors of diet, acid indigestion, indulgence in condiments, wines, and rich foods in general. Climatic changes, malarial infection, exposure to cold and dampness, etc. are indirectly causative of jaundice through the intermediation of gastro-duodenal catarrh.

Formerly, obstruction of the gall-ducts was supposed to be caused sometimes by a spasmodic contraction of the organic muscular fibre assumed to exist in the walls of the ducts. Although the presence of these muscular elements has been denied, Heidenhain has lately, apparently, demonstrated them. Audigé has made observations confirmatory of those of Heidenhain, and Dujardin-Beaumetz[24] has verified the statements of Audigé. It seems, therefore, in a high degree probable that organic muscular elements exist in the walls of the hepatic ducts, and that spasmodic icterus may therefore occur.

[Footnote 24: _Bull. gén. de Thérapeutique_, vol. lxxxv. p. 385, 1873.]

SYMPTOMS.--Simple icterus may exist without any other obvious symptoms than the yellow discoloration of the skin. In most cases, however, the yellowness is preceded for a week or more by the symptoms of a gastro-intestinal catarrh, or these symptoms accompany the jaundice. There is much mental depression and a general malaise is experienced. Headache, mental hebetude, a total loss of appetite, a furred tongue, and a bitter taste, nausea and sometimes vomiting, constipation or diarrhoea, precede or accompany the jaundice. When these symptoms precede for some time the appearance of yellowness, it is probable that the biliary derangement is secondary to the gastro-duodenal catarrh, but when they occur with the jaundice it is probable that they are due to the absence of bile from the intestine.

The yellowness first appears in the conjunctiva for a day or two before the skin is tinted, and within forty-eight hours after the flow of bile into the intestine has ceased. The face next becomes yellow, then the body, {978} and afterward the limbs, but in some cases the limbs remain free from discoloration. The lips do not exhibit any change of color, but the roof of the mouth, the palate, and the mucous membrane under the tongue are yellow. The saliva does not, as a rule, contain bile-pigment or exhibit any changes of color unless mercurial salivation is caused, when it becomes greenish in color and has a bitter taste.[25] A yellow tint of the sweat, especially under the arm-pits, is common. The milk very often contains bile-pigment or is changed in color in some way.

[Footnote 25: Legg, _On the Bile, etc._, _supra_.]

The feces are colorless or have a grayish or clay-colored tint, and are semi-solid, although sometimes hard and dry. In simple jaundice diarrhoea is very often present. There may be considerable flatulence, and more or less pain in consequence about the umbilicus, and the gas when discharged is very offensive. The stools also, in some cases, have an odor of decomposition, and if carefully examined particles of food, undigested and decomposing, will be found. The feces may have a parti-colored appearance--part whitish or grayish or clay-colored, and part of a normal color. This condition is not difficult of explanation. The obstruction to the flow of bile may be in a part, and indeed in a small part comparatively, of the liver, and hence there may be sufficient bile flow down to color the feces to a greater or less extent. But a small amount of bile-pigment in the blood suffices to tint the whole surface of the body.

The urine may exhibit changes in appearance before the conjunctiva becomes yellow. It is colored in all possible degrees, from a merely high normal hue to a deep brownish almost black tint. It may be deep red and clear like dark brandy or brown like porter, and thick with urates. Usually, the urine of jaundice deposits abundantly of urates, but this fact is more especially true of those patients retaining appetite or having a voracious appetite and indulging in a full diet without restraint. The reaction of the urine is acid, and the specific gravity does not often descend below 1010, and may be 1030. The amount passed in twenty-four hours varies, but does not differ materially from the normal. Toward the termination of some fatal cases the quantity of urine has greatly diminished, and in a few instances was suppressed, but in such examples other factors than hepatic disease were concerned. More or less albumen is nearly constantly present in the urine of jaundice, but the detection of a trace is very difficult when the urine, as is so often the case, is cloudy. The urine should be carefully filtered before applying the test, and a specimen for comparison should be placed alongside of that being examined. If on boiling no haze appears, it may be developed by dropping in some nitric acid. The nitric-acid test, so often employed by allowing some drops of urine to trickle down the test-tube and observing the reaction at the point of contact, is, in the writer's experience, very fallacious. The source of the albumen in jaundiced urine is obviously the blood-globules. As Von Dusch first demonstrated, and Kühne[26] afterward clearly confirmed, the bile acids dissolve the red corpuscles. As the quantity of albumen in the urine is small, it is reasonable to conclude, as suggested by Legg, that the bile acids are not present in the blood in any considerable amount.

[Footnote 26: _Archiv für path. Anat._, Band xiv. p. 333.]

When any large quantity of bile is contained in the urine, its detection is not difficult. A strip of muslin dipped in the urine will be stained, and the underclothing of the patient will have the yellowish spots {979} caused by bile. Gmelin's test is the most convenient. This is applied as follows: Some nitric acid containing nitrous--which is the case of the ordinary commercial article--is put into a test-tube, and some of the suspected urine is allowed to trickle down the side of the tube to come in contact, but not mix, with the acid. At the point of contact, when the urine contains bile-pigment, first a zone of green, then blue, violet, and finally red color, develops. As this play of colors takes place on the instant, the attention must be sharply fixed to see the changes. Rosenbach[27] suggests this test be applied by filtering some urine containing bile through filtering-paper and touching the paper with a drop of nitric acid. The result is, a green circle forms at the point of contact. The usual mode of applying Gmelin's test is to place on the bottom of a common white plate or on a porcelain dish a thin film of the urine, and carefully bring in contact with it a thin film of nitric acid. The color reaction mentioned above takes place at the margin of contact.

[Footnote 27: _Centralblatt für die medicin Wissenschaft_, 1876, p. 5.]

Besides the presence of bile and albumen, and some fatty epithelium from the tubules, there is no material change in the composition of the urine. At one time it was supposed that the amount of urea was greatly lessened, but later and more accurate investigations have shown that this excretion is in greater or less quantity according to the food taken, and bears no relation to the jaundice. On the other hand, Genevoix[28] maintains that the quantity of urea is increased in spasmodic icterus, and in the same ratio the uric acid declines. As regards the chlorides and other salts, there seems to be a tolerably constant ratio in their variations with the changes of quantity of urea and uric acid--are therefore nearly related to the amount of food taken.

[Footnote 28: _Essai sur les Variations de l'Urée et de l'Acide urique dans les Maladies du Foie_, Paris, 1876, p. 59 _et seq._]

As regards the condition of the liver, there is no apparent change. In topography, in the area of hepatic dulness, and in the dimensions of the right hypochondrium the local condition does not deviate from the normal in simple jaundice. There may be more or less tenderness over the epigastrium and along the inferior margin of the liver, but there is rarely any actual pain.

The circulation of bile in the blood and the action of the bile acids on the red corpuscles must have an influence on the functions of various organs. In some cases of jaundice, but by no means in all, the pulse is slow, in a few instances descending as low as 40 per minute, and, according to Frerichs,[29] as low as 21 per minute. Usually, the pulse-rate is not lower than 60. To observe the slowing of the heart the patient must be recumbent, for the pulse rises to the normal or above on assuming the erect posture and moving about. The occurrence of fever also prevents the depression of the circulation. The slowing of the heart is found to be due to the action of the bile acids on the cardiac ganglia. The other elements of the bile were ascertained to have no influence on the circulation. As the heart may be slowed by an increase of inhibition through stimulation of the vagi or by a paralyzing action on the cardiac muscle, it was necessary to eliminate these effects to establish the influence of the bile acids on the ganglia. By exclusion, and by ascertaining the effects {980} of the bile acids on a properly prepared Stannius heart, Steiner and Legg have succeeded in demonstrating this important point.[30]

[Footnote 29: _Diseases of the Liver_, Syd. Soc. ed., _supra_.]

[Footnote 30: _Archiv f. Anat. u. Physiol._, 1874, p. 474; Legg, _On the Bile, etc._, _loc. cit._]

The temperature of jaundice is normal usually, sometimes below. When a febrile affection occurs during the course of jaundice, the rise of temperature belonging to it is prevented in considerable part, sometimes entirely. The depression of temperature is referred by Legg to the lessened activity of the hepatic functions; but it seems to the writer more satisfactory to refer it to the action of the bile acids on the red corpuscles, the conveyors of oxygen. Röhrig[31] has shown experimentally that the injection of bile acids has this effect on the temperature of animals.

[Footnote 31: _Archiv der Heilkunde_, 1863, p. 418.]

The nutrition of the body early suffers in jaundice; more or less loss of flesh soon occurs, and debility and languor are experienced. There are several factors concerned in this result. The diversion of the bile from the intestine interferes in the digestion of certain materials; when jaundice occurs, glycogen ceases to be formed--and this substance has an important office in nutrition and force-evolution--and the injury done to the red blood-globules interferes with oxidation processes.

The functions of the nervous system are variously disturbed in jaundice. Headache, frontal, occipital, or general, is present in most cases to a greater or less extent. Hebetude of mind and despondency are nearly if not quite invariable, although it is not unusual to see men with jaundice engaged in their ordinary avocations. Drowsiness is a common symptom. More or less wakefulness at night, or sleep with disturbing dreams, not unfrequently coincide with drowsiness during the waking moments. In severe cases of icterus dependent on structural changes the cholæmia may produce stupor, delirium, convulsions, etc., but such formidable symptoms do not belong to the simple and merely functional jaundice.

Vision is sometimes colored yellow, or, rather, white objects appear yellow, but this must be a rare symptom, since Frerichs never met with an example. Murchison[32] narrates a case, and the writer has seen one. It is a fugitive symptom, rarely continuing longer than two or three days. The term xanthopsy has been applied to it.

[Footnote 32: _Clinical Lectures on Diseases of the Liver_, New York, 1877, p. 321.]

A nervous symptom of common occurrence is pruritus of the skin. This may be so severe as to prevent sleep, and in any case is a disagreeable and persistent affection, always worse at night. It may appear before the jaundice so long a period as ten days, as in a case mentioned by Graves,[33] and two months in a case narrated by Flint.[34] It is most severe at the beginning of the jaundice, and usually disappears before the jaundice ceases, but it may continue to the end. It is not limited to any particular part of the body. Pruritus is sometimes accompanied by urticaria, and the irritation caused by the friction of the skin may set up an eczema. Occasionally boils, and more rarely carbuncles, appear during the course of jaundice. Another curious affection of the skin which occurs during chronic jaundice is xanthelasma or vitiligoidea. First mentioned by Rayer, this disease was afterward well described by Addison and Gull[35] under the name vitiligoidea, and they recognized two varieties, v. plana and v. tuberosa. The plane variety is found on the {981} mucous membrane of the mouth, the eyelids, the palms of the hands, and the flexures of the joints, and consists of a yellowish-white soft eruption slightly raised above the surrounding skin and varying in size from a pin's point to a dime in size. The color is described as like that of a dead leaf or chamois-skin. The tuberose variety consists of small tubercles from a millet-seed to a pea in size. They have a yellowish color, are tense and shining, and are placed on the ears, neck, knuckles, elbows, knees, and other parts. Whilst the plane variety gives little if any uneasiness, the tuberose is apt to become irritated and painful. From the pathological point of view this eruption consists of proliferating connective-tissue corpuscles, some of which have undergone fatty degeneration.[36] The morbid process tends to occur symmetrically, as on the eyelids, to which it may be confined, but it usually develops in patches, and may indeed extend over the whole body, when it is called xanthelasma multiplex.

[Footnote 33: _Clinical Lectures on the Practice of Medicine_, 2d ed., by Neligan, p. 637.]

[Footnote 34: _Philada. Med. Times_, 1878, p. 507.]

[Footnote 35: _Guy's Hospital Reports_, 1851, p. 265.]

[Footnote 36: Waldeyer, _Archiv für path. Anatomie, etc._, vol. lii. p. 318.]

The disorganization of the blood caused by jaundice sets up a hemorrhagic diathesis. This result, however, is not usual in simple jaundice, but belongs rather to acute yellow atrophy, sclerosis, and other chronic affections of the liver. It will therefore be more appropriately considered in connection with those maladies.

COURSE, DURATION, AND TERMINATION.--When jaundice is a symptom merely, it pursues a course determined by the peculiarities of the disease. The duration of simple jaundice varies from one to four weeks, the average being about three weeks. If it continues longer than two months, suspicions may well be entertained that the case is of a more formidable character than simple jaundice. The termination of this form of the disease is always in health. A favorable prognosis can be given only in the case of an accurate diagnosis. Those cases may terminate more speedily which, being of malarial origin, are treated by efficient doses of quinine. If delirium and coma come on, the apparently mild case means, probably, acute yellow atrophy, which cannot at the onset be distinguished from simple jaundice. If any nervous symptoms occur or if hemorrhage appears, the case will prove to be serious. A rise of temperature usually indicates mischief. When the stools begin to exhibit the normal appearance from the presence of bile, a satisfactory termination of the case may be soon expected. The yellowness of the skin disappears slowly after the natural route of the bile has been restored, and the urine is the last to lose the pigment, as it was the first to exhibit its presence.

DIAGNOSIS.--The diagnosis of jaundice as a symptom is usually easy. It should be remembered that jaundice cannot be detected at night by any ordinary light, and when it is disappearing the tint varies, now being distinct, again absent. Mental emotion when the color is fading develops it. Browning by the sun's rays causes an appearance which might be mistaken by a superficial observer for jaundice, but it is only necessary to look at the parts protected and at the urine to discover the true state of the case. The detection of bile in the urine and the ocular evidence of its absence from the stools will be conclusive. In some cases of jaundice the stools are golden yellow, and in many instances they are offensive.

{982} It is important to mark out the limits of the gall-bladder, if it is of sufficient size to do so, for any accumulation of bile in this sac signifies an obstruction of the ductus communis choledochus. If the jaundice has come on after the symptoms of gastro-duodenal catarrh, is recent, continues but two or three weeks, and then subsides without any nervous symptoms or hemorrhage, it is a case of simple jaundice, probably due to catarrh or spasm of the bile-ducts. If the jaundice be preceded by attacks of severe pain, nausea, and vomiting, and disappears after a week or two, the case is one of hepatic calculi. If the jaundice persists months after such an attack of acute pain, and does not disappear after a year or more, it is probably due to an impacted calculus. The other diagnostic relations of jaundice are more properly considered in connection with the malady of which jaundice is a symptom.

TREATMENT.--For jaundice the symptom the treatment is included in that of the disease. Here the treatment of simple jaundice, the functional disorder, is to be discussed. If there is much nausea, the tongue is heavily coated, and, especially if the seizure has followed dietetic excesses, an emetic of ipecac may be highly serviceable. Recent experiments have proved the accuracy of the clinical observations which recognized the cholagogue property of ipecac, and hence the emetic effect of this remedy is aided by its power to promote the discharge of bile. Emetics are of course contraindicated when jaundice is due to an impacted calculus, to malignant disease, to echinococci or other kinds of tumor. If there is much irritability of the gastro-intestinal mucous membrane, as shown in vomiting and diarrhoea, small doses of calomel (1/12 to 1/4 grain) three or four times a day are highly useful. If calomel possessed the property ascribed to it of stimulating the liver, it would be injurious; it is beneficial here because it has a sedative effect at first, followed, when a sufficient amount has accumulated, by an eliminant action. Such hepatic stimulants as euonymin, sanguinarin, podophyllin, jalap, colocynth, rhubarb, etc. have long been used in cases of jaundice with the view that the liver is torpid and needs stimulating. It may be inquired, however, If the bile already formed has no outlet by the proper route, what utility can there be in making the organ produce more? The true reason for the administration of such remedies in any case of obstructive jaundice is to cause such downward pressure as to force out of the duct an obstructing plug of mucus. The writer has known this result to be accomplished by a dose of compound jalap powder when a great variety of remedies had been employed in vain. One of the most efficient remedies--in the writer's considerable experience the most efficient--is phosphate of sodium, of which a drachm or more is administered three times a day. This remedy liquefies mucous plugs and promotes the flow of bile without harshly and rudely forcing the biliary secretion, and it also has a marked curative effect in gastro-duodenal catarrh. It may be given advantageously with arseniate of soda--the latter in dose of 1/20 grain--and dissolved in a tumblerful of Vichy water or Saratoga Vichy water, or preferably in a wineglassful of hot water. Free use of alkaline and laxative mineral waters is desirable, for a double purpose--to act on the liver and on intestinal digestion, and to promote the excretion of biliary matters by the kidneys. In this country we have a number to select from--the Saratoga, Bethesda, Michigan, and others. Certain sulphurous waters, {983} as the Blue Lick of Kentucky, are highly useful in the more chronic cases. Sulphur baths may be conjoined to the internal administration of the waters.

Nitric and nitro-muriatic acids have long been celebrated for their good effects in jaundice. It is the presence of the acid chyme in the duodenum which excites the normal flow of bile, and Bernard found that applying acid to the orifice of the common duct in the intestine has the same effect. There is then a rational reason for the administration of this remedy. A nitro-muriatic bath, both local and general, was formerly more used than now. Its utility is questionable, and the difficulties in the way of applying it great.

Recently, Gerhardt[37] has proposed to faradize the gall-bladder, and by compression with the fingers to empty it, forcing the bile into the intestine, and thus clearing out obstructions. This seems to be very questionable if not dangerous practice, but repeated successes will justify it.

[Footnote 37: _Sammlung klinische Vorträge_, Volkmann, p. 112.]

Regulation of the diet is of the first importance. Fats, starches, and sweets cannot be well digested when no bile enters the small intestine, where they undergo conversion. These substances fermenting, much acid results, and hence if a catarrh exist it is increased. An exclusive diet of skimmed milk, kept up for two weeks or as long as possible, is the best mode of alimentation for this part of the treatment. Afterward, the diet should be composed of milk, meat-broth, lemonade, and subsequently of the succulent vegetables, acid fruits, and fresh meat. Indulgence in malt liquors, wines, and spirits should be strictly prohibited.

A new method of treating jaundice has been lately proposed by Krull,[38] which has the merit that no injury is done by it if no good is accomplished. It consists in injecting into the rectum from two to four pints of water at 60° F., which is retained as long as possible. Each time the injection is repeated the temperature is raised a little. Krull reports that he has uniformly succeeded, and has never found it necessary to repeat the injection more than seven times. It may be given twice or thrice a day.

[Footnote 38: _Berliner klinische Wochenschrift_, 1877, p. 159.]